106 research outputs found

    Lipidic characterization of Santa Ines lamb shoulder

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    The edible portion of the shoulder of 12 castrated and 12 non-castrated Santa Ines lambs slaughtered at different ages (84, 168, 210, 252 days) were used. The shoulders were chemically analyzed to determine the quantity of total lipids, cholesterol, and fatty acids composition. Castrated and non-castrated lambs gained body weight (p = 0.0393, p = 0.0017) and half carcass weight (p = 0.0240, p = 0.0017), respectively. The shoulder weight was increased in the carcasses of non-castrated lambs (p = 0.0110). The edible portion of the shoulder of castrated lambs presented higher total lipids (16.09 g.100 g(-1)). The cholesterol content was influenced by castration (p = 0.0001) reducing with age. Castrated animals presented higher content of C18:1 T11, CLA, and C18:0. The shoulder weight is only increased with increasing age in the carcasses of non-castrated lambs. Castration influences the cholesterol content of the shoulder; however, both castrated and non-castrated lambs had their cholesterol contents reduced with increasing age. Castration and age interfered in the estearic acid concentration of the edible portion of lamb shoulder.31250851

    Effects of post-exercise cooling on heart rate recovery in normotensive and hypertensive men

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    Background: Post-exercise heart rate recovery (HRR) is determined by cardiac autonomic restoration after exercise and is reduced in hypertension. Post-exercise cooling accelerates HRR in healthy subjects, but its effects in a population with cardiac autonomic dysfunction, such as hypertensives (HT), may be blunted. This study assessed and compared the effects of post-exercise cooling on HRR and cardiac autonomic regulation in HT and normotensive (NT) subjects. Methods: Twenty-three never-treated HT (43±8 ys) and 25 NT (45±8 ys) men randomly underwent two exercise sessions (30 min of cycling at 70%VO2peak) followed by 15 min of recovery. In one randomly allocated session, a fan was turned on in front of the subject during the recovery (cooling), while in the other session, no cooling was performed (control). HRR was assessed by heart rate reductions after 60 (HRR60s) and 300s (HRR300s) of recovery, short-term time constant of HRR (T30), and the time constant of the HRR after exponential fitting (HRRτ). HRV was assessed using time- and frequency-domain indices. Results: HRR and HRV responses in the cooling and control sessions were similar between the HT and NT. Thus, in both groups, post-exercise cooling equally accelerated HRR (HRR300s = 39±12 vs. 36±10 bpm, p≤0.05) and increased post44 exercise HRV (lnRMSSD = 1.8±0.7 vs. 1.6±0.7 ms, p≤0.05). Conclusion: Differently from the hypothesis, post-exercise cooling produced similar improvements in HRR in HT and NT men, likely by an acceleration of cardiac parasympathetic reactivation and sympathetic withdrawal. These results suggest that post-exercise cooling equally accelerates HRR in hypertensive and normotensive subjects

    Serum Activity of Platelet-Activating Factor Acetylhydrolase Is a Potential Clinical Marker for Leptospirosis Pulmonary Hemorrhage

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    Pulmonary hemorrhage has been recognized as a major, often lethal, manifestation of severe leptospirosis albeit the pathogenesis remains unclear. The Leptospira interrogans virulent serogroup Icterohaemorrhagiae serovar Lai encodes a protein (LA2144), which exhibited the platelet-activating factor acetylhydrolase (PAF-AH) activity in vitro similar to that of human serum with respect to its substrate affinity and specificity and thus designated L-PAF-AH. On the other hand, the primary amino acid sequence of L-PAF-AH is homologous to the α1-subunit of the bovine brain PAF-AH isoform I. The L-PAF-AH was proven to be an intracellular protein, which was encoded unanimously and expressed similarly in either pathogenic or saprophytic leptospires. Mongolian gerbil is an appropriate experimental model to study the PAF-AH level in serum with its basal activity level comparable to that of human while elevated directly associated with the course of pulmonary hemorrhage during severe leptospirosis. Mortality occurred around the peak of pulmonary hemorrhage, along with the transition of the PAF-AH activity level in serum, from the increasing phase to the final decreasing phase. Limited clinical data indicated that the serum activity of PAF-AH was likely to be elevated in the patients infected by L. interrogans serogroup Icterohaemorrhagiae, but not in those infected by other less severe serogroups. Although L-PAF-AH might be released into the micro-environment via cell lysis, its PAF-AH activity apparently contributed little to this elevation. Therefore, the change of PAF-AH in serum not only may be influential for pulmonary hemorrhage, but also seems suitable for disease monitoring to ensure prompt clinical treatment, which is critical for reducing the mortality of severe leptospirosis

    Vulnerability of women living with HIV/aids

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    OBJECTIVE: outline the profile of women living with the human immunodeficiency virus/aids in interior cities in São Paulo State, in the attempt to identify characteristics related to individual, social and programmatic vulnerability and to analyze the conditions in which they discovered their serological status. METHOD: between October 2008 and December 2010, a cross-sectional study was undertaken with 184 women attended at a specialized service. The data were collected through an interview and gynecological test, including the collection of samples for the etiological diagnosis of sexually transmissible conditions. RESULTS: the women were predominantly white, between 30 and 49 years of age, lived with a partner, had a low education level, multiple sexual partners across the lifetime and unsafe sexual practices. The prevalence of sexually transmitted diseases corresponded to 87.0%. CONCLUSION: the study suggests the need to offer gynecological care in specialized services and the accomplishment of multiprofessional actions to reinforce the female autonomy in protective decision making

    Association of the Gene Polymorphisms IFN-γ +874, IL-13 −1055 and IL-4 −590 with Patterns of Reinfection with Schistosoma mansoni

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    Approximately 200 million people have schistosomiasis in parts of Africa, South America, the Middle East, the Caribbean and Asia. Several studies of multiple treatments and reinfections indicate that some people develop resistance to reinfection. Of all the immunologic findings associated with such studies, the most consistent observation is that resistance (usually defined as lower levels of infection upon reinfection) correlates with high IgE and low IgG4 antibodies against schistosome antigens. Our studies test whether single nucleotide polymorphisms residing in the gene or promoter regions of cytokines pivotal in controlling production of these antibody isotypes are different amongst those that develop resistance to reinfection as opposed to those that do not. Through genotyping of these polymorphisms in a cohort of occupationally exposed car washers, we found that men with certain genotypic patterns of polymorphisms in IL-4, IFN-γ, and IL-13 were significantly more likely to be resistant to reinfection than those with different patterns. These data provide initial insights into the potential genetic foundation of propensities of people to develop resistance to reinfection by schistosomes, and offer a basis for further molecular studies of how these polymorphisms might work at the transcriptional and gene product level in cells stimulated by schistosome antigens

    Clostridium difficile infection.

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    Infection of the colon with the Gram-positive bacterium Clostridium difficile is potentially life threatening, especially in elderly people and in patients who have dysbiosis of the gut microbiota following antimicrobial drug exposure. C. difficile is the leading cause of health-care-associated infective diarrhoea. The life cycle of C. difficile is influenced by antimicrobial agents, the host immune system, and the host microbiota and its associated metabolites. The primary mediators of inflammation in C. difficile infection (CDI) are large clostridial toxins, toxin A (TcdA) and toxin B (TcdB), and, in some bacterial strains, the binary toxin CDT. The toxins trigger a complex cascade of host cellular responses to cause diarrhoea, inflammation and tissue necrosis - the major symptoms of CDI. The factors responsible for the epidemic of some C. difficile strains are poorly understood. Recurrent infections are common and can be debilitating. Toxin detection for diagnosis is important for accurate epidemiological study, and for optimal management and prevention strategies. Infections are commonly treated with specific antimicrobial agents, but faecal microbiota transplants have shown promise for recurrent infections. Future biotherapies for C. difficile infections are likely to involve defined combinations of key gut microbiota
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