Limpotter4989

Receiver operating curve (ROC) analyses revealed that a PPR value greater than 0.057 had 76% sensitivity and 51% specificity and a PDW higher than 16.2% had 80% sensitivity and 66% specificity in predicting inadequate CCD. CONCLUSION The present study suggests that PDW and PPR may be associated with the degree of collateral development in chronic stable coronary artery disease (CAD). Copyright © 2020 by Istanbul Northern Anatolian Association of Public Hospitals.OBJECTIVE Pump thrombosis in left ventricular assist device (LVAD) patients is an important cause of mortality and morbidity. Inflow cannula migration is a predisposing factor for pump thrombosis. Telecardiographic measurements can be used to follow up apical cannula deviation. In this study, we aimed to evaluate the migration of the inflow cannulas in patients with LVADs using angle measurements on telecardiograms. METHODS Twenty-three patients who were implanted left ventricular assist devices in our clinic between February 2013 and April 2016 were included in our study. During the first year of follow-up, changes in angle measurements on postoperative 1st, 3rd, 6th, and 12th month telecardiograms were compared against the incidence of device thrombus and serum Lactate Dehydrogenase (LDH) levels. RESULTS Patients who were diagnosed with device thrombosis had more change in inflow cannula angles than patients without device thrombus (p less then 0.05 at 6th and 12th months). Patients with higher LDH values had more parallel angular changes at all intervals, and the change in angle was statistically significant at 3rd, 6th and 12th months (p less then 0.05). CONCLUSION This study shows that it is possible to track the migration of inflow cannulas in patients with left ventricular heart failure using telecardiograms. The correlation between angle change and LDH levels and embolic events may suggest that telecardiographic follow up of angles may be a useful tool for ventricular assist devices teams for early detection of thrombus. Copyright © 2020 by Istanbul Northern Anatolian Association of Public Hospitals.OBJECTIVE This study aimed to evaluate the penetration of moxifloxacin and doripenem into the pleural fluid (PF) using a rabbit model of empyema. METHODS An empyema was induced using the intrapleural injection of turpentine (1 mL), followed 24 h later by instillation of 5 mL Klebsiella Pneumoniae (ATCC 33495), Fusobacterium nucleatum (ATCC 25586) and Streptokok Pneumoniae (ATCC 6305) into the pleural space. After an empyema was corroborated, Moxifloxacin (25 mg/kg-1) and Doripenem (20 mg/kg-1) were administered intraperitoneally. To determine the levels of antibiotics measured by High-Performance Liquid Chromatography in pleural and blood samples were obtained serially at 8, 24, 48 and 72nd hour. RESULTS The penetration of both antibiotics into the PF was very good. The penetration rate of doripenem (area under the curve (AUC) for PF/blood (AUCPF/AUCblood) ratio=1.68) was better than moxifloxacin (ratio=0.78). Equalization time between the PF and blood concentration of doripenem was more quickly than moxifloxacin. Tofacitinib molecular weight Peak PF concentration of moxifloxacin was 0,81 μg/mL-1 and occurred 8 h after infusion and then gradually decreased; at the beginning of the blood and pleural fluid concentrations of doripenem were equal. While the pleura concentration was increasing, blood concentration was almost the same. Doripenem reached a peak concentration (0.54 μg/ml) 24 h post-administration. CONCLUSION Differences were found in the penetration of the two antibiotics. Doripenem had convenient penetration PF compared to moxifloxacin. Due to the differences between human and rabbit pleural thickness, doripenem's pleural penetration should be examined in infection models in animals with equal pleura thickness and clinical trials. Copyright © 2020 by Istanbul Northern Anatolian Association of Public Hospitals.In response to signals associated with infection or tissue damage, macrophages undergo a series of dynamic phenotypic changes. Here we show that during the response to LPS and interferon-γ stimulation, metabolic reprogramming in macrophages is also highly dynamic. Specifically, the TCA cycle undergoes a two-stage remodeling the early stage is characterized by a transient accumulation of intermediates including succinate and itaconate, while the late stage is marked by the subsidence of these metabolites. The metabolic transition into the late stage is largely driven by the inhibition of pyruvate dehydrogenase complex (PDHC) and oxoglutarate dehydrogenase complex (OGDC), which is controlled by the dynamic changes in lipoylation state of both PDHC and OGDC E2 subunits and phosphorylation of PDHC E1 subunit. This dynamic metabolic reprogramming results in a transient metabolic state that strongly favors HIF-1α stabilization during the early stage, which subsides by the late stage; consistently, HIF-1α levels follow this trend. This study elucidates a dynamic and mechanistic picture of metabolic reprogramming in LPS and interferon-γ stimulated macrophages, and provides insights into how changing metabolism can regulate the functional transitions in macrophages over a course of immune response.The common forms of metabolic diseases are highly complex, involving hundreds of genes, environmental and lifestyle factors, age-related changes, sex differences and gut-microbiome interactions. Systems genetics is a population-based approach to address this complexity. In contrast to commonly used 'reductionist' approaches, such as gain or loss of function, that examine one element at a time, systems genetics uses high-throughput 'omics' technologies to quantitatively assess the many molecular differences among individuals in a population and then to relate these to physiologic functions or disease states. Unlike genome-wide association studies, systems genetics seeks to go beyond the identification of disease-causing genes to understand higher-order interactions at the molecular level. The purpose of this review is to introduce the systems genetics applications in the areas of metabolic and cardiovascular disease. Here, we explain how large clinical and omics-level data and databases from both human and animal populations are available to help researchers place genes in the context of pathways and networks and formulate hypotheses that can then be experimentally examined.