120 research outputs found

    Identification and antimicrobial resistance profile of bacteria isolated from the

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    The main cause of infertility in mares is endometritis, characterized by acute or chronic inflammation of the endometrium. One of the main causes of the occurrence of inflammation in the endometrium is the response to bacterial infection. When the infection overcomes the defense capacity of the host it leads to the development of bacterial endometritis, often caused by Streptococcus equi subsp. zooepidemicus, an opportunistic pathogen. The present study aimed to evaluate the presence of bacteria in the uterus of mares before insemination. For this purpose, uterine washings were performed with sterile saline solution. Samples were centrifuged at 8000 g for 10min at 4oC, and the pellet was streaked onto Blood Agar and MacConkey plates. The obtained isolates were identified using biochemical (VITEK 2 Compac and API, Biomerieux) and molecular identification methodologies (16S rRNA gene sequencing). Moreover, antimicrobial susceptibility tests (AST) were performed with VITEK 2 Compac, for fast growing bacteria and disc diffusion method, for fastidious bacteria. A total of 62 uterine washings were analyzed. A positive culture was obtained in 66% of the specimens, resulting in 57 isolates, with 57% of Gram-positive bacteria isolated. Regarding prevalence, the most frequently isolated genera were Streptococcus (33%), Escherichia (25%) and Staphylococcus (18%), while the most frequent species was Escherichia coli, followed by S. equi subsp. zooepidemicus. Most Gram-positive bacteria were sensitive to the following three antimicrobials, namely tetracycline, ceftiofur, and enrofloxacin. Regarding Gram-negative bacteria, over 90% of the isolates were sensitive to ceftiofur and gentamycin, while over 60% of the isolates were sensitive to enrofloxacin

    Food Patterns According to Sociodemographics, Physical Activity, Sleeping and Obesity in Portuguese Children

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    Our study aimed to describe the association between food patterns and gender, parental education, physical activity, sleeping and obesity in 1976 children aged 5−10 years old. Dietary intake was measured by a semi quantitative food frequency questionnaire; body mass index was calculated and categorized according to the IOTF classification. Factor analysis and generalized linear models were applied to identify food patterns and their associations. TV viewing and male gender were significant positive predictors for fast-food, sugar sweetened beverages and pastry pattern, while a higher level of maternal education and longer sleeping duration were positively associated with a dietary patterns that included fruit and vegetables

    TEAD and YAP regulate the enhancer network of human embryonic pancreatic progenitors.

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    The genomic regulatory programmes that underlie human organogenesis are poorly understood. Pancreas development, in particular, has pivotal implications for pancreatic regeneration, cancer and diabetes. We have now characterized the regulatory landscape of embryonic multipotent progenitor cells that give rise to all pancreatic epithelial lineages. Using human embryonic pancreas and embryonic-stem-cell-derived progenitors we identify stage-specific transcripts and associated enhancers, many of which are co-occupied by transcription factors that are essential for pancreas development. We further show that TEAD1, a Hippo signalling effector, is an integral component of the transcription factor combinatorial code of pancreatic progenitor enhancers. TEAD and its coactivator YAP activate key pancreatic signalling mediators and transcription factors, and regulate the expansion of pancreatic progenitors. This work therefore uncovers a central role for TEAD and YAP as signal-responsive regulators of multipotent pancreatic progenitors, and provides a resource for the study of embryonic development of the human pancreas

    Glutathione-Related Antioxidant Defense System in Elderly Patients Treated for Hypertension

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    The purpose of this study was to analyze glutathione antioxidant defense system in elderly patients treated for hypertension. Studies were carried out in the blood collected from 18 hypertensive and 15 age- and sex-matched controls, all subjects age over 60. Hypertensives were on their usual antihypertensive treatment at the time of blood collection. The concentration of glutathione (GSH) in whole blood and activities of glutathione peroxidase (GPx-1), glutathione transferase (GST), and glutathione reductase (GR) in erythrocytes were measured. The data from patients and controls were compared using independent-samples t test. P value of 0.05 and less was considered statistically significant. We observed increased glutathione-related antioxidant defense in treated hypertensive elderly patients (HT) when compared with healthy controls (C). Mean GSH concentration was significantly higher in HT when compared with C: 3.1 ± 0.29 and 2.6 ± 0.25 mmol/L, respectively, P < 0.001. Mean activity of GR was significantly higher in HT group if compared with C: 83.4 ± 15.25 U/g Hb versus 64.2 ± 8.26 U/g Hb, respectively, P < 0.001. Mean activity of GST was significantly higher in HT group compared with C: 3.0 ± 0.60 mmol CDNB-GSH/mgHb/min and 2.6 ± 0.36 mmol CDNB-GSH/mgHb/min, respectively, P < 0.05. No difference in GPx activity was observed between two groups. These results show that glutathione-related antioxidant defense system was enhanced in elderly hypertensive patients treated for their conditions. This suggests important role of glutathione system in blood pressure regulation. Alterations in concentration and activity of antioxidants observed during antihypertensive medication are likely to be related to the effect of the treatment on NO bioavailability

    Concepts of Cardiac Development in Retrospect

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    Recent research, enabled by powerful molecular techniques, has revolutionized our concepts of cardiac development. It was firmly established that the early heart tube gives rise to the left ventricle only, and that the remainder of the myocardium is recruited from surrounding mesoderm during subsequent development. Also, the cardiac chambers were shown not to be derived from the entire looping heart tube, but only from the myocardium at its outer curvatures. Intriguingly, many years ago, classic experimental embryological studies reached very similar conclusions. However, with the current scientific emphasis on molecular mechanisms, old morphological insights became underexposed. Since cardiac development occurs in an architecturally complex and dynamic fashion, molecular insights can only fully be exploited when placed in a proper morphological context. In this communication we present excerpts of important embryological studies of the pioneers of experimental cardiac embryology of the previous century, to relate insights from the past to current observations

    Antidepressants increase human hippocampal neurogenesis by activating the glucocorticoid receptor

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    Antidepressants increase adult hippocampal neurogenesis in animal models, but the underlying molecular mechanisms are unknown. In this study, we used human hippocampal progenitor cells to investigate the molecular pathways involved in the antidepressant-induced modulation of neurogenesis. Because our previous studies have shown that antidepressants regulate glucocorticoid receptor (GR) function, we specifically tested whether the GR may be involved in the effects of these drugs on neurogenesis. We found that treatment (for 3–10 days) with the antidepressant, sertraline, increased neuronal differentiation via a GR-dependent mechanism. Specifically, sertraline increased both immature, doublecortin (Dcx)-positive neuroblasts (+16%) and mature, microtubulin-associated protein-2 (MAP2)-positive neurons (+26%). This effect was abolished by the GR-antagonist, RU486. Interestingly, progenitor cell proliferation, as investigated by 5′-bromodeoxyuridine (BrdU) incorporation, was only increased when cells were co-treated with sertraline and the GR-agonist, dexamethasone, (+14%) an effect which was also abolished by RU486. Furthermore, the phosphodiesterase type 4 (PDE4)-inhibitor, rolipram, enhanced the effects of sertraline, whereas the protein kinase A (PKA)-inhibitor, H89, suppressed the effects of sertraline. Indeed, sertraline increased GR transactivation, modified GR phosphorylation and increased expression of the GR-regulated cyclin-dependent kinase-2 (CDK2) inhibitors, p27Kip1 and p57Kip2. In conclusion, our data suggest that the antidepressant, sertraline, increases human hippocampal neurogenesis via a GR-dependent mechanism that requires PKA signaling, GR phosphorylation and activation of a specific set of genes. Our data point toward an important role for the GR in the antidepressant-induced modulation of neurogenesis in humans
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