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Bulevar, Serbia

de Godoy J.M.P.,Medical School | de Godoy M.F.G.,FAMERP
International Journal of Medical Sciences | Year: 2010

The aim of this paper is to report new options in the treatment of lymphedema for under-privileged populations. Several articles and books have been published reporting recent advances and contributions. A new technique of manual lymph drainage, mechanisms of compression, development of active and passive exercising apparatuses and the adaptation of myolymphokinetic activities have been developed for the treatment of lymphedema. This novel approach can be adapted for the treatment of lymphedema in mass. © Ivyspring International Publisher. Source


Bertoletto P.R.,Medical School
Acta cirúrgica brasileira / Sociedade Brasileira para Desenvolvimento Pesquisa em Cirurgia | Year: 2012

To determine the profile of gene expressions associated with oxidative stress and thereby contribute to establish parameters about the role of enzyme clusters related to the ischemia/reperfusion intestinal injury. Twelve male inbred mice (C57BL/6) were randomly assigned: Control Group (CG) submitted to anesthesia, laparotomy and observed by 120 min; Ischemia/reperfusion Group (IRG) submitted to anesthesia, laparotomy, 60 min of small bowel ischemia and 60 min of reperfusion. A pool of six samples was submitted to the qPCR-RT protocol (six clusters) for mouse oxidative stress and antioxidant defense pathways. On the 84 genes investigated, 64 (76.2%) had statistic significant expression and 20 (23.8%) showed no statistical difference to the control group. From these 64 significantly expressed genes, 60 (93.7%) were up-regulated and 04 (6.3%) were down-regulated. From the group with no statistical significantly expression, 12 genes were up-regulated and 8 genes were down-regulated. Surprisingly, 37 (44.04%) showed a higher than threefold up-regulation and then arbitrarily the values was considered as a very significant. Thus, 37 genes (44.04%) were expressed very significantly up-regulated. The remained 47 (55.9%) genes were up-regulated less than three folds (35 genes - 41.6%) or down-regulated less than three folds (12 genes - 14.3%). The intestinal ischemia and reperfusion promote a global hyper-expression profile of six different clusters genes related to antioxidant defense and oxidative stress. Source


Introduction: Male live births occur slightly in excess of female births. The ratio of male divided by total births is referred to as M/F. Many factors reduce M/F including toxins, stress, and privation, with excess male foetal loss. “The Troubles” (1969-1998) of Northern Ireland (NI) and the economic downturn of Republic of Ireland (ROI) from 2007 posed stresses with corresponding controls. This study analysed M/F in NI and ROI. Methods: Annual male and female live births in NI and the ROI were compared using chi tests. Results: M/F was significantly higher in NI than in ROI. M/F in NI dropped after 1974. M/F rose in ROI up to 1994, then fell. Discussion: Violence-related stress may have been the cause for the M/F drop in NI. Economic improvement followed by recession may have caused parallel M/F changes in ROI. These findings agree with the stress hypothesis of M/F. © The Ulster Medical Society, 2015. Source


News Article | September 2, 2016
Site: http://www.chromatographytechniques.com/rss-feeds/all/rss.xml/all

Almost half our genes can be the starting point for diseases. Scientists have identified 11,000 genes that occur in the human genome in variants that can cause disease. Scientists from the Max Planck Institute for Evolutionary Biology in Plön and the Harvard Medical School have studied why such high-risk genes persist in the human genome instead of being eliminated by selection. Their analyses suggest that the continuous adaptation to new pathogens in the course of evolution has increased the diversity of our immune genes but also comes at a price. According to the researchers, such diversity also extends to neighbouring DNA segments, where it results in the persistence of harmful gene variants. Diversity in the genome is a good thing: it has allowed us humans to adjust to changing environmental conditions during the course of evolution. Such genetic variety generates diverse combinations with each new generation and can bring with it survival advantages. Besides the many variants that have no effect or even a beneficial effect on health, there are others that make their carriers susceptible to certain diseases. These harmful gene variants represent a survival disadvantage and should therefore have been weeded out by natural section in the course of evolution. Instead, some high-risk gene variants, such as those for Alzheimer's disease or cancer, have persisted in the population for a long time without disappearing. A group of researchers led by Tobias Lenz and Shamil Sunyaev has studied this phenomenon and found evidence that the occurrence of harmful gene variants could be the price we pay for the genetic diversity that is otherwise highly beneficial to our survival. They analyzed a group of immune system proteins that help detect foreign molecules. The genes for these proteins contain many variable sites and occur in a number of alternative forms in the population. This diversity ensures that our immune system is able to recognize a broad range of pathogens. A special form of selection preserves this variation within the group of immune proteins: scientists describe it as balancing selection. It arises, for example, when several alternative variants of a gene confer a survival advantage, and are therefore not eliminated by selection. The scientists suspect that balancing selection may sometimes also lead to the conservation of harmful gene variants. They ran computer simulations of different types of selection using the example of immune system genes. During these tests they discovered that balancing selection not only increases the diversity of immune proteins but also affects neighbouring DNA segments. There, while reducing the total number of variable sites, it increases the frequency with which these variants occur in the population – even if they are harmful. They then compared the simulation results with data from a genetic analysis of 6,500 people. And the analysis confirmed their suspicions: As in the simulation, fewer variable sites occurred in the immediate vicinity of the immune system genes; however, the remaining variants, including harmful mutations, were relatively more common in the population. Harmful genes are therefore able to evade natural selection. "I did expect that higher resistance to pathogens might lead to an accumulation of some harmful mutations. But the extent to which such mutations persist in the population really surprised me. It would be interesting to know how many genetic diseases in humans can be traced back to contact with pathogens we have encountered in the course of our evolution," says Tobias Lenz, group leader at the Max Planck Institute in Plön and member of the newly founded Kiel Evolution Center. In the next step, the researchers want to examine whether balancing selection at other sites in the genome are responsible for the fact that harmful gene variants occur so frequently in the population.


News Article | August 31, 2016
Site: http://www.biosciencetechnology.com/rss-feeds/all/rss.xml/all

New Jersey researchers have identified what is believed to be the first strain of Escherichia coli bacteria from a patient in the United States that harbored two mobile genes making it resistant to both broad spectrum carbapenem antibiotics as well as colistin, an older antibiotic increasingly used as a last resort for multidrug-resistant infections. Their report is published this week in mBio®, an online open-access journal of the American Society for Microbiology. The strain of bacteria, isolated in 2014 from a 76-year-old man with a complicated urinary tract infection but further analyzed in 2016, was found to carry the genes mcr-1 and blaNDM-5, which confer resistance to colistin and carbapenems, respectively. These genes exist on plasmids, small segments of DNA that are capable of moving from one bacterium to another, potentially spreading antibiotic resistance to other bacterial species. While this strain did respond to other antimicrobial agents and was treated successfully, investigators say the case presents a sound reminder to monitor and track multidrug-resistant organisms. "The good news is that this did not cause a major outbreak of drug-resistant infection," said senior study author Barry N. Kreiswirth, Ph.D., founding director of the Public Health Research Institute (PHRI) Tuberculosis Center at New Jersey Medical School, part of Rutgers University in Newark, N.J. "The bad news is that since this occurred two years ago, there are clearly other strains out there we haven't detected yet. Both the carbapenem resistance and the colistin resistance genes are on separate plasmids, which means in principle they could spread to other bacteria." In August 2014, the patient presented to University Hospital in Newark, N.J., with fever and pain in his side. He had emigrated from India to the United States a year prior to experiencing these symptoms. The man had a history of prostate cancer treated with radiation therapy and subsequently developed recurrent urinary tract infections. He had recently undergone a procedure called cystoscopy to examine the bladder. The procedure was complicated by a bladder perforation, requiring surgery to place rubber tubes to help drain the kidneys. Laboratory testing suggested the man had pyuria, or pus in the urine. The man was started on the antimicrobial drugs piperacillin/tazobactam and vancomycin. A urine sample tested positive for the bacteria Pseudomonas aeruginosa, Citrobacter koseri, and Enterococcus faecium; another urine sample from the tube tested positive for P. aeruginosa, E. coli, Klebsiella pneumoniae, Enterococcus spp., and methicillin-resistant Staphylococcus aureus (MRSA). After six days of antimicrobial therapy, a urine sample was clear of bacteria; the man returned home after another procedure to create a new conduit for urine flow. Kreiswirth's lab, which analyzes bacterial isolates from University Hospital, used various molecular techniques to identify and compare bacteria in the man's urine samples. Investigators found that the E. coli strain from the man's urine sample carried both mcr-1 and blaNDM-5 and harbored resistance to several classes of antibiotics, including aminoglycosides, beta-lactams, chloramphenicol, fluoroquinolones, rifampin, sulfonamides, and tetracycline. Additional testing found that the plasmids isolated were highly similar to others that have been reported to be associated with clinical infection in China. The lab identified the E. coli strain as a variant of ST405, one of the main disease-causing strains of the bacteria. "Worrisomely, ST405 has frequently been associated with community-onset urinary tract infections," Kreiswirth said. Most mcr-1 cases appear to be happening in E. coli, the most common cause of urinary tract infections, said lead study author José R. Mediavilla, MBS, MPH, a research teaching specialist at PHRI. "These strains are probably already in the community and could spread further, essentially building toward a situation where you're going to have difficult if not impossible to treat urinary infections," he said. "Active surveillance efforts involving all colistin- and carbapenem-resistant organisms are imperative to determine mcr-1 prevalence and prevent further dissemination."

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