Exercise Improves Elimination of Toxic Proteins from Muscles

A new study conducted by researchers at the University of Sao Paulo in Brazil in partnership with colleagues in the U.S. and Norway and published in Scientific Reports, has shown that lack of muscle stimulus results in a buildup of inadequately processed proteins in muscle cells which in turn leads to muscle wasting and weakness. This typical muscle dysfunction is a condition commonly effecting the elderly, individuals who sit for long periods of time without any exercise and bedridden patients.

Test results from rats with induced sciatic nerve injury which stopped receiving stimuli, showed the protein buildup was caused by impairment of autophagy which is the cellular machinery responsible for identifying then removing damaged toxins and proteins. The analysis of the tests on the rats subjected to a regime of aerobic exercise training which were previous to injury enabled the researchers to demonstrate that physical exercise can keep the autophagic system primed and then facilitate its activity as necessary. This is similar to muscle dysfunction due to the lack of stimulus.

Daily exercise will sensitize the autophagic system which facilitates the elimination of organelles (any of a variety of organized or specialized structures within a living cell) and proteins that are not functional in the muscles. It is important that removal of these dysfunctional components occur. When they accumulate they will become toxic and contribute to muscle cell impairment and death.

A good example of what muscle autophagy is, is by comparing muscles working in a similar manner as a refrigerator which runs on electricity. If the signal ceases due to someone pulling the plug on the frig or in the case of muscles blocks the neurons that innervate the muscles, it won’t take too long for food in a frig to spoil and proteins in muscles to spoil at different rates according to their composition. At this point an early warning mechanism in cells activates the autophagic system which will identify, isolate and then incinerate the defective material which prevents propagation of the damage. If the muscles do not receive the right electric signals for long periods of time, the early warning mechanism will stop working properly and cell collapse will occur. Without autophagy, a cascade effect will occur which leads to cell death.

In the current study, rats were submitted to sciatic nerve ligation surgery which created an effect equal to that of sciatic nerve compression in humans. The pain this injury can cause prevents people from using the leg affected by the injury which will lead to weakened muscles and eventually atrophy of those muscles.

Previous to surgery, the rats were divided into two groups. One group remained sedentary while the other group was given exercise training which consisted of running at 60% maximum aerobic capacity for one hour a day, five days per week. After four weeks of exercise training, surgery was performed. The muscular dysfunction induced by sciatic nerve injury was discovered to be less aggressive in the group which had aerobic exercise than the group of rats that were sedentary. Biochemical and functional parameters in the affected muscles were also evaluated. The aerobic training increased autophagic flux and therefore reduced dysfunctional protein levels in the muscles of the rats. Occurring at the same time was improvement in the muscle tissue’s contractility properties. Exercise is a transient stress which will leave memory in the organism and in this case via the autophagic system. When the organism is subjected to a variety of stress, it is better prepared to respond and combat the effects.

The team performed two other experiments which were designed to more thoroughly investigate the link between autophagy and exercise. One experiment involved mice in which the autophagy related gene ATG7 was silenced in the skeletal system. ATG7 encodes a particular protein responsible for synthesizing a vesicle called the autophagosome which forms around dysfunctional organelles and then transports them to the lysosome where they are broken down and then digested. This particular experiment validated the importance of autophagy in muscle biology. ATG7 will knockout mice that had not been subjected to sciatic nerve litigation although displayed muscular dysfunction.

In the second experiment, muscles from rats with sciatic nerve injury and control rats without injury were treated with chloroquine, a drug which inhibits autophagy by raising the lysosomal pH or alkalinity and therefore prevents the degradation of defective proteins. These tests showed less muscle strength in the control group of rats treated with the drug than in the untreated group. Chloroquine had no effect at all on the muscles of the rats with the sciatic nerve injury showing that the inhibition of autophagy is critical to muscular dysfunction caused by lack of stimulus.

Rather than aiming to find a treatment for people who are unable to exercise adequately, the goal of the studies was to use an experimental model for future research to help understand the cellular processes involved in muscle dysfunction. This will help facilitate the development of interventions capable of minimizing or even reversing an increasingly serious problem with muscle weakness and atrophy caused by lack of movement. By identifying a molecule that will selectively keep the autophagic system alert similar to what happens during physical exercise, treatments may be developed which can be given to people with this type of muscle disorder which includes people who are bedridden for extended periods of time, patients with degenerative muscular diseases and the elderly.

To view the original scientific study click here: Exercise prevents impaired autophagy and proteostasis in a model of neurogenic myopathy.

Artificial Sweeteners and Toxic Effects on Gut Microbes

A collaborative study conducted by researchers at Ben Burion University of the Negev and Nanyang Technological University in Singapore, has shown the relative toxicity of six different FDA approved artificial sweeteners (sucralose, aspartame, saccharine, neotame, advantame and acesulfame potassium k) and also 10 sport supplements that contain these ingredients. Bacteria found in the digestive system became toxic when exposed to high levels of the artificial sweeteners such as just one mg/ml.

The team modified bioluminescent E coli bacteria which will illuminate when toxicants are detected and thus become a sensing model representative of the complex microbial system. This provided evidence that artificial sweeteners consumed regulartly adversely affects the activity of gut microbe which can lead to a variety of health issues.

The gut microbial system plays an important role in human metabolism. The study found that mice treated with one artificial sweetener, neotame, had different patterns than those not treated and several important genes found in the human gut decreased. Also noted were high concentrations of several fatty acids, cholesterol and lipids in the mice treated with this artificial sweetener.

Artificial sweeteners are found in many food products and diet soft drink beverages. People consume these added ingredients without even knowing it. This is especially common with athletes who devote a lot of time to their diet which often includes sport supplements taken to improve their physical performance. Additionally, artificial sweeteners have emerged as environmental pollutants and are found in surface and drinking water and in groundwater aquifers.

The study results may help in understanding the toxicity of these sweeteners and the possible negative affects on the gut microbial community and the environment. The bioluminescent bacteria panel might also be used for finding artificial sweetners that could be in the environment.

To view the original scientific study click here: Measuring Artificial Sweeteners Toxicity Using a Bioluminescent Bacterial Panel.

Does Nutrition have More Impact on Bone Strength than Exercise?

Researchers at the University of Michigan have answered the question that fitness experts and scientists have wondered about. Does nutrition or exercise have the biggest impact on bone strength?

The tests were conducted on male, 16 week old mice which were assigned to 9 groups that were weight matched. This included a baseline group, an exercise with detraining group and a group that was non-exercised. 0.5% Calcium and 0.5% Phosphorus was fed to the control group and 5% Calcium and 1% Phosphorus was fed to the supplemented diet.

The exercise employed was treadmill running for 30 minutes at 12 metres per minute and this lasted for eight weeks. At the end of the eight week period, the mice that consumed the supplemented diet had more BMC (tibial cortical bone mineral content) and vBMD (bone mineral density) than the mice that were in the controlled diet group.

It was additionally noted that exercise was only able to increase BMC when the supplemented diet was also included. At the end of 16 weeks, both exercise and non-exercise groups of mice that were fed a supplemented diet were able to maintain greater tibial cortical BMC as well as vBMD as compared to the mice in the control group.

After looking at exercise and mineral supplementation in mice, they found some very interesting results. Nutrition played a much bigger role in bone strength and mass than exercise. Additionally, after exercise was stopped the mice continued to retain gains in bone strength if they continued to consume a diet supplemented with minerals.

David Kohn, a professor in the schools of engineering and dentistry, noted that long term mineral supplements will lead not only to increases in strength and bone mass, but also the ability to retain the increases even when training stops. And as people age, it is much easier to maintain diet over exercise.

Another finding was that diet alone will have positive effects on bone even when exercise isn’t happening. This was a big surprise to the team who anticipated exercise with a pretty ordinary diet to prove to have bigger gains in a persons bone strength.

Their data indicates that long term use of a mineral supplemented diet can be beneficial in the prevention of bone loss and strength even if you aren’t exercising. Combining both mineral supplementation and exercise serves to amplify the gains.

Previous studies looked at the effects of dietary calcium. The current study looked at increased calcium along with increased phosphorus and discovered benefits by increasing both. This doesn’t mean people should start running out and buying phosphorus and calcium supplements since their findings don’t directly correlate from mice to humans, but it does give the team a concept to study.

It is well known that peak bone mass occurs in people in the early twenties and then begins to decline. The goal then is to figure out how to maximize bone mass at an early age so when bone mass begins to decline, people are able to start in a better position.

The researchers also performed a variety of mechanical assessments that relate to the bone. The mechanical quality of bone tissue doesn’t always correlate with bone mass. The mice were tested following eight weeks of exercise training and a normal diet or a supplemented diet and then following another eight weeks of no training.

To view the original scientific study click here: Combined mineral-supplemented diet and exercise increases bone mass and strength after eight weeks and maintains increases after eight weeks detraining in adult mice.

Too Much Sleep can be Bad for the Brain

Neuroscientists from Western University’s Brain and Mind Institute have released early results from the world’s most intense sleep study which reveals that sleeping an average of 7-8 hours per night have better cognitive performance than people that sleep less than that or more.

The article published in SLEEP, shows results from the study which was started in June 2017 with more than 40,000 people from all over the world included in the scientific investigation that was online. The study involved a very detailed questionnaire including a list of cognitive performance activities. The goal was to find out the sleeping habits of people all around the world. Sleep studies of a smaller degree have been conducted in laboratories, however this study’s goal was to find out what sleep is really like.

The study involved a very diverse group of participants which allowed the researchers to compare sleep deprivation on people of different professions, lifestyles and ages. The extensive questionnaire asked questions about where they lived, education level, medications they took and other information that helped the team consider factors that would contribute to results of the study. The participants also underwent 12 established cognitive tests so that mental ability and amount of sleep could be correlated.

About one half of the participants reported that they slept less than 6.3 hours each night. This is about sixty minutes less than what the study recommends for healthy sleep habits. One very surprising revelant factor was that participants who had slept less than four hours performed like they were nine years older than they were.

An additional interesting discovery was the fact that adults were affected equally. People who got seven to eight hours of sleep per night showed the highest functional cognitive behavior and this was regardless of age. The impairment related to too much or too little sleep was not dependent on age. However, older adults were much more likely to have shorter sleep duration which meant they were much more impacted by sleep deprivation than the other age groups of people.

Less sleep and more sleep both negatively impacted several cognitive functions such as information manipulation for problem solving and recognizing complex patterns. Verbal ability and reasoning were the most impacted by sleep with short term memory ability being barely impacted.

The study confirmed that getting 7 to 8 hours of sleep per night is optimal. Data from a previous study conducted on about one million people showed that both sleep deprivation and too many hours sleeping should be avoided for optimal health of the heart. 7 to 8 hours of sleep is recommended to keep the brain performing at its very best.

The studies findings show how significant real world implications are. Many people including those in positions that require a lot of responsibility may operate on too little sleep which may impair problem solving, reasoning and communication skills on a regular basis. Getting too much sleep on the other hand can be just as damaging.

To view the original scientific study click here: Dissociable effects of self-reported daily sleep duration on high-level cognitive abilities.

Skeletal Stem Cells Identified

Researchers have isolated human skeletal stem cells from adult and fetal bones that become cartilage, bone or stroma cells. This is the first time that skeletal stem cells have been identified in humans. The team was also able to derive the skeletal stem cells from human induced pluripotent stem cells which opens up the possibility of therapeutic applications.

By identifying this human skeletal stem cell and elucidating its lineage map, the researchers believe molecular diagnosis and treatment of skeletal diseases will occur. There is a tremendous burden imposed by neoplastic, post traumatic, post surgical and degenerative skeletal disorders. Skeletal dysfunction can develop into a broad spectrum of health conditions and despite its significant impact on disease and health, treatments aimed at improving skeletal function are currently limited. A major hurdle is that stem cell regulation in the human skeletal system is largely unexplored.

Bones posses skeletal tissues which have exceptionally regenerative potential. Defects of the bone heal readily and some vertebrates can actually regenerate portions of their limbs. However, regenerative capacities of skeletal tissues in other vertebrates are much more restricted. Bones in humans and mice can recover from small to moderate sized defects. However, adult cartilage tissue possess little to no regenerative ability. Both humans and mice exhibit severe age related degeneration of skeletal tissues with aging.

In the recent study, the team addressed the knowledge gap by identifying and characterizing human skeletal stem cells and downstream cartilage and bone progeny in a variety of tissues. These self renewing and multipotent cells were present in both adult and fetal human bone marrow tissues. They could be derived from iPSCs (induced pluripotent stem cells). By identifying the relationships between downstream skeletal progenitors and human skeletal stem cells, the team was able to create a lineage map of stem cell mediated formation of human skeletal tissues.

Additionally, transcriptomic (the study of the complete set of RNA transcripts that are produced by the genome under specific circumstances or in a specific cell) and epigenetic (the study of changes in organisms caused by modification of gene expression) comparisons with mouse skeletal stem cells revealed evolutionary conserved pathways regulating stem cell mediated formation of skeletal tissues. Divergent molecular pathways which may regulate species specific differences in skeletal structure and bone development were also revealed.

Comparing functional and molecular differences in specific types of stem cells between different species of vertebrates may lead to the uncovering of divergent and convergent mechanisms which underlie tissue growth and regeneration. This understanding could be applied towards enhancing health and rejuvenation in humans.

To view the original scientific study click here: Identification of the Human Skeletal Stem Cell

Are BPA Free Plastics Any Better Than BPA?

Twenty years ago a research team discovered by accident that BPA had leached out of plastic cages that were used to house female lab mice which caused an increase in chromosomally abnormal eggs. They have now discovered that a variety of alternative bisphenols now being used to replace earlier BPA in BPA free cups, cages, bottles and other items appear to have similar problems with their mice. Patricia Hunt of Washington State University reports a strange deja vu experience in their laboratory.

The recent findings were uncovered very similarly as the team once again noticed changes in the data coming from studies on control animals. The problem was once again traced to contamination from damaged cages, however the effects were more subtle than what presented in the original discovery. That was due to not all of the cages being damaged and the contamination source remained less certain.

The team was able to determine that the mice were being exposed to bisphenol replacements. They also observed that the disturbance in the lab was causing problems in the production of both sperm and eggs. After getting the contamination under control, they conducted additional controlled studies to test the effects of a variety of replacement bisphenols including one of the more common replacements known as BPS. The studies confirmed that the dispenol replacements produce remarkably similar chromosomal abnormalities as those seen in the earlier BPA study.

Patricia Hunt noted that the initial accidental exposure of the mice was remarkably similar to what could happen in people who use plastics in that the exposure was highly variable and accidental. Not all of the mice’s cages were damaged therefore the findings differed among mice in different cages. She adds that although determining levels of human exposure is difficult, the controlled experiments were conducted using low doses of BPS and other disphenol replacements thought to be relevant in people who use BPA free plastics.

The problems if they remain true in people as has been shown with BPA, will carry to future generations through their effects on the germ line. The team has shown that if it were possible to completely eliminate bisphenol contaminants, the effects would still persist for about three generations.

The team says more work is needed to determine whether some bisphenol replacements might be safer than others as there are dozens of these types of chemicals now in use. They also suspect that other widely used and endocrine disrupting chemicals such as parabens, flame retardants and phthalates may have similar adverse affects on fertility and they warrant study also.

The team agrees that the ability to rapidly enhance properties of chemicals has tremendous potential for treating a variety of diseases, controlling dangerous infectious agents, and enhancing medical and structural materials. The technology has paved the way for green chemistry which is a healthier future achieved by engineering chemicals to protect against hazardous effects. Currently however, regulatory agencies which are charged with assessing chemical safety cannot keep up with the introduction of new chemicals. Furthermore, as disphenol replacements illustrate, it is more cost effective and easier under current regulations to replace a chemical of concern with structural analogs instead of determining the attributes that make it hazardous.

The teams advice to consumers is simple: BPA free or not, plastic products which show physical signs of aging or damage cannot be deemed safe.

To view the original scientific study click here: Replacement Bisphenols Adversely Affect Mouse Gametogenesis with Consequences for Subsequent Generations.

Stem Cell Fate Identified

Researchers at the University of California, Irvine, have made a discovery that may improve the ability to control the formation of mature cells after stem cell transplants. Intrinsic cell properties have been identified that affect the fate of neural stem cells. The discovery could help scientists in predicting or controlling the fate of stem cells thereby improving their use in transplant therapies.

Neural stem cells can become one of 3 types of brain cells: neurons, astrocytes or oligendrocytes. The study revealed that neural stem cells which differed in fate potential expressed distinct patterns of sugars on the cell’s surface. The sugars contribute to electrical properties of the neural cell membrane and ultimately result in cell fate. Stem cells which hold great promise for disease treatments, can also pose difficulties in knowing what a stem cell will become after transplantation. The same number of stem cells can be transplanted in different patients, but the outcomes can be significantly different if cells transplanted in one patient become astrocytes and the cells in another patient become neurons. With the new discovery, scientists were able to predict what a neural stem cell will become and potentially direct cell fate. This would greatly enhance the success of stem cell transplantation therapies for a variety of diseases.

By using electrical properties, the research team discovered a new way to identify and then sort neural stem cells. They built on these findings by showing that differences in cell surface sugars are the reason these cells have different electrical properties. This study examined a variety of pathways that add sugars to cells and were able to find one that differed between cells that make astrocytes and cells that made neurons. The team stimulated the pathway in neural cells, changed the cell electrical properties, and caused the cells to make more astrocytes and fewer neurons. This showed that cell surface sugars can control cell fate. This pathway is active in cells which are grown for transplants and also in cells of developing brains. This pathway could also control how neural stem cells form astrocytes and neurons when the brain is being formed during development.

The researchers are now studying whether this pathway changes how cells will behave in transplants or how a developing brain is formed. To see how the process is regulated, they are focusing on the machinery inside the cell which adds the sugars in the first place. They have also found that particular proteins on cell surfaces are altered by this pathway which will help them uncover how the sugars go about telling stem cells which type of cell to form. The long term goal of the studies is to find methods to improve the effectiveness stem cell transplants for treating disease and injury.

To view the original scientific study click here: The Long Noncoding RNA Lncenc1 Maintains Naive States of Mouse ESCs by Promoting the Glycolysis Pathway.

Another Step Towards Curing Spinal Cord Injury and Paralysis

Researchers at Boston Children’s Hospital have conducted a study that shows new insight as to why people with spinal cord injuries become paralyzed from the injury site down, even when the spinal cord has not become completely severed. Using paralyzed mice, they have shown that a small molecule compound when given systemically can revive these circuits and restore their ability to walk. They saw 80% of compound treated mice sleeping ability restored.

The researchers took a new approach from earlier studies from inspiration by the successful strategies of epidural electrical stimulation, the only treatment that was effective in treating patients with spinal cord injury. A current was applied to the lower position of the spinal cord in combination with rehabilitation training, some parties regained movement. The epidural stimulation seemed to affect the excitability of neurons. When the stimulation was turned off, the effect was gone. The researchers tried to find a pharmacologic reason to conduct the same stimulation and, therefore, understand how it can work.

The researchers selected some of the compounds previously known to change neuron excitabilit;y and able to move across the blood brain barrier. The compound was given to mice in groups of 10 by intraperitoneal injection. All the mice used in the study had spinal cord injuries but with some nerves still intact. Each group including a control group that was given a placebo were treated for 8 to 10 weeks.

One of the compounds used, called COP290, had the most powerful effect. It enabled the mice that had been paralyzed restore their stepping ability after 4 to 5 weeks of the treatment. Recordings of the electromyography were shown that the 2 relevant groups of hind limb muscles had become active. And the scores from walking remained higher than the control groups for up to 2 weeks after stopping treatment with minimal side effects.

CLP290 is shown to activate a protein called KCC2 found in cell membranes. It transports chloride out of neurons. The current research shows that neurons that inhibit an injured spinal cord are important to the recovery of the function of motor skills. These neurons produce drastically less KCC2 after a spinal cord injury and they are unable to respond properly to signals from the brain. They only respond to excitatory signals which tell them to keep firing. This results in too much inhibitory signaling in the overall spinal circuit. In other words, the brain is not commanding the limbs to move.

Restoring KCC2 with either genetic techniques or CLP290, the inhibitory neurons may receive signals inhibiting the brain which tells them to not to fire as often. The researchers found that this changes the overall circuit backward toward excitation, making it respond more to brain input. This had the same effect of reanimating spinal circuits which were disabled due to injury. By restoring inhibition, the whole system will be excited more easily. However, there does need to be a balance as too much excitation is not good and too much inhibition is not good either.

The team is now investigating other compounds that will act as agonists to KCC2. They believe such gene therapy to restore KCC2 might be combined with epidural stimulation to maximize function after spinal cord injuries.

To view the original scientific study click here: Reactivation of Dormant Relay Pathways in Injured Spinal Cord by KCC2 Manipulations

Dietary Fiber and Brain Inflammation

As all mammals age, microglia which are immune cells in the brain become chronically inflamed. When this occurs, they produce chemicals which can impair cognitive and motor functions. This is one explanation in regards to why the memory can fade and brain functions also decline during the aging process. According to a study at the University of Illinois College of Agricultural, Consumer and Environmental Sciences however, there might be a way to delay this inevitability and that is with dietary fiber.

Consuming dietary fiber will promote the growth of the good bacteria in the gut. As these bacteria digest ingested fiber, they produce SCFAs (short chain fatty acids) which includes butyrate, as byproducts. Butyrate is of particular interest as it has been shown to produce antiinflammatory properties on microglia. It has also been shown to improve memory in mice when it has been administered pharmacologically.

In previous studies, butyrate in drug form (sodium butyrate) showed positive outcomes although the mechanism wasn’t clear. The new study however reveals in old mice that butyrate inhibits the production of damaging chemicals produced by inflamed microglia. One of these damaging chemicals has been associated with Alzheimers disease in humans.

Researchers have been interested in how sodium butyrate works, however they are more interested in knowing whether similar effects can be obtained by feeding mice more fiber. People are highly unlikely to consume sodium butyrate due to its noxious odor, however a more practical way to get elevated butyrate is by consuming a diet high in soluble fiber. The idea goes directly to the fact that gut bacteria naturally convert fiber to butyrate.

Diet has a major influence on the function and composition of microbes found in the gut. Diets high in fiber benefit these good microbes. Diets high in fat and protein on the other hand, can have a negative influence on microbial function and composition. It was believed that butyrate which is derived from dietary fiber would have the same benefits in the brain as the drug form, sodium butyrate. However, it had not been previously tested. The research team fed low and high fiber diets to groups of both young and old mice. They then measured the levels of butyrate and other SCFAs contained in the blood and additionally, inflammatory chemicals in the intestine.

The diet high in fiber elevated butyrate and SCFAs in the blood in both the young and old mice. However, only the old mice showed intestinal inflammation on the low fiber diet. The young adult mice did not have the inflammatory response on the same low fiber diet as the old mice. This indicates the vulnerability of the aging process and diet. When the old mice were fed the high fiber diet, the intestinal inflammation was drastically reduced revealing that dietary fiber can manipulate the inflammatory environment in the gut.

The next step the researchers took was to look at signs of brain inflammation. They examined about 50 unique genes in microglia and discovered that high fiber diet reduced the inflammatory profile in older mice.

The next step for the researchers is to examine the effects of diet on behavior and cognition and the precise mechanisms in the gut brain axis. Although the current study was conducted on mice, the team is comfortable in extending the finding to humans if only in a general way. What we eat matters and it is known that older adults consume 40% less dietary fiber than is recommended. By not consuming enough fiber, negative consequences can occur. Most people do not make the connection to brain health and inflammation in general.

To view the original scientific study click here: Butyrate and Dietary Soluble Fiber Improve Neuroinflammation Associated With Aging in Mice. Frontiers in Immunology, 2018; 9 DOI: 10.3389/fimmu.2018.01832

Matrix to Heal Injured Elderly Muscles

Researchers at the Georgia Institute of Technology have engineered a molecular matrix which will deliver stem cells referred to as muscle satellite cells (MuSCs), directly to muscle tissue in patients such as the elderly whose muscles don’t regenerate very well. This molecular matrix, a hydrogel, has successfully delivered MuSCs to injured, aged muscles in mice. The hydrogel boosted the healing process while also protecting the stem cells from any harsh immune reactions.

The development has provided a new method by which an aging patient after a car accident for instance, can receive treatment to severe muscle injuries that won’t typically heal. Previously, muscle stem cells from a donor have not been able to be successfully delivered to restore damaged tissue. Simply injecting additional MuSCs into the inflamed, damaged tissue was inefficient. This was mostly due to the stem cells encountering an immune system on the warpath.

Muscle injuries attract immune cells and typically this would help with muscle stem cell repair. However, in the aged or dystropic muscles, immune cells will lead to the release of toxic chemicals such as cytokines and free radicals which kill the new stem cells. Young Jang, one of the researchers says that only about 1 and 20 percent of injected MuSCs actually make it to damaged tissue and those that do will arrive in a weakened state. Additionally, some tissue damage makes any injection unfeasible.

The new hydrogel will protect the cells which will multiply and thrive inside the matrix. The hydrogel is applied to the injured muscles with the cells engrafting onto the tissues which will help them heal. Hydrogels very often start out as a water-based solution of molecular components which resemble crosses and other components that make the ends of the crosses attach to each other. When these components come together, they will fuse into molecular nets suspended in water. This results in a material that resembles the consistency of a gel.

If stem cells are mixed into the solution, when the matrix forms it ensnares the treatment for delivery and also protects the payload from dissipation or death in the body. Researchers can custom engineer hydrogels and can reliably and easily synthesize them by tweaking their components. This physically traps the MuSCs in a net and the cells also grab onto chemical latches that have been engineered into the net or matrix.

The hydrogel’s added latches bond with proteins protruding from stem cells membranes and not only increase the cell’s adhesion to the net, but also hinder them from suicide. Stem cells will tend to kill themselves when they are detached and free floating.

The cells and chemical components are mixed in solution then applied to the muscle that has been injured. The mixture sets to a matrix gel patch which glues the stem cells in place. The gel is biodegradable and biocompatible. The stem cells thrive and multiply in the gel once it has been applied. The hydrogel then degrades and leaves behind the cells engrafted onto muscle tissue in much the same way natural stem cells would be.

In healthier, younger individuals MuSCs are part of the natural healing mechanism in the body. MuSCs are resident stem cells found in the skeletal muscles. They are key players in producing new muscle tissue and live on muscle strands like specks.

As people age they lose muscle mass and the number of satellite cells will also decrease. The ones that do remain get weaker. At very advanced age, a person stops regenerating muscle altogether.

With the new system the researchers engineered, donor cells can be introduced to enhance the repair mechanism in older, injured people. If the new method goes to clinical trials, researchers will most likely have to work around the possibility for donor cell rejection in human patients.

To view the original scientific study click here: Synthetic matrix enhances transplanted satellite cell engraftment in dystrophic and aged skeletal muscle with comorbid trauma

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