408 research outputs found
Assessing indicators of runoff and erosion by rain simulation in the Ben Ahmed watershed (Central Morocco)
The objective of this study was to investigate the risks of runoff and erosion of soils in the Ben Ahmed watershed, it's located in the region of casa-settat, 70 km south-east of Casablanca, and characterized by a semi-arid climate. The study consists of measuring on 1 m2 plot, the volumes of runoff and sediments, under the influence of rainfall generation (60mm/30 min). Soil samples were collected from each plot to determine texture, organic matter and humidity. Results obtained show that the detachability varies between 19 and 34 g/l, infiltrability oscillate between 15 and 37 mm.h-. Pearson correlation test shows that infiltration was negatively correlated with runoff and soil detachability (R=-0.99, R=-0.87 respectively). It‘s significantly correlated with the proportions of sand(R=0.69), silt (R= -0.98) an clay (R= 0.92), however, is weakly correlated with organic matter (R=-0.32). Infiltration and detachability were significantly correlated with humidity (R = -0.99, R = -0.63respectively)
Protein phosphatase 5 regulates titin phosphorylation and function at a sarcomere-associated mechanosensor complex in cardiomyocytes.
Serine/threonine protein phosphatase 5 (PP5) is ubiquitously expressed in eukaryotic cells; however, its function in cardiomyocytes is unknown. Under basal conditions, PP5 is autoinhibited, but enzymatic activity rises upon binding of specific factors, such as the chaperone Hsp90. Here we show that PP5 binds and dephosphorylates the elastic N2B-unique sequence (N2Bus) of titin in cardiomyocytes. Using various binding and phosphorylation tests, cell-culture manipulation, and transgenic mouse hearts, we demonstrate that PP5 associates with N2Bus in vitro and in sarcomeres and is antagonistic to several protein kinases, which phosphorylate N2Bus and lower titin-based passive tension. PP5 is pathologically elevated and likely contributes to hypo-phosphorylation of N2Bus in failing human hearts. Furthermore, Hsp90-activated PP5 interacts with components of a sarcomeric, N2Bus-associated, mechanosensor complex, and blocks mitogen-activated protein-kinase signaling in this complex. Our work establishes PP5 as a compartmentalized, well-controlled phosphatase in cardiomyocytes, which regulates titin properties and kinase signaling at the myofilaments
The emergence of antimicrobial resistance in enterococci isolates from infants: A review study
The emergence of antibiotic resistance in potential bacterial pathogens is considered as an important consequence of antibiotic misuse and overuse in humans and animals husbandry. In addition, lacks of adequate infection-control practice in hospital and medical care settings have led to the continuing development of extensive resistance problems worldwide. Certain multidrug-resistant commensal and potential pathogens are now   widely spread in community and hospital patients worldwide . Examples are meticillin-resistant Staphylococcus aureus (MRSA) and vancomycin-resistance enterococcci (VRE), extended-spectrum β-lactamase- and carbapenemase-producing coliforms, and toxin-hyperproducing Clostridium difficile. During the last decade, Enterococcus faecalis and Enterococcus faecium are the most prevalent species cultured from human infections. Incidence of enterococci resistant to multiple antibiotics has become increasingly common in the hospitalized patients all over the world. E. faecium is reported to be responsible for most vancomycin-resistant enterococci (VRE) infections.Â
Transmural Heterogeneity of Myofilament Function and Sarcomeric Protein Phosphorylation in Remodeled Myocardium of Pigs with a Recent Myocardial Infarction
Aim: Transmural differences in sarcomeric protein composition and function across the left ventricular (LV) wall have been reported. We studied in pigs sarcomeric function and protein phosphorylation in subepicardial (EPI) and subendocardial (ENDO) layers of remote LV myocardium after myocardial infarction (MI), induced by left circumflex coronary artery ligation. Methods: EPI and ENDO samples were taken 3 weeks after sham surgery (n = 12) or induction of MI (n = 12) at baseline (BL) and during β-adrenergic receptor (βAR) stimulation with dobutamine. Isometric force was measured in single cardiomyocytes at various [Ca2+] and 2.2 μm sarcomere length. Results: In sham hearts, no significant transmural differences were observed in myofilament function or protein phosphorylation. Myofilament Ca2+-sensitivity was significantly higher in both EPI and ENDO of MI compared to sham hearts. Maximal force was significantly reduced in MI compared to sham, but solely in ENDO cells. A higher passive force was observed in MI hearts, but only in EPI cells. The proportion of stiff N2B isoform was higher in EPI than in ENDO in both sham and MI hearts, and a trend toward increased N2B-proportion appeared in MI EPI, but not MI Endo. Analysis of myofilament protein phosphorylation did not reveal significant transmural differences in phosphorylation of myosin binding protein C, desmin, troponin T, troponin I (cTnI), and myosin light chain 2 (MLC-2) both at BL and during βAR stimulation with dobutamine infusion. A significant increase in MLC-2 phosphorylation was observed during dobutamine only in sham. In addition, the increase in cTnI phosphorylation upon dobutamine was twofold lower in MI than in sham. Conclusion: Myofilament dysfunction is present in both EPI and ENDO in post-MI remodeled myocardium, but shows a high degree of qualitative heterogeneity across the LV wall. These heterogeneous transmural changes in sarcomeric properties likely contribute differently to systolic vs. diastolic global LV dysfunction after MI
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