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Background: We aimed to determine the SSRP1's potential influence on the apoptosis and proliferation of gastric cancer (GC) cells and its regulatory mechanism. Methods: SSRP1 expression in GC cells and tissues was detected via quantitative reverse transcription-polymerase chain reaction (qRT-PCR). The interrelation between clinicopathological characteristics of GC patients and SSRP1 expression was analysed via x2 test, and the correlation between SSRP1 expression and overall survival rate was analysed using Kaplan-Meier survival analysis. After the knockdown of SSRP1 in AGS cells, the SSRP1 expression, colony formation ability, cell viability, cell cycle changes, apoptosis rate, and migration and invasion ability were detected through qRT-PCR, colony formation assay, CCK8 assay, flow cytometry and transwell test, respectively. Finally, the effects of down-regulation of SSRP1 on the expressions of phosphorylated-protein kinase B (p-AKT), B-cell lymphoma-2 (Bcl-2) and Bcl-2 associated X protein (Bax) were explored using Western blotting. Results: SSRP1 displayed a high expression in GC cells and tissues. SSRP1 expression was closely interrelated to the TNM stage, lymph node metastasis and tumour size. The survival rate of patients was markedly shorter in the high expression group than in the lower expression group. After the knockdown of SSRP1 in cells, the viability and colony formation ability of AGS cells were inhibited. In addition, the cell ratio in the G1 phase was increased, while that in the S phase declined, and the cell invasion and migration were obviously weakened. It was found from Western blotting that the knockdown of SSRP1 could evidently suppress the protein levels of Bcl-2 and p-AKT but promote the protein expression of Bax, indicating that silencing SSRP1 can inhibit the proliferative capacity and increase the number of GC cells through inactivating the AKT signalling pathway. Conclusions: SSRP1 rose up in GC tissues and cells. Reduction of SSRP1 can inhibit the proliferative capacity and increase the number of GC cells through inactivating the AKT signalling pathway.

Objective To assess the effects of dimethicone at different doses in bowel preparation for small bowel capsule endoscopy (SBCE) and explore the optimal dose for the examination. Methods A multicenter randomized controlled trial (RCT) was carried out on 132 patients from 4 different institutions from May 2016 to January 2019. They were randomly divided into 3 groups, with 44 cases in each group. All of them were given 2 liters of polyethylene glycol (PEG) solution orally 6 h before procedure, and then in 30 min before examination, the patients were asked to drink 100 mL pure water, 2.5 g and 5 g 100 mL dimethicone solution for those from group A, B and C, respectively. The primary evaluation indexes included small bowel bubble quantity (SBBQ), small bowel valid picture ratio (SBVPR), small bowel cleaning quality (SBCQ), and the secondary evaluation indexes contained gastric bubble quantity (GBQ), gastric cleaning quality (GCQ), completion rate (CR), diagnostic yield (DY), and small bowel transit time (SBTT) and gastric transit time(GTT) of the capsule. Results The SBBQ of group A was higher than those of the other 2 groups in the proximal, middle and distal segments of small intestine (P0.05). Similar results were seen in the SBIRP in the 3 groups. No statistical significances were found in other indexes among the 3 groups (P>0.05). Conclusion Dimethicone treatment can efficiently decrease intraluminal bubbles and improve the visibility of small bowel mucosa for SBCE, and the optimal dose of dimethicone is 2.5 g.

Silica-containing barium-rich BaTiO₃ ceramics for thermistors with a positive temperature coefficient of resistance are prepared by a tape-casting technique. The ceramics are sintered in a reducing atmosphere at low temperatures of 1175-1225°C. The influences of reoxidation are investigated after the reduced ceramics are reoxidized in air at 700-900°C. An anomalous correlation is illustrated between room temperature resistivity and reoxidation temperature. The anomaly results from the ferroelectricity rebuilding mechanism, which includes the spontaneous polarization theory and the ferroelectricity degradation caused by oxygen vacancies. The acceptor-state densities are estimated from the temperature-dependent resistivity. A critical temperature of 750-800°C is concluded for the grain boundary reoxidation.