StemCell Therapy

(EnviroNews World News) Kobe, Japan For more than two million Americans, straight lines may look wavy and the vision in the center of their eye may slowly disappear. Its called age-related macular degeneration (AMD), and there is no cure. But that may change soon.

A surgical team at Kobe City Medical Center General Hospital in Japan recently injected 250,000 retinal pigment epithelial (RPE) cells into the right eye of a man in his 60s. The cells were derived from donor stem cells stored at Kyoto University. It marked the first time that retinal cells derived from a donors skin have been implanted in a patients eye. The skin cells had been reprogrammed into induced pluripotent stem cells (iPS), which can be grown into most cell types in the body.

The procedure is part of a safety study authorized by Japans Ministry of Health that will involve five patients. Each will be followed closely for one year and continue to receive follow-up exams for three additional years. Project leader Dr. Masayo Takahashi at Riken, a research institution that is part of the study, told the Japan Times, A key challenge in this case is to control rejection. We need to carefully continue treatment.

A previous procedure on a different patient in 2014 used stem cells from the individuals own skin. Two years later, the patient reported showing some improvement in eyesight. But the procedure cost $900,000, leading the study team to move forward using donor cells. They expect the costs to come down to less than $200,000.

Among people over 50 in developed countries, AMD is the leading cause of vision loss. According to the National Eye Institute, 14 percent of white Americans age 80 or older will suffer some form of AMD. The condition is almost three times more common among white adults than among people of color. Women of all races comprise 65 percent of AMD cases.

The lack of a cure has led some to try unproven treatments. Three elderly women lost their sight after paying $5,000 each for a stem cell procedure at a private clinic in Florida. Clinic staff used liposuction to remove fat from the womens bellies. They then extracted stem cells from the fat, which were injected into both eyes of each patient in the same procedure, resulting in vision loss in both eyes. Two of the three victims agreed to a lawsuit settlement with the company that owned the clinic.

Stem cell therapy is still at an early stage. As of January 2016, 10 clinical uses have been approved around the world, all using adult stem cells. These include some forms of leukemia and bone marrow disease, Hodgkin and non-Hodgkin lymphoma and some rare inherited disorders including sickle cell anemia. Stem cell transplants are now often used to treat multiple myeloma, which strikes more than 24,000 people a year in the U.S.

Clinical trials to treat type 1 diabetes, Parkinsons disease, stroke, brain tumors and other conditions are being conducted. The first patient in a nationwide clinical study to receive stem cell therapy for heart failure recently underwent the procedure at the University of Wisconsin School of Medicine and Public Health. An experimental treatment at Keck Medical Center of USC last year on a paralyzed patient restored the 21-year-old mans use of his arms and hands. Harvard scientists see stem cell biology as a path to counter aging and extend human lifespans. But the International Society for Stem Cell Research warns that there are many challenges ahead before these treatments are proven safe and effective.

The U.S. Food and Drug Administration (FDA) regulates stem cells to ensure that they are safe and effective for their intended use. But, that doesnt stop some clinics from preying on worried patients. The FDA warns on its website that the hope that patients have for cures not yet available may leave them vulnerable to unscrupulous providers of stem cell treatments that are illegal and potentially harmful.

While there is yet no magic cure for AMD, the Japan study and others may one day lead there. The Harvard Stem Cell Institute (HSCI) in Boston is currently researching retina stem cell transplants. One approach uses gene therapy to generate a molecule that preserves healthy vision. Another involves Muller cells, which give fish the ability to repair an injured retina.

But these therapies are far off. We are at about the halfway mark, but there is still a precipitous path ahead of us, Takahashi said.

Originally posted here:
World's 1st Stem Cell Transplant from Donor to Man's Eye Shows Promise of Restoring Sight - EnviroNews (registration) (blog)

An adult stem cell is thought to be an undifferentiated cell, found among differentiated cells in a tissue or organ. The adult stem cell can renew itself and can differentiate to yield some or all of the major specialized cell types of the tissue or organ. The primary roles of adult stem cells in a living organism are to maintain and repair the tissue in which they are found. Scientists also use the term somatic stem cell instead of adult stem cell, where somatic refers to cells of the body (not the germ cells, sperm or eggs). Unlike embryonic stem cells, which are defined by their origin (cells from the preimplantation-stage embryo), the origin of adult stem cells in some mature tissues is still under investigation.

Research on adult stem cells has generated a great deal of excitement. Scientists have found adult stem cells in many more tissues than they once thought possible. This finding has led researchers and clinicians to ask whether adult stem cells could be used for transplants. In fact, adult hematopoietic, or blood-forming, stem cells from bone marrow have been used in transplants for more than 40 years. Scientists now have evidence that stem cells exist in the brain and the heart, two locations where adult stem cells were not at firstexpected to reside. If the differentiation of adult stem cells can be controlled in the laboratory, these cells may become the basis of transplantation-based therapies.

The history of research on adult stem cells began more than 60 years ago. In the 1950s, researchers discovered that the bone marrow contains at least two kinds of stem cells. One population, called hematopoietic stem cells, forms all the types of blood cells in the body. A second population, called bone marrow stromal stem cells (also called mesenchymal stem cells, or skeletal stem cells by some), were discovered a few years later. These non-hematopoietic stem cells make up a small proportion of the stromal cell population in the bone marrow and can generate bone, cartilage, and fat cells that support the formation of blood and fibrous connective tissue.

In the 1960s, scientists who were studying rats discovered two regions of the brain that contained dividing cells that ultimately become nerve cells. Despite these reports, most scientists believed that the adult brain could not generate new nerve cells. It was not until the 1990s that scientists agreed that the adult brain does contain stem cells that are able to generate the brain's three major cell typesastrocytes and oligodendrocytes, which are non-neuronal cells, and neurons, or nerve cells.

Adult stem cells have been identified in many organs and tissues, including brain, bone marrow, peripheral blood, blood vessels, skeletal muscle, skin, teeth, heart, gut, liver, ovarian epithelium, and testis. They are thought to reside in a specific area of each tissue (called a "stem cell niche"). In many tissues, current evidence suggests that some types of stem cells are pericytes, cells that compose the outermost layer of small blood vessels. Stem cells may remain quiescent (non-dividing) for long periods of time until they are activated by a normal need for more cells to maintain tissues, or by disease or tissue injury.

Typically, there is a very small number of stem cells in each tissue and, once removed from the body, their capacity to divide is limited, making generation of large quantities of stem cells difficult. Scientists in many laboratories are trying to find better ways to grow large quantities of adult stem cells in cell culture and to manipulate them to generate specific cell types so they can be used to treat injury or disease. Some examples of potential treatments include regenerating bone using cells derived from bone marrow stroma, developing insulin-producing cells for type1 diabetes, and repairing damaged heart muscle following a heart attack with cardiac muscle cells.

Scientists often use one or more of the following methods to identify adult stem cells: (1) label the cells in a living tissue with molecular markers and then determine the specialized cell types they generate; (2) remove the cells from a living animal, label them in cell culture, and transplant them back into another animal to determine whether the cells replace (or "repopulate") their tissue of origin.

Importantly, scientists must demonstrate that a single adult stem cell can generate a line of genetically identical cells that then gives rise to all the appropriate differentiated cell types of the tissue. To confirm experimentally that a putative adult stem cell is indeed a stem cell, scientists tend to show either that the cell can give rise to these genetically identical cells in culture, and/or that a purified population of these candidate stem cells can repopulate or reform the tissue after transplant into an animal.

As indicated above, scientists have reported that adult stem cells occur in many tissues and that they enter normal differentiation pathways to form the specialized cell types of the tissue in which they reside.

Normal differentiation pathways of adult stem cells. In a living animal, adult stem cells are available to divide for a long period, when needed, and can give rise to mature cell types that have characteristic shapes and specialized structures and functions of a particular tissue. The following are examples of differentiation pathways of adult stem cells (Figure 2) that have been demonstrated in vitro or in vivo.

Figure 2. Hematopoietic and stromal stem cell differentiation. Click here for larger image. ( 2008 Terese Winslow)

Transdifferentiation. A number of experiments have reported that certain adult stem cell types can differentiate into cell types seen in organs or tissues other than those expected from the cells' predicted lineage (i.e., brain stem cells that differentiate into blood cells or blood-forming cells that differentiate into cardiac muscle cells, and so forth). This reported phenomenon is called transdifferentiation.

Although isolated instances of transdifferentiation have been observed in some vertebrate species, whether this phenomenon actually occurs in humans is under debate by the scientific community. Instead of transdifferentiation, the observed instances may involve fusion of a donor cell with a recipient cell. Another possibility is that transplanted stem cells are secreting factors that encourage the recipient's own stem cells to begin the repair process. Even when transdifferentiation has been detected, only a very small percentage of cells undergo the process.

In a variation of transdifferentiation experiments, scientists have recently demonstrated that certain adult cell types can be "reprogrammed" into other cell types in vivo using a well-controlled process of genetic modification (see Section VI for a discussion of the principles of reprogramming). This strategy may offer a way to reprogram available cells into other cell types that have been lost or damaged due to disease. For example, one recent experiment shows how pancreatic beta cells, the insulin-producing cells that are lost or damaged in diabetes, could possibly be created by reprogramming other pancreatic cells. By "re-starting" expression of three critical beta cell genes in differentiated adult pancreatic exocrine cells, researchers were able to create beta cell-like cells that can secrete insulin. The reprogrammed cells were similar to beta cells in appearance, size, and shape; expressed genes characteristic of beta cells; and were able to partially restore blood sugar regulation in mice whose own beta cells had been chemically destroyed. While not transdifferentiation by definition, this method for reprogramming adult cells may be used as a model for directly reprogramming other adult cell types.

In addition to reprogramming cells to become a specific cell type, it is now possible to reprogram adult somatic cells to become like embryonic stem cells (induced pluripotent stem cells, iPSCs) through the introduction of embryonic genes. Thus, a source of cells can be generated that are specific to the donor, thereby increasing the chance of compatibility if such cells were to be used for tissue regeneration. However, like embryonic stem cells, determination of the methods by which iPSCs can be completely and reproducibly committed to appropriate cell lineages is still under investigation.

Many important questions about adult stem cells remain to be answered. They include:

Previous|IV. What are adult stem cells?|Next

More here:
Stem Cell Basics IV. | stemcells.nih.gov

As we age, our bodies go through a lot of changes and decline as time passes. Unfortunately, our cells healing abilities go down as well. If only it was easy to fix with glue or adhesive tape, right? There is, however, an investigational study for fat stem cell therapy being conducted by Innovations Medical to help us out of this predicament. Dr. Johnson talks about it in this video.

According to Dr. Johnson, a stem cell is a single cell that can replicate itself or differentiate into many cell types. The embryo is actually composed of stem cells that end up becoming the tissues and organs in our bodies. Every time our body needs a new cell, its the stem cells role to do that. Their ability to self-renew is very important in the healing process of our bodies. As we age, we lose a good supply of stem cells and that is where fat stem cell therapy comes in. It harnesses the stem cells ability to self-multiply and deliver to a part of our body that doesnt heal well.

It is quite surprising, but stem cells have been used for treatment for thirty (30) years already. The bone marrow transplants in the 1980s that treat patients with cancers and other problems use a similar technique. Dr. Johnson says that what they did at the time though, was to give a lot of bone marrow cells. And the stem cells within the bone marrow are what made the procedure work. With the advancement of the procedure through research, it is now known that you dont have to go to the bone marrow alone. Fat, which is easily harvested, is proven to contain more stem cells than the bone marrow.

When asked about the stem cell harvesting method, Dr. Johnson explained that the procedure does not take that long. The fat, where the stem cells are coming from, is harvested through liposuction. About three tablespoons of fat will be acquired and it would take at least an hour to get the stem cells out of it. After that, taking it back into the body can be done in a number of ways.

Whats great about the fat stem cell therapy is how wide the possibilities are in treating many diseases. Orthopedic conditions like arthritis can be treated using this procedure. Even though there is still a small number of long-term data, there are already cases where people avoid having knee surgery or knee replacement, because of fat stem cell therapy.

Neuropathy is another condition that is being explored as well. Dr. Johnson says that most of the time, what you can only do is mask the patients pain, but the nerves functions are hard to restore. With the help of stem cells, there can be real improvement in relieving pain and restoring the nerves functions. He also mentioned how stem cell therapy can help calm down the Trigeminal Neuralgia or severe facial pain condition.

Here are some other diseases with SVF Deployment protocols:

Presently, Innovations Medical is still on the investigational status so insurance firms are not yet covering this type of procedure. But Dr. Johnson says that they are collecting very good data and getting better with the procedure.

Have questions?

Email us at questions@innovationsmedical.com with any questions that you may have or if you want to know what special offers that Innovations Medical may have regarding fat transfer, liposuction and their other cosmetic procedures. Contact our Dallas branch at 214-420-7970.

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Many people opt for low-calorie sweeteners as a "healthful" alternative to sugar, but a new study suggests that they may not be so beneficial after all. Researchers have found that consuming high amounts of low-calorie sweeteners may promote fat formation, particularly for individuals who are already obese.

Principal study investigator Dr. Sabyasachi Sen, of George Washington University in Washington, D.C., and colleagues reached their findings by analyzing the effects of sucralose on stem cells derived from human fat tissue, as well as on abdominal fat samples.

The researchers recently presented their findings at ENDO 2017 - the 99th annual meeting of the Endocrine Society, held in Orlando, FL.

Sucralose is a zero-calorie, artificial sweetener that is up to 650 times sweeter than sugar. It is used as a sugar substitute in a wide variety of products, including diet sodas, table-top sweeteners (such as Splenda), baking mixes, gum, breakfast cereals, and even salad dressings.

Given the widely documented health implications of sugar consumption, an increasing number of people are turning to products containing sucralose and other artificial sweeteners, with the view that they are better for health.

"However, there is increasing scientific evidence that these sweeteners promote metabolic dysfunction," notes Dr. Sen.

For their study, the researchers sought to gain a better understanding of how low-calorie sweeteners affect the body's metabolism at a cellular level.

Firstly, Dr. Sen and team applied sucralose to stem cells derived from human fat tissue.

The stem cells were exposed to the artificial sweetener for a total of 12 days at a dose of 0.2 millimolars - a dose comparable to the blood concentration of people who drink around four cans of diet soda daily.

The researchers found that the stem cells showed an increase in the expression of genes that are indicators of fat production and inflammation. Additionally, the stem cells demonstrated an increase in the accumulation of fat droplets, especially when exposed to a higher sucralose dose of 1 millimolar.

Next, the researchers took biopsies of abdominal fat from eight adults, of whom four were obese and four were a healthy weight. All adults reported consuming low-calorie sweeteners, primarily sucralose and aspartame.

Abdominal fat samples were then compared with samples taken from adults who did not consume low-calorie sweeteners.

The team found that adults who consumed low-calorie sweeteners not only showed an increase in the transportation of glucose into cells, but they also demonstrated an overexpression of genes associated with fat production.

Furthermore, the researchers identified an overexpression of sweet taste receptors that was up to 2.5 times higher among the fat samples of adults who consumed low-calorie sweeteners. Such overexpression may play a part in the transportation of glucose into cells. From there, glucose is absorbed into the bloodstream.

The effects of low-calorie sweeteners were strongest among adults who were obese, the team notes.

Taken together, Dr. Sen and colleagues say that their findings indicate that low-calorie sweeteners may dysregulate the metabolism in a way that boosts the formation of fat.

The increase in transportation of glucose into cells may be of particular concern for adults who have prediabetes or diabetes, the researchers note, as these individuals already have higher levels of blood glucose.

Still, the researchers caution that further studies are required in larger samples of people before any concrete conclusions can be made about the effects of low-calorie sweeteners on metabolism.

"However, from our study, we believe that low-calorie sweeteners promote additional fat formation by allowing more glucose to enter the cells, and promotes inflammation, which may be more detrimental in obese individuals."

Dr. Sabyasachi Sen

Learn about the link between artificial sweetener aspartame and weight gain.

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Low-calorie sweeteners increase fat formation, study finds - Medical ... - Medical News Today

April 5, 2017 Stem cells (red) on polycaprolactone-based microcarriers. Credit: Elsevier

Bone tissue engineering is theoretically now possible at a large scale. A*STAR researchers have developed small biodegradable and biocompatible supports that aid stem cell differentiation and multiplication as well as bone formation in living animal models.

Mesenchymal stem cells self-renew and differentiate into fat, muscle, bone, and cartilage cells, which makes them attractive for organ repair and regeneration. These stem cells can be isolated from different sources, such as the human placenta and fatty tissue. Human early mesenchymal stem cells (heMSCs), which are derived from fetal bone marrow, were thought to be best suited for bone healing, but were not readily accessible for therapeutic use.

Existing approaches to expand stem cells for industrial applications tend to use two-dimensional materials as culture media, but their production yields are too low for clinical demand. Furthermore, stem cells typically need to be harvested with enzymes and attached to a scaffold before they can be implanted.

To bring commercially viable cell therapies to market, Asha Shekaran and Steve Oh, from the A*STAR Bioprocessing Technology Institute, have created directly implantable microscopic spheres in collaboration with the A*STAR Institute of Materials Research and Engineering. These spheres, which acted as heMSC microcarriers, consist of a biodegradable and biocompatible polymer called polycaprolactone.

According to Shekaran, their initial aim was to expand stem cells on microcarriers in bioreactors to scale up production. However, this strategy threw up difficulties, especially when attempting to effectively dissociate the cells from the microcarriers and transfer them to biodegradable scaffolds for implantation.

"A biodegradable microcarrier would have a dual purpose," Shekaran says, noting that it could potentially provide a substrate for cell attachment during scalable expansion in bioreactors, and a porous scaffold for cell delivery during implantation.

The researchers generated their microcarriers by synthesizing polycaprolactone spheres and coating them with two proteins polylysine and fibronectin. These proteins are found in the extracellular matrix that assists cell adhesion, growth, proliferation, and differentiation in the body.

Microcarriers that most induced cell attachment also promoted cell differentiation into bone-like matrix more strongly than conventional two-dimensional supports. In addition, implanted stem cells grown on these microcarriers produced an equivalent amount of bone to their conventionally-derived analogs.

"This is encouraging because microcarrier-based expansion and delivery are more scalable than two-dimensional culture methods," says Shekaran.

The team now plans to further investigate the therapeutic potential of these microcarrierstem cell assemblies in actual bone healing models.

Explore further: Study shows adipose stem cells may be the cell of choice for therapeutic applications

More information: Asha Shekaran et al. Biodegradable ECM-coated PCL microcarriers support scalable human early MSC expansion and in vivo bone formation, Cytotherapy (2016). DOI: 10.1016/j.jcyt.2016.06.016

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What Really Goes on When We "Burn Fat"? POPSUGAR Health and Fitness Australia In scientific terms, fat cells are known as adipocytyes, and everyone is born with a set number of them in their body. However over time, new cells have the ability to form from what's known as adipocyte precursor cells stem cell-like cells that can ...

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It might not seem to make sense, but consuming a lot of low-calorie, artificial sweetener could cause your body to accumulate more fat.

It might even accelerate fat formation in people who are obese, who are using artificial sweeteners in an effort to lose weight. Researchers who reached that conclusion presented their findings this week at the annual meeting of the Endocrine Society.

Many health-conscious individuals like to consume low-calorie sweeteners as an alternative to sugar. However, there is increasing scientific evidence that these sweeteners promote metabolic dysfunction, said Dr. Sabyasachi Sen, an Associate Professor of Medicine and Endocrinology at George Washington University, and the studys principal investigator.

Here's how Sen and his colleagues arrived at their conclusions: using sucralose, a widely-avaailable low-calorie sweetener, they introduced it to stem cells that could turn into fat, muscle, cartilage, or bone cells. The amount of sucralose was about equal to about four cans of diet soda per day. Then, they sat back at waited.

They observed an increase in the expression of genes that are markers of fat and inflammation. Sen says there was also an increase in fat droplets in the cells.

Artificial sweeteners, of course, are supposed to prevent you from getting fat. But the scientists say they found signs of metabolic dysregulation, a process in which cells actually changed to produce more fat.

Sen said he is most concerned because this was most evident in people who were already obese. They tended to produce more fat with artificial sweeteners than people who were of normal weight.

He's also concerned by the increase in glucose into the cells for consumers who have prediabetes, or who have already developed the disease.

From our study, we believe that low-calorie sweeteners promote additional fat formation by allowing more glucose to enter the cells, and promotes inflammation, which may be more detrimental in obese individuals, Sen said.

There have been other studies that suggest artificial sweeteners can have the opposite effect than intended. Last year, researchers at York University reported that obese people who consumed lot of artificial sweeteners had a harder time managing their glucose production.

The research team said it did not find this adverse effect in people consuming saccharin an early artificial sweetener or natural sugars.

Read more from the original source:
Researchers say some artificial sweeteners could promote fat ... - ConsumerAffairs

Stem cells collected from human fat may have the potential for use in anti-ageing treatments, as they are more stable than fibroblasts from the skin, scientists have found.

Researchers developed a new model to study chronological ageing of fat cells.

Chronological ageing shows the natural life cycle of the cells - as opposed to cells that have been unnaturally replicated multiple times or otherwise manipulated in a lab.

In order to preserve the cells in their natural state, researchers from the University of Pennsylvania in the US developed a system to collect and store them without manipulating them, making them available for this study.

They found stem cells collected directly from human fat - called adipose-derived stem cells (ASCs) - can make more proteins than originally thought.

This gives them the ability to replicate and maintain their stability, a finding that held true in cells collected from patients of all ages.

"Our study shows these cells are very robust, even when they are collected from older patients," said Ivona Percec, from University of Pennsylvania.

"It also shows these cells can be potentially used safely in the future, because they require minimal manipulation and maintenance," said Percec.

Stem cells are currently used in a variety of anti-ageing treatments and are commonly collected from a variety of tissues.

However, researchers specifically found ASCs to be more stable than other cells, a finding that can potentially open the door to new therapies for the prevention and treatment of ageing-related diseases.

"Unlike other adult human stem cells, the rate at which these ASCs multiply stays consistent with age," Percec said.

"That means these cells could be far more stable and helpful as we continue to study natural ageing," he said.

The research was published in the journal Stem Cells.

(This story has not been edited by Business Standard staff and is auto-generated from a syndicated feed.)

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'Stem cells from fat may have use in anti-ageing treatments' - Business Standard

UPI.com

Stem cells collected from fat may have use in anti-aging treatments Science Daily Adult stem cells collected directly from human fat are more stable than other cells -- such as fibroblasts from the skin -- and have the potential for use in anti-aging treatments, according to researchers from the Perelman School of Medicine at the ... Stem cells from fat could be used in anti-aging treatmentsUPI.com all 2 news articles »

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Stem cells collected from fat may have use in anti-aging treatments - Science Daily

Korea's aesthetic procedures have become a big export. Some are innovative, some are questionable. Local doctors discuss their merit and the alternatives.

What

Use your stem cells to generate new cells for brighter, firmer and younger-looking skin with improved elasticity and diminished fine lines and wrinkles.

How

There are two ways: Extract the cells from the bone marrow or from abdominal and thigh fat, using syringes.

The materials are processed and purified to separate the stem cells from the other stuff.

Sometimes, the stem cells may be further cultured to increase their numbers.

The concentrate is then injected into the targeted area.

In South Korea, fat-derived stem cells are injected on the same day while bone marrow-derived ones are injected after a four-week culture, said Dr Kim Byung Gun, a plastic surgeon and director of BK Plastic Surgery Hospital in Seoul.

Local doctors say

Stem-cell therapy is not available in Singapore except in clinical trials approved by the Ministry of Health (MOH).

It is not offered for aesthetic purposes.

In its stead, Dr Low Chai Ling, medical director of The Sloane Clinic, recommended treatments using the fractional CO2 laser.

Compared with other lasers, it reaches deeper into the skin where the collagen fibres are, to immediately tighten skin and boost collagen production over the next few months.

Its depth also enables more effective treatment of deep-set wrinkles and scars.

What

Inject your own blood platelets, which have proteins known as growth factors that contribute to wound healing.

This supposedly enhances the skin's repair process, thereby treating fine lines and wrinkles for a fresher, smoother complexion with fewer blemishes. The jury is still out on the effectiveness of PRP therapy, but that hasn't detracted from its popularity in Korea.

"Koreans are more willing to try new things earlier than others," said Dr Kim.

How

About 10ml of blood is taken from the patient and placed in a centrifuge, which separates the platelets from the rest of the blood. The platelet concentrate is then injected into the face.

According to Dr Kim, who offers PRP therapy in his Seoul clinic, patients can expect to see improvements after several days, with results lasting between six and 12 months.

Local doctors say

Like stem-cell therapy, PRP therapy is available here only in clinical trials approved by the MOH. Otherwise, it is mainly used in orthopaedic clinics to aid in the recovery of sprains and muscle tears.

Dr Low suggested an alternative, Sculptra, an injectable made from poly-L-lactic acid, which encourages collagen production.

Unlike hyaluronic acid fillers that create immediate volume to give the treated areas a supple appearance, Sculptra works gradually over a few months, reducing the severity of wrinkles and restoring facial contours as collagen levels increase.

This article is adapted from the February issue of Her World magazine.

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Health Beat: Stem cells treat...

LOS ANGELES - Roy Woelke knows how overwhelming hair loss can be.

"It's been 30 years of concern," Woelke said. "I noticed thinning in my late 20s, and it never stops. It seems like it just goes on and on."

Woelke has had three hair replacement surgeries, but that's really just moving hair around the head and, as he said, you run out of supply.

Dr. Kenneth Williams, a hair restoration surgeon at Orange County Hair Restoration in Los Angeles, may have new hope for Woelke and millions of others. He's running a clinical trial that uses stem cells and platelet-rich plasma, or PRP, to treat baldness.

"The study is taking cells that are in our body that help to regenerate or stimulate inactive or dormant hair follicles. That is the theory behind what we're doing this procedure on," Williams explained.

Williams takes fat from the abdomen, emulsifies it and separates the stem cells, mixes it with the patient's own plasma, which has been spun down to be super concentrated. Then, with 300 shots, he injects the mixture into the scalp, twice over a three-month period.

Woelke said he hopes to get into the trial, which has five participants so far. Williams already does the procedure for paying patients who've had promising results.

Research summary - Stem cells treat baldness

"Those patients are seeing some differences in the density of the hair," Williams said. "We're waiting for the final results, which take nine to 12 months after the administration. We look to see the final results of what we're doing."

Williams hopes to publish results in two years.

Williams' trial is supported by National Institutes of Health, but not by a major pharmaceutical company yet. That means his trial is patient-funded, meaning they'll pay a reduced cost of the $2,500 to $5,800 procedure, depending on which arm of the trial is chosen.

Contact the Irvine Institute of Medicine and Cosmetic Surgery at 949-333-2999 or visit straandstudy.com for more information.

Original post:
Health Beat: Stem cells treat baldness with PRP - WFMZ Allentown

Americans spend between one and four billion dollars a year treating hair loss.

Now, four surgeons in the U.S. are testing a stem cell treatment in a non-surgical procedure.

Overseas trials in Japan and Egypt are already showing some success.

Its been 30 years of concern, Roy Woelke said.

Woelke knows how overwhelming hair loss can be.

I noticed thinning in my late twenties, and it never stops. It seems like it just goes on and on, Woelke detailed.

Hes had three hair replacement surgeries, but thats really just moving hair around the head, and as he says, you run out of supply.

Kenneth Williams, D.O., a hair restoration surgeon at Orange County Hair Restoration in Los Angeles, California, may have new hope for Woelke and millions of others.

Hes running a clinical trial that uses stem cells and platelet-rich plasma, or PRP, to treat baldness.

The study is taking cells that are in our body that help to regenerate or stimulate inactive or dormant hair follicles," Williams explained. "That is the theory behind what were doing this procedure on.

Williams takes fat from the abdomen, emulsifies it and separates the stem cells, mixes it with the patients own plasma which has been spun down to be super concentrated. Then with 300 shots, injects the mixture into the scalp, twice over a three-month period.

Woelke hopes to get into the trial, which has five participants so far.

Williams already does the procedure for paying patients whove had promising results.

Those patients are seeing some differences in the density of the hair," Williams said. "Were waiting for the final results, which take nine to 12 months after the administration. We look to see the final results of what were doing.

He hopes to publish results in two years.

Williams trial is supported by NIH, but not by a major pharmaceutical company yet. That means his trial is patient-funded, meaning theyll pay a reduced cost of the $2,500 to $5,800 procedure, depending on which arm of the trial is chosen.

Contact the Irvine Institute of Medicine and Cosmetic Surgery at (949) 333-2999 or visit http://www.straandstudy.com for more information.

Published at 5:46 PM CST on Feb 17, 2017 | Updated at 5:50 PM CST on Feb 17, 2017

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Stem Cells Treat Baldness with PRP | NBC 5 Dallas-Fort Worth - NBC 5 Dallas-Fort Worth

The Conversation AU

Yes there's hope, but treating spinal injuries with stem cells is not a ... The Conversation AU Claims that stem cell treatments can repair spinal injuries right now are overblown. But it's not for lack of trying, and the science is certainly progressing. and more »

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A new clinical study is offering hope for folks who suffer from hair loss. The treatment: stem cells.

Americans spend between one and four billion dollars a year treating hair loss. It's a problem that affects around 56 million people in this country. Now, four surgeons in the U.S. are testing a stem cell treatment in a non-surgical procedure, and overseas trials in Japan and Egypt are already showing some success.

Roy Woelke knows how overwhelming hair loss can be. He's been dealing with it for 30 years.

I noticed thinning in my late 20s, and it never stops. It seems like it just goes on and on, he said.

Hes had three hair replacement surgeries, but thats really just moving hair around the head, and as he says, you run out of supply. Dr. Kenneth Williams may have new hope for Roy and millions of others. Hes running a clinical trial that uses stem cells and platelet-rich plasma, or PRP, to treat baldness.

The study is taking cells that are in our body that help to regenerate or stimulate inactive or dormant hair follicles. That is the theory behind what were doing this procedure on.

Doctor Williams takes fat from the abdomen, emulsifies it and separates the stem cells, mixes it with the patients own plasma which has been spun down to be super concentrated. Then with 300 shots, he injects the mixture into the scalp, twice over a three month period. Roy hopes to get into the trial, which has five participants so far. Dr. Williams already does the procedure for paying patients whove had promising results.

Those patients are seeing some differences in the density of the hair. Were waiting for the final results, which takes 9 to 12 months after the administration. We look to see the final results of what were doing," Dr. Williams explained.

Dr. Williams hopes to publish results in two years.

His trial is supported by National Institutes of Health, but not by a major pharmaceutical company yet. That means his trial is patient-funded, meaning theyll pay a reduced cost of the $2,500 to $5,800 procedure, depending on which arm of the trial is chosen.

-- Research Summary

Background: Around 70 percent of men and 40 percent of women are impacted by hair loss. Two- thirds of American men will suffer from some kind of hair loss by the age of 35. By the age of 50, 85 percent of American men will experience thinning of their hair. The process begins for 25 percent of men during their twenties, and even though it is a common process that occurs naturally, like aging, most men and women are unhappy and would do anything to fix or delay the process. Hair loss can occur for different reasons like disease, reaction to medications and stressful events; however, heredity is most often the cause of hair loss. (Source: http://www.americanhairloss.org/men_hair_loss/introduction.asp & http://www.straandstudy.com)

Treatments: American hair loss sufferers have spent around $3.5 billion combined in treatments. If a treatment is not FDA approved or recommended by the AHLA (American Hair Loss Association), it may not be a safe option for your scalp or hair. The key to treating hair loss or hair thinning is treating it early. The two popular options recommended by the AHLA are medication or surgery, like propecia, and/or surgical hair restoration. (Source: http://www.americanhairloss.org/men_hair_loss/treatment.asp)

Straand Study: Dr. Kenneth Williams is currently running a clinical trial that will hopefully help and delay hair loss. Unlike any other form of current treatment, Dr. Williams is focusing on stem cells and platelet-rich plasma, or PRP, to treat baldness. The study consists of taking stem cells that are already in the body to regenerate or stimulate inactive hair follicles. Studies show that stem cells residing in the scalp remain at recurrent numbers but in balding patients, the conversion of stem cells to progenitor cells required for follicle growth is reduced. The goal of this study is to stimulate hair to become active and to be able to grow again. In the non-surgical procedure, Dr. Williams takes fat from the abdomen of the patient. The stem cells are separated from the fat cells by emulsification. The stem cells are then mixed with the patients plasma and the mixture is injected 300 times into the scalp of the patient twice in the span of three months. With the current five participants in the study, the results have been very promising. The current trial is supported by National Institutes of Health and is patient-funded. For more information on the study or to become a participant, visit http://www.straandstudy.com. (Source: Dr. Kenneth Williams & http://www.straandstudy.com)

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In 2014, when Springer Publications published Stem Cells in Aesthetic Procedures, the first book ever published on the subject, Jacksonville physician Lewis Obi contributed a chapter, Specialized Stem Cell Fat Transfer to Face.

At places like the Mayo Clinic, researchers have been looking at the possibilities that stem cells could someday help repair damaged organs.

But Obi, a veteran plastic surgeon, already has been using stem cells, harvested from a patients own fat, in a number of procedures in recent years. He has become an ardent champion of the potential stem cells have in regenerative medicine. While stem cells extracted from bone marrow have been used in the past, Obi said there are actually more stem cells in fat than in bone marrow and they are easier to harvest

The current use of stem cells and the potential of stem cells will be the subject of a two day symposium by the Cell Surgical Network of Florida, an organization Obi founded. The symposium will be held Thursday and Friday at Memorial Hospital.

Presenters during the conference include three Jacksonville physicians, Obi, orthopedic surgeon David Heekin and anesthesiologist and pain management specialisit Orlando Florette. Heekin will talk about the orthopedic uses of stem cells and Florette will talk about the use of stem cells in pain management.

Another presenter will be Hee Young Lee, a Korean physician who invented Maxstem, a totally enclosed system which processes adult fat into large numbers of viable stem cells. Obi has used these cells in both his plastic surgery practice as well as in regenerative medicine.

Stuart Williams, a researcher with the University of Louisville, will discuss issues with the Food and Drug Administration, which has been reluctant to approve the use of stem cells to treat many conditions that stem cell advocates believe could be treated effectively with stem cells.

Mark Berman, co-author of the 2015 book The Stem Cell Revolution and co-founder of the Cell Surgical Network, the nations largest stem cell network, is scheduled to appear via Skype to talk about using stem cells to mitigate the effects of concussions.

Thursday will feature asesssions on preparing and storing stem cells and bioprinting. Friday will feature 12 presentations, the last being a panel discussion by nine faculty members.

For more about the conference and about the Cell Surgical Network of Florida, go to http://www.stemcellsurgeryflorida.com.

Charlie Patton: (904) 359-4413

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Over the past decade, studies have found that obesity and eating a high-fat, high-calorie diet are significant risk factors for many types of cancer.

Now, a study from MIT reveals how a high-fat diet makes the cells of the intestinal lining more likely to become cancerous.

The study of mice suggests that a high-fat diet drives a population boom of intestinal stem cells and also generates a pool of other cells that behave like stem cells.

This means they can reproduce themselves indefinitely and differentiate into other cell types.

These stem cells and stem-like cells are more likely to give rise to intestinal tumors, says Omer Yilmaz, an MIT assistant professor of biology and leader of the research team.

Not only does the high-fat diet change the biology of stem cells, it also changes the biology of non-stem-cell populations, which collectively leads to an increase in tumor formation, says Yilmaz, who is a member of MITs Koch Institute for Integrative Cancer Research and a gastrointestinal pathologist at Massachusetts General Hospital.

Under a high-fat diet, these non-stem cells acquire the properties of stem cells so that when they are transformed they become tumorigenic, says David Sabatini, an MIT professor of biology, member of the Whitehead Institute, and investigator with the Howard Hughes Medical Institute.

Sabatini and Yilmaz, who previously collaborated on research into the effects of caloric restriction on stem cell potential in the intestine, are the senior authors of the study, which appears in Nature.

Exploring cancer risk

People who are obese have a greater risk of developing colorectal cancer, according to previous studies.

Yilmaz lab, which studies the relationship between diet and cancer, set out to uncover the cellular mechanisms underpinning the enhanced risk of colon cancer.

Recent studies have shown that intestinal stem cells, which last a lifetime, are the cells most likely to accumulate the mutations that give rise to colon cancer.

These stem cells live in the lining of the intestine, known as the epithelium, and generate all of the different cell types that make up the epithelium.

To investigate a possible link between these stem cells and obesity-linked cancer, Yilmaz and colleagues fed healthy mice a diet made up of 60 percent fat for nine to 12 months.

This diet, Yilmaz noted, is much higher in fat than the typical American diet, which is usually about 20 to 40 percent fat.

During this period, the mice on the high-fat diet gained 30 to 50 percent more body mass than mice fed a normal diet, and they developed more intestinal tumors than mice on a normal diet.

These mice also showed some distinctive changes in their intestinal stem cells, the researchers discovered.

First, they found that the mice on a high-fat diet had many more intestinal stem cells than mice on a normal diet. These stem cells were also able to operate without input from neighboring cells.

Normally, intestinal stem cells are surrounded by support or niche cells, which regulate stem cell activity and tell them when to generate stem cells or differentiated cells.

However, the stem cells from mice on a high-fat diet were more able to function on their own;

when they were removed from the mice and grown in a culture dish without their niche cells, they gave rise to mini-intestines much more readily than intestinal stem cells from mice on a normal diet.

Expanding the pool

The researchers also found that another population known as progenitor cells differentiated daughter cells of stem cells started to behave like stem cells:

They began to live much longer than their usual lifespan of a few days, and they could also generate mini-intestines when grown outside of the body.

This is really important because its known that stem cells are often the cells in the intestine that acquire the mutations that go on to give rise to tumors, Yilmaz says.

Not only do you have more of the traditional stem cells (on a high-fat diet), but now you have non-stem-cell populations that have the ability to acquire mutations that give rise to tumors.

The researchers also identified a nutrient-sensing pathway that is hyperactivated by the high-fat diet.

The fatty acid sensor known as PPAR-delta responds to high levels of fat by turning on a metabolic process that enables cells to burn fat as an energy source instead of their usual carbohydrates and sugars.

Indeed, small-molecule agonists of PPAR-delta mimic the effects of a high-fat diet in animals fed a normal diet, Sabatini says.

In addition to activating this metabolic program, PPAR-delta also appears to turn on a set of genes that are important for stem cell identity, Yilmaz says.

His lab is now further investigating how this happens in hopes of identifying possible cancer drug targets for tumors that arise in obesity.

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Scientists have extracted stem cells from a 50-year-old test subjects fatty tissue and applied genetic reprogramming to make them mature into functional beta cells.

The feat brings them a step closer to a personalized repair kit for diabetes.

In the presence of glucose, the beta cells generated using this genetic software produce the hormone insulinjust like natural beta cells, which are found in the pancreas.

The researchers report the findings in Nature Communications.

The team, led by Martin Fussenegger, professor of biotechnology and bioengineering in ETH Zurichs department of biosystems science and engineering, took the stem cells and added a highly complex synthetic network of genesthe genetic software.

They designed this network to precisely recreate the key growth factors involved in this maturation process.

Central to the process are the growth factors Ngn3, Pdx1, and MafA. Concentrations of these factors change during the differentiation process. For instance, MafA is not present at the start of maturation.

Only on day four, in the final maturation step, does it appear, its concentration rising steeply and then remaining at a high level.

The changes in concentration of Ngn3 and Pdx1, however, are very complex: while the concentration of Ngn3 rises and then falls again, the level of Pdx1 rises at the beginning and towards the end of maturation.

Fussenegger stresses that it is essential to reproduce these natural processes as closely as possible in order to produce functioning beta cells: The timing and the quantities of these growth factors are extremely important.

In Fusseneggers opinion, it is a real breakthrough that a synthetic gene network has been successfully used to achieve genetic reprogramming that delivers beta cells.

Until now, scientists have controlled such stem cell differentiation processes by adding various chemicals and proteins using pipettes.

Its not only really hard to add just the right quantities of these components at just the right time, its also inefficient and impossible to scale up, Fussenegger says.

In contrast, the new process can successfully transform three out of four adipose stem cells into beta cells.

These beta cells look very similar to their natural counterpartsboth kinds contain dark spots known as granules, which store insulin. In addition, the artificial beta cells function in a very similar way.

At the present time, the quantities of insulin they secrete are not as great as with natural beta cells, he admits.

In the future, the new technique might make it possible to implant new functional beta cells in diabetes sufferers that are made from their own adipose tissue.

While beta cells have been transplanted in the past, this has always required subsequent suppression of the recipients immune systemas with any transplant of donor organs or tissue.

With our beta cells, there would likely be no need for this action, since we can make them using endogenous cell material taken from the patients own body, says Fussenegger.

This is why our work is of such interest in the treatment of diabetes.

To date, the ETH researchers have only cultured their beta cells; they have yet to implant them in someone with diabetes.

This is because they first wanted to test whether stem cells could be fully differentiated from start to finish using genetic programming.

Fussenegger is convinced that this new method could also be used to produce other cells.

Stem cells taken from adipose tissue could be differentiated into various cell types, he says, and most people have an overabundance of fat from which these stem cells can be harvested.

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No treatments using MSCs are yet available. However, several possibilities for their use in the clinic are currently being explored.

Bone and cartilage repair The ability of MSCs to differentiate into bone cells called osteoblasts has led to their use in early clinical trials investigating the safety of potential bone repair methods. These studies are looking at possible treatments for localized skeletal defects (damage at a particular place in the bone).

Other research is focussed on using MSCs to repair cartilage. Cartilage covers the ends of bones and allows one bone to slide over another at the joints. It can be damaged by a sudden injury like a fall, or over a long period by a condition like osteoarthritis, a very painful disease of the joints. Cartilage does not repair itself well after damage. The best treatment available for severe cartilage damage is surgery to replace the damaged joint with an artificial one. Because MSCs can differentiate into cartilage cells called chondrocytes, scientists hope MSCs could be injected into patients to repair and maintain the cartilage in their joints. Researchers are also investigating the possibility that transplanted MSCs may release substances that will tell the patients own cells to repair the damage.

Many hurdles remain before this kind of treatment can become a reality. For example, when MSCs are transplanted, most of them are rapidly removed from the body. Researchers are working on new techniques for transplanting the cells, such as developing three-dimensional structures or scaffolds that mimic the conditions in the part of the body where the cells are needed. These scaffolds will hold the cells and encourage them to differentiate into the desired cell type.

Heart and blood vessel repair Some studies in mice suggest that MSCs can promote formation of new blood vessels in a process called neovascularisation. MSCs do not make new blood vessel cells themselves, but they may help with neovascularisation in a number of ways. For example, they may release proteins that stimulate the growth of other cells called endothelial precursors cells that will develop to form the inner layer of blood vessels. They may also "guide" the assembly of new blood vessels from preexisting endothelial cells (those that line the blood vessel). Such studies on animals have led researchers to hope that MSCs may provide a way to repair the blood vessel damage linked to heart attacks or diseases such as critical limb ischaemia. A number of early stage clinical trials using MSCs in patients are currently underway but it is not yet clear whether the treatments will be effective.

Inflammatory and autoimmune diseases Several claims have been made that MSCs are able to avoid detection by the immune system and can be transplanted from one patient to another without risk of immune rejection by the body. However, these claims have not been confirmed by other studies. MSCs are rejected like any other "non-self" cell type. It has also been suggested that MSCs may be able to slow down the multiplication of immune cells in the body to reduce inflammation and help treat transplant rejection or autoimmune diseases. Again, this has yet to be proven and much more evidence is needed to establish whether MSCs could really be used for this kind of application.

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Muscle is a soft tissue found in most animals. Muscle cells contain protein filaments of actin and myosin that slide past one another, producing a contraction that changes both the length and the shape of the cell. Muscles function to produce force and motion. They are primarily responsible for maintaining and changing posture, locomotion, as well as movement of internal organs, such as the contraction of the heart and the movement of food through the digestive system via peristalsis.

Muscle tissues are derived from the mesodermal layer of embryonic germ cells in a process known as myogenesis. There are three types of muscle, skeletal or striated, cardiac, and smooth. Muscle action can be classified as being either voluntary or involuntary. Cardiac and smooth muscles contract without conscious thought and are termed involuntary, whereas the skeletal muscles contract upon command.[1] Skeletal muscles in turn can be divided into fast and slow twitch fibers.

Muscles are predominantly powered by the oxidation of fats and carbohydrates, but anaerobic chemical reactions are also used, particularly by fast twitch fibers. These chemical reactions produce adenosine triphosphate (ATP) molecules that are used to power the movement of the myosin heads.[2]

The term muscle is derived from the Latin musculus meaning "little mouse" perhaps because of the shape of certain muscles or because contracting muscles look like mice moving under the skin.[3][4]

The anatomy of muscles includes gross anatomy, which comprises all the muscles of an organism, and microanatomy, which comprises the structures of a single muscle.

Muscle tissue is a soft tissue, and is one of the four fundamental types of tissue present in animals. There are three types of muscle tissue recognized in vertebrates:

Cardiac and skeletal muscles are "striated" in that they contain sarcomeres that are packed into highly regular arrangements of bundles; the myofibrils of smooth muscle cells are not arranged in sarcomeres and so are not striated. While the sarcomeres in skeletal muscles are arranged in regular, parallel bundles, cardiac muscle sarcomeres connect at branching, irregular angles (called intercalated discs). Striated muscle contracts and relaxes in short, intense bursts, whereas smooth muscle sustains longer or even near-permanent contractions.

Skeletal (voluntary) muscle is further divided into two broad types: slow twitch and fast twitch:

The density of mammalian skeletal muscle tissue is about 1.06kg/liter.[8] This can be contrasted with the density of adipose tissue (fat), which is 0.9196kg/liter.[9] This makes muscle tissue approximately 15% denser than fat tissue.

All muscles are derived from paraxial mesoderm. The paraxial mesoderm is divided along the embryo's length into somites, corresponding to the segmentation of the body (most obviously seen in the vertebral column.[10] Each somite has 3 divisions, sclerotome (which forms vertebrae), dermatome (which forms skin), and myotome (which forms muscle). The myotome is divided into two sections, the epimere and hypomere, which form epaxial and hypaxial muscles, respectively. The only epaxial muscles in humans are the erector spinae and small intervertebral muscles, and are innervated by the dorsal rami of the spinal nerves. All other muscles, including those of the limbs are hypaxial, and inervated by the ventral rami of the spinal nerves.[10]

During development, myoblasts (muscle progenitor cells) either remain in the somite to form muscles associated with the vertebral column or migrate out into the body to form all other muscles. Myoblast migration is preceded by the formation of connective tissue frameworks, usually formed from the somatic lateral plate mesoderm. Myoblasts follow chemical signals to the appropriate locations, where they fuse into elongate skeletal muscle cells.[10]

Skeletal muscles are sheathed by a tough layer of connective tissue called the epimysium. The epimysium anchors muscle tissue to tendons at each end, where the epimysium becomes thicker and collagenous. It also protects muscles from friction against other muscles and bones. Within the epimysium are multiple bundles called fascicles, each of which contains 10 to 100 or more muscle fibers collectively sheathed by a perimysium. Besides surrounding each fascicle, the perimysium is a pathway for nerves and the flow of blood within the muscle. The threadlike muscle fibers are the individual muscle cells (myocytes), and each cell is encased within its own endomysium of collagen fibers. Thus, the overall muscle consists of fibers (cells) that are bundled into fascicles, which are themselves grouped together to form muscles. At each level of bundling, a collagenous membrane surrounds the bundle, and these membranes support muscle function both by resisting passive stretching of the tissue and by distributing forces applied to the muscle.[11] Scattered throughout the muscles are muscle spindles that provide sensory feedback information to the central nervous system. (This grouping structure is analogous to the organization of nerves which uses epineurium, perineurium, and endoneurium).

This same bundles-within-bundles structure is replicated within the muscle cells. Within the cells of the muscle are myofibrils, which themselves are bundles of protein filaments. The term "myofibril" should not be confused with "myofiber", which is a simply another name for a muscle cell. Myofibrils are complex strands of several kinds of protein filaments organized together into repeating units called sarcomeres. The striated appearance of both skeletal and cardiac muscle results from the regular pattern of sarcomeres within their cells. Although both of these types of muscle contain sarcomeres, the fibers in cardiac muscle are typically branched to form a network. Cardiac muscle fibers are interconnected by intercalated discs,[12] giving that tissue the appearance of a syncytium.

The filaments in a sarcomere are composed of actin and myosin.

The gross anatomy of a muscle is the most important indicator of its role in the body. There is an important distinction seen between pennate muscles and other muscles. In most muscles, all the fibers are oriented in the same direction, running in a line from the origin to the insertion. However, In pennate muscles, the individual fibers are oriented at an angle relative to the line of action, attaching to the origin and insertion tendons at each end. Because the contracting fibers are pulling at an angle to the overall action of the muscle, the change in length is smaller, but this same orientation allows for more fibers (thus more force) in a muscle of a given size. Pennate muscles are usually found where their length change is less important than maximum force, such as the rectus femoris.

Skeletal muscle is arranged in discrete muscles, an example of which is the biceps brachii (biceps). The tough, fibrous epimysium of skeletal muscle is both connected to and continuous with the tendons. In turn, the tendons connect to the periosteum layer surrounding the bones, permitting the transfer of force from the muscles to the skeleton. Together, these fibrous layers, along with tendons and ligaments, constitute the deep fascia of the body.

The muscular system consists of all the muscles present in a single body. There are approximately 650 skeletal muscles in the human body,[13] but an exact number is difficult to define. The difficulty lies partly in the fact that different sources group the muscles differently and partly in that some muscles, such as palmaris longus, are not always present.

A muscular slip is a narrow length of muscle that acts to augment a larger muscle or muscles.

The muscular system is one component of the musculoskeletal system, which includes not only the muscles but also the bones, joints, tendons, and other structures that permit movement.

The three types of muscle (skeletal, cardiac and smooth) have significant differences. However, all three use the movement of actin against myosin to create contraction. In skeletal muscle, contraction is stimulated by electrical impulses transmitted by the nerves, the motoneurons (motor nerves) in particular. Cardiac and smooth muscle contractions are stimulated by internal pacemaker cells which regularly contract, and propagate contractions to other muscle cells they are in contact with. All skeletal muscle and many smooth muscle contractions are facilitated by the neurotransmitter acetylcholine.

The action a muscle generates is determined by the origin and insertion locations. The cross-sectional area of a muscle (rather than volume or length) determines the amount of force it can generate by defining the number of "sarcomeres" which can operate in parallel. Each skeletal muscle contains long units called myofibrils, and each myofibril is a chain of sarcomeres. Since contraction occurs at the same time for all connected sarcomeres in a muscles cell, these chains of sarcomeres shorten together, thus shortening the muscle fiber, resulting in overall length change. [14]The amount of force applied to the external environment is determined by lever mechanics, specifically the ratio of in-lever to out-lever. For example, moving the insertion point of the biceps more distally on the radius (farther from the joint of rotation) would increase the force generated during flexion (and, as a result, the maximum weight lifted in this movement), but decrease the maximum speed of flexion. Moving the insertion point proximally (closer to the joint of rotation) would result in decreased force but increased velocity. This can be most easily seen by comparing the limb of a mole to a horse - in the former, the insertion point is positioned to maximize force (for digging), while in the latter, the insertion point is positioned to maximize speed (for running).

Muscular activity accounts for much of the body's energy consumption. All muscle cells produce adenosine triphosphate (ATP) molecules which are used to power the movement of the myosin heads. Muscles have a short-term store of energy in the form of creatine phosphate which is generated from ATP and can regenerate ATP when needed with creatine kinase. Muscles also keep a storage form of glucose in the form of glycogen. Glycogen can be rapidly converted to glucose when energy is required for sustained, powerful contractions. Within the voluntary skeletal muscles, the glucose molecule can be metabolized anaerobically in a process called glycolysis which produces two ATP and two lactic acid molecules in the process (note that in aerobic conditions, lactate is not formed; instead pyruvate is formed and transmitted through the citric acid cycle). Muscle cells also contain globules of fat, which are used for energy during aerobic exercise. The aerobic energy systems take longer to produce the ATP and reach peak efficiency, and requires many more biochemical steps, but produces significantly more ATP than anaerobic glycolysis. Cardiac muscle on the other hand, can readily consume any of the three macronutrients (protein, glucose and fat) aerobically without a 'warm up' period and always extracts the maximum ATP yield from any molecule involved. The heart, liver and red blood cells will also consume lactic acid produced and excreted by skeletal muscles during exercise.

At rest, skeletal muscle consumes 54.4 kJ/kg(13.0kcal/kg) per day. This is larger than adipose tissue (fat) at 18.8kJ/kg (4.5kcal/kg), and bone at 9.6kJ/kg (2.3kcal/kg).[15]

The efferent leg of the peripheral nervous system is responsible for conveying commands to the muscles and glands, and is ultimately responsible for voluntary movement. Nerves move muscles in response to voluntary and autonomic (involuntary) signals from the brain. Deep muscles, superficial muscles, muscles of the face and internal muscles all correspond with dedicated regions in the primary motor cortex of the brain, directly anterior to the central sulcus that divides the frontal and parietal lobes.

In addition, muscles react to reflexive nerve stimuli that do not always send signals all the way to the brain. In this case, the signal from the afferent fiber does not reach the brain, but produces the reflexive movement by direct connections with the efferent nerves in the spine. However, the majority of muscle activity is volitional, and the result of complex interactions between various areas of the brain.

Nerves that control skeletal muscles in mammals correspond with neuron groups along the primary motor cortex of the brain's cerebral cortex. Commands are routed though the basal ganglia and are modified by input from the cerebellum before being relayed through the pyramidal tract to the spinal cord and from there to the motor end plate at the muscles. Along the way, feedback, such as that of the extrapyramidal system contribute signals to influence muscle tone and response.

Deeper muscles such as those involved in posture often are controlled from nuclei in the brain stem and basal ganglia.

The afferent leg of the peripheral nervous system is responsible for conveying sensory information to the brain, primarily from the sense organs like the skin. In the muscles, the muscle spindles convey information about the degree of muscle length and stretch to the central nervous system to assist in maintaining posture and joint position. The sense of where our bodies are in space is called proprioception, the perception of body awareness. More easily demonstrated than explained, proprioception is the "unconscious" awareness of where the various regions of the body are located at any one time. This can be demonstrated by anyone closing their eyes and waving their hand around. Assuming proper proprioceptive function, at no time will the person lose awareness of where the hand actually is, even though it is not being detected by any of the other senses.

Several areas in the brain coordinate movement and position with the feedback information gained from proprioception. The cerebellum and red nucleus in particular continuously sample position against movement and make minor corrections to assure smooth motion.

The efficiency of human muscle has been measured (in the context of rowing and cycling) at 18% to 26%. The efficiency is defined as the ratio of mechanical work output to the total metabolic cost, as can be calculated from oxygen consumption. This low efficiency is the result of about 40% efficiency of generating ATP from food energy, losses in converting energy from ATP into mechanical work inside the muscle, and mechanical losses inside the body. The latter two losses are dependent on the type of exercise and the type of muscle fibers being used (fast-twitch or slow-twitch). For an overall efficiency of 20 percent, one watt of mechanical power is equivalent to 4.3 kcal per hour. For example, one manufacturer of rowing equipment calibrates its rowing ergometer to count burned calories as equal to four times the actual mechanical work, plus 300 kcal per hour,[16] this amounts to about 20 percent efficiency at 250 watts of mechanical output. The mechanical energy output of a cyclic contraction can depend upon many factors, including activation timing, muscle strain trajectory, and rates of force rise & decay. These can be synthesized experimentally using work loop analysis.

A display of "strength" (e.g. lifting a weight) is a result of three factors that overlap: physiological strength (muscle size, cross sectional area, available crossbridging, responses to training), neurological strength (how strong or weak is the signal that tells the muscle to contract), and mechanical strength (muscle's force angle on the lever, moment arm length, joint capabilities).

Vertebrate muscle typically produces approximately 2533N (5.67.4lbf) of force per square centimeter of muscle cross-sectional area when isometric and at optimal length.[17] Some invertebrate muscles, such as in crab claws, have much longer sarcomeres than vertebrates, resulting in many more sites for actin and myosin to bind and thus much greater force per square centimeter at the cost of much slower speed. The force generated by a contraction can be measured non-invasively using either mechanomyography or phonomyography, be measured in vivo using tendon strain (if a prominent tendon is present), or be measured directly using more invasive methods.

The strength of any given muscle, in terms of force exerted on the skeleton, depends upon length, shortening speed, cross sectional area, pennation, sarcomere length, myosin isoforms, and neural activation of motor units. Significant reductions in muscle strength can indicate underlying pathology, with the chart at right used as a guide.

Since three factors affect muscular strength simultaneously and muscles never work individually, it is misleading to compare strength in individual muscles, and state that one is the "strongest". But below are several muscles whose strength is noteworthy for different reasons.

Humans are genetically predisposed with a larger percentage of one type of muscle group over another. An individual born with a greater percentage of Type I muscle fibers would theoretically be more suited to endurance events, such as triathlons, distance running, and long cycling events, whereas a human born with a greater percentage of Type II muscle fibers would be more likely to excel at sprinting events such as 100 meter dash.[citation needed]

Exercise is often recommended as a means of improving motor skills, fitness, muscle and bone strength, and joint function. Exercise has several effects upon muscles, connective tissue, bone, and the nerves that stimulate the muscles. One such effect is muscle hypertrophy, an increase in size. This is used in bodybuilding.

Various exercises require a predominance of certain muscle fiber utilization over another. Aerobic exercise involves long, low levels of exertion in which the muscles are used at well below their maximal contraction strength for long periods of time (the most classic example being the marathon). Aerobic events, which rely primarily on the aerobic (with oxygen) system, use a higher percentage of Type I (or slow-twitch) muscle fibers, consume a mixture of fat, protein and carbohydrates for energy, consume large amounts of oxygen and produce little lactic acid. Anaerobic exercise involves short bursts of higher intensity contractions at a much greater percentage of their maximum contraction strength. Examples of anaerobic exercise include sprinting and weight lifting. The anaerobic energy delivery system uses predominantly Type II or fast-twitch muscle fibers, relies mainly on ATP or glucose for fuel, consumes relatively little oxygen, protein and fat, produces large amounts of lactic acid and can not be sustained for as long a period as aerobic exercise. Many exercises are partially aerobic and partially anaerobic; for example, soccer and rock climbing involve a combination of both.

The presence of lactic acid has an inhibitory effect on ATP generation within the muscle; though not producing fatigue, it can inhibit or even stop performance if the intracellular concentration becomes too high. However, long-term training causes neovascularization within the muscle, increasing the ability to move waste products out of the muscles and maintain contraction. Once moved out of muscles with high concentrations within the sarcomere, lactic acid can be used by other muscles or body tissues as a source of energy, or transported to the liver where it is converted back to pyruvate. In addition to increasing the level of lactic acid, strenuous exercise causes the loss of potassium ions in muscle and causing an increase in potassium ion concentrations close to the muscle fibres, in the interstitium. Acidification by lactic acid may allow recovery of force so that acidosis may protect against fatigue rather than being a cause of fatigue.[19]

Delayed onset muscle soreness is pain or discomfort that may be felt one to three days after exercising and generally subsides two to three days later. Once thought to be caused by lactic acid build-up, a more recent theory is that it is caused by tiny tears in the muscle fibers caused by eccentric contraction, or unaccustomed training levels. Since lactic acid disperses fairly rapidly, it could not explain pain experienced days after exercise.[20]

Independent of strength and performance measures, muscles can be induced to grow larger by a number of factors, including hormone signaling, developmental factors, strength training, and disease. Contrary to popular belief, the number of muscle fibres cannot be increased through exercise. Instead, muscles grow larger through a combination of muscle cell growth as new protein filaments are added along with additional mass provided by undifferentiated satellite cells alongside the existing muscle cells.[13]

Biological factors such as age and hormone levels can affect muscle hypertrophy. During puberty in males, hypertrophy occurs at an accelerated rate as the levels of growth-stimulating hormones produced by the body increase. Natural hypertrophy normally stops at full growth in the late teens. As testosterone is one of the body's major growth hormones, on average, men find hypertrophy much easier to achieve than women. Taking additional testosterone or other anabolic steroids will increase muscular hypertrophy.

Muscular, spinal and neural factors all affect muscle building. Sometimes a person may notice an increase in strength in a given muscle even though only its opposite has been subject to exercise, such as when a bodybuilder finds her left biceps stronger after completing a regimen focusing only on the right biceps. This phenomenon is called cross education.[citation needed]

Inactivity and starvation in mammals lead to atrophy of skeletal muscle, a decrease in muscle mass that may be accompanied by a smaller number and size of the muscle cells as well as lower protein content.[21] Muscle atrophy may also result from the natural aging process or from disease.

In humans, prolonged periods of immobilization, as in the cases of bed rest or astronauts flying in space, are known to result in muscle weakening and atrophy. Atrophy is of particular interest to the manned spaceflight community, because the weightlessness experienced in spaceflight results is a loss of as much as 30% of mass in some muscles.[22][23] Such consequences are also noted in small hibernating mammals like the golden-mantled ground squirrels and brown bats.[24]

During aging, there is a gradual decrease in the ability to maintain skeletal muscle function and mass, known as sarcopenia. The exact cause of sarcopenia is unknown, but it may be due to a combination of the gradual failure in the "satellite cells" that help to regenerate skeletal muscle fibers, and a decrease in sensitivity to or the availability of critical secreted growth factors that are necessary to maintain muscle mass and satellite cell survival. Sarcopenia is a normal aspect of aging, and is not actually a disease state yet can be linked to many injuries in the elderly population as well as decreasing quality of life.[25]

There are also many diseases and conditions that cause muscle atrophy. Examples include cancer and AIDS, which induce a body wasting syndrome called cachexia. Other syndromes or conditions that can induce skeletal muscle atrophy are congestive heart disease and some diseases of the liver.

Neuromuscular diseases are those that affect the muscles and/or their nervous control. In general, problems with nervous control can cause spasticity or paralysis, depending on the location and nature of the problem. A large proportion of neurological disorders, ranging from cerebrovascular accident (stroke) and Parkinson's disease to CreutzfeldtJakob disease, can lead to problems with movement or motor coordination.

Symptoms of muscle diseases may include weakness, spasticity, myoclonus and myalgia. Diagnostic procedures that may reveal muscular disorders include testing creatine kinase levels in the blood and electromyography (measuring electrical activity in muscles). In some cases, muscle biopsy may be done to identify a myopathy, as well as genetic testing to identify DNA abnormalities associated with specific myopathies and dystrophies.

A non-invasive elastography technique that measures muscle noise is undergoing experimentation to provide a way of monitoring neuromuscular disease. The sound produced by a muscle comes from the shortening of actomyosin filaments along the axis of the muscle. During contraction, the muscle shortens along its longitudinal axis and expands across the transverse axis, producing vibrations at the surface.[26]

The evolutionary origin of muscle cells in metazoans is a highly debated topic. In one line of thought scientists have believed that muscle cells evolved once and thus all animals with muscles cells have a single common ancestor. In the other line of thought, scientists believe muscles cells evolved more than once and any morphological or structural similarities are due to convergent evolution and genes that predate the evolution of muscle and even the mesoderm - the germ layer from which many scientists believe true muscle cells derive.

Schmid and Seipel argue that the origin of muscle cells is a monophyletic trait that occurred concurrently with the development of the digestive and nervous systems of all animals and that this origin can be traced to a single metazoan ancestor in which muscle cells are present. They argue that molecular and morphological similarities between the muscles cells in cnidaria and ctenophora are similar enough to those of bilaterians that there would be one ancestor in metazoans from which muscle cells derive. In this case, Schmid and Seipel argue that the last common ancestor of bilateria, ctenophora, and cnidaria was a triploblast or an organism with three germ layers and that diploblasty, meaning an organism with two germ layers, evolved secondarily due to their observation of the lack of mesoderm or muscle found in most cnidarians and ctenophores. By comparing the morphology of cnidarians and ctenophores to bilaterians, Schmid and Seipel were able to conclude that there were myoblast-like structures in the tentacles and gut of some species of cnidarians and in the tentacles of ctenophores. Since this is a structure unique to muscle cells, these scientists determined based on the data collected by their peers that this is a marker for striated muscles similar to that observed in bilaterians. The authors also remark that the muscle cells found in cnidarians and ctenophores are often contests due to the origin of these muscle cells being the ectoderm rather than the mesoderm or mesendoderm. The origin of true muscles cells is argued by others to be the endoderm portion of the mesoderm and the endoderm. However, Schmid and Seipel counter this skepticism about whether or not the muscle cells found in ctenophores and cnidarians are true muscle cells by considering that cnidarians develop through a medusa stage and polyp stage. They observe that in the hydrozoan medusa stage there is a layer of cells that separate from the distal side of the ectoderm to form the striated muscle cells in a way that seems similar to that of the mesoderm and call this third separated layer of cells the ectocodon. They also argue that not all muscle cells are derived from the mesendoderm in bilaterians with key examples being that in both the eye muscles of vertebrates and the muscles of spiralians these cells derive from the ectodermal mesoderm rather than the endodermal mesoderm. Furthermore, Schmid and Seipel argue that since myogenesis does occur in cnidarians with the help of molecular regulatory elements found in the specification of muscles cells in bilaterians that there is evidence for a single origin for striated muscle.[27]

In contrast to this argument for a single origin of muscle cells, Steinmetz et al. argue that molecular markers such as the myosin II protein used to determine this single origin of striated muscle actually predate the formation of muscle cells. This author uses an example of the contractile elements present in the porifera or sponges that do truly lack this striated muscle containing this protein. Furthermore, Steinmetz et al. present evidence for a polyphyletic origin of striated muscle cell development through their analysis of morphological and molecular markers that are present in bilaterians and absent in cnidarians, ctenophores, and bilaterians. Steimetz et al. showed that the traditional morphological and regulatory markers such as actin, the ability to couple myosin side chains phosphorylation to higher concentrations of the positive concentrations of calcium, and other MyHC elements are present in all metazoans not just the organisms that have been shown to have muscle cells. Thus, the usage of any of these structural or regulatory elements in determining whether or not the muscle cells of the cnidarians and ctenophores are similar enough to the muscle cells of the bilaterians to confirm a single lineage is questionable according to Steinmetz et al. Furthermore, Steinmetz et al. explain that the orthologues of the MyHc genes that have been used to hypothesize the origin of striated muscle occurred through a gene duplication event that predates the first true muscle cells (meaning striated muscle), and they show that the MyHc genes are present in the sponges that have contractile elements but no true muscle cells. Furthermore, Steinmetz et all showed that the localization of this duplicated set of genes that serve both the function of facilitating the formation of striated muscle genes and cell regulation and movement genes were already separated into striated myhc and non-muscle myhc. This separation of the duplicated set of genes is shown through the localization of the striated myhc to the contractile vacuole in sponges while the non-muscle myhc was more diffusely expressed during developmental cell shape and change. Steinmetz et al. found a similar pattern of localization in cnidarians with except with the cnidarian N. vectensis having this striated muscle marker present in the smooth muscle of the digestive track. Thus, Steinmetz et al. argue that the pleisiomorphic trait of the separated orthologues of myhc cannot be used to determine the monophylogeny of muscle, and additionally argue that the presence of a striated muscle marker in the smooth muscle of this cnidarian shows a fundamentally different mechanism of muscle cell development and structure in cnidarians.[28]

Steinmetz et al. continue to argue for multiple origins of striated muscle in the metazoans by explaining that a key set of genes used to form the troponin complex for muscle regulation and formation in bilaterians is missing from the cnidarians and ctenophores, and of 47 structural and regulatory proteins observed, Steinmetz et al. were not able to find even on unique striated muscle cell protein that was expressed in both cnidarians and bilaterians. Furthermore, the Z-disc seemed to have evolved differently even within bilaterians and there is a great deal diversity of proteins developed even between this clade, showing a large degree of radiation for muscle cells. Through this divergence of the Z-disc, Steimetz et al. argue that there are only four common protein components that were present in all bilaterians muscle ancestors and that of these for necessary Z-disc components only an actin protein that they have already argued is an uninformative marker through its pleisiomorphic state is present in cnidarians. Through further molecular marker testing, Steinmetz et al. observe that non-bilaterians lack many regulatory and structural components necessary for bilaterians muscle formation and do not find any unique set of proteins to both bilaterians and cnidarians and ctenophores that are not present in earlier, more primitive animals such as the sponges and amoebozoans. Through this analysis the authors conclude that due to the lack of elements that bilaterians muscles are dependent on for structure and usage, nonbilaterian muscles must be of a different origin with a different set regulatory and structural proteins.[28]

In another take on the argument, Andrikou and Arnone use the newly available data on gene regulatory networks to look at how the hierarchy of genes and morphogens and other mechanism of tissue specification diverge and are similar among early deuterostomes and protostomes. By understanding not only what genes are present in all bilaterians but also the time and place of deployment of these genes, Andrikou and Arnone discuss a deeper understanding of the evolution of myogenesis.[29]

In their paper Andrikou and Arnone argue that to truly understand the evolution of muscle cells the function of transcriptional regulators must be understood in the context of other external and internal interactions. Through their analysis, Andrikou and Arnone found that there were conserved orthologues of the gene regulatory network in both invertebrate bilaterians and in cnidarians. They argue that having this common, general regulatory circuit allowed for a high degree of divergence from a single well functioning network. Andrikou and Arnone found that the orthologues of genes found in vertebrates had been changed through different types of structural mutations in the invertebrate deuterostomes and protostomes, and they argue that these structural changes in the genes allowed for a large divergence of muscle function and muscle formation in these species. Andrikou and Arnone were able to recognize not only any difference due to mutation in the genes found in vertebrates and invertebrates but also the integration of species specific genes that could also cause divergence from the original gene regulatory network function. Thus, although a common muscle patterning system has been determined, they argue that this could be due to a more ancestral gene regulatory network being coopted several times across lineages with additional genes and mutations causing very divergent development of muscles. Thus it seems that myogenic patterning framework may be an ancestral trait. However, Andrikou and Arnone explain that the basic muscle patterning structure must also be considered in combination with the cis regulatory elements present at different times during development. In contrast with the high level of gene family apparatuses structure, Andrikou and Arnone found that the cis regulatory elements were not well conserved both in time and place in the network which could show a large degree of divergence in the formation of muscle cells. Through this analysis, it seems that the myogenic GRN is an ancestral GRN with actual changes in myogenic function and structure possibly being linked to later coopts of genes at different times and places.[29]

Evolutionarily, specialized forms of skeletal and cardiac muscles predated the divergence of the vertebrate/arthropod evolutionary line.[30][dead link] This indicates that these types of muscle developed in a common ancestor sometime before 700 million years ago (mya). Vertebrate smooth muscle was found to have evolved independently from the skeletal and cardiac muscle types.

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Muscle - Wikipedia

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