How intestine repairs itself

Researchers at Baylor College of Medicine, Johns Hopkins University School of Medicine and the University of California, San Francisco have gained new insights into how the small intestine, one of the fastest renewing tissues in the human body, repairs itself after injury caused by intestinal rotavirus infection. Their findings have led them to propose that, contrary to the current thinking, how the intestine repairs itself seems to depend on the type of damage, and they found that triggers that were previously thought to be unimportant are actually essential for repairing virus-caused injury.

They studied different damage model, damage caused by rotavirus, a common small intestinal viral infection that affects young children. Repair and turnover of the epithelium, the most external cellular layer of the small intestine responsible for absorption of nutrients and other functions, depend on the intestinal stem cells, regardless of the cause of the damage. There are two types of intestinal stem cells: CBCs (crypt-based columnar cells) and reserve intestinal stem cells. The type of injuries studied until now damages the highly proliferative CBCs, and when these stem cells are destroyed, the reserve intestinal stem cells respond to restore the damage. The response to injury caused by rotavirus, however, is different.

Rotavirus is an infection and has a very specific damage pattern, the virus specifically infects epithelial cells, but not the stem cells. The first finding refers to the type of stem cell involved in the repair of the epithelial cells damaged by the virus. Previous studies had shown that when CBC stem cells are damaged, the reserve stem cells come to their rescue leading the reconstitution of the damaged epithelium. When rotavirus damages the epithelium, but not the stem cells,  the CBCs, not the reserve stem cells, are the primary cell type involved in the restoration of the intestinal epithelium.

 CBCs were not considered important for the repair of intestinal epithelium, but the results show that they are crucial for injury repair after rotavirus-induced epithelial cell damage in contrast to previous studies supporting the reserve intestinal stem cells as the cell type involved in epithelial restitution. The second finding refers to the source of the signaling molecules-called WNTs that trigger the growth and activation of stem cells leading to injury repair. Scientists have described two sources of WNT molecules, epithelial cells and mesenchymal cells. Epithelial WNT molecules were essential to signal the stem cells to repair the damage caused by rotavirus infection.
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Links between high cholesterol diet and colon cancer

New UCLA research could help explain the link between a high-cholesterol diet and an elevated risk for colon cancer. In a study of mice, scientists from the David Geffen School of Medicine at UCLA discovered that boosting the animals' cholesterol levels spurred intestinal stem cells to divide more quickly, enabling tumors to form 100 times faster. The study identifies a molecular pathway that could serve as a new drug target for colon cancer treatment.

Cholesterol influences the growth of stem cells in the intestines, which in turn accelerates the rate of tumor formation. The connection between dietary cholesterol and colon cancer is well established. The scientists increased cholesterol in the intestinal stem cells in some of the mice by introducing more of the substance into their diets.

In others, the researchers altered a gene that regulates phospholipids, the primary type of fat in cell membranes, which spurred the cells into producing more cholesterol on their own. The stem cells ' ability to multiply increased in both groups.

As the animals' cholesterol levels rose, their cells divided more rapidly, causing the tissue lining their guts to expand and their intestines to lengthen. These changes significantly sped up the rate of tumor formation in their colons.
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How alcohol damages DNA and causes cancer

Scientists have shown how alcohol damages DNA in stem cells, helping to explain why drinking increases the risk of cancer, according to latest research. Researchers used mice to show how alcohol exposure leads to permanent genetic damage. Scientists at the MRC Laboratory of Molecular Biology, Cambridge, gave diluted alcohol, chemically known as ethanol, to mice.

They then used chromosome analysis and DNA sequencing to examine the genetic damage caused by acetaldehyde, a harmful chemical produced when the body processes alcohol. They found that acetaldehyde can break and damage DNA within blood stem cells leading to rearranged chromosomes and permanently altering the DNA sequences within these cells.

It is important to understand how the DNA blueprint within stem cells is damaged because when healthy stem cells become faulty, they can give rise to cancer. These new findings therefore help us to understand how drinking alcohol increases the risk of developing 7 types of cancer including common types like breast and bowel.

Some cancers develop due to DNA damage in stem cells while some damage occurs by chance. The study also examined how the body tries to protect itself against damage caused by alcohol. The first line of defence is a family of enzymes called aldehyde dehydrogenases (ALDH). These enzymes break down harmful acetaldehyde into acetate, which our cells can use as a source of energy.

In the study, when mice lacking the critical ALDH enzyme - ALDH2 - were given alcohol, it resulted in four times as much DNA damage in their cells compared to mice with the fully functioning ALDH2 enzyme. The second line of defence used by cells is a variety of DNA repair systems which, most of the time, allow them to fix and reverse different types of DNA damage. But they don't always work and some people carry mutations which mean their cells aren't able to carry out these repairs effectively.

The study highlights that not being able to process alcohol effectively can lead to an even higher risk of alcohol-related DNA damage and therefore certain cancers. But it's important to remember that alcohol clearance and DNA repair systems are not perfect and alcohol can still cause cancer in different ways, even in people whose defence mechanisms are intact.
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Gene therapy may kill HIV

Gene therapy may have the potential to eradicate HIV in people infected with the virus, new animal research suggests. The science centers around the use of "chimeric antigen receptor" (CAR) genes. In laboratory work with monkeys, these engineered cells have destroyed HIV-infected cells for more than two years, scientists reported.

T-cells are the cells that are largely responsible for human ability to fight off pathogens and get rid of infections in the body. Every T-cell has a unique receptor, or molecule, on it. That receptor allows the cell to recognize a specific target-a bacteria, or fungus or virus. And when it recognizes that target, it's called into duty to clear it from the body. Taking artificial receptors- CAR that can go on to these cells and allow them to recognize what we want them to recognize," he noted. "In this case that's HIV."

First, the team genetically engineered CAR to find and bind to simian/human immunodeficiency virus (SHIV), a lab-engineered HIV hybrid composed of human virus and monkey virus. Then the researchers modified the DNA of certain blood-forming stem cells so they would carry SHIV-killing CAR. The resulting cells were introduced into the bloodstream of four male juvenile SHIV-infected macaque monkeys.

The engineered cells successfully took up residence in each monkey's bone marrow. The cells moved widely throughout the body, targeting and killing SHIV-infected cells, without producing any notable adverse side effects. The advantage of the stem cell-based approach is that once these cells are grafted into the body, they continuously produce new T-cells that have this gene in them that can target HIV cells.

Plans are underway for a human trial, this study shows both that these cells will respond to HIV and that it's safe. This strategy is unlikely to fully work on its own, CAR will most likely need to be used with antiretroviral therapy. CAR therapy is already leading to impressive results in cancer and holds promise for HIV eradication.
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Gene therapy can destroy HIV infected cells

Through gene therapy, researchers engineered blood-forming stem cells (hematopoietic stem/progenitor cells, or HSPCs) to carry chimeric antigen receptor (CAR) genes to make cells that can detect and destroy HIV-infected cells. These engineered cells not only destroyed the infected cells, they persisted for more than two years, suggesting the potential to create long-term immunity from the virus that causes AIDS.

Antiviral drugs can suppress the amount of HIV in the body to nearly undetectable levels, but only an effective immune response can eradicate the virus. Researchers have been seeking a way to improve the body's ability to combat the virus by engineering blood-forming stem cells to specifically target and kill HIV-infected cells for the life of the individual.

 Although chimeric antigen receptor (CAR) T-cells have emerged as a powerful immunotherapy for various forms of cancer -- and show promise in treating HIV-1 infection -- the therapy may not impart long-lasting immunity. Researchers, physicians and patients need T cell-based products that can respond to malignant or infected cells that may reappear months or years after treatment.

Because HIV uses CD4 to infect cells, the researchers used a CAR molecule that hijacks the essential interaction between HIV and the cell surface molecule CD4 to make stem cell-derived T-cells target infected cells. When the CD4 on the CAR molecule binds to HIV, other regions of the CAR molecule signal the cell to become activated and kill the HIV infected cell.

The researchers found that, in test animals, modification of the blood-forming stem cells resulted in more than two years of stable production of CAR-expressing cells without any adverse effects. In addition, these cells were widely distributed throughout the lymphoid tissues and gastrointestinal tract, which are major anatomic sites for HIV replication and persistence in infected people. Most important, engineered CAR T-cells showed efficacy in attacking and killing HIV-infected cells.
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Diabetes in pregnancy affects fetus heart

Researchers have discovered how high glucose levels-whether caused by diabetes or other factors keep heart cells from maturing normally, this shows the reason why babies born to women with diabetes are more likely to develop congenital heart disease. When developing heart cells are exposed to high levels of glucose, the researchers found, the cells generate more building blocks of DNA than usual, which leads the cells to continue reproducing rather than mature.

High blood sugar levels are not only unhealthy for adults; they're unhealthy for developing fetuses.  the leading non-genetic risk factor for congenital heart disease is a mother having diabetes during pregnancy. Babies born to women with high levels of glucose in their blood during pregnancy are two to five times more likely to develop the disorder than other babies. However, researchers have never been able to define the precise effect of glucose on the developing fetus.

Researchers used human embryonic stem cells to grow heart cardiomyocin and then exposed them to varying levels of glucose. Cells that were exposed to small amounts of glucose matured normally. But cardiomyocytes that had been mixed with high levels of glucose matured late or failed to mature altogether, and instead generated more immature cells. The researchers discovered that, when exposed to extra glucose, the cardiomyocytes over-activated the pentose phosphate pathway -a cellular process that, among other things, generates nucleotides, the building blocks of DNA.

In cells with high glucose levels, the pentose phosphate pathway made more nucleotides than usual. The scientists showed that the excess of building blocks kept the cells from maturing. By depleting glucose at the right point in development, we can limit the proliferation of the cells, which coaxes them to mature and makes the heart muscle stronger, The same thing occurred in pregnant mice with diabetes-the heart cells of fetuses divided quickly but matured slowly.
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How Zika virus induces congenital microcephaly

Epidemiological studies show that in utero fetal infection with the Zika virus (ZIKV) may lead to microcephaly, an irreversible congenital malformation of the brain characterized by an incomplete development of the cerebral cortex. However, the mechanism of Zika virus-associated microcephaly remains unclear.

Combined analysis of human fetuses infected with Zika virus, cultures of human neuronal stem cells and mice embryos showed that ZIKV infection of cortical progenitors -stem cells for cortical neurons) controlling neurogenesis triggers stress in the endoplasmic reticulum -where some of the cellular proteins and lipids are synthesized in the embryonic brain, inducing signals in response to incorrect protein conformation.

When it reaches the brain, Zika virus infects neuronal stem cells, which will generate fewer neurons, and by inducing chronic stress in the endoplasmic reticulum, it promotes apoptosis-the early death of these neuronal cells. These two combined mechanisms explain why the cerebral cortex of infected fetuses becomes deficient in neurons and is therefore smaller in size.

 Researchers administered an inhibitors of protein-folding re-sponse in cortical progenitors and found that this inhibited the development of microcephaly in mice embryos infected with Zika virus. The defects observed are specific to an infection by ZIKV, as other neurotropical viruses of the flavivirus family- West Nile virus and yellow fever did not cause microcephaly, in contrast to Zika virus.
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Natural immune suppressor responsible for early death in leukemia patients

Patients diagnosed with the most common form of leukemia who also have high levels of an enzyme known to suppress the immune system are most likely to die early. High levels of this enzyme, indoleamine 2,3 dioxygenase, or IDO, at diagnosis also identify those who might benefit most by taking an IDO inhibitor along with their standard therapy.

A review of patients with acute myeloid leukemia, or AML, found increased IDO expression in the bone marrow biopsy, performed to diagnose their disease, correlated with lower overall survival rates and early mortality. It also indicates that IDO expression should routinely be measured when the diagnostic bone marrow biopsy is performed, Everyone has the IDO gene, it's the cancer cells in this scenario that activate the disabler of the immune response that is also used by the fetus and solid tumors.

 Stem cells in the bone marrow are supposed to mature into a variety of cells that enable human blood and immune system function. Instead in AML, stem cells get stuck in an in-between, undifferentiated state called blasts.In leukemia, stem cells get limboed in the blast state so you don't get any maturation. That means there are low platelets so you get clotting problems, you have low neutrophils so you have infections, you have less red blood cells so you get anemic.

Bleeding is a major cause of death for patients and often, significant gum bleeding is the first indicator. The patients who died at six months had a high expression of IDO while the blasts produced relatively little IDO in the patients who lived five years or more. During pregnancy, cells in the placenta trigger an isolated suppression of the mother's immune system so it won't reject the genetically foreign fetus. They showed that IDO locally disables the mother's immune system by degrading tryptophan, an amino acid essential to survival of T cells , orchestrators of the immune system's response.

Later work would show that tumors - and leukemia - also use IDO to hide from the immune response. Conversely, some organ transplant patients who inexplicably express higher levels of IDO, have lower rejection rates of their new organ. Induction therapy is given to get the patient into remission, and is typically followed by more chemotherapy to ensure it stays dormant.
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How Zika virus infects developing brain

Zika virus is transmitted from mother to fetus by infected cells that later develop into the brain's first and primary form of defense against invasive pathogens. During embryogenesis- the early stages of prenatal development cells called microglia form in the yolk sac and then disperse throughout the central nervous system CNS of the developing fetus.

In the brain, these microglia will become resident macrophages whose job is to constantly clear away plaques, damaged cells and infectious agents. The Zika virus can infect these early microglia, moving into the brain where they transmit the virus to other brain cells, leading to devastating neurological damage.

The Zika virus is transmitted to people through the bite of infected Aedes species mosquitoes. However, a pregnant woman can also pass the virus to her fetus, the researchers used human induced pluripotent stem cells to create two relevant CNS cell types: microglia and neural progenitor cells (NPCs), which generate the millions of neurons and glial cells required during embryonic development.

Then they established a co-culture system that mimicked the interactions of the two cell types in vitro when exposed to the Zika virus. They discovered that the microglia cells engulfed Zika-infected NPCs, doing their job. But when these microglia carrying the virus were placed in contact with non-infected NPCs, they transmitted the virus to the latter.
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Reversing damaged heart tissue

It is possible to change fibroblasts -scar tissue cells into cardiomyocytes -heart muscle cells. Researchers used single cell RNA sequencing technology in combination with mathematical modeling and genetic and chemical approaches to delineate the step-by-step molecular changes that occur during cell fate conversion from fibroblast to cardiomyocyte. They reconstructed the routes a single cell could take in this process but also identified underlying molecular pathways and key regulators important for the transformation from one cell type to another.

Embryonic stem cells throughout human body gradually changes into a variety of highly specialized cell types, such as neurons, blood cells, and heart muscle cells. New discovery showed that it is possible to revert terminally differentiated somatic cells to a pluripotent state- cell that can self-produce and potentially turn into any kind of cell in the body. Researchers have also figured out how to convert one kind of differentiated somatic cell type into another without detouring through the pluripotent stage or the original progenitor stage. Such findings shifted the paradigm of cellular hierarchy and revolutionized stem cell research and the field of regenerative medicine.


Direct cardiac reprogramming, a promising approach for cardiac regeneration and disease modeling that direct conversion of cardiac non-myocytes into induced cardiomyocytes (iCMs) that closely resemble endogenous CMs. Like any reprogramming process, the many cells that are being reprogrammed don't do so at the same time.

Cellular reprogramming is heterogeneous, which makes it difficult to study using traditional approaches.
Using microfluidic single-cell RNA sequencing techniques, addressed the two main issues of 'asynchronous' programming and heterogeneous cell populations. They analyzed global transcriptome changes during fate conversion from fibroblasts to iCMs.
Using mathematical algorithms, they identified molecularly distinct subpopulations of cells along the reprogramming pipeline.

After a heart attack, cardiac fibroblasts around the injured area are immediately activated and become highly proliferative but this proliferative capacity decreases over time. How to take advantage of the varied cell cycle status of fibroblasts over the progression of a heart attack and its aftermath would certainly broaden the application of cellular reprogramming for patients and optimize outcomes. The molecular features of subpopulations of fibroblasts were differentially suppressed during reprogramming, suggesting that the susceptibility of cells to be reprogrammed varies.

This susceptibility coincides with the timing of cardiomyocyte differentiation during heart development. The signatures in the intermediate populations that seem to appear earlier in heart development were more resistant to the alterations. This suggests that the recent epigenetic memories of cells might be more easily erased, and so the fibroblast subpopulations with such epigenetic features are more easily converted into cardiomyocytes. Adjusting epigenetic memories not just changing their current epigenetic status could be crucial for changing a cell fate for therapeutic value.
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How ultraviolet rays cause skin cancer

Melanoma is a cancer of skin pigment cells called melanocytes, a fraction of those melanomas come from existing moles. When melanocyte stem cells accumulate a sufficient number of genetic mutations, they can become the cells cancers originate.

Under normal conditions, ultraviolet UV radiation from the sun activates melanocytes to release melanin, a pigment that protects the skin from the sun's rays. But if melanocyte stem cells have surpassed a threshold of genetic mutations, a tumor can start to grow. The skin stem cells can be activated by exposure to sunlight.

Exposure to sunlight triggers mutations that are sufficient for melanoma. A gene known as Hgma2 was suspected to become expressed in the skin under UV radiation. When expressed, Hgma2 facilitates melanocyte stem cells to move from the base of skin hair follicles to the skin's surface-the epidermis, where the cells release melanin.

Researchers used mice engineered with melanocyte stem cell mutations. One set of mice had the mutations, while another set with the mutations had the Hgma2 gene deleted. They then gave the mice a very low dose of UV radiation, just enough to trigger a tanning response. Mice with tumor-causing mutations and the Hgma2 gene intact developed melanomas, but the mice with mutations and the deleted gene remained healthy.
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Inflammation heals skin faster

Wounds and harmful inflammation provoking experiences impart long lasting memories to stem cells in the skin, teaching them to heal subsequent injuries faster. These stem cells, which replenish the skin's outer layer take their cue from the body's response to injury or infection.

The first bout of inflammation sensitizes these cells: the next time they sense it coming, they respond more rapidly. Skin can form memories of an inflammatory response, enhancing responsiveness to inflammation, these memories help the skin maintain its integrity, a feature that is beneficial in healing wounds after an injury.

Whether burned by the sun, attacked by microbes, nicked by a cut, the skin quickly becomes inflamed, swollen, and painful as the body seeks to stop the damage and initiate repair. The immune system maintains a memory of inflammation to mount faster responses to recurrent infections.

 Skin is the body's protective barrier, most of the cells in the skin's outermost layer, the epithelium, don't stick around long enough to form such memories but they migrate up through the epithelium and eventually slough off. Deeper within the epithelium, however, reside the stem cells that are responsible for continually replenishing it. These stem cells remain in place long after the skin has recovered from inflammation; and this experience changes the skin.

In experiments with mice, researchers showed that wounds closed more than twice as fast in skin that had already experienced inflammation than in skin that had never been damaged even if the initial inflammatory experience had occurred as long as six months earlier, inflammation-experienced stem cells were better at moving into the wound to repair the breach.

Inflammation triggers a process that physically opens up distinct sites within the cell's chromosomes, making certain genes accessible for activation. Some of these sites remain open long after the skin has recovered, allowing the genes to be turned on faster during a second round of inflammation.

A gene called Aim2, which encodes damage-and-danger sensing protein, appeared particularly crucial: an initial bout of inflammation prompts a sustained increase in its expression. A second assault quickly activates the protein, resulting in the production of an inflammatory signal that boosts the stem cells' ability to migrate into the wound.
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Aspiring could reverse tooth decay

Tooth decay occurs when acid in the mouth dissolves the enamel and dentine of the teeth causing formation of holes or cavities. The acid is produced by bacteria that are found within the plaque and thin film that builds up on the teeth.

Aspirin could reverse the effects of tooth decay by triggering teeth to self-reported, reducing the need for filling.
The drug can form new dentine, the hard tooth structure that is usually damaged by decay.

When we eat sugar it interacts with the bacteria within the plaque to produce the destructive acid. If the plaque is allowed to build up, the acid can begin to break down the surface of tooth, causing holes.

After the damage, the cavity begins to eat away at the second level of tooth material that lies beneath the enamel: the dentin. Tooth decay can lead to tooth abscesses, which may result in the tooth having to be removed.

A filling can be used to stop the bacteria in order to prevent the cavity from reaching the tooth's pulp. Fillings may fail and may need to be replaced many times during the life time of the tooth.

Low dose of aspirin increased the rebuilding of minerals which restores strength and function of the tooth, it also stimulated existing stem cells in the tooth to regenerate the damaged tooth structure.
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Bone marrow protein may be used for stem cell transplant

Bone marrow contains hematopoetic stem cells, the precursors to every blood cell type. These cells become after bone marrow transplants, bone marrow injury and during systemic infection, creating new blood cells, including immune cells.

Del-1 is a protein that plays a role in gum disease, it regulate the production of blood cells. Targeting it could be an effective way to improve stem cell transplants for both donors and recipients. Modulate levels of Del-1 in patients with certain blood cancers can enhance immune cell production.

Because the hematopoetic stem cell niche is so important for the creation of bone marrow and blood cells and because Del-1 is a soluble protein and is easily manipulated, it could be a target in many potential applications.

The researchers' investigations revealed that Del-1 was expressed by at least three cell types in the bone marrow that support hematopoetic stem cells: endothelial cells, CAR cells and osteoblasts.

Using mice deficient in Del-1, they found that the protein promotes proliferation and differentiation of hematopoetic stem cells, sending more of these progenitor cells down a path toward becoming myeloid cells, such as macrophages and neutrophils, rather than lymphocytes, such as T cells and B cells.

In bone marrow transplant experiments, researchers discovered that the presence of Del-1 in recipient
bone marrow is required for the transplanted stem cells to engraft in the recipient and to facilitate the process of myelopoesis, the production of myeloid cells.

When the researchers mimicked a systemic infection in mice, animals deficient in Del-1 were slower to begin making myeloid cells again compared to those with normal Del-1 levels.

The scientists see potential applications in bone marrow and stem cell transplants, for both donors and recipients. In donors, blocking the interaction between Del-1 and hematopoetic stem cells could enhance the mobilization of those progenitors into the bloodstream. This could be helpful for increasing donor cell numbers for transplantation.

Transplant recipients, on the other hand, may need enhanced Del-1 interaction to ensure the transplanted cells engraft and begin making new blood cells more rapidly. People undergoing chemotherapy who develop febrile neutropenia, associated with low levels of white blood cells, might benefit from the role of Del-1 in supporting the production of immune-related blood cells such as neutrophils.
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Vitamin C can stop the spread of blood cancer

Faulty stem cells in bone marrow often multiply, increasing the growth of fatal tumours. The diseases can lead to anaemia and bleeding as abnormal stem cells multiply in the bone marrow and interfere with blood cell production.

Vitamin C can kill and prevents the spread of the tumours. Vitamin C found in high levels in kale, oranges and peppers could prevents blood cancer but it is impossible to get the required amount through fruits and vegetables in high quantities.

High quantities of vitamin C required for killing the tumours can be given by injecting cancer patients intravenously, the patients can get up to 500 times the amount they would get through eating fruit and vegetables.

Vitamin C prevents the breakdown of glucose, the mitochondria - the strength of the cancer cells are unable to gain vital energy it needs to grow with vitamin C injection.

Researchers discovered that vitamin C suppressed the growth of leukaemia cancer stem cells from human patients implanted into the mice. Combining vitamin C with a cancer drug is more effective in cancer treatment.
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New drug for hair loss

Increasing lactate production genetically increases the stem cells in dormant hair follicles to grow again.
Receding hairlines and thinning crowns can be caused by aging, genetics, hormone imbalance, stress, illness and medications. The metabolic process that takes place in hair follicle stem cells is different from that which takes place in other skin cells.

Cells convert glucose into pyruvate but this metabolite can take one of two paths; it can be sent to the mitochondria and used as energy, or the cells can convert it to a different metabolite known as lactate - the same substance produced during intense exercise that causes a burning sensation in muscles.

Changing the chemical course of the glucose metabolites could change the behavior of inactive follicles. Researchers examined mice that had been genetically engineered to not produce lactate along with those that had been altered to increase lactate production.

They discovered that blocking lactate prevented hair follicle stem cells from being activated while increasing lactate increased the production of hair. When the drugs - RCGD423 and UK5099 were applied to the skin of mice, both increased lactate production and
accelerate hair growth.
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Low calories diet prevents aging

Low-calorie diet and eating less keeps the body younger. Body's biological clock change as a result of physiological aging, the clock controlled circuit that directly connects to the process of aging is based on efficient metabolism of energy within cells.

Energy is metabolized within cells under precise circadian controls.
The researchers found that the 24-hour cycle in the circadian-controlled metabolic system of older mice remained the same, but there were notable changes in the circadian mechanism that turns genes on and off based upon the cells' energy usage.

Older cells processed energy inefficiently. Caloric restriction works by sprucing up the biological clock. According to scientists, low-calorie diet conserved most of the rhythmic functions in young people.

The low-calorie diet greatly contributes to preventing the effects of physiological aging. Keeping the rhythm of stem cells young is important because these cells renew and preserve day-night cycles in tissue.

Eating less prevent tissue aging, therefore, it prevents stem cells from reprogramming their circadian activities. Calorie restriction influences the body's circadian rhythms involvement with the aging process in cells. Circadian rhythm-metabolism link circadian enzyme protein called SIRT1 works.

 SIRT1 senses energy levels in cells; its activity is modulated by how many nutrients a cell is consuming. It helps cells resist oxidative and radiation-induced stress. SIRT1 has also been linked to the inflammatory response, diabetes and aging.
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Brain cells control aging

Scientists have discovered that stem cells in the brain's hypothalamus control how fast aging occurs in the body. This discovery could lead to new method of preventing diseases and increasing lifespan.

The hypothalamus regulates growth, development, reproduction, metabolism and aging. The number of hypothalamic neural stem cells naturally declines and this accelerates aging.
Replenishing stem cells can slow down the process of aging but the loss are not irreversible.

Researchers disrupted the hypothalamic stem cells in middle-aged mice and discovered that disruption accelerated aging. They injected hypothalamic stem cells into the brains of middle-aged mice whose stem cells had been destroyed as well as into the brains of normal old mice.

The treatment showed different measures of aging in both groups. Hypothalamic stem cells exert their anti-aging effects by releasing microRNAs (miRNAs).

The researchers extracted miRNA-containing exosomes from hypothalamic stem cells and injected them into the cerebrospinal fluid of middle-aged mice whose hypothalamic stem cells had been destroyed and normal middle-aged mice.

This treatment slowed aging in both groups of animals as measured by tissue analysis and behavioral testing that involved assessing changes in the animals' muscle endurance, coordination, social behavior and cognitive ability.
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