Behavior of large-scale rectangular columns confined with FRP composites

This paper focuses on axially loaded, large-scale rectangular RC columns confined with fiber-reinforced polymer (FRP) wrapping. Experimental tests are conducted to obtain the stress-strain response and ultimate load for three field-size columns having different aspect ratios and/or corner radii. Effective transverse FRP failure strain and the effect of increasing confining action on the stress-strain behavior are examined. Existing strength models, the majority of which were developed for small-scale specimens, are applied to predict the structural response. Since some of them fail to adequately characterize the test data and others are complex and require significant calculation, a simple design-oriented model is developed. The new model is based on the confinement effectiveness coefficient, an aspect ratio coefficient, and a corner radius coefficient. It accurately predicts the axial ultimate strength of the large-scale columns at hand and, when applied to the small-scale columns studied by other investigators, produces reasonable results

Nitric oxide function in atherosclerosis

Atherosclerosis is a chronic inflammatory process in the intima of conduit arteries, which disturbs the endothelium-dependent regulation of the vascular tone by the labile liposoluble radical nitric oxide (NO) formed by the constitutive endothelial nitric oxide synthase (eNOS). This defect predisposes to coronary vasospasm and cardiac ischaemia, with anginal pain as the typical clinical manifestation. It is now appreciated that endothelial dysfunction is an early event in atherogenesis and that it may also involve the microcirculation, in which atherosclerotic lesions do not develop. On the other hand, the inflammatory environment in atherosclerotic plaques may result in the expression of the inducible NO synthase (iNOS) isozyme. Whether the dysfunction in endothelial NO production is causal to, or the result of, atherosclerotic lesion formation is still highly debated. Most evidence supports the hypothesis that constitutive endothelial NO release protects against atherogenesis e.g. by preventing smooth muscle cell proliferation and leukocyte adhesion. Nitric oxide generated by the inducible isozyme may be beneficial by replacing the failing endothelial production but excessive release may damage the vascular wall cells, especially in combination with reactive oxygen intermediates

Муніципальні відзнаки: проблеми законодавчого регулювання в Україні

Актуальною проблемою законодавства є розробка, призначення, заснування та відзначення громадян нагородами органів місцевого самоврядування.Актуальной проблемой законодательства является разработка, назначение, основание и отмечание граждан наградами органов местного самоуправления.An urgent problem of legislation is treatment, assignment, establishment and to honour citizens by the rewards of organs of local self-government

Modulation of nitric oxide synthase activity in macrophages

L-Arginine is converted to the highly reactive and unstable nitric oxide (NO) and L-citrulline by an enzyme named nitric oxide synthase (NOS). NO decomposes into other nitrogen oxides such as nitrite (NO2-) and nitrate (NO2-), and in the presence of superoxide anion to the potent oxidizing agent peroxynitrite (ONOO−). Activated rodent macrophages are capable of expressing an inducible form of this enzyme (iNOS) in response to appropriate stimuli, i.e., lipopolysaccharide (LPS) and interferon-γ (IFNγ). Other cytokines can modulate the induction of NO biosynthesis in macrophages. NO is a major effector molecule of the anti-microbial and cytotoxic activity of rodent macrophages against certain micro-organisms and tumour cells, respectively. The NO synthesizing pathway has been demonstrated in human monocytes and other cells, but its role in host defence seems to be accessory. A delicate functional balance between microbial stimuli, host-derived cytokines and hormones in the microenvironment regulates iNOS expression. This review will focus mainly on the known and proposed mechanisms of the regulation of iNOS induction, and on agents that can modulate NO release once the active enzyme has been expressed in the macrophage

Effect of a serotonin blocking agent on renal hemodynamics in the normal rat

Effect of a serotonin blocking agent on renal hemodynamics in the normal rat. These studies were designed to explore the effects of ketanserin (K), a serotonergic S2-receptor blocker on glomerular filtration rate (GFR), renal plasma flow (RPF) and autoregulation of renal blood flow (RBF) in the normal, anesthetized rat. Two doses of ketanserin were used: a high dose that, in addition to its serotonin blocking effect, possessed alpha 1-adrenergic blocking capacities; and a low dose that acted only as a serotonin S2 blocking agent. The effects of the high dose were compared to the effects of phenotolamine. Both the high dose of K and phentolamine resulted in a similar fall of systemic blood pressure from 117 ± 4 to 78 ± 3 and from 121 ± 4.5 to 76 ± 5mm Hg, respectively (P < 0.01). Despite this fall, GFR and RPF remained unchanged from 2.36 ± 0.16 ± to 2.26 ± 0.12 ml/min, and from 5.33 ± 0.41 to 5.76 ± 0.5ml/min with K, while both parameters significantly decreased with phentolamine. A remarkable preservation of the autoregulation of RBF until a renal perfusion pressure (RPP) of 70 to 75mm Hg was noted with K, but not with phentolamine or Ringer infusion. With the low dose of K, a significant rise in GFR and PAH clearance was noted, from 2.12 ± 0.17 to 2.59 ± 0.18 and from 4.81 ± 0.35 to 5.66 ± 0.48 ml/min, respectively (P < 0.05). A similar preservation of autoregulation of RBF was observed. Our studies suggest that in the pressure ranges below normal autoregulation of RBF in the rat, serotonin blockade is associated with maintenance of both GFR and RBF

Effect of a serotonin blocking agent on renal hemodynamics in the normal rat

Effect of a serotonin blocking agent on renal hemodynamics in the normal rat. These studies were designed to explore the effects of ketanserin (K), a serotonergic S2-receptor blocker on glomerular filtration rate (GFR), renal plasma flow (RPF) and autoregulation of renal blood flow (RBF) in the normal, anesthetized rat. Two doses of ketanserin were used: a high dose that, in addition to its serotonin blocking effect, possessed alpha 1-adrenergic blocking capacities; and a low dose that acted only as a serotonin S2 blocking agent. The effects of the high dose were compared to the effects of phenotolamine. Both the high dose of K and phentolamine resulted in a similar fall of systemic blood pressure from 117 ± 4 to 78 ± 3 and from 121 ± 4.5 to 76 ± 5mm Hg, respectively (P < 0.01). Despite this fall, GFR and RPF remained unchanged from 2.36 ± 0.16 ± to 2.26 ± 0.12 ml/min, and from 5.33 ± 0.41 to 5.76 ± 0.5ml/min with K, while both parameters significantly decreased with phentolamine. A remarkable preservation of the autoregulation of RBF until a renal perfusion pressure (RPP) of 70 to 75mm Hg was noted with K, but not with phentolamine or Ringer infusion. With the low dose of K, a significant rise in GFR and PAH clearance was noted, from 2.12 ± 0.17 to 2.59 ± 0.18 and from 4.81 ± 0.35 to 5.66 ± 0.48 ml/min, respectively (P < 0.05). A similar preservation of autoregulation of RBF was observed. Our studies suggest that in the pressure ranges below normal autoregulation of RBF in the rat, serotonin blockade is associated with maintenance of both GFR and RBF