April 17, 2009, 5:04 AM CT
Laughter Coupled With Standard Diabetic Treatment
The correlation between the body, mind and spirit has been the subject of conventional scientific inquiry for some 20 years. The notion that psychosocial and societal considerations have a role in maintaining health and preventing disease became crystallized as a result of the experiences of a layman, Norman Cousins. In the 1970s, Cousins, then a writer and magazine editor of the popular Saturday Review, was diagnosed with an autoimmune disease. He theorized that if stress could worsen his condition, as some evidence suggested at the time, then positive emotions could improve his health. As a result, he prescribed himself, with the approval of his doctor, a regimen of humorous videos and shows like Candid Camera©. Ultimately, the disease went into remission and Cousins wrote a paper that was reported in the New England Journal (NEJM) and a book about his experience, Anatomy of an Illness: A Patient's Perspective, which was published in 1979. The book became a best seller and led to the investigation of a new field, known then as whole-person care or integrative medicine and now, lifestyle medicine.Background
The unscientific foundation that was laid down by Cousins was taken up by a number of medical scientists including the academic medical researcher Dr. Lee Berk in the l980s. In earlier work, Berk and colleagues discovered that the anticipation of "mirthful laughter" had surprising and significant effects. Two hormones - beta-endorphins (the family of chemicals that elevates mood state) and human growth hormone (HGH; which helps with optimizing immunity) - increased by 27% and 87 % respectively in study subjects who anticipated watching a humorous video. There was no such increase among the control group who did not anticipate watching the humorous film. In another study, they observed that the same anticipation of mirthful laughter reduced the levels of three detrimental stress hormones. Cortisol (termed "the steroid stress hormone"), epinephrine (also known as adrenaline) and dopac, (the major catabolite of dopamine), were reduced 39, 70 and 38%, respectively (statistically significant in comparison to the control group). Chronically released high levels of these stress hormones can be detremential to the immune system.........
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April 16, 2009, 5:11 AM CT
Patient's own stem cells to combat stroke
For the first time in the United States, a stroke patient has been intravenously injected with his own bone marrow stem cells as part of a research trial at The University of Texas Medical School at Houston.
Roland "Bud" Henrich, 61, was transferred to Memorial Hermann Texas Medical Center on March 25 after suffering a stroke while working on his farm in Liberty. He arrived too late to receive tissue plasminogen activator (tPA), the only therapy for ischemic strokes. He became the first patient in the trial.
The Phase I safety trial, funded with a pilot grant from The National Institutes of Health and support from the Notsew Orm Sands Foundation, will enroll nine more patients who have suffered a stroke and can be treated with the stem cell procedure within 24 to 72 hours of initial symptoms.
Stroke occurs when blood flow to the brain is interrupted by a blockage or a rupture in an artery, depriving brain tissue of oxygen. It is the third-leading cause of death behind heart disease and cancer. As per the American Stroke Association, nearly 800,000 Americans suffer a stroke each year one every 40 seconds. On average, someone dies of stroke every three to four minutes.
"It's still very early in this safety study, but this could be an exciting new therapeutic approach for people who have just suffered a stroke," said Sean Savitz, M.D., assistant professor of neurology at the medical school and the study's lead investigator. "Animal studies have shown that when you administer stem cells after stroke, the cells enhance the healing. We know that stem cells have some kind of guidance system and migrate to the area of injury. They're not making new brain cells but they appears to be enhancing the repair processes and reducing inflammatory damage."........
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April 16, 2009, 5:07 AM CT
How Alzheimer's destroy brain cells
For a decade, Alzheimer's disease scientists have been entrenched in debate about one of the mechanisms thought to beresponsible for brain cell death and memory loss in the illness.
Now scientists at the University of Michigan and the University of California, San Diego have settled the dispute. Resolving this controversy improves understanding of the disease and could one day lead to better therapys.
Michael Mayer, an assistant professor in the U-M departments of Biomedical Engineering and Chemical Engineering, and Jerry Yang, an assistant professor in the Department of Chemistry and Biochemistry at UCSD, and their colleagues found a flaw in earlier studies supporting one side of the debate. Their findings are published online in the Journal of Neurotoxicity Research
They will appear in the May print edition.
Their results clarify how small proteins called amyloid-beta peptides damage brain cell membranes, allowing extra calcium ions to enter the neurons. An ion is an electrically-charged particle. An ion imbalance in a cell can trigger its suicide.
Amyloid-beta peptides are the prime suspects for causing cell death in Alzheimer's, eventhough other mechanisms could also be to blame. The disease is not well understood.
The scientists confirmed evidence found by others that amyloid-beta peptides prick pores into brain cell membranes, opening channels where calcium ions can rush in. This was one mechanism the field had contemplated, but other evidence suggested a different scenario. Some scientists believed that the peptide caused a general thinning of the cell membranes and these thinned membranes lost their ability to keep calcium ions out of brain cells. Mayer and Yang disproved this latter theory.........
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April 16, 2009, 5:00 AM CT
New target for melanoma
A protein called Mcl-1 plays a critical role in melanoma cell resistance to a form of apoptosis called anoikis, as per research published this week in Molecular Cancer Research
The presence of Mcl-1 causes cell resistance to anoikis. This resistance to anoikis enables the melanoma cells to metastasize and survive at sites distant from the primary tumor, as per Andrew Aplin, Ph.D., an associate professor of Cancer Biology at Jefferson Medical College of Thomas Jefferson University, and a member of the Kimmel Cancer Center at Jefferson. The research was conducted at Albany Medical College in New York by Dr. Aplin and his colleagues.
Mcl-1 is part of the Bcl-2 protein family, and is regulated by B-RAF proteins, which are mutated in approximately 60 percent of all human melanomas. The Bcl-2 family includes several prosurvival proteins that are linked to the resistance of cancer cells to apoptosis, or cell death. Dr. Aplin and his colleagues analyzed three candidate Bcl-2 proteins: Mcl-1, Bcl-2 and Bcl-XL.
"When we depleted Mcl-1 from the tumor cells, they were susceptible to cell death," Dr. Aplin said. "Mcl-1 showed dramatic results in comparison to Bcl-2 and Bcl-XL, which was a surprise. Our findings show that targeting Mcl-1, which is upregulated in a majority of melanoma cells, could be a viable therapy strategy".........
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April 15, 2009, 5:19 AM CT
Low glycemic breakfast may increase benefits of working out
The benefits of physical activity and a balanced diet are well documented and form the basis of a number of public health recommendations. This is because each of these factors can independently influence risks for a number of chronic diseases such as obesity, type 2 diabetes, and some forms of cancer. Some research also suggests that exercise and diet interact to influence health. For instance, exercising after short-term fasting (such as before breakfast) may increase the amount of fat burned. Similarly, consumption of a meal eliciting a low blood glucose response previous to exercise may also boost the use of body fat (instead of glucose). However, most of these studies have used either trained athletes or recreational exercisers, and none has looked at effects of the type of pre-exercise meal on metabolism during and after exercise. To better understand the effects of pre-exercise meal composition on fat metabolism in more typical (sedentary) individuals, a group of scientists headed by Dr. Emma Stevenson at the University of Nottingham conducted a controlled human intervention trial. The results of their study are reported in the May 2009 issue of The Journal of Nutrition
As expected, blood glucose concentrations were higher after the HGI than the LGI meals and had returned to baseline levels by the time exercise was commenced, after which they were not influenced by breakfast type. Plasma free fatty acids (FFA; a marker for adipose oxidation) fell after consumption of both HGI and LGI breakfasts, but began to rise at ~2 h post-breakfast in the LGI (but not HGI) therapy. Exercise caused a rapid increase in FFA in both groups, but this was higher in the LGI trial in comparison to the HGI trial (P < 0.001). Circulating concentrations of FFA were not different between therapys following lunch. Overall, fat oxidation was higher in the LGI therapy than in the HGI therapy (P < 0.05) during the post-breakfast and exercise periods. Following lunch, fullness scores were higher in the LGI trial than in the HGI trial (P < 0.05). The authors concluded that consuming a LGI breakfast increases fat oxidation during subsequent exercise and improved satiety during recovery in sedentary females. As such, individuals trying to shed fat may consider choosing LGI foods eaten previous to when they exercise.........
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April 15, 2009, 5:14 AM CT
Is that chemotherapy working?
Oncologists often have to wait months before they can determine whether a therapy is working. Now, using a non-invasive method, scientists at UCLA's Jonsson Comprehensive Cancer Center have shown that they can determine after a single cycle of chemotherapy whether the toxic drugs are killing the cancer or not.
Using a combination Positron Emission Tomography (PET) and computed tomography (CT) scanner, scientists monitored 50 patients undergoing therapy for high-grade soft tissue sarcomas. The patients were receiving neoadjuvant chemotherapy therapys to shrink their tumors previous to surgery. The study observed that response could be determined about a week after the first dose of chemotherapy drugs. Typically, patients are scanned at about three months into chemotherapy to determine whether the therapy is working.
"The question was, how early could we pick up a response? We wanted to see if we could determine response after a single administration of chemotherapy," said Dr. Fritz Eilber, an assistant professor of surgical oncology, director of the Sarcoma Program at UCLA's Jonsson Cancer Center and senior author of the study. "There's no point in giving a patient a therapy that isn't working. These therapys make patients very sick and have long-term serious side effects. ".........
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April 15, 2009, 5:12 AM CT
Sleeplessness leads to increased cancer pain
A study in the April 15 issue of the Journal of Clinical Sleep Medicine
suggests that sleep problems lead to increased pain and fatigue in cancer patients. The results indicate that interventions aimed at trouble sleeping would be expected to improve both pain and fatigue in this patient population.
Results show that more than half the sample reported having trouble sleeping, with 26 percent reporting moderate or severe trouble sleeping. Compared with patients who reported no trouble sleeping, patients with moderate to severe trouble sleeping reported significantly more fatigue, pain and depressed mood. Using structural equation modeling analysis to evaluate causal relations and directions of effect, the best-fitting model indicates that trouble sleeping led to increased ratings of pain.
As per the authors, the relationship between pain and sleep often has been assumed to be reciprocal. In the present study, however, a model of reciprocal causation could not be fit to the data, and models in which pain caused trouble sleeping did not fit as well as the model in which trouble sleeping caused pain.
"We believed we would find a bi-directional relationship between insomnia and pain, but instead observed that trouble sleeping was more likely a cause, rather than a consequence, of pain in patients with cancer," said main author Edward J. Stepanski, chief operational officer at the Accelerated Community Oncology Research Network in Memphis, Tenn.........
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April 15, 2009, 5:10 AM CT
Melatonin for sleep problems in children with autism
Westchester, Ill. - A study in the April 15 issue of the Journal of Clinical Sleep Medicine
determined that over-the-counter melatonin medicine can shorted the length of time it takes for children with autistic spectrum disorder (ASD), Fragile X Syndrome (FXS), or both to fall asleep at the beginning of the night.
Results of the study indicated that children who received over-the-counter melatonin therapys experienced significant improvements in total night sleep durations, sleep latency times, and sleep-onset times. Mean sleep duration was longer on melatonin than placebo by 21 minutes, sleep-onset latency was shorter by 28 minutes and sleep-onset time was earlier by 42 minutes.
As per the senior author, Beth L. Goodlin-Jones, PhD of the M.I.N.D Institute at the University of California Davis Health System in Sacramento, Calif., therapy with over-the-counter melatonin supplements benefits children of all ages, which helps alleviate some of the additional stress that parents of special-needs children experience.
"Sleep onset problems at the beginning of the night are very troublesome for children and their families," said Goodlin-Jones. "Sometimes children may take one to two hours to fall asleep and often they disrupt the household during this time."........
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April 13, 2009, 2:07 PM CT
Omega-3 Fatty Acids May Benefit Cancer Patients
Omega 3 fats are essential fats found naturally in oily fish, with highest concentrations in salmon, herring, mackerel, and sardines. Recently food manufacturers have begun to add omega 3 to foods such as yogurt, milk, juice, eggs and infant formula
New research from Trinity College Dublin published in this month's Annals of Surgery points to a potentially significant advance in the therapy of patients undergoing major cancer surgery. The study was carried out by the oesophageal research group at Trinity College Dublin and St James's Hospital. A randomised controlled trial showed omega-3 fatty acids given as part of an oral nutritional supplement resulted in the preservation of muscle mass in patients undergoing surgery for oesopahageal cancer, a procedure normally linked to significant weight loss and quality of life issues.
The trial was designed by Professor John V Reynolds, Professor of Surgery at Trinity College Dublin and St James's Hospital, Dublin, and Dr Aoife Ryan PhD, a research dietitian at St James's Hospital, Dublin*.
Omega 3 fats are essential fats found naturally in oily fish, with highest concentrations in salmon, herring, mackerel, and sardines. Recently food manufacturers have begun to add omega 3 to foods such as yogurt, milk, juice, eggs and infant formula in light of a body of scientific evidence which suggests that they reduce cardiovascular disease risk, blood pressure, clot formations, and certain types of fat in the blood.
Prior studies had observed that nutritional supplements containing one form of omega 3 fat, eicosapentaenoic acid (EPA), significantly reduced weight loss among inoperable cancer patients. The scientists hypothesised that a nutritional supplement rich in calories and a high dose of EPA would stem the debilitating weight loss seen in patients following oesophageal surgery. The group chose to study patients undergoing surgery for oesophageal cancer as this surgery is one of the most stressful and serious operations a patient can undergo.........
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April 13, 2009, 1:54 PM CT
Insights into progressive hearing loss
In parallel studies in human and mouse, two groups of scientists have come to the same conclusion: that a new kind of gene is linked to progressive hearing loss. The new gene - called a microRNA - is a tiny fragment of RNA that affects the production of hundreds of other molecules within sensory hair cells of the inner ear.
The research provides important new genetic understanding of a condition that is common in humans but remains poorly understood.
One team, led by scientists from the Hospital Ramn y Cajal, Madrid, Spain, followed families who showed hearing loss. The second team, led by scientists from the Wellcome Trust Sanger Institute, Cambridge, UK, examined a new line of mice, called diminuendo, that showed progressive hearing loss from an early age. The two groups shared their emerging data.
"We were able quite quickly to show that if the mice carried one copy of the gene variant they suffered progressive hearing loss, if they carried two variants they were profoundly deaf," explains Professor Karen Steel, principal investigator of the programme at the Wellcome Trust Sanger Institute. "The important questions were could we determine what the variant is and how does it exert its effect on hearing?".
In their studies of families with progressive hearing loss, the Spanish team had proposed that the gene responsible lay on human chromosome 7. Both teams set about sequencing every gene in the equivalent genomic regions in human and mouse identified as implicated in hearing loss; the sequencing showed that most of the genes in the region could not be responsible for hearing loss.........
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