4,487 research outputs found

    Megfelelés, hasonlítás, tettenérés

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    This paper analyses the concepts Mészöly uses in his essays to describe an ethical stance. Without ever reaching a true conceptual consistency in his theoreticl writings, he reformulates from time to time how the writer has to compose a responsible answer to the insult of reality. Beyond his critical essays, his short stories are the primordial experimental medium in which these answers are realized. According to Mészöly, the task of the realist is not to imitate reality but to catch it in the act by way of an experimental situation

    Mechanisms of coronary microvascular adaptation to obesity.

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    The metabolic syndrome (MetS) is associated with clustering of cardiovascular risk factors in individuals that may greatly increase their risk of developing coronary artery disease. Obesity and related metabolic dysfunction are the driving forces in the prevalence of MetS. It is believed that obesity has detrimental effects on cardiovascular function, but its overall impact on the vasomotor regulation of small coronary arteries is still debated. Emerging evidence indicates that in obesity coronary arteries adapt to hemodynamic changes via maintaining and/or upregulating cellular mechanism(s) intrinsic to the vascular wall. Among other factors, endothelial production of cyclooxygenase-2-derived prostacyclin and reactive oxygen species, as well as increased nitric oxide sensitivity and potassium channel activation in smooth muscle cells, have been implicated in maintaining coronary vasodilator function. This review aims to examine studies that have been primarily focused on alterations in coronary vasodilator function in obesity. A better understanding of cellular mechanisms that may contribute to coronary microvascular adaptation may provide insight into the sequence of pathological events in obesity and may allow the harnessing of these effects for therapeutic purposes

    sj-docx-2-asn-10.1177_17590914221123138 - Supplemental material for Multispectral LEDs Eliminate Lipofuscin-Associated Autofluorescence for Immunohistochemistry and CD44 Variant Detection by in Situ Hybridization in Aging Human, non-Human Primate, and Murine Brain

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    Supplemental material, sj-docx-2-asn-10.1177_17590914221123138 for Multispectral LEDs Eliminate Lipofuscin-Associated Autofluorescence for Immunohistochemistry and CD44 Variant Detection by in Situ Hybridization in Aging Human, non-Human Primate, and Murine Brain by Philip A. Adeniyi, Katie-Anne Fopiano, Fatima Banine, Mariel Garcia, Xi Gong, C. Dirk Keene, Larry S. Sherman, Zsolt Bagi and Stephen A. Back in ASN Neuro</p

    sj-docx-1-asn-10.1177_17590914221123138 - Supplemental material for Multispectral LEDs Eliminate Lipofuscin-Associated Autofluorescence for Immunohistochemistry and CD44 Variant Detection by in Situ Hybridization in Aging Human, non-Human Primate, and Murine Brain

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    Supplemental material, sj-docx-1-asn-10.1177_17590914221123138 for Multispectral LEDs Eliminate Lipofuscin-Associated Autofluorescence for Immunohistochemistry and CD44 Variant Detection by in Situ Hybridization in Aging Human, non-Human Primate, and Murine Brain by Philip A. Adeniyi, Katie-Anne Fopiano, Fatima Banine, Mariel Garcia, Xi Gong, C. Dirk Keene, Larry S. Sherman, Zsolt Bagi and Stephen A. Back in ASN Neuro</p

    Activation of hexosamine pathway impairs nitric oxide (NO)-dependent arteriolar dilations by increased protein O-GlcNAcylation.

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    We hypothesized that under high glucose conditions, activation of the hexosamine pathway leads to impaired nitric oxide (NO)-dependent arteriolar dilation. Skeletal muscle arterioles (diameter: ~160μm) isolated from male Wistar rats were exposed to normal glucose (NG, 5.5mmol/L) or high glucose concentrations (HG, 30mmol/L, for 2h) and agonist-induced diameter changes were measured with videomicroscopy. Western blots were performed to identify the vascular levels of protein O-linked-N-acetyl-glucosamine (O-GlcNAc) and phosphorylated endothelial NO synthase (eNOS). In arterioles exposed to HG, dilations to histamine were abolished compared to those exposed to NG (max: -6±6% and 69±9%, respectively), while acetylcholine-induced responses were not affected. Inhibition of NO synthesis with N(G)-nitro-l-arginine methyl ester (L-NAME) reduced histamine-induced dilations in NG arterioles, but it had no effect on microvessels exposed to HG. Dilations to the NO donor, sodium nitroprusside and constrictions to norepinephrine and serotonin were similar in the two groups. In the presence of the inhibitor of hexosamine pathway, azaserine, histamine-induced dilations were significantly augmented in arterioles exposed to HG (max: 67±2%). Moreover, exposure of vessels to glucosamine (5mmol/L, for 2h) resulted in reduced histamine-induced arteriolar dilations (max: 26±3%). The level of protein O-GlcNAcylation was increased, whereas the P-eNOS (Ser-1177) was decreased in HG exposed vessels. These findings indicate that a high concentration of glucose may lead to glucosamine formation, which impairs histamine-induced, NO-mediated arteriolar dilations. We propose that interfering with the hexosamine pathway may prevent microvascular complications in diabetes

    Eldologiasodott élet : Lukács György társadalomelméleti fenomenológiája

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    Lukács György társadalomelméleti filozófiájának legfontosabb kontextusa a huszadik század elejének transzcendentális filozófiája. Ez az írás azt kívánja bemutatni, hogyan értelmezi a kapitalista világban-létet – kantiánus és fenomenológiai eszközökkel – a Történelem és osztálytudat. A világban-lét abban a történetileg és társadalmilag meghatározott korban, amelyet kapitalizmusnak nevezünk, három mozzanattal jellemezhető, amelyek az eldologiasodás elméletét specifikálják: absztrakció, véletlen és kontempláció. Ezen fogalmak mindegyike – külön-külön vagy együttvéve – preformálja a huszadik századi társadalomelmélet diskurzusát

    petunjuk bagi penulis

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    petunjuk bagi penulis</jats:p

    Vasculo-neuronal coupling and neurovascular coupling at the neurovascular unit: impact of hypertension

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    Components of the neurovascular unit (NVU) establish dynamic crosstalk that regulates cerebral blood flow and maintain brain homeostasis. Here, we describe accumulating evidence for cellular elements of the NVU contributing to critical physiological processes such as cerebral autoregulation, neurovascular coupling, and vasculo-neuronal coupling. We discuss how alterations in the cellular mechanisms governing NVU homeostasis can lead to pathological changes in which vascular endothelial and smooth muscle cell, pericyte and astrocyte function may play a key role. Because hypertension is a modifiable risk factor for stroke and accelerated cognitive decline in aging, we focus on hypertension-associated changes on cerebral arteriole function and structure, and the molecular mechanisms through which these may contribute to cognitive decline. We gather recent emerging evidence concerning cognitive loss in hypertension and the link with vascular dementia and Alzheimer’s disease. Collectively, we summarize how vascular dysfunction, chronic hypoperfusion, oxidative stress, and inflammatory processes can uncouple communication at the NVU impairing cerebral perfusion and contributing to neurodegeneration.Fil: Presa, Jessica Lorena. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Biología y Medicina Experimental. Fundación de Instituto de Biología y Medicina Experimental. Instituto de Biología y Medicina Experimental; ArgentinaFil: Saravia, Flavia Eugenia. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Biología y Medicina Experimental. Fundación de Instituto de Biología y Medicina Experimental. Instituto de Biología y Medicina Experimental; ArgentinaFil: Bagi, Zsolt. Augusta University; Estados UnidosFil: Filosa, Jessica A.. Augusta University; Estados Unido
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