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Potentially immortal flatworm species studied
February 29, 2012. An article published online on February 27, 2012 in the Proceedings of the National Academy of Sciences describes a mechanism by which a species of flatworm appears to have achieved an indefinitely extended life span.
Schmidtea mediterranea has strains that reproduce sexually or asexually, and may have an indefinite capacity to renew their tissues from a pool of potentially immortal stem cells. "We've been studying two types of planarian worms; those that reproduce sexually, like us, and those that reproduce asexually, simply dividing in two," explained Dr Abu Aboobaker of the University of Nottingham, who led the research. "Both appear to regenerate indefinitely by growing new muscles, skin, guts and even entire brains over and over again. Usually when stem cells divide — to heal wounds, or during reproduction or for growth — they start to show signs of aging. This means that the stem cells are no longer able to divide and so become less able to replace exhausted specialized cells in the tissues of our bodies. Our aging skin is perhaps the most visible example of this effect. Planarian worms and their stem cells are somehow able to avoid the aging process and to keep their cells dividing."
The researchers identified a gene in the flatworm that coded for telomerase, an enzyme that maintains the length of telomeres. Telomeres are caps at the ends of chromosomes that shorten with aging, and telomere length has been used as a marker for cellular aging. They found that flatworms that reproduce asexually show a significantly increase activity of the gene when they regenerate, which allows stem cells to maintain their telomeres while dividing to replace tissues. "Asexual planarian worms demonstrate the potential to maintain telomere length during regeneration," Dr Aboobaker stated. "Our data satisfy one of the predictions about what it would take for an animal to be potentially immortal and that it is possible for this scenario to evolve. The next goals for us are to understand the mechanisms in more detail and to understand more about how you evolve an immortal animal."
Vitamin D anti-inflammatory pathway identified
February 27, 2012. Writing in the March 1, 2012, issue of The Journal of Immunology, researchers at National Jewish Health in Denver report their discovery of a molecular pathway through which vitamin D inhibits inflammation.
Assistant professor of pediatrics Elena Goleva and her associates cultured human white blood cells with varying amounts of vitamin D or no vitamin D before exposing them to lipopolysaccharide, a pro-inflammatory compound. They found that cells incubated without vitamin D or with a reduced concentration of 15 nanograms per milliliter produced high amounts of the cytokines interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-a), both of which are involved in the inflammatory response. However, white blood cells that received concentrations of 30 nanograms per milliliter or more of vitamin D, which is a level considered by some researchers to be sufficient when measured in the bloodstream, had a decreased inflammatory response, with 50 nanograms per milliliter vitamin D resulting in the greatest reduction. Among other findings, the team observed that vitamin D treatment upregulated the expression of mitogen-activated protein kinase (MAPK) phosphatase-1, which interferes with inflammation. "This study goes beyond previous associations of vitamin D with various health outcomes," stated Dr Goleva. "It outlines a clear chain of cellular events, from the binding of DNA, through a specific signaling pathway, to the reduction of proteins known to trigger inflammation. Patients with chronic inflammatory diseases, such as asthma, arthritis and prostate cancer, who are vitamin D deficient, may benefit from vitamin D supplementation to get their serum vitamin D levels above 30 nanograms/milliliter."
"The fact that we showed a dose-dependent and varying response to levels commonly found in humans also adds weight to the argument for vitamin D's role in immune and inflammatory conditions," she added.
Greater flavanone intake linked to lower stroke risk in women
February 24, 2012. The American Heart Association journal Stroke published the finding of an association between a higher intake of a class of flavonoids known as flavanones and a reduced risk of stroke in women. The study is among the first to evaluate the impact of flavonoid subclasses on stroke risk.
Aedín Cassidy, PhD and colleagues analyzed data from 69,622 participants in the Nurse's Health Study for the current investigation. Responses to dietary questionnaires completed every four years during the fourteen year follow-up period were used to quantify the intake of six main flavonoid subclasses, which included flavanones, anthocyanins, flavan-3-ols, flavonoid polymers, flavonols and flavones. Nine hundred forty-three ischemic strokes, 253 hemorrhagic strokes and 607 strokes of unknown origin occurred over follow-up.
Although no association was observed between the risk of stroke and total flavonoid intake, among individual flavonoids, women whose flavanone consumption was among the top 20 percent of participants had a 19 percent lower risk of ischemic stroke compared to those whose intake was among the lowest fifth. Flavanone consumption in the current study was primarily derived from oranges and grapefruit, and their juices.
"Studies have shown higher fruit, vegetable and specifically vitamin C intake is associated with reduced stroke risk," stated Dr Cassidy, who is a professor of nutrition at Norwich Medical School at the University of East Anglia in Norwich, England. "Flavonoids are thought to provide some of that protection through several mechanisms, including improved blood vessel function and an anti-inflammatory effect."
"Our findings suggest that bioactive compounds present in citrus may potentially be associated with a reduced risk of stroke," the authors conclude. "Further prospective studies are needed to confirm these associations together with further molecular mechanistic data on flavanones to inform and optimize the design of randomized trials of flavanone and citrus-based foods to potentially reduce ischemic stroke risk."
Merely anticipating stress is aging
February 22, 2012. In addition to the negative effect that experiencing stress has on telomeres, research scheduled for publication in the May, 2012 issue of Brain, Behavior and Immunity reveals that anticipating a stressful event is also associated with a reduction in telomere length. Telomeres are protective caps at the ends of chromosomes that shorten with age and are a marker of cellular aging.
The research included 50 women, half of whom were caregivers of relatives with dementia. University of California San Francisco associate professor Elissa Epel and her colleagues found that when anticipating stressful tasks in the laboratory or tasks involving public speaking, the majority of participants underwent a reduction in telomere length. Women who were caregivers tended to anticipate a greater level of threat, which resulted in an increase risk of telomere shortening.
"We are getting closer to understanding how chronic stress translates into the present moment," Dr Epel stated. "As stress researchers, we try to examine the psychological process of how people respond to a stressful event and how that impacts their neurobiology and cellular health. And we're making some strides in that."
"How you respond to a brief stressful experience in the laboratory may reveal a lot about how you respond to stressful experiences in your daily life," remarked lead author Aoife O'Donovan, PhD. "Our findings are preliminary for now, but they suggest that the major forms of stress in your life may influence how your respond to more minor forms of stress, such as losing your keys, getting stuck in traffic or leading a meeting at work. Our goal is to gain better understanding of how psychological stress promotes biological aging so that we can design targeted interventions that reduce risk for disease in stressed individuals. We now have preliminary evidence that higher anticipatory threat perception may be one such mechanism."
Cooling prevents early death in septic shock
February 20, 2012. An article appearing online recently in the American Journal of Respiratory and Critical Care Medicine affirms a benefit for external cooling in sedated patients with septic shock. Septic shock is an inflammatory state resulting from the spread of infectious agents in the bloodstream, which can cause fever, low blood pressure and organ failure. The concept of cooling septic shock patients is controversial, as fever may play a role in the body's defense against pathogens, however, reducing fever can help elevate dangerously low blood pressure.
The current study included 200 adults with septic shock and fever who were receiving an infusion of vasopressor drugs to normalize their blood pressure. One hundred one subjects underwent external cooling under sedation for 48 hours, resulting in a reduction in body temperature to 36.5˚ to 37°C. Vasopressor dose was lowered to maintain normal blood pressure when indicated.
Participants undergoing cooling began to experience a reduction in body temperature after two hours. At twelve hours, those treated with cooling had a significantly greater need for a decrease in medication dose. This group also had a higher prevalence of shock reversal during their intensive care unit stay, and lower mortality at two weeks.
"The benefits and risks of fever control in patients with severe sepsis remains a matter of controversy," stated lead author Frédérique Schortgen, MD, PhD, of the Henri Mondor Hospital in Créteil, France. "In our study, external cooling to achieve normothermia in patients with septic shock was safe, accelerated hemodynamic stabilization, decreased vasopressor requirements, increased the rate of shock reversal, and decreased early mortality."
"Larger studies are needed to confirm the positive effects of cooling on mortality we observed and to examine whether fever control provides any additional benefits in patients with severe sepsis."
Curcumin prolongs life in model of Alzheimer's disease
February 17, 2012. Researchers from Sweden report a benefit for curcumin in fruit flies (Drosophila melanogaster) that have been genetically modified to develop a disorder similar to Alzheimer's disease. The findings were described in an article published on February 13, 2012 in the journal PLoS One.
For their research, Professor Per Hammarstrom and colleagues at Linköping University utilized four groups of fruit flies with different genetic modifications controlling the expression of amyloid beta, a toxic protein that accumulates in the brains of human Alzheimer's disease patients. Also included in the study was a group of flies bred to express Tau protein, which is also found in Alzheimer's diseased brains. Unmodified flies were used as controls.
With the exception of flies bred to express Tau, genetically modified flies that received curcumin lived up to 75 percent longer and maintained mobility longer compared to those that did not receive the compound. While curcumin was not associated with a decrease in amyloid plaque in the flies' brains or eyes, it appeared to reduce the amount of amyloid fibril precursors known as oligomers.
"Several theories have been established about how oligomers can instigate the disease process," the authors write. "According to one hypothesis, they become trapped at synapses, inhibiting nerve impulse signals. Others claim that they cause cell death by puncturing the cell membrane."
"The results confirm our belief that it is the oligomers that are most harmful to the nerve cells," Professor Hammarstrom stated. "We now see that small molecules in an animal model can influence the amyloid form. To our knowledge the encapsulation of oligomers is a new and exciting treatment strategy."
Curcumin may help in castration resistant prostate cancer
February 15, 2012. In an article published online on January 18, 2012 in Cancer Research, Professor of Cancer Biology, Urology and Radiation Oncology Karen Knudsen, PhD and her associates at Thomas Jefferson University report a benefit for curcumin, an isoflavone found in the spice turmeric, in reducing the growth of castration-resistant prostate cancer in men undergoing androgen deprivation therapy. Androgen deprivation therapy is a treatment for prostate cancer that works by inhibiting the androgen receptor. While androgen deprivation therapy is effective in many cases of prostate cancer, the disease often becomes resistant to therapy due to reactivation of the androgen receptor, necessitating other methods of treatment.
"Nuclear receptors and pioneer factors drive the development and progression of prostate cancer," the authors write. "In this disease, aggressive disease phenotypes and hormone therapy failures result from resurgent activity of androgen receptor and the upregulation of coactivator protein p300 and pioneer factors. Thus, a major current emphasis in the field is to identify mechanisms by which castrate-resistant androgen receptor activity and pioneer factor function can be combinatorially suppressed."
In preliminary research, curcumin was found to suppress the nuclear receptor activators p300 and CREB1-binding protein (CBP), which work against androgen deprivation therapy. For the current study, Dr Knudsen's team utilized prostate cancer cells subjected to androgen deprivation and found that the addition of physiologically attainable doses of curcumin resulted in cell cycle inhibition and a reduction in survival compared to cancer cells that did not receive curcumin. In another experiment using mice that were castrated and implanted with prostate tumors, animals that received curcumin experienced decreased tumor growth and mass compared with untreated mice.
"This study sets the stage for further development of curcumin as a novel agent to target androgen receptor signaling," Dr Knudsen stated. "It also has implications beyond prostate cancer since p300 and CBP are important in other malignancies, like breast cancer. In tumors where these play an important function, curcumin may prove to be a promising therapeutic agent."
Too many calories could increase memory loss
February 13, 2012. The latest findings from the Mayo Clinic in Scottsdale, Arizona could add yet another condition to the growing list of those that have been found to benefit from calorie restriction: a better memory. In research scheduled for presentation at the American Academy of Neurology's 64th Annual Meeting, to be held April 21 to April 28, 2012 in New Orleans, Yonas E. Geda, MD, MSc and associates discovered a link between decreased calorie intake and a lower risk of mild cognitive impairment, a condition that can precede Alzheimer's disease.
The current study included 1,233 participants in the Mayo Clinic Study of Aging, an ongoing population-based study centered in Olmsted County, Minnesota. The subjects, who were between the ages of 70 and 89, completed dietary questionnaires within one year of being interviewed. While the study excluded those with dementia, 163 subjects were determined to be cognitively impaired.
Although no significant difference was found between those whose calorie intake was among the lowest one-third at 600 to 1,526 calories per day and those whose intake was among the middle third at 1,527 to 2,142.5 calories, those whose intake was highest had 2.41 times the risk of cognitive impairment than those whose calorie consumption was lowest. The risk remained unchanged after adjustment for diabetes, stroke, education level and other factors.
"We observed a dose-response pattern which simply means; the higher the amount of calories consumed each day, the higher the risk of mild cognitive impairment," stated Dr Geda, MD who is a member of the American Academy of Neurology. "Cutting calories and eating foods that make up a healthy diet may be a simpler way to prevent memory loss as we age."
Trial will evaluate omega 3 fatty acids for the prevention of mental illness in teenagers
February 10, 2012. A double-blinded, randomized trial funded by the National Institute of Mental Health will examine the effect of omega-3 fatty acids from fish oil in young adults aged 12 to 25 who are at risk for severe psychiatric disorders. Omega-3 fatty acids, which include eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), are necessary for normal brain function, and have been recently studied as possible therapies for psychiatric disorders in addition to being widely recognized as helpful in depression, arrhythmias and other conditions.
The trial will be administered by researchers at Zucker Hillside Hospital's Recognition and Prevention (RAP) Program in Glen Oaks, New York. The RAP Program is a clinic and a research facility that works with adolescents and young adults to help prevent and treat psychiatric illnesses. The current study will compare the effects of six months of fish oil or a placebo on the subjects' clinical symptoms and school, work and social function. Participants will be monitored monthly at eight clinical sites.
"Of the 300 adolescents who have participated in the RAP Program, most have shown substantial improvement," stated Barbara Cornblatt, PhD, who is the director of the RAP Program and investigator at The Feinstein Institute for Medical Research, headquartered in Manhasset, New York. "If this study continues to show success, omega 3 could offer a natural alternative to the range of medications and therapies now offered to RAP participants. Ultimately, the goal of the RAP Program is to intervene and prevent illness before symptoms get worse."
Vitamin D levels reduced in trauma patients
February 8, 2012. The 2012 Annual Meeting of the American Academy of Orthopedic Surgeons was the site of the presentation of the finding of widespread vitamin D insufficiency among orthopedic trauma patients.
Brett D. Crist, MD of the University of Missouri and his associates evaluated data from 1,830 adult trauma center patients who were seen from January, 2009 through September, 2010. Deficient serum vitamin D levels, defined as less than 20 nanograms per milliliter, were detected in 39 percent of the men and women, and 38.4 had insufficient levels between 20 and 32 nanograms per milliliter. While those between the ages of 18 to 25 had the lowest incidence of deficiency, deficient levels were still found in 29 percent of this group, and 54.7 percent had vitamin D insufficiency.
The findings of the current study are significant "as vitamin D deficiency has been linked to increased incidences of fracture nonunions (bone breaks that fail to heal)," noted Dr Crist, who is codirector of the Orthopedic Trauma Service of the University of Missouri's Department of Orthopedic Surgery.
"Vitamin D deficiency affects patients of all ages and is more prevalent than we thought it was," he admitted. "Although we've gone to treating most patients with weekly high dose vitamin D, in addition to daily vitamin D and calcium, monitoring vitamin D levels can be done to diagnose and monitor levels."
He added that Vitamin D deficiency is "easy to manage," and "can prevent future fractures and improve healing of current fractures."
Vitamin and mineral supplementation prevents colon cancer in animal model
February 6, 2012. In the January, 2012 issue of the Canadian Journal of Physiology and Pharmacology, researchers from King Saud University in Riyadh, Saudi Arabia reveal the finding of a protective effect for vitamins and minerals against colon cancer in rats.
Two-thirds of a group of sixty male rats were injected with the colon-specific carcinogen DMH weekly for 15 weeks. Animals that did not receive DMH were subdivided to receive a regular diet or a diet enhanced with vitamins and minerals. While one group of carcinogen-treated animals received no supplementation, the remainder received supplemented diets during the 15 weeks DMH was administered, for 16 weeks after the carcinogen was administered, or throughout the 32-week treatment period. Lipid peroxidation products and antioxidant enzyme levels were measured in blood and tissue at the end of the experiment, and the animals were examined for aberrant crypt foci, a precursor of colorectal adenoma.
Rats that received DMH had higher levels of lipid peroxidation and lower antioxidant status in comparison with animals that did not receive the carcinogen; however, vitamin and mineral supplementation reversed these trends. Supplemented animals experienced a significant reduction in aberrant crypt foci compared to carcinogen-treated rats that received unsupplemented diets.
The authors conclude that "multivitamin and mineral supplements synergistically contribute to the cancer chemopreventative potential, and hence, regular supplements of multivitamins and minerals could reduce the risk of colon cancer."
"It has been unclear whether multivitamin supplementation to cancer patients is helpful, has no effect, or is even detrimental during therapy," remarked Canadian Journal of Physiology and Pharmacology editor Dr Grant Pierce. "This study is important because it gives some direction to cancer patients in desperate need of guidance on the value of multivitamins and minerals administered during cancer."
Calcium, magnesium reduce drug side effect in colon cancer patients
February 3, 2012. The addition of calcium and magnesium supplementation to a stop and go regimen of the drug oxaliplatin reduces the risk of potentially disabling neurological side effects, according to a review published recently in the Journal of Oncology.
"Many patients don't receive the necessary dose to try to keep their cancer in check, because their symptoms become too debilitating and their quality of life is reduced," explained Andrew Weickhardt, MD, who is a clinical fellow at the University of Colorado Cancer Center and coauthor of the review. "Before, when patients died in a few months, these symptoms were overlooked. Now they're living two to three years and the symptoms deserve closer attention."
Dr Weickhardt and colleagues recommend the addition of oxaliplatin to a standard colorectal cancer chemotherapy regimen for an initial period of two months, followed by a two month period in which oxaliplatin is discontinued. Oxaliplatin is then reintroduced at the end of the break or when disease progression is observed.
"After about six to nine months of total treatment, metastatic colorectal cancers tend to develop resistance to the drug," Dr Weickhardt remarked. "And also, no matter what we do, after this same six to nine months of total treatment, neurological side effects start to rise."
With the recommended regimen, five percent of the patients still experience significant persistent nerve damage. "There's room for improvement," Dr Weickhardt noted.
"An infusion of calcium and magnesium should be used as well because they've shown some benefit and they don't do any harm," he added. "They're popular in the community, and I'd encourage their use."
B vitamin lowers blood pressure in at risk population
February 1, 2012. In an article published online on January 25, 2012 in the American Journal of Clinical Nutrition, researchers from Northern Ireland report a benefit for the B vitamin riboflavin in men and women with a gene mutation that puts them at risk for elevated homocysteine and hypertension.
The study, conducted in 2008, included 83 participants in a 16 week placebo-controlled trial of riboflavin conducted in 2004. Thirty-one subjects who had the TT genotype of the gene encoding methylenetetrahydrofolate reductase (MTHFR, a folate-metabolizing enzyme), were again given 1.6 milligrams per day riboflavin or a placebo for 16 weeks, however, those who received riboflavin in 2004 were given a placebo in 2008, and vice-versa. (Riboflavin, in its coenzymatic form, is a cofactor for MTHFR.)
Those who had the TT genotype had higher systolic blood pressure in 2004 and 2008 than the remainder of the subjects. Although more subjects in this group were taking three or more antihypertensive medications, only 54 percent had achieved their goal blood pressure by 2008, compared to 70 percent of the other participants. For those that received riboflavin at either time point, systolic and diastolic blood pressure declined by an average of 9.2 mm Hg and 6.0 mm Hg.
"In this genetically at-risk group, significant lowering of blood pressure was achieved only with riboflavin treatment," the authors write. "To put these results into context, it would take approximately 10 kilograms of weight loss or an exercise regimen that burned 4200 kcal/week to achieve comparable decreases in blood pressure."
"Optimization of riboflavin status could be achieved in individuals through the use of low dose supplements or the consumption of foods naturally rich in riboflavin or in populations via food fortification," they note. "Such approaches could lower blood pressure in those genetically at risk without causing harm to those who are not."
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