Show of the Month September 10- 2012

Cynarin-rich sunflower (Helianthus annuus) sprouts possess both antiglycative and antioxidant activities   Ig Human and Soil Bacteria Swap Antibiotic-Resistance Genes   Aspirin May Lower the Risk of Pancreatic Cancer   Daily Aspirin Usage Linked to Lower Cancer Mortality   Growing Strong Muscles Without Working Out ************************************************************************** Cynarin-rich sunflower (Helianthus annuus) sprouts possess both antiglycative and antioxidant activities. J Agric Food Chem. 2012 Mar 28;60(12):3260-5 Authors: Sun Z, Chen J, Ma J, Jiang Y, Wang M, Ren G, Chen F Abstract
The present study examined the antiglycative and antioxidant properties of four edible sprouts popular in Chinese markets. In a protein-reducing sugar model, the sunflower sprout Helianthus annuus exhibited the strongest inhibitory effects against the formation of advanced glycation end products (AGEs).[U1]  At a concentration of 1.0 mg/mL, its inhibitory rate achieved 83.29%, which is stronger than that of aminoguanidine (1 mM), a well-known synthetic antiglycative agent (with an inhibitory rate of 80.88%). The antioxidant capacity of H. annuus was also much stronger than other sprout samples in terms of free radical scavenging and reducing properties. An active ingredient contributing to the observed activities was identified as cynarin (1,5-dicaffeoylquinic acid). This is the first report of the novel function of cynarin to intervene against glycoxidation. Given the key roles of AGEs and oxidation in the pathogenesis of diabetes, the sunflower sprout H. annuus rich in cynarin may be regarded as a beneficial food choice for diabetic patients.—PMID: 22394088 [PubMed – indexed for MEDLINE] ************************************************************************** Ig Human and Soil Bacteria Swap Antibiotic-Resistance Genes   Escherichia coli bacteria of the strain O157:H7. Soil bacteria and bacteria that cause human diseases have recently swapped at least seven antibiotic-resistance genes.)—-ScienceDaily (Aug. 30, 2012) — Soil bacteria and bacteria that cause human diseases have recently swapped at least seven antibiotic-resistance genes, researchers at Washington University School of Medicine in St. Louis report Aug. 31 in Science.According to the scientists, more studies are needed to determine how widespread this sharing is and to what extent it makes disease-causing pathogens harder to control.—-“It is commonplace for antibiotics to make their way into the environment,” says first author Kevin Forsberg, a graduate student. “Our results suggest that this may enhance drug resistance in soil bacteria in ways that could one day be shared with bacteria that cause human disease.”—[U2] Among the questions still to be answered: Did the genes pass from soil bacteria to human pathogens or vice versa? And are the genes just the tip of a vast reservoir of shared resistance? Or did some combination of luck and a new technique for studying genes across entire bacterial communities lead the scientists to discover the shared resistance genes?–Humans only mix their genes when they produce offspring, but bacteria regularly exchange genes throughout their lifecycles. This ability is an important contributor to the rapid pace of bacterial evolution. When a bacterial strain develops a new way to beat antibiotics, it can share the strategy not only with its descendants but also with other bacteria. Earlier studies by other scientists have identified numerous resistance genes in strains of soil bacteria. However, unlike the seven genes described in this report, the earlier genes were dissimilar to their analogs in disease-causing bacteria, implying that they had crossed between the bacterial communities a long time ago.—Most of the antibiotics used to fight illness today originated from the soil. Bacteria use the antibiotics, in part, as weapons to compete with each other for resources and survival. Scientists have long acknowledged that gives environmental bacteria an evolutionary incentive to find ways to beat antibiotics.–“We wanted to try to get a broader sense of how often and extensively antibiotic-resistance genes are shared between environmental bacteria and pathogens,” says senior author Gautam Dantas, PhD, assistant professor of pathology and immunology.—The researchers isolated bacteria from soil samples taken at various U.S. locations. The bacteria’s DNA was broken into small chunks and randomly inserted into a strain of Escherichia coli that is vulnerable to antibiotics. Scientists treated the altered E. coli with multiple antibiotics.—“We knew that any E. coli that continued to grow after these treatments had picked up a gene from the soil bacteria that was helping it fight the antibiotics,” Forsberg says. Scientists took the DNA from soil bacteria out of the surviving E. coli and prepared it for high-throughput sequencing. Dantas’ laboratory has developed techniques that make it possible to simultaneously sequence and analyze thousands of chunks of DNA from many diverse microorganisms. The DNA can be selected for a single function, such as antibiotic resistance. When the scientists compared antibiotic-resistance genes found in the soil bacteria to disease-causing bacteria, they were surprised to find some genes were identical not only in the sections of the genes that code for proteins but also in nearby non-coding sections that help regulate the genes’ activities.–Since bacteria have such large population sizes and rapid reproduction times, their DNA normally accumulates mutations and other alterations much more quickly than the DNA of humans. The lack of changes in the resistance genes identified in the study suggests that the transfers of the genes must have occurred fairly recently[U3] , according to Dantas.-In some soil bacteria, the genes are present in clusters that make the bacteria resistant to multiple classes of antibiotics, including forms of penicillin, sulfonamide and tetracycline.—“I suspect the soil is not a teeming reservoir of resistance genes,” Dantas says. “But if factory farms or medical clinics continue to release antibiotics into the environment, it may enrich that reservoir, potentially making resistance genes more accessible to infectious bacteria.”–Story Source-The above story is reprinted from materials provided by Washington University School of Medicine. The original article was written by Michael C. Purdy. —Journal Reference-K. J. Forsberg, A. Reyes, B. Wang, E. M. Selleck, M. O. A. Sommer, G. Dantas. The Shared Antibiotic Resistome of Soil Bacteria and Human Pathogens. Science, 2012; 337 (6098): 1107 DOI: 10.1126/science.1220761   ********************************************************************* Aspirin May Lower the Risk of Pancreatic Cancer ScienceDaily (Apr. 10, 2011) — The use of aspirin at least once per month is associated with a significant decrease in pancreatic cancer risk, according to results of a large case-control study presented at the AACR 102nd Annual Meeting 2011, held in Orlando, Florida, April 2-6.— For the current study, Tan and colleagues enrolled 904 patients who had documented pancreatic cancer and compared them with 1,224 healthy patients. All patients were at least 55 years old and reported their use of aspirin, NSAIDs and acetaminophen by questionnaire.–Results showed that people who took aspirin at least one day during a month had a 26 percent decreased risk of pancreatic cancer compared to those who did not take aspirin regularly. The effect was also found for those who took low-dose aspirin for heart disease prevention at 35 percent lower risk, according to Tan.—The researchers did not see a benefit from non-aspirin NSAIDs or acetaminophen. “This provides additional evidence that aspirin may have chemoprevention activity against pancreatic cancer,” said Tan. He added that more data must be gathered before we can prove a real benefit.–Story Source-The above story is reprinted from materials provided by American Association for Cancer Research. ********************************************************************** Daily Aspirin Usage Linked to Lower Cancer Mortality ScienceDaily (Aug. 10, 2012) — A large new observational study finds more evidence of an association between daily aspirin use and modestly lower cancer mortality, but suggests any reduction may be smaller than that observed in a recent analysis. The study, appearing early online in the Journal of the National Cancer Institute (JNCI), provides additional support for a potential benefit of daily aspirin use for cancer mortality[U4] , but the authors say important questions remain about the size of the potential benefit. —A recent analysis pooling results from existing randomized trials of daily aspirin for prevention of vascular events found an estimated 37% reduction in cancer mortality among those using aspirin for five years or more. But uncertainty remains about how much daily aspirin use may lower cancer mortality, as the size of this pooled analysis was limited and two very large randomized trials of aspirin taken every other day found no effect on overall cancer mortality.—For the current study, American Cancer Society researchers led by Eric J. Jacobs, Ph.D., analyzed information from 100,139 predominantly elderly participants in the Cancer Prevention Study II Nutrition Cohort who reported aspirin use on questionnaires, did not have cancer at the start of the study, and were followed for up to 11 years. They found daily aspirin use was associated with an estimated 16% lower overall risk of cancer mortality, both among people who reported taking aspirin daily for at least five years and among those who reported shorter term daily use. The lower overall cancer mortality was driven by about 40% lower mortality from cancers of the gastrointestinal tract (such as esophageal, stomach, and colorectal cancer) and about 12% lower mortality from cancers outside the gastrointestinal tract.———The reduction in cancer mortality observed in the current study is considerably smaller than the 37% reduction reported in the recent pooled analysis of randomized trials. The authors note that their study was observational, not randomized, and therefore could have underestimated or overestimated potential effects on cancer mortality if participants who took aspirin daily had different underlying risk factors for fatal cancer than those who did not. However, the study’s large size is a strength in determining how much daily aspirin use might lower cancer mortality.—“Expert committees that develop clinical guidelines will consider the totality of evidence about aspirin’s risks and benefits when guidelines for aspirin use are next updated,” said Dr. Jacobs. “Although recent evidence about aspirin use and cancer is encouraging, it is still premature to recommend people start taking aspirin specifically to prevent cancer. Even low-dose aspirin can substantially increase the risk of serious gastrointestinal bleeding. Decisions about aspirin use should be made by balancing the risks against the benefits in the context of each individual’s medical history. Any decision about daily aspirin use should be made only in consultation with a health care professional.”–Story Source-The above story is reprinted from materials provided by American Cancer Society, via EurekAlert!, a service of AAAS. -Journal Reference-Eric J. Jacobs, Christina C. Newton, Susan M. Gapstur, Michael J. Thun. Daily Aspirin Use and Cancer Mortality in a Large US Cohort. Journal of the National Cancer Institute, August 10, 2012 DOI: 10.1093/jnci/djs318 ************************************************************************* Growing Strong Muscles Without Working Out? ‘Hulk’ Protein, Grb10, Controls Muscle Growth ScienceDaily (Aug. 30, 2012) — Scientists have moved closer toward helping people grow big, strong muscles without needing to hit the weight room. Australian researchers have found that by blocking the function of a protein called Grb10 while mice were in the womb, they were considerably stronger and more muscular than their normal counterparts. This discovery appears in the September 2012 issue of The FASEB Journal. Outside of aesthetics, this study has important implications for a wide range of conditions that are worsened by, or cause muscle wasting, such as injury, muscular dystrophy, Type 2 diabetes, and problems produced by muscle inflammation.—“By identifying a novel mechanism regulating muscle development, our work has revealed potential new strategies to increase muscle mass,[U5] ” said Lowenna J. Holt, Ph.D., a study author from the Diabetes and Obesity Research Program at the Garvan Institute of Medical Research in Sydney, Australia. “Ultimately, this might improve treatment of muscle wasting conditions, as well as metabolic disorders such as Type 2 diabetes.”—To make this discovery, Holt and colleagues compared two groups of mice. Once group had disruption of the Grb10 gene, and were very muscular. The other group, where the Grb10 gene was functional, had normal muscles. Researchers examined the properties of the muscles in both adult and newborn mice and discovered that the alterations caused by loss of Grb10 function had mainly occurred during prenatal development. These results provide insight into how Grb10 works, suggesting that it may be possible to alter muscle growth and facilitate healing, as the processes involved in muscle regeneration and repair are similar to those for the initial formation of muscle.[U6] –“Don’t turn in your gym membership just yet,” said Gerald Weissmann, M.D., Editor-in-Chief of The FASEB Journal. “If you want big muscles, the classic prescription still applies: lift heavy things, eat and sleep right, and have your hormones checked. But this study shows that when we understand the basic science of how muscle fibers grow and multiply, we will be able to lift the burden — literally — of muscle disease for many of our patients.”—Story Source-The above story is reprinted from materials provided by Federation of American Societies for Experimental Biology, via EurekAlert!, a service of AAAS. –Journal Reference-L. J. Holt, N. Turner, N. Mokbel, S. Trefely, T. Kanzleiter, W. Kaplan, C. J. Ormandy, R. J. Daly, G. J. Cooney. Grb10 regulates the development of fiber number in skeletal muscle. The FASEB Journal, 2012; 26 (9): 3658 DOI: 10.1096/fj.11-199349   TOP B  

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