New Discovery for Reprogramming Lost Hearing Cells in the Inner Ear

Loss of hearing due to noise, certain cancer drugs and aging cannot be reversed due to researchers not being able to reprogram cells to evolve into the inner and outer ear sensory cells. This is fundamental for hearing after they have died. However, researchers have now found a particular master gene to program ear hair cells into an inner or outer cell. This overcomes a significant hurdle that has prevented these cells from developing and hearing to be restored.

The findings are the first time that it has been shown that a cell can switch to one type or the other type. It will supply a formerly unavailable tool that will make an outer and inner hair cell.

Approximately 8.5% of adults in the U.S. between the ages of 55-64 have disabling loss of hearing. In adults aged 65-74 it increases to almost 25% and 50% in adults who are older than 75.

Right now scientists can create an artificial hair cell. However, it is not able to tell the difference between an outer or inner cell which provides crucial functions in producing hearing. The findings are a major advancement to development of those specific cells.

When hair cells that are made by the cochlea die, hearing loss and deafness occur. The cell develops in the embryo but does not reproduce. Outer hair cells contract and expand responding to pressure of sound waves and turn up sound to the inner hair cells. They carry the vibrations to the neurons to make the sound that we hear.

The scientists found the master gene switch known as TBX2 which programs the ear cells. An inner cell is created when this gene is expressed. If the gene becomes blocked, it then becomes an outer hair cell. The capability to create one of these cells requires a gene mix. The GF1 and the ATOH1 genes are required to create a cochlear hair cell from a non-hair cell. TBX2 is then able to be turned off or on to create the needed outer or inner cell.

The aim is to reprogram the supporting cells that are laced among the hair cells to provide them with basic support into outer and inner hair cells.

The team can now work on how to make a specific inner cell and outer cell and why the outer cells are more susceptible to die and cause deafness. The scientists stress that the research is experimental.

To view the original scientific study click below:
Tbx2 is a master regulator of inner versus outer hair cell differentiation

As You Age Seven Hours of Sleep Is Optimal

A new study has shown that seven hours of sleep a night is optimal for those in their mid to older ages. And, too much or too little sleep is linked with poorer mental health and cognitive performance.

Sleep is important in maintaining great psychological health and cognitive performance. It additionally helps in keeping the brain healthy through removing products that are waste. As we age we often see changes in our patterns of sleep which includes trouble staying asleep and falling asleep and also decreased quality and quantity of sleep. It is thought that these disturbances of sleep might add to psychiatric disorders and cognitive decline in the older population.

In the study the scientists looked at data from almost 500,000 adults who were aged 38 to 73 years. Participants were questioned about their sleeping habits, well being and mental health and also participated in a group of cognitive tests. Genetic data and brain imaging were available for nearly 40,000 of the participants.

Through analyzing the data, the researchers discovered that both excessive and insufficient duration of sleep were linked with impaired performance of cognitive skills such as visual attention, processing speed, skills for problem solving and memory. Seven hours of sleep each night was the optimal quantity of sleep for performance of cognitive skills and also good for mental health. Participants experienced more symptoms of worse overall well being, depression and anxiety if they revealed sleeping for shorter and longer durations.

The team says one potential reason for the link between cognitive decline and insufficient sleep might be due to the disruption of deep sleep or slow wave sleep. This type of disruption has been known to have a close link to memory consolidation and also with the build up of amyloid. This is a significant protein that misfolds, causing “tangles” in the characteristics in the brain of some dementia forms. Also, lack of sleep may hinder the ability of the brain to get rid of toxins.

The researchers additionally discovered an association between the sleep amount and differences in the structure of regions in the brain that are involved in memory and cognitive processing. And, once again it also showed more changes linked to less or greater than seven hours of sleep.

Experiencing an unvarying seven hours of sleep every night without too much duration fluctuation was additionally important to good mental health, well being and performance of cognitive skills. Earlier research has also shown that sleep patterns that are interrupted are linked with increased inflammation which indicates a susceptibility to diseases that are age related.

While the team cannot say for sure that too much or too little sleep may cause cognitive problems, their analysis looking at participants over a longer time period seems to support this thought. However, the reasons why people who are older have poorer sleep appears to be complicated, influenced by a combination of brain structure and genetic makeup.

The findings have suggested that excessive or insufficient duration of sleep might be a risk factor for decline in cognition with aging. This is supported by earlier research that has reported an association between the risk of developing dementia and Alzheimer’s Disease and duration of sleep in which decline in cognition is a hallmark symptom.

Getting a good night of sleep is important during all the stages of life, but is particularly important as people age. Finding ways that will improve sleep for the older population could be imperative to helping them keep up good well being and mental health and in addition avoiding decline in cognition skills and particularly for people with dementias and psychiatric disorders.

To view the original scientific study click below:
The brain structure and genetic mechanisms underlying the nonlinear association between sleep duration, cognition and mental health

Hallmarks of Aging Reversed with Fecal Transplants

As we search for the fountain of youth, fecal transplants might seem to be an unlikely method in the process of reversing aging. However, researchers have shown evidence from their study on mice, that fecal microbiota transplanting from young mice into older mice may reverse signs of aging in the brain, eyes, and gut.

In the study, microbes from older mice created inflammation in young recipient’s brains and reduced an important protein which is needed for correct vision. The discoveries have shown that gut microbes have a part in the regulation of some negative effects of aging and opens up the opportunity of therapies that are gut microbe based to combat the decline in older life.

The ground breaking work provided exciting realizations for the involvement of microbes in the gut in aging and the decline of brain and vision function. It also provides a possible solution from replacement therapy with gut microbes.

It is known that the microbe population that people carry in the gut, which is collectively known as gut microbiota, is associated with health. Many diseases are linked to changes in the behavior and types of viruses, fungi, bacteria and other microbes in a person’s gut.

Some changes in the composition of the microbiota occur as people age, negatively affecting immunity and metabolism. This can be directly linked to age related disorders such as cardiovascular, inflammatory bowel disease, metabolic, neurodegenerative and autoimmune disorders.

In understanding the results of the changes as we age in the microbiota, the team transferred gut microbes from older mice into young healthy mice and vice versa. Then they observed what affects it had on inflammation of aging in the brain, vision and gut which all suffer from the decline of function as a person gets older.

This study discovered that the microbiota from the older donor mice led to a loss of stability of the gut lining. This allowed bacterial products to incorporate into circulation, which caused inflammation in the eyes, brain and the immune system.

Inflammaging which is chronic age related inflammation, has been linked with activation of very specific immune cells that are in the brain. These particular cells became greatly activated in the younger mice who had received microbiome transplants that were aged.

The researchers additionally noted specific proteins in the eye linked with degeneration of the retina that were at higher levels in the younger mice who had received microbiota from the older donors.

In aged mice, these negative developments in the eye, brain and gut could be restored through transplanting gut microbiota from the younger mice.

In continuing studies, the researchers are in the process to try and understand the long term effects that were positive can last. They also hope to identify the components that are beneficial of the young mice microbiota and what the impact is on organs that are far off from the gut.

The microbiota of the younger mice, and the older mice who had been given younger transplants of microbiota, were fortified in bacteria that was beneficial and had previously been linked with good health in both humans and mice.

The team also analyzed the products that these bacteria are producing by breaking down certain elements of what we eat. This has shown major changes in certain fats (lipids) and metabolism of vitamins which could be associated to the shifts that are seen in cells that are in the brain and eyes.

The same pathways live in people and the gut microbiota of humans also will change greatly as we get older, but the team caution that extrapolating the results of their research to humans until studies that are similar in older people can be made.

A new facility for MRT (Microbiota Replacement Therapy) which is also known as FMT (Fecal Microbiota Transplantation) is being built that will enable these trials in addition to new trials for conditions that are microbiota related.

The team was excited to discover that through changing the gut microbiota of older people, they could rescue indicators of age related decline which is commonly seen in conditions that are degenerative in the eye and brain.

The results provide additional evidence of the major links between gut microbes and the healthy aging of organs and tissues of the body. They hope their findings ultimately contribute to understanding how manipulation of diet and gut bacteria can maximize better health as we age.

Fecal transplants are relatively safe and rarely spread disease as long as they are lab tested for diseases and are from very healthy donors. At one time doctors could order them for their patients, however the FDA in the US now requires extreme illness before they are allowed. This is sad since side effects and complications have been rare.

To view the original scientific study click below:
Fecal microbiota transfer between young and aged mice reverses hallmarks of the aging gut, eye, and brain

Driving Risky as Common Sleep Disorders Worsen

Close to half of older adults might have sleep apnea, which is a condition where sleep and breathing are briefly interrupted many times throughout the night. A recent study has shown that this chronic tiredness may have serious implications for safety on the road.

People who have sleep apnea will wake up feeling tired in the morning and it doesn’t matter how many hours they actually slept. Sleep apnea causes people to stop briefly and restart breathing dozens and even hundreds of times in a night. Even those with breathing interruptions often won’t awaken a person that has sleep apnea and will prevent them from getting into a refreshing, deep sleep.

A recent study shows a variety of how dangerous chronic tiredness from sleep apnea can be when it comes to driving. For every eight added breathing interruptions each hour, the odds of making dangerous driving moves such as braking hard, speeding and suddenly accelerating increase by 27% according to the research.

Older adults are much more likely to develop sleep apnea. In addition, they are more likely to be killed or seriously injured in an automobile accident. This discovery, has suggested that screening adults that are older for sleep apnea and then for treatment if needed, might help the older population continue driving safely for a longer period.

The percentage of adults who are older with mild sleep apnea is 30% to 50%. However, if these adults do not have sleepiness during the day or any other proof of impairment, they may not become aware they need medical attention. The findings have suggested that it might be wise to lower the threshold to evaluate adults who are older for sleep apnea and track their interruptions in breathing. If their conditions are worse by just eight interruptions per hour, that might have significant negative effects on their driving and the risk of serious injury.

People 65 and older are the more responsible drivers on our roads. They tend to obey speed limits and drive defensively. They tend to avoid driving in bad weather, at night and in places that are unfamiliar. However, changes that come with the advancement of age such as slower reflexes, deteriorating vision and sleep difficulty, can undermine even some of the safest habits.

The researchers teamed up with a driving researcher to study the relationship between risky driving behaviors and sleep apnea.

96 older adult participants were recruited and had their sleep habits and driving monitored under real world situations. The team used a commercially available test that was taken at home to identify participants with sleep apnea and then measure its severity. Fewer than five interruptions of breathing an hour is considered normal. Five to 15 interruptions per hour is considered mild sleep apnea. 15 to 30 interruptiond is considered moderate, and greater than 30 is considered severe.

To assess the driving habits, the team installed a chip into the participant’s personal cars and monitored their driving for one year with focus on episodes of sudden acceleration, braking hard, and speeding. In total, they collected data on more than 100,000 participant’s trips. Additionally, the participants were evaluated by the team for molecular evidence of early Alzheimer’s Disease and cognitive impairments.

Although all participants were cognitively normal, almost one third had changes in their brain which was indicative of early Alzheimers. The team discovered that the frequency that the drivers made with moves that were dangerous behind the wheel increased in parallel with the frequency that their sleep had been interrupted at night. This was even though their brains did not show any markers of early Alzheimers.

Since there weren’t cameras in the participant’s vehicles, the team doesn’t know exactly what occurred that caused a participant to suddenly brake hard. An example would be not noticing a light that turned red until they got close and had to brake suddenly. The more tired a person is, the less attention they have to handle the task going on, particularly if it is constantly changing and is novel.

The study does help untangle the way risk factors that are age related, such as poor sleep and Alzheimers put older adults into danger when driving. It also might assist efforts to discover new ways to maximize safe driving for years.

To view the original scientific study click below:
Adverse driving behaviors are associated with sleep apnea severity and age in cognitively normal older adults at risk for Alzheimer’s disease

Breakthrough Tendon Repair with Stem Cells and Silk Protein

Many people know that an injury to tendons can be difficult, lengthy and many times an incomplete process of healing. As an example, repetitive or sudden motion which can be experienced by factory workers and athletes can increase the risk of ruptures or tears in the tendons. 30% of people will experience an injury to the tendon with the highest risk in women. Additionally, people who endure this type of injury are more likely to experience a future injury at the same site or never fully recover from the injury.

Muscles which are attached to bone are tendons which are fibrous connective tissues. The tissues are soft and connected to rigid bones which makes for a difficult interface that is a very defined structure. After an injury occurs, the structure becomes obstructed and the tissues that connect the muscle to the bone change from a linear formation to one that is kinked. Excessive scarring may additionally occur which changes the tendon’s natural properties and the capacity to bear loads.

While the body is going through its natural process of healing, tendons and other cells initiate to reconstruct the primary matrix of connective parallel tissue fibers. However, this process can take weeks and even months and the resulting tendon is very often not perfect. This will result in chronic pain, weakness and a lesser quality of life.

Potential treatments for injuries to the tendons include grafts from the tendon tissue taken from donors or patients. However these have a risk of infection, necrosis or transplant rejection. Transplants that are synthetic have been tried, but biocompatibility, bio-degradation and mechanical problems have hindered these attempts.

An alternative approach is to use MSCs (mesenchymal stem cells) which are specialized cells whose pivotal role is in regeneration of tissue. At the site of the wound, they can tell the difference between various cell types. They then produce molecules that signal which will regulate cellular migration, immune response, and new formation of blood vessels which enables regeneration of tissue.

However, methods of treatment that use direct injection, systemic infusion or MSCs being genetic modified have their own problems. Infusion that is systemic does not target specifically to the site of injury. An injection that is direct requires a prohibitively large number of cells, and modification that is genetic is insufficient and will produce cells that can be hard to isolate.

Another approach has been constructing bio-material scaffolds or frameworks, and then let in MSCs and growth factors to create new tissue in the tendon. A team has used this method in developing a procedure that is showing important advances in MSC regeneration of tissue.

The team initially looked to silk fibroin which is a silk protein that is produced by the Bombyx mori silkworm. It is used in silk fabrics and additionally used in electrical and optical material and in a variety of biomedical applications such as suture materials to bone, bio-engineered ligaments, and corneal tissue. Due to its superior durability, strength, bio-degradative, and bio-compatibility aspects, silk fibroin is perfect to use in frameworks for tendons.

To enhance the ability of the framework for regeneration of tissue, the team combined silk fibroin with GelMA, a gel that is gelatin based. It retains water due to the GelMA’s controllable degradation, biocompatiblity, stiffness and the ability to promote cell growth and attachment.

The synergistic results of GelMA’s capacity for the support of formation of regenerative tissue and the structural advantages of the silk fibroin make the composite material very well suited for repair of tendons.

The team prepared mixtures of a variety of ratios of silk fibroin and GelMA (SG) and created thin nanofiber sheets. Next they tested the sheets for fiber stretchiness and structure and chose the best formulation with the optimal mechanical properties. They noticed that the silk fibroin passed on an increased permeability to the material which enhanced repair of the tissue.

The improved SG sheets were then implanted with MSCs and put through a variety of tests measuring MSC production of growth factor, differentiation and compatibility, and gene activity that triggered matrix formulation.

The MSCs that were on the SG sheets indicated a rise in proliferation and viability of cells compared to those on silk fibroin sheets that did not have the GelMA (SF). Genetic analysis indicated that pertinent gene activity in SG MSCs was greatly increased as contrasted to those on SF sheets which was shown to be decreased.

Using stained test procedures it was shown that the MSCs on the SG sheets indicated a rate higher than 80% of attachment and showed an oblong shape which is similar to cells that are attached to surfaces. This was in comparison to a 60% rate of attachment on SF and GelMA only surfaces with spherically shaped cells.

Additional tests on a growth factor that was secreted by MSCs implanted onto nanofiber sheets indicated that the growth factors produced had the best ability to repair tendon tissue that was injured.

Experiments on live rats with injuries to their Achilles tendons were also performed. MSC implanted nanofiber sheets were attached to the site of injury and the SG sheets promoted the best healing acceleration with reduced sites of injury and remodeled muscle component and the formation of densely packed, well-aligned fiber.

Remodeling of tissue for repair of tendons is very challenging to achieve. The research done has significantly advanced that achievement.

To view the original scientific study click below:
Co-Electrospun Silk Fibroin and Gelatin Methacryloyl Sheet Seeded with Mesenchymal Stem Cells for Tendon Regeneration

Your Gut Microbiome Can Influence Your Food Cravings

Every day we all make decisions about what we consume, however our choices might not be totally our own. Research on mice has shown that the microbes in their guts have an influence on what they choose to eat, creating substances that will prompt urges for a variety of foods.

Everyone has urges for certain foods like really needing to eat a salad or some meat. The team’s work has shown that mice with different varieties of microbes in the gut choose different foods.

Although it has long been speculated by researchers as to whether microbes can influence what we prefer to eat, the thought has not been tested directly on animals larger that a fruit fly. Investigating this, 30 mice that had a lack of gut microbes were given a combination of microorganisms coming from 3 species of wild rodents that had contrasting natural diets.

They discovered that each group of mice had chosen foods flush in a variety of different nutrients which showed that their microbiome had changed what they preferred to eat.

While the thought that microbiome can affect a person’s behavior may appear somewhat far fetched, it wasn’t a surprise for the team. Our gut and our brain are in ongoing contact, with particular kinds of molecules acting as mediators. Byproducts from digestion signal that you have consumed enough food or that maybe you need certain types of nutrients. However, microbes can emit some of these same molecules, possibly hijacking lines of communication which can change the meaning of their message benefitting themselves.

For example, one messenger might be needing a nap following a turkey dinner due to its content of tryptophan. This is an essential amino acid that is found in turkey, however it is also formed by microbes in the gut. It travels to the brain and is transformed into serotonin which sends an important signal for feeling satisfied following a meal. It then eventually becomes converted into melatonin making you sleepy.

From this study, it was shown that the mice that had contrasting microbiomes also had varying levels of tryptophan in their blood. This was before they had the choice to choose a different diet. Those with more of this molecule in their blood also showed more bacteria that could produce it in their gut.

Tryptophan is only one thread of what is a complicated web of chemical communication. There are most likely dozens of signals that influence eating behavior day to day. Tryptophan which is produced by microbes might be one aspect of that. However, it does establish a credible way that microscopic organisms can alter what we prefer to eat. This is one of a few rigorous experiments showing such a link between the brain and the gut despite quite a few years of theorizing by researchers.

There is still more science that needs to be done before a person should begin distrusting their cravings for certain foods. Without a way to test the idea on humans, the researchers could not measure the significance of microbes in determining diet when compared to anything else.

It might be that what a person has eaten the day before is more significant than just the microbes they have. People have a lot more going on that can’t be ignored in the team’s experiment.

It is just one behavior that microbes might be tweaking without our knowledge. The field is young and there is a lot still to learn. The team is just amazed at the role they are finding that microbes play in animal and human biology.

To view the original scientific study click below:
The gut microbiome influences host diet selection behavior

Meditation Can Help Improve Mental Awareness

If you make mistakes or are forgetful when hurried, a new study which is the largest in this field to date, has found that meditation can help a person be less error prone.

The study tested ways that open monitoring meditation altered activity in the brain in a way that has suggested increased recognition of error. This is meditation that puts the focus on awareness of thoughts, feelings, or sensations as they occur in a person’s body and mind.

Interest in mindfulness and meditation is currently passing what science is able to prove in relation to benefits and effects. The team noted how amazing it was to be able to observe how just one course of a managed meditation is able to make changes to activity in the brain in non-meditators.

The discovery has suggested that a variety of meditation forms can produce contrasting neurocognitive outcomes. The team explains that there isn’t much research in regards to the reason why open monitoring meditation can impact error recognition.

In some kinds of meditation the person will focus on a single thing, such as breathing. However, there is a difference with open monitoring meditation. With it a person turns inward and then places their attention on everything that is happening with their body and mind. The aim is for the person to sit quietly while noticing where the mind goes without getting too caught up in what is going on around them.

The team recruited over 200 non-meditation participants to test how open monitoring affected how people detect and then respond to errors.

The non-meditation participants were put through an open monitored meditation exercise that lasted 20 minutes. During this session the team measured activity in the brain through EEG. Afterwards, a computerized distraction test was completed.

The EEG measures activity in the brain at the millisecond level so the team could get exact measurements of neural activity immediately following mistakes compared to responses that were correct. A particular neural signal will occur about half a second following an error which is called error positivity which is associated with conscious recognition of error. They discovered that the strength of the signal is increased in the mediators compared to controls.

Even though the mediators did not have immediate improvements to real task performance, the team’s discoveries show a promising window into the possibility of sustained meditation.

The findings show a powerful demonstration of how meditating for just 20 minutes can strengthen the ability of the brain to realize and note a mistake. This shows how mindfulness meditation could potentially be capable of use in daily functioning and performance from moment to moment.

While mindfulness and meditation have shown more mainstream interest in the past few years, the study group is a relatively small group that use a neuroscientific approach to evaluating their performance and psychological effects.

To view the original scientific study click below:
On Variation in Mindfulness Training: A Multimodal Study of Brief Open Monitoring Meditation on Error Monitoring

Vitamin D The Sunshine Vitamin That Supports Cardio Health

Vitamin D is naturally produced when you are exposed to the sun. It is a natural source of a hormone essential to us and especially to our bones. However, according to new research, when you are low on this vitamin, not only do the bones take a hit but also cardio health.

The study which is the first of it kind, has identified genetic evidence that a deficiency of Vitamin D is causing cardiovascular disease. It indicates that people with low Vitamin D are most likely to have heart disease and high blood pressure. Participants who had the lower concentrations of the vitamin were shown to have a heart disease risk that was more than two times higher than participants in the normal range.

Worldwide cardiovascular diseases (CVD’s) are the leading cause of death. Low levels of Vitamin D are common in many places in the world. The team says the role of the deficiency of the vitamin for health of the heart could reduce CVD’s globally.

A severe deficiency is rare, but where is does occur it is important to be proactive and decrease negative affects on the heart.

We can get Vitamin D from food sources which include eggs, oily fish and fortified drinks and food. Unfortunately, food is a relativity poor source of the vitamin and a diet that is healthy typically does not contain enough.

If you don’t get enough from the sun, then supplementation will help keep up the requirements.

The results of the study are important as they suggest that Vitamin D levels can be raised to be within the normal range that will also affect rates of CVD’s. By increasing Vitamin D deficient levels at least 50 nmol/L it is estimated 4.4% of all CVD cases could have been prevented.

The study utilized a new genetic approach that made it able for them to assess how increasing the levels of the vitiman could effect CVD risk based on how high vitamin D levels were. The study utilized information from close to 267,980 participants which allowed them to provide strong statistical evidence for the association between CVD and Vitamin D.

To view the original scientific study click below:
Non-linear Mendelian randomization analyses support a role for vitamin D deficiency in cardiovascular disease risk

Lab Grown Muscle Cells Repair Disease and Injury

Researchers have cultivated successfully human stem cells that have the ability to renew themselves and repair damage to muscle tissue in mice. This potentially advances attempts to treat disorders that are muscle wasting and muscle injuries in humans.

To create the stem cells that are self-renewing, the team started with lab grown human skin cells that had been genetically changed to a more undeveloped state where the cells had the possibility of becoming just about any cell type found in the body. These are IPS (induced pluripotent stem) cells and they are combined with a mixture of standard cell nutrients and growth factors that prod them to transform into cells types that are specific.

In the lab, researchers have been able for a long time to alter IPS cells to become a variety of cell types, including brain and skin cells. The more difficult task is being able to change IPS cells to become a cell that self-renews itself for a specific organ.

The team coerced IPS cells to transform into stem cells that are muscle by the use of a nutrient rich blend. Additional research is planned to determine the particular recipe in the future to establish which ingredients might be key to brewing the stem cells that are muscle.

The hope is to be able to make muscle cell therapies to use for muscle wasting diseases such as muscular dystrophy. The team points out that these kind of stem cell treatments are not available at this time.

In proof concept experiments using mice, the team set out to establish where the newly transformed cells settle in living animals and whether or not they could mend tissue that was damaged.

The team showed that after injecting the muscle stem cells into the mice muscles, they moved to an area of the muscles which is called the niche and remained there for over four months. This is where various natural muscle stem cells are normally found.

The team utilized two different techniques to see if the muscle stem cells would mend tissue that was damaged.

In one of the methods, the team transplanted the stem cells that are muscle into genetically engineered mice that were bred without an immune system to keep away from rejection of the transplanted cells. Then they exposed the mice to a toxin that is muscle degrading and also radiation to eradicate muscle stem cells that are already in the mice.

At the area of the radiation damage and toxin in the tissue that was muscle, they found that the transplanted human stem cells developed into mycoblasts. These are a kind of muscle construction cell that will repair damage through fusing together and developing microfibers that look like ordinary muscle. Additionally, they discovered that several of the transplanted human stem cells that are muscle migrated to the niche and behaved like stem cells that are muscle and naturally found in the mice.

In the second method, the team transplanted stem cells that are muscle into genetically engineered mice with a mutation in the dystrophin gene. This results in Duchenne muscular dystrophy which is a wasting disorder in humans and mice.

The team found that the transplanted stem cells that are muscle traveled to the area of the muscle niche. Over many months, tests indicated that the transplanted mice could run twice as long on treadmills than the untreated mice which is a measure of strength of muscles.

The team says that the stem cells that are muscle could possibly be made as therapies for a variety of disorders of the muscles.

The team will continue to study the use of the cells in the mice models of other conditions that are muscle related and their potential for use in trauma, sports injuries and age related loss of muscle.

To view the original scientific study click below:
Human pluripotent stem cell-derived myogenic progenitors undergo maturation to quiescent satellite cells upon engraftment

New Discovery Enhances Recovery of Injured Muscle

Researchers have developed a promising new approach to combat age related muscle atrophy that is associated with immobility following illness or injury. The technique which was shown in mice, arrests the processes through which muscle will begin to deteriorate at the start of exercise following a period of inactivity.

Exercise and activities that particularly are load bearing, help retain muscle mass which is especially important as we age. Illness and injury can lead to periods of decline in the quality of muscle mass and inactivity.

When we don’t have the ability to contract a muscle, it atrophies. If that immobility remains for very long, there is going to be a significant loss of strength and muscle mass.

Muscles of younger adults and children will tend to quickly recover resuming exercise. However, for older adults, they are deficient in the ability to recover muscles mass following a period of disuse.

The typical prescription is physical therapy to promote the healing process following immobility and injury. However, studies have shown that cellular dysfunction and inflammation in the muscles accumulate and hamper healing.

The team focused on the factors that degrade or enhance muscle mass in the aging process. In an earlier study, the team discovered that injecting pericytes, which are support cells, contributed to restoration of muscle in young mice following an episode of immobility. But the response was not as good in the older mice to these injections and the recovery was impeded.

In the current study the researchers obtained pericytes from the muscles of healthy, young mice and cultivated them in a cell culture. These cells were exposed to hydrogen peroxide. It is a strong oxidant that will promote the creation of extracellular vesicles (EVs) that contain factors that will battle stress and promote the healing process. They also collected EVs to use in therapy.

Extracellular vesicles are required to intercellular communication and can be utilized as biological markers of disease and health. Earlier studies have shown that in addition they are powerful biological mediators of healing and stress. As an example, blood can be taken from young mice, EVs from the blood collected and then injected into older mice and they would then have a younger collection of traits which are known as phenotypes. You can also take healthy EVs from the blood of mice, introduce them into a mouse with diabetes and it will reverse the diabetes.

However there hasn’t been any studies exploring the use of EVs in support of muscle recovery.

Pericyte-derived EVs were injected into the muscles of mice that were young and old that had gone through sustained immobility of muscle in one leg and were starting to reuse these muscles again.

They were successful. The mice that were treated with the stimulated EVs were able to recover skeletal muscle fiber size in both the young and older mice. The research also showed for the fist time EVs that had been derived from muscle pericytes produced a diversity of factors that could combat oxidative stress and inflammation.

To view the original scientific study click below:
Development of a cell-free strategy to recover aged skeletal muscle after disuse

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