Проект реконструкции подстанции 35/6 кВ Правобережная

Дипломная работа 74 с., 1 рисунков, 10 таблиц, 22 источника. Объектом исследования является подстанция «Правобережная». В работе проводится реконструкция подстанции, напряжением 35/6 кВ. Осуществляется установка трансформатора ТДНС 16000/35/6, для увеличения мощности. Для определения затрат на реконструкцию был произведен экономический расчет. Так же был произведен анализ производственной и экологической безопасности. Выпускная квалификационная работа выполнена с помощью программ Mathcad 15 и текстовом редакторе MS Word 2007 и представлена на компакт - диске (в конверте на обороте обложки).Thesis 74 p., 1 pictures, 10 tables, 22 source. The object of this study is to substation "Right-Bank". The work is carried out the reconstruction of substations 35/6 kV voltage. Implemented by installing the transformer TDNS 16000/35/6, ​​to increase capacity. To determine the costs for the reconstruction of economic calculation was made. The same was made the analysis of industrial and environmental safety. Final qualifying work done with Mathcad 15 programs and MS Word 2007 text editor, and is represented on the CD - ROM (in an envelope on the back cover)

Riccardin D Exerts Its Antitumor Activity by Inducing DNA Damage in PC-3 Prostate Cancer Cells <i>In Vitro</i> and <i>In Vivo</i>

<div><p>We recently reported that Riccardin D (RD) was able to induce apoptosis by targeting Topo II. Here, we found that RD induced cell cycle arrest in G2/M phase in PC-3 cells, and caused remarkable DNA damage as evidenced by induction of γH2AX foci, micronuclei, and DNA fragmentation in Comet assay. Time kinetic and dose-dependent studies showed that ATM/Chk2 and ATR/Chk1 signaling pathways were sequentially activated in response to RD. Blockage of ATM/ATR signaling led to the attenuation of RD-induced γH2AX, and to the partial recovery of cell proliferation. Furthermore, RD exposure resulted in the inactivation of BRCA1, suppression of HR and NHEJ repair activity, and downregulation of the expressions and DNA-end binding activities of Ku70/86. Consistent with the observations, microarray data displayed that RD triggered the changes in genes responsible for cell proliferation, cell cycle, DNA damage and repair, and apoptosis. Administration of RD to xenograft mice reduced tumor growth, and coordinately caused alterations in the expression of genes involved in DNA damage and repair, along with cell apoptosis. Thus, this finding identified a novel mechanism by which RD affects DNA repair and acts as a DNA damage agent in prostate cancer.</p> </div

RD inhibits tumor growth in xenograft mice.

<p><i>A</i>-<i>C</i>, Effect of RD on tumor growth and body weight of nude mice. <i>D</i>, western blot analysis of DNA damage and repair, and apoptosis proteins from tumor tissues. <i>E</i>, immunofluorescence staining of p-BRCA1 and γH2AX in RD-treated and placebo tissues. Nuclei were stained with DAPI. Scale bars, 100 µm. <i>F</i>, <i>a</i>, H&E staining of tissues from RD- and placebo-treated nude mice. <i>b</i>, Tissues were fixed and stained by TUNEL followed by DAB staining. Nuclei were counterstained with methyl green. Brown stain around green nuclei indicates apoptotic cells.</p

Effect of RD on DNA damage response signalings.

<p><i>A</i>, Changes of DNA damage proteins in RD-treated cells were analyzed by western blotting. <i>B</i>, After treatment with chemicals for 4h or 12h, protein levels of DNA damage proteins were detected by western blotting. <i>C</i>, Immunofluorescence staining of γH2AX foci and p-BRCA1 foci in PC-3 cells. <i>D</i>, <i>a</i>, Neutral comet assay of PC-3 cells treated with RD for 4h and 12h. <i>b</i>, Comet length was analyzed by box and whisker plot method (100 cells per sample). <i>E</i>, Associations of γH2AX, PP2AC, and PPP4C were determined by coimmunoprecipitation using anti-γH2AX, anti-PP2AC, anti-PPP4C, or normal IgG. <i>F</i>, PC-3 cells were pretreated with 10 mmol/L caffeine for 1h, and exposed to RD for 4h and 12h, <i>a</i>, cell viability measured by MTT assay; bars, SD. *, ^#, P < 0.05, significant difference from control. <i>b</i>, changes of γH2AX were detected by western blotting.</p