ObjectiveThis study was to evaluate the changes of inflamatory mediators in patients undergoing tension free hernioplasty(LH) using expanded polytetrafluoroethylene (e PTFE) mycromesh biomaterial or conventional Bassini hernia repair(BH). MethodTwenty one patients randomized into two groups receiving LH or BH. Peripheral venous blood samples were collected 24 hours prior to surgery and then 6,24,48 and 168 hours postoperatively.ResultLH patients showed a higher increased serum level of fibringen,C reactive protein,alpha 1 antitrypsin, and interleukin 6 than BH patients. Postoperative visual analogue scales for pain reduced on mobilization for patients undergoing LH compared with BH. Neutrophils significantly increased only in LH compared with baseline. ConclusionOur data show that although LH induces less pain and rapid postoperative recovery,it is associated with an higher inflammatory response compared with BH, likely due to mycromesh biomaterial.

Objective To investigate the effect of the replication-deficient adenovirus carrying miR-138(Ad-miR138) on the pro-liferation of human gastric cancer cell line BGC-823 and the possible mechanism .Methods The human gastric cancer cell line BGC-823 was infected with Ad-miR138 .Then the expression level of miR-138 was measured by RT-PCR .The growth curve of BGC-823 was measured using CCK-8 method .The ability of cell invasion was measured using Transwell chambers .Results After infected with Ad-miR138 ,the expression of miR-138 in BGC-823 cells was up -regulated significantly (1 .07 ± 0 .07 vs .4 .89 ± 0 .45 ,P<0 .05) .Absorbance of the 6th day decreased significantly (0 .52 ± 0 .06 vs .0 .77 ± 0 .06 ,P<0 .05) ,and the invasion ability was de-creased obviously (32 .00 ± 11 .00 vs .56 .00 ± 12 .00 ,P<0 .05) .Conclusion miR-138 can effectively suppress the proliferation and invasion of human gastric cancer cell line BGC-823 in vitro .

Bone remodelling keeps going through the lifespan of human by bone formation and bone resorption. In the craniofacial region, mandibles act as the main force for biting and chewing, and also become susceptible to a common bone-loss disease, namely, apical periodontitis, once infected dental pulp is not treated timely, during which bone resorption occurs from the apical foramen to the apical bone area. Although conventional root canal treatment (RCT) can remove the most of the infection, chronical apical periodontitis due to incomplete removal of dental pulp and subsequent microleakage will become refractory and more challenging, and this process has scarcely been specifically studied as a bone remodelling issue in rat models. Therefore, to study chronical and refractory apical periodontitis owing to incomplete cleaning of infected dental pulp and microleackage in vivo, we establish a modified rat model of gradually progressive apical periodontitis by sealing residual necrotic dental pulp and introducing limited saliva, which simulates gradually progressive apical periodontitis, as observed in the clinical treatment of chronical and refractory apical periodontitis. We show that bone-loss is inevitable and progressive in this case of apical periodontitis, which confirms again that complete and sound root canal treatment is crucial to halt the progression of chronical and refractory apical periodontitis and promote bone formation. Interestingly, bone remodelling was enhanced at the initial stage of apical periodontitis in this model while reduced with a high osteoblast number afterwards, as shown by the time course study of the modified model. Suggesting that the pathological apical microenvironment reserve its hard tissue formation ability to some degree but in a disturbed manner. Hopefully, our findings can provide insights for future bone regenerative treatment for apical periodontitis-associated bone loss.