目的探讨保留胃管对重型颅脑损伤气管切开患者气管套管拔管后切口闭合及肺部感染的影响。方法64例重症颅脑损伤气管切开患者,按是否保留原有胃管分成实验组(保留原有胃管)和对照组(不保留原有胃管),对两组患者气管套管拔出后切口闭合时间、肺部再次感染等情况进行观察。结果实验组切口闭合时间(2.26±1.94)d较对照组(3.83±3.82)d缩短(P<0.05);实验组肺部再次感染率(14.70%)少于对照组(40%,P<0.05)。结论重型颅脑损伤气管切开患者选择在拔气管套管时保留原有胃管可使切口早期愈合,减少肺部再次感染。

Objective To evaluate advantages of the Herbert screw in treating displaced radial head fractures. Methods The Herbert screw was used to treat 25 segmental fractures of the radial head from since 1991 and the results were compared with those of other treatment methods mentioned in the literature. Results A follow up averaging 6 years and 8 months showed that postoperative function was all excellent or good and that most cases recovered to normal absolutely, without complications. Conclusions The Herbert screw provides such rigid internal fixation for displaced radial head fractures that, after operation, a plaster cast is rarely required and most patients are able to return to work within a few weeks. This method of treatment appears to offer significant advantages over conventional techniques.

Phospholipase D (PLD) hydrolyzes phosphocholine into choline and phosphatide acid, and these metabolites play an important role in regulating cell physiology and biochemistry. To study the biological function of phospholipase D3 (PLD3) during the insulin stimulation in C2C12 myoblasts, we constructed PLD3 over-expressed cell lines (C2C12/pPLD3) and investigated the phosphorylation of Akt. The results showed that the level of phosphorylated Akt (P-Akt) was significantly increased in control C2C12 cells when insulin concentration was elevated during cell treatment, whereas the level of P-Akt in C2C12/pPLD3 cells was not changed. When extending the time of insulin treatment, P-Akt level in C2C12/pPLD3 cells was increased around 2 folds, but the total level of P-Akt in C2C12/pPLD3 was still lower than that in control group. 1-Butanol, a PLD inhibitor, could completely block Akt phosphorylation in C2C12 cells that even stimulated by insulin. However, 1-Butanol did not inhibit the Akt phosphorylation in C2C12/pPLD3 cells, but increased the phosphorylation up to 6 folds higher than control cells. The level of Akt phosphorylation in control C2C12 cells was increased significantly when stimulated by phosphatidic acid (PA), while there was no change in C2C12/pPLD3 cells with the similar treatment. When cells simulated by both PA and insulin, P-Akt level in both C2C12/pPLD3 cells and C2C12 cells were down regulated. Our observations indicated that PLD3 over expression may inhibit Akt phosphorylation and further block the transduction of insulin signaling in C2C12 cells.
Cell Line ; Humans ; Insulin ; pharmacology ; Myoblasts ; cytology ; metabolism ; Phosphatidylinositol 3-Kinases ; metabolism ; Phospholipase D ; biosynthesis ; Phosphorylation ; Proto-Oncogene Proteins c-akt ; chemistry ; drug effects ; Signal Transduction