Category Archives: Papers

Drug Could Rejuvenate Aging Brain And Muscle Tissue

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After 15+ years as an IT professional. Jonathon decided to return to school in hopes of one day troubleshooting the most universal problem effecting all. Death, pain, and suffering by aging. As an undergraduate he is currently performing research in Dr. Richard Bennetts lab at the University of Southern Indiana, as well as volunteering for various organizations including the Buck Institute for research on Aging.
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proteins

The ability of adult stem cells to renew themselves decline as we age, but researchers have discovered a small molecular drug that could ‘rejuvenate’ brain and muscle tissue. The study, published in the journal Oncotarget, successfully interrupted the activity of a growth factor in mice that has been previously shown to affect a stem cell’s ability to regenerate.

Previous research has shown that molecular changes in a stem cell microenvironment contributes to the tissues’ ability to repair damage and maintain homeostasis. Researchers found the transforming growth factor beta 1 (TGF-beta1) pathway to play a significant role in the aging of multiple stem cells. In the new study, researchers reduced TGF-beta1 activity by inserting genetic blockers into the brains of old mice. The results found tissue regeneration of stem cells to be ‘enhanced’ in old mice.

“Based on our earlier papers, the TGF-beta1 pathway seemed to be one of the main culprits in multi-tissue aging,” said co-author David Schaffer, director of the Berkeley Stem Cell Center and a professor of chemical and biomolecular engineering, in a statement. “That one protein, when upregulated, ages multiple stem cells in distinct organs, such as the brain, pancreas, heart and muscle. This is really the first demonstration that we can find a drug that makes the key TGF-beta1 pathway, which is elevated by aging, behave younger, thereby rejuvenating multiple organ systems.”

The research team injected a small molecule called Alk5 kinase inhibitor, which is known to reduce the influence of TGF-beta1, into the blood of old mice once a day for 11 days. Researchers found the small molecule had ‘perked up’ the stem cells’ ability to regenerate both brain and muscle tissue in old mice.

Researchers hope this research could result in effective treatments for combating multiple age-related degenerative disorders, which can have a range of debilitating effects

“The challenge ahead is to carefully retune the various signaling pathways in the stem cell environment, using a small number of chemicals, so that we end up recalibrating the environment to be youth-like,” Conboy said. “Dosage is going to be the key to rejuvenating the stem cell environment.”

Have a sense of purpose in life? It may Extend it.

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After 15+ years as an IT professional. Jonathon decided to return to school in hopes of one day troubleshooting the most universal problem effecting all. Death, pain, and suffering by aging. As an undergraduate he is currently performing research in Dr. Richard Bennetts lab at the University of Southern Indiana, as well as volunteering for various organizations including the Buck Institute for research on Aging.
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important person

New study by Mount Sinai St. Luke’s and Mount Sinai Roosevelt shows having a high sense of purpose may lower your risk of death, heart disease, or stroke

THE MOUNT SINAI HOSPITAL / MOUNT SINAI SCHOOL OF MEDICINE

Having a high sense of purpose in life may lower your risk of heart disease and stroke, according to a new study led by researchers at Mount Sinai St. Luke’s and Mount Sinai Roosevelt and presented on March 6 at the American Heart Association’s EPI/Lifestyle 2015 Scientific Sessions in Baltimore.

The new analysis defined purpose in life as a sense of meaning and direction, and a feeling that life is worth living. Previous research has linked purpose to psychological health and well-being, but the new Mount Sinai analysis found that a high sense of purpose is associated with a 23 percent reduction in death from all causes and a 19 percent reduced risk of heart attack, stroke, or the need for coronary artery bypass surgery (CABG) or a cardiac stenting procedure.

“Developing and refining your sense of purpose could protect your heart health and potentially save your life,” says lead study author Randy Cohen, MD, a preventive cardiologist at Mount Sinai St. Luke’s and Mount Sinai Roosevelt. “Our study shows there is a strong relationship between having a sense of purpose in life and protection from dying or having a cardiovascular event. As part of our overall health, each of us needs to ask ourselves the critical question of ‘do I have a sense of purpose in my life?’ If not, you need to work toward the important goal of obtaining one for your overall well-being.”

The research team reviewed 10 relevant studies with the data of more than 137,000 people to analyze the impact of sense of purpose on death rates and risk of cardiovascular events. The meta-analysis also found that those with a low sense of purpose are more likely to die or experience cardiovascular events.

“Prior studies have linked a variety of psychosocial risk factors to heart disease, including negative factors such as anxiety and depression and positive factors such as optimism and social support,” says Alan Rozanski, MD, study co-author and Director of Wellness and Prevention Programs for Mount Sinai Heart at the Mount Sinai Health System. “Based on our findings, future research should now further assess the importance of life purpose as a determinant of health and well-being and assess the impact of strategies designed to improve individuals’ sense of life purpose.”

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About the Mount Sinai Health System

The Mount Sinai Health System is an integrated health system committed to providing distinguished care, conducting transformative research, and advancing biomedical education. Structured around seven member hospital campuses and a single medical school, the Health System has an extensive ambulatory network and a range of inpatient and outpatient services–from community based facilities to tertiary and quaternary care.

The System includes approximately 6,600 primary and specialty care physicians, 12minority owned free standing ambulatory surgery centers, over 45 ambulatory practices throughout the five boroughs of New York City, Westchester, and Long Island, as well as 31 affiliated community health centers. Physicians are affiliated with the Icahn School of Medicine at Mount Sinai, which is ranked among the top 20 medical schools both in National Institutes of Health funding and by U.S. News & World Report.

For more information, visit http://www.mountsinai.org or find Mount Sinai on Facebook, Twitter and YouTube

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Study reveals molecular genetic mechanisms driving breast cancer progression

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Original Source Here

UT SOUTHWESTERN MEDICAL CENTER

DALLAS – April 3, 2015 – Researchers at UT Southwestern Medical Center have uncovered how the body’s inflammatory response can alter how estrogen promotes the growth of breast cancer cells. IMAGE

UT Southwestern researchers identified how a combination of signaling molecules inhibits the growth of breast cancer cells, improving clinical outcomes for some subtypes of breast cancers.

The combination — the steroid hormone estradiol and the proinflammatory cytokine tumor necrosis factor alpha (TNFα) — act to expand the number of sites where estrogen receptor alpha (ERα) can bind to the genome in breast cancer cells. The new sites of ERα binding turn new genes on and off, which alters the growth response of the breast cancer cells, inhibiting their growth and improving clinical outcomes in certain cases.

The newly identified gene set can be used as a biomarker that can help physicians determine who is at risk and how they might react to certain therapies.

“Our study uncovered the molecular mechanisms that alter the expression of the new set of genes in response to estradiol and TNFα, and identified potential target genes for future therapy,” said senior author Dr. W. Lee Kraus, Director of the Cecil H. and Ida Green Center for Reproductive Biology Sciences, Professor of Obstetrics and Gynecology, and a member of the Harold C. Simmons Comprehensive Cancer Center. “Since the altered pattern of gene expression can predict outcomes in breast cancer, there are important diagnostic and prognostic implications.”

The findings are published online and in the journal Molecular Cell.

Approximately 12.3 percent of women will be diagnosed with breast cancer at some point during their lifetime, and nearly 2.9 million women are living with breast cancer in the United States, according to statistics from the National Cancer Institute (NCI). About 232,670 new cases were reported in 2014, constituting about 14 percent of all new cancer cases. About 40,000 deaths were attributed to breast cancer in 2014.

Cancer cells release signals that can prompt the body to respond with an inflammatory response. As part of this response, TNFα is released and can impact the growth of the cancer cells. Previous studies suggested that inflammation might exacerbate the cancer, while the present study suggests that, in some cases, it might actually promote a better outcome. The study revealed that, when present together, TNFα and estradiol cause ERα, a nuclear transcription factor that is present in about two-thirds of breast cancers (so-called ER+ cancers), to bind to new sites in the genome where the protein does not bind with either TNFα or estradiol alone. These new ERα binding sites allow altered gene expression and, for some subtypes of breast cancers, inhibit the growth of cancer cells.

Since the effect only happens when the two are combined, researchers can use the altered gene expression patterns as an indicator that both agents are at work in the cancer and as a biomarker that may help determine who might be more at risk and how they might react to therapy, said Dr. Kraus, Professor and Vice Chair for Basic Sciences in Obstetrics and Gynecology, Professor of Pharmacology, and holder of the Cecil H. and Ida Green Distinguished Chair in Reproductive Biology Sciences.

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The mission of the Cecil H. and Ida Green Center for Reproductive Biology Sciences, endowed by Cecil and Ida Green in 1974, is to promote and support cutting-edge, integrative, and collaborative basic research in female reproductive biology, with a focus on signaling, gene regulation, and genome function.

Other UT Southwestern researchers involved in the work were postdoctoral researcher Dr. Hector Franco and computational biologist Anusha Nagari.

The work was supported by a postdoctoral fellowship from the American Cancer Society – Lee National Denim Day Fellowship and a grant from the National Institute of Diabetes and Digestive and Kidney Diseases, part of the National Institutes of Health.

UT Southwestern’s Harold C. Simmons Comprehensive Cancer Center is the only National Cancer Institute-designated cancer center in North Texas and one of just 68 NCI-designated cancer centers in the nation. The Simmons Cancer Center includes 13 major cancer care programs with a focus on treating the whole individual with innovative treatments, while fostering groundbreaking research that has the potential to improve patient care and prevention of cancer worldwide. In addition, the Center’s education and training programs support and develop the next generation of cancer researchers and clinicians.

The Simmons Cancer Center is among only 30 U.S. cancer research centers to be named a National Clinical Trials Network Lead Academic Participating Site, a prestigious new designation by the NCI, and the only Cancer Center in North Texas to be so designated. The designation and associated funding is designed to bolster the cancer center’s clinical cancer research for adults and to provide patients access to cancer research trials sponsored by the NCI, where promising new drugs often are tested.

About UT Southwestern Medical Center

UT Southwestern, one of the premier academic medical centers in the nation, integrates pioneering biomedical research with exceptional clinical care and education. The institution’s faculty includes many distinguished members, including six who have been awarded Nobel Prizes since 1985. Numbering approximately 2,800, the faculty is responsible for groundbreaking medical advances and is committed to translating science-driven research quickly to new clinical treatments. UT Southwestern physicians provide medical care in 40 specialties to about 92,000 hospitalized patients and oversee approximately 2.1 million outpatient visits a year.

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A new antibiotic kills pathogens without detectable resistance – Posted at the request of a friend

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After 15+ years as an IT professional. Jonathon decided to return to school in hopes of one day troubleshooting the most universal problem effecting all. Death, pain, and suffering by aging. As an undergraduate he is currently performing research in Dr. Richard Bennetts lab at the University of Southern Indiana, as well as volunteering for various organizations including the Buck Institute for research on Aging.
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new antibiotic

Abstract

Full Paper Here

Antibiotic resistance is spreading faster than the introduction of new compounds into clinical practice, causing a public health crisis. Most antibiotics were produced by screening soil microorganisms, but this limited resource of cultivable bacteria was overmined by the 1960s. Synthetic approaches to produce antibiotics have been unable to replace this platform. Uncultured bacteria make up approximately 99% of all species in external environments, and are an untapped source of new antibiotics. We developed several methods to grow uncultured organisms by cultivation in situ or by using specific growth factors. Here we report a new antibiotic that we term teixobactin, discovered in a screen of uncultured bacteria. Teixobactin inhibits cell wall synthesis by binding to a highly conserved motif of lipid II (precursor of peptidoglycan) and lipid III (precursor of cell wall teichoic acid). We did not obtain any mutants of Staphylococcus aureus or Mycobacterium tuberculosis resistant to teixobactin. The properties of this compound suggest a path towards developing antibiotics that are likely to avoid development of resistance.

Bursts of fasting may be key to longevity and health

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After 15+ years as an IT professional. Jonathon decided to return to school in hopes of one day troubleshooting the most universal problem effecting all. Death, pain, and suffering by aging. As an undergraduate he is currently performing research in Dr. Richard Bennetts lab at the University of Southern Indiana, as well as volunteering for various organizations including the Buck Institute for research on Aging.
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Andrea Cannon

Andrea Cannon

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Hunger. People go to great lengths to keep their stomachs full, but research dating back more than 60 years suggests that temporarily depriving oneself of food may be the key to a long and healthy life.

Clinical research from as early as 1945 reveals that restricting calories in animal test subjects results in a longer life—up to 20 percent longer in mice—and significantly decreases the likelihood of developing age-related disease. At the time the researchers might not have known the mechanisms behind the disease-fighting and life-extending qualities mustered by the missing calories, but recent science has suggested a handful of potential answers for why an energy-scarce environment might result in

health benefits.

In a February 2015 paper published in the journal Rejuvenation Research, scientists from the University of Florida recruited a group of healthy individuals to fast intermittently for two three-week periods. On “fasting” days, the group had their caloric intake restricted to 25 percent of their average diet. Conversely, on alternating “feasting” days, they were required to eat 175 percent of their normal intake to control for fluctuating weight as a confounding variable. Researchers hypothesized that this intermittent fasting approach might be a more sustainable eating pattern for the long-term than a consistently calorie-restricted diet.

“Most of the evidence in terms of caloric restriction in humans is typically in an observational context where you have people who choose to do it because that’s the kind of lifestyle they want to live,” said Martin Wegman, the lead author of the study and an M.D.-Ph.D. student at the University of Florida. “There’s anecdotal evidence in those arenas that those who [fast]  tend to slow down some aging-related diseases, tend to live longer.”

When cells in the body shift from an energy-rich environment to an energy-poor environment, like when the energy stored from food runs out, it produces reactive oxygen species—or chemically reactive oxygen-containing molecules—Wegman said. Researchers suspect the presence of these molecules creates stress in the cell that promotes the genetic changes that result in a kind of cellular-protective action, including the production of antioxidants in the body.

“We’ve postulated that in certain scenarios they can actually serve a beneficial role in many different pathways,” Wegman said. “We’re considering whether or not the intermittent fasting regimen may be an effective way to upregulate [reactive oxygen species] intermittently to trigger a kind of

protective mechanism.”

Post-study blood tests showed that certain genes, which have been linked to anti-aging characteristics, were expressed in greater numbers while circulating insulin decreased. The study also included a dietary satisfaction survey component.

“That’s actually one of the bigger surprises,” said Michael Guo, co-author and graduate student in the Hirschhorn Lab at Harvard Medical School. “On one day someone is fasting at 25 percent of their normal intake and on feasting days eating 175 percent of normal caloric intake. We expected the fasting days to be more difficult but found it to be exactly the opposite. Participants had more trouble eating the full 175 percent and found little trouble with the fasting days.”

According to Mark Mattson, chief of the Laboratory of Neurosciences at the National Institute on Aging in Baltimore, Maryland, the surprising ease with which participants ate so few calories on fasting days may have an evolutionary adaptive basis, which could explain the resulting health benefits.

“In pathological conditions, there’s an abnormal accumulation of damaged and dysfunctional proteins in the cells,” Mattson said. “What’s happening is that fasting and calorie restriction and exercise activate a pathway called autophagy—an old term meaning ‘self-eating.’ It’s a mechanism whereby cells remove garbage and that protects them from building up these damaging proteins. It also increases the production of neurotropic factors which we’ve seen lead to cognitive improvements in animals.”

Intuitively, our ancestors did not have a constant supply of food and would have likely fasted for extended periods of time, Mattson said. When we eat three or more regular meals per day, our livers primarily store energy as glucose. Mattson said it takes at least 10–12 hours of fasting to deplete those stores before the body uses fatty acids from cells as energy, which can translate to weight loss, improvements in body composition and, possibly, cognitive benefits.

“We think that intermittent fasting is superior to counting calories at each meal or eating regular smaller meals,” Mattson said. “During the fasting period you activate the garbage disposal mechanisms, the neurotropic factor mechanisms, the mechanisms that suppress inflammation. When you do eat, when you catch your prey, your cells are ready to grow and function better. We think cycles of mild stress-and-recovery—which is kind of what the evolutionary situation was—might be better for health than a more constant intake of calories.”

Memory loss associated with Alzheimer’s reversed for first time

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Original Source Here

Patient 1 had two years of progressive memory loss. She was considering quitting her job, which involved analyzing data and writing reports, she got disoriented driving, and she mixed up the names of her pets.

Patient 2 kept forgetting once-familiar faces at work, forgot his gym locker combination and had to have his assistants constantly remind him of his work schedule.

Patient 3’s memory was so bad that she used an iPad to record everything, then forgot her password. Her children noticed she commonly lost her train of thought in mid-sentence, and often asked them if they had carried out the tasks that she mistakenly thought she had asked them to do.

— “Reversal of cognitive decline: A novel therapeutic program,” UCLA/Buck Institute, 2014

Since it was first described over 100 years ago, Alzheimer’s disease causes a ton of pain in the nervous system and involves medication about which you can find everything on Neuropathy Help, but till today it has been without an effective treatment.

That may finally be about to change: In the first, small study of a novel, personalized and comprehensive program to reverse memory loss, nine of 10 participants, including those described above, displayed subjective or objective improvement in their memories beginning within three to six months.

Six patients had discontinued working or had been struggling at their jobs at the time they joined the study; all were able to return to their jobs or continue working with improved performance, and their improvements have been sustained. (The patient in treatment the longest has been receiving the therapy for two-and-a-half years.)

Among the 10 were patients with memory loss associated with Alzheimer’s disease, amnestic mild cognitive impairment or subjective cognitive impairment (in which the patient reports cognitive problems). One patient who had been diagnosed with late stage Alzheimer’s did not improve.

The study was conducted Dr. Dale Bredesen of the UCLA Mary S. Easton Center for Alzheimer’s Disease Research and the Buck Institute for Research on Aging. It is the first to suggest that memory loss in patients may be reversed — and improvement sustained — using a complex, 36-point therapeutic program that involves comprehensive diet changes, brain stimulation, exercise, sleep optimization, specific pharmaceuticals and vitamins, and multiple additional steps that affect brain chemistry.

The findings are published in the current online edition of the journal Aging.

Bredesen, UCLA’s Augustus Rose Professor of Neurology, director of the Easton Center and the paper’s author, said the findings are “very encouraging,” but he added that the results are anecdotal, and a more extensive, controlled clinical trial is needed.

No single drug has been found to stop or even slow the progression of Alzheimer’s, and drugs have only had modest effects on symptoms. “In the past decade alone, hundreds of clinical trials have been conducted for Alzheimer’s, without success, at an aggregate cost of over $1 billion,” said Bredesen, who also is a professor at the Buck Institute.

Although other chronic illnesses such as cardiovascular disease, cancer and HIV have been improved through the use of combination therapies, comprehensive combination therapies have not been explored for Alzheimer’s and other memory disorders. However, over the past few decades, genetic and biochemical research has revealed an extensive network of molecular interactions involved in the development of Alzheimer’s.

“That suggested that a broader-based therapeutic approach, rather than a single drug that aims at a single target, may be feasible and potentially more effective for the treatment of cognitive decline due to Alzheimer’s,” Bredesen said.

While extensive preclinical studies in numerous other laboratories have identified single pathogenic targets for potential intervention, in human studies, such single target therapeutic approaches have not borne out. But, said Bredesen, it’s possible that addressing multiple targets within the network underlying Alzheimer’s may be successful even when each target is affected in a relatively modest way. “In other words,” he said, “the effects of the various targets may be additive, or even synergistic.”

The uniform failure of drug trials in Alzheimer’s influenced Bredesen’s desire to better understand the fundamental nature of the disease. His laboratory has found evidence that Alzheimer’s stems from an imbalance in nerve cell signaling. In the normal brain, specific signals foster nerve connections and memory making, while balancing signals support memory loss, allowing irrelevant information to be forgotten. But in people with Alzheimer’s, the balance of these opposing signals is disturbed, nerve connections are suppressed and memories are lost.

That finding is contrary to the popular belief that Alzheimer’s is caused by the accumulation of sticky plaques in the brain. Bredesen believes the amyloid beta peptide, the source of the plaques, has a normal function in the brain, as part of a larger set of molecules that promote signals that cause nerve connections to lapse. Thus, the increase in the peptide that occurs in Alzheimer’s shifts the balance in favor of memory loss.

Bredesen therefore thought that, rather than a single targeted agent, the solution might be a multiple-component system approach, in line with the approach for other chronic illnesses.

“The existing Alzheimer’s drugs affect a single target, but Alzheimer’s disease is more complex. Imagine having a roof with 36 holes in it, and your drug patched one hole very well,” he said. “The drug may have worked, and a single hole may have been fixed, but you still have 35 other leaks, and so the underlying process may not be affected much.”

Bredesen’s approach is personalized to the patient, based on extensive testing to determine what is affecting the brain’s plasticity signaling network. In the case of the patient with the demanding job who was forgetting her way home, her therapy consisted of some, but not all, of the components of Bredesen’s program, including:

  • eliminating all simple carbohydrates, gluten and processed food from her diet, and eating more vegetables, fruits and non-farmed fish
  • meditating twice a day and beginning yoga to reduce stress
  • sleeping seven to eight hours per night, up from four to five
  • taking melatonin, methylcobalamin, vitamin D3, fish oil and coenzyme Q10 each day
  • optimizing oral hygiene using an electric flosser and electric toothbrush
  • reinstating hormone replacement therapy, which had previously been discontinued
  • fasting for a minimum of 12 hours between dinner and breakfast, and for a minimum of three hours between dinner and bedtime
  • exercising for a minimum of 30 minutes, four to six days per week

Bredesen said the program’s downsides are its complexity and that the burden falls on patients and caregivers to follow it. In the study, none of the patients was able to stick to the entire protocol. Their most common complaints were the diet and lifestyle changes, and having to take multiple pills each day.

The good news, though, said Bredesen, are the side effects: “It is noteworthy that the major side effects of this therapeutic system are improved health and an improved body mass index, a stark contrast to the side effects of many drugs.”

The results suggest that memory loss may be reversed and improvement sustained with the therapeutic program, but Bredesen cautioned that the results need to be replicated.

“The current, anecdotal results require a larger trial, not only to confirm or refute the results reported here, but also to address key questions raised, such as the degree of improvement that can be achieved routinely, how late in the course of cognitive decline reversal can be effected, whether such an approach may be effective in patients with familial Alzheimer’s disease, and last, how long improvement can be sustained,” he said.

Cognitive decline is a major concern of the aging population. Alzheimer’s affects approximately 5.4 million Americans and 30 million people globally. By 2050, without effective prevention and treatment, an estimated 160 million people globally would have the disease, including 13 million Americans, which could potentially bankrupt the Medicare system. Unlike several other chronic illnesses, the incidence of Alzheimer’s is on the rise; recent estimates suggest that it has become the third leading cause of death in the U.S. behind cardiovascular disease and cancer.

Multiple entities provided support for the study, including the National Institutes of Health (AG16570, AG034427 and AG036975). The complete list is included in the paper.

Building artificial body parts with particle beams

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After 15+ years as an IT professional. Jonathon decided to return to school in hopes of one day troubleshooting the most universal problem effecting all. Death, pain, and suffering by aging. As an undergraduate he is currently performing research in Dr. Richard Bennetts lab at the University of Southern Indiana, as well as volunteering for various organizations including the Buck Institute for research on Aging.
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Companies are using an electron-beam 3-D printing process to manufacture medical implants.

Think antioxidants will make you live longer? Think again: We spend millions on them but now researchers say supplements may make our bodies age FASTER

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After 15+ years as an IT professional. Jonathon decided to return to school in hopes of one day troubleshooting the most universal problem effecting all. Death, pain, and suffering by aging. As an undergraduate he is currently performing research in Dr. Richard Bennetts lab at the University of Southern Indiana, as well as volunteering for various organizations including the Buck Institute for research on Aging.
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By JOHN NAISH – Courtesy of Dailymail.co.uk

For years we’ve swallowed the line from scientists that antioxidants could slow the rate at which our cells————————————————————————————————————————–

We all want to stay as healthy and young-looking as possible, which is why millions of us dutifully take antioxidant supplements such as vitamins C, E and beta-carotene, as well as splashing out on costly antioxidant ‘superfoods’ such as blueberries.

For years we’ve swallowed the line from scientists that antioxidants could slow the rate at which our cells – and therefore our bodies – age.

The theory is that antioxidants reduce the ‘oxidising’ damage caused by free radicals – corrosive molecules produced by our bodies as we process oxygen, and which we also breathe in from polluted air and smoking.

We all want to stay as healthy and young-looking as possible, which is why millions of us dutifully take antioxidant supplements such as vitamins C, E and beta-carotene, as well as splashing out on costly antioxidant ‘superfoods’ such as blueberries.

For years we’ve swallowed the line from scientists that antioxidants could slow the rate at which our cells – and therefore our bodies – age.

The theory is that antioxidants reduce the ‘oxidising’ damage caused by free radicals – corrosive molecules produced by our bodies as we process oxygen, and which we also breathe in from polluted air and smoking.

It is thought that when these free radicals attack proteins and lipids (fats in the cells), it breaks down the cell membrane and damages the DNA inside. This in turn may cause cancerous mutations, as well as making the cells age more rapidly. Free-radical damage to brain cells is also believed to cause the sort of drops in cognitive functioning associated with ageing.

In Britain, we spend £175 million a year on antioxidant supplements – but a new study suggests we might be wasting our money. Not only do free radicals not cause ageing, say researchers at McGill University in Canada, but taking antioxidant pills may actually make our bodies age faster- making them a short cut to an early grave. So what is going on?

More…

Read more: http://www.dailymail.co.uk/health/article-2639929/Think-antioxidants-make-live-longer-Think-We-spend-millions-researchers-say-supplements-make-bodies-age-FASTER.html#ixzz337MEvKBP
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Researchers use light to coax stem cells to regrow teeth

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After 15+ years as an IT professional. Jonathon decided to return to school in hopes of one day troubleshooting the most universal problem effecting all. Death, pain, and suffering by aging. As an undergraduate he is currently performing research in Dr. Richard Bennetts lab at the University of Southern Indiana, as well as volunteering for various organizations including the Buck Institute for research on Aging.
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Researchers use light to coax stem cells to repair teeth

These tooth models show the relative size comparison of a human tooth versus a rat tooth — to give an idea of the technical challenges involved with performing dentistry on such a small scale. NOTE: The small “rat tooth” is not an actual rat …more

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Article Courtesy of edicalxpress.com

A Harvard-led team is the first to demonstrate the ability to use low-power light to trigger stem cells inside the body to regenerate tissue, an advance they reported inScience Translational Medicine. The research, led by Wyss Institute Core Faculty member David Mooney, Ph.D., lays the foundation for a host of clinical applications in restorative dentistry and regenerative medicine more broadly, such as wound healing, bone regeneration, and more.

The team used a low-power laser to trigger human dental  to form dentin, the hard tissue that is similar to bone and makes up the bulk of teeth. What’s more, they outlined the precise molecular mechanism involved, and demonstrated its prowess using multiple laboratory and animal models.

A number of biologically active molecules, such as regulatory proteins called growth factors, can trigger stem cells to differentiate into different cell types. Current regeneration efforts require scientists to isolate stem cells from the body, manipulate them in a laboratory, and return them to the body—efforts that face a host of regulatory and technical hurdles to their clinical translation. But Mooney’s approach is different and, he hopes, easier to get into the hands of practicing clinicians.

“Our treatment modality does not introduce anything new to the body, and lasers are routinely used in medicine and dentistry, so the barriers to clinical translation are low,” said Mooney, who is also the Robert P. Pinkas Family Professor of Bioengineering at Harvard’s School of Engineering and Applied Sciences (SEAS). “It would be a substantial advance in the field if we can regenerate teeth rather than replace them.”

The team first turned to lead author and dentist Praveen Arany, D.D.S., Ph.D., who is now an Assistant Clinical Investigator at the National Institutes of Health (NIH). At the time of the research, he was a Harvard graduate student and then postdoctoral fellow affiliated with SEAS and the Wyss Institute.

Researchers use light to coax stem cells to repair teeth

The team used high-resolution x-ray imaging and microscopy techniques to assess the formation of reparative (tertiary) dentin 12 weeks after the low-power laser treatment. In the microscopy images shown here, the yellow hashtags (#) sit atop …more

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Arany took rodents to the laboratory version of a dentist’s office to drill holes in their molars, treat the tooth pulp that contains adult dental stem cells with low-dose laser treatments, applied temporary caps, and kept the animals comfortable and healthy. After about 12 weeks, high-resolution x-ray imaging and microscopy confirmed that the laser treatments triggered the enhanced dentin formation.

“It was definitely my first time doing rodent dentistry,” said Arany, who faced several technical challenges in performing oral surgery on such a small scale. The dentin was strikingly similar in composition to normal dentin, but did have slightly different morphological organization. Moreover, the typical reparative dentin bridge seen in human teeth was not as readily apparent in the minute rodent teeth, owing to the technical challenges with the procedure.

“This is one of those rare cases where it would be easier to do this work on a human,” Mooney said.

Next the team performed a series of culture-based experiments to unveil the precise molecular mechanism responsible for the regenerative effects of the laser treatment. It turns out that a ubiquitous regulatory cell protein called transforming growth factor beta-1 (TGF-β1) played a pivotal role in triggering the dental stem cells to grow into dentin. TGF-β1 exists in latent form until activated by any number of molecules.

Here is the chemical domino effect the team confirmed: In a dose-dependent manner, the laser first induced reactive oxygen species (ROS), which are chemically active molecules containing oxygen that play an important role in cellular function. The ROS activated the latent TGF-β1complex which, in turn, differentiated the stem cells into dentin.

Researchers use light to coax stem cells to regrow teeth

Scanning electron microscopy images of a polymeric scaffold used for 3D cultures. Credit: Arany PR et al.

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Nailing down the mechanism was key because it places on firm scientific footing the decades-old pile of anecdotes about low-level light therapy (LLLT), also known as Photobiomodulation (PBM).

Since the dawn of medical laser use in the late 1960s, doctors have been accumulating anecdotal evidence that low-level light therapy can stimulate all kind of biological processes including rejuvenating skin and stimulating hair growth, among others. But interestingly enough, the same laser can be also be used to ablate skin and remove hair—depending on the way the clinician uses the laser. The clinical effects of low-power lasers have been subtle and largely inconsistent. The new work marks the first time that scientists have gotten to the nub of how low-level laser treatments work on a molecular level, and lays the foundation for controlled treatment protocols.

“The scientific community is actively exploring a host of approaches to using stem cells for tissue regeneration efforts,” said Wyss Institute Founding Director Don Ingber, M.D., Ph.D., “and Dave and his team have added an innovative, noninvasive and remarkably simple but powerful tool to the toolbox.”

Next Arany aims to take this work to human clinical trials. He is currently working with his colleagues at the National Institute of Dental and Craniofacial Research (NIDCR), which is one of the National Institutes of Health (NIH), to outline the requisite safety and efficacy parameters. “We are also excited about expanding these observations to other regenerative applications with other types of stem cells,” he said.

More information: “Photoactivation of Endogenous Latent Transforming Growth Factor–β1 Directs Dental Stem Cell Differentiation for Regeneration,” by P.R. Arany et al. Science Translational Medicine, 2014.stm.sciencemag.org/lookup/doi/10.1126/scitranslmed.3008234

First Complete Mapping Of Human Proteome Discovers 193 New Proteins Read more at http://www.iflscience.com/health-and-medicine/first-complete-mapping-human-proteome-discovers-193-new-proteins#HxRpFzk4Hch5orSR.99

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After 15+ years as an IT professional. Jonathon decided to return to school in hopes of one day troubleshooting the most universal problem effecting all. Death, pain, and suffering by aging. As an undergraduate he is currently performing research in Dr. Richard Bennetts lab at the University of Southern Indiana, as well as volunteering for various organizations including the Buck Institute for research on Aging.
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catalog of human proteins

 

Article Courtesy Of IFLSCIENCE.COM

 

In separate papers published this week, two independent teams have drafted the first maps of the human proteome — which charts all of the proteins that make up a person. And both teams discovered that proteins do come from “noncoding” DNA sequences.

The proteome is an important complement to the genome and transcriptome, and together they create a more complete resource for researching health and diseases. While genes determine many of our characteristics, they’re able to do that by providing instructions for making proteins. So these draft maps — which you can think of as the Human Genome Project for proteins — consist of profiles of proteins expressed in all sorts of different human cell types. Both drafts were generated using mass spectrometry.

One of the teams, led by Akhilesh Pandey from Johns Hopkins University, identified and annotated proteins encoded by 17,294 genes – that accounts for around 84 percent of all the genes in the human genome that are predicted to encode proteins (that number is estimated at 19,629, if you’re curious). The team extracted proteins from samples of 30 different tissues, then used enzymes to cut them into small pieces called peptides. They ran the peptides through a series of instruments to identify and measure their relative abundance.

They also discovered 193 novel proteins that come from regions of the genome that haven’t been predicted to code for proteins. Within the genome, there are stretches of DNA whose sequences don’t follow a conventional protein-coding gene pattern – these have been labeled as noncoding. “The fact that 193 of the proteins came from DNA sequences predicted to be noncoding means that we don’t fully understand how cells read DNA, because clearly those sequences do code for proteins,” Pandey explains in a news release.

The other team, led by Bernhard Kuster of Technische Universität München (TUM) in Germany, assembled protein evidence for over 18,000 genes (or 92 percent of the entire proteome) by compiling raw mass spec data from databases and other analyses that were already available. These include a core of 10,000–12,000 proteins expressed in several different tissues, and to fill in the gaps, they generated their own mass spec data by analyzing 60 human tissues, 13 body fluids, and 147 cancer cell lines.

Like the Hopkins team, they also found evidence of translation from DNA regions that were not thought to be translated. This includes more than 400 translated long, intergenic non-coding RNAs (lincRNAs). “While we have a good idea of what the genome looks like, we didn’t know how many of those potentially 20,000 protein-coding genes would actually make protein,” Kuster tells BBC. The team also identified protein markers that may predict an individual’s resistance or sensitivity to drugs for diseases like cancer.

“You can think of the human body as a huge library where each protein is a book,” Pandey says. “The difficulty is that we don’t have a comprehensive catalog that gives us the titles of the available books and where to find them.” Now it looks like we’ve got two first drafts of that comprehensive catalog. Each group has built a publicly accessible, interactive database of their datasets: Human Proteome Map and ProteomicsDB.

Although they had seen each other’s work at conferences, both Pandey and Kuster tell BBC they had “no idea” they were headed towards publishing simultaneously. And now they share a Nature cover. “We never saw this as a race to be first,” Kuster says. “My interpretation is that when the time is right, somebody’s going to just do it. And perhaps two people are going to do it!” Here’s the human body map of protein expression.


Read more at http://www.iflscience.com/health-and-medicine/first-complete-mapping-human-proteome-discovers-193-new-proteins#HxRpFzk4Hch5orSR.99

The findings [here and here] were published in Nature this week.

[Johns HopkinsTUM via The ScientistBBC]

Images: H. Hahne, TUM

Read more at http://www.iflscience.com/health-and-medicine/first-complete-mapping-human-proteome-discovers-193-new-proteins#HxRpFzk4Hch5orSR.99