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Archive for November, 2016

Risks – Bone marrow transplant – Mayo Clinic

Friday, November 18th, 2016

A bone marrow transplant poses many risks of complications, some potentially fatal.

The risk can depend on many factors, including the type of disease or condition, the type of transplant, and the age and health of the person receiving the transplant.

Although some people experience minimal problems with a bone marrow transplant, others may develop complications that may require treatment or hospitalization. Some complications could even be life-threatening.

Complications that can arise with a bone marrow transplant include:

Your doctor can explain your risk of complications from a bone marrow transplant. Together you can weigh the risks and benefits to decide whether a bone marrow transplant is right for you.

If you receive a transplant that uses stem cells from a donor (allogeneic transplant), you may be at risk of developing graft-versus-host disease (GVHD). This condition occurs when the donor stem cells that make up your new immune system see your body's tissues and organs as something foreign and attack them.

Many people who have an allogeneic transplant get GVHD at some point. The risk of GVHD is a bit greater if the stem cells come from an unrelated donor, but it can happen to anyone who gets a bone marrow transplant from a donor.

GVHD may happen at any time after your transplant. However, it's more common after your bone marrow has started to make healthy cells.

There are two kinds of GVHD: acute and chronic. Acute GVHD usually happens earlier, during the first months after your transplant. It typically affects your skin, digestive tract or liver. Chronic GVHD typically develops later and can affect many organs.

Chronic GVHD signs and symptoms include:

Oct. 13, 2016

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Transplantation of Hypoxia-preconditioned Mesenchymal Stem …

Friday, November 18th, 2016

OBJECTIVES:

This study explored the novel strategy of hypoxic preconditioning of bone marrow mesenchymal stem cells before transplantation into the infarcted heart to promote their survival and therapeutic potential of mesenchymal stem cell transplantation after myocardial ischemia.

Mesenchymal stem cells from green fluorescent protein transgenic mice were cultured under normoxic or hypoxic (0.5% oxygen for 24 hours) conditions. Expression of growth factors and anti-apoptotic genes were examined by immunoblot. Normoxic or hypoxic stem cells were intramyocardially injected into the peri-infarct region of rats 30 minutes after permanent myocardial infarction. Death of mesenchymal stem cells was assessed in vitro and in vivo after transplantation. Angiogenesis, infarct size, and heart function were measured 6 weeks after transplantation.

Hypoxic preconditioning increased expression of pro-survival and pro-angiogenic factors including hypoxia-inducible factor 1, angiopoietin-1, vascular endothelial growth factor and its receptor, Flk-1, erythropoietin, Bcl-2, and Bcl-xL. Cell death of hypoxic stem cells and caspase-3 activation in these cells were significantly lower compared with that in normoxic stem cells both in vitro and in vivo. Transplantation of hypoxic versus normoxic mesenchymal stem cells after myocardial infarction resulted in an increase in angiogenesis, as well as enhanced morphologic and functional benefits of stem cell therapy.

Hypoxic preconditioning enhances the capacity of mesenchymal stem cells to repair infarcted myocardium, attributable to reduced cell death and apoptosis of implanted cells, increased angiogenesis/vascularization, and paracrine effects.

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CD34 – Wikipedia

Friday, November 18th, 2016

Hematopoietic progenitor cell antigen CD34 also known as CD34 antigen is a protein that in humans is encoded by the CD34 gene.[3][4][5]

CD34 is a cluster of differentiation first described independently by Civin et al. and Tindle et al.[6][7][8][9] in a cell surface glycoprotein and functions as a cell-cell adhesion factor. It may also mediate the attachment of stem cells to bone marrow extracellular matrix or directly to stromal cells.

The CD34 protein is a member of a family of single-pass transmembrane sialomucin proteins that show expression on early hematopoietic and vascular-associated tissue.[10] However, little is known about its exact function.[11]

CD34 is also an important adhesion molecule and is required for T cells to enter lymph nodes. It is expressed on lymph node endothelia, whereas the L-selectin to which it binds is on the T cell.[12][13] Conversely, under other circumstances CD34 has been shown to act as molecular "Teflon" and block mast cell, eosinophil and dendritic cell precursor adhesion, and to facilitate opening of vascular lumens.[14][15] Finally, recent data suggest CD34 may also play a more selective role in chemokine-dependent migration of eosinophils and dendritic cell precursors.[16][17] Regardless of its mode of action, under all circumstances CD34, and its relatives podocalyxin and endoglycan, facilitates cell migration.[10][16]

Cells expressing CD34 (CD34+ cell) are normally found in the umbilical cord and bone marrow as hematopoietic cells, a subset of mesenchymal stem cells, endothelial progenitor cells, endothelial cells of blood vessels but not lymphatics (except pleural lymphatics), mast cells, a sub-population dendritic cells (which are factor XIIIa-negative) in the interstitium and around the adnexa of dermis of skin, as well as cells in soft tissue tumors like DFSP, GIST, SFT, HPC, and to some degree in MPNSTs, etc. The presence of CD34 on non-hematopoietic cells in various tissues has been linked to progenitor and adult stem cell phenotypes.[18]

It is important to mention that Long-Term Hematopoietic Stem Cells [LT-HSCs] in mice and humans are the hematopoietic cells with the greatest self-renewal capacity.[citation needed] Human HSCs express CD34 marker.[citation needed]

CD34 is expressed in roughly 20% of murine hematopoietic stem cells,[19] and can be stimulated and reversed.[20]

CD34+ cells may be isolated from blood samples using immunomagnetic or immunofluorescent methods.

Antibodies are used to quantify and purify hematopoietic progenitor stem cells for research and for clinical bone marrow transplantation. However, counting CD34+ mononuclear cells may overestimate myeloid blasts in bone marrow smears due to hematogones (B lymphocyte precursors) and CD34+ megakaryocytes.

Cells observed as CD34+ and CD38- are of an undifferentiated, primitive form; i.e., they are multipotential hemopoietic stem cells. Thus, because of their CD34+ expression, such undifferentiated cells can be sorted out.

In tumors, CD34 is found in alveolar soft part sarcoma, preB-ALL (positive in 75%), AML (40%), AML-M7 (most), dermatofibrosarcoma protuberans, gastrointestinal stromal tumors, giant cell fibroblastoma, granulocytic sarcoma, Kaposis sarcoma, liposarcoma, malignant fibrous histiocytoma, malignant peripheral nerve sheath tumors, mengingeal hemangiopericytomas, meningiomas, neurofibromas, schwannomas, and papillary thyroid carcinoma.

A negative CD34 may exclude Ewing's sarcoma/PNET, myofibrosarcoma of the breast, and inflammatory myofibroblastic tumors of the stomach.

Injection of CD34+ hematopoietic Stem Cells has been clinically applied to treat various diseases including Spinal Cord Injury,[21] Liver Cirrhosis[22] and Peripheral Vascular disease.[23] Research has shown that CD34+ cells are relatively more in men than in women in the reproductive age among Spinal Cord Injury victims.[24]

CD34 has been shown to interact with CRKL.[25] It also interacts with L-selectin, important in inflammation.

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Stem Cell Therapy – Premier Stem Cell Institute

Friday, November 18th, 2016

The Re-Brand Premier Regenerative Stem Cell and Wellness Centers, recently rebranded their business from Premier Stem Cell Institute, in response to expanding locations, technology, and treatments. This move reflects the growth and success this company has undergone recently and goals for the future.

PRSC and Wellness Centers President, Kandace Stolz said, This rebrand is the culmination of the years of work weve put into stem cell medicine. Were growing and healing more patients than we ever have before, this new name reflects those accomplishments and gives us room grow. We are so thrilled for this move and cant wait to do even more for our patients going forward.

Premier Regenerative Stem Cell and Wellness Centers will continue to partner with the NFL Alumni Association and treat current and former professional athletes. PRSC remains dedicated to studying stem cell treatment by collecting and tracking data to further stem cell progress and maximize results for all patients. PRSCs commitment to being a leader in stem cell and regenerative medicine is unwavering and will continue to innovate and learn to heal and improve the quality of life for all patients.

About Premier Regenerative Stem Cell and Wellness Centers: PRSC is the leading research and treatment facility in Colorado, providing innovative medicine and therapies for those in pain by harnessing the bodys own natural healing power of stem cells. As team of cutting-edge medical experts, PRSC is dedicated to treating patients by using their own stem cells to heal, improve quality of life, and battle the acute pain of chronic illnesses. Premier Regenerative Stem Cell and Wellness Center locations include Loveland Colorado, Dallas Texas, St. Louis, Missouri, and Jacksonville, Florida. PRSC has plans to expand to other major cities across the United States in the near future.

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Population Reference Bureau (PRB)

Thursday, November 17th, 2016

Regions / Countries

Select Country Afghanistan Albania Algeria American Samoa Andorra Angola Anguilla Antigua and Barbuda Argentina Armenia Aruba Australia Austria Azerbaijan Bahamas Bahrain Bangladesh Barbados Belarus Belgium Belize Benin Bermuda Bhutan Bolivia Bosnia-Herzegovina Botswana Brazil Brunei Bulgaria Burkina Faso Burundi Cambodia Cameroon Canada Cape Verde Central African Republic Chad Channel Islands Chile China Hong Kong, SAR Macao, SAR Colombia Comoros Congo Congo, Dem. Rep. of Costa Rica Cote d'Ivoire Croatia Cuba Cyprus Czech Republic Denmark Djibouti Dominica Dominican Republic Timor-Leste Ecuador Egypt El Salvador Equatorial Guinea Eritrea Estonia Ethiopia Fiji Finland France French Guiana French Polynesia Gabon Gambia Georgia Germany Ghana Greece Greenland Grenada Guadeloupe Guam Guatemala Guinea Guinea-Bissau Guyana Haiti Honduras Hungary Iceland India Indonesia Iran Iraq Ireland Israel Italy Jamaica Japan Jordan Kazakhstan Kenya Kiribati Korea, North Korea, South Kuwait Kyrgyzstan Laos Latvia Lebanon Lesotho Liberia Libya Liechtenstein Lithuania Luxembourg Macedonia Madagascar Malawi Malaysia Maldives Mali Malta Marshall Islands Martinique Mauritania Mauritius Mexico Federated States of Micronesia Moldova Monaco Mongolia Montenegro Morocco Mozambique Myanmar Namibia Nauru Nepal Netherlands New Caledonia New Zealand Nicaragua Niger Nigeria Norway Oman Pakistan Palau Palestinian Territory Panama Papua New Guinea Paraguay Peru Philippines Poland Portugal Puerto Rico Qatar Reunion Romania Russia Rwanda Samoa Sao Tome and Principe Saudi Arabia Senegal Serbia Seychelles Sierra Leone Singapore Slovakia Slovenia Solomon Islands Somalia South Africa Spain Sri Lanka St. Kitts-Nevis St. Lucia St. Vincent & the Grenadines Sudan Suriname Swaziland Sweden Switzerland Syria Taiwan Tajikistan Tanzania Thailand Togo Tonga Trinidad and Tobago Tunisia Turkey Turkmenistan Tuvalu Uganda Ukraine United Arab Emirates United Kingdom United States Uruguay Uzbekistan Vanuatu Venezuela Vietnam Western Sahara Yemen Zambia Zimbabwe

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Genetically Modified Organisms – European Commission

Thursday, November 17th, 2016

Food and feed generally originates from plants and animals grown and bred by humans for several thousand years. Over time, those plants and animals with the most desirable characteristics were chosen for breeding the next generations of food and feed. This was, for example, the case for plants with an increased resistance to environmental pressures such as diseases or with an increased yield.

These desirable characteristics appeared through naturally occurring variations in the genetic make-up of those plants and animals. In recent times, it has become possible to modify the genetic make-up of living cells and organisms using techniques of modern biotechnology called gene technology. The genetic material is modified artificially to give it a new property (e.g. a plant's resistance to a disease, insect or drought, a plant's tolerance to a herbicide, improving a food's quality or nutritional value, increased yield).

Such organisms are called "genetically modified organisms" (GMOs). Food and feed which contain or consist of such GMOs, or are produced from GMOs, are called "genetically modified (GM) food or feed".

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Dr. Geeta Shroff’s Stem Cell Technology | Healthcare Hacks

Tuesday, November 15th, 2016

About Dr. Geeta Shroff and her technology

Dr. Geeta Shroff is an infertility expert located in Delhi, India, and the first individual in the world to develop an infinite number of pure human embryonic stem cell lines from using just one donated embryo. The single donated embryo originated from an IVF donor, which negates the debate over destroying numerous embryos for therapy.

Her partnering physician and anesthesiologist is Dr. Ashish Verma. The two have been working together since before the discovery of this technology in 1999. They have recently filed a patent with the World Intellectual Property Organization, covering over 126 countries including India and the United States.

Every day we hear of treatments around the world using stem cells (fetal, umbilical cord, adult, nasal, rats, etc.). Dr. Geeta Shroff has developed the only purely human embryonic stem cell lines that do not show any immune reaction in the body. Embryonic stem cells do not have any antigenic proteins on their surface and therefore do not require immunosuppressant drugs to combat rejection.

Importantly, despite the theoretical risks of human embryonic stem cells, no side effects have been reported from her therapy. Dr. Geeta Shroff practices under the guise of the Indian Health Council, which allows her to conduct clinical trials on incurable or terminal patients. She operates out of two hospitals in Delhi, India, which have ISO certifications (International Organization for Standardization) and BCI certifications (awarded by a British independent agency). Her lab is in compliance with Good Manufacturing Practice and Good Labratory Practice.

Scientific explanation of this technology

The following text was extracted from an article by Dr. Laurance Johnston Ph.D. "Embryonic Stem Cell Therapy" was published on the Healing Therapies website.

Basically, after an egg is fertilized, an embryo is formed, which then splits into a two cells. In Stem Cell Now (2006), author Christopher Scott compares the process to dividing a soap bubble with a knife, creating two smaller bubbles within the confines of the original. Cut again, and it becomes four bubbles or a four-cell embryo. This division goes on, successively creating 8, 16, 32, 64, 128-cell embryo, the total volume changing little.

Between four and six days, the cells rearrange into two layers: an outer layer that will develop into placental and amniotic tissue and a few dozen cells called the inner-cell mass (ICM) which turns into everything else. Now labeled a blastocyst, the embryo is about 0.1-mm across or the size of the period at the end of this sentence.

As the cells continue to develop, they increasingly lose their omnipotent nature. After about two weeks, the ICM starts to organize into three specific layers that become our various tissues: 1) ectodermal layer (developing into nerve, skin, etc), 2) mesodermal (turning into blood, muscle, bone, etc), and 3) endodermal (differentiating into the gut, liver, pancreas, bladder, etc.).

To obtain ESCs, the ICM cells are isolated before they start turning into these layers, and grown in culture. The culturing technology has only recently emerged and requires sophisticated methodology and skill. For example, scientists have had to grow the cells on a layer of animal cells to provide nutrients and the signals needed to keep the cells from further differentiating.

In this regard, Shroffs breakthrough is that she has grown ESCs without using any animal products, including these feeder cells. By keeping the cells purely human in nature, she makes them more amenable to transplantation. The cells from her mother culture are further adapted or primed to create daughter cultures targeting specific disorders. Hence, a more specialized cell line will be used to treat individuals with SCI, stroke, diabetes, etc.

According to Dr. Shroff, the transplanted cells will home into the tissue where they are needed, to begin regeneration. Thus, even when introduced by more remote intravenous or intramuscular routes, the cells' physiological affinity for the target tissue will cause them to migrate where they are needed.

The Potential

It can be said that the complete effect of human embryonic stem cells transplanted into a patient closely resembles the time frame of the human embryos development. This includes nine months of gestation, and then the growth of a newborn baby after delivery up until five years of age where the nervous system reaches its full potential. Although often response in patients is seen immediately after transplantation, the embryonic stem cells continue their developmental process as per their pre-programmed time frame.

This human embryonic stem cell treatment has been used in a number of conditions in clinical trials on patients from all over the world at Dr. Geeta Shroffs clinics. All have shown improvement of some kind. Some of these conditions include Diabetes, spinal cord injury, Parkinsons, Multiple Sclerosis, ALS, Chronic Lyme Disease, cerebral palsy, autism, etc. Patients with complete spinal injuries as old as 16 years are seeing dramatic results such as regaining bowel and bladder control and function in their legs; Diabetics are weaning off their insulin or have been able to withdraw from medication completely; and neurodegenerative disease patients with brain lesions are seeing reversals.

*Some of this information has been used with permission from Amanda Boxtel's blog, Awakenings.

To read more....

Here's a Global Post Article on Dr. Shroff and Amy's treatment.

For related information, please read Stem Cell Cheat Sheet.

For an interview with Dr. Ashish from the clinic, read Stem Cell Curiosity: Answers From India.

Amy answers frequently asked questions about her India treatment.

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Dr. Geeta Shroff's Stem Cell Technology | Healthcare Hacks

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Stem Cell Therapy for COPD | Mexico Stem Cell Therapy

Tuesday, November 15th, 2016

The increasing trend of smoking and air pollution has affected human health badly; more and more people are succumbing to diseases of airways and lungs. Air pollution and smoking are commonly present in every country especially in industrialized centers. Significant numbers of people complaining of chronic cough, breathlessness and repeated chest infections are diagnosed having airway or lung disease. When we go behind the causes of such complaints, bronchial asthma and chronic obstructive pulmonary disease come on the top. COPD is especially dangerous because it gradually causes lung damage and results in respiratory failure and heat failure.

Chronic Obstructive Pulmonary Disease is actually a disease of lung as well as airways. It is caused by chronic irritation of airways (by smoking, dust, air pollution) that sets an inflammatory response resulting in narrowing of airways and damage to the lungs. The suffers complain of cough with sputum, shortness of breath, wheezing and in advance stages body swelling due to heart failure. It is a terrifying fact that around 200 million people worldwide are suffering from chronic obstructive pulmonary disease or COPD and approximately 3 million deaths annually are attributed to this deadly disease. With so much disease burden worldwide, COPD stands among the major health problems. The question arises is there some curative treatment for COPD or not?

Previously available treatments for COPD have their only limitations and complications; they dont have curative potential rather they only improve the situation for some times. Conventional medical therapy is not effective at restoring lung function while on the other hand heart lung transplantation (an option for patients which advanced COPD and respiratory failure/heart failure) is not available to each patient due to higher cost, higher mortality and limited number of donors. This necessitates an innovative treatment of COPD; a treatment which is both curative and safely available to every patient. Such a treatment for COPD is stem cell therapy.

Stem cell therapy stands high on the list as a definite and curative treatment with potential availability for almost every person. It has passed through stages of animal experimentation and clinical trials on humans to be declared a safe treatment for chronic obstructive pulmonary disorder (COPD), emphysema, chronic bronchitis, pulmonary fibrosis and interstitial lung disease. Many countries of the world have tested stem cell therapy for cure or remission of COPD patients.

Stem cells, as we know, have the potential to differentiate into different types of cells including cells present in the lungs. When we inject stem cells in a patient with COPD and administer some specific type of factors that help cell differentiation and growth, they reach at the site of damaged cells and replace them. Stem cells take the function of damaged cells and help in healing the injury and setting off the fire of destruction. Lung function is improved gradually after stem cell transplantation and patient gets his complaints allayed in matter of months. Stem cell therapy has several advantages over heart/lung transplant and these include:

Mexico Stem Cell Therapy is among the top rated places in the world for stem cell transplantation. Our hospitals especially are registered for this purpose and comply with the guidelines of safety and standard. Latest technology and experienced stem cell physicians make the therapy happen in a very pleasant and successful environment. Patients around the world enjoy these facilities and a high standard of care.

We offer stem cell therapy for a number of diseases including lung-related diseases, such as COPD, pulmonary fibrosis, chronic bronchitis, emphysema and interstitial lung disease.

The best regenerative medicine option will be based on your medical history and health condition. Remember, the sooner you get treatment the better the results.

If you would like to find out more about treatment options, contact our patient coordinators today at (855) 768-7247. We work with you and your pulmonologist to improve your condition.

Updated Dec 29, 2015

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Regenerative Medicine | The Future of Plastic Surgery …

Tuesday, November 15th, 2016

Regenerative medicine is the science of replacing, engineering or regenerating human cells, tissues or organs to restore or establish normal form and function. This broadly encompasses the use of cells, tissues, drugs, synthetic biomaterials, and devices to help patients heal more effectively from trauma, cancer therapy, other disease processes, and birth anomalies. Regenerative medicine therapies can have goals of both healing damaged tissues and forming new tissue.

While many clinicians and scientists across all fields of medicine have been involved in regenerative medicine research and clinical advances over the last two decades, plastic surgeons have been especially instrumental in moving new therapies into the clinical arena and having a leadership role in new scientific discoveries.

Areas of ongoing research and clinical care:

Burn care: Plastic surgeons have been pioneers in the use of protein scaffolds to generate the dermal layer, or innermost layer of the skin, following burn injury.

Nerve regeneration: Plastic surgeons, in the practice of hand and upper extremity surgery, as well as lower extremity surgery, are forging new paths in the science of regenerating nerves and restoring optimal function after nerve injury. These therapies involve the use of special growth factors to stimulate nerve healing, as well as special biomaterials to serve as guides to direct the growth of nerve fibers.

Breast reconstruction: Breast reconstruction is a vital part of cancer therapy for many women. Plastic surgeons are achieving better outcomes through the use of decellularized tissue scaffolds to regenerate new tissue layers over implants in breast cancer survivors.

Wound care: Complex wounds that are difficult to heal represent a major focus for tissue engineering and regenerative medicine strategies. Skin substitutes, composed of living cells grown in a laboratory, are used to heal these types of wounds. Additionally, growth factors are being explored for improving wound healing. One of the most significant breakthroughs in regenerative therapy for wound healing has been the use of negative pressure devices. Discovered by a plastic surgeon, these devices use negative pressure and micro-mechanical forces to stimulate wound healing.

Fat grafting and adipose stem cell therapy: A significant advance in surgical regenerative medicine has been the development and refinement of techniques to transfer fat tissue in a minimally invasive manner. This allows the regeneration of fat tissue in other parts of the body, using a patient's own extra fat tissue. This technique is revolutionizing many reconstructive procedures, including breast reconstruction. Importantly, fat tissue is an important source of adult mesenchymal stem cells. Discovered by plastic surgeons, adipose derived stem cells, are easy to isolate from fat tissue, and hold tremendous promise for treating many disorders across the body.

Scar treatment: Plastic surgeons are experts in the biology of scar formation and the molecular signals that impact healing. Regenerative therapies are being developed using energy-based devices, such as laser and intense pulsed light, to improve the healing of scars.

Hand and face transplantation: The ultimate in "Tissue replacement therapy," hand and face transplantation represents a life-restoring therapy for patients with severe trauma or other disease processes that result in loss of the hands or face. Most people aren't aware of this fact, but the very first successful human organ transplant was performed by a plastic surgeon. Dr. Joseph Murray performed the first kidney transplant in 1954. Plastic surgeons have been building up on his legacy in developing this new field of hand and face transplantation. This field also blends elements of cell therapy in order to control the immune response and reduce the need for toxic immunosuppressive drugs.

Bioprosthetic interfaces connecting humans and machine: This very interesting area of regenerative practice is directed at methods of connecting severed nerve endings with powered artificial limbs. This often involves "rerouting" the severed nerve endings to different muscles so that sensors over the skin can detect the signals and transmit them to a computer that controls the artificial limb.

Bone regeneration: For patients suffering extensive face or a limb trauma, large segments of bone may be missing. Plastic surgeons are using calcium based scaffolds and biomaterials derived from bone to form new bone tissue for reconstructive purposes.

"Custom made tissue flaps." For deformities that involve complex structures such as a major part of the nose, plastic surgeons are engineering new replacement parts at another site on the body. In a process called "flap prefabrication," the structure is assembled using tissue grafts and then transferred to the deformity after healing.

Generation of new skin by tissue expansion: Another technique pioneered by plastic surgeons is the use of gradual expansion of implanted balloon devices to generate new skin tissue that can cover a deformity. This technique is revolutionizing breast reconstruction and the treatment of many birth anomalies.

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Aegean Regenerative Medicine by Dr. Angelo Tellis

Tuesday, November 15th, 2016

Dr. Angelo Tellis Regenerative Medicine Specialist

Regenerative Medicine is an exciting new field of medicine that helps the body renew itself by using powerful natural agents like Platelet Rich Plasma and adult stem cells. It is much less invasive than surgery, which can often lead to even more tissue damage. It is all natural without placing any foreign substances in the body and has much less risk and downtime compared to surgery. Aegean Regenerative Medicine specializes in two different types of services including orthopedic and cosmetic procedures.

Orthopedic:Healing agents are delivered directly to the site of tissue injury. This restarts and maximizes the healing process in a natural way. New cartilage is formed, tendons and ligaments are repaired, and joints are restored.

Cosmetic:Tumescent Liposuction is performed for shaping and sculpting areas of the body while collecting adipose tissue rich in stem cells (Liposculpting). Stem cell rich adipose tissue can be combined with Platelet Rich Plasma to naturally enhance or augment other areas of the body (breasts, buttocks, hands, face, etc.) where desired (Lipotransfer).

Aegean Regenerative Medicine is available at Crystal Coast Pain Management offices located in New Bern, Morehead City and Jacksonville, North Carolina. Call 252-636-0300 to schedule a consultation with Dr. Tellis and explore your natural options.

Advantages Tumescent liposuction and breast enhancement in one procedure. All natural- nothing artificial is used. Safe and gentle procedure. Enhancement looks and feels like natural breasts. Future breast feeding not affected. Rapid recovery. Permanent, selective treatment of problem areas with smooth, even results. Virtually no scarring at insertion sites. Significantly reduced risk of complications. Comfortable outpatient procedure. Less bleeding, bruising and swelling.

Three locations to serve you Aegean Regenerative Medicine is located in Morehead City, New Bern, and Jacksonville, NC and operates under the Crystal Coast Pain Management system and supporting providers .

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UT Southwestern, Dallas, Texas – UTSW Medicine (Patient …

Tuesday, November 15th, 2016

We Are Magnet

UT Southwestern has achieved Magnet designation, the highest honor bestowed by the American Nurses Credentialing Center (ANCC).

We've brought the leading-edge therapies and world-class care of UT Southwestern to Richardson/Plano, Las Colinas, and the Park Cities.

Clinical Center at Las Colinas The Las Colinas Obstetrics/Gynecology Clinic is a full-service practice, treating the full range of obstetric and gynecologic conditions.

Clinical Center at Park Cities The Clinical Center at Park Cities features cardiology, general internal medicine, obstetric/gynecologic, and rheumatology services.

Clinical Center at Richardson/Plano The Clinical Center at Richardson/Plano features behavioral health, cancer, neurology, obstetric/gynecologic, primary care, sports medicine, and urology services.

UT Southwestern Medical Center is honored frequently for the quality of our care and the significance of our discoveries. Some of our recent awards include the Press Ganey Beacon of Excellence Award for patient satisfaction and the National Research Consultants' Five Star National Excellence Award.

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Molecular Genetics Service – Great Ormond Street Hospital …

Tuesday, November 15th, 2016

Diagnostic, carrier and predictive testing is offered for a comprehensive range of single gene disorders as well as a DNA banking service whereby samples can be forwardedto external laboratories for approved requests providing funding is available.

A complete list oftesting services offeredis providedon this web site see:

Molecular Genetics Tests

or is available to download as a service pack:

Click here to download the price list for NHS patients

It is the responsibility of the patient's clinician to request a laboratory service/test and to ensure that all samples are correctly labelled and request forms completed to a minimum standard.

Consent is not required for DNA storage. It is the responsibility of the clinician to obtain consent before requesting a genetic test.

Click here for a copy of our Test Request Form

Click here for a copy of the Delay-Seizure (EIEE)panel proforma

Click here for a copy of the Hearing Loss panel proforma

Click here for a copy of the Immunodeficiency (PID/SCID)panel proforma

Click here for a copy of the Inflammatory Bowel Disease panel proforma

Click here for information about new NIPD tests

5ml venous blood in plastic EDTA bottles (>1ml from neonates)

Sample must be labelled with:

Tissue type and date of biopsy should be clearly documented on the referral information.

In the case of twins, special attention must be given to the identity of each sample.

Minimum criteria:

The Association for Clinical Genetic Science (ACGS)guidelines recommend at least two pieces of identifying information on every sample tube.

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Molecular phylogenetics – Wikipedia

Tuesday, November 15th, 2016

Molecular phylogenetics ([1][2]) is the branch of phylogeny that analyses hereditary molecular differences, mainly in DNA sequences, to gain information on an organism's evolutionary relationships. The result of a molecular phylogenetic analysis is expressed in a phylogenetic tree. Molecular phylogenetics is one aspect of molecular systematics, a broader term that also includes the use of molecular data in taxonomy and biogeography.

The theoretical frameworks for molecular systematics were laid in the 1960s in the works of Emile Zuckerkandl, Emanuel Margoliash, Linus Pauling, and Walter M. Fitch.[3] Applications of molecular systematics were pioneered by Charles G. Sibley (birds), Herbert C. Dessauer (herpetology), and Morris Goodman (primates), followed by Allan C. Wilson, Robert K. Selander, and John C. Avise (who studied various groups). Work with protein electrophoresis began around 1956. Although the results were not quantitative and did not initially improve on morphological classification, they provided tantalizing hints that long-held notions of the classifications of birds, for example, needed substantial revision. In the period of 19741986, DNA-DNA hybridization was the dominant technique.[4]

Every living organism contains DNA, RNA, and proteins. In general, closely related organisms have a high degree of agreement in the molecular structure of these substances, while the molecules of organisms distantly related usually show a pattern of dissimilarity. Conserved sequences, such as mitochondrial DNA, are expected to accumulate mutations over time, and assuming a constant rate of mutation, provides a molecular clock for dating divergence. Molecular phylogeny uses such data to build a "relationship tree" that shows the probable evolution of various organisms. With the invention of Sanger sequencing in 1977 it became possible to isolate and identify these molecular structures.[5][6]

The most common approach is the comparison of homologous sequences for genes using sequence alignment techniques to identify similarity. Another application of molecular phylogeny is in DNA barcoding, wherein the species of an individual organism is identified using small sections of mitochondrial DNA or chloroplast DNA. Another application of the techniques that make this possible can be seen in the very limited field of human genetics, such as the ever-more-popular use of genetic testing to determine a child's paternity, as well as the emergence of a new branch of criminal forensics focused on evidence known as genetic fingerprinting.

A comprehensive step-by-step protocol on constructing phylogenetic tree, including DNA/Amino Acid contiguous sequence assembly, multiple sequence alignment, model-test (testing best-fitting substitution models) and phylogeny reconstruction using Maximum Likelihood and Bayesian Inference, is available at Nature Protocol[7]

Early attempts at molecular systematics were also termed as chemotaxonomy and made use of proteins, enzymes, carbohydrates, and other molecules that were separated and characterized using techniques such as chromatography. These have been replaced in recent times largely by DNA sequencing, which produces the exact sequences of nucleotides or bases in either DNA or RNA segments extracted using different techniques. In general, these are considered superior for evolutionary studies, since the actions of evolution are ultimately reflected in the genetic sequences. At present, it is still a long and expensive process to sequence the entire DNA of an organism (its genome). However, it is quite feasible to determine the sequence of a defined area of a particular chromosome. Typical molecular systematic analyses require the sequencing of around 1000 base pairs. At any location within such a sequence, the bases found in a given position may vary between organisms. The particular sequence found in a given organism is referred to as its haplotype. In principle, since there are four base types, with 1000 base pairs, we could have 41000 distinct haplotypes. However, for organisms within a particular species or in a group of related species, it has been found empirically that only a minority of sites show any variation at all and most of the variations that are found are correlated, so that the number of distinct haplotypes that are found is relatively small.

In a molecular systematic analysis, the haplotypes are determined for a defined area of genetic material; a substantial sample of individuals of the target species or other taxon is used, however many current studies are based on single individuals. Haplotypes of individuals of closely related, but different, taxa are also determined. Finally, haplotypes from a smaller number of individuals from a definitely different taxon are determined: These are referred to as an out group. The base sequences for the haplotypes are then compared. In the simplest case, the difference between two haplotypes is assessed by counting the number of locations where they have different bases: This is referred to as the number of substitutions (other kinds of differences between haplotypes can also occur, for example the insertion of a section of nucleic acid in one haplotype that is not present in another). The difference between organisms is usually re-expressed as a percentage divergence, by dividing the number of substitutions by the number of base pairs analysed: the hope is that this measure will be independent of the location and length of the section of DNA that is sequenced.

An older and superseded approach was to determine the divergences between the genotypes of individuals by DNA-DNA hybridisation. The advantage claimed for using hybridisation rather than gene sequencing was that it was based on the entire genotype, rather than on particular sections of DNA. Modern sequence comparison techniques overcome this objection by the use of multiple sequences.

Once the divergences between all pairs of samples have been determined, the resulting triangular matrix of differences is submitted to some form of statistical cluster analysis, and the resulting dendrogram is examined in order to see whether the samples cluster in the way that would be expected from current ideas about the taxonomy of the group, or not. Any group of haplotypes that are all more similar to one another than any of them is to any other haplotype may be said to constitute a clade. Statistical techniques such as bootstrapping and jackknifing help in providing reliability estimates for the positions of haplotypes within the evolutionary trees.

Molecular systematics is an essentially cladistic approach: it assumes that classification must correspond to phylogenetic descent, and that all valid taxa must be monophyletic.

The recent discovery of extensive horizontal gene transfer among organisms provides a significant complication to molecular systematics, indicating that different genes within the same organism can have different phylogenies.

In addition, molecular phylogenies are sensitive to the assumptions and models that go into making them. They face problems like long-branch attraction, saturation, and taxon sampling problems: This means that strikingly different results can be obtained by applying different models to the same dataset.[8]

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Saccharomyces Genome Database

Monday, November 14th, 2016

Rap1-GFP and Calcofluor White staining of stationary phase cells. Image courtesy of M. Guidi, M. Ruault and A. Taddei, Institut Curie (Paris).

Pma1-mCherry and Vma1-GFP localization in mitotic cells. Image courtesy of M. Eastwood, Fred Hutch and M. Meneghini, University of Toronto.

CCCP-induced decrease of mitochondrial membrane potential (below) or control treatment (above) as measured by MitoLoc. Image courtesy of Dr. Jakob Vowinckel, Ralser Lab, University of Cambridge.

Redistribution of Msn5 pools from the nucleus to the cytoplasm upon glucose deprivation. Image courtesy of H. Huang and A. Hopper, Ohio State University.

Floccule of yeast rho0 cells expressing PTS1-GFP as a peroxisomal marker, stained with calcofluor white. Image courtesy of Dr. Jakob Vowinckel, University of Cambridge

S. cerevisiae membrane proteins visualized by RFP and GFP. Image courtesy of Masur. Wikimedia Commons.

Peroxisome (red) and mitochondrial (green) fission defects in vps1 fis1 double deletion strain transformed with FIS1. Image courtesy of S. Lefevre, S. Kumar and I. van der Klei, University of Groningen.

Yeast cells expressing TRK1/GFP. Image courtesy of V. Zayats and J. Ludwig, Center of Nanobiology and Structural Biology, AV CR.

The distribution of mtDNA (green) within the mitochondrial network (red). Image courtesy of Christof Osman and Peter Walter, University of California, San Francisco

The distribution of ER exit sites (ERES, green) within the ER (red). Image courtesy of A. Nakano and K. Kurokawa, RIKEN.

Cell, actin and nuclear morphology of yeast cells treated with DMSO (left) and poacic acid (right). Images courtesy of Hiroki Okada and Yoshikazu Ohya, University of Tokyo.

Localization of active Ras in a wild type strain Image courtesy of S. Colombo and E. Martegani, University Milano Bicocca

Sectored colonies showing loss of silencing at the HML locus Image courtesy of Anne Dodson, UC Berkeley

Pma1p imaged using the RITE tagging system in mother (green) and daughter cells (red) Image courtesy of Dan Gottschling Ph.D., Fred Hutchinson Cancer Research Center

Lipid droplets in fld1 mutant images by CARS Image courtesy of Heimo Wolinski, Ph.D. and Sepp D. Kohlwein, Ph.D., University of Graz, Austria

Fpr3p accumulation in the nucleolus of S. cerevisiae Image courtesy of Amy MacQueen, Ph.D., Wesleyan University anti-Fpr3 antibody courtesy of Jeremy Thorner, Ph.D., UC Berkeley

San1 strain visualized with FUN and calcofluor white Image courtesy of the Bruschi lab, ICGEB, Trieste, Italy

Single MDN1 mRNAs detected by FISH Image courtesy of the Zenklusen Lab, Universit de Montral

Localization of Ace2-GFP to daughter cell nuclei Image courtesy of Eric Weiss, Ph.D. Northwestern University

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Monday, November 14th, 2016

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Molecular evolution – Wikipedia

Saturday, November 12th, 2016

Molecular evolution is the process of change in the sequence composition of cellular molecules such as DNA, RNA, and proteins across generations. The field of molecular evolution uses principles of evolutionary biology and population genetics to explain patterns in these changes. Major topics in molecular evolution concern the rates and impacts of single nucleotide changes, neutral evolution vs. natural selection, origins of new genes, the genetic nature of complex traits, the genetic basis of speciation, evolution of development, and ways that evolutionary forces influence genomic and phenotypic changes.

The content and structure of a genome is the product of the molecular and population genetic forces which act upon that genome. Novel genetic variants will arise through mutation and will spread and be maintained in populations due to genetic drift or natural selection.

Mutations are permanent, transmissible changes to the genetic material (DNA or RNA) of a cell or virus. Mutations result from errors in DNA replication during cell division and by exposure to radiation, chemicals, and other environmental stressors, or viruses and transposable elements. Most mutations that occur are single nucleotide polymorphisms which modify single bases of the DNA sequence, resulting in point mutations. Other types of mutations modify larger segments of DNA and can cause duplications, insertions, deletions, inversions, and translocations.

Most organisms display a strong bias in the types of mutations that occur with strong influence in GC-content. Transitions (A G or C T) are more common than transversions (purine (adenine or guanine)) pyrimidine (cytosine or thymine, or in RNA, uracil))[1] and are less likely to alter amino acid sequences of proteins.

Mutations are stochastic and typically occur randomly across genes. Mutation rates for single nucleotide sites for most organisms are very low, roughly 109 to 108 per site per generation, though some viruses have higher mutation rates on the order of 106 per site per generation. Among these mutations, some will be neutral or beneficial and will remain in the genome unless lost via genetic drift, and others will be detrimental and will be eliminated from the genome by natural selection.

Because mutations are extremely rare, they accumulate very slowly across generations. While the number of mutations which appears in any single generation may vary, over very long time periods they will appear to accumulate at a regular pace. Using the mutation rate per generation and the number of nucleotide differences between two sequences, divergence times can be estimated effectively via the molecular clock.

Recombination is a process that results in genetic exchange between chromosomes or chromosomal regions. Recombination counteracts physical linkage between adjacent genes, thereby reducing genetic hitchhiking. The resulting independent inheritance of genes results in more efficient selection, meaning that regions with higher recombination will harbor fewer detrimental mutations, more selectively favored variants, and fewer errors in replication and repair. Recombination can also generate particular types of mutations if chromosomes are misaligned.

Gene conversion is a type of recombination that is the product of DNA repair where nucleotide damage is corrected using an homologous genomic region as a template. Damaged bases are first excised, the damaged strand is then aligned with an undamaged homolog, and DNA synthesis repairs the excised region using the undamaged strand as a guide. Gene conversion is often responsible for homogenizing sequences of duplicate genes over long time periods, reducing nucleotide divergence.

Genetic drift is the change of allele frequencies from one generation to the next due to stochastic effects of random sampling in finite populations. Some existing variants have no effect on fitness and may increase or decrease in frequency simply due to chance. "Nearly neutral" variants whose selection coefficient is close to a threshold value of 1 / the effective population size will also be affected by chance as well as by selection and mutation. Many genomic features have been ascribed to accumulation of nearly neutral detrimental mutations as a result of small effective population sizes.[2] With a smaller effective population size, a larger variety of mutations will behave as if they are neutral due to inefficiency of selection.

Selection occurs when organisms with greater fitness, i.e. greater ability to survive or reproduce, are favored in subsequent generations, thereby increasing the instance of underlying genetic variants in a population. Selection can be the product of natural selection, artificial selection, or sexual selection. Natural selection is any selective process that occurs due to the fitness of an organism to its environment. In contrast sexual selection is a product of mate choice and can favor the spread of genetic variants which act counter to natural selection but increase desirability to the opposite sex or increase mating success. Artificial selection, also known as selective breeding, is imposed by an outside entity, typically humans, in order to increase the frequency of desired traits.

The principles of population genetics apply similarly to all types of selection, though in fact each may produce distinct effects due to clustering of genes with different functions in different parts of the genome, or due to different properties of genes in particular functional classes. For instance, sexual selection could be more likely to affect molecular evolution of the sex chromosomes due to clustering of sex specific genes on the X,Y,Z or W.

Selection can operate at the gene level at the expense of organismal fitness, resulting in a selective advantage for selfish genetic elements in spite of a host cost. Examples of such selfish elements include transposable elements, meiotic drivers, killer X chromosomes, selfish mitochondria, and self-propagating introns. (See Intragenomic conflict.)

Genome size is influenced by the amount of repetitive DNA as well as number of genes in an organism. The C-value paradox refers to the lack of correlation between organism 'complexity' and genome size. Explanations for the so-called paradox are two-fold. First, repetitive genetic elements can comprise large portions of the genome for many organisms, thereby inflating DNA content of the haploid genome. Secondly, the number of genes is not necessarily indicative of the number of developmental stages or tissue types in an organism. An organism with few developmental stages or tissue types may have large numbers of genes that influence non-developmental phenotypes, inflating gene content relative to developmental gene families.

Neutral explanations for genome size suggest that when population sizes are small, many mutations become nearly neutral. Hence, in small populations repetitive content and other 'junk' DNA can accumulate without placing the organism at a competitive disadvantage. There is little evidence to suggest that genome size is under strong widespread selection in multicellular eukaryotes. Genome size, independent of gene content, correlates poorly with most physiological traits and many eukaryotes, including mammals, harbor very large amounts of repetitive DNA.

However, birds likely have experienced strong selection for reduced genome size, in response to changing energetic needs for flight. Birds, unlike humans, produce nucleated red blood cells, and larger nuclei lead to lower levels of oxygen transport. Bird metabolism is far higher than that of mammals, due largely to flight, and oxygen needs are high. Hence, most birds have small, compact genomes with few repetitive elements. Indirect evidence suggests that non-avian theropod dinosaur ancestors of modern birds [3] also had reduced genome sizes, consistent with endothermy and high energetic needs for running speed. Many bacteria have also experienced selection for small genome size, as time of replication and energy consumption are so tightly correlated with fitness.

Transposable elements are self-replicating, selfish genetic elements which are capable of proliferating within host genomes. Many transposable elements are related to viruses, and share several proteins in common.

DNA transposons are cut and paste transposable elements which excise DNA and move it to alternate sections of the genome.

non-LTR retrotransposons

LTR retrotransposons

Helitrons

Alu elements comprise over 10% of the human genome. They are short non-autonomous repeat sequences.

The number of chromosomes in an organism's genome also does not necessarily correlate with the amount of DNA in its genome. The ant Myrmecia pilosula has only a single pair of chromosomes[4] whereas the Adders-tongue fern Ophioglossum reticulatum has up to 1260 chromosomes.[5]Cilliate genomes house each gene in individual chromosomes, resulting in a genome which is not physically linked. Reduced linkage through creation of additional chromosomes should effectively increase the efficiency of selection.

Changes in chromosome number can play a key role in speciation, as differing chromosome numbers can serve as a barrier to reproduction in hybrids. Human chromosome 2 was created from a fusion of two chimpanzee chromosomes and still contains central telomeres as well as a vestigial second centromere. Polyploidy, especially allopolyploidy, which occurs often in plants, can also result in reproductive incompatibilities with parental species. Agrodiatus blue butterflies have diverse chromosome numbers ranging from n=10 to n=134 and additionally have one of the highest rates of speciation identified to date.[6]

Different organisms house different numbers of genes within their genomes as well as different patterns in the distribution of genes throughout the genome. Some organisms, such as most bacteria, Drosophila, and Arabidopsis have particularly compact genomes with little repetitive content or non-coding DNA. Other organisms, like mammals or maize, have large amounts of repetitive DNA, long introns, and substantial spacing between different genes. The content and distribution of genes within the genome can influence the rate at which certain types of mutations occur and can influence the subsequent evolution of different species. Genes with longer introns are more likely to recombine due to increased physical distance over the coding sequence. As such, long introns may facilitate ectopic recombination, and result in higher rates of new gene formation.

In addition to the nuclear genome, endosymbiont organelles contain their own genetic material typically as circular plasmids. Mitochondrial and chloroplast DNA varies across taxa, but membrane-bound proteins, especially electron transport chain constituents are most often encoded in the organelle. Chloroplasts and mitochondria are maternally inherited in most species, as the organelles must pass through the egg. In a rare departure, some species of mussels are known to inherit mitochondria from father to son.

New genes arise from several different genetic mechanisms including gene duplication, de novo origination, retrotransposition, chimeric gene formation, recruitment of non-coding sequence, and gene truncation.

Gene duplication initially leads to redundancy. However, duplicated gene sequences can mutate to develop new functions or specialize so that the new gene performs a subset of the original ancestral functions. In addition to duplicating whole genes, sometimes only a domain or part of a protein is duplicated so that the resulting gene is an elongated version of the parental gene.

Retrotransposition creates new genes by copying mRNA to DNA and inserting it into the genome. Retrogenes often insert into new genomic locations, and often develop new expression patterns and functions.

Chimeric genes form when duplication, deletion, or incomplete retrotransposition combine portions of two different coding sequences to produce a novel gene sequence. Chimeras often cause regulatory changes and can shuffle protein domains to produce novel adaptive functions.

De novo origin. Novel genes can also arise from previously non-coding DNA.[7] For instance, Levine and colleagues reported the origin of five new genes in the D. melanogaster genome from noncoding DNA.[8][9] Similar de novo origin of genes has been also shown in other organisms such as yeast,[10] rice[11] and humans.[12] De novo genes may evolve from transcripts that are already expressed at low levels.[13] Mutation of a stop codon to a regular codon or a frameshift may cause an extended protein that includes a previously non-coding sequence.

Molecular systematics is the product of the traditional fields of systematics and molecular genetics. It uses DNA, RNA, or protein sequences to resolve questions in systematics, i.e. about their correct scientific classification or taxonomy from the point of view of evolutionary biology.

Molecular systematics has been made possible by the availability of techniques for DNA sequencing, which allow the determination of the exact sequence of nucleotides or bases in either DNA or RNA. At present it is still a long and expensive process to sequence the entire genome of an organism, and this has been done for only a few species. However, it is quite feasible to determine the sequence of a defined area of a particular chromosome. Typical molecular systematic analyses require the sequencing of around 1000 base pairs.

Depending on the relative importance assigned to the various forces of evolution, three perspectives provide evolutionary explanations for molecular evolution.[14]

Selectionist hypotheses argue that selection is the driving force of molecular evolution. While acknowledging that many mutations are neutral, selectionists attribute changes in the frequencies of neutral alleles to linkage disequilibrium with other loci that are under selection, rather than to random genetic drift.[15] Biases in codon usage are usually explained with reference to the ability of even weak selection to shape molecular evolution.[16]

Neutralist hypotheses emphasize the importance of mutation, purifying selection, and random genetic drift.[17] The introduction of the neutral theory by Kimura,[18] quickly followed by King and Jukes' own findings,[19] led to a fierce debate about the relevance of neodarwinism at the molecular level. The Neutral theory of molecular evolution proposes that most mutations in DNA are at locations not important to function or fitness. These neutral changes drift towards fixation within a population. Positive changes will be very rare, and so will not greatly contribute to DNA polymorphisms.[20] Deleterious mutations will also not contribute very much to DNA diversity because they negatively affect fitness and so will not stay in the gene pool for long.[21] This theory provides a framework for the molecular clock.[20] The fate of neutral mutations are governed by genetic drift, and contribute to both nucleotide polymorphism and fixed differences between species.[22][23]

In the strictest sense, the neutral theory is not accurate.[24] Subtle changes in DNA very often have effects, but sometimes these effects are too small for natural selection to act on.[24] Even synonymous mutations are not necessarily neutral [24] because there is not a uniform amount of each codon. The nearly neutral theory expanded the neutralist perspective, suggesting that several mutations are nearly neutral, which means both random drift and natural selection is relevant to their dynamics.[24] The main difference between the neutral theory and nearly neutral theory is that the latter focuses on weak selection, not strictly neutral.[21]

Mutationists hypotheses emphasize random drift and biases in mutation patterns.[25] Sueoka was the first to propose a modern mutationist view. He proposed that the variation in GC content was not the result of positive selection, but a consequence of the GC mutational pressure.[26]

Protein evolution describes the changes over time in protein shape, function, and composition. Through quantitative analysis and experimentation, scientists have strived to understand the rate and causes of protein evolution. Using the amino acid sequences of hemoglobin and cytochrome c from multiple species, scientists were able to derive estimations of protein evolution rates. What they found was that the rates were not the same among proteins.[21] Each protein has its own rate, and that rate is constant across phylogenies (i.e., hemoglobin does not evolve at the same rate as cytochrome c, but hemoglobins from humans, mice, etc. do have comparable rates of evolution.). Not all regions within a protein mutate at the same rate; functionally important areas mutate more slowly and amino acid substitutions involving similar amino acids occurs more often than dissimilar substitutions.[21] Overall, the level of polymorphisms in proteins seems to be fairly constant. Several species (including humans, fruit flies, and mice) have similar levels of protein polymorphism.[20]

Protein evolution is inescapably tied to changes and selection of DNA polymorphisms and mutations because protein sequences change in response to alterations in the DNA sequence. Amino acid sequences and nucleic acid sequences do not mutate at the same rate. Due to the degenerate nature of DNA, bases can change without affecting the amino acid sequence. For example, there are six codons that code for leucine. Thus, despite the difference in mutation rates, it is essential to incorporate nucleic acid evolution into the discussion of protein evolution. At the end of the 1960s, two groups of scientistsKimura (1968) and King and Jukes (1969)-- independently proposed that a majority of the evolutionary changes observed in proteins were neutral.[20][21] Since then, the neutral theory has been expanded upon and debated.[21]

There are sometimes discordances between molecular and morphological evolution, which are reflected in molecular and morphological systematic studies, especially of bacteria, archaea and eukaryotic microbes. These discordances can be categorized as two types: (i) one morphology, multiple lineages (e.g. morphological convergence, cryptic species) and (ii) one lineage, multiple morphologies (e.g. phenotypic plasticity, multiple life-cycle stages). Neutral evolution possibly could explain the incongruences in some cases.[27]

The Society for Molecular Biology and Evolution publishes the journals "Molecular Biology and Evolution" and "Genome Biology and Evolution" and holds an annual international meeting. Other journals dedicated to molecular evolution include Journal of Molecular Evolution and Molecular Phylogenetics and Evolution. Research in molecular evolution is also published in journals of genetics, molecular biology, genomics, systematics, and evolutionary biology.

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Human Molecular Genetics – amazon.com

Saturday, November 12th, 2016

Tom Strachan is Scientific Director of the Institute of Human Genetics and Professor of Human Molecular Genetics at Newcastle University, UK, and is a Fellow of the Academy of Medical Sciences and a Fellow of the Royal Society of Edinburgh. Tom's early research interests were in multigene family evolution and interlocus sequence exchange, notably in the HLA and 21-hydroxylase gene clusters. While pursuing the latter, he became interested in medical genetics and disorders of development. His most recent research has focused on developmental control of the vertebrate cohesion regulators Nipbl and Mau-2.

Andrew Read is Emeritus Professor of Human Genetics at the University of Manchester, UK and a Fellow of the Academy of Medical Sciences. Andrew has been particularly concerned with making the benefits of DNA technology available to people with genetic problems. He established one of the first DNA diagnostic laboratories in the UK over 20 years ago (it is now one of two National Genetics Reference Laboratories), and was founder chairman of the British Society for Human Genetics, the main professional body in this area. His own research is on the molecular pathology of various hereditary syndromes, especially hereditary hearing loss.

Drs. Strachan and Read were recipients of the European Society of Human Genetics Education Award.

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Why I Hope to Die at 75 – The Atlantic

Saturday, November 12th, 2016

Seventy-five.

Thats how long I want to live: 75 years.

This preference drives my daughters crazy. It drives my brothers crazy. My loving friends think I am crazy. They think that I cant mean what I say; that I havent thought clearly about this, because there is so much in the world to see and do. To convince me of my errors, they enumerate the myriad people I know who are over 75 and doing quite well. They are certain that as I get closer to 75, I will push the desired age back to 80, then 85, maybe even 90.

I am sure of my position. Doubtless, death is a loss. It deprives us of experiences and milestones, of time spent with our spouse and children. In short, it deprives us of all the things we value.

But here is a simple truth that many of us seem to resist: living too long is also a loss. It renders many of us, if not disabled, then faltering and declining, a state that may not be worse than death but is nonetheless deprived. It robs us of our creativity and ability to contribute to work, society, the world. It transforms how people experience us, relate to us, and, most important, remember us. We are no longer remembered as vibrant and engaged but as feeble, ineffectual, even pathetic.

By the time I reach 75, I will have lived a complete life. I will have loved and been loved. My children will be grown and in the midst of their own rich lives. I will have seen my grandchildren born and beginning their lives. I will have pursued my lifes projects and made whatever contributions, important or not, I am going to make. And hopefully, I will not have too many mental and physical limitations. Dying at 75 will not be a tragedy. Indeed, I plan to have my memorial service before I die. And I dont want any crying or wailing, but a warm gathering filled with fun reminiscences, stories of my awkwardness, and celebrations of a good life. After I die, my survivors can have their own memorial service if they wantthat is not my business.

Let me be clear about my wish. Im neither asking for more time than is likely nor foreshortening my life. Today I am, as far as my physician and I know, very healthy, with no chronic illness. I just climbed Kilimanjaro with two of my nephews. So I am not talking about bargaining with God to live to 75 because I have a terminal illness. Nor am I talking about waking up one morning 18 years from now and ending my life through euthanasia or suicide. Since the 1990s, I have actively opposed legalizing euthanasia and physician-assisted suicide. People who want to die in one of these ways tend to suffer not from unremitting pain but from depression, hopelessness, and fear of losing their dignity and control. The people they leave behind inevitably feel they have somehow failed. The answer to these symptoms is not ending a life but getting help. I have long argued that we should focus on giving all terminally ill people a good, compassionate deathnot euthanasia or assisted suicide for a tiny minority.

I am talking about how long I want to live and the kind and amount of health care I will consent to after 75. Americans seem to be obsessed with exercising, doing mental puzzles, consuming various juice and protein concoctions, sticking to strict diets, and popping vitamins and supplements, all in a valiant effort to cheat death and prolong life as long as possible. This has become so pervasive that it now defines a cultural type: what I call the American immortal.

I reject this aspiration. I think this manic desperation to endlessly extend life is misguided and potentially destructive. For many reasons, 75 is a pretty good age to aim to stop.

What are those reasons? Lets begin with demography. We are growing old, and our older years are not of high quality. Since the mid-19th century, Americans have been living longer. In 1900, the life expectancy of an average American at birth was approximately 47 years. By 1930, it was 59.7; by 1960, 69.7; by 1990, 75.4. Today, a newborn can expect to live about 79 years. (On average, women live longer than men. In the United States, the gap is about five years. According to the National Vital Statistics Report, life expectancy for American males born in 2011 is 76.3, and for females it is 81.1.)

In the early part of the 20th century, life expectancy increased as vaccines, antibiotics, and better medical care saved more children from premature death and effectively treated infections. Once cured, people who had been sick largely returned to their normal, healthy lives without residual disabilities. Since 1960, however, increases in longevity have been achieved mainly by extending the lives of people over 60. Rather than saving more young people, we are stretching out old age.

The American immortal desperately wants to believe in the compression of morbidity. Developed in 1980 by James F. Fries, now a professor emeritus of medicine at Stanford, this theory postulates that as we extend our life spans into the 80s and 90s, we will be living healthier livesmore time before we have disabilities, and fewer disabilities overall. The claim is that with longer life, an ever smaller proportion of our lives will be spent in a state of decline.

Compression of morbidity is a quintessentially American idea. It tells us exactly what we want to believe: that we will live longer lives and then abruptly die with hardly any aches, pains, or physical deteriorationthe morbidity traditionally associated with growing old. It promises a kind of fountain of youth until the ever-receding time of death. It is this dreamor fantasythat drives the American immortal and has fueled interest and investment in regenerative medicine and replacement organs.

But as life has gotten longer, has it gotten healthier? Is 70 the new 50?

Not quite. It is true that compared with their counterparts 50 years ago, seniors today are less disabled and more mobile. But over recent decades, increases in longevity seem to have been accompanied by increases in disabilitynot decreases. For instance, using data from the National Health Interview Survey, Eileen Crimmins, a researcher at the University of Southern California, and a colleague assessed physical functioning in adults, analyzing whether people could walk a quarter of a mile; climb 10 stairs; stand or sit for two hours; and stand up, bend, or kneel without using special equipment. The results show that as people age, there is a progressive erosion of physical functioning. More important, Crimmins found that between 1998 and 2006, the loss of functional mobility in the elderly increased. In 1998, about 28 percent of American men 80 and older had a functional limitation; by 2006, that figure was nearly 42 percent. And for women the result was even worse: more than half of women 80 and older had a functional limitation. Crimminss conclusion: There was an increase in the life expectancy with disease and a decrease in the years without disease. The same is true for functioning loss, an increase in expected years unable to function.

This was confirmed by a recent worldwide assessment of healthy life expectancy conducted by the Harvard School of Public Health and the Institute for Health Metrics and Evaluation at the University of Washington. The researchers included not just physical but also mental disabilities such as depression and dementia. They found not a compression of morbidity but in fact an expansionan increase in the absolute number of years lost to disability as life expectancy rises.

How can this be? My father illustrates the situation well. About a decade ago, just shy of his 77th birthday, he began having pain in his abdomen. Like every good doctor, he kept denying that it was anything important. But after three weeks with no improvement, he was persuaded to see his physician. He had in fact had a heart attack, which led to a cardiac catheterization and ultimately a bypass. Since then, he has not been the same. Once the prototype of a hyperactive Emanuel, suddenly his walking, his talking, his humor got slower. Today he can swim, read the newspaper, needle his kids on the phone, and still live with my mother in their own house. But everything seems sluggish. Although he didnt die from the heart attack, no one would say he is living a vibrant life. When he discussed it with me, my father said, I have slowed down tremendously. That is a fact. I no longer make rounds at the hospital or teach. Despite this, he also said he was happy.

As Crimmins puts it, over the past 50 years, health care hasnt slowed the aging process so much as it has slowed the dying process. And, as my father demonstrates, the contemporary dying process has been elongated. Death usually results from the complications of chronic illnessheart disease, cancer, emphysema, stroke, Alzheimers, diabetes.

Take the example of stroke. The good news is that we have made major strides in reducing mortality from strokes. Between 2000 and 2010, the number of deaths from stroke declined by more than 20 percent. The bad news is that many of the roughly 6.8 million Americans who have survived a stroke suffer from paralysis or an inability to speak. And many of the estimated 13 million more Americans who have survived a silent stroke suffer from more-subtle brain dysfunction such as aberrations in thought processes, mood regulation, and cognitive functioning. Worse, it is projected that over the next 15 years there will be a 50 percent increase in the number of Americans suffering from stroke-induced disabilities. Unfortunately, the same phenomenon is repeated with many other diseases.

So American immortals may live longer than their parents, but they are likely to be more incapacitated. Does that sound very desirable? Not to me.

The situation becomes of even greater concern when we confront the most dreadful of all possibilities: living with dementia and other acquired mental disabilities. Right now approximately 5 million Americans over 65 have Alzheimers; one in three Americans 85 and older has Alzheimers. And the prospect of that changing in the next few decades is not good. Numerous recent trials of drugs that were supposed to stall Alzheimersmuch less reverse or prevent ithave failed so miserably that researchers are rethinking the whole disease paradigm that informed much of the research over the past few decades. Instead of predicting a cure in the foreseeable future, many are warning of a tsunami of dementiaa nearly 300 percent increase in the number of older Americans with dementia by 2050.

Half of people 80 and older with functional limitations. A third of people 85 and older with Alzheimers. That still leaves many, many elderly people who have escaped physical and mental disability. If we are among the lucky ones, then why stop at 75? Why not live as long as possible?

Even if we arent demented, our mental functioning deteriorates as we grow older. Age-associated declines in mental-processing speed, working and long-term memory, and problem-solving are well established. Conversely, distractibility increases. We cannot focus and stay with a project as well as we could when we were young. As we move slower with age, we also think slower.

It is not just mental slowing. We literally lose our creativity. About a decade ago, I began working with a prominent health economist who was about to turn 80. Our collaboration was incredibly productive. We published numerous papers that influenced the evolving debates around health-care reform. My colleague is brilliant and continues to be a major contributor, and he celebrated his 90th birthday this year. But he is an outliera very rare individual.

American immortals operate on the assumption that they will be precisely such outliers. But the fact is that by 75, creativity, originality, and productivity are pretty much gone for the vast, vast majority of us. Einstein famously said, A person who has not made his great contribution to science before the age of 30 will never do so. He was extreme in his assessment. And wrong. Dean Keith Simonton, at the University of California at Davis, a luminary among researchers on age and creativity, synthesized numerous studies to demonstrate a typical age-creativity curve: creativity rises rapidly as a career commences, peaks about 20 years into the career, at about age 40 or 45, and then enters a slow, age-related decline. There are some, but not huge, variations among disciplines. Currently, the average age at which Nobel Prizewinning physicists make their discoverynot get the prizeis 48. Theoretical chemists and physicists make their major contribution slightly earlier than empirical researchers do. Similarly, poets tend to peak earlier than novelists do. Simontons own study of classical composers shows that the typical composer writes his first major work at age 26, peaks at about age 40 with both his best work and maximum output, and then declines, writing his last significant musical composition at 52. (All the composers studied were male.)

This age-creativity relationship is a statistical association, the product of averages; individuals vary from this trajectory. Indeed, everyone in a creative profession thinks they will be, like my collaborator, in the long tail of the curve. There are late bloomers. As my friends who enumerate them do, we hold on to them for hope. It is true, people can continue to be productive past 75to write and publish, to draw, carve, and sculpt, to compose. But there is no getting around the data. By definition, few of us can be exceptions. Moreover, we need to ask how much of what Old Thinkers, as Harvey C. Lehman called them in his 1953 Age and Achievement, produce is novel rather than reiterative and repetitive of previous ideas. The age-creativity curveespecially the declineendures across cultures and throughout history, suggesting some deep underlying biological determinism probably related to brain plasticity.

We can only speculate about the biology. The connections between neurons are subject to an intense process of natural selection. The neural connections that are most heavily used are reinforced and retained, while those that are rarely, if ever, used atrophy and disappear over time. Although brain plasticity persists throughout life, we do not get totally rewired. As we age, we forge a very extensive network of connections established through a lifetime of experiences, thoughts, feelings, actions, and memories. We are subject to who we have been. It is difficult, if not impossible, to generate new, creative thoughts, because we dont develop a new set of neural connections that can supersede the existing network. It is much more difficult for older people to learn new languages. All of those mental puzzles are an effort to slow the erosion of the neural connections we have. Once you squeeze the creativity out of the neural networks established over your initial career, they are not likely to develop strong new brain connections to generate innovative ideasexcept maybe in those Old Thinkers like my outlier colleague, who happen to be in the minority endowed with superior plasticity.

Maybe mental functionsprocessing, memory, problem-solvingslow at 75. Maybe creating something novel is very rare after that age. But isnt this a peculiar obsession? Isnt there more to life than being totally physically fit and continuing to add to ones creative legacy?

One university professor told me that as he has aged (he is 70) he has published less frequently, but he now contributes in other ways. He mentors students, helping them translate their passions into research projects and advising them on the balance of career and family. And people in other fields can do the same: mentor the next generation.

Mentorship is hugely important. It lets us transmit our collective memory and draw on the wisdom of elders. It is too often undervalued, dismissed as a way to occupy seniors who refuse to retire and who keep repeating the same stories. But it also illuminates a key issue with aging: the constricting of our ambitions and expectations.

We accommodate our physical and mental limitations. Our expectations shrink. Aware of our diminishing capacities, we choose ever more restricted activities and projects, to ensure we can fulfill them. Indeed, this constriction happens almost imperceptibly. Over time, and without our conscious choice, we transform our lives. We dont notice that we are aspiring to and doing less and less. And so we remain content, but the canvas is now tiny. The American immortal, once a vital figure in his or her profession and community, is happy to cultivate avocational interests, to take up bird watching, bicycle riding, pottery, and the like. And then, as walking becomes harder and the pain of arthritis limits the fingers mobility, life comes to center around sitting in the den reading or listening to books on tape and doing crossword puzzles. And then

Maybe this is too dismissive. There is more to life than youthful passions focused on career and creating. There is posterity: children and grandchildren and great-grandchildren.

But here, too, living as long as possible has drawbacks we often wont admit to ourselves. I will leave aside the very real and oppressive financial and caregiving burdens that many, if not most, adults in the so-called sandwich generation are now experiencing, caught between the care of children and parents. Our living too long places real emotional weights on our progeny.

Unless there has been terrible abuse, no child wants his or her parents to die. It is a huge loss at any age. It creates a tremendous, unfillable hole. But parents also cast a big shadow for most children. Whether estranged, disengaged, or deeply loving, they set expectations, render judgments, impose their opinions, interfere, and are generally a looming presence for even adult children. This can be wonderful. It can be annoying. It can be destructive. But it is inescapable as long as the parent is alive. Examples abound in life and literature: Lear, the quintessential Jewish mother, the Tiger Mom. And while children can never fully escape this weight even after a parent dies, there is much less pressure to conform to parental expectations and demands after they are gone.

Living parents also occupy the role of head of the family. They make it hard for grown children to become the patriarch or matriarch. When parents routinely live to 95, children must caretake into their own retirement. That doesnt leave them much time on their ownand it is all old age. When parents live to 75, children have had the joys of a rich relationship with their parents, but also have enough time for their own lives, out of their parents shadows.

But there is something even more important than parental shadowing: memories. How do we want to be remembered by our children and grandchildren? We wish our children to remember us in our prime. Active, vigorous, engaged, animated, astute, enthusiastic, funny, warm, loving. Not stooped and sluggish, forgetful and repetitive, constantly asking What did she say? We want to be remembered as independent, not experienced as burdens.

At age 75 we reach that unique, albeit somewhat arbitrarily chosen, moment when we have lived a rich and complete life, and have hopefully imparted the right memories to our children. Living the American immortals dream dramatically increases the chances that we will not get our wishthat memories of vitality will be crowded out by the agonies of decline. Yes, with effort our children will be able to recall that great family vacation, that funny scene at Thanksgiving, that embarrassing faux pas at a wedding. But the most-recent yearsthe years with progressing disabilities and the need to make caregiving arrangementswill inevitably become the predominant and salient memories. The old joys have to be actively conjured up.

Of course, our children wont admit it. They love us and fear the loss that will be created by our death. And a loss it will be. A huge loss. They dont want to confront our mortality, and they certainly dont want to wish for our death. But even if we manage not to become burdens to them, our shadowing them until their old age is also a loss. And leaving themand our grandchildrenwith memories framed not by our vivacity but by our frailty is the ultimate tragedy.

Seventy-five. That is all I want to live. But if I am not going to engage in euthanasia or suicide, and I wont, is this all just idle chatter? Dont I lack the courage of my convictions?

No. My view does have important practical implications. One is personal and two involve policy.

Once I have lived to 75, my approach to my health care will completely change. I wont actively end my life. But I wont try to prolong it, either. Today, when the doctor recommends a test or treatment, especially one that will extend our lives, it becomes incumbent upon us to give a good reason why we dont want it. The momentum of medicine and family means we will almost invariably get it.

My attitude flips this default on its head. I take guidance from what Sir William Osler wrote in his classic turn-of-the-century medical textbook, The Principles and Practice of Medicine: Pneumonia may well be called the friend of the aged. Taken off by it in an acute, short, not often painful illness, the old man escapes those cold gradations of decay so distressing to himself and to his friends.

My Osler-inspired philosophy is this: At 75 and beyond, I will need a good reason to even visit the doctor and take any medical test or treatment, no matter how routine and painless. And that good reason is not It will prolong your life. I will stop getting any regular preventive tests, screenings, or interventions. I will accept only palliativenot curativetreatments if I am suffering pain or other disability.

This means colonoscopies and other cancer-screening tests are outand before 75. If I were diagnosed with cancer now, at 57, I would probably be treated, unless the prognosis was very poor. But 65 will be my last colonoscopy. No screening for prostate cancer at any age. (When a urologist gave me a PSA test even after I said I wasnt interested and called me with the results, I hung up before he could tell me. He ordered the test for himself, I told him, not for me.) After 75, if I develop cancer, I will refuse treatment. Similarly, no cardiac stress test. No pacemaker and certainly no implantable defibrillator. No heart-valve replacement or bypass surgery. If I develop emphysema or some similar disease that involves frequent exacerbations that would, normally, land me in the hospital, I will accept treatment to ameliorate the discomfort caused by the feeling of suffocation, but will refuse to be hauled off.

What about simple stuff? Flu shots are out. Certainly if there were to be a flu pandemic, a younger person who has yet to live a complete life ought to get the vaccine or any antiviral drugs. A big challenge is antibiotics for pneumonia or skin and urinary infections. Antibiotics are cheap and largely effective in curing infections. It is really hard for us to say no. Indeed, even people who are sure they dont want life-extending treatments find it hard to refuse antibiotics. But, as Osler reminds us, unlike the decays associated with chronic conditions, death from these infections is quick and relatively painless. So, no to antibiotics.

Obviously, a do-not-resuscitate order and a complete advance directive indicating no ventilators, dialysis, surgery, antibiotics, or any other medicationnothing except palliative care even if I am conscious but not mentally competenthave been written and recorded. In short, no life-sustaining interventions. I will die when whatever comes first takes me.

As for the two policy implications, one relates to using life expectancy as a measure of the quality of health care. Japan has the third-highest life expectancy, at 84.4 years (behind Monaco and Macau), while the United States is a disappointing No. 42, at 79.5 years. But we should not care about catching up withor measure ourselves againstJapan. Once a country has a life expectancy past 75 for both men and women, this measure should be ignored. (The one exception is increasing the life expectancy of some subgroups, such as black males, who have a life expectancy of just 72.1 years. That is dreadful, and should be a major focus of attention.) Instead, we should look much more carefully at childrens health measures, where the U.S. lags, and shamefully: in preterm deliveries before 37 weeks (currently one in eight U.S. births), which are correlated with poor outcomes in vision, with cerebral palsy, and with various problems related to brain development; in infant mortality (the U.S. is at 6.17 infant deaths per 1,000 live births, while Japan is at 2.13 and Norway is at 2.48); and in adolescent mortality (where the U.S. has an appalling recordat the bottom among high-income countries).

A second policy implication relates to biomedical research. We need more research on Alzheimers, the growing disabilities of old age, and chronic conditionsnot on prolonging the dying process.

Many people, especially those sympathetic to the American immortal, will recoil and reject my view. They will think of every exception, as if these prove that the central theory is wrong. Like my friends, they will think me crazy, posturingor worse. They might condemn me as being against the elderly.

Again, let me be clear: I am not saying that those who want to live as long as possible are unethical or wrong. I am certainly not scorning or dismissing people who want to live on despite their physical and mental limitations. Im not even trying to convince anyone Im right. Indeed, I often advise people in this age group on how to get the best medical care available in the United States for their ailments. That is their choice, and I want to support them.

And I am not advocating 75 as the official statistic of a complete, good life in order to save resources, ration health care, or address public-policy issues arising from the increases in life expectancy. What I am trying to do is delineate my views for a good life and make my friends and others think about how they want to live as they grow older. I want them to think of an alternative to succumbing to that slow constriction of activities and aspirations imperceptibly imposed by aging. Are we to embrace the American immortal or my 75 and no more view?

I think the rejection of my view is literally natural. After all, evolution has inculcated in us a drive to live as long as possible. We are programmed to struggle to survive. Consequently, most people feel there is something vaguely wrong with saying 75 and no more. We are eternally optimistic Americans who chafe at limits, especially limits imposed on our own lives. We are sure we are exceptional.

I also think my view conjures up spiritual and existential reasons for people to scorn and reject it. Many of us have suppressed, actively or passively, thinking about God, heaven and hell, and whether we return to the worms. We are agnostics or atheists, or just dont think about whether there is a God and why she should care at all about mere mortals. We also avoid constantly thinking about the purpose of our lives and the mark we will leave. Is making money, chasing the dream, all worth it? Indeed, most of us have found a way to live our lives comfortably without acknowledging, much less answering, these big questions on a regular basis. We have gotten into a productive routine that helps us ignore them. And I dont purport to have the answers.

But 75 defines a clear point in time: for me, 2032. It removes the fuzziness of trying to live as long as possible. Its specificity forces us to think about the end of our lives and engage with the deepest existential questions and ponder what we want to leave our children and grandchildren, our community, our fellow Americans, the world. The deadline also forces each of us to ask whether our consumption is worth our contribution. As most of us learned in college during late-night bull sessions, these questions foster deep anxiety and discomfort. The specificity of 75 means we can no longer just continue to ignore them and maintain our easy, socially acceptable agnosticism. For me, 18 more years with which to wade through these questions is preferable to years of trying to hang on to every additional day and forget the psychic pain they bring up, while enduring the physical pain of an elongated dying process.

Seventy-five years is all I want to live. I want to celebrate my life while I am still in my prime. My daughters and dear friends will continue to try to convince me that I am wrong and can live a valuable life much longer. And I retain the right to change my mind and offer a vigorous and reasoned defense of living as long as possible. That, after all, would mean still being creative after 75.

Go here to read the rest:
Why I Hope to Die at 75 - The Atlantic

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Google Health Google

Saturday, November 12th, 2016

Google Health has been permanently discontinued. All data remaining in Google Health user accounts as of January 2, 2013 has been systematically destroyed, and Google is no longer able to recover any Google Health data for any user. To learn more about this announcement, see our blog post, or answers to frequently-asked questions below.

Is there any way to retrieve my Google Health data from Google?

No -- all remaining user data has been permanently and irrevocably deleted from the Google Health system starting on January 2, 2013. Google is no longer able to recover any Google Health data for any user.

What happened to my Google Health data after January 1, 2013?

All Google Health user accounts have been deactivated, and all data stored in them has been systematically deleted from Google's systems.

I want to keep tracking my health online. What can I use to do this?

There are a number of options available. For example, you can continue tracking your health data via another personal health record provider such as Microsoft(R) HealthVault(TM).

Why was Google Health discontinued?

Please see our blog post for more information on this decision.

More here:
Google Health Google

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Human Stem Cells Institute – Wikipedia

Friday, November 11th, 2016

Human Stem Cells Institute Public Tradedas MCX:ISKJ Industry Biotech Research and Pharmaceutical Founded 2003(2003) Headquarters Moscow, Russia

Key people

Human Stem Cells Institute OJSC (HSCI) ( or ) is a Russian public biotech company founded in 2003. HSCI engages in R&D as well as commercialization and marketing of innovative proprietary products and services in the areas of cell-based, gene and post-genome technologies. HSCI aims to foster a new culture of medical care developing new health care opportunities in such areas as personalized and preventive medicine.

Today, HSCIs projects encompass the five main focus areas of modern biomedical technologies: regenerative medicine, bio-insurance, medical genetics, gene therapy, biopharmaceuticals (within the international project SynBio).

HSCI owns the largest family cord blood stem cell bank in Russia Gemabank, as well as the reproductive cell and tissue bank Reprobank (personal storage, donation).

The Company launched Neovasculgen, the first-in-class gene-therapy drug for treating Peripheral Arterial Disease, including Critical Limb Ischemia, and also introduced the innovative cell technology SPRS-therapy, which entails the use of autologous dermal fibroblasts to repair skin damage due to aging and other structural changes.

HSCI is implementing a socially significant project to create its own Russia-wide network of Genetico medical genetics centers to provide genetic diagnostics and consulting services for monogenic inherited diseases as well as multifactorial disorders (Ethnogene, PGD and other services).

The Company actively promotes its products on the Russian market and intends to open new markets throughout the world.

HSCI is listed on the Innovation & Investment Market (iIM) of the Moscow Exchange (ticker ISKJ). The Company conducted its IPO in December 2009, becoming the first Russian biotech company to go public.

In 2003, the Human Stem Cells Institute and Gemabank were established.[1] Over the next few years, the Company increased its client base while expanding its technological abilities. In 2008, HSCI gained a blocking stake in the German biotech company, SymbioTec GmbH, which owns international patents for a new generation of drugs to treat cancer and infectious diseases. In 2009, HSCI successfully raised RUB 142.5 million in an IPO on MICEX and became the first publicly traded biotech company in Russia.[2] The Company continued to expand in 2010, when it gained a 50% stake in Hemafund, Ukraines largest family cord blood bank. In 2011, HSCI initiated the SynBio Project, as a long-term partnership with RUSNANO (a state-owned fund for supporting nanotechnologies) and some major R&D companies from Russia and Europe including Pharmsynthez, Xenetic Biosciences and SymbioTec (which was acquired by Xenetic Biosciences pursuant to the SynBio project agreement ).[3] The project is founded on strong principles of international scientific cooperation, as participating research centers are found in England, Germany, and Russia.[4]

HSCI is engaged in scientific studies and research in the main fields of biomedical technology with the aim of creating innovative products (drugs, medical devices, technologies, services, etc.) which are capable of solving urgent and complex challenges faced by clinical medicine today and which could be incorporated into contemporary healthcare practices. Within of each of the main fields of biomedical technology cell (regenerative medicine), gene (genetic medicine) and post-genome (biopharmaceuticals) technologies the Company is currently undertaking several scientific research projects. [5]

See original here:
Human Stem Cells Institute - Wikipedia

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