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Objective To compare the effect of laparoscopic and open surgery in treatment of rectal cancer. Methods 80 cases of patients with rectal cancer from May 2008 to May 2013 were selected, they were randomly divided into laparoscopy surgery group (n = 40) and open surgery group (n = 40), the operation time, intraoperative blood loss, length of incision, lymph node dissection, number for the first time, ventilation time, ambulation time, hospitalization time, cost of hospitalization, postoperative complications, treatment satisfaction of the two groups were statistically analyzed. Results The operation time of the laparoscopic surgery group was significantly longer (P < 0.05), the amount of bleeding was significantly less (P < 0.05), the incision length was significantly shorter (P < 0.05), the first time, ventilation time, ambulation time, hospitalization time were significantly shorter (P < 0.05), the hospitalization cost was significantly higher (P < 0.05), the rate of postoperative complications 15.0% (6/40) was significantly lower than the open surgery group 35.0% (14/40) (P < 0.05) 97.5% (39/40), the treatment satisfaction was significantly higher than the open surgery group 67.5% (27/40)(P < 0.05). Conclusion The effect of laparoscopic and open surgery in treatment of rectal cancer is better than open surgery.
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<p><b>BACKGROUND</b>Tubulointerstitial renal fibrosis is the common end point of progressive kidney diseases, and tubular epithelial-myofibroblast transdifferentiation (TEMT) plays a key role in the progress of tubulointerstitial renal fibrosis. Anaphylatoxin C3a and C5a are identified as novel profibrotic factors in renal disease and as potential new therapeutic targets. The aim of this study was to investigate whether C3a, C5a can regulate TEMT by transforming growth factor-β1 (TGF-β)/connective tissue growth factor (CTGF) signaling pathway and the effects of C3a and C5a receptor antagonists (C3aRA and C5aRA) on C3a- and C5a-induced TEMT.</p><p><b>METHODS</b>HK-2 cells were divided into C3a and C5a groups which were subdivided into four subgroups: control group, 10 ng/ml TGF-β1 group, 50 nmol/L C3a group, 50 nmol/L C3a plus 1 µmol/L C3aRA group; control group, 10 ng/ml TGF-β1 group, 50 nmol/L C5a group, 50 nmol/L C5a plus 2.5 µmol/L C5aRA group. TGF-β1 receptor antagonist (TGF-β1RA) 10 µg/ml was used to investigate the mechanism of C3a- and C5a-induced TEMT. Electron microscopy was used to observe the morphological changes. Immunocytochemistry staining, real-time PCR and Western blotting were used to detect the expressions of a smooth muscle actin (α-SMA), E-cadherin, Col-I, C3a receptor (C3aR), C5aR, CTGF and TGF-β1.</p><p><b>RESULTS</b>HK-2 cells cultured with C3a and C5a for 72 hours exhibited strong staining of α-SMA, lost the positive staining of E-cadherin, and showed a slightly spindle-like shape and loss of microvilli on the cell surface. The expressions of α-SMA, E-cadherin, Col-I, C3aR, C5aR, TGF-β1 and CTGF in C3a- and C5a-treated groups were higher than normal control group (P < 0.05). C3aRA and C5aRA inhibited the expressions of α-SMA, Col-I, C3aR, C5aR, and up-regulated the expression of E-cadherin (P < 0.05). TGF-β1 and CTGF mRNA expressions induced by C3a and C5a were partly blocked by TGF-β1RA (P < 0.05).</p><p><b>CONCLUSION</b>C3a and C5a can induce TEMT via the up-regulations of C3aR and C5aR mRNA and the activation of TGF-β1/CTGF signaling pathway in vitro.</p>