1,643 research outputs found

    Do statins increase and Mediterranean diet decrease the risk of breast cancer?

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    BACKGROUND: Physical exercise and healthy dietary habits are recommended to prevent breast cancer. DISCUSSION: Increased intake of omega-3 fatty acids associated with decreased omega-6 - resulting in higher omega-3 to omega-6 ratio compared with Western-type diet - is inversely associated with breast cancer risk. The modernized Mediterranean diet with high omega-3 to omega-6 ratio, high fiber and polyphenol intake, and consumption of low-glycemic index foods reduces overall cancer risk and specifically breast cancer risk. It has been suggested that consuming no more than one alcoholic drink per day, preferably wine, is preferable. Eliminating environmental contaminants, including endocrine disruptors, and favoring organic foods to increase polyphenol intake and the omega-3 to omega-6 ratios were also shown to be beneficial. Cholesterol-lowering statins may decrease antitumor defenses; are toxic for the mitochondria; decrease the omega-3 to omega-6 ratio; increase body mass index, insulin resistance and diabetic risk; and have been associated with an increased breast cancer risk. SUMMARY: Therefore, as well as making lifestyle changes to decrease breast cancer risk, we argue that physicians should carefully consider (and often avoid) therapies that may increase breast cancer or diabetes risk in high-risk women and women who wish to decrease their breast cancer risk

    Is it smoking or related lifestyle variables that increase metabolic syndrome risk?

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    Metabolic syndrome is considered as mainly caused by a deleterious lifestyle (sedentarity and diet). That smoking contributes to metabolic syndrome had been suggested by several small studies and a meta-analysis. The interesting study by Slagter et al. published in BMC Medicine is the first very large study confirming this association in both genders, in all classes of body mass index, and in a dose-related manner. Surprisingly, smoking is even associated with increased abdominal fat. Rather than a direct causal effect of smoking, the reason for these associations is most probably the frequent presence of other lifestyle components in smokers. For example, physical inactivity and alcohol drinking are known to be more often present in smokers and could completely explain the observations of the Slagter et al. study. Unfortunately, these factors, already not properly checked in the first studies, were not assessed at all in the present one. However, as it is still on-going, we hope that other lifestyle factors will be included in future publications. Please see related research: http://www.biomedcentral.com/1741-7015/11/195

    Modelling of metal matrix syntactic foams - Description of the compressive stress-strain curves

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    This paper deals with the mathematical description of metal matrix syntactic foams (MMSFs). MMSFs are advanced materials having promising application fields in aviation, transport and automotive industry, in civil engineering and in many other industrial fields. They are porous materials having low density and relatively high compression strength especial compared to ´conventional´ metallic foams. The characterization of MMSFs is continuously developing but the mathematical description of the compressive stress - strain curves is still missing partially. However these formulas are needed to numerically model the non-linear response and energy absorption of the MMSFs in case of compressive loading. According to this the aim of this paper is to give a full, but relatively simple method to handle the compressive stress - strain curves

    Acute influence of cigarette smoke in platelets, catecholamines and neurophysins in the normal conditions of daily life

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    Cigarette smoking is firmly linked to the occurrence of acute coronary events. In twenty-two healthy volunteers in normal conditions of daily life we studied the acute influence of smoking on the following parameters: beta-thromboglobulin, thromboxane B2, epinephrine, norepinephrine, estrogen-stimulated neurophysin, and nicotine-stimulated-neurophysin. Our results show that in our population and following our protocol, smoking did not induce platelet activation, thromboxane formation, catecholamine release or estrogen-stimulated-neurophysin secretion. However, smoking did provoke a significant increase of nicotine-stimulated-neurophysin (p<0.05) which reflects vasopressin increase and which might explain the high incidence of ischaemic accidents in cigarette smoking via the vasoactive properties of vasopressi

    Molecular diversity of antimicrobial effectors in the oyster Crassostrea gigas

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    Background: To gain insight into the molecular diversity of antimicrobial peptides and proteins in the oyster Crassostrea gigas, we characterized and compared the sequence polymorphism of the antimicrobial peptides (AMPs), Cg-Defensins (Cg-Defs) and Cg-Proline Rich peptide (Cg-Prp), and of the bactericidal permeability increasing protein, Cg-BPI. For that, we analyzed genomic and transcript sequences obtained by specific PCR amplification and in silico searches. Results: High diversification among the three antimicrobial effectors was evidenced by this polymorphism survey. On the basis of sequence phylogenies, each AMP aggregates into clearly defined groups of variants and is the product of a multigenic family displaying a variety of gene structures. In contrast, Cg-bpi forms a single group and is encoded by a single gene copy. Moreover, we identified for both AMPs several genetic mechanisms of diversification such as recombination, parallel mutations leading to phylogenetic homoplasy and indel events. In addition, the non synonymous to synonymous substitutions ratio by codon (dN/dS) revealed several negatively and positively selected sites for both AMPs, suggesting that directional selection pressures have shaped their sequence variations. Conclusions: This study shows for the first time in a mollusc that antimicrobial peptides and proteins have been subject to distinct patterns of diversification and we evidence the existence of different evolutionary routes leading to such sequence variability

    Beyond confusion and controversy, can we evaluate the real efficacy and safety of cholesterol-lowering with statins?

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    A strong controversy has emerged about the reality of safety and efficacy of statins as stated by company-sponsored reports. However, physicians need credible data to make medical decisions, in particular about the benefit/harm balance of any prescription. This study aimed to test the validity of data on the company-sponsored statin trial by comparing them over time and then comparing statins with each other. Around the years 2005/2006, new stricter Regulations were introduced in the conduct and publication of randomized controlled trials (RCTs). This would imply that RCTs were less reliable before 2006 than they were later on. To evaluate this, we first reviewed RCTs testing the efficacy of statins versus placebo in preventing cardiovascular complications and published after 2006. Our systematic review thereby identified four major RCTs, all testingrosuvastatin. They unambiguously showed that rosuvastatin is not effective in secondary prevention, while the results are highly debatable in primary prevention. Because of the striking clinical heterogeneity and the inconsistency of the published data in certain RCTs, meta-analysis was not feasible. We then examined the most recent RCTs comparing statins to each other: all showed that no statin is more effective than any other, including rosuvastatin. Furthermore, recent RCTs clearly indicate that intense cholesterol-lowering (including those with statins) does not protect high-risk patients any better than less-intense statin regimens. As for specific patient subgroups, statins appear ineffective in chronic heart failure and chronic kidney failure patients. We also conducted a MEDLINE search to identify all the RCTs testing a statin against a placebo in diabetic patients, and we found that once secondary analyses and subgroup analyses are excluded, statins do not appear to protect diabetics. As for the safety of statin treatment – a major issue for medical doctors – it is quite worrisome to realize that it took 30 years to bring to light the triggering effect of statins on new-onset diabetes, manifestly reflecting a high level of bias in reporting harmful outcomes in commercial trials, as has been admitted by the recent confession of prominent experts in statin treatment. In conclusion, this review strongly suggests that statins are not effective for cardiovascular prevention. The studies published before 2005/2006 were probably flawed, and this concerned in particular the safety issue. A complete reassessment is mandatory. Until then, physicians should be aware that the present claims about the efficacy and safety of statins are not evidence based
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