Электрооборудование и электропривод подъема кислородной фурмы

В выпускной квалификационной работе был произведён расчёт и выбор силового оборудования для электропривода подъёма кислородной фурмы. Выполнен расчёт параметров силовой цепи. Результатом расчёта является выбор асинхронного электродвигателя фирмы SIEMENS серии 1LG4310-8AB-Z мощностью 55 кВт; преобразователь частоты типа MICROMASTER 440 фирмы SIEMENS шкафного исполнения мощностью 75кВт. Исследованы переходные процессы в программе MATLAB, динамические показатели качества при отработке воздействий по управлению и возмущению во всем диапазоне регулирования скорости полностью удовлетворяют требованиям технического задания.In the final qualifying work, the calculation and selection of power equipment for the electric drive of lifting the oxygen lance was made. The parameters of the power circuit are calculated. The result of the calculation is the selection of an asynchronous electric motor from SIEMENS series 1LG4310-8AB-Z with a power of 55 kW; frequency converter type MICROMASTER 440 firm SIEMENS cabinet version 75kW. The transient processes in the MATLAB program have been studied, the dynamic quality indices during the development of control and disturbance influences in the whole range of speed regulation fully satisfy the requirements of the technical assignment

Basic fibroblast growth factor contributes to a shift in the angioregulatory activity of retinal glial (Müller) cells.

Basic fibroblast growth factor (bFGF) is a pleiotropic cytokine with pro-angiogenic and neurotrophic effects. The angioregulatory role of this molecule may become especially significant in retinal neovascularization, which is a hallmark of a number of ischemic eye diseases. This study was undertaken to reveal expression characteristics of bFGF, produced by retinal glial (Müller) cells, and to determine conditions under which glial bFGF may stimulate the proliferation of retinal microvascular endothelial cells. Immunofluorescence labeling detected bFGF in Müller cells of the rat retina and in acutely isolated Müller cells with bFGF levels, which increased after ischemia-reperfusion in postischemic retinas. In patients with proliferative diabetic retinopathy or myopia, the immunoreactivity of bFGF co-localized to glial fibrillary acidic protein (GFAP)-positive cells in surgically excised retinal tissues. RT-PCR and ELISA analyses indicated that cultured Müller cells produce bFGF, which is elevated under hypoxia or oxidative stress, as well as under stimulation with various growth factors and cytokines, including pro-inflammatory factors. When retinal endothelial cells were cultured in the presence of media from hypoxia (0.2%)-conditioned Müller cells, a distinct picture of endothelial cell proliferation emerged. Media from 24-h cultured Müller cells inhibited proliferation, whereas 72-h conditioned media elicited a stimulatory effect. BFGF-neutralizing antibodies suppressed the enhanced endothelial cell proliferation to a similar extent as anti-VEGF antibodies. Furthermore, phosphorylation of extracellular signal-regulated kinases (ERK-1/-2) in retinal endothelial cells was increased when the cells were cultured in 72-h conditioned media, while neutralizing bFGF attenuated the activation of this signaling pathway. These data provide evidence that retinal (glial) Müller cells are major sources of bFGF in the ischemic retina. Müller cells under physiological conditions or transient hypoxia seem to provide an anti-angiogenic environment, but long-lasting hypoxia causes the release of bFGF, which might significantly co-stimulate neovascularization in the retina

Müller cells express bFGF in retinal tissue.

<p>Panel <b>A</b> demonstrates glial localization of bFGF (<i>green</i> immunostaining) in a surgically excised fibrovascular membrane from a subject with non-hypoxic pathologic myopia and a patient with PDR (scale bar, 25 µm). <b>B</b>: Freshly dissociated human Müller cells express bFGF (<i>red</i>) and GFAP (<i>green;</i> scale bar, 50 µm). Co-staining of GFAP in panel <b>A</b> yielded a <i>yellow</i> merge signal. Parallel tissue samples or cells stained with nonimmune IgG did not fluoresce (not shown).</p

Increased immunostaining of bFGF is a hallmark of ischemia-reperfusion in the rat retina.

<p>The images display representative slices of a control retina (<i>upper panel</i>) and a retina obtained 3 d after reperfusion (<i>lower panel</i>). Specimens were labeled with antibodies against bFGF (<i>red</i>) and vimentin (<i>green</i>). Co-labeling yielded a <i>yellow</i> merge signal, and cell nuclei were labeled with Hoechst 33258 (<i>blue</i>, scale bar, 20 µm). Note increasing vimentin and bFGF labeling in the outer nuclear layer (ONL) after ischemia as compared to the control tissue. <i>Unfilled arrowhead</i>, ganglion cell soma; <i>arrow</i>, Müller cell soma; <i>filled arrowhead</i>, Müller cell process. GCL, ganglion cell layer; INL, inner nuclear layer; IPL, inner plexiform layer; OPL, outer plexiform layer; PRS, photoreceptor segments.</p

Effects of Müller-cell-derived soluble factors on growth-related activities of retinal microvascular endothelial cells.

<p>Hypoxia (0.2% O₂)-conditioned media from different cultures of Müller cells were employed. Note that proliferation-inducing properties might have varied from one particular medium to another, with different numbers of Müller cells that may have governed a different level of growth factors in these media. (<b>A</b>) The proliferation rate of BRECs was determined in the presence of media conditioned for 24, 48, and 72 h under hypoxia. The effects of corresponding media, conditioned under normoxia for 48 and 72 h, were not markedly different from those obtained after 24 h, which caused an approximate 80% reduction of BREC proliferation (<i>data not shown</i>). (<b>B</b>) and (<b>C</b>) Endothelial cell growth-related effects induced by the hypoxia (72 h)-conditioned media was altered in the presence of neutralizing antibodies. (<b>B</b>) The proliferation-stimulatory effect of the media on BRECs is significantly attenuated by antibodies directed to bFGF (a-bFGF; 2 µg/ml) or VEGF (a-VEGF; 1 µg/ml), or simultaneous application of both. Significant differences <i>vs</i>. hypoxic control cultures maintained in the presence of normal goat immunoglobulin (^•<i>P</i><0.05) or cultures in the presence of a-bFGF (^o<i>P</i><0.05) are indicated. Data are means ± SEM of 3 independent experiments and are expressed in relative units, i.e., as proportions to basal cellular proliferation in EBM (*<i>P</i><0.05). (<b>C</b>) An increase of ERK-1/−2 phosphorylation is induced by 72-h conditioned media from Müller cells (2,3, normoxia; 3,4, hypoxia) and is reversed by the neutralizing anti-bFGF antibody (+) compared to samples (−), to which normal goat IgG was added. ERK-1/-2 phosphorylation was analyzed by Western blotting.</p