Acute physical exercise increases growth hormone (GH) secretion, and GH regulates the expression of insulin-like growth factor I (IGF-I) and IGF-binding protein (IGFBP) 3. IGFBP-1 is a local modulator of IGF activity with rapid dynamic regulation that is downregulated by insulin. The IGF system mediates the metabolic actions of GH, and possibly it regulates glucose metabolism. We hypothesize that strenuous exercise causes changes in the IGF system. We studied the effects of the marathon run on the circulating levels of IGF-I, IGFBP-1, IGFBP-3, and insulin in 23 participants. Immediately after the run, the most striking change was an 11.6-fold median increase in serum IGFBP-1 level (from 63.7 +/- 50.5 to 736 +/- 408 micrograms/l; P < 0.001). Because the insulin level remained unchanged, the elevation of serum IGFBP-1 level cannot be explained by changes in insulin. One day after the run, the IGFBP-1 level had returned to baseline. The physiological role of this increment could be the inhibition of hypoglycemic effects of IGF-I and/or regulation of glucose availability to the muscles. The changes in IGF-I and IGFBP-3 levels were less dramatic: the IGF-I and IGFBP-3 levels were lower 1 and 3 days after the run. This report provides an important basis for authentic effects of strenuous exercise on the IGF-system.
Selenium compounds influence cell growth and are highly interesting candidate compounds for cancer chemotherapy. Over decades an extensive number of publications have reported highly efficient growth inhibitory effects with a number of suggested mechanisms f especially for redox-active selenium compounds. However, the studies are difficult to compare due to a high degree of variations in half-maximal inhibitor concentration (IC50) dependent on cultivation conditions and methods to assess cell viability. Among other factors, the variability in culture conditions may affect the experimental outcome. To address this, we have compared the maintenance effects of four commonly used cell culture media on two cell lines, A549 and HepG2, evaluated by the toxic response to selenite and seleno-methylselenocysteine, cell growth and redox homeostasis. We found that the composition of the cell culture media greatly affected cell growth and sensitivity to selenium cytotoxicity. We also provided evidence for change of phenotype in A549 cells when maintained under different culture conditions, demonstrated by changes in cytokeratin 18 (CK18) and vimentin expression. In conclusion, our results have shown the importance of defining the cell culture medium used when comparing results from different studies.
AIMTo study the effects of warm ischemia-reperfusion (I/R) injury on hepatic morphology at the ultrastructural level and to analyze the expression of the thioredoxin (TRX) and glutaredoxin (GRX) systems.METHODSEleven patients undergoing liver resection were subjected to portal triad clamping (PTC). Liver biopsies were collected at three time points; first prior to PTC (baseline), 20 min after PTC (post-ischemia) and 20 min after reperfusion (post-reperfusion). Electron microscopy and morphometry were used to study and quantify ultrastructural changes, respectively. Additionally, gene expression analysis of TRX and GRX isoforms was performed by quantitative PCR. For further validation of redox protein status, immunogold staining was performed for the isoforms GRX1 and TRX1.RESULTSPost-ischemia, a significant loss of the liver sinusoidal endothelial cell (LSEC) lining was observed (P = 0.0003) accompanied by a decrease of hepatocyte microvilli in the space of Disse. Hepatocellular morphology was well preserved apart from the appearance of crystalline mitochondrial inclusions in 7 out of 11 patients. Post-reperfusion biopsies had similar features as post-ischemia with the exception of signs of a reactivation of the LSECs. No changes in the expression of redox-regulatory genes could be observed at mRNA level of the isoforms of the TRX family but immunoelectron microscopy indicated a redistribution of TRX1 within the cell.CONCLUSIONAt the ultrastructural level, the major impact of hepatic warm I/R injury after PTC was borne by the LSECs with detachment and reactivation at ischemia and reperfusion, respectively. Hepatocytes morphology were well preserved. Crystalline inclusions in mitochondria were observed in the hepatocyte after ischemia.
cohort was 85%, 43% and 27% respectively; disease free survival was 55%, 27% and 21% respectively. Patients with negative nodal histology had a significant overall and disease free survival advantage (median overall survival 43.9 vs 19.7 months (p < 0.01), median disease free survival 19.6 vs 10.8 months (p < 0.01)). Conclusions: Combined hepatectomy and lymph node resection in CRLM is justified as imaging and operative findings are poor guides in determining positive lymph node disease.
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