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The primary function of the arterial microvasculature is to ensure that regional perfusion of blood flow is matched to the needs of the tissue bed. This critical physiological mechanism is tightly controlled and regulated by a variety of vasoactive compounds that are generated and released from the vascular endothelium. While these substances are required for modulating vascular tone, they also influence the surrounding tissue and have an overall effect on vascular as well as parenchymal homeostasis. Bioactive lipids, fatty acid derivatives that exert their effects through signaling pathways, are included in the list of vasoactive compounds that modulate the microvasculature. Although lipids were identified as important vascular messengers over three decades ago, their specific role within the microvascular system is not well defined. Thorough understanding of these pathways and their regulation is not only essential to gain insight of their role in cardiovascular disease but is also important for preventing vascular dysfunction following cancer treatment, a rapidly growing problem in medical oncology. The purpose of this review is to discuss how biologically-active lipids contribute to vascular function and signaling within the endothelium. Methods for quantifying lipids will be briefly discussed, followed by an overview of the various lipid families. The crosstalk in signaling between classes of lipids will be discussed in the context of vascular disease. Finally, the potential clinical implications of these lipid families will be highlighted.In the embryonic heart, blood flow is distributed through a bilaterally paired artery system composed of the aortic arches (AA). The purpose of this study is to establish an understanding of the governing mechanism of microstructural maturation of the AA matrix and its reversibility, towards the desired macroscopic vessel lumen diameter and thickness for healthy, abnormal and in ovo repaired abnormal mechanical loading. While matrix-remodeling mechanisms were significantly different for normal vs. conotruncal banding (CTB), both led to an increase in vessel lumen. Correlated with right-sided flow increase at Hamburger & Hamilton stages (HH) 21, intermittent load switching between Collagen-I and III with Elastin and Collagen-IV defines the normal process. However, decreases in COL-I, Elastin, VEGF and FBN-1 in CTB were recovered almost fully following CTB-release model (CTB-R), primarily due to the pressure load changes. The complex temporal changes in matrix proteins are illustrated through a predictive finite-element model based on elastin and collagen load-sharing mechanism to achieve lumen area increase and thickness increase due to wall shear stress and tissue strain respectively. The effect of embryonic timing in cardiac interventions on AA microstructure was established where abnormal mechanical loading was selectively restored at the key stage of development. Recovery of the normal mechanical loading via early fetal intervention resulted in delayed microstructural maturation. Temporal elastin increase, correlated with wall shear stress, is required for continuous lumen area growth.Cardiovascular disease is a major cause of morbidity and mortality among patients with chronic kidney disease (CKD). Trimethylamine-N-oxide (TMAO), a uremic metabolite that is elevated in the setting of CKD, has been implicated as a nontraditional risk factor for cardiovascular disease. While association studies have linked elevated plasma levels of TMAO to adverse cardiovascular outcomes, its direct effect on cardiac and smooth muscle function remains to be fully elucidated. We hypothesized that pathological concentrations of TMAO would acutely increase cardiac and smooth muscle contractility. These effects may ultimately contribute to cardiac dysfunction during CKD. High levels of TMAO significantly increased paced, ex vivo human cardiac muscle biopsy contractility (P0.05). We conclude that TMAO directly increases the force of cardiac contractility, which corresponds with TMAO-induced increases in intracellular calcium, but does not acutely affect vascular smooth muscle or endothelial function of the aorta. It remains to be determined if this acute inotropic action on cardiac muscle is ultimately beneficial or harmful in the setting of CKD.Bullying is a serious public health issue among children and adolescents in the United States. The purpose of this study was to estimate the prevalence of bullying victimization (defined as a child being bullied, picked on, or excluded by children) in the 50 states and the District of Columbia. We used data on bullying victimization from the 2016-2017 National Survey of Children's Health (NSCH). We stratified the sample by age children aged 6-11 years (n = 21 142) and adolescents aged 12-17 years (n = 29 011). check details We conducted bivariate analyses to determine the prevalence of bullying victimization by state for each age group. In the survey, parents/caregivers responded to a question about whether it was "definitely true," "somewhat true," or "not true" that their child "is being bullied, picked on, or excluded by other children." We combined "definitely true" and "somewhat true" responses to create a dichotomous variable for bullying victimization. Parents reported 22.4% of children aged 6-11 years and 21.0% of adolescents aged 12-17 years as experiencing bullying victimization during 2016-2017. The prevalence of bullying victimization among children ranged from 16.5% in New York State to 35.9% in Wyoming and among adolescents ranged from 14.9% in Nevada to 31.6% in Montana. The prevalence of bullying victimization among children or adolescents was >30% in 7 states Arkansas, Kentucky, Maine, Montana, North Dakota, South Dakota, and Wyoming. These data can be used to inform state programs and policies to support bullying prevention efforts and services for children and adolescents who experience bullying. NSCH will continue to collect data on bullying victimization to track annual trends in national and state-level prevalence rates among children and adolescents.The Imperial Academy of Medicine of Paris met in the spring of 1865 to discuss the localization of speech. One of the participants was Maximien Parchappe (1800-1866), an alienist whose research interests lay in the cerebral cortex. This article addresses Maximien Parchappe's concept that the cognitive elements of language-such as the translation of thoughts into words, the will to express them, and the means to do so-reside within the cortical gray matter, and that they are integrated through white-matter fibers. In so doing, Parchappe anticipated Carl Wernicke's linking of the posterior aspects of the dominant frontal and temporal lobes in verbal expression, and Jules Dejerine's linking of the angular gyrus and Wernicke's area in the understanding of written language. Functional imaging has revived interest in language as a network of neuronal aggregates and has given new relevance to Parchappe's concept of the functional organization of language.

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