StemCell Therapy

Representative imageBy Priyanka V Gupta

New Delhi: Indian Council of Medical Research (ICMR) will soon release the final document on guidelines for stem cell research, the draft of which was available on the ICMR and the DBT (Department of Biotechnology) websites for public reviews till July 31 this year. The guidelines are expected to help in curbing the unethical practices in regenerative medicine. The information was shared by Dr Geeta Jotwani, deputy director general, ICMR, at a recent event where MoU was signed between ABLE (Association of Biotechnology Led Enterprise) and FIRM (Forum for Innovative Regenerative Medicine) for industry research collaborations.

Dr Jotwani said, On the directives of DCGI (Drug Controller General of India), ICMR has been framing the guidelines for stem cell research and therapy since 2001. Unfortunately, there is no therapy available other than bone marrow transplantation, for which also no standard of care has been laid out. In that direction, we have been making periodic efforts by releasing the guideline documents in 2002, 2007, 2013 and now the updated documentation for 2017 is under finalization.

ICMR has been proactively working towards educating the stakeholders about the ethical practices in stem cell research and therapy, for which a special committee, called National Apex Committee for Stem Cell Research and Therapy (NAC-SCRT), has been formed to advise the scientists community. Regenerative medicine is an innovative science. As part of ICMR, more research is involved than getting into conclusion that we are ready for application. We are proactively making efforts to educate, create awareness and give directions to our scientists community and clinicians on how they should go about the research part of stem cell therapy, said Dr Jotwani.

There are many clinicians entering into unethical practices and promising general public about the available care in almost all sorts of incurable conditions, including autism, according to Dr Jotwani.

She said, We are always concerned about what the end users are getting and the promises that are being made to them. Hence, we are proactively being involved in interacting with different government agencies as well as the industry to curb the unethical practices for which we also established NAC-SCRT under the Department of Health Research, Government of India. The committee, which comprises of different government agencies as well as ethics and social groups, legal experts, representatives of drug controllers office and CDSCO (Central Drug Standard Control Organization), deliberates on the issues of upcoming technologies and takes proactive role in the regenerative medicine.

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ICMR's stem cell research guidelines soon to be released - ETHealthworld.com

Global Nanomedicine Market Research Report 2017 to 2022 provides a unique tool for evaluating the market, highlighting opportunities, and supporting strategic and tactical decision-making. This report recognizes that in this rapidly-evolving and competitive environment, up-to-date marketing information is essential to monitor performance and make critical decisions for growth and profitability. It provides information on trends and developments, and focuses on markets and materials, capacities and technologies, and on the changing structure of the Nanomedicine Market.

Companies Mentioned are GE Healthcare, Johnson & Johnson, Mallinckrodt plc, Merck & Co. Inc., Nanosphere Inc., Pfizer Inc., Sigma-Tau Pharmaceuticals Inc., Smith & Nephew PLC, Stryker Corp, Teva Pharmaceutical Industries Ltd., UCB (Union chimique belge) S.A.

Primary sources are mainly industry experts from core and related industries, and suppliers, manufacturers, distributors, service providers, and organizations related to all segments of the industrys supply chain. The bottom-up approach was used to estimate the global market size of Nanomedicine based on end-use industry and region, in terms of value. With the data triangulation procedure and validation of data through primary interviews, the exact values of the overall parent market, and individual market sizes were determined and confirmed in this study.

Sample/Inquire at: https://www.marketinsightsreports.com/reports/08308548/global-nanomedicine-market-research-report-2017/inquiry

This report segments the global Nanomedicine market on the basis of types Regenerative Medicine, In-vitro & In-vivo Diagnostics, Vaccines, Drug Delivery. On the basis of application Clinical Cardiology, Urology, Genetics, Orthopedics, Ophthalmology.

Essential points covered in Global Nanomedicine Market 2017 Research are:-

This independent 116 page report guarantees you will remain better informed than your competition. With over 170 tables and figures examining the Nanomedicine market, the report gives you a visual, one-stop breakdown of the leading products, submarkets and market leaders market revenue forecasts as well as analysis to 2022.

The global Nanomedicine market consists of different international, regional, and local vendors. The market competition is foreseen to grow higher with the rise in technological innovation and M&A activities in the future. Moreover, many local and regional vendors are offering specific application products for varied end-users. The new vendor entrants in the market are finding it hard to compete with the international vendors based on quality, reliability, and innovations in technology.

Browse Full Report at: https://www.marketinsightsreports.com/reports/08308548/global-nanomedicine-market-research-report-2017

Geographically, this report is segmented into several key Regions, with production, consumption, revenue (million USD), and market share and growth rate of Storage Area Network Switch in these regions, from 2012 to 2022 (forecast), covering

by Regions

The report provides a basic overview of the Nanomedicine industry including definitions, classifications, applications and industry chain structure. And development policies and plans are discussed as well as manufacturing processes and cost structures.

Then, the report focuses on global major leading industry players with information such as company profiles, product picture and specifications, sales, market share and contact information. Whats more, the Nanomedicine industry development trends and marketing channels are analyzed.

The research includes historic data from 2012 to 2016 and forecasts until 2022 which makes the reports an invaluable resource for industry executives, marketing, sales and product managers, consultants, analysts, and other people looking for key industry data in readily accessible documents with clearly presented tables and graphs. The report will make detailed analysis mainly on above questions and in-depth research on the development environment, market size, development trend, operation situation and future development trend of Nanomedicine on the basis of stating current situation of the industry in 2017 so as to make comprehensive organization and judgment on the competition situation and development trend of Nanomedicine Market and assist manufacturers and investment organization to better grasp the development course of Nanomedicine Market.

The study was conducted using an objective combination of primary and secondary information including inputs from key participants in the industry. The report contains a comprehensive market and vendor landscape in addition to a SWOT analysis of the key vendors.

There are 15 Chapters to deeply display the global Nanomedicine market.

Chapter 1, to describe Nanomedicine Introduction, product scope, market overview, market opportunities, market risk, market driving force;

Chapter 2, to analyze the top manufacturers of Nanomedicine, with sales, revenue, and price of Nanomedicine, in 2016and 2017;

Chapter 3, to display the competitive situation among the top manufacturers, with sales, revenue and market share in 2016and 2017;

Chapter 4, to show the global market by regions, with sales, revenue and market share of Nanomedicine, for each region, from 2012to 2017;

Chapter 5, 6, 7,8and 9, to analyze the key regions, with sales, revenue and market share by key countries in these regions;

Chapter 10and 11, to show the market by type and application, with sales market share and growth rate by type, application, from 2012 to 2017;

Chapter 12, Nanomedicine market forecast, by regions, type and application, with sales and revenue, from 2017to 2022;

Chapter 13, 14 and 15, to describe Nanomedicine sales channel, distributors, traders, dealers, Research Findings and Conclusion, appendix and data source.

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Nanomedicine Market Growth Opportunities for Distributers 2017 - Equity Insider (press release)

You probably know the Nietzsche quote: That which does not kill us makes us stronger.

One University of South Florida researcher is studying that adage in nature.

University Beat report on USF Health research into venom peptides.

Craig Doupnik looks at how components of venom the toxic secretions of dozens of animals like spiders and snakes can actually be bio-engineered to treat diseases.

Venom peptides have been recognized as potential therapeutics for a variety of different disorders in fact, several have made their way into clinical trials of currently FDA-approved drugs, saidDoupnik, an associate professor in the USF Morsani College of Medicines Department of Molecular Pharmacology and Physiology.

He explained that venom peptides are strings of amino acids that can be manipulated by scientists so they can be used to target ion channels. Those are proteins that help control things like how your heart beats and how neurons fire within your brain.

As a result, a lot of the FDA-approved venom peptides are used to treat problems with those systems.

Captopril, which is a drug that was originally derived from a viper venom, is used to treat hypertension and congestive heart failure," Doupnik said. "There's a peptide thats released from the venom of a cone snail thats used for treating chronic pain.

Other venom peptides target seizure-related disorders and other cardiac arrhythmias.

Doupniks research focuses on peptides from the venom of honeybees. He re-engineers those peptides so they can interact with different ion channels. His work doesnt create specific treatments but instead turns the venom into something a chemist can create a treatment from.

This kind of work on bee venom has been going on for more than thirty years but has really been advanced as technology approves.

Whats really kind of transformed the field for myself is how structural biology, in terms of how we can see these peptides and ion channels at atomic level resolution and some of the computational tools that are now available allow us to do the type of peptide engineering that otherwise wouldnt have been possible 10 years ago," Doupnik said.

Doupnik also studies nano-medicines, which treat diseases at the atomic level.

What it does is it provides computational engineers an opportunity to redesign molecules like peptides or even small molecules that can target these areas and either enhance their activity or reduce their activity, whatever the beneficial or therapeutic direction would be, and it can go in either direction, so thats part of the trick of the trade," he said.

"It gives us whats often referred to as rational drug design or rational peptide design," he added. "At least we have some rational understanding of what were trying to target versus just throwing a soup of chemicals onto a preparation and seeing what happens and then trying to sift through that soup to find out what the magic bullet might be or what the active ingredient might be.

Of course, there are ethical concerns when talking about bio-engineering. Doupnik believes sharing information with the public about this kind of work helps allay some of their fears.

There clearly are areas of concern and I think its important for scientists to effectively communicate to the lay public what the goals and intentions of this type of research are," he said.

And what about perhaps the most obvious question, one that comes back to the Nietzsche quote we started with: how in the world would someone think that deadly venom could be used to actually save lives?

Basic science is a crazy business!" Doupniksaid, laughing. "It takes you down a lot of different paths and a lot of those paths are dead ends. But it never the less is where a lot of our fundamental discoveries come from and when they do lead down paths towards therapeutics and helping us better understand human disease, we see the value in it obviously.

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Deadly Venom Can Be Turned Into Disease Treatments | WLRN - WLRN

eHealth Magazine | Elets

Innovation in cancer treatment multimodality therapy eHealth Magazine | Elets Nano medicine as a multimodality treatment of cancer is the latest evolution in this field. The advantage of nano delivery system is that it simultaneously delivers different agents to the active site, causing a special interaction between the agents ... and more »

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Innovation in cancer treatment multimodality therapy - eHealth Magazine | Elets

Bone marrow contains hematopoetic stem cells, the precursors to every blood cell type. These cells spring into action following bone marrow transplants, bone marrow injury and during systemic infection, creating new blood cells, including immune cells, in a process known as hematopoiesis.

A new study led by University of Pennsylvania and Technical University of Dresden scientists has identified an important regulator of this process, a protein called Del-1. Targeting it, the researchers noted, could be an effective way to improve stem cell transplants for both donors and recipients. There may also be ways to modulate levels of Del-1 in patients with certain blood cancers to enhance immune cell production. The findings are reported this week in The Journal of Clinical Investigation.

Because the hematopoetic stem cell niche is so important for the creation of bone marrow and blood cells and because Del-1 is a soluble protein and is easily manipulated, one can see that it could be a target in many potential applications, said George Hajishengallis, the Thomas W. Evans Centennial Professor in the Department of Microbiology in Penns School of Dental Medicine and a senior author on the work.

I think that Del-1 represents a major regulator of the hematopoetic stem cell niche, said Triantafyllos Chavakis, co-senior author on the study and a professor at the Technical University of Dresden. It will be worthwhile to study its expression in the context of hematopoetic malignancy.

For Hajishengallis, the route to studying Del-1 in the bone marrow began in his field of dental medicine. Working with Chavakis, he had identified Del-1 as a potential drug target for gum disease after finding that it prevents inflammatory cells from moving into the gums.

Both scientists and their labs had discovered that Del-1 was also expressed in the bone marrow and began following up to see what its function was there.

In the beginning, I thought it would have a simple function, like regulating the exit of mature leukocytes [white blood cells] from the marrow into the periphery, Hajishengallis said, something analogous to what it was doing in the gingiva. But it turned out it had a much more important and global role than what I had imagined.

The researchers investigations revealed that Del-1 was expressed by at least three cell types in the bone marrow that support hematopoetic stem cells: endothelial cells, CAR cells and osteoblasts. Using mice deficient in Del-1, they found that the protein promotes proliferation and differentiation of hematopoetic stem cells, sending more of these progenitor cells down a path toward becoming myeloid cells, such as macrophages and neutrophils, rather than lymphocytes, such as T cells and B cells.

In bone marrow transplant experiments, the team discovered that the presence of Del-1 in recipient bone marrow is required for the transplanted stem cells to engraft in the recipient and to facilitate the process of myelopoesis, the production of myeloid cells.

When the researchers mimicked a systemic infection in mice, animals deficient in Del-1 were slower to begin making myeloid cells again compared to those with normal Del-1 levels.

We saw roles for Del-1 in both steady state and emergency conditions, Hajishengallis said.

Hajishengallis, Chavakis and their colleagues identified the protein on hematopoetic stem cells with which Del-1 interacts, the 3 integrin, perhaps pointing to a target for therapeutic interventions down the line.

The scientists see potential applications in bone marrow and stem cell transplants, for both donors and recipients. In donors, blocking the interaction between Del-1 and hematopoetic stem cells could enhance the mobilization of those progenitors into the bloodstream. This could be helpful for increasing donor cell numbers for transplantation. Transplant recipients, on the other hand, may need enhanced Del-1 interaction to ensure the transplanted cells engraft and begin making new blood cells more rapidly.

In addition, people undergoing chemotherapy who develop febrile neutropenia, associated with low levels of white blood cells, might benefit from the role of Del-1 in supporting the production of immune-related blood cells such as neutrophils.

Its easy to think of practical applications for these findings, said Hajishengallis. Now we need to find out whether it works in practice, so our studies continue.

Ioannis Mitroulis, Lan-Sun Chen and Rashim Pal Singh of TU-Dresden were co-lead authors on the study, and Ben Wielockx of TU-Dresden was a co-senior author along with Hajishengallis and Chavakis. They were joined by coauthors Tetsuhiro Kajikawa, Kavita Hosur, Tomoki Maekawa and Baomei Wang of Penn Dental Medicine; Ioannis Kourtzelis, Matina Economopoulou, Maria Troullinaki, Athanasios Ziogas, Klara Ruppova, Pallavi Subramanian, Panayotis Verginis, Malte Wobus, Martin Bornhuser and Tatyana Grinenko of TU-Dresden; Torsten Tonn of the German Red Cross Blood Donation Service in Dresden; and Marianna Di Scala and Andrs Hidalgo of the Spanish National Center for Cardiovascular Research.

The study was supported by the Deutsche Forschungsgemeinschaft, European Commission, European Research Council and National Institutes of Health (grants AI068730, DE024153, DE024716, DE0152 54 and DE026152).

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Bone Marrow Protein May Be Target for Improving Stem Cell Transplants - Penn: Office of University Communications

A new University of Michigan study found the combination of traditional chemotherapy drug, cisplatin, with an experimental drug destroys a rare type of salivary gland tumor and prevents it from reoccurring within 300 days after treatment. The study was conducted on mice as well as primary human adenoid cystic carcinoma cells in the Nr Lab at the School of Dentistry.

The salivary gland tumor is a product of ACC, which is a rare cancer of the salivary glands and of surrounding head and neck areas. The cancer typically arises in adulthood and affects about 3,000 to 4,000 people per year. Treatment of advanced ACC with traditional chemotherapy has only had limited success.

LSA sophomore Leo Thompson, a pre-dental student, found the results to be inspiring for the future of ACC cancer care. As someone looking forward to attending dental school, Thompson was very interested in the studys results.

The study gives a promising outlook towards defeating ACC, Thompson said. Hopefully the prevention of recurrence can be achieved in the long term, and we see the treatment curing humans in a few years.

ACC is known to grow slowly; however, it is often discovered in the late, aggressive stages. There is no cure for the cancer, and the tumor cells have a tendency to reappear later at their original site. This is a serious concern for physicians treating ACC patients. The cancer tends to spread to other parts of the body, especially the lungs, leading to additional life-threatening issues.

The study found mice treated with the experimental drug, MI-773, combined with cisplatin had shrunken tumors, ranging from being the size of an acorn to being nonexistent. Next, the acorn-sized tumors were removed from the mice and subjects continued to take MI-773 for another month. This treatment group eradicated tumor recurrences for more than 300 days.

On the other hand, 62.5 percent of control mice that only received surgical removal of the tumor saw recurrences. These results suggest this combination treatment may be more effective in treating human patients with ACC.

LSA senior Samantha Sciancalepore, a pre-dental student, said she was eager to see what the future holds for this kind of research.

I think its really (admirable) that this research is being done on our campus, she said. I feel lucky that we have the tools to research solutions to cancer, especially in facial tumors. As a dentist, I think one of your ultimate goals is to provide help and comfort to your patients, and I think this sort of conclusive research is exactly what they need to advance.

Most cancers attempt to block the cancer-fighting protein p53 so the protein can no longer kill the cancer. However, this is not the case with ACC tumors, which tend to leave p53 untouched. This makes MI-773 suitable for treating ACC, which works by preventing the tumor from attacking p53.

Primary investigator Jacques Nr, professor of dentistry, otolaryngology and biomedical engineering, explained in an interview with Michigan News the importance of MI-773 in staving off the cancer. MI-773 stops the interaction between cancer cells and p53, which might otherwise be fatal for the patient.

This drug MI-773 prevents that interaction, so p53 can induce cell death, Nr said. In this study, when researchers activated p53 in mice with salivary gland cancer, the cancer stem cells died.

MI-773 was discovered by study co-author Shaomeng Wang, professor of medicine, pharmacology and medical chemistry. The drug is licensed to Sanofi, a French pharmaceutical company known to engage in the research and development aspects of medicine.

A major drawback of the study is that it was conducted over a 300-day period, whereas studies show ACC tumors tend to reappear after 10 years.

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Dentistry school uncovers new treatment for gland cancer - The Michigan Daily

Diabetesis a chronic disease that occurs when the pancreas is no longer able to make insulin, or when the body cannot make good use of the insulin it produces. Insulin is a hormone made by the pancreas, that acts like a key to let glucose from the food we eat pass from the blood stream into the cells in the body to produce energy. All carbohydrate foods are broken down into glucose in the blood. Insulin helps glucose get into the cells.

Not being able to produce insulin or use it effectively leads to raised glucose levels in the blood (known as hyperglycaemia). Over the long-term high glucose levels are associated with damage to the body and failure of various organs and tissues.

Type 1 diabetes used to be called juvenile-onset diabetes. It is usually caused by an auto-immune reaction where the bodys defence system attacks the cells that produce insulin. The reason this occurs is not fully understood. People with type 1 diabetes produce very little or no insulin. The disease may affect people of any age, but usually develops in children or young adults. People with this form of diabetes need injections of insulin every day in order to control the levels of glucose in their blood. If people with type 1 diabetes do not have access to insulin, they will die.

Type 2 diabetes used to be called non-insulin dependent diabetes or adult-onset diabetes, and accounts for at least 90% of all cases of diabetes. It is characterised by insulin resistance and relative insulin deficiency, either or both of which may be present at the time diabetes is diagnosed. The diagnosis of type 2 diabetes can occur at any age. Type 2 diabetes may remain undetected for many years and the diagnosis is often made when a complication appears or a routine blood or urine glucose test is done. It is often, but not always, associated with overweight or obesity, which itself can cause insulin resistance and lead to high blood glucose levels. People with type 2 diabetes can often initially manage their condition through exercise and diet. However, over time most people will require oral drugs and or insulin.

Both type 1 and type 2 diabetes are serious. There is no such thing as mild diabetes.

Gestational diabetes (GDM) is a form of diabetes consisting of high blood glucose levels during pregnancy. It develops in one in 25 pregnancies worldwide and is associated with complications to both mother and baby. GDM usually disappears after pregnancy but women with GDM and their children are at an increased risk of developing type 2 diabetes later in life. Approximately half of women with a history of GDM go on to develop type 2 diabetes within five to ten years after delivery.

Other specific types of diabetes also exist.

The risk factors for type 1 diabetes are still being researched. However, having a family member with type 1 diabetes slightly increases the risk of developing the disease. Environmental factors and exposure to some viral infections have also been linked to the risk of developing type 1 diabetes.

Several risk factors have been associated with type 2 diabetes and include:

*Impaired glucose tolerance (IGT) is a category of higher than normal blood glucose, but below the threshold for diagnosing diabetes.

Changes in diet and physical activity related to rapid development and urbanisation have led to sharp increases in the numbers of people developing diabetes.

Pregnant women who are overweight, have been diagnosed with IGT, or have a family history of diabetes are all at increased risk of developing gestational diabetes mellitus (GDM). In addition, having been previously diagnosed with gestational diabetes or being of certain ethnic groups puts women at increased risk of developing GDM.

Brief questionnaires are simple, practical and inexpensive ways to quickly identify people who may be at a higher risk of type 2 diabetes and who need to have their level of risk further investigated. The Finnish Type 2 Diabetes Risk Assessment Form, developed in 2001, is an example of an effective questionnaire that can be used as the basis for developing national questionnaires which take into account local factors. It has eight scored questions, with the total test score providing a measure of the probability of developing type 2 diabetes over the following 10 years. The reverse of the form contains brief advice on what the respondent can do to lower their risk of developing the disease, and whether they should seek advice or have a clinical examination. The test takes only a couple of minutes to complete and can be done online, in pharmacies or at various public campaign events. The questionnaire is available for download in several languages.

IDF has developed an IDF type 2 diabetes online diabetes risk assessment which aims to predict an individuals risk of developing type 2 diabetes within the next ten years. The test is based on the Finnish Diabetes Risk Score (FINDRISC) developed and designed by Adj. Prof Jaana Lindstrom and Prof. Jaakko Tuomilehto from the National Institute for Health and Welfare, Helsinki, Finland.

People with diabetes have an increased risk of developing a number of serious health problems. Consistently high blood glucose levels can lead to serious diseases affecting the heart and blood vessels, eyes, kidneys, nerves and teeth. In addition, people with diabetes also have a higher risk of developing infections. In almost all high-income countries, diabetes is a leading cause of cardiovascular disease, blindness, kidney failure, and lower limb amputation.

Maintaining blood glucose levels, blood pressure, and cholesterol at or close to normal can help delay or prevent diabetes complications. Therefore people with diabetes need regular monitoring.

Cardiovascular disease: affects the heart and blood vessels and may cause fatal complications such as coronary artery disease (leading to heart attack) and stroke. Cardiovascular disease is the most common cause of death in people with diabetes. High blood pressure, high cholesterol, high blood glucose and other risk factors contribute to increasing the risk of cardiovascular complications.

Kidney disease (diabetic nephropathy): caused by damage to small blood vessels in the kidneys leading to the kidneys becoming less efficient or to fail altogether. Kidney disease is much more common in people with diabetes than in those without diabetes. Maintaining near normal levels of blood glucose and blood pressure can greatly reduce the risk of kidney disease.

Nerve disease (diabetic neuropathy): diabetes can cause damage to the nerves throughout the body when blood glucose and blood pressure are too high. This can lead to problems with digestion, erectile dysfunction, and many other functions. Among the most commonly affected areas are the extremities, in particular the feet. Nerve damage in these areas is called peripheral neuropathy, and can lead to pain, tingling, and loss of feeling. Loss of feeling is particularly important because it can allow injuries to go unnoticed, leading to serious infections and possible amputations. People with diabetes carry a risk of amputation that may be more than 25 times greater than that of people without diabetes. However, with comprehensive management, a large proportion of amputations related to diabetes can be prevented. Even when amputation takes place, the remaining leg and the persons life can be saved by good follow-up care from a multidisciplinary foot team. People with diabetes should regularly examine their feet.

Eye disease (diabetic retinopathy): most people with diabetes will develop some form of eye disease (retinopathy) causing reduced vision or blindness. Consistently high levels of blood glucose, together with high blood pressure and high cholesterol, are the main causes of retinopathy. It can be managed through regular eye checks and keeping glucose and lipid levels at or close to normal.

Pregnancy complications: Women with any type of diabetes during pregnancy risk a number of complications if they do not carefully monitor and manage their condition. To prevent possible organ damage to the fetus, women with type 1 diabetes or type 2 diabetes should achieve target glucose levels before conception. All women with diabetes during pregnancy, type 1, type 2 or gestational should strive for target blood glucose levels throughout to minimize complications. High blood glucose during pregnancy can lead to the foetus putting on excess weight. This can lead to problems in delivery, trauma to the child and mother, and a sudden drop in blood glucose for the child after birth. Children who are exposed for a long time to high blood glucose in the womb are at higher risk of developing diabetes in the future.

At present, type 1 diabetes cannot be prevented. The environmental triggers that are thought to generate the process that results in the destruction of the bodys insulin-producing cells are still under investigation.

While there are a number of factors that influence the development of type 2 diabetes, it is evident that the most influential are lifestyle behaviours commonly associated with urbanization. These include consumption of processed foods, for example foods with a high fat contentm sugar-sweetened beverages and highly refined carbohydrates. At the same time, modern lifestyles are characterized by physical inactivity and long sedentary periods. Together, these behaviours are associated with an increased risk of being overweight or obese and the development of type 2 diabetes.

A number of prevention programmes have shown that modifying such behaviours, by eating healthier foods and increasing physical activity, can greatly reduce the risk of developing type 2 diabetes. In order to halt the increase of type 2 diabetes, whole populations must change their lifestyle behaviours by modifying diet and increasing physical activity levels. To support this, IDF has reviewed the evidence on which types of food predispose to type 2 diabetes and has released nine recommendations for a healthy diet for the general population.

A particular threat in terms of the associated risk of developing type 2 diabetes is the consumption of high sugar foods, particularly sugar-sweetened beverages, In 2014, the World Health Organization (WHO) issued new recommendations to limit sugar intake. IDF fully supports these recommendations and in response published the IDF Framework for Action on Sugar.

The IDF Diabetes Atlas, Seventh Edition 2015 provides the latest figures, information and projections on the current and future magnitude of the diabetes epidemic.

Original post:
International Diabetes Federation - What is diabetes

The importance of both diabetes and these comorbidities will continue to increase as the population ages. Therapies that have proven to reduce microvascular and macrovascular complications will need to be assessed in light of the newly identified comorbidities.

Lifestyle change has been proven effective in preventing or delaying the onset of type 2 diabetes in high-risk individuals. Based on this, new public health approaches are emerging that may deserve monitoring at the national level. For example, the Diabetes Prevention Program research trial demonstrated that lifestyle intervention had its greatest impact in older adults and was effective in all racial and ethnic groups. Translational studies of this work have also shown that delivery of the lifestyle intervention in group settings at the community level are also effective at reducing type 2 diabetes risk. The National Diabetes Prevention Program has now been established to implement the lifestyle intervention nationwide.

Another emerging issue is the effect on public health of new laboratory based criteria, such as introducing the use of A1c for diagnosis of type 2 diabetes or for recognizing high risk for type 2 diabetes. These changes may impact the number of individuals with undiagnosed diabetes and facilitate the introduction of type 2 diabetes prevention at a public health level.

Several studies have suggested that process indicators such as foot exams, eye exams, and measurement of A1c may not be sensitive enough to capture all aspects of quality of care that ultimately result in reduced morbidity. New diabetes quality-of-care indicators are currently under development and may help determine whether appropriate, timely, evidence-based care is linked to risk factor reduction. In addition, the scientific evidence that type 2 diabetes can be prevented or delayed has stimulated new research into the best markers and approaches for identifying and referring high-risk individuals to prevention programs in community settings.

Finally, it may be possible to achieve additional reduction in the risk of type 2 diabetes or its complications by influencing various behavioral risk factors, such as specific dietary choices, which have not been tested in large randomized controlled trials.

1Nathan DM. Diabetes: Advances in diagnosis and treatment. JAMA. 2015;314(10):1052-62.

2Knowler WC, Fowler SE, Hamman RF, et al; Diabetes Prevention Program Research Group. Ten-year followup of diabetes incidence and weight loss in the Diabetes Prevention Program Outcomes Study. Lancet. 2009 Nov 14;374(9702):1677-86.

3Centers for Disease Control and Prevention. National Diabetes Statistics Report: Estimates of Diabetes and Its Burden in the United States, 2014. Atlanta, GA: US Department of Health and Human Services; 2014. Available from: http://www.cdc.gov/diabetes/data/statistics/2014StatisticsReport.html.

4Centers for Disease Control and Prevention. Diabetes Report Card 2014. Atlanta, GA: Centers for Disease Control and Prevention, US Dept of Health and Human Services; 2015.

5Emerging Risk Factors Collaboration, Seshasai SR, Kaptoge S, Thompson A, Di Angelantonio E, Gao P, et al. Diabetes mellitus, fasting glucose, and risk of cause-specific death. N Engl J Med. 2011;364(9):829-41.

6Menke A, Casagrande S, Geiss L, Cowie CC. Prevalence of and trends in diabetes among adults in the United States, 1988-2012. JAMA. 2015;314(10):1021-9.

7Danaei G, Finucane MM, Lu Y, Singh GM, Cowan MJ, Paciorek CJ, et al. National, regional, and global trends in fasting plasma glucose and diabetes prevalence since 1980: systematic analysis of health examination surveys and epidemiological studies with 370 country-years and 2.7 million participants. Lancet. 2011;378(9785):31-40.

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Diabetes | Healthy People 2020

In BriefHealth care startup Virta is proposing a new type of treatment for type 2 diabetes, which revolves around personalized nutrition and constant contact with a medical professional.

More than 29 million people suffer from diabetes in the United States alone. Now, a new healthcare startup called Virta claims that it can stamp out the condition for good and whats more, it plans to do so using little more than a sensible diet plan and a smartphone app.

Virta puts its patients on a nutrition plan that cuts out sugar and bad carbohydrates. To make sure that they can stick to this diet safely, theyre kept in constant contact with a trained physician, exchanging text messages and engaging in video calls as often as every day.

Each patients plan is highly individualized, with everything from their food intake, to their recommended activity levels, to their medication being tailored to their specific situation. Preliminary test have been very promising, with a recent trial of 262 people allowing 87 percent of participants to stop using insulin completely or at least reduce their dosage.

Virta founder Sami Inkinen had good reason to get into diabetes care. In 2007, he had just started competing in Ironman triathlon events, when he was told that he was pre-diabetic.Click to View Full Infographic

I started reading research and thats what kind of led me to meet my scientific co-founders, said Inkinen in a recent interview with Tech Crunch. The bottom line, what these guys had shown is that there is a way to nutritionally reverse type 2 diabetes without starving you to death. They had published all these papers. I was like this is nuts. This is 30 years-old science.

Diabetes has a huge impact on the lives of people affected, not least when theyre forced to administer their own insulin injections. Fortunately, researchers are finding ways to avoid this process, from CRISPR skin grafts to cell implants, to a smartphone app.

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Healthcare Startup Claims It Can Defeat Diabetes With Nutrition Alone - Futurism

Q My neighbor told me she went to an all-day event last year that was great for people with diabetes. Do you happen to know what, where, when? M.J., Greenville

A I asked Angie Watson, registered dietitian nutritionist and certified diabetes educator at ECU Endocrinology, to tell you about this wonderful program that is scheduled for 9 a.m. to 3 p.m. Nov. 1. Here is what Angie wants you to know about the popular event, Winning With Diabetes. The event is for people living with diabetes, at risk for diabetes, or wanting to support someone with diabetes. It is definitely worth the time, attention and admission charge to attend. This years event will be at a new location, the Edwin W. Monroe Conference Center, 2000 Venture Tower Drive (adjacent to the Vidant hospital campus).

Diabetes can be a very demanding and complex disease, so I love it when people living with diabetes or prediabetes, as well as their friends and family members, are excited about learning how to better manage the condition. For the last 16 years, Greenville has played host to a daylong event for people with diabetes and their loved ones where folks come out to learn, laugh, engage and empower themselves to manage their health. I have had the privilege to be a part of the planning committee for the past two years and have seen first-hand the impact this event can have. Winning With Diabetes is a day filled with guest speakers in the morning, healthy snacks and lunch, interactive screenings, diabetes information booths and opportunities to ask questions to experts.

Our theme this year is Risky Business. The event will highlight some of the health risks that come with having diabetes and ways to reduce these risks. Among these risks are heart disease and stroke, nerve damage, damage to the feet, eye disease, kidney disease and dental problems.

Morning speakers include Kathy Kolasa, professor emeritus and Registered Dietitian Nutritionist and columnist, who will present Sweeteners, Smoothies, Supplements, and Sugars ... Oh My to help people sort out which foods and drinks help or hinder blood sugar levels. Following that will be Nancy Leggett Fraser, diabetes nurse educator at Greenvilles Veterans Affairs Clinic, who will present Risky Business Reducing Complications. Closing the morning sessions will be Dr. Robert Tanenberg of ECU Physicians-Endocrinology,a longtime supporter of Winning With Diabetes. His presentation, Diabetic Neuropathy: the Forgotten Complication, will focus on nerve damage.

The healthy snacks and lunch provided give those attending a chance to review carbohydrate counting basics that can help control blood sugars and reduce risks in the long term.

Afternoon events include foot and kidney screenings, as well as Know Your Numbers and Sugar Shockers stations. Afternoon displays will showcase some diabetes resources in the Pitt County area, including medications, devices and tools. Diabetes experts will be available throughout the event to answer questions and concerns that relate to diabetes self-management skills.

Registration is required; the cost is $30 per person. The charge to register a spouse or friend is $25. Mention The Daily Reflector when you register, and the cost is $20. Free parking is available. Those attending will receive a passport booklet that when stamped at each station makes the person eligible to win prizes. Call 847-8265 to register or for more information.

The program is supported by local volunteers and health-care professionals and receives financial support from Medtronic, Sanofi, Lily, NovoNordisk and Tandem.

Professor emeritus Kathy Kolasa, a registered dietitian nutritionist and Ph.D., is an Affiliate Professor in the Brody School of Medicine at ECU. Contact her at kolasaka@ecu.edu.

IF YOU GO!

WHAT: Winning with Diabetes

WHEN: 9 a.m.-3 p.m. Nov. 1. (doors open at 8:30 a.m.)

WHERE: Edwin W. Monroe Conference Center, 2000 Venture Tower Drive

COST: $30 per person; $25 per each additional person; mention the Daily Reflector and registration is $20.

TO REGISTER: Call 847-8265

Continue reading here:
Winning With Diabetes - Greenville Daily Reflector

Credit: CC0 Public Domain

Regular and early lifestyle changes key to reducing type 2 diabetes and cardiovascular disease in young South Asians, study suggests

Regular and early one-to-one educational sessions on healthy diet and lifestyle could reduce the risk of developing type 2 diabetes and cardiovascular disease (CVD) in young South Asians, a new research published today in BMC Medicine suggests.

Unlike previous studies which have focussed on high risk older people, researchers from King's College London and the Diabetes Association of Sri Lanka looked at almost 4000 people aged between 5 and 40. The results suggest regular and realistic interventions with high risk younger people - especially if done before 18- may be more successful, and cost-effective than less-intensive and irregular sessions.

Asia is a major site of Type 2 diabetes, accounting for 60 per cent of people with the disease worldwide. South Asians are predisposed to develop the disease early on, with a third of future cases predicted to occur in those aged below 45 years old.

Participants in the study from Colombo, Sri Lanka had been screened out of a total of 23,298 people, and identified as being at a higher risk of developing type 2 diabetes and CVD, but not yet diagnosed. Out of the 4672 participants aged between five and 40 who began the study, 3539 were eligible for analysis after three years.

Participants were randomised into two groups; pragmatic lifestyle modification (P-LSM) programme and control lifestyle modification programme (C-LSM). There were no significant differences in age, gender, clinical or biochemical characteristics between the two groups at time of randomisation.

Both groups received an identical lifestyle education programme, aimed at reducing weight, improving diet, reducing psychological stress and increasing physical activity. Those in the P-LSM group received one-to-one advice, assessment and education sessions every three months for an average of three years. Those in C-LSM in comparison received these sessions only once a year for an average of three years. For participants younger than 16 the advice and guidance in both groups was also given to the child's parents. The programme was delivered by 'peer educators', i.e. educators aged between 18 to 40 years old. They were trained by experts from the University of Colombo and the MV diabetes research centre in Chennai India with regular refresher sessions.

The groups were monitored throughout the period for several risk factors that lead to cardio-metabolic disease in later life: new type 2 diabetes, hypertension, cardiovascular disease and renal disease.

After three years, the researchers found that overall, these risk factors occurred less in the P-LSM group than in the control group (479 compared to 562), a significant risk reduction of 11%. New occurrences of hypertension were significantly reduced with those in the P-LSM group (115 participants) versus the control group (152 participants). The researchers found further reductions in the occurrence of type 2 diabetes between the two groups (58 in the P-LSM group versus 72 in the C-LSM group). The reduction was especially pronounced in participants aged under 18; when looked at overall, the risk factors occurred less in the P-LSM group versus C-LSM, with 140 versus 174, a 17% risk reduction.

Participants in the P-LSM also improved their physical activity and their behaviour towards increasing activity during the study to a greater extent than those in the C-LSM group.

Lead author Dr Janaka Karalliedde, Clinical Senior Lecturer at King's College London said: 'This study highlights that even small changes in lifestyle could lead to changes in health. We suggest that early and regular interventions can have a significant impact in delaying or preventing the onset of type 2 diabetes and other cardiovascular disease.'

Dr Mahen Wijesuriya, co-lead author, the Diabetes Association of Sri Lanka, said: 'The impact of this research could hold huge benefits for young South Asians at risk of type 2 diabetes and other cardiovascular disease. Importantly it is a low-cost intervention that could be translated into parts of the community in Sri Lanka and other low to middle income countries. The use of peer educators to deliver interventions could be a more pragmatic, cost-effective approach than registered dietitians or counsellors.'

The researchers state that further research is required to establish the longer-term impact of such lifestyle changes in a younger population. The trial does not explain the mechanisms behind the reductions in risk factors rather establishes associations that require further research. Additionally, the results in this young urban population may not be generalizable to other groups.

Explore further: Intensive lifestyle intervention provides modest improvement in glycemic control, reduced need for medication

More information: Mahen Wijesuriya et al. A pragmatic lifestyle modification programme reduces the incidence of predictors of cardio-metabolic disease and dysglycaemia in a young healthy urban South Asian population: a randomised controlled trial, BMC Medicine (2017). DOI: 10.1186/s12916-017-0905-6

Journal reference: BMC Medicine

Provided by: King's College London

Original post:
Regular, early lifestyle changes key to reducing type 2 diabetes & cardiovascular disease - Medical Xpress

DUBLIN--(BUSINESS WIRE)--The "Global Cartilage Repair Market 2017-2021" report has been added to Research and Markets' offering.

The global cartilage repair market to grow at a CAGR of 11.59 % during the period 2017-2021.

The treatment of articular cartilage has evolved tremendously in the past decade. Reparative and restorative methods have been developed to address the significant source of morbidity in the young and active patients. Articular cartilage injury can be focal, which is localized or systemic. Procedures are being developed not only to alleviate the symptoms associated with articular cartilage defects but also to limit the progression of cartilage damages into degenerative diseases.

According to the report, one of the major drivers for this market is Rising incidence of accidental injuries. Globally, the road traffic injuries are increasing, with post complicated symptoms such as weakening of tendons, cartilage tear, and orthopedic issues.

The latest trend gaining momentum in the market is Gene therapy and stem cell therapy. Gene therapy is one of the promising fields in the cartilage repair. Many clinical studies have been performed for cartilage repair. The researchers are trying to develop gene therapy for cartilage repair and currently been investigated for clinical application.

Further, the report states that one of the major factors hindering the growth of this market is Product side effects. Surgeons use cartilage repair products such as tissue scaffold to improve the recovery. These products once grafted in the body may cause serious complications, resulting in their increased scrutiny for safety and efficacy. In many autologous chondrocyte implantation, there were common complications such as graft rejection, symptomatic hypertrophy, disturbed fusion and delamination.

Key vendors

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For more information about this report visit https://www.researchandmarkets.com/research/rjx284/global_cartilage

Originally posted here:
Global Cartilage Repair Market 2017-2021 - Gene Therapy and Stem Cell Therapy is the latest Market Trend Making ... - Business Wire (press release)

RACHEL THOMAS

Last updated19:30, August 30 2017

SUPPLIED

Tiny rat hearts growing in dishes in a move that Australian plastic surgeon Wayne Morrison hopes will one day be able to help humans.

"We're growing little beating hearts in dishes," Professor Wayne Morrison says, deadpan.

The man behind Australia's first hand transplanthas spent his life reattaching and transplanting body parts. Now he's working to see if we can regrow them ourselves.

As part of his work as director of Melbourne's BernardO'Brien Instituteof Microbiology, Morrison hasgrown hearts to maturity on the legs of rats and retransplanted them inside their bodies.

RACHEL THOMAS/STUFF

Morrison with leading Kiwi plastic surgeon Swee Tan at the Gillies McIndoe Research Institute in Wellington.

The next step is humans:"Our core interestis in trying to grow fat tissue and skin to repair people."

READ MORE:*Christchurch research key to printing human body parts*Scientists convert spinach leaves into human hearttissue that beats*Grant for NZ scientist seeking ways to use fish eyes to repair human corneas

With this in mind, he has been in Wellington to talk tissue engineering with leading plastic surgeon SweeTan, founder of the Gillies McIndoe Research Institute (GMRI) in Newtown, as well as to give a public lecture on his work.

RACHEL THOMAS/STUFF

The cell and tissue culture lab at the Gillies McIndoe Research institute, where Tan is engineering tissue.

We're "miles away" from growing a fully functional heart for humans, Morrison said, but the work could have a massive impactfor burns victims, mastectomy patients, and those waiting for vital organs such as lungs and hearts in the future.

"First, you want to be able to grow tissue that will not be rejected."

It all comes down tofiguring out how the building blocks of the body stem cells lead to growth of new tissue.

REUTERS

A rat with a human ear growing on its back, reportedly pictured by a Shanghai university in the 1990s. Morrison hopes a similar process can be used to grow vital organs for human transplants in the future.

New developments mean expertscan take a piece of skin and recreate the embryo which means it can be manipulated and growninto any type of tissue, he said.

Tanhas pioneered research at GMRIon targeting specific cancer stem cellswhich if manipulated properly would mean doctors could nip certain types of cancer in the bud.

InMelbourne, Morrison recentlytrialleda way ofregrowingbreastsin four mastectomy patients.

About 30mlof fatty tissue was inserted under the skin in a 200ml special chamber,and in one patient, that chamber filled completely with new tissue.

The key is to understand how that happened, and why it didn't work in the three other patients. "It is a principle, that you can grow or expand tissue."

A long-time plastic surgeon, Morrison has always been in the business of putting people back together.

He cited a "face amputation" about 20 years ago as the most complex and rewardingprocedures he's ever done.

An Australian womangot her ponytail caught in a milking machine near Melbourne. She was scalped from the back of her head down to her jawline.

"This one, extraordinarily, took the whole face off. I think there's only one other ever been reported in the world.

"Reattachingthat took 24 hours or so, and we didn't know if it would surviveor not. Fortunately the face did;a lot of the scalp tissue did not."

It's those horrifying cases thatled to both him and Tan seekingmore solutions for victims of cancer or freak accidents.

"Thecomplications of the drugs you have to take are morbid, and they will eventually kill you."

Frenchwoman IsabelleDinoirewas theworld's first recipient of afacialtransplant in 2005, butdied last year after developing two kinds ofof cancer.

But as Morrison says: "If you see someone with facial injuries or burns, you'd need a hard heart to say, 'No, you can't have a transplant' that would be horrendous."

-Stuff

More here:
Recreating breasts and beating hearts: how tissue engineering is changing medicine - The Dominion Post

The Independent Citizens Oversight Committee of the California Institute for Regenerative Medicine (CIRM) today unanimously approved an $18.29 million grant to University of California San Diego School of Medicine researchers to fund a phase Ib/IIa clinical trial of a novel combination drug therapy for B-cell cancers.

Scanning electron micrograph of B lymphocyte. Image courtesy of National Cancer Institute.

The approach combines an experimental monoclonal antibody-based drug called cirmtuzumab with ibrutinib, a small molecule drug that inhibits a protein called Brutons tyrosine kinase. Ibrutinib, marketed as Imbruvica, is already approved to treat B cell cancers, like chronic lymphocytic leukemia (CLL) and mantle cell lymphoma (MCL). Cirmtuzumab targets ROR1, a cell surface protein present on tumors but not in normal adult tissues a distinction that makes it an attractive target for anticancer therapy. Cirmtuzumab is currently in clinical trials for the treatment of CLL.

The new combined drug trial, intended to study both safety and efficacy, is headed by Thomas Kipps, MD, PhD, Distinguished Professor of Medicine and deputy director of research at UC San Diego Moores Cancer Center, in collaboration with colleagues at the UC San Diego CIRM Alpha Stem Cell Clinic the cell therapy arm of the Sanford Stem Cell Clinical Center at UC San Diego Health.

We are very excited about evaluating this combination of targeted therapies in the clinic, said Kipps. Although ibrutinib has been approved for treatment of patients with CLL or MCL, it is exceptionally rare for this drug by itself to get rid of all the leukemia cells or cause long-lasting remissions without continuous therapy.

As a result, patients are recommended to take ibrutinib indefinitely until they develop intolerance or resistance to this drug. By blocking a survival/growth-stimulating pathway that provides a lifeline to the leukemia cells of patients taking ibrutinib, cirmtuzumab can work together with ibrutinib to potentially kill all the leukemia cells, allowing patients to achieve a complete remission and stop therapy altogether.

Kipps noted, too that cirmtuzumab targets cancer stem cells, which behave somewhat like the roots of the disease, resisting many forms of treatment and allowing a malignancy to grow back after apparently successful therapy. By targeting cancer stem cells, said Kipps, cirmtuzumab may improve our capacity to achieve more complete and longer lasting remissions when used in combination with targeted drugs, such as ibrutinib, or other anti-cancer drugs for the treatment of patients with many different types of cancer.

B cell malignancies are cancers of the blood. B cells are a type of white blood cell or lymphocyte, part of the immune system. Some B cells produce antibodies to immediately help fight off infections while others, called memory B cells, remember the pathogen in case of future infections. In B cell cancers, mutated B cells dysfunction or grow in an uncontrolled manner, resulting in diseases like CLL (the most common type of leukemia) and most non-Hodgkins lymphomas.

Cirmtuzumab was developed in Kipps laboratory under the auspices of CIRMs HALT leukemia grant awarded to Dennis Carson, MD, principal investigator, and Catriona Jamieson, MD, PhD, deputy director of the Sanford Stem Cell Clinical Center and director of stem cell research at Moores Cancer Center. Kipps led one of the six projects, generating antibodies against ROR1 that, ultimately, led to the cirmtuzumab trials in patients with CLL.

Every year around 20,000 Americans are diagnosed with CLL, said Maria Millan, MD, interim president and CEO of CIRM. For those who have run out of treatment options, the only alternative is a bone marrow transplant. Since CLL afflicts individuals in their 70's who often have additional medical problems, bone marrow transplantation carries a higher risk of life-threatening complications. The combination approach of cirmtuzumab and Ibrutinib seeks to offer a less invasive and more effective alternative for these patients.

Cirmtuzumab has also shown efficacy against solid tumors. A clinical trial is planned to test it, in combination with the drug paclitaxel, for treating metastatic breast cancer. That trial is not yet recruiting participants. Cirmtuzumabs name is a nod to CIRMs long-standing support and research funding.

CIRM was created in 2004 by California voters with $3 billion in funding support to accelerate stem cell research and treatments. Since 2004, UC San Diego researchers have received at least 96 CIRM awards, totaling more than $182 million.

Continued here:
State's Stem Cell Agency Awards $18.2 Million Grant for B Cell Cancer Clinical Trial - UC San Diego Health

An Indianapolis-based startup believes its device could be groundbreaking in the world of ophthalmologyand life-changing for patients with glaucoma. The disease is the second-leading cause of blindness, but Purdue-affiliated startup Bionode says its noninvasive technologyenveloped in off-the-shelf contact lenses and glassesreverses the physical cause of glaucoma. Driven by the vision of researchers at Purdue, the technology could be on the market in a matter of months.

Glaucoma is caused by fluid buildup in the front part of the eye; the extra fluid increases the pressure in the eye, damaging the optic nerve and ultimately causing blindness. Bionodes technology involves adding a gold trace to an off-the-shelf contact lens, which then works hand-in-hand with specially-equipped glasses.

The glasses generate a magnetic field, the contact picks it up, turns it into a current and drives the current into the structures of the eye, says Bionode Chief Technology Officer Dr. Pedro Irazoqui, who is also an electrical and computer engineering and biomedical engineering professor at Purdue.

By electrically stimulating the muscles around the canal where fluid leaves the eye, pressure on the optic nerve is relieved, preventing vision loss. Irazoqui likens the fluid-filled interior chamber of the eye to a clogged sink, and says Bionode does some expert plumbing.

Think of it as a sink filled with water, and the drain is closed. You open it up so the water can now flow around that clog, says Irazoqui. If you look at the pressure in the eye, its actually going down a lot faster than we would expect just from that opening of the drain.

Even more important than relieving the clog, says Irazoqui, is that Bionodes technology also turns down the faucet while opening the draina double whammy that relieves pressure in the eye.

Its interesting to think that using these electrical currents, we can actually get much more specific control down to whether we [manipulate] the drain, the faucet or both, says Irazoqui, and to what extent we [manipulate] themand we can really dial it in.

Because most glaucoma patients are over 40, when the eyes naturally produce less tearsand contacts exacerbate dry eyesBionode has improved the technology in recent months to produce the same effect with glasses only.

The new design works as well as the old design, but it has no contact lens, says Irazoqui. We can still use the contact lens to give the patient an even bigger kick, but I think most patients wont need the contact lens. And now, we have a deeper understanding of how it all works.

Bionode believes the result is a therapy thats far superior to existing glaucoma treatments; medicated eye drops eventually stop working and have low patient compliance, laser eye surgery can only be performed a limited number of times, and a blood procedure that allows liquid to leak out of an open wound in the eye carries a high risk of infection.

Bionode says the device relieves eye pressure in a matter of minutes, but an upcoming clinical trial will answer a looming question: how long will the effect last? In the coming weeks, Bionode will begin a human clinical trial involving 30 patients in Canada to evaluate how long the therapy is effective and generate data that could eliminate the need for additional trials in the U.S.

[The FDA] is going to ask some very specific questions, so we will structure this study [in Canada] in such a way that it answers the questions the FDA is going to ask, says Irazoqui. Were partnering with the right people who have the experience in putting together these clinical trials in ophthalmology for devices that have been approved by the FDA.

Irazoqui says commercializing the device by late summer 2018 is optimistic, but not crazy. Bionodes funding includes $100,000 from the Elevate Purdue Foundry Fund and $1 million from an anonymous investor.

The goal is to build medical devices that are clinically relevantthats what gets me out of bed in the morning. I want a device that we invented at Purdue to make it all the way to the clinic and change peoples lives, says Irazoqui. [Glaucoma] is the second leading cause of blindness, so the impact is huge. Thats a lot to be excited about.

Continue reading here:
Purdue Visionaries Build Device to Prevent Blindness - Inside INdiana Business

What Barrita Sue "Susie" Holverson lacks in sight, she makes up for in admiration from those who know her.

Holverson has been blind almost her whole life. That's also about the amount of time she's been attending Anoka United Methodist Church, where she serves as pianist. Parishioners there praise Holverson for her musical talent, sharp memory and wit, pleasant personality and positive attitude in the face of her inability to see.

In her Kokomo home, with her cane leaning against a wall and her piano standing in the living room, Holverson recalled having to be given oxygen after being born premature. Getting too much oxygen is likely what led to her blindness, she said.

"But that was what kept me alive," she added.

She went on to remember how it wasn't uncommon for people to sue hospitals for such sight-robbing treatments, but said her own experience doesn't leave her bitter.

"I thought, well, you know what? There could've been worse things," she said. "I have a relatively good mind."

"I'm no genius," she added with a laugh. "Compared to what could've been, I'm fine."

Holverson said she could see early on in life, but not really well. Before reaching age 3, her vision was reduced to just being able to sense light and dark before that ability went away too, she continued.

"I've just grown up with it, so to me it was no big deal," she said.

Holverson said she attended the Indiana School for the Blind in Indianapolis, where she learned how to read Braille and Braille music and took piano and voice lessons.

She said she went on to work in medical transcription for St. Vincent Hospital in Kokomo for about 20 years.

"I cook, I clean, I do just about the same things that everybody else does," she said. "The only thing I guess I don't do, and everybody should thank God that I don't, I don't drive," she added with a laugh.

Her music lessons started before she went off to school, she said, and she currently plays the piano for services at Anoka United Methodist Church.

"It's my way of serving," she said.

Holverson said her mother, who was an avid pianist too, got her interested in music. She recalled how they used to play together at Anoka United Methodist Church, which she grew up down the street from. Her grandmother helped start the church in 1913, Holverson said.

"It's just always been a part of my life, the church," she said. "There are friends and family there and I don't know how else to put it. It's a special place to be."

With the help of the speech software on her computer, Holverson said she does a lot of emailing for the church's prayer chain. She said she also likes to listen to audio books and relies on Siri, the voiced personal assistant developed by Apple Inc., to use her iPhone.

"Sometimes I'd like to smack her," she admitted with a laugh.

Ruth Mayhill, organist for Anoka United Methodist Church, has known Holverson since she was born. She, like several others at the church, is in awe of Holverson's ability to recall hymns by their numbers across multiple hymnals.

Mayhill said she's also fond of Holverson's ability to play the piano.

"She can sit down and play a song and it just blows us away," she said. "She is amazing."

Holverson's friendly personality is another one of her qualities, Mayhill said.

"She is fun to be around," Mayhill said. "They torment and tease her and she takes it and dishes it right back."

Mayhill said she also admires Holverson's ability to live alone and take care of herself despite not being able to see.

"It's amazing," Mayhill said. "I know they are taught that in the blind school, all the blind people are taught how to take care of themselves, but to witness it, she has been eye-opening for all of us around here."

Joyce Propes, who sings in the church's choir, said one of her favorite stories about Holverson is when she was picked up one summer to perform at the church's vacation Bible school. A song was played in the car and Holverson was asked about playing it at vacation Bible school, Propes continued.

"And Susie would listen to it on the way from Kokomo and be able to play it for the kids when she got here," Propes said. "Just that fast she can pick up and play."

Holverson reacts to the praise with humility.

"I just do what I can and to me I don't do anymore than anybody else, the only difference is that I can't look at what I'm doing," she said.

She said her faith, family and friends are the source of her positive attitude.

"I guess I don't see myself the way other people see me," she said. "I'm just plain me and that's all I really am."

Reach Mitchell Kirk at mitchell.kirk@pharostribune.com or 574-732-5130

Link:
Out of sight: Area woman doesn't let blindness darken her spirit - pharostribune.com

Tree death, like tree sex, can reveal deeper truths. You may have seen bare trunks with branches that fork over and over in perfect symmetry (that opposite branching again). These are ash trees, victims of the deadly emerald ash borer, which is thought to have arrived in shipping pallets from Asia. Beyond the aesthetic and ecological loss, and just plain tragedy, the ash carnage costs society a huge amount of money, as parks departments and homeowners must either treat ash trees or have them cut down.

The borer is a consequence of global trade, and its only the latest iteration of this sad story; chestnuts, hemlocks and elms have already taken major hits from foreign pests.

Luckily, not everything in tree world is so dismal. The trees around us can uncover forgotten history. Sometimes a huge oak rises in a yard or in the midst of a much younger woods. These witness trees once marked the edges of farm fields. An oddly straight line of junipers or locusts likely signals an old fence row. Neighborhoods built in the 1960s might be lined with once-loved, now-hated Bradford pears; older ones may feature towering willow oaks with roots bulging out of undersized tree boxes. Parts of Paris, New York and, appropriately, London, are practically monocultures of London plane trees, once favored because they could survive these cities fetid air.

Trees can also tell us how well were managing our environment today. Many eastern forests, including Rock Creek Park, the wild green vein running down Washingtons center, have an understory dominated by American beech. Beeches are slow to get going, but theyre almost unmatched at growing in shade and being unappetizing to deer, which are wildly overpopulated in much of the country. Unless we find a way to manage our woods, using predators and periodic fires, were probably on our way to species-poor forests dominated by beeches. As much as I love the trees smooth, elephant-skin bark and brittle leaves shivering on their branches through the winter, I dont think an all-beech future is one I want to see.

Some may want more practical reasons for learning trees. If so, I offer that knowing your trees opens up an abundant and entirely free food source. Those in the know can gorge on juicy native mulberries and serviceberries in the spring, and persimmons and pawpaws in late summer. Thats to say nothing of tree nuts, which carpet the forest floor in fall. Pecans, walnuts, hickory nuts, beech nuts; with proper preparation, theyre all edible. For Native Americans living in California before European contact, acorns were a staple more important than corn. Yet today theyre a specialty item, largely limited to the occasional D.I.Y. foraging workshop.

Were so used to eating domesticated plants that the idea of eating wild tree parts seems strange, primitive and possibly dangerous. As a result, were letting billions of dollars worth of free, high-quality food go to waste. This, reader, is madness! Ill admit, however, that Im among the mad. Roadside tree fruit is just an occasional supplement to my diet, and I havent yet found the patience to leach the bitter tannins out of acorns. For me, learning about trees is more about seeing, and knowing. Its about not being a stranger in my own country.

And its about not letting the built environment make me too tame. When you engage with a tree, you momentarily leave the human-created world. Look at an American elm in winter, its limbs waving like Medusas snaky hair. The elm may grow along streets and sidewalks, but there is nothing tame about that tree. In cities, where animals feast on human gardens or garbage and most landscape plants are domesticated cultivars, native trees are the last truly wild beings.

Yes, people may look curiously if you stop to study a tree. But so what? Let yourself go a little wild.

Read the rest here:
Cure Yourself of Tree Blindness - New York Times

New wearable technology is changing the view for color blind patients.

Amity Addrisi and NBC News , KING 6:24 PM. PDT August 25, 2017

Tyler Gore has red/green color blindness, but with new glasses, hes able to see those colors properly for the first time in his life.

Wearable technology is changing everything for color-blind patients.

"I have red/green color blindness, and reds and greens look more brown and tan to me. It makes it hard to see," says Tyler Gore,.

He found out he was color blind from a test at the optometrist office in first grade. Now 16 years old, it affects the way he drives.

"Mostly when they're mixed together, like stop lights. I can't see stop light colors," said Gore.

Roughly 13 million people in the United States have this genetic condition.

"Because it doesn't prevent vision it just alters the way we perceive color in vision it's very difficult for anyone to understand the effect, said Dr. Raquel Strange, Gores optometrist.

But technology is changing that. Gore heard about Enchroma glasses that allows him to see color, such as red and green, for the first time.

"Everything was so beautiful. All of the colors popped out. All of the colors were exaggerated, and I could see color. It was awesome," said Gore.

"We've had people break down and cry. We've seen lots of parents cry and girlfriends and wives cry because they had no idea the difference that it makes. It allows them to perceive those differences. That's what they're missing. It's this kind of one-ness to so many of those colors, said Strange.

So, for his birthday, Gore is getting his own pair. It's the only thing he asked for, so he can experience a brighter version of the world he knows.

There are several different versions of glasses to help correct color blindness. The Enchroma brand costs from $250 to $300 and can be made with corrective prescription lenses for indoors or out.

2017 NBCNEWS.COM

Read the original:
Corrective lenses minimize color blindness - KING5.com

Scientists are still a long way from creating a visual prosthesis that works as well as a real human eye. But, engineers are making steady progress in what was once the realm of science fiction.

One of their promising new devices, a bionic vision system based on photovoltaic implants, is awaiting approval for human clinical trials in Europe. A second system, based on in vitro studies of the retina, could be ready for animal testing within four or five years. Both inventions have the same goal: to give back some measure of sight to people with progressive diseases of the retinaespecially retinitis pigmentosa and macular degeneration.

The new device doesnt require the implantation of a bulky electronics case and antenna, or a cable coming out of the eye.

According to the National Institutes of Health, retinitis pigmentosa is the leading cause of inherited blindness, affecting 1 in about 4,000 people in the United States. The disease usually begins with a loss of night vision in childhood, and progresses to involve peripheral and then central vision, gradually robbing young people of the ability to read, drive, recognize faces, and do routine daily tasks.

Macular degeneration, in contrast, is one of the leading causes of vision loss in Americans 60 and older. By 2020, the NIH estimates that as many as 3 million people in the United States may be living with various stages of the disease, which gradually destroys the densely packed light-sensitive cells, called photoreceptors, in the retinas center, or macula.

Many of these folks are going to be losing their central vision, says Chip Goehring, president of the American Macular Degeneration Foundation, so it is absolutely vital that we have options for the restoration of sight, including biological and mechanical approachesstem cell therapies for photoreceptor replacement, gene therapies to restore dysfunctional retinal tissues, and prosthetic retinas that can serve an even wider population of people with vision loss.

Normal retinal tissue consists of photoreceptors: light-sensitive cells resembling rods and cones at the base of the eye, topped by interconnected layers of neurons. The signal travels from the rods and cones, through bipolar cells to ganglion cells, then via the optic nerve to several brain areas, including the visual cortex. Scientists still arent exactly sure why the rods and cones break down in patients with retinal diseases, nor have they figured out ways to prevent, slow, or reverse the process.

There is one silver lining: Retinitis pigmentosa and macular degeneration tend to spare some of the bipolar and ganglion cells. This means that the neurons in these patients retinas can be stimulated artificially, with micro-electrodes, bypassing the damaged rods and cones altogether.

Daniel Palanker, a professor of ophthalmology at Stanford University, has developed and patented numerous devices over the years to diagnose and treat eye diseases. Among them are a neurostimulator for enhancement of tear secretion in patients with dry eye syndrome, a femtosecond laser for cataract surgery, and a patterned laser scanning photocoagulator that surgeons use to treat multiple retinal disorders, including diabetic retinopathy, without excessive damage to the delicate tissues around the treatment spots.

Palankers new prosthetic device, called PRIMA, features a tiny video camera mounted atop futuristic-looking augmented reality goggles, connected to a video processor about the size of a cell phone. It doesnt require the implantation of a bulky electronics case and antenna, or a cable coming out of the eye, like a German system that has been used successfully by a handful of patients in Europe.

Instead it relies on multiple arrays of photodiodes, each about a millimeter in diameter and containing hundreds of pixels, which work like the solar panels on a rooftop. Surgeons can lay down these tiny chips, like tiles, replacing the missing light-sensitive rods and cones in the central retina.

When PRIMAs camera captures an image of, say, a flower, the video processor transmits that picture to a microdisplay mounted inside the goggles. Powerful pulses of near-infrared light illuminate this display and are projected from the goggles into the eye, like the invisible rays of a TV remote control.

The implanted photodiodes pick up these signals and convert them into tiny pulses of electrical current, which stimulate the bipolar cells directly above them. The signals propagate to the ganglion cells and then to the brain, which perceives them as patterns of light: a flower!

To test the system, researchers implanted PRIMA chips in laboratory rodents and exposed them to flashes of light, or to flickering patterns on a computer screen. By recording the resulting electrical activity in the animals visual cortices, the scientists measured their visual acuity.

It turned out that the prosthetic acuity exactly matched the 70-micron resolution of the implant, which is half the acuity of the rats natural vision, Palanker says. Since the stimulation thresholds were much lower than the safety limits, we decided to develop even smaller pixels to enable better vision. More recent behavioral tests, conducted by the French collaborators in primates, have confirmed our results with rodents.

Of course, until the implants are done in human patients, we wont know for sure.

But when human clinical trials do start later this year in Europe, they hope to achieve resolution corresponding to 20/250 vision with 70-micron pixels. That still is worse than the standard for legal blindness, 20/200, but it may be enough for a user to read very large print, or to see the face of a newborn grandchild.

In the next generation of the device, Palanker says, We should be able to put more than 12,000 pixels within 15 degrees of the visual field, taking the system to 20/150 or even better.

And while PRIMA cant reproduce color vision yetonly various shades of grayWe are working on single-cell selectivity in retinal stimulation, which might enable color perception, he says. With more experience, surgeons also might be able to expand the visual field to about 20 degrees.

Scientists ultimate dream is to build a visual prosthesis so small and powerful that it can stimulate specific neurons inside the retina, rather than sundry patches of them. Thats the goal of E.J. Chichilnisky, a Stanford professor of neurosurgery and of ophthalmology.

Think of the retina as an orchestra, Chichilnisky says. When you try to make music, you need the violins to play one score, the oboes to play a different score, and so on. Likewise, the retinas 1 million or so ganglion cells are composed of about 20 distinct types. Each plays a slightly different role in transmitting the perception of shape, color, depth, motion, and other visual features to the brain.

Since the mid-1990s, Chichilnisky has worked with a variety of physicists and engineers to develop small but powerful electrode arrays capable of measuring neural activity at the cellular level.

To better understand the patterns of electrical activity in the retina, Chichilnisky and colleagues use eye tissue taken from primates that have been euthanized for other medical studies. By placing small pieces of retinal tissue atop the microchip arrays, then exposing those samples to various patterns of light, theyve been able to record and study the distinctive electrical responses of five different types of retinal ganglion cells, which together account for 75 percent of the visual signal sent to the brain.

Theyve also developed techniques to replicate those electrical patterns, artificially stimulating the ganglion cells with high precision, comparable to the natural signals elicited by the rods and cones.

By learning how to replicate these complex signals, researchers are one step closer to their ultimate goal: a high-acuity visual prosthesis that behaves like an orchestra conductor, signaling the retinas myriad neurons to fire in precisely the right ways, at precisely the right times. Im not saying weve got it nailed, he says, but we certainly now have proof of concept for how to make a better device in the future.

The next challenge will be to fit the computing power onto an implantable electrode array that can do its job safely inside the eye, without overheating surrounding tissues, and autonomously, without any graduate students or postdocs running it, he says, laughing. If all goes well, a prototype of the implant could be ready for testing in lab animals in four to five years.

Chichilnisky and Palanker have the sense that they are pushing scientific boundariesand that their work someday may help more than blind people. Electro-neural interfaces already are being used to assist in the control of several vital organs, including the heart, bladder, and limbs. Before long, they even may be hooked up to different parts of the brain, helping people with memory loss, for example or, incredible as it sounds, even enabling telepathic communication.

We live in an era when we are starting to overcome the limitations imposed on us by our biological nature, Palanker says. This is how evolution goes.

Source:Theresa Johnston for Stanford University

Continued here:
Scientists aim to ease blindness with video goggles - Futurity: Research News

Your DNA may predict more about you than the way you look. According to the genetic theory of aging, your genes (as well as mutations in those genes) are responsible for how long you'll live. Here's what you should know about genes and longevity, and where genetics fits in among the various theories of aging.

The genetic theory of aging states that lifespan is largely determined by the genes we inherit.

According to the theory, our longevity is primarily determined at the moment of conception, and is largely reliant on our parents and their genes.

The basis behind this theory is that segments of DNA that occur at the end of chromosomes, called telomeres, determine the maximum lifespan of a cell. Telomeres are pieces of "junk" DNA at the end of chromosomes which become shorter every time a cell divides. These telomeres become shorter and shorter and eventually the cells cannot divide without losing important pieces of DNA.

Before delving into the tenets of how genetics affects aging, and the arguments for and against this theory, it's helpful to briefly discuss the primary categories of aging theories and some of the specific theories in these categories. At the current time there is not one theory or even one category of theories which can explain everything we observe in the aging process.

There are two primary categories of aging theories which differ fundamentally in what can be referred to as the "purpose" of aging. In the first category, aging is essentially an accident; an accumulation of damage and wear and tear to the body which eventually leads to death. In contrast, programmed aging theories view aging as an intentional process, controlled in a way that can be likened to other phases of life such as puberty.

Error theories include several separate theories including:

Programmed theories of aging are also broken down into different categories based on the method in which our body's are programmed to age and die.

There is significant overlap between these theories and even categories of aging theories.

Before discussing the key concepts related to aging and genetics, let's review what our DNA is and some of the basic ways in which genes affect our lifespan.

Our genes are contained in our DNA which is present in the nucleus (inner area) of each cell in our bodies. (There is also mitochondrial DNA present in the organelles called mitochondria which are present in the cytoplasm of the cell.) We each have 46 chromosomes making up our DNA, 23 of which come from our mothers and 23 which come from our fathers. Of these, 44 are autosomes, and two are the sex chromosomes, which determine if we are to be male or female.

(Mitochondrial DNA, in contrast, carries much less genetic information and is received from only our mothers.)

Within these chromosomes lie our genes, our genetic bluepirint responsible for carrying the information for every process which will take place in our cells. Our genes can be envisioned as a series of letters which make up words and sentences of instructions. These words and sentences code for the manufacturing of proteins which control every cellular process.

If any of these genes are damaged, for example, by a mutation which alters the series of "letters and words" in the instructions, an abnormal protein may be manufactured, which in turn, performs a defective function.

If a mutation occurs in proteins which regulate the growth of a cell, cancer may result. If these genes are mutated from birth, various hereditary syndromes may occur. For example, cystic fibrosis is a condition in which a child inherits two mutated genes controlling a protein which regulates channels responsible for the movement of chloride across cells in the sweat glands, digestive glands, and more. The result of this single mutation results in a thickening of mucus produced by these glands, and the resultant problems which are associated with this condition.

It doesn't take an elaborate study to determine that our genes play at least some role in longevity. People whose parents and ancestors have lived longer, tend to live longer and vice versa. At the same time, we know that genetics alone are not the sole cause of aging. Studies looking at identical twins reveal that there is clearly something else going on; identical twins who have identical genes do not always live an identical number of years.

Some genes are beneficial and enhance longevity. For example, the gene that helps a person metabolize cholesterolwould reduce a person's risk of heart disease.

Some gene mutations are inherited, and may shorten lifespan. However, mutations also can happen after birth, since exposure to toxins, free radicals and radiation can cause gene changes. (Gene mutations acquired after birth are referred to as acquired or somatic gene mutations.) Most mutations are not bad for you, and some can even be beneficial. That's because genetic mutations create genetic diversity, which keeps populations healthy. Other mutations, called silent mutations, have no effect on the body at all.

Some genes, when mutated are harmful, like those that increase the risk of cancer. Many people are familiar with the BRCA1 and BRCA2 mutations which predispose to breast cancer. These genes are referred to as tumor suppressor genes which code for proteins that control the repair of damaged DNA (or the elimination of the cell with damaged DNA if repair is not possible.)

Various disease and conditions related to heritable gene mutations can directly impact lifespan. These include cystic fibrosis, sickle cell anemia, Tay-Sachs disease and Huntington's disease, to name a few.

The key concepts in genetics and aging include several important concepts and ideas ranging from telomere shortening to theories about the role of stem cells in aging.

Telomeres - At the end of each of our chromosomes lies a piece of "junk" DNA called telomeres. Telomeres do not code for any proteins but appear to have a protective function, keeping the ends of DNA from attaching to other pieces of DNA or forming a circle. Each time a cell divides a little more of a telemore is snipped off. Eventually. there is none of this junk DNA left, and further snipping can damage the chromosomes and genes so that the cell dies.

In general, the average cell is able to divide 50 times before the telomere is used up (the Hayflick limit). Cancer cells have figured out a way to not remove, and sometimes even add to, a section of the telomere. In addition, some cells such as white blood cells do not undergo this process of telomere shortening. It appears that while genes in all of our cells have the code word for the enzyme telomerase which inhibits telomere shortening and possibly even results in lengthening, the gene is only "turned on" or "expressed" as geneticists say, in cells such as white blood cells and cancer cells. Scientists have theorized that if this telomerase could somehow be turned on in other cells (but not so much that their growth would go haywire as in cancer cells) our age limit could be expanded.

Studies have found that some chronic conditions such as high blood pressure are associated with less telomerase activity whereas a healthy diet and exercise are linked with longer telomeres. Being overweight is also associated with shorter telomeres.

Longevity genes - Longevity genes are specific genes which are associated with living longer. Two genes that are directly associated with longevity are SIRT1 (sirtruin 1) and SIRT2. Scientists looking at a group of over 800 people age 100 or older, found three significant differences in genes associated with aging.

Cell senescence - Cell senescence refers to the process by which cells decay over time. This can be related to shortening of the telomeres, or the process of apoptosis (or cell suicide) in which old or damaged cells are removed.

Stem cells - Pluripotent stem cells are immature cells which have the potential to become any type of cell in the body. It is theorized that aging may be related to either the depletion of stem cells or the loss of the ability of stem cells to differentiate or mature into different kinds of cells. It's important to note that this theory refers to adult stem cells, not embryonic stem cells. Unlike embryonic stem cells, adult stem cells cannot mature into any type of cell but rather only a certain number of cell types. Most cells in our bodies are differentiated, or fully mature, and stem cells are only a small number of the cells present in the body.

An example of a tissue type in which regeneration is possible by this method is the liver. This is in contrast to brain tissue which usually lacks this regenerative potential. There is now evidence that stem cells themselves may be affected in the aging process, but these theories are similar to the chicken-and-the-egg issue. It's not certain of aging occurs due to changes in stem cells, or, if instead, changes in stem cells are due to the process of aging.

Epigenetics - Epigenetics refers to the expression of genes. In other words, a gene may be present, but can either be turned on or turned off. We know that there are some genes in the body that are turned on for only a certain period of time. The field of epigenetics is also helping scientists understand how environmental factors may work within the constraints of genetics to either protect or predispose to disease.

As noted above, there is a significant amount of evidence that looks at the importance of genes in expected survival. When looking at genetic theories, these are broken down into three primary schools of thought.

There are several avenues of evidence that support a genetic theory of aging, at least in part.

Perhaps the strongest evidence in support of the genetic theory are the considerable species-specific differences in maximal survival, with some species (such as butterflies) having very short lifespans, and others, such as elephants and whales, being similar to ours. Within a single species, survival is similar, but survival can be very different between two species that are otherwise similar in size..

Twins studies also support a genetic component, as identical twins (monozygotic twins) are much more similar in terms of life expectancy than are non-identical or dizygotic twins. Evaluating identical twins who have been raised together and contrasting this with identical twins who are raised apart can help to separate out behavior factors such as diet and other lifestyle habits as a cause of family trends in longevity.

Further evidence on a broad scale has been found by looking at the effect of genetic mutations in other animals. In some worms as well as some mice, a single gene mutation may lengthen survival by over 50 percent.

In addition, we are finding evidence for some of the specific mechanisms involved in the genetic theory. Direct measurements of telomere length has shown that telomeres are vulnerable to genetic factors that can speed up the rate of aging.

One of the stronger arguments against a genetic theory of aging or a "programmed lifespan" comes from an evolutionary perspective. Why would there by a specified lifespan beyond reproduction? In other words, what "purpose" is there for life after a person has reproduced and been alive long enough to raise their progeny to adulthood?

It's also clear from what we know about lifestyle and disease that there are many other factors in aging. Identical twins may have very different lifespans depending on their exposures, their lifestyle factors (such as smoking) and physical activity patterns.

Its been estimated that genes can explain a maximum of 35 percent of lifespan, but there is still more we do not understand about aging than which we do understand. Overall, it's likely that aging is a multifactorial process, meaning that it is probably a combination of several of the theories. It's also important to note that the theories discussed here are not mutually exclusive. The concept of epigenetics, or whether or not a gene that is present is "expressed" can further muddy our understanding.

In addition to genetics, there are other determinants in aging such as our behaviors, exposures, and just plain luck. You are not doomed if your family members tend to die young, and you can't ignore your health even if your family members tend to live long.

We are taught to eat a healthy diet and be active and these lifestyle factors are likely just as important no matter how much our genetics are involved in aging. The same practices which seem to keep the organs and tissues of our body's healthy may also keep our genes and chromosomes healthy.

Regardless of the particular causes of aging, it can make a difference to:

Sources:

Jin, K. Modern Biological Theories of Aging. Aging and Disease. 2010. 1(2):72-74.

Kasper, Dennis, Anthony Fauci, Stephen Hauser, Dan Longo, and J. Jameson. Harrison's Principles of Internal Medicine. New York: McGraw-Hill Education, 2015. Print.

Kumar, Vinay, Abul K. Abbas, Jon C. Aster, and James A. Perkins. Robbins and Cotran Pathologic Basis of Disease. Philadelphia, PA: Elsevier/Saunders, 2015. Print.

Leung, C., Laraia, B., Needham, B. et al. Soda and Cell Aging: Associations Between Sugar-Sweetened Beverage Consumption and Leukocyte Telomere Length in Healthy Adults From the National Health and Nutrition Examination Surveys. American Journal of Public Health. 2014. 104(12):2425-31.

Smith, J., and R. Daniel. Stem Cells and Aging: A Chicken-Or-The-Egg Issue?. Aging and Disease. 2012. 3(3):260-267.

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The Genetic Theory of Aging - Concepts and Evidence