|Posted by Pacific J Med Sci on September 8, 2015 at 8:40 AM||comments ()|
The Pacific Journal of Medical Sciences (Pac. J. Med. Sci.) participated in the 2015 Convention of the Asia Pacific Association of Medical Journal Editors (APAME) held in Manila Philippines from 24 to 26 August 2015. The Managing Editor of the Pacific Journal of Medical Sciences was enrolled as a member of the APAME during the APAME 2015 Convention and Joint Meeting with the Western Pacific Region Index Medicus Regional Journal Selection Committee Meeting. The Pacific Journal of Medical Sciences is now officially recognised as one of the Journals linked to APAME and listed in the Index Medicus of the Western Pacific Region Index Medicus (WPRIM).
|Posted by Pacific J Med Sci on July 21, 2013 at 1:30 PM||comments ()|
From SCIENCE NEWS
New Functions for Autoimmune Disease 'Risk' Gene Identified
July 19, 2013 — Researchers at the University of Minnesota have identified infection-fighting and inflammation-suppressing functions for a gene associated with human autoimmune disease.
The discovery, centered on a gene known as PTPN22, could set into motion new treatment approaches for autoimmune diseases like lupus, rheumatoid arthritis and type 1 diabetes. The key to these advances may lie with a better understanding of how a variant of PTPN22, known as a "risk variant," impacts autoimmune disease development and the behavior of myeloid cells that act as the body's "first responders."
The study appears in the journal Immunity.
In launching their latest research project, University of Minnesota Center for Immunology researchers set out to determine how PTPN22 could regulate immune system function in health and disease.
"Almost a decade ago, researchers at the University of Minnesota and other institutions discovered that people carrying a variant form of the PTPN22 gene bear an increased risk of becoming sick with certain autoimmune diseases. However, we have lacked a deep understanding how the variant creates that increased risk," said Erik J. Peterson, M.D., one of the study's lead authors and a University of Minnesota Medical School associate professor in the Division of Rheumatic and Autoimmune Diseases. "We wanted to understand the molecular basis for PTPN22 association with disease."
Much of the work carried out in the latest study took place in Peterson's laboratory, which utilizes genetic, biochemical, and primary human sample-based approaches to investigate how "risk" genes predispose to development of autoimmune disease. According to the study's authors, previous research showed that PTPN22 works in immune cells, but few studies had specifically examined PTPN22's function in infection-fighting cells called myeloid cells. "Myeloid cells are among the body's 'first responders' to a challenge with a virus or bacterium," said Yaya Wang, Ph.D., one of the study's co-first authors and a research associate in the Center for Immunology. "Upon recognizing the presence of an infection, myeloid cells produce chemicals that increase inflammation and help fight the invading microbe. We were intrigued by the idea that PTPN22 and its disease-associated variant might have a role in myeloid cell functions." Researchers found that both mouse and human myeloid cells carrying the PTPN22 "risk" variant show decreased production of molecules called type 1 Interferons. Type 1 Interferons are needed to boost immune responses to viruses and other infections. In mice lacking the PTPN22 gene, reduced type 1 Interferon production correlates with an impaired ability to fight infections. But the PTPN22 gene does more than simply fight infection, the study showed. "Unexpectedly, we also found that PTPN22 suppresses inflammation," said Wang. "Furthermore, we showed that the PTPN22 risk variant is defective in suppressing inflammatory arthritis." "We anticipate that our findings will open new lines of investigation into how PTPN22 and other autoimmune disease 'risk' genes could work in infection-fighting and anti-inflammatory processes. Ultimately, we hope that the research will accelerate the drive toward better treatments and cures for autoimmune disorders," said Peterson. More research is underway to determine the impact of the PTPN22 variant in the function of myeloid blood cells, particularly in patients suffering from lupus. Researchers are also comparing immune responses to influenza A vaccines between carriers and non-carriers of the PTPN22 variant. The goal is to understand the role of the disease-associated variant in mounting a normal response to immunizations against viruses.
Story Source: The above story is reprinted from materials provided by University of Minnesota Academic Health Center, via EurekAlert!, a service of AAAS.
• Yaya Wang, Iftach Shaked, Stephanie M. Stanford, Wenbo Zhou, Julie M. Curtsinger, Zbigniew Mikulski, Zachary R. Shaheen, Genhong Cheng, Kristy Sawatzke, Amanda M. Campbell, Jennifer L. Auger, Hatice Bilgic, Fernanda M. Shoyama, David O. Schmeling, Henry H. Balfour, Kiminori Hasegawa, Andrew C. Chan, John A. Corbett, Bryce A. Binstadt, Matthew F. Mescher, Klaus Ley, Nunzio Bottini, Erik J. Peterson. The Autoimmunity-Associated Gene PTPN22 Potentiates Toll-like Receptor-Driven, Type 1 Interferon-Dependent Immunity. Immunity, 2013; DOI: 10.1016/j.immuni.2013.06.013
• University of Minnesota Academic Health Center (2013, July 19). New functions for autoimmune disease 'risk' gene identified. ScienceDaily. Retrieved July 21, 2013, from http://www.sciencedaily.com; /releases/2013/07/130719140008.htm
|Posted by Pacific J Med Sci on July 21, 2013 at 1:25 PM||comments ()|
From SCIENCE NEWS
Calcium Linked to Increased Risk of Heart Disease and Death in Patients with Kidney Disease
July 19, 2013 — Kidney patients who take calcium supplements to lower their phosphorus levels may be at a 22 per cent higher risk of death than those who take other non-calcium based treatments, according to a new study by Women's College Hospital's Dr. Sophie Jamal.
The study, published today in the Lancet, calls into question the long-time practice of prescribing calcium to lower phosphate levels in patients with chronic kidney disease. The researchers suggest some of the calcium is absorbed into the blood stream and may expedite hardening of the arteries, leading to a higher risk of heart disease and even death. Cardiovascular disease is a leading cause of death for people with chronic kidney disease. "Doctors commonly prescribe calcium supplements to prevent elevated phosphate levels, which can damage the body, but a growing number of studies have shown calcium supplements may actually increase the risk of heart disease," explains Dr. Sophie Jamal, a physician at Women's College Hospital and an associate professor of medicine at the University of Toronto. "Our study validates these claims and, for the first time, shows the long-term consequences of taking calcium supplements can be dangerous for patients with kidney disease." As part of their analysis, researchers reviewed 11 randomized, controlled studies that included more than 4,600 patients. The researchers assessed the risk of heart disease, including heart attack, stroke, and hardening of the arteries, along with death among individuals prescribed the medication containing calcium and those prescribed the medication without calcium. They found:
• A 22% reduction in death among patients who took non-calcium based treatments sevelamer and lanthanum.
• Less artery calcification (hardening) in patients who did not take calcium supplements.
"Some researchers and physicians have been saying for years that kidney disease patients need to get off calcium, now we think our review shows there is much more solid evidence to argue for that change to clinical practice," the study's senior author Ross Tsuyuki from the University of Alberta's faculty of medicine and dentistry. In the meantime, given the study's findings, the researchers suggest non-calcium containing treatments be used as a first line of treatment to lower phosphate for patients with chronic kidney disease.
"The findings of our study provides the best evidence as to what doctors should be prescribing their patients, but further research is necessary to help us understand how exactly calcium increases the risk of death, if non calcium-based treatments reduce the risk of death, and whether certain types of treatments may be more effective and beneficial than others," says Dr. Jamal.
Story Source: The above story is reprinted from materials provided by Women's College Hospital, via EurekAlert!, a service of AAAS.
• Sophie A Jamal, Ben Vandermeer, Paolo Raggi, David C Mendelssohn, Trish Chatterley, Marlene Dorgan, Charmaine E Lok, David Fitchett, Ross T Tsuyuki. Effect of calcium-based versus non-calcium-based phosphate binders on mortality in patients with chronic kidney disease: an updated systematic review and meta-analysis. The Lancet, 2013; DOI: 10.1016/S0140-6736(13)60897-1
• Women's College Hospital (2013, July 19). Calcium linked to increased risk of heart disease and death in patients with kidney disease. Science Daily. Retrieved July 21, 2013, from http://www.sciencedaily.com; /releases/2013/07/130719112136.htm
|Posted by Pacific J Med Sci on July 16, 2013 at 10:30 AM||comments ()|
FROM SCIENCE NEWS:
Link between Omega-3 Fatty Acids and Increased Prostate Cancer Risk Confirmed
July 10, 2013 — A second large, prospective study by scientists at Fred Hutchinson Cancer Research Center has confirmed the link between high blood concentrations of omega-3 fatty acids and an increased risk of prostate cancer.
Published July 11 in the online edition of the Journal of the National Cancer Institute, the latest findings indicate that high concentrations of EPA, DPA and DHA -- the three anti-inflammatory and metabolically related fatty acids derived from fatty fish and fish-oil supplements -- are associated with a 71% increased risk of high-grade prostate cancer. The study also found a 44% increase in the risk of low-grade prostate cancer and an overall 43 % increase in risk for all prostate cancers.
The increase in risk for high-grade prostate cancer is important because those tumors are more likely to be fatal. The findings confirm a 2011 study published by the same Fred Hutch scientific team that reported a similar link between high blood concentrations of DHA and a more than doubling of the risk for developing high-grade prostate cancer. The latest study also confirms results from a large European study.
"The consistency of these findings suggests that these fatty acids are involved in prostate tumorigenesis and recommendations to increase long-chain omega-3 fatty acid intake, in particular through supplementation, should consider its potential risks," the authors wrote.
"We've shown once again that use of nutritional supplements may be harmful," said Dr. Alan Kristal, the paper's senior author and member of the Fred Hutch Public Health Sciences Division. Kristal also noted a recent analysis published in the Journal of the American Medical Association that questioned the benefit of omega-3 supplementation for cardiovascular diseases. The analysis, which combined the data from 20 studies, found no reduction in all-cause mortality, heart attacks or strokes.
"What's important is that we have been able to replicate our findings from 2011 and we have confirmed that marine omega-3 fatty acids play a role in prostate cancer occurrence," said corresponding author Theodore Brasky, Ph.D., a research assistant professor at The Ohio State University Comprehensive Cancer Center who was a postdoctoral trainee at Fred Hutch when the research was conducted. "It's important to note, however, that these results do not address the question of whether omega-3 fatty acids play a detrimental role in prostate cancer prognosis," he said.
Kristal said the findings in both Fred Hutch studies were surprising because omega-3 fatty acids are believed to have a host of positive health effects based on their anti-inflammatory properties. Inflammation plays a role in the development and growth of many cancers.
It is unclear from this study why high levels of omega-3 fatty acids would increase prostate cancer risk, according to the authors, however the replication of this finding in two large studies indicates the need for further research into possible mechanisms. One potentially harmful effect of omega-3 fatty acids is their conversion into compounds that can cause damage to cells and DNA, and their role in immunosuppression. Whether these effects impact cancer risk is not known.
The difference in blood concentrations of omega-3 fatty acids between the lowest and highest risk groups was about 2.5 percentage points (3.2% vs. 5.7%), which is somewhat larger than the effect of eating salmon twice a week, Kristal said. The current study analyzed data and specimens collected from men who participated in the Selenium and Vitamin E Cancer Prevention Trial (SELECT), a large randomized, placebo-controlled trial to test whether selenium and vitamin E, either alone or combined, reduced prostate cancer risk. That study showed no benefit from selenium intake and an increase in prostate cancers in men who took vitamin E.
The group included in the this analysis consisted of 834 men who had been diagnosed with incident, primary prostate cancers (156 were high-grade cancer) along with a comparison group of 1,393 men selected randomly from the 35,500 participants in SELECT. The National Cancer Institute and the National Center for Complementary and Alternative Medicine funded the research.
Also participating in the study were additional Fred Hutch scientists and researchers from the University of Texas, University of California, University of Washington, National Cancer Institute and the Cleveland Clinic.
According to Science News: The above story was reprinted from materials provided by Fred Hutchinson Cancer Research Center, via Newswise
http://www.sciencedaily.com/releases/2013/07/130710183637.htm (downloaded 16th July 2013)
• T. M. Brasky, C. Till, E. White, M. L. Neuhouser, X. Song, P. Goodman, I. M. Thompson, I. B. King, D. Albanes, A. R. Kristal. Serum Phospholipid Fatty Acids and Prostate Cancer Risk: Results from the Prostate Cancer Prevention Trial. American Journal of Epidemiology, 2011; 173 (12): 1429 DOI: 10.1093/aje/kwr027
• Fred Hutchinson Cancer Research Center (2013, July 10). Link between omega-3 fatty acids and increased prostate cancer risk confirmed. ScienceDaily. Retrieved July 16, 2013, from http://www.sciencedaily.com; /releases/2013/07/130710183637.htm
People Who Eat Nuts More Than Three Times a Week Have Reduced Risk of Dying from Cancer or Cardiovascular Disease
|Posted by Pacific J Med Sci on July 16, 2013 at 10:30 AM||comments ()|
FROM SCIENCE NEWS:
People Who Eat Nuts More Than Three Times a Week Have Reduced Risk of Dying from Cancer or Cardiovascular Disease
July 16, 2013 — People who eat nuts, particularly walnuts, are more likely to live longer, finds research in BioMed Central's open access journal BMC.
Medicine. In a longitudinal study, researchers suggest that those who eat nuts more than three times a week have a reduced risk of dying from cancer or cardiovascular disease than non-nut eaters.
The PREDIMED nutrition trial based in Spain looked at the effect on the primary prevention of cardiovascular disease of over 7000 older people (aged 55 to 90) randomized to a Mediterranean Diet supplemented with extra virgin olive oil or nuts, compared to a control group following a low fat diet. In Mediterranean regions, nut consumption is relatively high compared to other countries. People who ate nuts tended to have a lower BMI and smaller waist. They were also less likely to smoke and were more physically active than those who rarely or never ate nuts. Nut eating was associated with a better diet in general as these people ate more vegetables, fruit and fish.
There were fewer people with type 2 diabetes or people taking medicine for hypertension in the group of people who ate the most nuts. Overall, nut eaters had a 39% lower mortality risk and walnut eaters 45% lower -- meaning that they were less likely to die than the non-nut eaters.
People eating more than 3 servings (1 serving -- 28 g) a week of nuts reduced risk of death due to cardiovascular disease by 55% and cancer by 40%. A similar effect was demonstrated for walnuts.
Prof Jordi Salas-Salvadó, from the Universitat Rovira i Virgili who led this study explained, "Quite how nuts are able to prevent premature mortality is not entirely clear, nor why walnut should be better for you than other nuts. Walnuts have particularly high content of alpha-linoleic acid and phytochemicals, especially in their 'skin' both of which, along with fibre and minerals such as calcium, magnesium and potassium, may contribute to their healthy effect."
According to Science News: The above story is reprinted from materials provided by BioMed Central Limited http://www.sciencedaily.com/releases/2013/07/130710183637.htm (downloaded 16th July 2013)
• BioMed Central Limited (2013, July 16). People who eat nuts more than three times a week have reduced risk of dying from cancer or cardiovascular disease. ScienceDaily. Retrieved July 16, 2013, from http://www.sciencedaily.com; /releases/2013/07/130715202458.htm
• Marta Guasch-Ferré, Mònica Bulló, Miguel Ángel Martínez-González, Emilio Ros, Dolores Corella, Ramon Estruch, Montserrat Fitó, Fernando Arós, Julia Wärnberg, Miquel Fiol, José Lapetra, Ernest Vinyoles, Rosa Lamuela-Raventós, Lluís Serra-Majem, Xavier Pintó, Valentina Ruiz-Gutierrez, Josep Basora and Jordi Salas-Salvado. Frequency of nut consumption and mortality risk in the PREDIMED nutrition intervention trial. BMC Medicine, 2013; 11: 164 DOI: 10.1186/1741-7015-11-164
• Sabine Rohrmann and David Faeh. Should we go nuts about nuts? BMC Medicine, 2013; 11: 165 DOI: 10.1186/1741-7015-11-165
|Posted by Pacific J Med Sci on July 16, 2013 at 10:30 AM||comments ()|
FROM BBC NEWS
Three-parent embryo formed in lab IVF treatment
Scientists believe they have made a potential breakthrough in the treatment of serious disease by creating a human embryo with three separate parents.
The Newcastle University team believes the technique could help to eradicate a whole class of hereditary diseases, including some forms of epilepsy. The embryos have been created using DNA from a man and two women in lab tests. It could ensure women with genetic defects do not pass the diseases on to their children. The technique is intended to help women with diseases of the mitochondria - mini organelles that are found within individual cells. They are sometimes described as "cellular power plants" because they generate most of the cell's energy. Faults in the mitochondrial DNA can cause around 50 known diseases, some of which lead to disability and death.
About one in every 6,500 people is affected by such conditions, which include fatal liver failure, stroke-like episodes, blindness, muscular dystrophy, diabetes and deafness. At present, no treatment for mitochondrial diseases exists.
Genetic transplant: The Newcastle team has effectively given the embryos a mitochondria transplant. They experimented on 10 severely abnormal embryos left over from traditional fertility treatment. Within hours of their creation, the nucleus, containing DNA from the mother and father, was removed from the embryo, and implanted into a donor egg whose DNA had been largely removed. The only genetic information remaining from the donor egg was the tiny bit that controls production of mitochondria - around 16,000 of the three billion component parts that make up the human genome. The embryos then began to develop normally, but were destroyed within six days.
Appearance: Experiments using mice have shown that the offspring with the new mitochondria carry no information that defines any human attributes. So while any baby born through this method would have genetic elements from three people, the nuclear DNA that influences appearance and other characteristics would not come from the woman providing the donor egg. However, the team only has permission to carry out the lab experiments and as yet this would not be allowed to be offered as a treatment.
Professor Patrick Chinnery, a member of the Newcastle team, said: "We believe that from this work and work we have done on other animals that in principle we could develop this technique and offer treatment in the for seeable future that will give families some hope of avoiding passing these diseases to their children."
Dr Marita Pohlschmidt, of the Muscular Dystrophy Campaign, which has funded the Newcastle research, was confident it would lead to a badly needed breakthrough in treatment. "Mitochondrial myopathies are a group of complex and severe diseases," she said. "This can make it very difficult for clinicians to provide genetic counselling and give patients an accurate prognosis."
However, the Newcastle work has attracted opposition.
Josephine Quintavalle, of the pro-life group Comment on Reproductive Ethics, said it was "risky, dangerous" and a step towards "designer babies". "It is human beings they are experimenting with," she said. "We should not be messing around with the building blocks of life." Mrs Quintavalle said embryo research in the US using DNA from one man and two women was discontinued because of the "huge abnormalities" in some cases.
Dr David King, of Human Genetics Alert, expressed concern about a "drift towards GM babies".
Source: http://news.bbc.co.uk/2/hi/health/7227861.stm. (downloaded 15th July 2013)
|Posted by Pacific J Med Sci on February 27, 2012 at 8:45 AM||comments ()|
Contact: Craig Brierley email@example.com
44-207-611-7329. Wellcome Trust
New candidate vaccine neutralizes all tested strains of malaria parasite
A new candidate malaria vaccine with the potential to neutralise all strains of the most deadly species of malaria parasite has been developed by a team led by scientists at the University of Oxford. The results of this new vaccine independently confirm the utility of a key discovery reported last month from scientists at the Wellcome Trust Sanger Institute who had identified this target within the parasite as a potential 'Achilles' heel' that could hold significant promise for vaccine development.According to the World Malaria Report 2010, malaria killed an estimated 781,000 people in 2009, mainly young children and pregnant women. It is caused by parasites that are injected into the bloodstream by infected mosquitoes. The most deadly form, Plasmodium falciparum, is responsible for nine out of ten deaths from malaria. Vaccinating against malaria is likely to be the most cost-effective way of protecting populations against disease; however, no licensed vaccine is currently available. Another vaccine is achieving promising but incomplete levels of protection in clinical trials in Africa; scientists believe a new and more effective vaccine will be required to eradicate the disease. In early November, research published in the journal Nature* showed that the P. falciparum parasite relies on a single receptor, known as 'basigin', on the surface of red blood cells to invade the cell. The parasite attaches a protein – the antigen RH5 – to the receptor, in a sense 'unlocking' the doorway for the parasite to enter the red blood cell. Once there, it grows and replicates, causing potentially life-threatening disease.Today, in a paper published in the journal Nature Communications, a team of scientists from the Jenner Institute at the University of Oxford led by Dr Simon Draper, working with colleagues from the Wellcome Trust Sanger Institute and the Kenyan Medical Research Institute-Wellcome Trust Programme in Kilifi, Kenya, demonstrate that a vaccine they have developed induces an antibody response in animal models capable of neutralising all the tested strains of the P. falciparum parasite."Our initial finding, reported last month, was unexpected and completely changed the way in which we view how the malaria parasite invades red blood cells," says Dr Gavin Wright from the Wellcome Trust Sanger Institute, a co-author on both studies. "It revealed what we think is the parasite's Achilles' heel in the way it invades our cells and provided a target for potential new vaccines."Dr Sandy Douglas, a Wellcome Trust Clinical Research Training Fellow from the University of Oxford and first author on the new study, adds: "We have created a vaccine that confirms the recent discovery relating to the biology of RH5, given it can generate an immune response in animal models capable of neutralising many – and potentially all – strains of the P. falciparum parasite, the deadliest species of malaria parasite. This is an important step towards developing a much-needed vaccine against one of the world's major killers."The antigens of the malaria parasite are often genetically very diverse as they are forced to evolve to stay one step ahead of the immune system and avoid recognition by antibodies. However, the RH5 antigen appears to have little genetic diversity. The researchers believe that this is because even people who have been naturally and repeatedly exposed to malaria have low or undetectable levels of antibodies that target this particular antigen; these very low levels of antibody would be insufficient to kill the parasites, and hence would not exert a selective pressure for the antigen to evolve variability. Professor Adrian Hill, a Wellcome Trust Senior Investigator at the University of Oxford, says: "Vaccines against malaria are notoriously difficult to develop because the parasites' antigens – the target of vaccines – tend to be genetically so diverse. The RH5 antigen doesn't show this diversity, making it a particularly good target for a vaccine to exploit. Our next step will be to begin safety tests of this vaccine. If these prove successful, we could see clinical trials in patients beginning within the next two to three years."
The Jenner Institute is funded through a Strategic Award from the Wellcome Trust, whose goals include combating infectious diseases. Other support for the research came from organisations including the Medical Research Council.
|Posted by Pacific J Med Sci on December 10, 2010 at 10:03 AM||comments ()|
AFP/Getty Images/File – A small, daily dose of aspirin significantly diminishes the risk of death from a wide range of cancers, …
By MARIA CHENG, AP Medical Writer Tue Dec 7, 9:23 am ET
LONDON – A new report from British scientists suggests that long-term, low-dose aspirin use may modestly reduce the risk of dying of certain cancers, though experts warn the study isn't strong enough to recommend healthy people start taking a pill that can cause bleeding and other problems. In a new observational analysis published online Tuesday in the medical journal Lancet, Peter Rothwell of the University of Oxford and colleagues looked at eight studies that included more than 25,000 patients and estimated that aspirin use cut the risk of death from certain cancers by 20 percent. While some experts said the analysis adds to evidence of aspirin's potential to cut cancer risk, others said it falls short of changing advice to healthy people, and it failed to show the benefits apply equally to women. The trials mostly compared men who took a daily dose of at least 75 milligrams of aspirin for heart problems to people who took a placebo or another drug. On average, the studies lasted at least four years. Researchers used national cancer registries to get information on participants after the studies ended, though they weren't sure how many aspirin takers continued using it or how many people in the comparison groups may have started. The researchers said that the projected risk after two decades of dying from cancers like lung and prostate would be 20 percent lower in groups who had taken aspirin and 35 percent lower for gastrointestinal cancers like colon cancer. These odds are figured from smaller numbers — there were 326 lung cancer deaths in all, for example.
Only one-third of people in the analysis were women — not enough to calculate any estimates for breast cancer. There appeared to be no benefit to taking more than 75 milligrams daily — roughly the amount in a European dose of baby aspirin and a bit less than the baby aspirin dose in the U.S. The analysis left out a high-quality experiment that tested aspirin every other day in nearly 40,000 U.S. women. No reduction in cancer risk was seen except for lung cancer deaths in that trial. No funding was provided for the new Lancet analysis but several of the authors have been paid for work for companies that make aspirin and similar drugs. Scientists said it would take some time to digest the study results and figure out which people should take aspirin. Eric Jacobs, an American Cancer Society epidemiologist, called it a "major contribution" and said the study results, in addition to previous research, suggested aspirin's effects on the risk of dying from several cancers "appear likely." Others said the study wasn't strong enough for doctors to start recommending aspirin. "I definitely think we wouldn't want to make any treatment decisions based on this study," said Dr. Raymond DuBois, a cancer prevention specialist who is provost of the University of Texas M.D. Anderson Cancer Center. One concern is that the studies were designed to look at cardiovascular risks, so the groups of people being compared may differ on things that affect cancer risk, such as family history of the disease. DuBois also questioned drawing conclusions about people's cancer risk beyond the several years they were tracked.
Aspirin has long been recommended for some people with heart problems. But it can have serious side effects, like bleeding in the stomach and intestines, and poses risks in groups like the elderly who are prone to falls. "Balancing the risks and benefits of aspirin is really important and probably something that needs to be done on an individual basis," said Ed Yong, Cancer Research U.K.'s head of health evidence and information. He was not linked to the study.
"If anyone is considering aspirin on a regular basis, they should talk to their doctor first," Yong said. He warned people should not think of aspirin as a guarantee against cancer and other prevention strategies like not smoking and keeping a healthy body weight were essential.
A U.S. health task force specifically recommends against aspirin for people with an average cancer risk. AP Medical Writer Marilynn Marchione in Milwaukee contributed to this report
|Posted by Pacific J Med Sci on December 10, 2010 at 10:00 AM||comments ()|
Lipids Online (http://www.LipidsOnline.org)
August 27, 2009
MedWire News: Diagnosing myocardial infarction (MI) in patients presenting with chest pains could be improved with a new generation of cardiac troponin assays, study results demonstrate.
Two large, multicenter trials published in the New England Journal of Medicine compared the diagnostic performance of current cardiac troponin assays with a new wave of more biochemically sensitive assays. Since 1999, professional societies worldwide have recommended the use of troponin as the preferred biomarker for evaluation of patients with suspected MI.
The major limitation of current cardiac troponin assays is their low sensitivity at patient presentation, owing to a delayed increase in circulating levels of troponin. In the first of two studies evaluating a new generation of assays, Christian Mueller (University Hospital, Basel, Switzerland) and colleagues analyzed blood samples from 718 consecutive patients admitted to hospital with chest pains. A diagnosis of acute MI was confirmed in 123 (17%) patients. The researchers found that accuracy for detecting MI was higher in four novel cardiac troponin assays than in the standard test, with area under the receiver-operating characteristic (AUC) scores of 0.96 (Abbot-Architect Troponin I, Abbott Diagnostics, Abbott Park, Illinois, USA); 0.96 (Roche High-Sensitive Troponin T, F Hoffmann-La Roche AG, Basel Switzerland); 0.95 (Roche Troponin I); 0.96 (Siemens Troponin I Ultra, Siemens AG, Munich, Germany ) versus 0.90 (Roche Troponin T). Notably, the new generation cardiac troponin assays retained much of their diagnostic accuracy in patients who presented within 3 hours of the onset of chest pains, whereas the standard assay lost substantial power (AUCs: 0.93; 0.92; 0.92; 0.94 versus 0.76, respectively).
In a second study of 1818 patients presenting with chest pain, Stefan Blankenberg (Johannes Gutenberg University, Mainz, Germany) and colleagues similarly found a superior diagnostic accuracy for one new cardiac troponin assay over the standard test, with AUCs of 0.96 (Siemens Troponin I Ultra) versus 0.85 (Roche Troponin T). Blankenberg et al additionally went on to evaluate the effect of the new generation troponin assays on clinical management. Using the 99th percentile as a cut-off value, the clinical sensitivity for detecting MI was 63.7% for the standard assay and 90.7% for the new generation assay. However this was accompanied by a diminished specificity of the new generation assay compared with the standard test at 90.2% versus 97.2%.
Commenting on the findings in an accompanying editorial, David Morrow (Brigham and Women’s Hospital, Boston, Massachusetts, USA) said: “In these studies, the two groups of investigators showed that a new generation of sensitive assays for troponin improved overall diagnostic accuracy and thus functioned as a better test.
“However, their results also confirm a trade-off of superior clinical sensitivity for diminished clinical specificity for the diagnosis of MI.”
MedWire (www.medwire-news.md) is an independent clinical news service provided by Current Medicine Group, a part of Springer Science+Business Media. © Current Medicine Group Ltd; 2009
|Posted by Pacific J Med Sci on December 10, 2010 at 9:56 AM||comments ()|
28 Mar 2007
Don't drink alcohol. Take vitamins. Avoid eating eggs. We've heard these pieces of nutritional advice for years - but are they accurate? Not necessarily, say two exercise physiologists presenting at the American College of Sports Medicine (ACSM) 11th-annual Health & Fitness Summit & Exposition in Dallas, Texas. Wendy Repovich, Ph.D., FACSM, and Janet Peterson, Dr. P.H., FACSM, set out to debunk the "Top 10 Nutrition Myths."
According to Repovich and Peterson, these nutrition myths are:
10. Eating carbohydrates makes you fat. Cutting carbs from your diet may have short-term weight loss benefits due to water loss from a decrease in carbohydrate stores, but eating carbs in moderation does not directly lead to weight gain. The body uses carbs for energy, and going too long without them can cause lethargy.
9. Drink eight, 8-oz. glasses of water per day. You should replace water lost through breathing, excrement and sweating each day - but that doesn't necessarily total 64 ounces of water. It's hard to measure the exact amount of water you have consumed daily in food and drink, but if your urine is pale yellow, you're doing a good job. If it's a darker yellow, drink more H2O.
8. Brown grain products are whole grain products. Brown dyes and additives can give foods the deceiving appearance of whole grain. Read labels to be sure a food is whole grain, and try to get three-ounce equivalents of whole grains per day to reduce the risk of heart disease, diabetes, and stroke.
7. Eating eggs will raise your cholesterol. This myth began because egg yolks have the most concentrated amount of cholesterol of any food. However, there's not enough cholesterol there to pose health risks if eggs are eaten in moderation. Studies suggest that eating one egg per day will not raise cholesterol levels and that eggs are actually a great source of nutrients.
6. All alcohol is bad for you. Again, moderation is key. Six ounces of wine and 12 ounces of beer are considered moderate amounts, and should not pose any adverse health effects to the average healthy adult. All alcohol is an anticoagulant and red wine also contains antioxidants, so drinking a small amount daily can be beneficial.
5. Vitamin supplements are necessary for everyone. If you eat a variety of fruits, vegetables, and whole grains, along with moderate amounts of a variety of low-fat dairy and protein and the right quantity of calories, you don't need to supplement. Most Americans do not, so a multi-vitamin might be good. Special vitamin supplements are also recommended for people who are pregnant or have nutritional disorders.
4. Consuming extra protein is necessary to build muscle mass. Contrary to claims of some protein supplement companies, consuming extra protein does nothing to bulk up muscle unless you are also doing significant weight training at the same time. Even then the increased requirement can easily come from food. A potential problem with supplements is the body has to work overtime to get rid of excess protein, and can become distressed as a result.
3. Eating fiber causes problems if you have irritable bowel syndrome (IBS). There are two kinds of fiber: soluble and insoluble. Insoluble fiber can cause problems in IBS sufferers; soluble fiber, however, is more easily absorbed by the body and helps prevent constipation for those with IBS. Soluble fiber is found in most grains.
2. Eating immediately after a workout will improve recovery. Endurance athletes need to take in carbohydrates immediately after a workout to replace glycogen stores, and a small amount of protein with the drink enhances the effect. Drinking low-fat chocolate milk or a carbohydrate drink, like Gatorade, is better for the body, as they replace glycogen stores lost during exercise. Protein is not going to help build muscle, so strength athletes do not need to eat immediately following their workout.
1. Type 2 diabetes can be prevented by eating foods low on the glycemic index. High levels of glucose are not what "cause" diabetes; the disease is caused by the body's resistance to insulin. Foods high on the glycemic index can cause glucose levels to spike, but this is just an indicator of the presence of diabetes, not the root cause.
The American College of Sports Medicine is the largest sports medicine and exercise science organization in the world. More than 20,000 International, National and Regional members are dedicated to promoting and integrating scientific research, education and practical applications of sports medicine and exercise science to maintain and enhance physical performance, fitness, health and quality of life.
Source: American College of Sports Medicine
Article URL: http://www.medicalnewstoday.com/articles/66363.php
Main News Category: Nutrition / Diet
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