Objective To investigate the influence of thrombospondin 1 (TSP-1) on the expression of vascular endothelial growth factor (VEGF) in human renal tubular epithelial cells. Methods Human renal tubular epithelial cell (HKCs) line was cultured in vitro with DMEM/F12 1∶1 medium. HKCs were divided into four groups as follows: normal control group [HKCs were cultured with serum free medium (FSM), C group], TGF-? 1 group (HKCs were treated with FSM containing TGF-? 1, T group), antisense oligonucleotide group [HKCs were treated with FSM contained TGF-? 1 and TSP-1 antisense oligonucleotide (AS), TA group], missense oligonucleotide groups [HKCs were treated with FSM contained TGF-? 1 and TSP-1 missense oligonucleotide (SC), TS group]. Cells were cultured 72 hours in the conditioned media. The expressions of TSP-1 and VEGF were detected with immunohistochemistry. The expressions of TSP-1 mRNA and VEGF mRNA were assayed by RT-PCR. The correlation between the relative expressions of VEGF mRNA and TSP-1 mRNA was analyzed. Results There were significantly increased expressions of VEGF and VEGF mRNA in TA groups (P0.05) compared with T groups. The expressions of VEGF and VEGF mRNA were decreased significantly in T groups and TS groups (P0.05) compared with T groups. The expressions of TSP-1 and TSP-1 mRNA were increased significantly in T groups and TS groups (P

Objective To assess the effect of different treatment complex on portoazygous shunt in portal hypertensive patients. Methods Patients (115 cases) with esophageal varices were randomized to receive either endoscopic variceal ligation ( EVL) alone (54 cases ) , pericardial devascularization procedure (PDP) alone(30 cases) or a combination of EVL and PDP(31 cases) for variceal eradication. Esophageal vascular structures were examined with miniature ultrasonic probe and azygos blood flow (ABF) was measured with color Doppler ultrasonography. Results Esophageal varices were obliterated and collateral veins remained unchanged in patients treated by EVL, esophageal varices were diminished in size and collateral veins were obliterated by PDP and both esophageal varices and collateral veins were obliterated by the combination of EVL and PDP. EVL,PDP alone and a combination of the two modalities decreased ABF by 31% ,32% and 43% respectively. Conclusions The combination of EVL and PDP most effectively blocks esophageal collateral shunts.

OBJECTIVETo observe the changes of metabotropic glutamate receptor 1a in rat brain in a rodent model of diffuse head injury with secondary insults and the effects of 2-methyl-4-carboxyphenylglycine (MCPG).

METHODSBased on Marmarous rodent model of diffuse brain injury (DBI), hypotension was made by blood withdrawal as secondary brain insults (SBI). 105 male SD rats were randomized into A and B groups. The changes of mGluR(1a) in cerebral cortex were studied by immunohistochemistry and the effect of MCPG by HE. Each group was divided into different subgroups at different time after injury.

RESULTSCompared with that of sham group, the number of mGluR(1a) positive neuron increased by 12.9+/-3.2 (P<0.05) 1 day after injury in the injured cerebral cortex in DBI group. However, in DBI and SBI group there was a more significant increase in the number of mGluR(1a) positive neuron at 4 hours after injury (15.6+/-3.0, P<0.05) and then the number of mGluR(1a) positive neuron gradually decreased. Administration of MCPG reduced total cortical necrotic neurons counts on the 7th day after injury (5.21+/-2.52, P<0.05).

CONCLUSIONSBrain injury can increase the gene expression of mGluR(1a) and the role of mGluR(1a) may be a key factor in the aggravation of head injury with SBI, and that MCPG may have therapeutic potential in head injury.

Analysis of Variance ; Animals ; Benzoates ; pharmacology ; Blood Pressure ; drug effects ; Brain Injuries ; metabolism ; physiopathology ; Glycine ; analogs & derivatives ; pharmacology ; Male ; Rats ; Rats, Sprague-Dawley ; Receptors, Metabotropic Glutamate ; metabolism

Acute hypobaric hypoxic brain damage is a potentially fatal high-altitude sickness. Autophagy plays a critical role in ischemic brain injury, but its role in hypobaric hypoxia (HH) remains unknown. Here we used an HH chamber to demonstrate that acute HH exposure impairs autophagic activity in both the early and late stages of the mouse brain, and is partially responsible for HH-induced oxidative stress, neuronal loss, and brain damage. The autophagic agonist rapamycin only promotes the initiation of autophagy. By proteome analysis, a screen showed that protein dynamin2 (DNM2) potentially regulates autophagic flux. Overexpression of DNM2 significantly increased the formation of autolysosomes, thus maintaining autophagic flux in combination with rapamycin. Furthermore, the enhancement of autophagic activity attenuated oxidative stress and neurological deficits after HH exposure. These results contribute to evidence supporting the conclusion that DNM2-mediated autophagic flux represents a new therapeutic target in HH-induced brain damage.
Mice ; Animals ; Hypoxia ; Oxidative Stress ; Autophagy ; Cognition ; Sirolimus/therapeutic use*