StemCell Therapy

Volume 50, Issue 6 - selected pp. A1-A10, e163-e194, 677-810 (June 2016)

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American Journal of Preventive Medicine - ScienceDirect.com

We specialize in Primary Care Medicine with a focus on natural/alternative medicine and hormone replacement. It is our desire to treat the root cause of your medical problems, and not just the symptoms, so that you can live the healthiest, longest, and most enjoyable life possible. We take a different approach to your healthcare and believe strongly in treating our patients with natural, safe, and effective treatments that help the body to heal and repair. This involves taking the time to sit and listen to our patients and gathering all the information we need to really figure out what is going on. We try and avoid a rushed office visit where there is not enough time to really discuss the full extent of the problems you may be having. This type of medicine is known as Functional Medicine and goes much deeper into the cause of your health problems than standard approaches to health care.

We know that the body is very capable of healing itself and with the right knowledge, supplements, hormones, natural treatments, and lifestyle changes, you can start to overcome chronic disease and worsening health issues. You can begin to feel healthy again with a new energy and vitality for life that you may not have thought was possible. We believe you can feel young, energetic, and joyous about life at any age, and would love to help you achieve this. Please contact our office at one of our two locations to get some more information on how you can start feeling great again.

Altanta, GA 678-705-2118 5505 Peachtree Dunwoody Rd Suite 410 Atlanta, GA 30342

Ringgold, GA 706-891-1200 148 Cobb Parkway Ringgold, GA 30736

We Accept the following insurance plans: Cigna, Medicare, United, Blue Cross Blue Shield, and Humana We also offer very reasonable cash options for those who are uninsured, please call for more information.

What To Expect: We discover the root cause of many of your health problems by various methods. First, we gather a very detailed health history and review all of your concerns so that we can treat you as a holistic being. Then we gather information through various diagnostics that are appropriate for your conditions. These may include: comprehensive blood work, in depth hormone and full thyroid testing, salivary adrenal testing, micronutrient and immune testing, comprehensive stool analysis, heavy metal testing, bacterial and yeast overgrowth urine analysis, and other various tests. After we have collected the needed information, we than meet with you and review all the findings in detail to create a comprehensive treatment plan. This plan will include therapies such as nutrition, supplements, detox, exercise programs, and medications and hormones. You will have full input as to what testing you would like to pursue and what will go into your treatment plan. We will work with you closely to achieve your health goals and keep you headed in the right direction for optimal health and well being!

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Preventive Medicine - Home

By Mark Nichol

When you wish to refer to something that serves to prevent, which is the correct adjectival or noun form, preventative, or preventive? The latter word is more commonly cited, appearing by a ratio of three to one, but the longer variant is also widely employed, and with increasing frequency. Might, however, does not necessarily make right. So, which one is better?

Both words date back to the 1600s, and the latter predates the former by a mere several decades. It retains the upper hand, however, for two reasons: First, the extra syllable is superfluous, and second, it is supported both by quality as well as quantity: The most respected publications favor preventive, while preventative is more likely to appear in print and online sources with less rigorous editorial standards. Thats a good enough reason to favor preventive.

What about similar word pairs such as exploitative and exploitive, which both refer to underhandedly using someone or something to ones advantage? Like preventative and preventive, the first attestations of these words are only a few decades apart, though they are much more recent coinages; exploitative goes back only to the late nineteenth century, and exploitive is less than a hundred years old. But theres a significant difference between this word pair and the previous one: In this case, the longer form is widely considered the standard, and exploitive is the inferior alternative.

Fortunately, the correct form of most words ending in -ive is obvious, as with cumulative, formative, and representative. But other endings can confuse, such as with the question of whether to use orient or orientate as a verb. In this case, each refers to facing the east, though only orient correctly applies to other references to setting or directing.

Likewise, there is the case of systematic and systemic, both of which are valid terms, but with mostly distinct senses: Though both terms obviously pertain to systems, only systematic also refers to classification and to coherent, methodical, thorough procedures. Systemic generally connotes only biological systems and is neutral in value, as opposed to the qualitative senses of systematic.

In summary, as a careful writer, research proper usage for word endings in order to avoid employing the incorrect of two similar words or a less favored variant.

And alternatively and alternately, different meanings.

Preventive is an adjective. E.g. Take preventive action and wear a helmet. Preventative is a noun. E.g. A helmet is a preventative.

Or, He places a preventive plug in the hole, to prevent water from leaking into the room, just in case it rains. The plug is now a preventative

This seems simple enough to me. Most dictionaries do not make this distinction, but then dictionaries are not there to preserve, but rather to publish what is popular (which, of course, has little to do with good language).

Oy, I rage against orientate. And on the subject, commentate. Yes, I know that this is a losing battle and that by now, commentating has come to have a specific and separate meaning from comment. But its soself-serving. What do you do for a living? Im a commentator. Ewwwwww.

Oh, please tell me orientate isnt winning!

Its just wrong, wrong, wrong For some reason wronger than other errors which are slipping into common usage.

Had to laugh about thebluebird11s commentary about commentating.

I believe preventive is more correct for use as an adjective, such as preventive medicine, but preventative works better as a noun, he used the potion as a preventative.

Ive subscribed to Daily Writing Tips for several weeks now, and I look forward to your discussions from an etymological perspective.

Regarding todays post, I agree that preventive is preferable as an adjective, e.g. preventive medicine. But Ive come across preventative as a noun: an agent or a procedure that acts to prevent something from occurring. E.g.: Daily doses of Vitamin C (1000 mg) is recommended as a preventative for viral infections.

What do you think?

SO glad I found this site today. And timely, too: Orientate is on my worst words list!

I feel like Ive found my roots. Nice to find others that cherish the language as I do. I guess, in this group, I wont be the lone grammar-nazi. Nice!

I think theres a clear distinction between both the words as illustrated by Francois, and for some reason orient sounds better than orientate!

Systemic simply means inherent in the system itself.

I can quite logically write, The failures of capitalism can be ascribed to its systemic contradictions (overproduction and underconsumption brought on by the drive to maximize profits while minimizing the wage-bill and then attempting to bridge the gap through credit) and its systemic assumptions (self-interest, greed, aggressive competition).

These factors lead to systemic crises constant boom-and-bust cycles, the fall in the rate of capital (which causes capitalists to step-up the rate of exploitation) and the ever-increasing concentration of capital into fewer hands (which no quantity of anti-trust laws can halt, especially when capitalists can buy er, lobby the politicians who make those laws) and to systemic behaviours like imperialism and war (over resources, markets and cheap labour).

Im not sure what comparison you are making with systemic vs. systematic. They are distinct words with quite distinct meanings. Preventive vs preventative not so much. Despite the somewhat useful difference proposed by Francois, I dont know of any authority for it. Compare healthy and healthful. A nice distinction can and practically should be made between the 2, but it is simply not there historically. In SAE, at least, preventive is strongly preferred in all cases.

Orientate is different still. It is sub-standard, simply incorrect in American English. BUT, I think it IS standard in British. So, IFand only ifthe speaker/writer is using British English (or another that also accepts the -ATE ending), it has to be considered fine. Admittedly, to American ears it sounds as awful and illiterate as transportate or declarate.

This whole phenomenon has always made me want to claw at my face.

LOL@mordantkitten! -Definitely a difference between systemic (system-wide) and systematic (possessing a system; methodical). -Im not keen on preventative; I will never use that word. I declarate, let me go transportate myself downstairs for something to ingestate.

The discussion of orientate vs. orient ignores the difference between British and American usage. A Brit will normally use the back-formation orientated, for all that those of us on the other side of the pond might find it jarring.

The first time I heard preventative on network television is during a press coverage of one Royal Son who use the phrase preventative measures. The word preventative then became viral among the media. I took American English lessons from primary school to high school. Thereafter, I studied one year of college level English Literature based on British literary books that covered a wide range of era from the Legend of Beowulf to early Twentieth Century collections. At first, the sound of preventative was repulsive.

From the root verb: to prevent, we normally add -ive to construct and adjective. So, the word preventative appears to originate from the verb: to preventate. I still have hope that humanity will preventate such a decline of a living language like English.

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Preventative vs. Preventive - Daily Writing Tips

The History of the Highland Breed

Highland cattle are unique among British breeds of cattle in that they have remained virtually unchanged since records began. The western Highlands and Islands of Scotland have always been regarded as their true home where they formed a vital part of the economy. It was this hardy Highland breed that first brought commerce to the Highlands of Scotland. Arguably it could be said that cattle brought about the beginning of end of clan system and the traditional Scottish Highland way of life.

There are accounts of the droving trade in Highland cattle as early as 1359 and it was to continue well into the nineteenth century. This highly lucrative trade was at its height from 1760 to 1820. At that time, tens of thousands of 2-3 year old cattle left the Highlands and Islands throughout the summer and autumn and made their long and treacherous journey south to the great cattle fayres in Muir of Ord in the northeast Highlands and then they went on to, gathering in numbers, to the major fayres in the towns of Crieff, Falkirk and Dumbarton in the southern Highlands and then travelled a further three hundred miles south, across the border to be fattened on the lush pastures of England. Eventually, these cattle were sold as prime beef in the ever-expanding cities such as Manchester and London.

To quote the well known writer Daniel Defoe in 1724 referring to the cattle of the Highlands of Scotland These Scots runts as they call them, coming out of the cold barren mountains of the Highlands of Scotland, feed so eagerly on the rich pastures of its marshes that they thus in an unusual manner grow monstrously fat and the beef is so delicious for taste that the inhabitants prefer them to the English cattle. Another well known writer of the same period, Thomas Hurtley in 1786, when referring to the cattle of the West Highlands was quoted as saying To say the truth, when fattened on these rich old pastures there is no beef equal to them in fineness either of grain or flavour.

In order to reach their destination good feet and legs were essential. The cattle were expected to travel between ten and fifteen miles in one day over the roughest terrain and even on occasion, swim rivers that had swollen after days of torrential rain.

The drovers were every bit as hardy as the cattle under their care. They slept with their droves at night just in case they should stray or be stolen in the dead of night by the likes of Rob Roy MacGregor or by those other renowned cattle thieves the Loch Earnhead Stewarts of Ardvorlich to name but a few. These hardy drovers would also drive the hardest of bargains when selling their cattle to the English dealers at the annual fayres. It was the descendants of those tough Highland drovers that helped to establish the great cattle trails of the western United States and Australia, through the long journeys to the rail heads during the nineteenth century, at a time when only the very toughest men and cattle would survive. One of the earliest pioneers in America to develop commercial cattle droving was called John Chisholm whose forefathers once droved cattle from Skye to the Lowlands. And Australian readers may recognize the line from 1889 For the drovers life has pleasures that the townsfolk never know which was written by the son of Scottish immigrants.

What is it about this great Highland breed of cattle that has allowed them to endure over the centuries not only in their homeland but also throughout the world? They can be ideal where the terrain and climatic conditions demand a breed which can thrive on low quality vegetation whilst enduring long and hard winters and rearing calves every year well into the dams teens. If cared for correctly the quality of the beef has without question, as Thomas Hurtley put it there is no equal in fineness of grain or flavour. It is this fact about the Highland Breed that has attracted beef producers throughout the world today, that is to say those producers who listen to the customer. Todays consumer has a far greater awareness of how they want their beef to taste and a far greater interest in the manner in which it is reared. There can be few breeds of cattle which lend themselves better to a grass based system of production, whether in the breeding herd or finishing system. The Highlander is the master of utilising low quality roughage and turning it into the finest beef. This has been proven over the centuries.

There are many reasons why Highland genetics should be used to improve the efficiency in beef production throughout the world today:

*improvements in feed conversion

*long productive lives lowering replacement costs

*utilisation of land that was once considered unsuitable for livestock production

*improvement in the quality of the end product

. Which is to say, beef that is so delicious for taste

Why not let the Hardy Highlander help you whatever your system?

For more information, see the Gallery pages.

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The History of the Highland Breed | Scottish Genetics

Abstract Objectives

Stem cells have the ability to rescue and/or repair injured tissue. In humans, it is possible to isolate different types of stem cells from the body. Among these, dental pulp stem cells (DPSCs) are relatively easily obtainable and exhibit high plasticity and multipotential capabilities. In particular they represent a gold standard for neural-crest-derived bone reconstruction in humans and can be used for the repair of body defects in low-risk autologous therapeutic strategies.

An electronic search was conducted on PubMed databases and supplemented with a manual study of relevant references.

All research described in this review highlight that DPSCs are mesenchymal stem cells that could be used in clinical applications. Unfortunately, very few clinical trials have been reported. Major obstacles imposed on researchers are hindering the translation of potentially effective therapies to the clinic. Both researchers and regulatory institutions need to develop a new approach to this problem, drawing up a new policy for good manufacturing practice (GMP) procedures. We strongly suggest that only general rules be standardized rather than everything. Importantly, this would not have an effect on the safety of patients, but may very well affect the results, which cannot be identical for all patients, due to physiological diversity in the biology of each patient. Alternatively, it would be important to study the role of specific molecules that recruit endogenous stem cells for tissue regeneration. In this way, the clinical use of stem cells could be successfully developed.

DPSCs are mesenchymal stem cells that differentiate into different tissues, maintain their characteristics after cryopreservation, differentiate into bone-like tissues when loaded on scaffolds in animal models, and regenerate bone in human grafts. In summary, all data reported up to now should encourage the development of clinical procedures using DPSCs.

The stem cell field represents an area of particular interest for scientific research. The results so far obtained give good expectations for the use of stem cells in clinical trials. New therapeutic strategies have been made possible thanks to great advancements in stem cell biology, with the aim of regenerating tissues injured by disease.1and2 Based on their ability to rescue and/or repair injured tissue and partially restore organ function, multiple types of stem/progenitor cells have been speculated. A primary goal is to identify how different tissues and organs can arise from undifferentiated stem cells.

Stemness is the capability of undifferentiated cells to undergo an indefinite number of replications (self-renewal) and give rise to specialized cells (differentiation). Therefore, stem cells differ from other types of cells in the body because they are capable of sustaining self-renewal, are unspecialized, and can give rise to differentiated cell types. Differentiation can be recognized by a change in the morphology of the cell and by the detection of tissue-specific proteins.3 Stem cells may remain quiescent (non-dividing) for long periods of time until they are activated by a physiological need for more cells to maintain tissues, by disease, or by tissue injury. Thus, the primary role of adult stem cells is to maintain and repair the tissue in which they are found. They are thought to reside in specific areas termed stem cell niches.4 Adult stem cells have been identified in many organs and tissues, including brain, bone marrow, peripheral blood, blood vessels, skeletal muscle, skin, teeth, heart, gut, liver, ovarian epithelium, and testis.5 Among these tissues, dental pulp is considered a rich source of mesenchymal stem cells suitable for tissue engineering applications and, for this reason, many studies are performed with the final aim of obtaining new bone.6, 7and8

Tissue engineering is a multidisciplinary field that combines biology, engineering, and clinical science in order to generate new tissues and organs. This science involves different steps, such as the identification of appropriate cells, the development of scaffolds, and the study of morphogenic signals required to induce cells to regenerate a tissue or organ.9 After having discussed the state of the art in the field of dental pulp stem cells research and their potential use in bone engineering, here we try to suggest how to overcome the problems limiting the translationability of research, with the aim of improving the health of patients.

Dental pulp, a soft connective tissue within the dental crown, is an interesting source of adult stem cells because of the large amount of cells present and the non invasiveness of the isolation methods compared to other adult tissue sources.8, 10and11 Dental pulp contains mesenchymal stem cells defined as dental pulp stem cells (DPSCs). DPSCs are obtained from human permanent and primary teeth, human wisdom teeth, human exfoliated deciduous teeth (SHEDs), and apical papilla.7, 12, 13and14 Moreover, DPSCs can be also isolated from supernumerary teeth, which are generally discarded.15 Other sources of dental stem cells are the periodontal ligament, which houses periodontal ligament stem cells (PDLSCs),16 and the dental follicle, which contains dental follicle progenitor cells (DFPCs).17and18 DPSCs have been isolated from different organisms, including humans, mouse, rat, sheep, chimpanzee, and pig.19, 21, 22and23

DPSCs differentiate into different kinds of cells and tissues24, 25, 26, 27and28 and their multipotency has been compared to those of bone marrow stem cells (BMSCs). It has been demonstrated that proliferation, availability, and cell number of DPSCs are greater than BMSCs.20

See more here:
Dental pulp stem cells: State of the art and suggestions ...

PLC Staff Bios

David A. Fein, MD Internal Medicine Medical Director Locations: Princeton, Shelton, Fairfax

Founder of the Princeton Longevity Center, Dr. David Fein practiced general Internal Medicine in Morristown, NJ for 16 years. He has traveled extensively to research the latest medical advances to incorporate them into the Princeton Longevity Center. Dr Fein is a Founding Member of the Society for Cardiovascular CT. He lectures on topics in preventive medicine and the safe use of nutritional supplements. Dr. Fein has also been involved in developing health-related legislation in New Jersey.

Dr. Fein is on the Attending Staff at Morristown Memorial Hospital.

A graduate of Franklin & Marshall College in Lancaster, PA, Dr. Fein received his medical degree from New York University School of Medicine and was elected to the Alpha Omega Alpha Medical Honor Society. Dr. Fein completed his residency training at Bellevue Hospital- New York University Medical Center and is Board Certified in Internal Medicine.

John Rumberger , PhD, MD, FACC Cardiology Director of Cardiac Imaging Locations: Princeton

Dr. Rumberger is recognized as one of the world's leading authorities on cardiac and vascular imaging using CT Scanning. His notable credentials make him uniquely qualified to provide interpretation of Coronary CT Angiography.

Dr. Rumberger has been Professor of Medicine and Consultant in the Department of Cardiovascular Diseases at the Mayo Clinic in Rochester, Minnesota. It was during this time that his reputation as a leader in the development and application of computed tomography of the heart was established. He has published extensively and continues to lecture and train other physicians in the United States, Europe, and Asia.

Dr. Rumberger received his doctorate in engineering from The Ohio State University in 1976 and graduated from the University Of Miami School Of Medicine in 1978. He completed his internship and residency in internal medicine at The Ohio State University Hospitals, and completed a cardiovascular diseases fellowship and early faculty development at the University of Iowa. Dr. Rumberger is currently Director of Cardiac Imaging and Lipid Management at PLC and is Board Certified in Internal Medicine and Cardiovascular Diseases.

During his over 25 year career as a clinician, educator, and researcher, Dr. Rumberger has published nearly 500 scientific papers and book chapters. He has lectured worldwide on Cardiac CT, early disease diagnosis, and wellness. He is an Established Investigator of the American Heart Association and a Founding Member of the International Society of Atherosclerosis Imaging. Dr Rumberger is an active Reviewer for the Journal of the American Medical Association, Archives of Internal Medicine, publications of both the American Heart Association and American College of Cardiology, and the New England Journal of Medicine.

Charles Miner MD Internal Medicine Locations: Shelton

Dr. Miner is board-certified in Internal Medicine and has been in practice since 1982.

He is on the Board of Directors of The Stamford Hospital and the Stamford Hospital Foundation, on the medical staff of The Norwalk Hospital, and is on the Board of Directors of Misonix, Inc. He is listed in Castle Connolly Medical Ltd.s Top Doctors New York Metro Area and is an instructor in Clinical Medicine at Columbia University.

Dr. Miner performed his residency at Lenox Hill Hospital in New York, received his medical degree from the University of Cincinnati College of Medicine and holds a Bachelor of Science degree from Lehigh University.

Dr. Miner has particular expertise in personal services that emphasize prevention and screening, with a special interest in patient care during travel. He has developed a unique system that provides patients instant, secure access to their medical records via the web along with 24/7 access via cell phone, email or "BlackBerry" should a problem arise anywhere in the world. For physicians who wish to engage Dr. Miner's practice model, Dr. Miner has founded Lifestream MD, LLC, a physician-practice consulting company.

Dr. Miner serves as a member of the board of directors for Misonix, Inc., an ultrasonic medical device company based in Farmingdale, Long Island, and on the strategy and business development committee for Stamford Hospital. He previously served as director of web-based health and wellness

Oscar Ellison, III MD Internal Medicine Locations: Fairfax

Dr. Oscar Ellison, III, graduated from Harvard College and Georgetown University School of Medicine.

His focus has always been on personalized medical care, wellness and prevention. He has extensive experience treating hypertension, diabetes and hyperlipidemia.

Dr. Ellison has served on numerous boards, including the Arlington Hospital Physicians Organization and the Arlington County Medical Society. He has also served as Vice Chair/Chairman of the Virginia Hospital Center Department of Family Practice. Dr. Ellison is experienced in Phase 3 Clinical Research, and is the Medical Director of Atlantic Medical Associates.

Dr Ellison has been recognized as a Top Doctor by Washingtonian Magazine, Northern Virginia Magazine, and Washington Checkbook Magazine, and has been listed in the Leading Physicians of the World by the IAHCP. An accomplished athlete, Dr. Ellison competed in the Henley Royal Regatta and has won the Oxford triathlon.

Affiliated Medical Staff:

Yaakov Applbaum, MD Radiologist Medical Director and Acting Chairman Department of Radiology Capital Health System

Dr. Applbaum received his MD degree from the Albert Einstein College of Medicine. His esidency in Radiology at Maimonides Medical Center was followed by a fellowship in Interventional Radiology at the University of California at Irvine Medical Center. He previously served as Chief, Vascular and Interventional Radiology, at Staten Island University Hospital. He is board certified in Diagnostic Radiology, with Certificates of Added Qualification in both Interventional Radiology and Neuroradiology, by the American Board of Radiology (ABR.)

Ajay Choudhri, MD Radiologist, Vascular and Interventional Radiology Department of Radiology Capital Health System

Dr. Choudhri received his MD degree from the New Jersey Medical School, UMDNJ, Newark. His residency in Radiology at Albert Einstein College of Medicine, Montefiore Medical Center, was followed by a fellowship in Interventional Radiology at the Miami Cardiac and Vascular Institute. He previously served as Chief, Interventional Radiology at Jackson South Hospital in Miami. He is board certified in Radiology by the ABR.

Amin Chaoui, MD Radiologist The Center for Virtual Colonoscopy Boston Diagnostics

Dr. Amin Chaoui is an Associate radiologist at Faulkner/Brigham & Womens hospital, Department of Radiology, Harvard University School of Medicine. A graduate of the University of Geneva School of Medicine, Dr. Chaoui's graduate training included a research fellowship in Body Imaging at University of Florida College of Medicine and a Fellowship in Body Imaging at Boston Medical Center, Boston University School of Medicine. Dr. Chaoui is certified by the American Board of Radiology. From 1999-2002, he served as the Director of the Center for Virtual Colonoscopy at Boston Medical Center and is currently Medical Director of the Boston Diagnostics Center for Virtual Colonoscopy.

Dr. Chaoui has published numerous articles and studies, as well as lectured across the USA and internationally, on Virtual Colonoscopy and other areas of radiology.

Internal

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Princeton Longevity Center :: Staff Bios

Without it, we would all be forced to live in sterile environments, never touching each other, never feeling a spring breeze, never tasting rain. The immune system is that complex operation within our bodies that keeps us healthy and disease-free.

Few systems in nature are as complicated as the human immune system. It exists apart from, and works in concert with, every other system in the body. When it works, people stay healthy. When it malfunctions, terrible things happen.

The main component of the system is the lymphatic system. Small organs called lymph nodes help carry lymph fluid throughout the body. These nodes are located most prominently in the throat, armpit and groin. Lymph fluid contains lymphocytes and other white blood cells and circulates throughout the body.

The white blood cells are the main fighting soldiers in the body's immune system. They destroy foreign or diseased cells in an effort to clear them from the body. This is why a raised white blood cell count is often an indication of infection. The worse the infection, the more white blood cells the body sends out to fight it.

White and red blood cells are produced in the spongy tissue called bone marrow. This substance, rich in nutrients, is crucial for properly functioning immunity. Leukemia, a cancer of the bone marrow, causes greatly increased production of abnormal white blood cells and allows immature red blood cells to be released into the body. Other features, such as the lowly nose hair and mucus lining in the lungs, help trap bacteria before it gets into the bloodstream to cause an infection.

B cells and T cells are the main kinds of lymphocytes that attack foreign cells. B cells produce antibodies tailored to different cells at the command of the T cells, the regulators of the body's immune response. T cells also destroy diseased cells.

Many diseases that plague mankind are a result of insufficient immunity or inappropriate immune response. A cold, for instance, is caused by a virus. The body doesn't recognize some viruses as being harmful, so the T cell response is, "Pass, friend," and the sneezing begins.

Allergies are examples of inappropriate immune response. The body is hyper-vigilant, seeing that evil pollen as a dangerous invader instead of a harmless yellow powder. Other diseases, such as diabetes and AIDS, suppress the immune system, reducing the body's ability to fight infection.

Vaccines are vital in helping the body fend off certain diseases. The body is injected with a weakened or dead form of the virus or bacteria and produces the appropriate antibodies, giving complete protection against the full-strength form of the disease. This is the reason such disorders as diphtheria, mumps, tetanus and pertussis are so rarely seen today. Children have been vaccinated against them, and the immune system is on the alert. Vaccines have also been instrumental in eradicating plagues such as smallpox and polio.

Antibiotics help the body fight disease as well, but doctors are more cautious about prescribing the broad-spectrum variety, since certain bacteria are starting to show resistance to them. The next time you hug a loved one or smell a rose, thank your immune system.

Read the original here:
What is the Immune System? (with pictures) - wiseGEEK

A1 Stem Cells makes available the potency of Embryonic Stem Cells to treat major degenerative diseases. We offer tumor treatment and cancer treatments. We also address treatment for diabetes, treatment for depression, treatment for stroke and many more. (see our stem cells treatment page) Further more we encourage a proactive approach to heath care. Our team developed an anti aging therapy program to help your body rejuvenate.

A1 Stem Cells, beyond addressing the symptoms of your condition, cares to address its causes. We take it as our mission to find the source of your ailments, whether there are metal, pollutants or parasites of all sorts, then free you from these accumulated toxins, and finally restore the functionality of your organs thanks to our embryonic stem cells treatment. We will also counsel you so that you can maintain your regained well being and vitality once back home.

It is now understood that most diseases are the result of an accumulation of toxins and parasites that ineluctably damage our organs through time. It is also the major cause of aging and all its related ailments. The proposed embryonic stem cell treatment reverses the damages caused to the body. Upon injection, the cells trigger the body to repair itself, one organ at a time, bringing youth and wellness back from the inside out. The stem cell therapy have also been found more efficient if the toxins that caused the ailment at first have been thoroughly removed, thus preventing a possible future set-back. This is especially clear for all our cancer treatment.

The A1 Stem Cells offer is a complete and unique treatment that includes:

Each of the diseases listed here have been thoroughly studied by our medical partners and biochemists. You can browse our testimony page to see the extent of what can be achieved when an ill body is relieved from the toxins accumulated through time and then recharged with the regenerative power of the stem cells.

If you don't find your ailment described in our site, please inquire with our repre-sentative who will get back to you shortly with the advise of our experts.

When I first consulted with A1 Stem Cells doctor, they diagnosed a tumor that they quickly removed with their cleanse protocol and stem cell treatment. I dont remember when was the time I felt like I feel now. I have gained at least 20 years worth of energy.

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Stem Cell Therapy, Anti-Aging and Prevention

What Are Stem Cells?

Stem cells are your bodys repair team. They divide limitlessly and go around your body providing nourishment to all your other cells. As long as youre alive, stem cell ensure all the cells in your body are healthy, happy, and serving you well. There are two types of stem cells embryonic stem cells and adult stem cells.

As the name suggest, these stem cells come from the embryos that develop from eggs that have been fertilized in vitro. In vitro fertilization clinics donate these stem cells for research purposes with the informed consent of the donors. Its important to note that these eggs are not derived from eggs fertilized in a womans body. These particular cells are isolated from the inner mast of a blastocyst. These pluripotent stem cells can give rise to any type of cell in the fully developed body. In the lab, embryonic stem cells keep reproducing themselves until they are turned into specific types of cells. In the body, these cells eventually disappear, so a human adult body no longer contains cells that can generate any kind of cell. A problem often encountered with embryonic stem cells is tissue rejection, which is similar to the rejection in a liver or blood transplant. This can limit the therapeutic usefulness of these particular stem cells.

Adult stem cells are found in small numbers within most adult tissues like bone marrow or fat. They are the maintenance crew of your body they make sure everything is in tip-top shape by being multipotent in that they give rise to several kinds of cells in their home tissues. They regenerate cells damaged by disease, injury, and everyday wear and tear. By dividing, they become specialized to repair or replace surrounding differentiated cells. Just like embryonic stem cells, adult stem cells have the ability to differentiate into more than one cell type, but unlike embryonic stem cells, they are often restricted to certain lineages. There are three types of adult stem cells. Two types are located within the bone marrow, and the other type is known as a fat stem cell.

Stem cells are removed from the bone marrow at the back of the patients pelvis via suction. The substance is then removed using a syringe. The process is only slightly uncomfortable with local anesthetic. Typically, only 2 oz. of bone marrow aspirate is required. This aspirate contains platelets, mesenchymal stem cells, and other kinds of stem cells that are used in adult stem cell therapy. After its taken, it is placed inside a special container, which is then placed into a machine known as a centrifuge. This begins spinning at a high speed until the platelets and stem cells separate from the other blood products. This particular concentration of bone marrow is called BMAC or Bone Marrow Aspiration Concentrate. This is then re-introduced into the injured area during stem cell therapy.

Once the BMAC is reintroduced into the injured area, the platelets are released and start to go to work repairing the area. They signal proteins and growth factors that activate the stem cells. These signal proteins and growth factors are called cytokines, which are sort of the traffic directors of the operation, telling the stem cells where to go to repair your body.

The typical repair process is two to three months. However, in most cases, great improvement can be seen before then. About four to six weeks after the stem cell injection, the patient will receive a platelet-rich plasma injection on the afflicted area followed by another injection four to six weeks after that. Patients are advised to minimize alcohol consumption as it can deter healing. To boost healing, patients are advised to take a compound called StemXcell, which contains supplements such as carnosine, blueberry extract, vitamin D3, and green tea extract.

Excerpt from:
Stem Cell Therapy - Stem MD I Advanced Orthopedics

Can Stem Cell Studies help treat Chronic Obstructive Pulmonary Disease (COPD)?

Today, new COPD stem cell treatments and advances in research are giving new hope to people affected by this disease. The COPD treatments for Stem Cell Clinical Studies are being studied for their efficacy in improving the complications in patients with Chronic Obstructive Pulmonary Disease, through the use of stem cells. These stem cell COPD treatments may help patients who dont respond to typical drug treatment.

To learn more about becoming a patient and receiving stem cell therapy through StemGenex Medical Group, please contact one of our patient advocates at (800) 609-7795 or fill out the contact form on this page.

Chronic obstructive lung disease (COPD) describes a group of lung conditions (diseases) that make it difficult to empty the air out of the lungs. This difficulty can lead to shortness of breath (also called breathlessness) or the feeling of being tired. COPD is a word that can be used to describe a person with chronic bronchitis, emphysema or a combination of these. COPD is a different condition from asthma, but it can be difficult to distinguish between COPD and chronic asthma.

The most common cause of Chronic Obstructive Pulmonary Disease is cigarette smoking, but there are many other causes. Inhaling smoke or air pollutants can cause the mucus glands that line the bronchial tubes (bronchi) to produce more mucus than normal, and can cause the walls of the bronchi to thicken and swell (inflame). This increase in mucus causes you to cough, frequently resulting in raising mucus (or phlegm). COPD can develop if small amounts of these irritants are inhaled over a long period of time or if large amounts are inhaled over a short period of time.

Environmental factors and genetics may also cause COPD. For example, heavy exposure to certain dusts at work, chemicals and indoor or outdoor air pollution can contribute to COPD. The reason why some smokers never develop COPD and why some non-smokers get COPD is not fully understood. Family genes or heredity probably play a major role in who develops COPD.

There are 4 stages of COPD. They are :

The diagnosis of COPD depends upon the presence of one or more of the symptoms of the disease.

The following are facts cited from the American Lung Association(www.lungusa.org) and U.S. Centers for Disease Control and Prevention(www.cdc.gov)

Stem cells are unprogrammed cells in the human body that can be described as "shape shifters." These cells have the ability to change or differentiate into other types of cells. Stem cells are at the center of a new field of science called regenerative medicine. Because stem cells can become bone, muscle, cartilage and other specialized types of cells, they have the potential to treat many diseases, including Parkinson's, Alzheimer's, COPD, Diabetes and more.

StemGenex offers stem cell therapy using Adult stem cells only.There are four known types of stem cells:

Stem cell therapy is an intervention strategy that introduces new adult stem cells into damaged tissue in order to treat disease or injury. Many medical researchers believe that stem cell treatments have the potential to change the face of human disease and alleviate suffering. The ability of stem cells to self-renew and give rise to subsequent generations with variable degrees of differentiation capacities, offers significant potential for generation of tissues that can potentially replace diseases and damaged areas in the body, with minimal risk of rejection and side effects.

StemGenex is currently studying adipose stem cell therapy as a new alternative treatment to help manage the complications of COPD. The stem cells harvested from a patient have the potential to replace countless cells of the body, lung tissue included. These stem cells may heal the body by replacing ones plagued with disease, regenerating new cells, and suppressing the immune systems macrophage response which engulf and digest the dying cells of the lungs. Current research in adult stem cell therapy has shown that restoration of damaged cells through this treatment is possible. This breakthrough in regenerative medicine shines a light of hope on those battling this degenerative disease. Improvements have been seen in the following symptoms after treatment:

StemGenex is studying potential ways to directly target the conditions and complications themselves. These studies consist of multiple ways to deliver the highest amount of activated stem cells to the areas patients need them most. When stem cells are studied through StemGenex, as potential therapy for COPD, there are multiple ways they can be administered:

Yes. Scientists around the world believe there is enough evidence to suggest that stem cells hold real potential as a therapy for COPD. This evidence comes from research in animals and from a handful of early clinical trials. They believe that it is now time for a concerted effort in stem cell research and an international effort to support clinical trials of stem cells for COPD.

No. There are currently no FDA approved stem cell therapies for COPD disease. All stem cell therapies for COPD disease are currently unproven, experimental therapies. This means that the FDA does not know whether stem cells are effective for people with COPD disease. The only way to determine the effectiveness of stem cell therapy is through the type of clinical studies and trials which are currently being conducted in the US.

One of the goals of StemGenex, through our stem cell studies, is to understand what a particular stem cell therapy might be able to achieve. For example, does it have the potential for slowing the disease's progression, replacing damaged cells and memories, or both? With this goal in mind, StemGenex continues to study these diseases and the full effect of stem cell therapy on each disease. Anecdotally, these results have been overwhelmingly positive but there is more that needs to be done to determine the exact effectiveness of these therapies.

After stem cells have been administered into someones body they have to make their way to the correct place (e.g. area of damage) and then have their desired effect. This process takes time and although it is difficult to predict exactly how long, it is likely that it will take several weeks or months on average to see the full desired effect.

Yes, a stem cell therapy may be repeated. Current studies indicate the strong possibility of a cumulative effect from multiple stem cell therapies a patient received for their condition. Long-term studies will attempt to better understand this in detail.

Original post:
Stem Cell Therapy Studies for COPD - StemGenex

Redesigning the World Ethical Questions about Genetic Engineering

Ron Epstein 1

INTRODUCTION

Until the demise of the Soviet Union, we lived under the daily threat of nuclear holocaust extinguishing human life and the entire biosphere. Now it looks more likely that total destruction will be averted, and that widespread, but not universally fatal, damage will continue to occur from radiation accidents from power plants, aging nuclear submarines, and perhaps the limited use of tactical nuclear weapons by governments or terrorists.

What has gone largely unnoticed is the unprecedented lethal threat of genetic engineering to life on the planet. It now seems likely, unless a major shift in international policy occurs quickly, that the major ecosystems that support the biosphere are going to be irreversibly disrupted, and that genetically engineered viruses may very well lead to the eventual demise of almost all human life. In the course of the major transformations that are on the way, human beings will be transformed, both intentionally and unintentionally, in ways that will make us something different than what we now consider human.

Heedless of the dangers, we are rushing full speed ahead on almost all fronts. Some of the most powerful multinational chemical, pharmaceutical and agricultural corporations have staked their financial futures on genetic engineering. Enormous amounts of money are already involved, and the United States government is currently bullying the rest of the world into rapid acceptance of corporate demands concerning genetic engineering research and marketing.

WHAT IS GENETIC ENGINEERING

What are genes?

Genes are often described as 'blueprints' or 'computer programs' for our bodies and all living organisms. Although it is true that genes are specific sequences of DNA (deoxyribonucleic acid) that are central to the production of proteins, contrary to popular belief and the now outmoded standard genetic model, genes do not directly determine the 'traits' of an organism.1a They are a single factor among many. They provide the 'list of ingredients' which is then organized by the 'dynamical system' of the organism. That 'dynamical system' determines how the organism is going to develop. In other words, a single gene does not, in most cases, exclusively determine either a single feature of our bodies or a single aspect of our behavior. A recipe of ingredients alone does not create a dish of food. A chef must take those ingredients and subject them to complex processes which will determine whether the outcome is mediocre or of gourmet quality. So too the genes are processed through the self-organizing ('dynamical') system of the organism, so that the combination of a complex combination of genes is subjected to a variety of environmental factors which lead to the final results, whether somatic or behavioral.2

a gene is not an easily identifiable and tangible object. It is not only the DNA sequence which determines its functions in the organisms, but also its location in a specific chromosomal, cellular, physiological and evolutionary context. It is therefore difficult to predict the impact of genetic material transfer on the functioning of the extremely tightly controlled, integrated and balanced functioning of all the tens of thousands of structures and processes that make up the body of any complex organism.3

Genetic engineering refers to the artificial modification of the genetic code of a living organism. Genetic engineering changes the fundamental physical nature of the organism, sometimes in ways that would never occur in nature. Genes from one organism are inserted in another organism, most often across natural species boundaries. Some of the effects become known, but most do not. The effects of genetic engineering which we know are ususally short-term, specific and physical. The effects we do not know are often long-term, general, and also mental. Long-term effects may be either specific4 or general.

Differences between Bioengineering and Breeding

The breeding of animals and plants speeds up the natural processes of gene selection and mutation that occur in nature to select new species that have specific use to humans. Although the selecting of those species interferes with the natural selection process that would otherwise occur, the processes utilized are found in nature. For example, horses are bred to run fast without regard for how those thoroughbreds would be able to survive in the wild. There are problems with stocking streams with farmed fish because they tend to crowd out natural species, be less resistant to disease, and spread disease to wild fish.5

The breeding work of people like Luther Burbank led to the introduction of a whole range of tasty new fruits. At the University of California at Davis square tomatoes with tough skins were developed for better packing and shipping. Sometimes breeding goes awry. Killer bees are an example. Another example is the 1973 corn blight that killed a third of the crop that year. It was caused by a newly bred corn cultivar that was highly susceptible to a rare variant of a common leaf fungus.6

Bioengineers often claim that they are just speeding up the processes of natural selection and making the age-old practices of breeding more efficient. In some cases that may be true, but in most instances the gene changes that are engineered would never occur in nature, because they cross natural species barriers.

HOW GENETIC ENGINEERING IS CURRENTLY USED

Here is a brief summary of some of the more important, recent developments in genetic engineering.7

1) Most of the genetic engineering now being used commercially is in the agricultural sector. Plants are genetically engineered to be resistant to herbicides, to have built in pesticide resistance, and to convert nitrogen directly from the soil. Insects are being genetically engineered to attack crop predators. Research is ongoing in growing agricultural products directly in the laboratory using genetically engineered bacteria. Also envisioned is a major commercial role for genetically engineered plants as chemical factories. For example, organic plastics are already being produced in this manner.8

2) Genetically engineered animals are being developed as living factories for the production of pharmaceuticals and as sources of organs for transplantation into humans. (New animals created through the process of cross-species gene transfer are called xenographs. The transplanting of organs across species is called xenotransplantation.) A combination of genetic engineering and cloning is leading to the development of animals for meat with less fat, etc. Fish are being genetically engineered to grow larger and more rapidly.

3) Many pharmaceutical drugs, including insulin, are already genetically engineered in the laboratory. Many enzymes used in the food industry, including rennet used in cheese production, are also available in genetically engineered form and are in widespread use.

4) Medical researchers are genetically engineering disease carrying insects so that their disease potency is destroyed. They are genetically engineering human skin9 and soon hope to do the same with entire organs and other body parts.

5) Genetic screening is already used to screen for some hereditary conditions. Research is ongoing in the use of gene therapy in the attempt to correct some of these conditions. Other research is focusing on techniques to make genetic changes directly in human embryos. Most recently research has also been focused on combining cloning with genetic enginering. In so-called germline therapy, the genetic changes are passed on from generation to generation and are permanent.

6) In mining, genetically engineered organisms are being developed to extract gold, copper, etc. from the substances in which it is embedded. Other organisms may someday live on the methane gas that is a lethal danger to miners. Still others have been genetically engineered to clean up oil spills, to neutralize dangerous pollutants, and to absorb radioactivity. Genetically engineered bacteria are being developed to transform waste products into ethanol for fuel.

SOME DISTINGUISHED SCIENTISTS' OPINIONS

In the 1950's, the media was full of information about the great new scientific miracle that was going to make it possible to kill all of the noxious insects in the world, to wipe out insect-born diseases and feed the world's starving masses. That was DDT. In the 1990's, the media is full of information about the coming wonders of genetic engineering. Everywhere are claims that genetic engineering will feed the starving, help eliminate disease, and so forth. The question is the price tag. The ideas and evidence presented below are intended to help evaluate that central question.

Many prominent scientists have warned against the dangers of genetic engineering. George Wald, Nobel Prize-winning biologist and Harvard professor, wrote:

Recombinant DNA technology [genetic engineering] faces our society with problems unprecedented not only in the history of science, but of life on the Earth. It places in human hands the capacity to redesign living organisms, the products of some three billion years of evolution.

Such intervention must not be confused with previous intrusions upon the natural order of living organisms; animal and plant breeding, for example; or the artificial induction of mutations, as with X-rays. All such earlier procedures worked within single or closely related species. The nub of the new technology is to move genes back and forth, not only across species lines, but across any boundaries that now divide living organisms The results will be essentially new organisms. Self-perpetuating and hence permanent. Once created, they cannot be recalled

Up to now living organisms have evolved very slowly, and new forms have had plenty of time to settle in. Now whole proteins will be transposed overnight into wholly new associations, with consequences no one can foretell, either for the host organism or their neighbors.

It is all too big and is happening too fast. So this, the central problem, remains almost unconsidered. It presents probably the largest ethical problem that science has ever had to face. Our morality up to now has been to go ahead without restriction to learn all that we can about nature. Restructuring nature was not part of the bargain For going ahead in this direction may be not only unwise but dangerous. Potentially, it could breed new animal and plant diseases, new sources of cancer, novel epidemics.10

Erwin Chargoff, an eminent geneticist who is sometimes called the father of modern microbiology, commented:

The principle question to be answered is whether we have the right to put an additional fearful load on generations not yet born. I use the adjective 'additional' in view of the unresolved and equally fearful problem of the disposal of nuclear waste. Our time is cursed with the necessity for feeble men, masquerading as experts, to make enormously far-reaching decisions. Is there anything more far-reaching than the creation of forms of life? You can stop splitting the atom; you can stop visiting the moon; you can stop using aerosals; you may even decide not to kill entire populations by the use of a few bombs. But you cannot recall a new form of life. Once you have constructed a viable E. coli cell carry a plasmid DNA into which a piece of eukaryotic DNA has been spliced, it will survive you and your children and your children's children. An irreversible attack on the biosphere is something so unheard-of, so unthinkable to previous generations, that I could only wish that mine had not been guilty of it.11

It appears that the recombination experiments in which a piece of animal DNA is incorporated into the DNA of a microbial plasmid are being performed without a full appreciation of what is going on. Is the position of one gene with respect to its neighbors on the DNA chain accidental or do they control and regulate each other? Are we wise in getting ready to mix up what nature has kept apart, namely the genomes of eukaryotic and prokaryotic cells.

The worst is that we shall never know. Bacteria and viruses have always formed a most effective biological underground. The guerrilla warfare through which they act on higher forms of life is only imperfectly understood. By adding to this arsenal freakish forms of life-prokyarotes propagating eukaryotic genes-we shall be throwing a veil of uncertainties over the life of coming generations. Have we the right to counteract, irreversibly, the evolutionary wisdom of millions of years, in order to satisfy the ambition and curiosity of a few scientists?

This world is given to us on loan. We come and we go; and after a time we leave earth and air and water to others who come after us. My generation, or perhaps the one preceding mine, has been the first to engage, under the leadership of the exact sciences, in a destructive colonial warfare against nature. The future will curse us for it.12

In contrast, here are two examples of prominent scientists who support genetic engineering. Co-discoverer of the DNA code and Nobel Laureate Dr. James D. Watson takes this approach:

On the possible diseases created by recombinant DNA, Watson wrote in March 1979: 'I would not spend a penny trying to see if they exist' (Watson 1979:113). Watson's position is that we must go ahead until we experience serious disadvantages. We must take the risk of even a catastrophe that might be hidden in recombinant DNA technology. According to him that is how learning works: until a tiger devours you, you don't know that the jungle is dangerous.13

What is wrong with Watson's analogy? If Watson wants to go off into the jungle and put himself at risk of being eaten by a tiger, that is his business. What gives him the right to drag us all with him and put us at risk of being eaten? When genetically engineered organisms are released into the environment, they put us all at risk, not just their creators.

The above statement by a great scientist clearly shows that we cannot depend on the high priests of science to make our ethical decisions for us. Too much is at stake. Not all geneticists are so cavalier or unclear about the risks. Unfortunately the ones who see or care about the potential problems are in the minority. That is not really surprising, because many who did see some of the basic problems would either switch fields or not enter it in the first place. Many of those who are in it have found a fascinating playground, not only in which to earn a livelihood, but also one with high-stake prizes of fame and fortune.

Watson himself saw some of the problems clearly when he stated:

This [genetic engineering] is a matter far too important to be left solely in the hands of the scientific and medical communities. The belief thatscience always moves forward represents a form of laissez-faire nonsense dismally reminiscent of the credo that American business if left to itself will solve everybody's problems. Just as the success of a corporate body in making money need not set the human condition ahead, neither does every scientific advance automatically make our lives more 'meaningful'.14

Although not a geneticist, Stephen Hawking, the world-renowned physicist and cosmologist and Lucasian Professor of Mathematics at Cambridge University in England (a post once held by Sir Isaac Newton), has commented often and publicly on the future role of genetic engineering. For example:

Hawking, known mostly for his theories about the Big Bang and black holes, is focusing a lot these days on how humanity fits into the future of the universe--if indeed it fits at all. One possibility he suggests is that once an intelligent life form reaches the stage we're at now, it proceeds to destroy itself. He's an optimist, however, preferring the notion that people will alter DNA, redesigning the race to minimize our aggressive nature and give us a better chance at long-term survival. ``Humans will change their genetic makeup to give them more intelligence and better memory,'' he said.15

Hawking assumes that, even though humans are about to destroy themselves, they have the wisdom to know how to redesign themselves. If that were the case, why would we be about to destroy ourselves in the first place? Is Hawking assuming that genes control IQ and memory, and that they are equivalent to wisdom, or is Hawking claiming there is a wisdom gene? All these assumptions are extremely dubious. The whole notion that we can completely understand what it means to be human with a small part of our intellect, which is in turn a small part of who we are is, in its very nature, extremely suspect. If we attempt to transform ourselves in the image of a small part of ourselves, what we transform ourselves into will certainly be something smaller or at least a serious distortion of our human nature.

Those questions aside, Hawking does make explicit that, for the first time in history, natural evolution has come to an end and has been replaced by humans meddling with their own genetic makeup. With genetic engineering science has moved from exploring the natural world and its mechanisms to redesigning them. This is a radical departure in the notion of what we mean by science. As Nobel Prize winning biologist Professor George Wald was quoted above as saying: "Our morality up to now has been to go ahead without restriction to learn all that we can about nature. Restructuring nature was not part of the bargain."16

Hawking's views illustrate that even brilliant scientists, whose understanding of science should be impeccable, can get caught in the web of scientism. "Scientism"17 refers to the extending of science beyond the use of the scientific method and wrongly attempting to use it as the foundation for belief systems. Scientism promotes the myth that science is the sole source of truth about ourselves and the world we live in.

Most scientific research is dependent on artificial closed system models, yet the cosmos is an open system. Therefore, there are a priori limitations to the relevance of scientific data to the open system of the natural world. What seems to be the case in the laboratory may or may not be valid in the natural world.17a Therefore, we cannot know through scientific methodology the full extent of the possible effects of genetic alterations in living creatures.18

If science is understood in terms of hypotheses from data collected according to scientific method, then the claims of Hawking in the name of science extend far beyond what science actually is. He is caught in an unconscious web of presuppositions and values that deeply affect both his hypotheses and his interpretation of data. It is not only Hawking who is caught in this web but all of us, regardless of our philosophical positions, because scientism is part of our cultural background that is very hard to shake. We all have to keep in mind that there is more to the world than what our current crop of scientific instruments can detect.

Hawking's notions are at least altruistic. Perhaps more dangerous in the short run are projected commercial applications of so-called 'designer genes': gene alterations to change the physical appearance of our offspring to more closely match cultural values and styles. When we change the eye-color, height, weight, and other bodily characteristics of our offspring, how do we know what else is also being changed? Genes are not isolated units that have simple one-to-one correspondences.19

SOME SPECIFIC DIFFICULTIES WITH GENETIC ENGINEERING

Here are a few examples of current efforts in genetic engineering that may cause us to think twice about its rosy benefits.

The Potential of Genetic Engineering for Disrupting the Natural Ecosystems of the Biosphere

At a time when an estimated 50,000 species are already expected to become extinct every year, any further interference with the natural balance of ecosystems could cause havoc. Genetically engineered organisms, with their completely new and unnatural combinations of genes, have a unique power to disrupt our environment. Since they are living, they are capable of reproducing, mutating and moving within the environment. As these new life forms move into existing habitats they could destroy nature as we know it, causing long term and irreversible changes to our natural world.20

Any child who has had an aquarium knows that the fish, plants, snails, and food have to be kept in balance to keep the water clear and the fish healthy. Natural ecosystems are more complex but operate in a similar manner. Nature, whether we consider it to be conscious or without consciousness, is a self-organizing system with its own mechanisms.21 In order to guarantee the long-term viability of the system, those mechanisms insure that important equilibria are maintained. Lately the extremes of human environmental pollution and other human activities have been putting deep strains on those mechanisms. Nonetheless, just as we can clearly see when the aquarium is out of kilter, we can learn to sensitize ourselves to Nature's warnings and know when we are endangering Nature's mechanisms for maintaining equilibria. We can see an aquarium clearly. Unfortunately, because of the limitations of our senses in detecting unnatural and often invisible change, we may not become aware of serious dangers to the environment until widespread damage has already been done.

Deep ecology22 and Gaia theory have brought to general awareness the interactive and interdependent quality of environmental systems.22a No longer do we believe that isolated events occur in nature. Each event is part of a vast web of inter-causality, and as such has widespread consequences within that ecosystem.

If we accept the notion that the biosphere has its own corrective mechanisms, then we have to look at how they work and the limitations of their design. The more extreme the disruption to the self-organizing systems of the biosphere, the stronger the corrective measures are necessary. The notion that the systems can ultimately deal with any threat, however extreme, is without scientific basis. No evidence exists that the life and welfare of human beings have priority in those self-organizing systems. Nor does any evidence exist that anything in those systems is equipped to deal with all the threats that genetically engineered organisms may pose. Why? The organisms are not in the experience of the systems, because they could never occur naturally as a threat. The basic problem is a denial on the part of many geneticists that genetically engineered organisms are radical, new, and unnatural forms of life, which, as such, have no place in the evolutionarily balanced biosphere.

Viruses

Plant, animal and human viruses play a major role in the ecosystems that comprise the biosphere. They are thought by some to be one of the primary factors in evolutionary change. Viruses have the ability to enter the genetic material of their hosts, to break apart, and then to recombine with the genetic material of the host to create new viruses. Those new viruses then infect new hosts, and, in the process, transfer new genetic material to the new host. When the host reproduces, genetic change has occurred.

If cells are genetically engineered, when viruses enter the cells, whether human, animal, or plant, then some of the genetically engineered material can be transferred to the newly created viruses and spread to the viruses' new hosts. We can assume that ordinary viruses, no matter how deadly, if naturally produced, have a role to play in an ecosystem and are regulated by that ecosystem. Difficulties can occur when humans carry them out of their natural ecosystems; nonetheless, all ecosystems in the biosphere may presumably share certain defense characteristics. Since viruses that contain genetically engineered material could never naturally arise in an ecosystem, there is no guarantee of natural defenses against them. They then can lead to widespread death of humans, animals or plants, thereby temporarily or even permanently damaging the ecosystem. Widespread die-off of a plant species is not an isolated event but can affect its whole ecosystem. For many, this may be a rather theoretical concern. The distinct possibility of the widespread die-off of human beings from genetically engineered viruses may command more attention.23

Biowarfare

Secret work is going forward in many countries to develop genetically engineered bacteria and viruses for biological warfare. International terrorists have already begun seriously considering their use. They are almost impossible to regulate, because the same equipment and technology that are used commercially can easily and quickly be transferred to military application.

The former Soviet Union had 32,000 scientists working on biowarfare, including military applications of genetic engineering. No one knows where most of them have gone, or what they have taken with them. Among the more interesting probable developments of their research were smallpox viruses engineered either with equine encephalitis or with Ebola virus. In one laboratory, despite the most stringent containment standards, a virulent strain of pneumonia, which had been stolen from the United State military, infected wild rats living in the building, which then escaped into the wild.24

There is also suggestive evidence that much of the so-called Gulf War Syndrome may have been caused by a genetically engineered biowarfare agent which is contagious after a relatively long incubation period. Fortunately that particular organism seems to respond to antibiotic treatment.25 What is going to happen when the organisms are purposely engineered to resist all known treatment?

Nobel laureate in genetics and president emeritus of Rockefeller University Joshua Lederberg has been in the forefront of those concerned about international control of biological weapons. Yet when I wrote Dr. Lederberg for information about ethical problems in the use of genetic engineering in biowarfare, he replied, "I don't see how we'd be talking about the ethics of genetic engineering, any more than that of iron smelting - which can be used to build bridges or guns."26 Like most scientists, Lederberg fails to acknowledge that scientific researchers have a responsibility for the use to which their discoveries are put. Thus he also fails to recognize that once the genie is out of the bottle, you cannot coax it back in. In other words, research in genetic engineering naturally leads to its employment for biowarfare, so that before any research in genetic engineering is undertaken, its potential use in biowarfare should be clearly evaluated. After they became aware of the horrors of nuclear war, many of the scientists who worked in the Manhattan project, which developed the first atomic bomb, underwent terrible anguish and soul-searching. It is surprising that more geneticists do not see the parallels.

After reading about the dangers of genetic engineering in biowarfare, the president of the United States, Bill Clinton, became extremely concerned, and, in the spring of 1998, made civil defense countermeasures a priority. Yet, his administration has systematically opposed all but the most rudimentary safety regulations and restrictions for the biotech industry. By doing so, Clinton has unwittingly created a climate in which the production of the weapons he is trying to defend against has become very easy for both governments and terrorists.27

Plants

New crops may breed with wild relatives or cross breed with related species. The "foreign" genes could spread throughout the environment causing unpredicted changes which will be unstoppable once they have begun. Entirely new diseases may develop in crops or wild plants. Foreign genes are designed to be carried into other organisms by viruses which can break through species barriers, and overcome an organism's natural defenses. This makes them more infectious than naturally existing parasites, so any new viruses could be even more potent than those already known.

Ordinary weeds could become "Super-weeds": Plants engineered to be herbicide resistant could become so invasive they are a weed problem themselves, or they could spread their resistance to wild weeds making them more invasive. Fragile plants may be driven to extinction, reducing nature's precious biodiversity. Insects could be impossible to control. Making plants resistant to chemical poisons could lead to a crisis of "super pests" if they also take on the resistance to pesticides.

The countryside may suffer even greater use of herbicides and pesticides: Because farmers will be able to use these toxic chemicals with impunity their use may increase threatening more pollution of water supplies and degradation of soils.

Plants developed to produce their own pesticide could harm non-target species such as birds, moths and butterflies. No one - including the genetic scientists - knows for sure the effect releasing new life forms will have on the environment. They do know that all of the above are possible and irreversible, but they still want to carry out their experiment. THEY get giant profits. All WE get is a new and uncertain environment - an end to the world as we know it.29

When genetically engineered crops are grown for a specific purpose, they cannot be easily isolated both from spreading into the wild and from cross-pollinating with wild relatives. It has already been shown30 that cross-pollination can take place almost a mile away from the genetically engineered plantings. As has already occurred with noxious weeds and exotics, human beings, animals and birds may accidentally carry the genetically engineered seeds far vaster distances. Spillage in transport and at processing factories is also inevitable. The genetically engineered plants can then force out plant competitors and thus radically change the balance of ecosystems or even destroy them.

Under current United States government regulations, companies that are doing field-testing of genetically engineered organisms need not inform the public of what genes have been added to the organisms they are testing. They can be declared trade secrets, so that the public safety is left to the judgment of corporate scientists and government regulators many of whom switch back and forth between working for the government and working for the corporations they supposedly regulate.31 Those who come from academic positions often have large financial stakes in biotech companies, 32 and major universities are making agreements with biotech corporations that compromise academic freedom and give patent rights to the corporations. As universities become increasingly dependent on major corporations for funding, the majority of university scientists will no longer be able to function as independent, objective experts in matters concerning genetic engineering and public safety.32a

Scientists have already demonstrated the transfer of transgenes and marker genes to both bacterial pathogens and to soil fungi. That means genetically engineered organisms are going to enter the soil and spread to whatever grows in it. Genetically engineered material can migrate from the roots of plants into soil bacteria, in at least one case radically inhibiting the ability of the soil to grow plants.33 Once the bacteria are free in the soil, no natural barriers inhibit their spread. With ordinary soil pollution, the pollution can be confined and removed (unless it reaches the ground-water). If genetically engineered soil bacteria spreads into the wild, the ability of the soil to support plant life may seriously diminish.33a It does not take much imagination to see what the disastrous consequences might be.

Water and air are also subject to poisoning by genetically engineered viruses and bacteria.

The development of new genetically engineered crops with herbicide resistance will affect the environment through the increased use of chemical herbicides. Monsanto and other major international chemical, pharmaceutical, and agricultural corporations have staked their financial futures on genetically engineered herbicide-resistant plants.33b

Recently scientists have found a way to genetically engineer plants so that their seeds lose their viability unless sprayed with patented formulae, most of which turn out to have antibiotics as their primary ingredient. The idea is to keep farmers from collecting genetically engineered seed, thus forcing them to buy it every year. The corporations involved are unconcerned about the gene escaping into the wild, with obvious disastrous results, even though that is a clear scientific possibility.34

So that we would not have to be dependent on petroleum-based plastics, some scientists have genetically engineered plants that produce plastic within their stem structures. They claim that it biodegrades in about six months.35 If the genes escape into the wild, through cross-pollination with wild relatives or by other means, then we face the prospect of natural areas littered with the plastic spines of decayed leaves. However aesthetically repugnant that may seem, the plastic also poses a real danger. It has the potential for disrupting entire food-chains. It can be eaten by invertebrates, which are in turn eaten, and so forth. If primary foods are inedible or poisonous, then whole food-chains can die off.36

Another bright idea was to genetically engineer plants with scorpion toxin, so that insects feeding on the plants would be killed. Even though a prominent geneticist warned that the genes could be horizontally transferred to the insects themselves, so that they might be able to inject the toxin into humans, the research and field testing is continuing.37

Animals

The genetic engineering of new types of insects, fish, birds and animals has the potential of upsetting natural ecosystems. They can displace natural species and upset the balance of other species through behavior patterns that are a result of their genetic transformation.

One of the more problematic ethical uses of animals is the creation of xenographs, already mentioned above, which often involve the insertion of human genes. (See the section immediately below.) Whether or not the genes inserted to create new animals are human ones, the xenographs are created for human use and patented for corporate profit with little or no regard for the suffering of the animals, their felings and thoughts, or their natural life-patterns.

Use of Human Genes

As more and more human genes are being inserted into non-human organisms to create new forms of life that are genetically partly human, new ethical questions arise. What percent of human genes does an organism have to contain before it is considered human? For instance, how many human genes would a green pepper38 have to contain before one would have qualms about eating it? For meat-eaters, the same question could be posed about eating pork. If human beings have special ethical status, does the presence of human genes in an organism change its ethical status? What about a mouse genetically engineered to produce human sperm39 that is then used in the conception of a human child?

Several companies are working on developing pigs that have organs containing human genes in order to facilitate the use of the organs in humans. The basic idea is something like this. You can have your own personal organ donor pig with your genes implanted. When one of your organs gives out, you can use the pig's.

The U.S. Food and Drug Administration (FDA) issued a set of xenotransplant guidelines in September of 1996 that allows animal to human transplants, and puts the responsibility for health and safety at the level of local hospitals and medical review boards. A group of 44 top virologists, primate researchers, and AIDS specialists have attacked the FDA guidelines, saying, "based on knowledge of past cross-species transmissions, including AIDS, Herpes B virus, Ebola, and other viruses, the use of animals has not been adequately justified for use in a handful of patients when the potential costs could be in the hundreds, thousands or millions of human lives should a new infectious agent be transmitted."40

England has outlawed such transplants as too dangerous.41

Humans

Genetically engineered material can enter the body through food or bacteria or viruses. The dangers of lethal viruses containing genetically engineered material and created by natural processes have been mentioned above.

The dangers of generating pathogens by vector mobilization and recombination are real. Over a period of ten years, 6 scientists working with the genetic engineering of cancer-related oncogenes at the Pasteur Institutes in France have contracted cancer.42

Non-human engineered genes can also be introduced into the body through the use of genetically engineered vaccines and other medicines, and through the use of animal parts genetically engineered with human genes to combat rejection problems.

Gene therapy, for the correction of defective human genes that cause certain genetic diseases, involves the intentional introduction of new genes into the body in an attempt to modify the genetic structure of the body. It is based on a simplistic and flawed model of gene function which assumes a one-to-one correspondence between individual gene and individual function. Since horizontal interaction43 among genes has been demonstrated, introduction of a new gene can have unforeseen effects. Another problem, already mentioned, is the slippery slope that leads to the notion of designer genes. We are already on that slope with the experimental administration of genetically engineered growth hormone to healthy children, simply because they are shorter than average and their parents would like them to be taller.44

A few years ago a biotech corporation applied to the European Patent Office for a patent on a so-called 'pharm-woman,' the idea being to genetically engineer human females so that their breast-milk would contain specialized pharmaceuticals.44a Work is also ongoing to use genetic engineering to grow human breasts in the laboratory. It doesn't take much imagination to realize that not only would they be used for breast replacement needed due to cancer surgery, but also to foster a vigorous commercial demand by women in search of the "perfect" breasts.45 A geneticist has recently proposed genetically engineering headless humans to be used for body parts. Some prominent geneticists have supported his idea.46

Genetically Engineered Food

Many scientists have claimed that the ingestion of genetically engineered food is harmless because the genetically engineered materials are destroyed by stomach acids. Recent research47 suggests that genetically engineered materials are not completely destroyed by stomach acids and that significant portions reach the bloodstream and also the brain-cells. Furthermore, it has been shown that the natural defense mechanisms of body cells are not entirely effective in keeping the genetically engineered substances out of the cells.48

Some dangers of eating genetically engineered foods are already documented. Risks to human health include the probable increase in the level of toxins in foods and in the number of disease-causing organisms that are resistant to antibiotics.49 The purposeful increase in toxins in foods to make them insect-resistant is the reversal of thousands of years of selective breeding of food-plants. For example when plants are genetically engineered to resist predators, often the plant defense systems involve the synthesis of natural carcinogens.50

Industrial mistakes or carelessness in production of genetically engineered food ingredients can also cause serious problems. The l-tryptophan food supplement, an amino acid that was marketed as a natural tranquilizer and sleeping pill, was genetically engineered. It killed thirty-seven people and permanently disabled 1,500 others with an incurable nervous system condition known as eosinophilia myalgia syndrome (EMS).51

Dr. John Fagan has summarized some major risks of eating genetically engineered food as follows:

the new proteins produced in genetically engineered foods could: a) themselves, act as allergens or toxins, b) alter the metabolism of the food producing organism, causing it to produce new allergens or toxins, or c) causing it to be reduced in nutritional value.a) Mutations can damage genes naturally present in the DNA of an organism, leading to altered metabolism and to the production of toxins, and to reduced nutritional value of the food. b) Mutations can alter the expression of normal genes, leading to the production of allergens and toxins, and to reduced nutritional value of the food. c) Mutations can interfere with other essential, but yet unknown, functions of an organisms DNA.52

Basically what we have at present is a situation in which genetically engineered foods are beginning to flood the market, and no one knows what all their effects on humans will be. We are all becoming guinea pigs. Because genetically engineered food remains unlabeled, should serious problems arise, it will be extremely difficult to trace them to their source. Lack of labeling will also help to shield the corporations that are responsible from liability.

MORE BASIC ETHICAL PROBLEMS

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Zip codes: 88240, 88242.

Hobbs city income, earnings, and wages data

Estimated median house or condo value in 2013: $106,484 (it was $48,400 in 2000)

Median gross rent in 2013: $927.

Hobbs, NM residents, houses, and apartments details

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Ancestries: Irish (5.9%), German (5.7%), United States (5.0%), English (4.8%), Italian (1.0%).

Current Local Time: MST time zone

Incorporated in 1929

Elevation: 3621 feet

Land area: 18.9 square miles.

Population density: 1,961 people per square mile (low).

3,094 residents are foreign born (10.2% Latin America).

According to our research of New Mexico and other state lists there were 48 registered sex offenders living in Hobbs, New Mexico as of May 15, 2016. The ratio of number of residents in Hobbs to the number of sex offenders is 729 to 1. The number of registered sex offenders compared to the number of residents in this city is near the state average.

Median real estate property taxes paid for housing units with mortgages in 2013: $698 (0.5%) Median real estate property taxes paid for housing units with no mortgage in 2013: $410 (0.4%)

Nearest city with pop. 50,000+: Odessa, TX (74.2 miles , pop. 90,943).

Nearest city with pop. 200,000+: El Paso, TX (202.3 miles , pop. 563,662).

Nearest city with pop. 1,000,000+: San Antonio, TX (354.9 miles , pop. 1,144,646).

Nearest cities: North Hobbs, NM (2.1 miles ), Nadine, NM (2.5 miles ), Monument, NM (3.1 miles ), Eunice, NM (4.3 miles ), Lovington, NM (4.5 miles ), Denver City, TX (5.0 miles ), Seminole, TX (5.3 miles ), Seagraves, TX (6.1 miles ).

Number of permits per 10,000 residents

Latitude: 32.71 N, Longitude: 103.14 W

Daytime population change due to commuting: +2,335 (+6.5%) Workers who live and work in this city: 11,466 (75.4%)

Area code: 505

(click on a table row to update graph)

Crime rate in Hobbs detailed stats: murders, rapes, robberies, assaults, burglaries, thefts, arson Full-time law enforcement employees in 2012, including police officers: 84 (75 officers).

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Hobbs, New Mexico accommodation, waste management, arts - Economy and Business Data

Work and jobs in Hobbs: detailed stats about occupations, industries, unemployment, workers, commute

Based on data reported by over 4,000 weather stations

Hobbs-area historical tornado activity is significantly above New Mexico state average. It is 36% smaller than the overall U.S. average.

On 5/17/1954, a category F3 (max. wind speeds 158-206 mph) tornado 22.3 miles away from the Hobbs city center .

On 4/19/1969, a category F3 tornado 27.4 miles away from the city center caused between $500 and $5000 in damages.

On 4/14/1995 at 00:32:56, a magnitude 5.7 (5.6 MB, 5.7 MS, 5.7 MW, Depth: 11.1 mi, Class: Moderate, Intensity: VI - VII) earthquake occurred 168.8 miles away from the city center On 1/2/1992 at 11:45:35, a magnitude 5.0 (4.6 MB, 5.0 LG, Depth: 3.1 mi) earthquake occurred 26.2 miles away from Hobbs center On 6/16/1978 at 11:46:54, a magnitude 5.3 (4.4 MB, 4.6 UK, 5.3 ML) earthquake occurred 139.7 miles away from the city center On 12/19/2005 at 20:27:40, a magnitude 4.3 (4.3 MB, 4.1 MW, Depth: 3.1 mi, Class: Light, Intensity: IV - V) earthquake occurred 83.0 miles away from the city center On 5/23/2004 at 09:22:05, a magnitude 4.0 (4.0 MB, 4.0 LG, Depth: 3.1 mi) earthquake occurred 84.0 miles away from Hobbs center On 3/14/1999 at 22:43:17, a magnitude 4.0 (4.0 MD, 4.0 LG, Depth: 0.6 mi) earthquake occurred 87.1 miles away from the city center Magnitude types: regional Lg-wave magnitude (LG), body-wave magnitude (MB), duration magnitude (MD), local magnitude (ML), surface-wave magnitude (MS), moment magnitude (MW)

Causes of natural disasters: Fires: 2, Hurricane: 1 (Note: Some incidents may be assigned to more than one category).

Birthplace of: Colt McCoy - College football player, Ryan Bingham - Male singer, Rob Evans - College basketball coach, Bill Bridges (basketball) - Basketball player, Mike Chenault - Politician, Allen Haynes - College basketball player (New Mexico State Aggies), Mike May (Iowa politician) - Politician, Ronald Ross - College basketball player (Texas Tech Red Raiders), Scott Terry - Baseball player, Timmy Smith - Former professional football player.

Political contributions by individuals in Hobbs, NM

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Notable locations in Hobbs: Dal Paso Center (A), Heritage Square (B), Hobbs Weather Station (C), New Mexico Junior College Parnell Library (D), College of the Southwest Scarborough Memorial Library (E), Hobbs Public Library (F), City of Hobbs Fire Department Station 3 (G), City of Hobbs Fire Department Station 1 (H), City of Hobbs Fire Department Station 2 (I). Display/hide their locations on the map

Shopping Centers: Broadmoor Shopping Center and Mall (1), Broadmoor Shopping Center (2), Bel Aire Shopping Center (3), Downtown Mini Mall (4). Display/hide their locations on the map

Churches in Hobbs include: Church of the Nazarene (A), Grace Lutheran Church (B), First Church of Christ Scientist (C), Church of Christ (D), Taylor Saint Church of Christ (E), Christian Center (F), Aldersgate Church (G), Nadine Baptist Church (H), Calvary Baptist Church (I). Display/hide their locations on the map

Cemeteries: Memdry Gardens (1), Memorial Park Cemetery (2). Display/hide their locations on the map

Parks in Hobbs include: Harry McAdams State Park (1), Oil County Historical Marker (2), Heizer Park (3), Eagle Stadium (4), Bender Park (5), Humble Park (6), Green Acre Park (7), Hobbs Historical Marker (8), Bensing Park (9). Display/hide their locations on the map

Tourist attractions: Lea CO Cowboy Hall of Fame & Western Heritage Center (Museums; 5317 North Lovington Highway) (1), New Mexico Junior College - Cowboy Hall of Fame & Museum- Public-Community Serv (5317 North Lovington Highway) (2), Libraries-Public - Hobbs (Cultural Attractions- Events- & Facilities; 509 North Shipp Street) (3), M & M Tours (Tours & Charters; Po Box 247) (4), New Mexico Discus (Tours & Charters; 6401 North Lovington Highway) (5). Display/hide their approximate locations on the map

Hotels: Lamplighter Motel (110 East Marland Street) (1), Best Western Executive Inn (309 North Marland Boulevard) (2), Best Inn (501 North Marland Boulevard) (3), Hobbs Inn (722 North Marland Boulevard) (4), Sands Motel (1300 East Broadway Street) (5), Western Holiday Motel (2724 West Marland Street) (6), Desert Hills Motel (129 South Marland Place) (7), Relax Inn (509 N Marlan Blvd) (8), Econo Lodge (619 North Marland Boulevard) (9). Display/hide their approximate locations on the map

Courts: New Mexico - State - Magistrate Court- Division No 2- Employment Services Divi (2110 North Alto Drive) (1), Social Security Administration (501 East Bender) (2), Lea - County - Hobbs- Teen Court (801 North Linam Street) (3). Display/hide their approximate locations on the map

Air pollution and air quality trends (lower is better)

Air Quality Index (AQI) level in 2013 was 64.5. This is about average.

Nitrogen Dioxide (NO2) [ppb] level in 2013 was 4.19. This is significantly better than average. Closest monitor was 0.7 miles away from the city center.

Ozone [ppb] level in 2013 was 30.9. This is about average. Closest monitor was 1.4 miles away from the city center.

Particulate Matter (PM10) [g/m3] level in 2013 was 18.9. This is about average. Closest monitor was 0.7 miles away from the city center.

Particulate Matter (PM2.5) [g/m3] level in 2013 was 8.34. This is about average. Closest monitor was 1.1 miles away from the city center.

Detailed information about poverty and poor residents in Hobbs, NM

Educational Attainment (%) in 2013

School Enrollment by Level of School (%) in 2013

Presidential Elections Results

1996 Presidential Elections Results

2000 Presidential Elections Results

2004 Presidential Elections Results

2008 Presidential Elections Results

2012 Presidential Elections Results

Graphs represent county-level data. Detailed 2008 Election Results

5.81% of this county's 2011 resident taxpayers lived in other counties in 2010 ($37,469 average adjusted gross income)

6.07% of this county's 2010 resident taxpayers moved to other counties in 2011 ($40,120 average adjusted gross income)

Fatal accident count (per 100,000 population)

Most commonly used house heating fuel:

Top Patent Applicants

Total of 13 patent applications in 2008-2016.

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Hobbs, New Mexico - City-Data.com

Are applicants for a driver's license asked questions about diabetes?

Yes. The driver's license application (first-time and renewal) asks an applicant whether he or she has diabetes. If an applicant answers yes to this question, he or she is required to have a physician complete a medical report form. N.M. Stat. Ann. 66-5-14(A) (2013) (generally authorizing the licensing agency to examine driver's license applicants for "anyphysical and mental examination as [it] finds necessary to determine the applicant's fitness to operate a motor vehicle or motorcycle safely upon the highways").

What other ways does the state have to find out about people who may not be able to drive safely because of a medical condition?

The state accepts reports of potentially unsafe drivers from police officers, physicians, family members, friends, other citizens, and hospitals. The licensing agency accepts anonymous reports and does not investigate reports before a driver is contacted for medical review. Drivers also may be required to have medical evaluations if they are involved in a given number of at-fault crashes within a given time period, if they are involved in at-fault crashes resulting in a fatality, or if they have impairments which are observed by licensing agency personnel during the licensing process. N.M. Stat. Ann. 66-5-30(A)(2), (B) (2013) (authorizing the licensing agency to suspend or revoke a driver's license because of his or her involvement in an accident and providing for reinstatement after reexamination); N.M. Stat. Ann. 66-5-31 (2013) (authorizing the licensing agency to compel a medical evaluation if it has good cause to believe that a driver is incompetent or otherwise unqualified to be licensed).

What is the process for medical evaluations of drivers?

Individuals with diabetes must undergo medical evaluations when applying for driver's licenses for the first time and at all subsequent renewals. A Medical Report Form (MVD10124) is sent to an individual, which must be completed by his or her physician within 30 days. The Medical Report Form asks the physician whether the patient has diabetes, hypoglycemia, loss of consciousness, or other conditions. N.M. Motor Vehicle Division, "Medical Report," Form MVD10124 (Rev. 06/2013). If so, the physician must describe the condition and its treatment (including any medications that the patient is taking); to state whether the condition is currently controlled; and to provide test results that may be relevant. The physician also is asked to give an opinion on the following 1) whether, medically speaking, the individual is capable of safe and competent driving; 2) whether the individual suffers from any abnormal personality traits; 3) whether there should be any appropriate licensing restrictions; and 4) how often follow up any medical evaluations should be required. N.M. Motor Vehicle Division, "Medical Report," Form MVD10124 (Rev. 06/2013). Medical Report Forms are returned to the licensing agency for review and a licensing decision.

Are physicians required by law to report drivers who have medical conditions that could affect their ability to drive safely?

There is no statutory authority requiring physicians to report drivers with medical conditions that could affect their ability to drive safely to a central state agency.

Are physicians who report drivers with medical conditions immune from legal action by the patient?

There is no statutory authority providing immunity from civil or criminal liability for physicians who report or fail to report drivers with conditions that could affect their ability to drive safely to a central state agency.

Who makes decisions about whether drivers are medically qualified?

For individuals that do not take insulin or take insulin and have been under treatment for at least eight years, licensing agency personnel will issue a license so long as an individual's physician indicates on the medical evaluation form that he or she is medically fit to drive. Individuals that do not meet this condition, i.e., that have been taking insulin for less than eight years, are referred to the state's independent Health Standards Advisory Board. When diabetes cases are referred to the board, one membera general medical doctor, not an endocrinologistgenerally makes decisions, and the process generally takes four to eight weeks. The board may require additional on-the-road examinations or any other physical tests recommended by the Board. N.M. Stat. Ann. 66-5-6(B)-(C) (2013) (board may require road tests or other examinations). Although the Health Standards Advisory Board may advise licensing agency personnel with regard to licensing decisions, N.M. Stat. Ann. 66-5-6(B)-(C) (2013), ultimate authority over licensing decisions resides with the licensing agency itself. N.M. Stat. Ann. 66-5-24(A), -30(A)(1)-(11) (2013).

What are the circumstances under which a driver may be required to undergo a medical evaluation?

Upon five days' written notice, a driver may be required to undergo a medical evaluation if the licensing agency has good cause to believe that he or she is incompetent or otherwise unqualified to be licensed. N.M. Stat. Ann. 66-5-31 (2013). A driver may be required to undergo a medical evaluation if, upon review of his or her case, the Health Standards Advisory Board determines that such an evaluation is necessary to making a recommendation as to a licensing decision. N.M. Stat. Ann. 66-5-6(C) (2013). Drivers also may be required to have medical evaluations if they are involved in a given number of at-fault crashes within a given time period, if they are involved in at-fault crashes resulting in a fatality, or if they have impairments which are observed by licensing agency personnel during the licensing process. N.M. Stat. Ann. 66-5-30(A)(2), (B) (2013) (authorizing the licensing agency to suspend or revoke a driver's license because of his or her involvement in an accident and providing for reinstatement conditioned upon reexamination); N.M. Stat. Ann. 66-5-31 (2013) (authorizing the licensing agency to compel a medical evaluation if it has good cause to believe that a driver is incompetent or otherwise unqualified to be licensed).

Has the state adopted specific policies about whether people with diabetes are allowed to drive?

No. New Mexico has adopted no specific medical guidelines related to diabetes since most diabetes cases are decided on a case-by-case basis by the Health Standards Advisory Board.

What is the state's policy about episodes of altered consciousness or loss of consciousness that may be due to diabetes?

New Mexico has not adopted a policy about episodes of loss of consciousness but is working to develop such a policy. The state has adopted a policy regarding seizures, however, which requires that an individual who has had a seizure submit to the licensing agency a statement from a physician indicating that he or she has been seizure or episode-free for at least one year and that he or she either is not under medication or is taking medication without side effects before he or she will be licensed. N.M. Code R. 18.19.5.34(B) (2013). If an individual that has had a seizure has been issued a restricted license, the licensing agency may remove any restrictions early if the individual is able to produce a satisfactory physician's statement. N.M. Code R. 18.19.5.34(A) (2013).

Does the state allow for waivers of this policy, e.g., a waiver for a one-time episode of severe hypoglycemia that has mitigating factors (e.g., recent change in medication, illness, etc.) or that has been addressed with a physician?

No. There is no statutory authority providing for exceptions to New Mexico's policy regarding episodes of loss of consciousness and driver licensing. Again, if an individual that has had a seizure has been issued a restricted license, the licensing agency may remove any restrictions early if the individual is able to produce a satisfactory physician's statement, as described above. N.M. Code R. 18.19.5.34(A) (2013).

What is the process for appealing a decision of the state regarding a driver's license?

An individual may make a written request for a hearing in the county in which he or she resides, which must be received by the licensing agency within 20 days of the suspension notice. N.M. Stat. Ann. 66-5-30(B) (2013) (describing hearing process in detail). The licensing agency, in its discretion, may extend the 20-day request period. A hearing then is held so that an individual may provide proof as to his or her ability to operate a motor vehicle safely. Both the individual and the licensing agency may present evidence and testimony, and the individual may be required to undergo a driver examination. The licensing agency then will rescind, continue, modify, or extend the suspension. N.M. Stat. Ann. 66-5-30(B) (2013). Except in cases of mandatory suspension or revocation, decisions of the licensing agency also may be appealed to the district court. N.M. Stat. Ann. 66-5-36 (2013). For more information, see N.M. Motor Vehicle Division, "Hearing Requests," (Accessed 2013); N.M. Motor Vehicle Division, "Request for Hearing," Form MVD-10792 (Rev. 12/2008).

May an individual whose license is suspended or denied because of diabetes receive a probationary or restricted license?

No. However, the licensing agency may, whenever good cause appears, issue a license with restrictions, including the shortening of the licensure period, appropriate to ensure the safe operation of a motor vehicle by the licensee. N.M. Stat. Ann. 66-5-19(A) (2013); N.M. Code R. 18.19.5.32, 18.19.5.3(A) (2013) (providing for the issuance of restricted licenses, or licenses with shorter licensure periods).

Is an identification card available for non-drivers?

Yes, with proper identification, proof of residency, and payment of a fee. See N.M. Stat. Ann. 66-5-402 (2013) (describing identification and proof of residency requirements); N.M. Code R. 18.19.5.12(A) (2013) (same). An individual may not hold an identification card and a driver's license concurrently. N.M. Stat. Ann. 66-5-401(A), -402(A) (2013). An identification card is valid for a period of four years or, at the election of the holder, a period of eight years if he or she pays the applicable fee for an eight-year period. N.M. Stat. Ann. 66-5-403(A), (C) (2013). A $5.00 fee is required upon application for an identification card with a four-year term, and a $10.00 fee is required upon application for an identification card with an eight-year term. N.M. Stat. Ann. 66-5-408(A) (2013). Individuals 75 years of age or older may obtain identification cards free of charge. N.M. Stat. Ann. 66-5-408(A) (2013).

Resources

Driver licensing in New Mexico is administered by the Motor Vehicle Division of the State Taxation and Revenue Department.

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New Mexico: American Diabetes Association

Gene therapy is the therapeutic delivery of nucleic acid polymers into a patients cells as a drug to treat disease. Until September 1990, it had never been successfully done, and it is still an experimental and emerging medical technology that has seen new promise in the 2010s after extensive challenges and setbacks in the first two decades of its existence.

Between September 1990 and January 2014 some 2,000 clinical trials had been conducted or approved.[1][2]

It should be noted that not all medical procedures that introduce alterations to a patients genetic makeup can be considered gene therapy. Bone marrow transplantation, and organ transplants in general have been found to introduce foreign DNA into patients. [3] Gene therapy is defined by the precision of the procedure and the intention of direct therapeutic effects.

Gene therapy was conceptualized in 1972, by authors who urged caution before commencing human gene therapy studies.

The first attempt, albeit an unsuccessful one, at gene therapy was performed by Martin Cline on 10 July 1980.[4][5]

After extensive research on animals throughout the 1980s and a May 1989 bacterial gene tagging trial on humans, transitory (non-permanent) somatic (non-inheritable) gene therapy was first successfully demonstrated in a trial that started on September 14, 1990, when Ashi DeSilva was treated for ADA-SCID.[6]

The first somatic treatment that produced a permanent genetic change was performed in 1993. [7]

The first germ line gene therapy consisted of producing a genetically engineered embryo in October of 1996. The baby was born on July 21, 1997 and was produced by taking a donors egg with healthy mitochondria, removing its nuclear DNA and filling it with the nuclear DNA of the biological mother a procedure known as cytoplasmic transfer.[8]

This procedure was referred to sensationally and somewhat inaccurately in the media as a three parent baby, though mtDNA is not the primary human genome and has little effect on an organisms individual characteristics beyond powering their cells.

Gene therapy is a way to fix a genetic problem at its source. The polymers are either expressed as proteins, interfere with protein expression, or possibly correct genetic mutations.

The most common form uses DNA that encodes a functional, therapeutic gene to replace a mutated gene. The polymer molecule is packaged within a vector, which carries the molecule inside cells.

Early clinical failures led to dismissals of gene therapy. Clinical successes since 2006 regained researchers attention, although as of 2014, it was still largely an experimental technique.[9] These include treatment of retinal disease Lebers congenital amaurosis,[10][11][12][13]X-linked SCID,[14] ADA-SCID,[15][16]adrenoleukodystrophy,[17]chronic lymphocytic leukemia (CLL),[18]acute lymphocytic leukemia (ALL),[19]multiple myeloma,[20]haemophilia[16] and Parkinsons disease.[21] Between 2013 and April 2014, US companies invested over $600 million in the field.[22]

The first commercial gene therapy, Gendicine, was approved in China in 2003 for the treatment of certain cancers.[23] In 2011 Neovasculgen was registered in Russia as the first-in-class gene-therapy drug for treatment of peripheral artery disease, including critical limb ischemia.[24] In 2012 Glybera, a treatment for a rare inherited disorder, became the first treatment to be approved for clinical use in either Europe or the United States after its endorsement by the European Commission.[9][25]

Following early advances in genetic engineering of bacteria, cells and small animals, scientists started considering how to apply it to medicine. Two main approaches were considered replacing or disrupting defective genes.[26] Scientists focused on diseases caused by single-gene defects, such as cystic fibrosis, haemophilia, muscular dystrophy, thalassemia and sickle cell anemia. Glybera treats one such disease, caused by a defect in lipoprotein lipase.[25]

DNA must be administered, reach the damaged cells, enter the cell and express/disrupt a protein.[27] Multiple delivery techniques have been explored. The initial approach incorporated DNA into an engineered virus to deliver the DNA into a chromosome.[28][29]Naked DNA approaches have also been explored, especially in the context of vaccine development.[30]

Generally, efforts focused on administering a gene that causes a needed protein to be expressed. More recently, increased understanding of nuclease function has led to more direct DNA editing, using techniques such as zinc finger nucleases and CRISPR. The vector incorporates genes into chromosomes. The expressed nucleases then edit the chromosome. As of 2014 these approaches involve removing cells from patients, editing a chromosome and returning the transformed cells to patients.[31]

Other technologies employ antisense, small interfering RNA and other DNA. To the extent that these technologies do not alter DNA, but instead directly interact with molecules such as RNA, they are not considered gene therapy per se.[citation needed]

Gene therapy may be classified into two types:

In somatic cell gene therapy (SCGT), the therapeutic genes are transferred into any of any cell other than a gamete, germ cell, gametocyte or undifferentiated stem cell. Any such modifications affect the individual patient only, and are not inherited by offspring. Somatic gene therapy represents mainstream basic and clinical research, in which therapeutic DNA (either integrated in the genome or as an external episome or plasmid) is used to treat disease.

Over 600 clinical trials utilizing SCGT are underway in the US. Most focus on severe genetic disorders, including immunodeficiencies, haemophilia, thalassaemia and cystic fibrosis. Such single gene disorders are good candidates for somatic cell therapy. The complete correction of a genetic disorder or the replacement of multiple genes is not yet possible. Only a few of the trials are in the advanced stages.[32]

In germline gene therapy (GGT), germ cells (sperm or eggs) are modified by the introduction of functional genes into their genomes. Modifying a germ cell causes all the organisms cells to contain the modified gene. The change is therefore heritable and passed on to later generations. Australia, Canada, Germany, Israel, Switzerland and the Netherlands[33] prohibit GGT for application in human beings, for technical and ethical reasons, including insufficient knowledge about possible risks to future generations[33] and higher risks versus SCGT.[34] The US has no federal controls specifically addressing human genetic modification (beyond FDA regulations for therapies in general).[33][35][36][37]

The delivery of DNA into cells can be accomplished by multiple methods. The two major classes are recombinant viruses (sometimes called biological nanoparticles or viral vectors) and naked DNA or DNA complexes (non-viral methods).

In order to replicate, viruses introduce their genetic material into the host cell, tricking the hosts cellular machinery into using it as blueprints for viral proteins. Scientists exploit this by substituting a viruss genetic material with therapeutic DNA. (The term DNA may be an oversimplification, as some viruses contain RNA, and gene therapy could take this form as well.) A number of viruses have been used for human gene therapy, including retrovirus, adenovirus, lentivirus, herpes simplex, vaccinia and adeno-associated virus.[1] Like the genetic material (DNA or RNA) in viruses, therapeutic DNA can be designed to simply serve as a temporary blueprint that is degraded naturally or (at least theoretically) to enter the hosts genome, becoming a permanent part of the hosts DNA in infected cells.

Non-viral methods present certain advantages over viral methods, such as large scale production and low host immunogenicity. However, non-viral methods initially produced lower levels of transfection and gene expression, and thus lower therapeutic efficacy. Later technology remedied this deficiency[citation needed].

Methods for non-viral gene therapy include the injection of naked DNA, electroporation, the gene gun, sonoporation, magnetofection, the use of oligonucleotides, lipoplexes, dendrimers, and inorganic nanoparticles.

Some of the unsolved problems include:

Three patients deaths have been reported in gene therapy trials, putting the field under close scrutiny. The first was that of Jesse Gelsinger in 1999.[44] One X-SCID patient died of leukemia in 2003.[6] In 2007, a rheumatoid arthritis patient died from an infection; the subsequent investigation concluded that the death was not related to gene therapy.[45]

In 1972 Friedmann and Roblin authored a paper in Science titled Gene therapy for human genetic disease?[46] Rogers (1970) was cited for proposing that exogenous good DNA be used to replace the defective DNA in those who suffer from genetic defects.[47]

In 1984 a retrovirus vector system was designed that could efficiently insert foreign genes into mammalian chromosomes.[48]

The first approved gene therapy in the US took place on 14 September 1990, at the National Institutes of Health (NIH), under the direction of William French Anderson.[49] Four-year-old Ashanti DeSilva received treatment for a genetic defect that left her with ADA-SCID, a severe immune system deficiency. The effects were temporary, but successful.[50]

Cancer gene therapy was introduced in 1992/93.[51] The treatment of glioblastoma multiforme, the malignant brain tumor whose outcome is always fatal, was done using a vector expressing antisense IGF-I RNA (clinical trial approved by NIH n 1602, and FDA in 1994). The therapy proved to be effective due to the anti-tumor mechanism of IGF-I antisense, which is related to strong immune and apoptotic phenomena. For this reason this strategy can be considered also as immunotherapy.[52]

In 1992 Claudio Bordignon, working at the Vita-Salute San Raffaele University, performed the first gene therapy procedure using hematopoietic stem cells as vectors to deliver genes intended to correct hereditary diseases.[53] In 2002 this work led to the publication of the first successful gene therapy treatment for adenosine deaminase-deficiency (SCID). The success of a multi-center trial for treating children with SCID (severe combined immune deficiency or bubble boy disease) from 2000 and 2002, was questioned when two of the ten children treated at the trials Paris center developed a leukemia-like condition. Clinical trials were halted temporarily in 2002, but resumed after regulatory review of the protocol in the US, the United Kingdom, France, Italy and Germany.[54]

In 1993 Andrew Gobea was born with SCID following prenatal genetic screening. Blood was removed from his mothers placenta and umbilical cord immediately after birth, to acquire stem cells. The allele that codes for adenosine deaminase (ADA) was obtained and inserted into a retrovirus. Retroviruses and stem cells were mixed, after which the viruses inserted the gene into the stem cell chromosomes. Stem cells containing the working ADA gene were injected into Andrews blood. Injections of the ADA enzyme were also given weekly. For four years T cells (white blood cells), produced by stem cells, made ADA enzymes using the ADA gene. After four years more treatment was needed.[citation needed]

Jesse Gelsingers death in 1999 impeded gene therapy research in the US.[55][56] As a result, the FDA suspended several clinical trials pending the reevaluation of ethical and procedural practices.[57]

The modified cancer gene therapy strategy of antisense IGF-I RNA (NIH n 1602)[58] using antisense / triple helix anti IGF-I approach was registered in 2002 by Wiley gene therapy clinical trial n 635 and 636. The approach has shown promising results in the treatment of six different malignant tumors: glioblastoma, cancers of liver, colon, prostate, uterus and ovary (Collaborative NATO Science Programme on Gene Therapy USA, France, Poland n LST 980517 conducted by J. Trojan) (Trojan et al., 2012). This antigene antisense/triple helix therapy has proven to be efficient, due to the mechanism stopping simultaneously IGF-I expression on translation and transcription levels, strengthening anti-tumor immune and apoptotic phenomenons (Trojan et al., 2013).[59]

Sickle-cell disease can be treated in mice.[60] The mice which have essentially the same defect that causes human cases used a viral vector to induce production of fetal hemoglobin (HbF), which normally ceases to be produced shortly after birth. In humans, the use of hydroxyurea to stimulate the production of HbF temporarily alleviates sickle cell symptoms. The researchers demonstrated this treatment to be a more permanent means to increase therapeutic HbF production.[61]

A new gene therapy approach repaired errors in messenger RNA derived from defective genes. This technique has the potential to treat thalassaemia, cystic fibrosis and some cancers.[62]

Researchers created liposomes 25 nanometers across that can carry therapeutic DNA through pores in the nuclear membrane.[63]

In 2003 a research team inserted genes into the brain for the first time. They used liposomes coated in a polymer called polyethylene glycol, which, unlike viral vectors, are small enough to cross the bloodbrain barrier.[64]

Short pieces of double-stranded RNA (short, interfering RNAs or siRNAs) are used by cells to degrade RNA of a particular sequence. If a siRNA is designed to match the RNA copied from a faulty gene, then the abnormal protein product of that gene will not be produced.[65]

Gendicine is a cancer gene therapy that delivers the tumor suppressor gene p53 using an engineered adenovirus. In 2003, it was approved in China for the treatment of head and neck squamous cell carcinoma.[23]

In March researchers announced the successful use of gene therapy to treat two adult patients for X-linked chronic granulomatous disease, a disease which affects myeloid cells and damages the immune system. The study is the first to show that gene therapy can treat the myeloid system.[66]

In May a team reported a way to prevent the immune system from rejecting a newly delivered gene.[67] Similar to organ transplantation, gene therapy has been plagued by this problem. The immune system normally recognizes the new gene as foreign and rejects the cells carrying it. The research utilized a newly uncovered network of genes regulated by molecules known as microRNAs. This natural function selectively obscured their therapeutic gene in immune system cells and protected it from discovery. Mice infected with the gene containing an immune-cell microRNA target sequence did not reject the gene.

In August scientists successfully treated metastatic melanoma in two patients using killer T cells genetically retargeted to attack the cancer cells.[68]

In November researchers reported on the use of VRX496, a gene-based immunotherapy for the treatment of HIV that uses a lentiviral vector to deliver an antisense gene against the HIV envelope. In a phase I clinical trial, five subjects with chronic HIV infection who had failed to respond to at least two antiretroviral regimens were treated. A single intravenous infusion of autologous CD4 T cells genetically modified with VRX496 was well tolerated. All patients had stable or decreased viral load; four of the five patients had stable or increased CD4 T cell counts. All five patients had stable or increased immune response to HIV antigens and other pathogens. This was the first evaluation of a lentiviral vector administered in a US human clinical trial.[69][70]

In May researchers announced the first gene therapy trial for inherited retinal disease. The first operation was carried out on a 23-year-old British male, Robert Johnson, in early 2007.[71]

Lebers congenital amaurosis is an inherited blinding disease caused by mutations in the RPE65 gene. The results of a small clinical trial in children were published in April.[72] Delivery of recombinant adeno-associated virus (AAV) carrying RPE65 yielded positive results. In May two more groups reported positive results in independent clinical trials using gene therapy to treat the condition. In all three clinical trials, patients recovered functional vision without apparent side-effects.[10][11][12][13]

In September researchers were able to give trichromatic vision to squirrel monkeys.[73] In November 2009, researchers halted a fatal genetic disorder called adrenoleukodystrophy in two children using a lentivirus vector to deliver a functioning version of ABCD1, the gene that is mutated in the disorder.[74]

An April paper reported that gene therapy addressed achromatopsia (color blindness) in dogs by targeting cone photoreceptors. Cone function and day vision were restored for at least 33 months in two young specimens. The therapy was less efficient for older dogs.[75]

In September it was announced that an 18-year-old male patient in France with beta-thalassemia major had been successfully treated.[76] Beta-thalassemia major is an inherited blood disease in which beta haemoglobin is missing and patients are dependent on regular lifelong blood transfusions.[77] The technique used a lentiviral vector to transduce the human -globin gene into purified blood and marrow cells obtained from the patient in June 2007.[78] The patients haemoglobin levels were stable at 9 to 10 g/dL. About a third of the hemoglobin contained the form introduced by the viral vector and blood transfusions were not needed.[78][79] Further clinical trials were planned.[80]Bone marrow transplants are the only cure for thalassemia, but 75% of patients do not find a matching donor.[79]

In 2007 and 2008, a man was cured of HIV by repeated Hematopoietic stem cell transplantation (see also Allogeneic stem cell transplantation, Allogeneic bone marrow transplantation, Allotransplantation) with double-delta-32 mutation which disables the CCR5 receptor. This cure was accepted by the medical community in 2011.[81] It required complete ablation of existing bone marrow, which is very debilitating.

In August two of three subjects of a pilot study were confirmed to have been cured from chronic lymphocytic leukemia (CLL). The therapy used genetically modified T cells to attack cells that expressed the CD19 protein to fight the disease.[18] In 2013, the researchers announced that 26 of 59 patients had achieved complete remission and the original patient had remained tumor-free.[82]

Human HGF plasmid DNA therapy of cardiomyocytes is being examined as a potential treatment for coronary artery disease as well as treatment for the damage that occurs to the heart after myocardial infarction.[83][84]

n 2011 Neovasculgen was registered in Russia as the first-in-class gene-therapy drug for treatment of peripheral artery disease, including critical limb ischemia.[24] Neovasculogen is a plasmid encoding the CMV promoter and the 165 amino acid form of VEGF.[85][86]

The FDA approved Phase 1 clinical trials on thalassemia major patients in the US for 10 participants in July.[87] The study was expected to continue until 2015.[88]

In July 2012, the European Medicines Agency recommended approval of a gene therapy treatment for the first time in either Europe or the United States. The treatment used Alipogene tiparvovec (Glybera) to compensate for lipoprotein lipase deficiency, which can cause severe pancreatitis.[89] The recommendation was endorsed by the European Commission in November 2012[9][25][90][91] and commercial rollout began in late 2014.[92]

In December 2012, it was reported that 10 of 13 patients with multiple myeloma were in remission or very close to it three months after being injected with a treatment involving genetically engineered T cells to target proteins NY-ESO-1 and LAGE-1, which exist only on cancerous myeloma cells.[20]

In March researchers reported that three of five subjects who had acute lymphocytic leukemia (ALL) had been in remission for five months to two years after being treated with genetically modified T cells which attacked cells with CD19 genes on their surface, i.e. all B-cells, cancerous or not. The researchers believed that the patients immune systems would make normal T-cells and B-cells after a couple of months. They were also given bone marrow. One patient relapsed and died and one died of a blood clot unrelated to the disease.[19]

Following encouraging Phase 1 trials, in April, researchers announced they were starting Phase 2 clinical trials (called CUPID2 and SERCA-LVAD) on 250 patients[93] at several hospitals to combat heart disease. The therapy was designed to increase the levels of SERCA2a protein in heart muscles, improving muscle function.[94] The FDA granted this a Breakthrough Therapy Designation to accelerate the trial and approval process.[95]

In July researchers reported promising results for six children with two severe hereditary diseases had been treated with a partially deactivated lentivirus to replace a faulty gene and after 732 months. Three of the children had metachromatic leukodystrophy, which causes children to lose cognitive and motor skills.[96] The other children had Wiskott-Aldrich syndrome, which leaves them to open to infection, autoimmune diseases and cancer.[97] Follow up trials with gene therapy on another six children with Wiskott-Aldrich syndrome were also reported as promising.[98][99]

In October researchers reported that two children born with adenosine deaminase severe combined immunodeficiency disease (ADA-SCID) had been treated with genetically engineered stem cells 18 months previously and that their immune systems were showing signs of full recovery. Another three children were making progress.[16] In 2014 a further 18 children with ADA-SCID were cured by gene therapy.[100] ADA-SCID children have no functioning immune system and are sometimes known as bubble children.[16]

Also in October researchers reported that they had treated six haemophilia sufferers in early 2011 using an adeno-associated virus. Over two years later all six were producing clotting factor.[16][101]

Data from three trials on Topical cystic fibrosis transmembrane conductance regulator gene therapy were reported to not support its clinical use as a mist inhaled into the lungs to treat cystic fibrosis patients with lung infections.[102]

In January researchers reported that six choroideremia patients had been treated with adeno-associated virus with a copy of REP1. Over a six-month to two-year period all had improved their sight. Choroideremia is an inherited genetic eye disease with no approved treatment, leading to loss of sight.[103][104]

In March researchers reported that 12 HIV patients had been treated since 2009 in a trial with a genetically engineered virus with a rare mutation (CCR5 deficiency) known to protect against HIV with promising results.[105][106]

Clinical trials of gene therapy for sickle cell disease were started in 2014[107][108] although one review failed to find any such trials.[109]

In February LentiGlobin BB305, a gene therapy treatment undergoing clinical trials for treatment of beta thalassemia gained FDA breakthrough status after several patients were able to forgo the frequent blood transfusions usually required to treat the disease.[110]

In March researchers delivered a recombinant gene encoding a broadly neutralizing antibody into monkeys infected with simian HIV; the monkeys cells produced the antibody, which cleared them of HIV. The technique is named immunoprophylaxis by gene transfer (IGT). Animal tests for antibodies to ebola, malaria, influenza and hepatitis are underway.[111][112]

In March scientists, including an inventor of CRISPR, urged a worldwide moratorium on germline gene therapy, writing scientists should avoid even attempting, in lax jurisdictions, germline genome modification for clinical application in humans until the full implications are discussed among scientific and governmental organizations.[113][114][115][116]

Also in 2015 Glybera was approved for the German market.[117]

Speculated uses for gene therapy include:

Athletes might adopt gene therapy technologies to improve their performance.[118]Gene doping is not known to occur, but multiple gene therapies may have such effects. Kayser et al. argue that gene doping could level the playing field if all athletes receive equal access. Critics claim that any therapeutic intervention for non-therapeutic/enhancement purposes compromises the ethical foundations of medicine and sports.[119]

Genetic engineering could be used to change physical appearance, metabolism, and even improve physical capabilities and mental faculties such as memory and intelligence. Ethical claims about germline engineering include beliefs that every fetus has a right to remain genetically unmodified, that parents hold such rights, and that every child has the right to be born free of preventable diseases.[120][121][122] For adults, genetic engineering could be seen as another enhancement technique to add to diet, exercise, education, cosmetics and plastic surgery.[123][124] Another theorist claims that moral concerns limit but do not prohibit germline engineering.[125]

Possible regulatory schemes include a complete ban, provision to everyone, or professional self-regulation. The American Medical Associations Council on Ethical and Judicial Affairs stated that genetic interventions to enhance traits should be considered permissible only in severely restricted situations: (1) clear and meaningful benefits to the fetus or child; (2) no trade-off with other characteristics or traits; and (3) equal access to the genetic technology, irrespective of income or other socioeconomic characteristics.[126]

As early in the history of biotechnology as 1990, the scientific community was opposed to attempts to modify the human germline using these new tools,[127] and such cautions continued as technology progressed.[128] With the advent of new techniques like CRISPR, in March 2015 scientists urged a worldwide ban on clinical use of gene editing technologies to edit the human genome in a way that can be inherited.[113][114][115][116] In April 2015, researchers sparked controversy when they reported results of basic research to edit the DNA of non-viable human embryos using CRISPR.[129][130] Additionally, it has been suggested that 3D printing can be implemented in the rapid development of bioresorbable scaffolds capable of implanting stem cells.[131]

Regulations covering genetic modification are part of general guidelines about human-involved biomedical research.

The Helsinki Declaration (Ethical Principles for Medical Research Involving Human Subjects) was amended by the World Medical Associations General Assembly in 2008. This document provides principles physicians and researchers must consider when involving humans as research subjects. The Statement on Gene Therapy Research initiated by the Human Genome Organization (HUGO) in 2001 provides a legal baseline for all countries. HUGOs document emphasizes human freedom and adherence to human rights, and offers recommendations for somatic gene therapy, including the importance of recognizing public concerns about such research.[132]

No federal legislation lays out protocols or restrictions about human genetic engineering. This subject is governed by overlapping regulations from local and federal agencies, including the Department of Health and Human Services, the FDA and NIHs Recombinant DNA Advisory Committee. Researchers seeking federal funds for an investigational new drug application, (commonly the case for somatic human genetic engineering), must obey international and federal guidelines for the protection of human subjects.[133]

NIH serves as the main gene therapy regulator for federally funded research. Privately funded research is advised to follow these regulations. NIH provides funding for research that develops or enhances genetic engineering techniques and to evaluate the ethics and quality in current research. The NIH maintains a mandatory registry of human genetic engineering research protocols that includes all federally funded projects.

An NIH advisory committee published a set of guidelines on gene manipulation.[134] The guidelines discuss lab safety as well as human test subjects and various experimental types that involve genetic changes. Several sections specifically pertain to human genetic engineering, including Section III-C-1. This section describes required review processes and other aspects when seeking approval to begin clinical research involving genetic transfer into a human patient.[135]

The FDA regulates the quality and safety of gene therapy products and supervises how these products are used clinically. Therapeutic alteration of the human genome falls under the same regulatory requirements as any other medical treatment. Research involving human subjects, such as clinical trials, must be reviewed and approved by the FDA and an Institutional Review Board.[136][137]

Gene therapy is the basis for the plotline of the film I Am Legend[138] and the TV show Will Gene Therapy Change the Human Race?[139]

See original here: Gene therapy Wikipedia, the free encyclopedia

Read the original here:
StemCell Therapy MD

Stem cells are primal cells found in all multi-cellular organisms.

They retain the ability to renew themselves through mitotic cell division and can differentiate into a diverse range of specialized cell types.

The three broad categories of mammalian stem cells are: embryonic stem cells, derived from blastocysts, adult stem cells, which are found in adult tissues, and cord blood stem cells, which are found in the umbilical cord.

In a developing embryo, stem cells can differentiate into all of the specialized embryonic tissues.

In adult organisms, stem cells and progenitor cells act as a repair system for the body, replenishing specialized cells.

As stem cells can be grown and transformed into specialized cells with characteristics consistent with cells of various tissues such as muscles or nerves through cell culture, their use in medical therapies has been proposed.

In particular, embryonic cell lines, autologous embryonic stem cells generated through therapeutic cloning, and highly plastic adult stem cells from the umbilical cord blood or bone marrow are touted as promising candidates.

Medical researchers believe that stem cell therapy has the potential to change radically the treatment of human disease.

A number of adult stem cell therapies already exist, particularly bone marrow transplants that are used to treat leukemia.

Excerpt from:
Stem cell - Science Daily

Chronic renal failure is an important clinical problem with significant socioeconomic impact worldwide. Despite advances in renal replacement therapies and organ transplantation, poor quality of life for dialysis patients and long transplant waiting lists remain major concerns for nephrologists treating this condition. There is therefore a pressing need for novel therapies to promote renal cellular repair and tissue remodeling. Over the past decade, advances in the field of regenerative medicine allowed development of cell therapies suitable for kidney repair. Mesenchymal stem cells (MSCs) are undifferentiated cells that possess immunomodulatory and tissue trophic properties and the ability to differentiate into multiple cell types. Studies in animal models of chronic renal failure have uncovered a unique potential of these cells for improving function and regenerating the damaged kidney. Nevertheless, several limitations pertaining to inadequate engraftment, difficulty to monitor, and untoward effects of MSCs remain to be addressed. Adverse effects observed following intravascular administration of MSCs include immune rejection, adipogenic differentiation, malignant transformation, and prothrombotic events. Nonetheless, most studies indicate a remarkable capability of MSCs to achieve kidney repair. This review summarizes the regenerative potential of MSCs to provide functional recovery from renal failure, focusing on their application and the current challenges facing clinical translation.

Chronic kidney disease (CKD) is a prevalent condition (8 to 16%) associated with all-cause and cardiovascular mortality [1]. Importantly, CKD can progress towards end-stage renal disease (ESRD), requiring renal replacement therapy. ESRD currently accounts for 6.3% of the Medicare spending in the United States, and is projected to increase by 85% by 2015 [2]. Furthermore, ESRD has a tremendous impact on quality of life and life expectancy of affected individuals [3]. Therefore, it is imperative to develop therapeutic interventions to prevent, alleviate, or decelerate progression of renal failure.

Diabetes mellitus and hypertension represent major causes of CKD and initiation of dialysis in the United States [4]. In addition, glomerular diseases, malnutrition, infectious diseases, and acute kidney injury can progress to ESRD, contributing to the increased global burden of death associated with this condition [5]. Current treatment modalities often fail to target the major underlying contributors for progression of renal disease [6]. Chronic glomerular and tubulointerstitial fibrosis is a common pathway to ESRD, often associated with apoptosis, oxidative damage, and microvascular rarefaction. In fact, renal dysfunction is postulated to better correlate with the degree of tubulointerstitial than with glomerular damage [7].

Importantly, the kidney possesses intrinsic regenerative capacity that allows the organ to recover after limited insults [8]. Unfortunately, this regenerative potential is limited under chronic conditions and thus inefficient to prevent progressive glomerulosclerosis and tubulointerstitial fibrosis [9]. Treatment strategies that boost cellular regeneration might therefore offer good alternatives for patients with CKD.

Mesenchymal stem cells (MSCs) can be isolated from a variety of tissues, differentiate into multiple cell lineages, and possess unique immunomodulatory properties that ameliorate inflammation and immune responses, constituting a promising tool to facilitate renal repair. MSCs are defined by the presence of plastic-adherent cells under standard culture conditions, capacity to differentiate into osteoblasts, adipocytes and chondroblasts in vitro, expression of typical surface markers (CD29, CD44, CD73, CD90, CD105, and CD166), and the lack of CD45, CD34, CD14 or CD11b, CD79 or CD19 and HLA-DR surface molecules [10]. In recent years, experimental studies have uncovered the potential of MSCs to improve renal function in several models of CKD, and several clinical studies have indicated their safety and efficacy in CKD. Nevertheless, a number of hurdles need to be addressed before clinical translation. This review summarizes the current state of MSC transplantation for CKD, focusing on their mechanisms of renal repair, complications, obstacles for clinical translation, and potential approaches to overcome them.

Over the past few years, MSCs have been successfully applied in experimental models of CKD such as diabetes, hypertension, and chronic allograft nephropathy (Table

). For example, a single intravenous dose of MSCs resulted in beta-pancreatic islet regeneration, prevented renal damage in streptozotocin-induced type 1 diabetes in C57BL/6 mice [

], and decreased hyperglycemia and glycosuria that persisted for 2months after injection. Furthermore, MSC-treated diabetic mice showed histologically normal glomeruli, and albuminuria fell. Although the authors did not assess cellular mechanisms associated with MSC therapeutic effects, the long-lasting persistence of injected MSCs may suggest a direct effect to elicit kidney regeneration.

Preclinical studies using mesenchymal stem cells for the treatment of chronic kidney disease

Diabetic nephropathy

Mice bone marrow

0.5106

Intravenous

Engraftment/direct effect

None

[11]

Diabetic nephropathy

Human bone marrow

2106

Intracardiac

Engraftment/direct effect

None

[12]

Partial nephrectomy

Rat bone marrow

1106

Intravenous

Paracrine effect

None

[13]

Chronic allograft nephropathy

Rat bone marrow

0.5106

Intravenous

Immunomodulatory effect

None

[14]

Renal revascularization

Allogeneic swine adipose tissue

10106

Intrarenal

Engraftment/direct effect/paracrine

None

[16, 17]

Renal artery stenosis

Autologous swine adipose tissue

10106

Intrarenal

Engraftment/direct effect/paracrine

None

[15]

Similarly, Lee and colleagues tested the effectiveness of intracardiac infusions of MSCs from human bone marrow in immunodeficient mice with type 2 diabetes produced with multiple low doses of streptozotocin [12]. MSCs lowered blood glucose levels and decreased mesangial thickening and macrophage infiltration, suggesting their potential for improving renal lesions in subjects with diabetes mellitus. Interestingly, in kidneys of MSC-treated diabetic mice, a few injected human MSCs differentiated into glomerular endothelial cells.

Additionally, in rats with modified 5/6 nephrectomy, a single venous injection of MSCs 1day after nephrectomy preserved renal function and attenuated renal injury [13]. Despite unchanged blood urea nitrogen and creatinine levels, MSC-treated animals showed attenuated progression of proteinuria. The scarce engraftment of MSCs in the kidneys of rats with chronic renal failure suggests that paracrine secretion of mediators, such as cytokines or growth factors, may have accounted for their beneficial effects. Indeed, vascular endothelial growth factor (VEGF) levels were substantially higher in MSC-treated animals 1month after MSC injection.

Furthermore, a single dose of bone marrow-derived MSCs 11weeks after kidney transplantation in rats decreased interstitial fibrosis, tubular atrophy, T-cell and macrophage infiltration, and the expression of inflammatory cytokines [14]. Interestingly, a decrease over time in the inflammatory and profibrotic cytokine levels in MSC-treated animals was associated with an increase in the anti-inflammatory cytokine IL-10, although none of the injected MSCs were detected 7days after delivery. These observations imply that the beneficial effect of these cells in this setting is primarily attributable to their paracrine immunomodulatory properties rather than long-term engraftment.

We have previously shown in swine atherosclerotic renovascular disease that intrarenal delivery of MSCs isolated from subcutaneous adipose tissue protected the stenotic kidney despite sustained hypertension [

]. Notably, MSCs also attenuated renal inflammation, endoplasmic-reticulum stress, and apoptosis through mechanisms involving cell contact. Furthermore, adjunctive MSCs improved renal function and structure after renal revascularization and reduced inflammation, oxidative stress, apoptosis, microvascular remodeling, and fibrosis in the stenotic kidney [

] (Figure

). This strategy also restores oxygen-dependent tubular function in the stenotic-kidney medulla, extending their value to preserving medullary structure and function in chronic ischemic conditions [

].

Stenotic-kidney microvascular loss and fibrosis decreased in animals treated with mesenchymal stem cells. Top: representative microcomputed tomography three-dimensional images of kidney segments, showing improved microvascular architecture in pigs with atherosclerotic renal artery stenosis (ARAS) treated with percutaneous transluminal renal angioplasty (PTRA) and an adjunct intrarenal infusion of adipose tissue-derived mesenchymal stem cells (MSC) 4weeks earlier. Bottom: representative renal trichrome staining (40, blue) showing decreased fibrosis in ARAS + PTRA + MSC pigs.

While preclinical studies have established the safety and efficacy of MSCs in different models of CKD, these results need cautious translation into routine clinical practice. Trials using MSCs for CKD patients may face various challenges, including selecting the optimal route of MSC delivery, scant homing and engraftment, immune rejection, ensuring thriving, and tracking of injected cells. Addressing these challenges may bolster the success of MSC therapy in improving renal function in CKD patients.

The route of MSC delivery may influence the cells capacity to home and engraft the damaged tissue, and thereby their efficacy for renal repair. Commonly used experimental methods to deliver MSCs include systemic intravenous, intra-arterial, or intraparenchymal delivery. When intravenously delivered in normal SpragueDawley rats, the majority of MSCs are initially trapped in the lungs [18], but in nonhuman primates the cells distribute broadly into the kidneys, skin, lung, thymus, and liver with estimated levels of engraftment ranging from 0.1 to 2.7% [19]. In contrast, direct delivery of MSCs into the renal artery of an ischemic kidney is associated with retention rates of 10 to 15% [16, 17], although the normal swine kidney retains only around 4%, due to the low tonic release of injury signals. However, injection of human MSCs into the mouse abdominal aorta may lead to occlusion in the distal vasculature due to their relatively large cell size (16 to 53m), suggesting that this approach should be used cautiously [20]. Injections of MSCs into the renal parenchyma or their local subcapsular implantation confer renoprotective effects [21, 22], but are difficult to implement in the human injured kidney.

In experimental models of CKD, the optimal dose of MSCs is often empirical, with doses ranging from 0.5106 to 10106[11, 16]. Despite variability in dose regimens and route of delivery, the safety and beneficial effects of MSCs were consistent among studies. Nevertheless, the use of escalating doses is strongly recommended in clinical trials, and chronic adverse events should be evaluated prior to enrollment at the next dose level.

Circulating hematopoietic progenitor cells home to the damaged kidney by responding to injury signals that correspond to cognate surface receptors which they express [23]. Accumulating evidence indicates that exogenously infused MSCs respond to similar homing signals. In mice, expression of CD44 and its major ligand hyaluronic acid mediates MSC migration to the injured kidney [24], and hyaluronic acid also promotes MSC dose-dependent migration in vitro. Moreover, renal homing of intravenously injected MSCs was blocked by preincubation with the CD44 blocking antibody or by soluble hyaluronic acid, suggesting that CD44 and hyaluronic acid interactions recruit exogenous MSCs to the injured kidney. In addition, Liu and colleagues found that, when administered systemically, MSCs home to the ischemic kidney, improving renal function, accelerating mitogenic response, and reducing cell apoptosis, but these effects were abolished by either CXCR4 or CXCR7 inhibition, implicating the stromal derived factor-1CXCR4/CXCR7 axis in kidney repair [25].

Collectively, these observations suggest that strategies aimed to enhance MSC expression of homing signals may improve their capacity to attenuate renal dysfunction. Studies have shown that selective manipulation of MSCs before transplantation (preconditioning) enhances their ability to protect damaged tissues [26, 27]. The rationale underpinning this approach is that transplanted MSCs encounter a hostile microenvironment that mitigates their reparative capabilities and survival. Indeed, preconditioning with the mitogenic and prosurvival factor insulin-like growth factor (IGF)-1 before systemic infusion of bone marrow-derived MSCs (2105) upregulates the expression of CXCR4 and restores normal renal function in a mice model of cisplatin-induced acute kidney injury [28].

Some studies suggest that MSCs have the capacity to engraft the damaged tissue, integrate into tubular cells, and differentiate into mesangial cells [2931]. In swine renovascular disease, 4weeks after intrarenal infusion, MSCs (10106) were detected in all regions of the kidney, but mostly at the renal interstitium [16, 17]. On the other hand, intravenous infusion of bone marrow-derived MSCs (2105) in mice with cisplatin-induced acute renal failure reduced the severity of renal injury, but none were detected within the renal tubules and only few cells within the renal interstitium at 1 to 4days after infusion [32], suggesting that MSC engraftment is not necessary to achieve renoprotection. Likewise, despite significant improvement in renal function, within 3days of intracarotid infusion in a rat model of ischemiareperfusion-induced acute renal failure, none of the MSCs differentiated into the tubular or endothelial cell phenotype, indicating that their beneficial effects are primarily mediated via paracrine actions rather than differentiation into target cells [33].

Methods to increase MSC engraftment may therefore enhance their utility in regenerative cellular therapy. Temporary obstruction of the renal artery following intrarenal delivery [16, 17] may prevent cell washout, and is associated with significant retention rates in the postischemic kidney. Alternatively, in a rat model of acute kidney injury, s-nitroso N-acetyl penicillamine preconditioning enhances MSC engraftment, ultimately associated with a significant improvement in renal function [34].

Despite the crucial role attributed to MSC engraftment in potentiating the cells beneficial effect at the site of injury, there is currently consensus that the chief mechanism by which MSCs protect the damaged kidney is the release of growth factors, proangiogenic factors, and anti-inflammatory cytokines. Cultured MSCs release large amounts of the proangiogenic factor VEGF, which facilitates glomerular and tubular recovery [16, 35]. MSCs can also produce IGF-1, while administration of IGF-1 gene-silenced MSCs limits their protective effect on renal function and tubular structure in murine cisplatin-induced kidney injury, indicating that MSCs exert their beneficial effects by producing IGF-1 [36].

Importantly, these paracrine actions of MSCs seem to mediate their immunomodulatory properties. In ischemiareperfusion-induced acute kidney injury, infusion of MSCs downregulates renal expression of proinflammatory cytokines and adhesion molecules such as IL-1, tumor necrosis factor alpha, interferon gamma, monocyte chemoattractant protein-1, and intercellular adhesion molecule-1, but upregulates the expression of the anti-inflammatory IL-10 [26, 33]. Likewise, we have shown in swine renovascular disease that intrarenal delivery of MSCs during renal revascularization decreased renal expression of tumor necrosis factor alpha and monocyte chemoattractant protein-1, but increased IL-10 expression [17]. Moreover, MSCs induced a shift in the macrophage phenotype from inflammatory (M1) to reparative (M2), uncovering their immunomodulatory potential [37]. Taken together, these observations underscore the contribution of paracrine actions of MSCs to induce a shift from an inflammatory to an anti-inflammatory microenvironment. It is not unlikely that the type, number, and expansion methods used to secure MSCs alter their engraftment capacity.

For many years, MSCs have been considered immune privileged because of the lack of expression of co-stimulatory molecules and their capacity to decrease renal release and expression of inflammatory mediators [17, 33, 37]. These attributes engendered the hope that MSCs could engraft in allogeneic nonimmunosuppressed recipients, and stimulated development of off-the-shelf allogeneic MSC products [38], which allow rapid generation of large amounts of cells from few donors. Nevertheless, in vivo and in vitro studies have demonstrated that MSCs may occasionally induce an immune switch transitioning from an immunoprivileged to an immunogenic phenotype that triggered cellular cytotoxicity or immune rejection [39]. Moreover, implantation of murine MSCs engineered to release erythropoietin in major histocompatibility complex-mismatched allogeneic mice increased the proportion of host-derived lymphoid CD8+ and natural killer infiltrating cells, suggesting that MSCs are not intrinsically immunoprivileged [40]. Taken together, these observations do not support the use of allogeneic MSCs as a universal cellular platform, at least until development of unequivocally immunoprivileged MSCs. Therefore, at this point, administration of autologous MSCs seems to be the safest strategy.

An important feature of MSCs is their capacity to induce proliferation of renal glomerular and tubular cells, increasing cellular survival. By secreting proangiogenic and trophic factors, injected MSCs not only can enhance proliferation, but also can decrease apoptosis of tubular cells [32]. We have shown in swine renovascular disease that a single intrarenal delivery of MSCs in conjunction with renal revascularization increased proliferation of renal cells [16], and recently confirmed in vitro that MSCs blunt apoptosis by decreasing the expression of caspase-3 [15].

However, whether MSCs remain in the circulation long enough to exert any long-lasting effect is a matter of debate. Ezquer and colleagues showed that intravenous MSCs home into the kidney of type 1 diabetic mice, and some donor MSCs remained in the kidney up to 2months later [11]. Similarly, we found that 4weeks after intrarenal delivery a significant number of MSCs were retained in the injected kidney [16, 17], whereas by 12weeks after cell transfer only a few cells were observed in the kidney, yet their beneficial effects were sustained [15]. Longitudinal studies are needed to document the chronology of MSC retention and beneficial benefits in the kidney. Additionally, development of novel interventions such as preconditioning may enhance survival and potency of MSCs in renal failure. For instance, MSCs exposed to hypoxic conditions in culture sustain viability and function through preservation of oxidant status [41], and preconditioning with kallikrein [26] or melatonin [27] enhances their therapeutic potential.

An important challenge for clinical translation is the risk for long-term MSC maldifferentiation. While intrarenal injection of rat MSCs initially preserves renal function in a rat model of glomerulonephritis, a significant proportion of the glomeruli subsequently contained large adipocytes with glomerular sclerosis [42]. Furthermore, reports of sarcoma [43] and teratoma [44] arising from exogenous MSCs illustrate their potential for transformation into tumors, underscoring the requirement for closely monitoring human MSCs in clinical studies. Alternatively, complications and maldifferentiation of live replicating MSCs warrant development of safer tactics and interventions.

Considerable evidence shows that MSCs release microvesicles which exhibit characteristics of their parental cells, and transfer proteins, lipids, and genetic material to target cells. We have recently shown that endothelial outgrowth cells release microvesicles [

], which may mediate their intercellular communications. Similarly, MSCs are avid producers of microvesicles [

] (Figure

) that shuttle functional components for their paracrine action [

]. Delivery of microvesicles instead of their parent MSCs could avoid concerns about extensive expansion, cryopreservation, complications, and maldifferentiation of live replicating cells. Indeed, microvesicles derived from preconditioned MSCs promoted recovery in a rat hind-limb ischemia model [

]. However, questions regarding their composition and potency relative to their parent MSCs remain unanswered, underscoring the need for studies to clarify the potential of this promising therapeutic modality.

Mesenchymal stem cell release microvesicles. Transmission electron microscopy image (left) and scanning electron microscopy image (right) showing release of microvesicles (arrows) from adipose tissue-derived mesenchymal stem cells (26,500).

Uremic conditions may also affect the efficacy of MSCs, limiting their potential use in patients with CKD. Uremia induced by partial kidney ablation in C57Bl/6J mice leads to MSC functional incompetence, characterized by decreased expression of VEGF, VEGF receptor-1, and stromal derived factor-1, increased cellular senescence, and decreased proliferation [49]. Conversely, MSCs isolated from subcutaneous adipose tissue of healthy controls and patients with renal disease show similar characteristics and functionality, underscoring the feasibility of autologous cell therapy in patients with renal disease [50]. Indeed, a recent meta-analysis of prospective clinical trials that used intravascular delivery of MSCs concluded that these cells have an excellent safety record [51].

Although it is accepted that MSCs from different species are capable of differentiation into various lineages and express common MSC markers, species-dependent variability in their expression has been reported among different species [52]. Furthermore, the mechanism of MSC-mediated immunosuppression varies among different species. For example, while immunosuppression by human-derived or monkey-derived MSCs is mediated by indoleamine 2,3-dioxygenase, the molecular mechanisms underlying immunosuppression in mouse MSCs utilize nitric oxide [53]. Several immune barriers have been also encountered in experimental xenotransplantation, the transplantation of MSCs from one species to another, warranting the development of genetic alternatives to overcome these obstacles [54]. Clearly, results from experimental studies need to be carefully validated before clinical translation.

There is also a pressing need for better methods for detection and monitoring the fate of MSCs. Despite improvement in direct (fluorescent probe) [55] and indirect (reporter genes) [56] labeling techniques, questions regarding interactions of MSCs with tissue, differentiation, or migration remain unanswered. While fluorescent probes such as membrane tracers or microspheres need to be detected with histological techniques in a cell or organelle, reporter genes such as bioluminescence or fluorescent proteins can be used to identify different cell populations using imaging in vivo[57, 58]. However, these detection methods have little tissue penetration, limiting their use in large animal models or humans [59].

Conceivably, imaging modalities such as single-photon emission computed tomography or magnetic resonance imaging may address some of these deficiencies by providing high-resolution anatomical detail and tracking of cell viability [60, 61]. Several types of agents are currently used for labeling MSCs for their detection with magnetic resonance imaging. Among them, superparamagnetic iron oxide particles are the most commonly applied, because of their capacity to induce changes in T2 relaxivity in vivo[62]. However, the transfection agents used for superparamagnetic iron oxide particle internalization may also affect cell viability, and dying cells accumulate iron until dissolved or eliminated by phagocytosis, impeding their application as indices of cell viability. Further methods are therefore needed to better assess engraftment, survival, and function of MSCs in human subjects.

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Posted on April 9, 2014 by Dan Buettner

By Dan Buettner

Life expectancy of an American born today averages 78.2 years. But this year, over 70,000 Americans have reached their 100thbirthday. What are they doing that the average American isnt (or wont?)

To answer the question, we teamed up with National Geographic to find the worlds longest-lived people and study them. We knew most of the answers lied within their lifestyle and environment (The Danish Twin Study established that only about 20% of how long the average person lives is determined by genes.). Then we worked with a team of demographers to find pockets of people around the world with the highest life expectancy, or with the highest proportions of people who reach age 100.

We found five places that met our criteria:

We then assembled a team of medical researchers, anthropologists, demographers, and epidemiologists to search for evidence-based common denominators among all places. We found nine:

1. Move NaturallyThe worlds longest-lived people dont pump iron, run marathons or join gyms. Instead, they live in environments that constantly nudge them into moving without thinking about it. They grow gardens and dont have mechanical conveniences for house and yard work.

2. Purpose. The Okinawans call it Ikigai and the Nicoyans call it plan de vida; for both it translates to why I wake up in the morning. Knowing your sense of purpose is worth up to seven years of extra life expectancy

3. Down Shift Even people in the Blue Zones experiencestress. Stress leads to chronic inflammation, associated with every major age-related disease. What the worlds longest-lived people have that we dont are routines to shed that stress. Okinawans take a few moments each day to remember their ancestors, Adventists pray, Ikarians take a nap and Sardinians do happy hour.

4. 80% Rule Hara hachi bu the Okinawan, 2500-year old Confucian mantra said before meals reminds them to stop eating when their stomachs are 80 percent full. The 20% gap between not being hungry and feeling full could be the difference between losing weight or gaining it. People in the Blue Zones eat their smallest meal in the late afternoon or early evening and then they dont eat any more the rest of the day.

5. Plant Slant Beans, including fava, black, soy and lentils, are the cornerstone of most centenarian diets. Meatmostly porkis eaten on average only five times per month. Serving sizes are 3-4 oz., about the size of deck or cards.

6. Wine @ 5 People in all Blue Zones (except Adventists) drink alcohol moderately and regularly. Moderate drinkers outlive non-drinkers. The trick is to drink 1-2 glasses per day (preferably Sardinian Cannonau wine), with friends and/or with food. And no, you cant save up all weekend and have 14 drinks on Saturday.

7. Belong All but five of the 263 centenarians we interviewed belonged to some faith-based community. Denomination doesnt seem to matter. Research shows that attending faith-based services four times per month will add 4-14 years of life expectancy.

8. Loved Ones FirstSuccessful centenarians in the Blue Zones put their families first. This means keeping aging parents and grandparents nearby or in the home (It lowers disease and mortality rates of children in the home too.). They commit to a life partner (which can add up to 3 years of life expectancy) and invest in their children with time and love (Theyll be more likely to care for you when the time comes).

9. Right TribeThe worlds longest lived people choseor were born intosocial circles that supported healthy behaviors, Okinawans created moaisgroups of five friends that committed to each other for life. Research from the Framingham Studies shows that smoking, obesity, happiness, andeven loneliness are contagious.So the social networks of long-lived people have favorably shaped their health behaviors.

To make it to age 100, you have to have won the genetic lottery. But most of us have the capacity to make it well into our early 90s and largely without chronic disease. As the Adventists demonstrate, the average persons life expectancy could increase by 10-12 years by adopting a Blue Zones lifestyle.

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Conference Series LLC cordially invite you to participate at the 10th International Conference on Clinical and Experimental Ophthalmology to be held during November 21-23, 2016 at Dubai, UAE. The theme of the conference is Insights of Ophthalmology which focuses on the significance of vision and also explore the spectrum of latest technological developments in the field of Ophthalmology.

Retina and Retinal Disorders

The retina is a layer of tissue present in the interior of your eye. Retina disorders are mainly due to lack of light-delicate cells and other nerve cells which transform the impulse into visual information. Retina sends this visual data to the cerebrum through your optic nerve and process the information into an image and empowering you to see. Different age group generations, races and ethnicities are effected from Retinal degenerative disorders, for instance, Age-related macular degeneration and myopic macular degeneration.

Relevant Conferences:

6th Global Ophthalmologists Annual Meeting, May 16-18, 2016 Osaka, Japan, Global Pediatric Ophthalmology Congress, June 06-7, 2016 London, UK; 8th Global Ophthalmology Meeting July 18-20, 2016 Chicago, USA; International Conference and Expo on Cataract & Refractive Surgery Aug 04-05, 2016 Manchester, UK; 9thGlobal Ophthalmology Summit, August 24-26, 2016 Sao Paulo, Brazil; 7thEuropean Ophthalmology Conference, September 21-23, 2016 Amsterdam, Netherlands; 2nd International Conference on Eye and Vision September 26-28, 2016 Orlando, Florida, USA; Global Ophthalmology & Glaucoma Conference, October 13-15, 2016 Kuala Lumpur, Malaysia; International Conference & Expo on Optometry and Vision Science October 27-29, 2016 Rome, Italy; World Ophthalmology Conference, November 24-26, 2016 Melbourne, Australia ;Retina 2016, Hawaii, January 16-22, 2016, USA; 16thEURETINA Congress, September 08-11, 2016 Copenhagen, Denmark; American Society of Retina Specialists (ASRS) 34th Annual Meeting, August 10-14, 2016, California, USA; 19thRetina International World Congress, July 06-10, 2016, Taipei, Taiwan; 18th Annual: The Business of Retina Meeting, April 09-10, 2016 Texas, USA; American Academy of Ophthalmology (AAO 2016- Innovate), October 15-18, 2016 Chicago, USA; American Glaucoma Society Annual Meeting, March 03-06, 2016 Fort Lauderdale, USA; Asia Pacific Glaucoma Society Congress, July 14-16, 2016 Chiang Mai, Thailand; for more meetings visit Ophthalmology Meetings

Clinical Ophthalmology

Clinical Ophthalmology indicates the duties of practitioner in an eye clinic and it also covers the broad spectrum of research from beside to bench side and plays a crucial in screening, diagnosis and therapeutics to treat eye illness. There are various common eye problems that needs to treated in a same day and hence that can be achieved through community ophthalmology so that you can be treated near where you live or work rather than hospital.

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6th Global Ophthalmologists Annual Meeting, May 16-18, 2016 Osaka, Japan, Global Pediatric Ophthalmology Congress, June 06-7, 2016 London, UK; 8th Global Ophthalmology Meeting July 18-20, 2016 Chicago, USA; International Conference and Expo on Cataract & Refractive Surgery Aug 04-05, 2016 Manchester, UK; 9thGlobal Ophthalmology Summit, August 24-26, 2016 Sao Paulo, Brazil; 7thEuropean Ophthalmology Conference, September 21-23, 2016 Amsterdam, Netherlands; 2nd International Conference on Eye and Vision September 26-28, 2016 Orlando, Florida, USA; Global Ophthalmology & Glaucoma Conference, October 13-15, 2016 Kuala Lumpur, Malaysia; International Conference & Expo on Optometry and Vision Science October 27-29, 2016 Rome, Italy; World Ophthalmology Conference, November 24-26, 2016 Melbourne, Australia; 8thOcular Diseases Drug Discovery Conference, March 21-22, 2016, San Diego, USA; World Ophthalmology Congress, February 5-9, 2016, Guadalajara, Mexico; Retina 2016, Hawaii, January 16-22, 2016, USA; World Cornea Congress VIII, May 06-10, 2016, New Orleans, USA; 8th International Congress on Glaucoma Surgery, February 17-20, 2016, Muscat, Oman; American Academy of Ophthalmology (AAO 2016- Innovate), October 15-18, 2016 Chicago, USA; American Glaucoma Society Annual Meeting, March 03-06, 2016 Fort Lauderdale, USA; Asia Pacific Glaucoma Society Congress, July 14-16, 2016 Chiang Mai, Thailand; for more meetings visit Ophthalmology Meetings

Pediatric Ophthalmology

Pediatric ophthalmology is a sub-branch of ophthalmology associated with eye ailments, visual functions, and vision care in kids. The pediatric ophthalmologist gets further training to provide supervision to young patients. Neurologic improvement of vision happens up until around age 12 years. Misalignment of the eyes (strabismus), uncorrected refractive mistake (nearsightedness, hyperopia, and astigmatism), and asymmetry of refractive errors between the two eyes can contrarily influence this advancement. If these conditions not treated on time than it will affect the vision permanently. Pediatric ophthalmologists are eligible to perform ocular surgery along with the management of childrens eye diseases with glasses and pharmacological approach.

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6th Global Ophthalmologists Annual Meeting, May 16-18, 2016 Osaka, Japan, Global Pediatric Ophthalmology Congress, June 06-7, 2016 London, UK; 8th Global Ophthalmology Meeting July 18-20, 2016 Chicago, USA; International Conference and Expo on Cataract & Refractive Surgery Aug 04-05, 2016 Manchester, UK; 9thGlobal Ophthalmology Summit, August 24-26, 2016 Sao Paulo, Brazil; 7thEuropean Ophthalmology Conference, September 21-23, 2016 Amsterdam, Netherlands; 2nd International Conference on Eye and Vision September 26-28, 2016 Orlando, Florida, USA; Global Ophthalmology & Glaucoma Conference, October 13-15, 2016 Kuala Lumpur, Malaysia; International Conference & Expo on Optometry and Vision Science October 27-29, 2016 Rome, Italy; World Ophthalmology Conference, November 24-26, 2016 Melbourne, Australia; ICODDD 2016: 18th International Conference on Ocular Diseases Drug Discovery, April 22-23, 2016, London, UK; Vail Vitrectomy 2016, February 20-21, 2016, Colorado, USA; 8th Ocular Diseases Drug Discovery Conference, March 21-22, 2016, San Diego, USA; The 7th International Conference on Ocular Infections, September 3-4, 2016 Barcelona, Spain; 2nd San Raffaele OCT FORUM, April 12-13, 2016, Milan Italy; American Academy of Ophthalmology (AAO 2016- Innovate), October 15-18, 2016 Chicago, USA; American Glaucoma Society Annual Meeting, March 03-06, 2016 Fort Lauderdale, USA; Asia Pacific Glaucoma Society Congress, July 14-16, 2016 Chiang Mai, Thailand; for more meetings visit Ophthalmology Meetings

Ophthalmology Practice

It is a practice of an ophthalmologists, researchers and scientist to deal with the various eye health issues with an aim to treat the illness.

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6th Global Ophthalmologists Annual Meeting, May 16-18, 2016 Osaka, Japan, Global Pediatric Ophthalmology Congress, June 06-7, 2016 London, UK; 8th Global Ophthalmology Meeting July 18-20, 2016 Chicago, USA; International Conference and Expo on Cataract & Refractive Surgery Aug 04-05, 2016 Manchester, UK; 9thGlobal Ophthalmology Summit, August 24-26, 2016 Sao Paulo, Brazil; 7thEuropean Ophthalmology Conference, September 21-23, 2016 Amsterdam, Netherlands; 2nd International Conference on Eye and Vision September 26-28, 2016 Orlando, Florida, USA; Global Ophthalmology & Glaucoma Conference, October 13-15, 2016 Kuala Lumpur, Malaysia; International Conference & Expo on Optometry and Vision Science October 27-29, 2016 Rome, Italy; World Ophthalmology Conference, November 24-26, 2016 Melbourne, Australia; American Academy of Ophthalmology (AAO 2016- Innovate), October 15-18, 2016 Chicago, USA; American Glaucoma Society Annual Meeting, March 03-06, 2016 Fort Lauderdale, USA; Asia Pacific Glaucoma Society Congress, July 14-16, 2016 Chiang Mai, Thailand; for more meetings visit Ophthalmology Meetings

Ophthalmology Surgery

Translational Ophthalmology is a latest trend that bridges the gap by achieving breakthrough discoveries to patients faster than ever. Translational Research is a new initiative of the National Institutes of Health (NIH) which aims to translate basic research into more advanced form to yield the better results. The research trend discoveries maximize the opportunities to investigate the issues very minutely to decrease the risk of failure especially during surgical procedure like cataract and refractive surgery. Many fruitful facts have been discovered which indirectly helps in treating the respective conditions such as Age-Related Eye Disease Study (AREDS) proved that nutritional supplements (nutrition and ophthalmology) could minimize the risk of AMD. The American Health Assistance Foundation, dedicated to eradicating age-related degenerative diseases, estimates that up to 11 million people in the United States have some form of AMD - a number expected to double by 2050. Estimates of the global cost of visual impairment AMD causes are $343 billion, including $255 billion in direct health care costs, according to the foundation. Ophthalmology represents 18 percent of the average case volume in surgery centers, second behind GI/endoscopy (25 percent). The average surgery center performs 4,869 cases annually, which would average to around 876 ophthalmology cases annually, according to VMG Health's 2009 Intellimarker.

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International Conference and Expo on Cataract & Refractive Surgery August 04-06, 2016 Manchester, UK; 6th Global Ophthalmologists Annual Meeting, May 16-18, 2016 Osaka, Japan; 7th European Ophthalmology Conference, June 16-18, 2016, Alicante, Spain; 8th Global Ophthalmology Meeting July 18-20, 2016 Chicago, USA; World Ophthalmology Conference September 15-17, 2016 Berlin, Germany; 2nd International Conference on Eye and Vision September 26-28, 2016 Miami, USA; International Conference & Expo on Optometry and Vision Science October 27-29, 2016 Rome, Italy; 9th World Ophthalmic Conference October 24-26, 2016 Istanbul, Turkey; Global Ophthalmology and Glaucoma Conference November 7-9, 2016 Melbourne, Australia; Cataract Surgery Meeting, January 13-17, 2016 Florida, USA; American Society of Retina Specialists (ASRS) 34th Annual Meeting, August 10-14, 2016, California, USA; ASCRS 2016, May 610, 2016, New Orleans, USA; 34th Annual Meeting of ESOPRS, September 10-12, 2016 Brussels, Belgium; 7th International course on ophthalmic and oculoplastic reconstruction and trauma surgery, January, 13-15, 2016 Vienna, Austria; American Academy of Ophthalmology (AAO 2016- Innovate), October 15-18, 2016 Chicago, USA; American Glaucoma Society Annual Meeting, March 03-06, 2016 Fort Lauderdale, USA; Asia Pacific Glaucoma Society Congress, July 14-16, 2016 Chiang Mai, Thailand; for more meetings visit Ophthalmology Meetings

Optometry and Vision Science

Optometry is an eye care profession associated with the vision and visual system where information is processed to produce an image. Optometrists also called as ophthalmic optician and are qualified to diagnose & treat eye diseases. This scientific track welcomes the participant to participate and explore the insights of optometry and vision science.

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International Conference & Expo on Optometry and Vision Science Oct 27-29, 2016 Rome, Italy; 6th Global Ophthalmologists Annual Meeting, May 16-18, 2016 Osaka, Japan; 7th European Ophthalmology Conference, June 16-18, 2016, Alicante, Spain; 8th Global Ophthalmology Meeting July 18-20, 2016 Chicago, USA; International Conference and Expo on Cataract & Refractive Surgery Aug 4-6, 2016 Manchester, UK ; World Ophthalmology Conference Sept 15-17, 2016 Berlin German; 2nd International Conference on Eye and Vision Sept 26-28, 2016 Miami, USA; 9th World Ophthalmic Conference Oct 24-26, 2016 Istanbul, Turkey; Global Ophthalmology and Glaucoma Conference Nov 7-9, 2016 Melbourne, Australia; American Optometric Association Meeting, June 29 - July 3, 2016 Boston, USA; Global Specialty Lens Symposium, January 21-24, 2016 Las Vegas, USA; American Academy of Ophthalmology (AAO 2016- Innovate), October 15-18, 2016 Chicago, USA; American Glaucoma Society Annual Meeting, March 03-06, 2016 Fort Lauderdale, USA; Asia Pacific Glaucoma Society Congress, July 14-16, 2016 Chiang Mai, Thailand; for more meetings visit Ophthalmology Meetings

Cornea & Corneal Diseases

The cornea is the transparent exterior part of the eye that covers the iris, pupil, and foremost chamber. The cornea, with the front chamber and lens, refracts light, with the cornea representing around 66% of the eye's aggregate optical force. Corneal diseases, for example, corneal ulceration, epithelial keratitis and drug-induced epithelial keratitis, corneal degeneration, repetitive corneal disintegration and different corneal issue can influence the cornea and at last prompt the external eye disease that could wind up with perpetual visual impairment.

Relevant Conferences:

International Conference and Expo on Cataract & Refractive Surgery August 04-06, 2016 Manchester, UK; 6th Global Ophthalmologists Annual Meeting, May 16-18, 2016 Osaka, Japan; 7th European Ophthalmology Conference, June 16-18, 2016, Alicante, Spain; 8th Global Ophthalmology Meeting July 18-20, 2016 Chicago, USA; World Ophthalmology Conference September 15-17, 2016 Berlin, Germany; 2nd International Conference on Eye and Vision September 26-28, 2016 Miami, USA; International Conference & Expo on Optometry and Vision Science October 27-29, 2016 Rome, Italy; 9th World Ophthalmic Conference October 24-26, 2016 Istanbul, Turkey; Global Ophthalmology and Glaucoma Conference November 7-9, 2016 Melbourne, Australia; Cornea Day 2016, May 06, 2016, New Orleans, USA; Gordon Research Conference (GRC) on "Biology and Pathobiology of the Cornea, February 27-29, 2016, California, USA; World Cornea Congress VIII, May 06-10, 2016, New Orleans, USA; EUCORNEA September 12-14, 2016, Barcelona, Spain; Macula of Paris, January 15, 2016 Paris; American Academy of Ophthalmology (AAO 2016- Innovate), October 15-18, 2016 Chicago, USA; American Glaucoma Society Annual Meeting, March 03-06, 2016 Fort Lauderdale, USA; Asia Pacific Glaucoma Society Congress, July 14-16, 2016 Chiang Mai, Thailand; for more meetings visit Ophthalmology Meetings

Neuro-Ophthalmology

The incorporation of neurology and ophthalmology leads to Neuro-Ophthalmology. The nervous system diseases which affect the pupillary reflexes, vision, eye movements are taken into consideration under the branch of neuro-ophthalmology. Diplopia, ocular myasthenia gravis, optic neuritis, optic neuropathy, papilledema, idiopathic intracranial hypertension, brain tumors or stroke affecting vision, unexplained visual loss, headaches, blepharospasm or hemifacial spasm are the few commonly diseases associated with neuro-ophthalmology.

Relevant Conferences:

6th Global Ophthalmologists Annual Meeting, May 16-18, 2016 Osaka, Japan; 7th European Ophthalmology Conference, June 16-18, 2016, Alicante, Spain; 8th Global Ophthalmology Meeting July 18-20, 2016 Chicago, USA; International Conference and Expo on Cataract & Refractive Surgery August 04-06, 2016 Manchester, UK; World Ophthalmology Conference September 15-17, 2016 Berlin, Germany; 2nd International Conference on Eye and Vision September 26-28, 2016 Miami, USA; International Conference & Expo on Optometry and Vision Science October 27-29, 2016 Rome, Italy; 9th World Ophthalmic Conference October 24-26, 2016 Istanbul, Turkey; Global Ophthalmology and Glaucoma Conference November 7-9, 2016 Melbourne, Australia; 42nd North American Neuro-Ophthalmology Society Annual Meeting, February 27-March 03, 2016, Tucson, USA; 8th Annual Asian Neuro-Ophthalmology Society Congress (ASNOS), October 23-25, 2016, Beijing, China; The Royal College Of Ophthalmologists Annual Congress, May 24-26, 2016 Birmingham, UK; World Ophthalmology Congress, February 5-9, 2016, Guadalajara, Mexico; American Academy of Ophthalmology (AAO 2016- Innovate), October 15-18, 2016 Chicago, USA; American Glaucoma Society Annual Meeting, March 03-06, 2016 Fort Lauderdale, USA; Asia Pacific Glaucoma Society Congress, July 14-16, 2016 Chiang Mai, Thailand; for more meetings visit Ophthalmology Meetings

Glaucoma: Visual Field Loss

The damage of the optic nerve due to high intraocular pressure causes the glaucoma and if it is untreated than it will progresses to vision loss with the initiation of unobserved blind spots at the edges of visual field followed by tunnel vision and finally to blindness. The causes of glaucoma include optic nerve damage along with the several underlying causes which are unknown. According to world health organization (WHO) glaucoma is the 2nd major cause of blindness across the globe.

Relevant Conferences:

Global Ophthalmology and Glaucoma Conference November 7-9, 2016 Melbourne, Australia; 6th Global Ophthalmologists Annual Meeting, May 16-18, 2016 Osaka, Japan; 7th European Ophthalmology Conference, June 16-18, 2016, Alicante, Spain; 8th Global Ophthalmology Meeting July 18-20, 2016 Chicago, USA; International Conference and Expo on Cataract & Refractive Surgery August 04-06, 2016 Manchester, UK; World Ophthalmology Conference September 15-17, 2016 Berlin, Germany; 2nd International Conference on Eye and Vision September 26-28, 2016 Miami, USA; International Conference & Expo on Optometry and Vision Science October 27-29, 2016 Rome, Italy; 9th World Ophthalmic Conference October 24-26, 2016 Istanbul, Turkey; American Glaucoma Society Annual Meeting, March 03-06, 2016, Fort Lauderdale, USA; 3rd Asia-Pacific Glaucoma Conference, July 14-16, 2016, Chiang Mai, Thailand; European Glaucoma Society Conference, June 19-22, 2016, Prague, Czech Republic; Glaucoma 360 Annual Gala, January 28-29, 2016, California, USA; 8th International Congress on Glaucoma Surgery, February 17-20, 2016, Muscat, Oman; American Academy of Ophthalmology (AAO 2016- Innovate), October 15-18, 2016 Chicago, USA; American Glaucoma Society Annual Meeting, March 03-06, 2016 Fort Lauderdale, USA; Asia Pacific Glaucoma Society Congress, July 14-16, 2016 Chiang Mai, Thailand; for more meetings visit Ophthalmology Meetings

The Science of Orthoptics

Orthoptics is the study and treatment of improper or defective vision (binocular vision), abnormal functioning and action of ocular muscles or inappropriate visual habits. A clinical approach of vision therapy has been practiced to treat the binocular vision defects, nystagmus, strabismus, amblyopia and certain visual disorders.

Relevant Conferences:

6th Global Ophthalmologists Annual Meeting, May 16-18, 2016 Osaka, Japan; 7th European Ophthalmology Conference, June 16-18, 2016, Alicante, Spain; 8th Global Ophthalmology Meeting July 18-20, 2016 Chicago, USA; International Conference and Expo on Cataract & Refractive Surgery August 04-06, 2016 Manchester, UK; World Ophthalmology Conference September 15-17, 2016 Berlin, Germany; 2nd International Conference on Eye and Vision September 26-28, 2016 Miami, USA; International Conference & Expo on Optometry and Vision Science October 27-29, 2016 Rome, Italy; 9th World Ophthalmic Conference October 24-26, 2016 Istanbul, Turkey; Global Ophthalmology and Glaucoma Conference November 7-9, 2016 Melbourne, Australia; Association for Research in Vision and Ophthalmology 2016 (ARVO), May 1-5, 2016, Seattle, USA; IOA XIIIth International Orthoptic Congress, June 27-30, 2016, Rotterdam, The Netherlands; European Association for Vision and Eye Research (EVER), October 5-8, 2016, Nice, France; American Academy of Ophthalmology Meeting, October 15-18, 2016, Chicago, USA; The 12th European Glaucoma Society Congress, June 19-22, 2016 Prague, Czech Republic; American Academy of Ophthalmology (AAO 2016- Innovate), October 15-18, 2016 Chicago, USA; American Glaucoma Society Annual Meeting, March 03-06, 2016 Fort Lauderdale, USA; Asia Pacific Glaucoma Society Congress, July 14-16, 2016 Chiang Mai, Thailand; for more meetings visit Ophthalmology Meetings

Ophthalmology Novel Approaches

Novel approaches are referred to the techniques and procedure which is used to treat the ailment in specific manner to gain the maximum therapeutic effect. The novel approaches could be development in the ophthalmic formulation of drugs to reach out the desired site of action through different drug delivery systems and also usage of biomaterials, tissue science technologies, stem science technology to eradicate the various eye diseases.

Relevant Conferences:

6th Global Ophthalmologists Annual Meeting, May 16-18, 2016 Osaka, Japan, Global Pediatric Ophthalmology Congress, June 06-7, 2016 London, UK; 8th Global Ophthalmology Meeting July 18-20, 2016 Chicago, USA; International Conference and Expo on Cataract & Refractive Surgery Aug 04-05, 2016 Manchester, UK; 9thGlobal Ophthalmology Summit, August 24-26, 2016 Sao Paulo, Brazil; 7thEuropean Ophthalmology Conference, September 21-23, 2016 Amsterdam, Netherlands; 2nd International Conference on Eye and Vision September 26-28, 2016 Orlando, Florida, USA; Global Ophthalmology & Glaucoma Conference, October 13-15, 2016 Kuala Lumpur, Malaysia; International Conference & Expo on Optometry and Vision Science October 27-29, 2016 Rome, Italy; World Ophthalmology Conference, November 24-26, 2016 Melbourne, Australia; Association for Research in Vision and Ophthalmology 2016 (ARVO), May 1-5, 2016, Seattle, USA; IOA XIIIth International Orthoptic Congress, June 27-30, 2016, Rotterdam, The Netherlands; European Association for Vision and Eye Research (EVER), October 5-8, 2016, Nice, France; American Academy of Ophthalmology Meeting, October 15-18, 2016, Chicago, USA; The 12th European Glaucoma Society Congress, June 19-22, 2016 Prague, Czech Republic; American Academy of Ophthalmology (AAO 2016- Innovate), October 15-18, 2016 Chicago, USA; American Glaucoma Society Annual Meeting, March 03-06, 2016 Fort Lauderdale, USA; Asia Pacific Glaucoma Society Congress, July 14-16, 2016 Chiang Mai, Thailand; for more meetings visit Ophthalmology Meetings

Ocular Microbiology and Immunology

Fungi, parasites, bacteria and virus can enter the human body and are capable enough to spread to attack the interior surface of an eye thus spreading the infection. The immune system plays a crucial role to inhibit the effect of infections of eye and also during the corneal transplantation since transplantation is increasing rapidly. This scientific track highlights the significance and connection of ocular microbiology and immunology.

Relevant Conferences:

6th Global Ophthalmologists Annual Meeting, May 16-18, 2016 Osaka, Japan, Global Pediatric Ophthalmology Congress, June 06-7, 2016 London, UK; 8th Global Ophthalmology Meeting July 18-20, 2016 Chicago, USA; International Conference and Expo on Cataract & Refractive Surgery Aug 04-05, 2016 Manchester, UK; 9thGlobal Ophthalmology Summit, August 24-26, 2016 Sao Paulo, Brazil; 7thEuropean Ophthalmology Conference, September 21-23, 2016 Amsterdam, Netherlands; 2nd International Conference on Eye and Vision September 26-28, 2016 Orlando, Florida, USA; Global Ophthalmology & Glaucoma Conference, October 13-15, 2016 Kuala Lumpur, Malaysia; International Conference & Expo on Optometry and Vision Science October 27-29, 2016 Rome, Italy; World Ophthalmology Conference, November 24-26, 2016 Melbourne, Australia; ICODDD 2016: 18th International Conference on Ocular Diseases Drug Discovery, April 22-23, 2016, London, UK; Vail Vitrectomy 2016, February 20-21, 2016, Colorado, USA; 8th Ocular Diseases Drug Discovery Conference, March 21-22, 2016, San Diego, USA; The 7th International Conference on Ocular Infections, September 3-4, 2016 Barcelona, Spain; 2nd San Raffaele OCT FORUM, April 12-13, 2016, Milan, Italy; American Academy of Ophthalmology (AAO 2016- Innovate), October 15-18, 2016 Chicago, USA; American Glaucoma Society Annual Meeting, March 03-06, 2016 Fort Lauderdale, USA; Asia Pacific Glaucoma Society Congress, July 14-16, 2016 Chiang Mai, Thailand; for more meetings visit Ophthalmology Meetings

Ophthalmic Research & Drug Delivery

The aim and scope of ophthalmic research is to study the diseases minutely to eradicate the problems associated with vision and eye health. With the latest technological development and modern treatments in the field of ophthalmology the new techniques have been significantly improvising the life of humans. The detection of diseases through biomarkers aid the efficacy of treatment and new technological procedure such as stem cell, tissue science and use of biomaterial can change the perception of human vision. This scientific track dedicated to the latest technology, amendments, techniques and procedures in the field of Ophthalmology.

Relevant Conferences:

6th Global Ophthalmologists Annual Meeting, May 16-18, 2016 Osaka, Japan, Global Pediatric Ophthalmology Congress, June 06-7, 2016 London, UK; 8th Global Ophthalmology Meeting July 18-20, 2016 Chicago, USA; International Conference and Expo on Cataract & Refractive Surgery Aug 04-05, 2016 Manchester, UK; 9thGlobal Ophthalmology Summit, August 24-26, 2016 Sao Paulo, Brazil; 7thEuropean Ophthalmology Conference, September 21-23, 2016 Amsterdam, Netherlands; 2nd International Conference on Eye and Vision September 26-28, 2016 Orlando, Florida, USA; Global Ophthalmology & Glaucoma Conference, October 13-15, 2016 Kuala Lumpur, Malaysia; International Conference & Expo on Optometry and Vision Science October 27-29, 2016 Rome, Italy; World Ophthalmology Conference, November 24-26, 2016 Melbourne, Australia; 8thOcular Diseases Drug Discovery Conference, March 21-22, 2016, San Diego, USA; World Ophthalmology Congress, February 5-9, 2016, Guadalajara, Mexico; Retina 2016, Hawaii, January 16-22, 2016, USA; World Cornea Congress VIII, May 06-10, 2016, New Orleans, USA; 8th International Congress on Glaucoma Surgery, February 17-20, 2016, Muscat, Oman; American Academy of Ophthalmology (AAO 2016- Innovate), October 15-18, 2016 Chicago, USA; American Glaucoma Society Annual Meeting, March 03-06, 2016 Fort Lauderdale, USA; Asia Pacific Glaucoma Society Congress, July 14-16, 2016 Chiang Mai, Thailand; for more meetings visit Ophthalmology Meetings

Entrepreneurs Investment Meet

A global platform aimed to connect ophthalmic industries, Proposers, Entrepreneurs and the Investors worldwide. With a vision to provide and facilitate the most efficient and viable business meeting place for engaging people in constructive discussions, evaluation and execution for a promising future in the field of ophthalmology.

Relevant Conferences:

6th Global Ophthalmologists Annual Meeting, May 16-18, 2016 Osaka, Japan, Global Pediatric Ophthalmology Congress, June 06-7, 2016 London, UK; 8th Global Ophthalmology Meeting July 18-20, 2016 Chicago, USA; International Conference and Expo on Cataract & Refractive Surgery Aug 04-05, 2016 Manchester, UK; 9thGlobal Ophthalmology Summit, August 24-26, 2016 Sao Paulo, Brazil; 7thEuropean Ophthalmology Conference, September 21-23, 2016 Amsterdam, Netherlands; 2nd International Conference on Eye and Vision September 26-28, 2016 Orlando, Florida, USA; Global Ophthalmology & Glaucoma Conference, October 13-15, 2016 Kuala Lumpur, Malaysia; International Conference & Expo on Optometry and Vision Science October 27-29, 2016 Rome, Italy; World Ophthalmology Conference, November 24-26, 2016 Melbourne, Australia; American Academy of Ophthalmology (AAO 2016- Innovate), October 15-18, 2016 Chicago, USA; American Glaucoma Society Annual Meeting, March 03-06, 2016 Fort Lauderdale, USA; Asia Pacific Glaucoma Society Congress, July 14-16, 2016 Chiang Mai, Thailand; for more meetings visit Ophthalmology Meetings

OMICS International played host to a diverse panel of key members of the Ophthalmology community from research lab, industry, academia and financial investment practices, discussing the future of Ophthalmology specialties. This event was really aimed for examining where the real ophthalmological specialties are going in the future and purpose of the event was to provide an opportunity for cross fertilization of ideas and development of ideas, in the field of Ophthalmology.

The conference had multiple sessions, Keynote presentations, panel discussions and poster sessions. We received active participation from various scientists, researchers, students and leaders from the field of Ophthalmology who made this event successful.

The conference aimed a parallel rail with theme Scientific eye for visual intelligence. Focusing on

Ophthalmology 2015 Organizing Committee would like to thank the Moderators of the conference, Dr. Vijaya Juturu, Omni Active Health Technologies Inc., USA, Dr. Emmanuel S Buys, Massachusetts General Hospital, USA and Dr. Yoko Miura, University of Luebeck, Germany for their contributions which resulted in the smooth functioning of the conference.

The conference was initiated with a series of eponymous lectures delivered by both Honorable Guests and members of the Keynote forum. The list includes:

Instruction course carried by Dr. Atul Bansal, Consultant Ophthalmologist, University Hospital Coventry & Warwickshire, UK customising surgical glaucoma treatment to the patient and their disease

OMICS 5th International Conference on Clinical & Experimental Ophthalmology was a great success with the support of international, multiprofessional steering committee and coordinated by the Journal of Clinical & Experimental Ophthalmology, International Journal of Ophthalmic Pathology and Biological Systems: Open Access.

Ophthalmology-2014

In the presence of inter professional researchers and practitioners involved in the development of high quality education in all aspects of clinical skills, OMICS 4th International Conference on Clinical & Experimental Ophthalmology was held during July 14-16, 2014 in Baltimore, USA

OMICS Group played host to a diverse panel of key members of the Ophthalmology community from research lab, industry, academia and financial investment practices, discussing the future of Ophthalmology specialties. This event was really aimed for examining where the real ophthalmological specialties are going in the future and purpose of the event was to provide an opportunity for cross fertilization of ideas and development of ideas, in the field of Ophthalmology.

Focusing on Cornea and External Eye Disease, Retina and Retinal Disorders, Glaucoma: Visual Field Loss, Neuro-Ophthalmology, Ocular Microbiology and Immunology, Research Trends in Surgical and Medical Ophthalmology,Ophthalmic Research and Drug Development, and Novel Approaches to Ophthalmology Therapeutics as well, the three days of discussions enabled professionals to gain an insight into the current innovations and opened up networking opportunities.

Ophthalmology-2014 Organizing Committee would like to thank the Moderator of the conference, Dr. Rebecca M. Sappington, Vanderbilt University School of Medicine, USA who contributed a lot for the smooth functioning of this event. We are also thank full to all the speakers who made this event a grand success, our special thanks to Dr. Chris Hekimian, Inventor of the Quantitative Retina Test Grid for exhibiting at the conference, many thanks to all the media partners for the promotion of our event.

The highlights of the meeting were the eponymous lectures, delivered by Chi-Chao Chan from National Institutes of Health, USAand Ashim K Mitra from University of Missouri-Kansas City, USA, Sayon Roy from Boston University School of Medicine, USA, Jayne S. Weiss fromLouisiana State University Health Sciences Center, USA. These talks were of great interest to the general ophthalmologists and were enormously informative.

OMICS 4th International Conference on Clinical & Experimental Ophthalmology was a great success with the support of international, multiprofessional steering committee and coordinated by the Journal of Clinical & Experimental Ophthalmology, International Journal of Ophthalmic Pathology and Biological Systems: Open Access.

Ophthalmology-2013

The 3rd International Conference on Clinical & Experimental Ophthalmology, hosted by the OMICS Group was successfully held during April 15-17, 2013 in Chicago/Northbrook, USA. Outstanding response and active participation received from the Researchers, Leaders from Pharmaceutical R&D sectors, Government Organizations, and Principal Investigators. And Editorial Board Members of OMICS Group helped in making this meeting an ostentatious success.

Keynote Speakers:

Dr. Chi-Chao Chan, National Institutes of Health, USA

Dr. Lea Hyvarinen, Technical University of Dortmund, Germany

Dr. Christopher Hekimian, dxdt Engineering and Research, USA

Dr. Sayon Roy, University of Naples, Italy

A series of invited lectures by Honorable guests and members of the Keynote forum marked the commencement of the event. Keynote session was very prolific to the scientific community and they lifted up solutions and illustrated a way on the theme "Intolerable Disparity in Vision and Novel Therapies"

Scientific sessions established active contribution from researchers and principal investigators, and the Poster presentations were phenomenally excellent with the enthusiastic students and fellow researchers. It established a new prospect and hopes on ongoing projects in field of Ophthalmology.

OMICS Group felicitated all the Organizing Committee Members and Editorial Board Members who enthusiastically participated in the conference and made this meeting a huge success.

OMICS Group on behalf of OCMs and EBMs congratulates all the Best Poster Awardees for their outstanding contribution in the field of Ophthalmology and simultaneously encourage all the participants who tried to put their efforts in poster presentations and wish them success for their future research.

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