Runoff extremity in the Upper Lužnice catchment area

Thesis subject is the evaluation of runoff and flood regime of rivers Lužnice and Skřemelice at the closing profiles just before their confluences. The results are compared with findings from the profile Pilař, which were published in the past by other authors. More attention is paid to the evaluation of the hydrological year 2013 and in detail is described the flood in June of the same year. Daily flow data from the years 1971 - 2014 were used for evaluating of runoff conditions. The assessment of the runoff regime in terms of daily, monthly and annual flows were compared with the runoff regime in Pilař gauge station. The source regions with dominating influence on the resulting runoff were discovered. Analysis of the flood regime confirmed that spring floods in Lužnice came mainly from upland and hilly parts of catchment and large summer floods have main source area in the catchment of Lužnice river itself, before the confluence of the Lužnice river and Skřemelic river. When assessing flood in 2013, the main source areas of flood flows that hit Lužnice river basin were founded. The flood extremity was compared in each closing profiles

Additional file 3: of Chemerin in peritoneal sepsis and its associations with glucose metabolism and prognosis: a translational cross-sectional study

Figure S2. Correlation of fasting and intra-operative glucose levels with circulating chemerin in controls. a Correlation of circulating chemerin levels with fasting glucose levels (r = 0.216, p = 0.034, n = 17). b Correlation of circulating chemerin levels with OP glucose (r = 0.549, p = 0.023, n = 17). (PDF 44 kb

Modulation of insulin degrading enzyme activity and liver cell proliferation

<p>Diabetes mellitus type 2 (T2DM), insulin therapy, and hyperinsulinemia are independent risk factors of liver cancer. Recently, the use of a novel inhibitor of insulin degrading enzyme (IDE) was proposed as a new therapeutic strategy in T2DM. However, IDE inhibition might stimulate liver cell proliferation via increased intracellular insulin concentration. The aim of this study was to characterize effects of inhibition of IDE activity in HepG2 hepatoma cells and to analyze liver specific expression of <i>IDE</i> in subjects with T2DM. HepG2 cells were treated with 10 nM insulin for 24 h with or without inhibition of IDE activity using <i>IDE</i> RNAi, and cell transcriptome and proliferation rate were analyzed. Human liver samples (n = 22) were used for the gene expression profiling by microarrays. In HepG2 cells, <i>IDE</i> knockdown changed expression of genes involved in cell cycle and apoptosis pathways. Proliferation rate was lower in <i>IDE</i> knockdown cells than in controls. Microarray analysis revealed the decrease of hepatic <i>IDE</i> expression in subjects with T2DM accompanied by the downregulation of the p53-dependent genes <i>FAS</i> and <i>CCNG2</i>, but not by the upregulation of proliferation markers <i>MKI67, MCM2</i> and <i>PCNA</i>. Similar results were found in the liver microarray dataset from GEO Profiles database. In conclusion, <i>IDE</i> expression is decreased in liver of subjects with T2DM which is accompanied by the dysregulation of p53 pathway. Prolonged use of IDE inhibitors for T2DM treatment should be carefully tested in animal studies regarding its potential effect on hepatic tumorigenesis.</p