Aging Reversed / ABC News

Now researchers have found a way not just to stop, but, reverse the aging process. The key is something called a telomere. We all have them. They are the tips or caps of your chromosomes. They are long and stable in young adults, but, as we age they become shorter, damaged and frayed. When they stop working we start aging and experience things like hearing and memory loss.

In a recent study published in the peer reviewed journal Nature scientists took mice that were prematurely aged to the equivalent of 80-year-old humans, added an enzyme and essentially turned their telomeres back on. After the treatment they were the physiological equivalent of young adults. You can see the before and after pictures in the videos above. Brain function improved, their fertility was restored it was a remarkable reversal of the aging process. In the top video the untreated mouse shows bad skin, gray hair and it is balding. The mouse with it’s telomeres switched back on has a dark coat color, the hair is restored and the coat has a nice healthy sheen to it. Even more dramatic is the change in brain size. Before treatment the aged mice had 75% of a normal size brain like a patient with severe Alzheimers. After the telomeres were reactivated the brain returned to normal size. As for humans while it is just one factor scientists say the longer the telomeres the better the chances for a more graceful aging.

The formal study Telomere dysfunction induces metabolic and mitochondrial compromise was published in Nature.

Additional information published by Harvard can be found in the following articles.

Scientists Find Root Molecular Cause of Declining Health in the Old

Decoding Immortality – Smithsonian Channel Video about the Discovery of Telomerase

While scientists are not yet able to accomplish the same results in humans we believe we have developed a nutraceutical to help prolong youth and possibly extend life until age reversal therapy for humans becomes available.

Stem Cell Secret’s of 115 Year Old Woman

New evidence that adult stem cells are critical to human aging has recently been published on a study done on a super-centenarian woman that lived to be 115 years. At death, her circulating stem cell pool had declined to just two active stem cells from stem cell counts that are typically more than a thousand in younger adults. Super-centenarians have survived all the normal diseases that kill 99.9% of us before 100 years of age, so it has been a mystery as to what actually kills these hardy individuals. This recent data suggest that stem cell decline may be the main contributor to aging. If so, stabilizing stem cells may be the best thing one can do to slow your rate of aging.

There are many theories of aging that have been proposed. For example, damage to cells and tissues from oxidative stress has been one of the most popular fundamental theories of aging for more than half a century. Yet antioxidant substances or genes that code antioxidant enzymes have proven largely ineffective in slowing aging when tested in model animals. Thus, interest by scientists has shifted to other hypotheses that might provide a better explanation for the slow declines in function with age.

Stem cells provide one such promising mechanism of aging. Of course, we all know that babies are young and vigorous, independent of the age of their parents. This is because adults have embryonic stem cells that can generate young new cells needed to form a complete young baby. Indeed, these embryonic stem cells are the product of continuously evolving stem cell populations that go back to the beginning of life on earth over 3.5 billion years ago!

In adults, the mostly immortal embryonic stem cells give rise to mortal adult stem cells in all the tissues of the body. These adult stem cells can regenerate your cells and tissues as they wear out and need replacement. Unfortunate, adult stem cells also age, which leads to fewer cells and/or loss of function in cell replacement. As functional stem cells decline, skin and organs decline with age.

Blood from world’s oldest woman suggests life limit

Time Magazine: Long-Life Secrets From The 115-Year-Old Woman

Somatic mutations found in the healthy blood compartment of a 115-yr-old woman demonstrate oligoclonal hematopoiesis

The somatic mutation burden in healthy white blood cells (WBCs) is not well known. Based on deep whole-genome sequencing, we estimate that approximately 450 somatic mutations accumulated in the nonrepetitive genome within the healthy blood compartment of a 115-yr-old woman. The detected mutations appear to have been harmless passenger mutations: They were enriched in noncoding, AT-rich regions that are not evolutionarily conserved, and they were depleted for genomic elements where mutations might have favorable or adverse effects on cellular fitness, such as regions with actively transcribed genes. The distribution of variant allele frequencies of these mutations suggests that the majority of the peripheral white blood cells were offspring of two related hematopoietic stem cell (HSC) clones. Moreover, telomere lengths of the WBCs were significantly shorter than telomere lengths from other tissues. Together, this suggests that the finite lifespan of HSCs, rather than somatic mutation effects, may lead to hematopoietic clonal evolution at extreme ages.

Burning Fat with Strength Training

A new UNSW meta-analysis and systematic review has shown that a person can lose about 1.4% of their entire body fat just through strength training. This is similar to how much a person could lose through aerobics or cardio. Even when strength training is done solely on its own, it will still lead to favorable body fat loss without having to go running or dieting.

Until now the association between fat loss and strength training has not been clear. Previous research used a small sample size. This made it difficult to discover significant statistical results in addition to analyzing the different responses people had to an exercise program.

When looking at just one study it becomes difficult to see what the effect would be. However, when all the studies results are combined, it is easier for the researchers to get a better picture of what is going on.

The team looked at findings from 58 research papers which all utilized very accurate forms of measurement of body fat (more like body scans which differentiate lean mass from fat mass) to measure the results from programs of strength training. A total of 3,000 participants were included and none of them had any previous experience with weight training.

Each workout session averaged from 45 to 60 minutes and was performed on an average of 2.7 times each week with the program lasting about five months.

Following the training program, it was found that on average the participants lost 1.4% of their total body fat. And while the findings are encouraging for people who love strength training, the team still says the best approach for losing weight is a nutritious diet along with a routine that includes both strength training and aerobic/cardio. However, if cardio and aerobics aren’t for you, there is the option of strength training as well.

One reason people don’t think strength training lives up to cardio when it comes to fat loss is due to inexact methods of measuring body fat. Many people will focus on their total weight on a scale. But this measurement does not differentiate mass that is fat from everything else that the body is made of such as bone, muscles, and water.

Typically with aerobic training a person doesn’t gain muscle mass. We gain other functional and health benefits along with cardio respiratory fitness and fat loss. However, with strength training, a person loses fat and gains muscle mass which weighs more. Therefore, numbers on a weight scale don’t look as low as they would after aerobics training.

The researchers mainly focused on measuring the amount of a person’s body that is comprised of fat mass and how it changed after strength training. The measurement indicated loss of fat seems to be as effective as that with cardio and aerobics training despite the number on the weight scale.

With part of their study the researchers conducted a sub-analysis which compared how different methods of measuring fat could influence their findings. When more precise measurements like body scans were used, they tended towards showing lower overall body fat changes. Utilizing more precise body measurements gives a more realistic look at what changes in the body. Exercise studies in the future can be improved with the more accurate measurements.

If you have the desire to try strength training to change the way your body looks, then don’t focus on the number on the weight scale since it will not show all the results. Instead, consider whole body composition such as how your body will start to move and feel different and how your clothes fit. It is also helpful to use a scale that measures percent body fat in addition to weight.

To view the original scientific study click below:
The Effect of Resistance Training in Healthy Adults on Body Fat Percentage, Fat Mass and Visceral Fat: A Systematic Review and Meta-Analysis

Do Age or Gender Affect the Benefits of Time Restricted Eating

(TRE) or time restricted eating is a dietary system that works by restricting eating to a specific set of hours. Typically this involves eating during a period of 8 – 10 consecutive hours and then fasting for 14 – 16 hours each day. While TRE is often utilized to lose weight a recent study has shown that TRE confers a variety of additional health benefits. This study also illustrates that some of the benefits may be dependent on age or gender.

Most of the TRE studies have focused on weight loss in young male mice. The research team wanted to find out if TRE can confer added benefits on other populations. The findings indicate that while gender and age do affect outcomes of TRE, the TRE eating strategy can deliver a variety of benefits for both genders, old and young. It showed that TRE could be an important intervention to help with type 2 diabetes, fatty liver disease and possibly infectious diseases.

Intolerance to glucose is the initial step to non-alcoholic fatty liver disease. Also more than 40% of Americans are prediabetic or diabetic based on statistics from the American Diabetic Assoc. which forecasts 1.5 million new cases every year. The trend makes discovering an easy treatment option a significant priority for glucose intolerance.

The team decided to break from the conventional mice that are young males, by feeding a high sugar, high-fat diet to both female and male mice in two age groups that are age equivalent to 20 and 42 year old humans. They restricted eating to nine hours each day.

The researchers conducted tests to determine how gender and age affect the outcomes of TRE with a variety of health factors including glucose regulation, fatty liver disease, performance, endurance, muscle mass, and response to a life threatening infection known as sepsis. The team also took the step of matching the animals’ circadian clocks to conditions in the lab. Mice normally are active at night and sleep during the day. They often worked using night vision googles along with specialized lighting.

After analyzing the tissue of the mice on TRE the team discovered that no matter the gender, age, or weight loss profile, TRE very strongly protected the mice against fatty liver disease. This condition affects close to 100 million Americans and has no approved medication.

This study was the first time female mice were studied and the team wasn’t sure what they would discover. There were surprised to find that the females were not protected against weight gain however, the female mice still showed metabolic benefits including better controlled blood sugar and less fatty liver.

After sixteen hours of fasting, oral glucose tolerance tests were given to the mice and TRE was shown to be linked to less increase in blood glucose and also a quicker return to blood sugar levels that were normal both in the middle aged mice and the younger mice. Also there was a substantial improvement of glucose intolerance in both the middle aged and younger female mice. Middle aged male and female mice on TRE had the ability to bring back normal blood sugar levels much better than the controlled mice who had food available at all times. The findings indicate TRE may be a no cost or low cost and user friendly way to treat or prevent diabetes and supports the 2019 study on TRE for metabolic syndrome in people.

The team also discovered that TRE may protect both females and males from sepsis induced death which is a particular danger found in ICUs. Following administration of a toxin that would induce sepsis like conditions in mice, the team monitored 13 day survival rates and discovered that TRE did protect both female and male mice from death.

TRE also enabled the male mice to add and preserve muscle mass and improve their muscle performance. This effect did not hold up for the female mice. This discovery is especially important for the older population for whom improvement in muscle performance can assist in guarding against falls.

The researchers next want to determine if the increase in muscle mass for male mice on TRE shows improved muscle regeneration, repair and metabolism.

To view the original scientific study click below:
Sex- and age-dependent outcomes of 9-hour time-restricted feeding of a Western high-fat high-sucrose diet in C57BL/6J mice

Improve Memory Function with Mild Physical Activity

Research has shown that mild physical workouts can increase the link between parts of the brain that are responsible for storage and memory formation. Yoga or Tai Chi helps people remember things such as where they put their keys.

The study involved 36 healthy young adults. The team found that just ten minutes of mild exertion provides substantial cognitive benefits. By using high resolution functional magnetic resonance imaging, the researchers looked at the participant’s brains following exercise sessions and noted better connectivity between the cortical and hippocampal dentate gyrus areas which are associated with detailed processing of memory.

The hippocampus is crucial for creating new memories. It is one of the initial areas of the brain that deteriorates with aging. Improvement of the hippocampus function reveals great promise for enhancing memory of every day functions.

The scientists discovered that the level of the heightened connectivity foretold the degree of recall improvement.

Previous research centered around the way exercise promotes the generation of new brain cells in the regions of memory. The recent study shows a more immediate impact through strengthened transmission between the brain’s memory focused parts.

The team does not discount the possibility that new cells are being made, but that process takes longer to achieve. What they discovered is that just a ten minute exercise period showed immediate results.

Even mild physical activity such as short walking breaks throughout a day have considerable effects on cognition and memory improvement. It is encouraging to see people tracking their steps.

The team is now extending this research to testing adults who may be at a higher risk of mental impairment due to aging. This is to show if light, regular or brief exercise conducted daily for several months or weeks will have a positive affect on the brain’s function and structure.

There is great value in understanding the benefits different types of exercise in the older population so recommendations can be made to prevent cognitive decline.

To view the original scientific study click below:
Rapid stimulation of human dentate gyrus function with acute mild exercise

Benefits of Bone Marrow Stem Cells

New research from the University of Cologne has found that stem cell function reduces as we age due to changes in our epigenome. Because our bones become thinner as we age, fractures and bone diseases occur more often. One reason this may happen may be impaired function of bone-marrow stem cells, which are necessary for bone maintenance integrity.

The team wanted to know why these stem cells don’t produce as much material for developing and maintaining bones as a person ages, which can cause more fat in the bone marrow to accumulate.  To find out they compared the epigenome in bones of young and old mice.

They found that the epigenome can change naturally with aging. The genes that are significant for the production of bone are especially affected.  The epigenome had differences that were from proteins called histones.  Histones combine the DNA in cells controlling access to DNA and make certain genes active or inactive. Histone modification in stem cells reduces over time which lowers activity of bone forming genes.

The research group studied the epigenome of mesenchymal stem cells. These can be found in a person’s bone marrow and can produce cells of different types such as bone, cartilage and fat cells.  This was to find out if the change in the epigenome might be a cause of higher risk to osteoporosis or bone fractures in humans. Older aged patients with osteoporosis had presented the same epigenetic changes as they had noticed in the mice.

They wondered if the epigenome stem cells could be rejuvenated. They used a nutrient solution that contained sodium acetate to treat isolated stem cells that were from mouse bone marrow. The result was the cell converting the acetate into a sequence where the enzyme attaches to histones which can promote access to genes, thus increasing their activity. This successfully rejuvenated the epigenome which improved the activity of the stem cells and led to a higher accumulation of stem cells.

They did note that treating osteoporosis with the form of sodium acetate that is a food additive is not advisable since their observation of certain cells was very specific. But stem cell therapies for treating osteoporosis are currently being undergone. It may be possible to use sodium acetate in these cases. More research is needed to determine the outcome on the whole organism to reduce possible side effects and risks.

To view the original scientific study click below:
Chromatin remodeling due to degradation of citrate carrier impairs osteogenesis of aged mesenchymal stem cells

Harvested Stem Cells for Creating Cartilage Tissue

Research from the Univ. of Southampton has invented a novel way to use stem cells to generate tissue from human cartilage. This new technique could open up pathways for developing a much needed treatment for cartilage damage in people.

Cartilage serves as a shock buffer for the joints, however it is vulnerable to joint damage through trauma from falls or sports injuries or just daily wear and tear. The current surgical approach is to restore damaged cartilage regions utilizing cartilage cells but this has not been successful so far. This is due to the fact that survival of the cartilage tissue repair, which is caused by cartilage type cells at the damage site, has been shown to decrease just 5 to 10 years after the repair. There is a vital requirement for a new way to encourage long-term, robust repair through cartilage tissue implantation rather than to cartilage cells at the location of the damage.

Researchers believe they have discovered the answer to the dilemma. They generated tissue from cartilage in the lab through the success of transforming embryonic stem cells to cartilage cells. They then utilized these cells to generate 3-dimensional pieces of tissue from cartilage without using any natural or synthetic supporting substances. This is known as a cartilage engineering technique that is scaffold free. This new generated cartilage tissue produced is mechanically and structurally comparable to normal human cartilage and has the potential for a long lasting and stable repair that isn’t currently available to people.

The researchers for the study were the initial team to use this scaffold-free engineering technique to produce cartilage tissue which has been scaled up 1 mm with no adverse affects to its mechanical and structural properties. They hope that eventually following more research, the laboratory created tissue could routinely be used in surgery to heal damaged cartilage.

The research is exciting because the team’s ability to generate cartilage with properties similar to normal human cartilage will have the potential to provide vigorous tissue that has been engineered for repair of damaged cartilage.

The team thinks this tissue based approach of replacing like-for-like cartilage has the ability to form a step-by-step change improvement in the current cell based surgeries for the repair of damaged cartilage and improve the patient’s long term future and outcomes from the cartilage repairs.

To view the original scientific study click below:
A scaffold-free approach to cartilage tissue generation using human embryonic stem cells

Where You Live May Have An Effect on Your Longevity

There are certain locations in the US that seem to have a significant impact on longevity of seniors. Where a person lives and not just how they choose to live, can make a huge difference. This was discovered by an innovative study which examined seniors across the US and concluded that some places enhance longevity more than others.

The study showed that when a 65 year old person moves from a metro area in the 10th percentile of locations that enhance longevity to a metro area in the 90th percentile it will enhance longevity by an average of 1.1 years. That is an important boost since live expectancy for a 65 year old in the US is 83.3 years. Where an older person lives is important in relation to life expectancy and mortality in the US.

Research have observed important US regional variation in life expectancy and credited it to “health capital” which includes smoking, obesity and other behavioral factors in the regional population. By analyzing the impact of moving the recent study can quantify and isolate the effect the location has on its residents.

The research delivers valuable new information about large scale drivers of health outcomes in different locations. One clear possibility is available medical care. Other possibilities include pollution, climate, traffic safety, crime and a variety of other factors. The goal was to separate out what the role of senior’s previous behaviors and experiences were, or health capital, from the role of environment or place.

The study analyzed Medicare records from 1999 to 2014 with the focus on US residents between the ages 65 and 99. The team studied 6.3 million Medicare beneficiaries. Almost 2 million of them moved from one US commuting zone to another, and the rest were samples from a random 10% of seniors who had moved over the 15 year study.

The central elements of this study involved seeing how different seniors who were originally from identical locations did when they moved to different destinations. The plan was to take different people from a given area and compare some moving to a low mortality location and others to a high mortality location. The seniors health conditions and Medicare records include detailed claims data so the team applied records of 27 different conditions and illnesses ranging from diabetes to cancer to depression.

The study discovered that many urban areas on the West and East Coasts have positive effects on the longevity of seniors who moved there. Some Midwestern metro areas also scored well. In contrast, a belt of the deep South showed negative effects on longevity for seniors. This included much of Arkansas, Alabama, Louisiana, and northern Florida. Much of the Southwest fared similarly poor.

The researchers estimate that health capital will account for almost 70% of the difference in longevity in areas across the US and that location effects account for almost 15% of the variation. Health capital is important, but location also matters.

The life expectancy of an area’s population is not the same thing as that area’s longevity effect. In areas where smoking is high, population wide longevity of survival could be subpar. But there are other factors that could make it a location where people of average health live longer. The question becomes why?

The hard evidence is in regards to the location. The next step in the research is to think about specific factors that are at work. They know something about specific locations, but don’t know what. They are now working on two studies about practices in health care to see what can be observed that would impact these location-based differences might have. One of the studies will focus on doctors and the other will look at the opioid epidemic.

To view the original scientific study click below:
Place-Based Drivers of Mortality: Evidence from Migration

Weight Loss, Obesity and Calorie Intake

Standard scientific opinion has blamed weight gain on an excess of calories which is due to burning fewer than taken in. In opposition to this viewpoint, the carbohydrate-insulin model shows that the quality of diet matters more than calorie intake for weight loss. The model’s position is that eating processed carbohydrates and starchy foods leads to changes in hormone and insulin levels which results in an increase in fat deposition.

The increase in fat storage leads to hunger and the consumption of more foods rich in calories which then leads to obesity. This model has suggested that staying away from starchy and sugar rich foods might be necessary for losing weight instead of calorie restriction.

The WHO says that the worldwide prevalence of obesity and overweight has increased during the past 10 decades. There is an important consensus in the scientific community that the easy availability of these detrimental foods and also a sedentary lifestyles have contributed to the increase in obesity rates. However, there is a lot of disagreement as to how these environmental factors contribute to the problem.

According to the predominant EBM (energy balance model) eating more calories than those that are burned will result in weight gain due to a positive energy balance. The EBM has suggested that successful weight loss will require the reduction of total calorie consumption which means fewer calories and an increase in physical activity.

The CIM (carbohydrate insulin model) postulates that the quality of food eaten plays an important and critical role in management of body weight rather than the total caloric intake.

The EMB regards all calories in the exact way regardless of the their source. The problem is that the consumption of starchy and processed carbohydrates causes an increase in blood glucose which results in fat storage. As a result increased fat accumulation starts a feedback loop which results in increased hunger and the consumption of more foods rich in calories.

According to CIM it is the increased fat storage due to the consumption of processed carbohydrates and not the increased consumption of calories that actually leads to weight gain and is mostly responsible for elevated rates of obesity. Hormonal and metabolic changes which will occur due to eating specific foods are the main cause of weight gain with the excess calories being the outcome.

Reducing caloric intake tends to cause weight loss only in the short term. The is because the body adapts to the lower intake of calories which results in increased hunger and a lower metabolic rate.

The CIM postulates that food quality plays a more important role in the weight gain than the overall intake of calories. The intake of of carbohydrates has increased since the 1980’s and is likely because of the perception that eating fat causes weight gain.

The GI (glycemic index) rates carbohydrates due to how rapidly they increase blood glucose levels after consumption. The glycemic load is also a measure that can provide more comprehensive information about the surge in blood sugar levels.

The consumption of starchy and highly processed foods that have rapidly digestible carbs result in a blood glucose level surge. Foods with a high glycemic load such as potato products, refined grains and other foods high in starch are turned rapidly into free sugars.

As a contrast, proteins and fats have a minor impact on blood sugar level. Minimally processed grains, nuts, legumes, whole fruits and non-starchy vegetables typically have a moderate or low glycemic load.

A rapid surge of the glucose level after eating high glycemic foods will result in insulin secretion which regulates blood sugar and helps the liver, muscles, and fat tissue absorb glucose. At the same time, eating carbs that are rapidly digestible suppresses the level of glucagon, a hormone. The pancreas will secrete glucagon to counteract low  blood sugar which occur between meals. The secretion of glucagon which is stored in the liver raises blood glucose levels.

In the course of the first 3 hours following the consumption of high glycemic foods, low glucagon and high insulin lead to glucose and fat storage. As a result, the body absorbs nutrients that are present in high glycemic foods in the first 3 to 4 hours and the low glucagon and insulin levels persist.

The hormonal state then slows down the breakdown of energy stored in the liver and adipose tissue which is required to fuel other critical body tissues. That causes low levels of fatty acids, glucose, and a variety of metabolites in the blood which resembles a fast-like state.

This drop in blood metabolites signal the brain that tissues are being deprived of energy. When the brain distinguishes the fast-like state, it evokes hormonal changes that lead to craving and hunger for foods that are high energy such as the foods that are high on the GI.

In animals it has been shown that all calories are not alike and that weight gain and obesity can also develop without an increase food intake. There is not yet proof of this in humans.

The CIM theory of weight gain has created a sizable amount of controversy which includes how carbs and insulin affect weight gain. There is a lot of individual variability in the changes and physiology that occur in individuals as they develop obesity. There could be some role for insulin, but there could be a lot of other factors. This makes it more challenging to identify the causes and then the potential treatments to help to prevent weight gain and obesity.

The implications of counting calories then subtracting those that may have been burned with physical activity, has challenges in terms of accuracy. This can be easily gamed so that a person thinks they are doing the right thing, but in fact they are not really accurately assessing the two components which can lead to poor results.

It is suggested that adhering to a diet that consists of low GI foods can lead to weight loss through increasing energy levels and reducing hunger. An important strategy is to replace high glycemic foods with high fat foods and allowing for a moderate consumption of whole fruits, legumes, nuts, whole grains and non-starchy vegetables.

To view the original scientific study click below:
The carbohydrate-insulin model: a physiological perspective on the obesity pandemic

Stem Cell Research to Treat Muscle Related Conditions

Researchers who have previously discovered a method that turns skin cells into primitive like muscle cells that can be left in a lab indefinitely without losing their potential to turn into mature muscle, have now discovered how this method works and also what molecular changes it prompts within cells.

MyoD gene expression that was added and exposed to 3 chemicals may cause skin cells to turn into primitive progenitors and maintained in a lab indefinitely. Later they can be coaxed into turning into mature muscle cells that can be used to treat muscle related diseases. Skin derived muscle progenitors are molecularly the same as muscle tissue stem cells. Muscle cells which are obtained by these progenitors tend to be more mature and stable than muscle cells that have been converted directly from skin cells.

The study by researchers at Massachusetts General Hosp. (MGH) could let clinicians generate muscle cells matched to patients to help treat a variety of muscle diseases and injuries such as muscle degeneration due to aging, muscular dystrophy and injuries to the muscles.

It is already known that the MyoD gene expresses muscle regulatory and can directly change skin cells into mature muscle cells. However, muscle cells that are mature do not self-renew and divide and cannot be propagated for purposes clinically. To tackle this shortcoming, the team developed a system a few years ago to to convert skin cells into self-renewing muscle stem like cells they coined induced iMPCs (induced myogenic progenitor cells). Their system utilizes MyoD combined with 3 chemicals they had previously identified as promoters of cell plasticity in other situations.

With the latest research the team uncovered the details as to how this combination converted skin cells into iMPCs. They discovered that while MyoD expression alone allows skin cells to become mature muscle cells, by adding the three chemicals caused the skin cells to acquire a more primitive stem cell like state. IMPCs are molecularly highly like muscle tissue stem cells and muscle stem cells from iMPCs are more mature and stable than muscle cells that have been produced with MyoD expression alone. Mechanically, they showed that MyoD and the three chemicals aid in removal of certain marks on DNA called DNA methylation. DNA methylation will typically maintain the identification of specialized cells and the team shows that its removal was key for acquiring an identity of a muscle stem cell.

The team’s findings may be applicable to a variety of other tissue types besides the muscles that have different regulatory genes. Through combining the expression of these genes with the three chemicals that were utilized in this particular study could help future research bring about different types of stem cells that closely bare resemblance to a variety of body tissues.

To view the original scientific study click below:
Dissecting dual roles of MyoD during lineage conversion to mature myocytes and myogenic stem cells