Ten years ago there was a lot of controversy about the use of human embryonic stem cells in scientific research. The problem was solved with the creation of IPS Cells (induced pluripotent stem cells) which are made by turning adult skin or other cells back into embryonic like stem cells. The process has been time consuming and manual so robotic equipment has now been produced to make it much faster and more efficient.

The New York Stem Cell Foundation designed and has built a revolutionary, high-throughput robotic platform that automates and standardizes the process of transforming patient samples into stem cells. This one-of-a-kind system addresses challenges that face the entire field, and is now an essential resource that NYSCF provides in collaborations with leading academic and industry partners around the world.

In the paper published in Nature Methods, NYSCF scientists demonstrated how the NYSCF Global Stem Cell Array?, for the first time ever, gives researchers the scale to look at diverse populations and draw meaningful conclusions. This breakthrough technology will allow researchers to better understand the underlying causes of disease and, ultimately, create individually tailored treatments for patients.

Induced pluripotent stem cells (iPSCs) are an essential tool for modeling how causal genetic variants impact cellular function in disease, as well as an emerging source of tissue for regenerative medicine. The preparation of somatic cells, their reprogramming and the subsequent verification of iPSC pluripotency are laborious, manual processes limiting the scale and reproducibility of this technology. This process can not be automated using a modular, robotic platform for iPSC reprogramming, high-throughput conversion of skin biopsies into iPSCs and differentiated cells with minimal manual intervention. Automated reprogramming and the pooled selection of polyclonal pluripotent cells results in high-quality, stable iPSCs. These lines display less line-to-line variation than either manually produced lines or lines produced through automation followed by single-colony subcloning. The robotic platform will enable the application of iPSCs to population-scale biomedical problems including the study of complex genetic diseases and the development of personalized medicines.

Each new paradigm goes through three stages. The first is outright rejection, the second is discussion and the third is when it is accepted as self evident. For development of significant life extension technologies we are now in the second stage. Even five years ago the scientific consensus was that aging research was interesting but unlikely to lead to anything practical. Now Google is funding it’s Calico life extension startup with hundreds of millions of dollars and a number of other billonaires and Silicon Valley startups are also seriously funding or working on anti-aging research.

At Life Code we have taken the approach of using the scientific knowledge that is already available to develop nutraceutical supplements to help extend both the quality and quantity of life now. Combining these with a healthy diet and exercise program will yield even better results. We want to enjoy life as we get older and not end up shuffling around a nursing home with a walker. We also want to be alive when even more effective anti-aging therapies become available whether from our parent biotechnology companies or from others.

An excellent article with the title Live for ever: Scientists say they?ll soon extend life ?well beyond 120? appeared in the Guardian earlier this year. It gives an overview of some of the high profile people involved with life extension research.

When does aging really begin? Two Northwestern University scientists now have a molecular clue. In a study of the transparent roundworm C. elegans, they found that adult cells abruptly begin their downhill slide when an animal reaches reproductive maturity.

A genetic switch starts the aging process by turning off cell stress responses that protect the cell by keeping important proteins folded and functional. The switch is thrown by germline stem cells in early adulthood, after the animal starts to reproduce, ensuring its line will live on.

While the studies were conducted in worms, the findings have implications for humans, the researchers report. The genetic switch and other components identified by the scientists as playing a role in aging are conserved in all animals, including humans, offering targets for future study. (C. elegans has a biochemical environment similar to that of humans and is a popular research tool for the study of the biology of aging and as a model of human disease.)

Knowing more about how the quality control system works in cells could help researchers one day figure out how to provide humans with a better cellular quality of life and therefore delay degenerative diseases related to aging, such as neurodegenerative diseases.

“Wouldn’t it be better for society if people could be healthy and productive for a longer period during their lifetime?” said Richard I. Morimoto, the senior author of the study. “I am very interested in keeping the quality control systems optimal as long as we can, and now we have a target. Our findings suggest there should be a way to turn this genetic switch back on and protect our aging cells by increasing their ability to resist stress.”

Morimoto is the Bill and Gayle Cook Professor of Molecular Biosciences and director of the Rice Institute for Biomedical Research in Northwestern’s Weinberg College of Arts and Sciences.

The study, built on a decade of research, will be published in the July 23 issue of the journal Molecular Cell. Johnathan Labbadia, a postdoctoral fellow in Morimoto’s lab, is the first author of the paper.

In C. elegans, the decline begins eight hours into adulthood — all the switches get thrown to shut off an animal’s cell stress protective mechanisms. Morimoto and Labbadia found it is the germline stem cells responsible for making eggs and sperm that control the switch.

In animals, including C. elegans and humans, the heat shock response is essential for proper protein folding and cellular health. Aging is associated with a decline in quality control, so Morimoto and Labbadia looked specifically at the heat shock response in the life of C. elegans.

“We saw a dramatic collapse of the protective heat shock response beginning in early adulthood,” Morimoto said.

Morimoto and Labbadia found the genetic switch occurs between two major tissues in an organism that determine the future of the species: the germline and the soma (the body tissues of the animal, such as muscle cells and neurons). Once the germline has completed its job and produced eggs and sperm — necessary for the next generation of animals — it sends a signal to cell tissues to turn off protective mechanisms, starting the decline of the adult animal.

“C. elegans has told us that aging is not a continuum of various events, which a lot of people thought it was,” Morimoto said.

“In a system where we can actually do the experiments, we discover a switch that is very precise for aging,” he said. “All these stress pathways that insure robustness of tissue function are essential for life, so it was unexpected that a genetic switch is literally thrown eight hours into adulthood, leading to the simultaneous repression of the heat shock response and other cell stress responses.”

Using a combination of genetic and biochemical approaches, Morimoto and Labbadia found the protective heat shock response declines steeply over a four-hour period in early adulthood, precisely at the onset of reproductive maturity. The animals still appear normal in behavior, but the scientists can see molecular changes and the decline of protein quality control.

In one experiment, the researchers blocked the germline from sending the signal to turn off cellular quality control. They found the somatic tissues remained robust and stress resistant in the adult animals.

“This was fascinating to see,” Morimoto said. “We had, in a sense, a super stress-resistant animal that is robust against all kinds of cellular stress and protein damage. This genetic switch gives us a target for future research.”

Reference: Johnathan Labbadia, Richard I. Morimoto. Repression of the Heat Shock Response Is a Programmed Event at the Onset of Reproduction. Molecular Cell, 2015; DOI: 10.1016/j.molcel.2015.06.027

Summary: Prebiotics are digestion-resistant compounds that feed the “good bacteria” in the GI tract. The agave plant contains inulin, a polysaccharide for which some previous studies suggest a physiologic effect. Kelly Swanson, from the University of Illinois (Illinois, USA), and colleagues enrolled 29 healthy adults in a 3-period crossover double-blind study in which subjects were randomized to 1of 3 groups: 0, 5.0, or 7.5 grams per day of agave inulin; each period was followed by a 7-day washout before crossover. Fecal samples were collected and fermented, then analyzed to determine gut bacteria populations. Data analysis revealed that Bifidobacterium levels increased 4-fold after 5.0 and 7.5 grams per day agave inulin; as well, Desultivibrio levels decreased 40%. Agave inulin consumption also associated with reduced fecal pH and increased butyrate ? suggesting increased saccharolytic fermentation and reduced proteolytic fermentation. The study authors observe that: “Agave inulin supplementation shifted the gastrointestinal microbiota composition and activity in healthy adults.”

Background: Prebiotics resist digestion, providing fermentable substrates for select gastrointestinal bacteria associated with health and well-being. Agave inulin differs from other inulin type fibers in chemical structure and botanical origin. Preclinical animal research suggests these differences affect bacterial utilization and physiologic outcomes. Thus, research is needed to determine whether these effects translate to healthy adults.

Objective: We aimed to evaluate agave inulin utilization by the gastrointestinal microbiota by measuring fecal fermentative end products and bacterial taxa.

Methods: A randomized, double-blind, placebo-controlled, 3-period, crossover trial was undertaken in healthy adults (n = 29). Participants consumed 0, 5.0, or 7.5 g agave inulin/d for 21 d with 7-d washouts between periods. Participants recorded daily dietary intake; fecal samples were collected during days 16?20 of each period and were subjected to fermentative end product analysis and 16S Illumina sequencing.

Results: Fecal Actinobacteria and Bifidobacterium were enriched (P < 0.001) 3- and 4-fold after 5.0 and 7.5 g agave inulin/d, respectively, compared with control. Desulfovibrio were depleted 40% with agave inulin compared with control. Agave inulin tended (P < 0.07) to reduce fecal 4-methyphenol and pH. Bivariate correlations revealed a positive association between intakes of agave inulin (g/kcal) and Bifidobacterium (r = 0.41, P < 0.001). Total dietary fiber intake (total fiber plus 0, 5.0, or 7.5 g agave inulin/d) per kilocalorie was positively associated with fecal butyrate (r = 0.30, P = 0.005), tended to be positively associated with Bifidobacterium (r = 0.19, P = 0.08), and was negatively correlated with Desulfovibrio abundance (r = ?0.31, P = 0.004). Conclusions: Agave inulin supplementation shifted the gastrointestinal microbiota composition and activity in healthy adults. Further investigation is warranted to determine whether the observed changes translate into health benefits in human populations.

Summary: If you want to live longer and stay healthy your chances are better if you substantially reduce or eliminate sugar-sweetened beverages from your diet.

Consumption of sugary drinks may lead to an estimated 184,000 adult deaths each year worldwide, according to research published today in the journal Circulation and previously presented as an abstract at the American Heart Association Council on Epidemiology and Prevention in 2013.

“Many countries in the world have a significant number of deaths occurring from a single dietary factor, sugar-sweetened beverages. It should be a global priority to substantially reduce or eliminate sugar-sweetened beverages from the diet,” said Dariush Mozaffarian, M.D., Dr.P.H., senior author of the study and dean of the Friedman School of Nutrition Science & Policy at Tufts University in Boston.

In the first detailed global report on the impact of sugar-sweetened beverages, researchers estimated deaths and disabilities from diabetes, heart disease, and cancers in 2010. In this analysis, sugar sweetened beverages were defined as any sugar-sweetened sodas, fruit drinks, sports/energy drinks, sweetened iced teas, or homemade sugary drinks such as frescas, that contained at least 50 kcal per 8oz serving. 100 percent fruit juice was excluded.

Estimates of consumption were made from 62 dietary surveys including 611,971 individuals conducted between 1980 and 2010 across 51 countries, along with data on national availability of sugar in 187 countries and other information. This allowed capture of geographical, gender and age variation in consumption levels of sugar-sweetened beverages in different populations. Based on meta-analyses of other published evidence on health harms of sugar-sweetened beverages, the investigators calculated the direct impact on diabetes and the obesity-related effects on cardiovascular disease, diabetes and cancer.

In 2010, the researchers estimate that sugar-sweetened beverages consumption may have been responsible for approximately:

? 133,000 deaths from diabetes

? 45,000 deaths from cardiovascular disease

? 6,450 deaths from cancer

“Some population dietary changes, such as increasing fruits and vegetables, can be challenging due to agriculture, costs, storage, and other complexities. This is not complicated. There are no health benefits from sugar-sweetened beverages, and the potential impact of reducing consumption is saving tens of thousands of deaths each year,” Mozaffarian said.

The impact of sugar-sweetened beverages varied greatly between populations. At the extremes, the estimated percentage of deaths was less than 1 percent in Japanese over 65 years old, but 30 percent in Mexican adults younger than 45. Of the 20 most populous countries, Mexico had the highest death rate attributable to sugar-sweetened beverages with an estimated 405 deaths per million adults (24,000 total deaths) and the U.S. ranked second with an estimated 125 deaths per million adults (25,000 total deaths).

About 76 percent of the estimated sugar-sweetened beverage-related deaths occurred in low- or middle-income countries.

In nations of the Caribbean and Latin America, such as Mexico, homemade sugary drinks (e.g. frescas) are popular and consumed in addition to commercially prepared sugar-sweetened beverages. “Among the 20 countries with the highest estimated sugar-sweetened beverage-related deaths, at least 8 were in Latin America and the Caribbean, reflecting the high intakes in that region of the world,” said Gitanjali Singh, Ph.D., lead author of the study and a research assistant professor at the Friedman School.

Overall, in younger adults, the percent of chronic disease attributed to sugar-sweetened beverages was higher than the percent in older adults. “The health impact of sugar-sweetened beverage intake on the young is important because younger adults form a large sector of the workforce in many countries, so the economic impact of sugar-sweetened beverage-related deaths and disability in this age group can be significant. It also raises concerns about the future. If these young people continue to consume high levels as they age, the effects of high consumption will be compounded by the effects of aging, leading to even higher death and disability rates from heart disease and diabetes than we are seeing now,” Singh said.

CORVALLIS, Ore. – A study at Oregon State University indicates that both a high-fat and a high-sugar diet, compared to a normal diet, cause changes in gut bacteria that appear related to a significant loss of “cognitive flexibility,” or the power to adapt and adjust to changing situations.

This effect was most serious on the high-sugar diet, which also showed an impairment of early learning for both long-term and short-term memory.

The findings are consistent with some other studies about the impact of fat and sugar on cognitive function and behavior, and suggest that some of these problems may be linked to alteration of the microbiome – a complex mixture in the digestive system of about 100 trillion microorganisms.

The research was done with laboratory mice that consumed different diets and then faced a variety of tests, such as water maze testing, to monitor changes in their mental and physical function, and associated impacts on various types of bacteria. The findings were published in the journal Neuroscience, in work supported by the Microbiology Foundation and the National Science Foundation.

“It’s increasingly clear that our gut bacteria, or microbiota, can communicate with the human brain,” said Kathy Magnusson, a professor in the OSU College of Veterinary Medicine and principal investigator with the Linus Pauling Institute.

“Bacteria can release compounds that act as neurotransmitters, stimulate sensory nerves or the immune system, and affect a wide range of biological functions,” she said. “We’re not sure just what messages are being sent, but we are tracking down the pathways and the effects.”

Mice have proven to be a particularly good model for studies relevant to humans, Magnusson said, on such topics as aging, spatial memory, obesity and other issues.

In this research, after just four weeks on a high-fat or a high-sugar diet, the performance of mice on various tests of mental and physical function began to drop, compared to animals on a normal diet. One of the most pronounced changes was in what researchers call cognitive flexibility.

“The impairment of cognitive flexibility in this study was pretty strong,” Magnusson said. “Think about driving home on a route that’s very familiar to you, something you’re used to doing. Then one day that road is closed and you suddenly have to find a new way home.”

A person with high levels of cognitive flexibility would immediately adapt to the change, determine the next best route home, and remember to use the same route the following morning, all with little problem. With impaired flexibility, it might be a long, slow, and stressful way home.

This study was done with young animals, Magnusson said, which ordinarily would have a healthier biological system that’s better able to resist pathological influences from their microbiota. The findings might be even more pronounced with older animals or humans with compromised intestinal systems, she said.

What’s often referred to as the “Western diet,” or foods that are high in fat, sugars and simple carbohydrates, has been linked to a range of chronic illnesses in the United States, including the obesity epidemic and an increased incidence of Alzheimer’s disease.

“We’ve known for a while that too much fat and sugar are not good for you,” Magnusson said. “This work suggests that fat and sugar are altering your healthy bacterial systems, and that’s one of the reasons those foods aren’t good for you. It’s not just the food that could be influencing your brain, but an interaction between the food and microbial changes.”

There currently are 53 supercentenarians ? people age 110 years and over, alive today; and 51 of them are female. Ben Dulken, from Stanford University (California, USA), and colleagues explored the potential underlying reasons why no other demographic factor comes remotely close to gender in predicting the likelihood of achieving such an advanced age. With consideration for current knowledge about stem cell behavior and gender, the researchers submit that there are key differences in regenerative decline between men and women: particularly involving the sex hormones estrogen and testosterone in modifying lifespan. Previous studies report that estrogen has direct effects on stem cell populations in female mice, from increasing the number of blood stem cells to enhancing the regenerative capacity of brain stem cells. Further, other recent studies suggest that estrogen supplementation may increase the lifespan of male mice. Observing that: ?Longevity differs between sexes, with females being longer-lived in most mammals, including humans. One hallmark of aging is the functional decline of stem cells,? the authors consider that: ?a key question is whether the aging of stem cells differs between males and females and whether this has consequences for disease and lifespan.?

It’s known that estrogen has direct effects on stem cell populations in female mice, from increasing the number of blood stem cells (which is very helpful during pregnancy) to enhancing the regenerative capacity of brain stem cells at the height of estrus. Whether these changes have a direct impact on lifespan is what’s yet to be explored. Recent studies have already found that estrogen supplements increase the lifespan of male mice, and that human eunuchs live about 14 years longer than non-castrated males.

More work is also needed to understand how genetics impacts stem cell aging between the sexes. Scientists have seen that knocking out different genes in mice can add longevity benefits to one gender but not the other, and that males in twin studies have shorter telomeres–a sign of shorter cellular lifespan–compared to females.

“It is likely that gender plays a role in defining both lifespan and healthspan, and the effects of gender may not be identical for these two variables,” the authors write. “As the search continues for ways to ameliorate the aging process and maintain the regenerative capacity of stem cells, let us not forget one of the most effective aging modifiers is gender.”

A study confirms a link between peanut and nut intake and lower mortality rates, but finds no protective effect for peanut butter. Men and women who eat at least 10 grams of nuts or peanuts per day have a lower risk of dying from several major causes of death than people who don’t consume nuts or peanuts.

A paper published in the International Journal of Epidemiology confirms a link between peanut and nut intake and lower mortality rates, but finds no protective effect for peanut butter. Men and women who eat at least 10 grams of nuts or peanuts per day have a lower risk of dying from several major causes of death than people who don’t consume nuts or peanuts.

The reduction in mortality was strongest for respiratory disease, neurodegenerative disease, and diabetes, followed by cancer and cardiovascular diseases. The effects are equal in men and women. Peanuts show at least as strong reductions in mortality as tree nuts, but peanut butter is not associated with lower mortality, researchers from Maastricht University found.

This study was carried out within the Netherlands Cohort Study, which has been running since 1986 among over 120,000 Dutch 55-69 year old men and women. Nut consumption was assessed by asking about portion size and frequency of intake of peanuts, other nuts (tree nuts), and peanut butter. The researchers from Maastricht University analyzed the relationship with overall and cause-specific mortality since 1986.

The associations between nuts and peanut intake and cardiovascular death confirm earlier results from American and Asian studies that were often focused on cardiovascular diseases. However, in this new study, it was found that mortality due to cancer, diabetes, respiratory, and neurodegenerative diseases was also lowered among users of peanuts and nuts. Project leader and epidemiologist Professor Piet van den Brandt commented: “It was remarkable that substantially lower mortality was already observed at consumption levels of 15 grams of nuts or peanuts on average per day (half a handful). A higher intake was not associated with further reduction in mortality risk. This was also supported by a meta-analysis of previously published studies together with the Netherlands Cohort Study, in which cancer and respiratory mortality showed this same dose-response pattern.”

Peanuts and tree nuts both contain various compounds such as monounsaturated and polyunsaturated fatty acids, various vitamins, fiber, antioxidants, and other bioactive compounds, that possibly contribute to the lower death rates. In contrast to peanuts, no association was found between peanut butter intake and mortality risk. However, besides peanuts, peanut butter contains also added components like salt and vegetable oils. In the past, it has been shown that peanut butter contains trans fatty acids and therefore the composition of peanut butter is different from peanuts. The adverse health effects of salt and trans fatty acids could inhibit the protective effects of peanuts.

Cutting calories through dietary restriction has been shown to lower cholesterol, improve insulin sensitivity, and even prolong life in mammals. Now, new research publishing on May 28th in Cell Reports shows that, at least in mice, low protein, high carbohydrate diets can provide benefits similar to those obtained with calorie restriction.

“We’ve shown that when compared head-to-head, mice got the same benefits from a low protein, high carbohydrate diet as a 40% caloric restriction diet,” says senior author Stephen Simpson, Academic Director of the University of Sydney’s Charles Perkins Centre. “Except for the fanatical few, no one can maintain a 40% caloric reduction in the long term, and doing so can risk loss of bone mass, libido, and fertility.”

The investigators compared three 8-week diets varying in protein-to-carbohydrate ratio under conditions where food was restricted or food was available at all times. Of the three, low protein, high carbohydrate (LPHC) diets offered when food was always available delivered similar benefits as calorie restriction in terms of insulin, blood sugar, and cholesterol levels, despite increased food intake.

Even though the mice on LPHC diets ate more when food was always available, their metabolism was higher than that of mice on the calorie-restricted diet, and they did not gain more weight. Calorie restriction did not provide any additional benefits for LPHC mice.

Additional research is needed to determine how LPHC diets affect long-term metabolic health and survival, as well as to what extent the type and quality of proteins and carbohydrates matter. “An important next step will be to determine exactly how specific amino acids, the building blocks of proteins, contribute to overall health span and lifespan,” says lead author Samantha Solon-Biet, also of the Charles Perkins Centre.

If the study’s results apply to humans, adjusting protein and carbohydrate intake could lead to healthier aging in a more realistic manner than drastically cutting calories. “It still holds true that reducing food intake and body weight improves metabolic health and reduces the risk of diseases like type 2 diabetes, obesity, and fatty liver disease,” says Simpson. “However, according to these mouse data and emerging human research, it appears that including modest intakes of high-quality protein and plenty of healthy carbohydrates in the diet will be beneficial for health as we age.”

Scientists at McMaster University have discovered how to make adult sensory neurons from human patients simply by having them roll up their sleeve and providing a blood sample.

Specifically, stem cell scientists at McMaster can now directly convert adult human blood cells to both central nervous system (brain and spinal cord) neurons as well as neurons in the peripheral nervous system (rest of the body) that are responsible for pain, temperature and itch perception. This means that how a person’s nervous system cells react and respond to stimuli, can be determined from his blood.

The breakthrough, published online today and featured on the cover of the journal Cell Reports, was led by Mick Bhatia, director of the McMaster Stem Cell and Cancer Research Institute. He holds the Canada Research Chair in Human Stem Cell Biology and is a professor in the Department of Biochemistry and Biomedical Sciences of the Michael G. DeGroote School of Medicine. Also playing a key role was Karun Singh, a co-author in the study and holder of the David Braley Chair in Human Stem Cell Research.

Currently, scientists and physicians have a limited understanding of the complex issue of pain and how to treat it. The peripheral nervous system is made up of different types of nerves — some are mechanical (feel pressure) and others detect temperature (heat). In extreme conditions, pain or numbness is perceived by the brain using signals sent by these peripheral nerves.

“The problem is that unlike blood, a skin sample or even a tissue biopsy, you can’t take a piece of a patient’s neural system. It runs like complex wiring throughout the body and portions cannot be sampled for study,” said Bhatia.

“Now we can take easy to obtain blood samples, and make the main cell types of neurological systems — the central nervous system and the peripheral nervous system — in a dish that is specialized for each patient,” said Bhatia. “Nobody has ever done this with adult blood. Ever.

“We can actually take a patient’s blood sample, as routinely performed in a doctor’s office, and with it we can produce one million sensory neurons, that make up the peripheral nerves in short order with this new approach. We can also make central nervous system cells, as the blood to neural conversion technology we developed creates neural stem cells during the process of conversion.”

His team’s revolutionary, patented direct conversion technology has “broad and immediate applications,” said Bhatia, adding that it allows researchers to start asking questions about understanding disease and improving treatments such as: Why is it that certain people feel pain versus numbness? Is this something genetic? Can the neuropathy that diabetic patients experience be mimicked in a dish?

It also paves the way for the discovery of new pain drugs that don’t just numb the perception of pain. Bhatia said non-specific opioids used for decades are still being used today.

“If I was a patient and I was feeling pain or experiencing neuropathy, the prized pain drug for me would target the peripheral nervous system neurons, but do nothing to the central nervous system, thus avoiding non-addictive drug side effects,” said Bhatia.

“You don’t want to feel sleepy or unaware, you just want your pain to go away. But, up until now, no one’s had the ability and required technology to actually test different drugs to find something that targets the peripheral nervous system and not the central nervous system in a patient specific, or personalized manner.”

Bhatia’s team successfully tested their process using fresh blood, but also cryopreserved (frozen) blood. Since blood samples are taken and frozen with many clinical trials, this allows them “almost a bit of a time machine” to go back and explore questions around pain or neuropathy to run tests on neurons created from blood samples of patients taken in past clinical trials where responses and outcomes have already been recorded.”

In the future, the process may have prognostic potential, explained Bhatia, in that one might be able to look at a patient with Type 2 Diabetes and predict whether they will experience neuropathy by running tests in the lab using their own neural cells derived from their blood sample.

“This bench to bedside research is very exciting and will have a major impact on the management of neurological diseases, particularly neuropathic pain,” said Akbar Panju, medical director of the Michael G. DeGroote Institute for Pain Research and Care, a clinician and professor of medicine.

“This research will help us understand the response of cells to different drugs and different stimulation responses, and allow us to provide individualized or personalized medical therapy for patients suffering with neuropathic pain.”