Objective To observe noninvasive positive pressure ventilation with type Ⅱ respiratory failure treatment effect in the combined treatment of acute exacerbations of chronic obstructive pulmonary disease( COPD) . To explore the application value of noninvasive positive pressure ventilation in the treatment of COPD with type Ⅱrespiratory failure.And to provide clinical indications guidance for the better application of noninvasive positive pres-sure ventilation.Methods 60 cases of COPD with typeⅡrespiratory failure patients were collected as the research object.30 cases in each group were randomly divided into the control group and treatment group.Two groups of patients were given the treatment of expectorant,anti infection,thearapy according to the basis of disease and compli-cations.The control group were given nasal catheter oxygen.In the treatment group therapy and routine therapy com-bined with noninvasive positive pressure ventilation.Acute Physiology and Chronic Health Evaluation Ⅱ ( APACHE score Ⅱ) was used as the standard.The two groups were observed before and after treatment in the heart rate,respira-tory rate,blood gas analysis and clinical index changes.Results The patients in the two groups after treatment pH, PaO2,PaCO2 of blood gas indexes were better than before treatment,the difference was statistically significant(P<0.05).The treatment group improved more obviously compared with the control group (P<0.05).Compared with the control group,the treatment group patients hospitalization days,tracheal intubation and mortality declined or shorten, the differences were statistically significant (P<0.05).Conclusion Chronic obstructive pulmonary disease com-bined with type Ⅱ respiratory failure by using of noninvasive positive pressure ventilation at the same time, can improve the therapeutic effect in the conventional treatment.Noninvasive positive pressure ventilation reduces the inci-dence of complications and mortality.It is worthy of clinical reference.

OBJECTIVETo analyze the distribution and significance of occludin mRNA expression in human gastric cancer, as well as its relationship with gastric cancer pathology and multidrug resistance (MDR) in vivo.

METHODSIn situ hybridization (ISH) technique was used to evaluate the expression of occludin mRNA in 42 gastric carcinoma specimens obtained by surgery and 23 relatively normal gastric mucosa obtained by gastric endoscopy. All specimens had been stored in cryostatic section.

RESULTSOccludin mRNA was found positive in the cytoplasm of gastric glandulous epithelia as blue particles with intensive stain in 14 of 42 gastric carcinomas (33.3%), 23 of 42 paracancerous gastric tissues (54.8%), 14 of 23 relatively normal gastric tissues (60.9%), 9 of 16 well differentiated carcinomas (56.3%), 4 of 14 moderately differentiated carcinomas (28.6%), 1 of 10 poorly differentiated carcinomas (10.0%) and none of 2 mucosal carcinomas. There were significant differences in occludin mRNA positive rate between relatively normal gastric tissue and gastric cancer as well as between paracancerous gastric tissue and gastric cancer. The expression of occludin mRNA in moderately and poorly differentiated groups was gradually reduced when compared with well differentiated group, which suggests that there be a significant correlation between tumor differentiation and the expression of occludin mRNA. Furthermore, the positive signals of occludin mRNA distributed extensively in the cytoplasm of SGC7901/VCR cell, being vincristine resistant, derived from parental gastric cell line SGC7901. The positive signals of SGC7901/VCR were stronger than those of SGC7901 cells.

CONCLUSIONOccludin mRNA, being mainly located in epithelial cells and its expression correlated with tumor differentiation, may be involved in the development of multi-drug resistance in gastric cancer.

Drug Resistance, Multiple ; physiology ; Drug Resistance, Neoplasm ; physiology ; Humans ; In Situ Hybridization ; Membrane Proteins ; genetics ; metabolism ; Occludin ; RNA, Messenger ; metabolism ; Stomach Neoplasms ; metabolism ; Tight Junctions ; metabolism

Metabolic reprogramming is a hallmark of cancer, including lung cancer. However, the exact underlying mechanism and therapeutic potential are largely unknown. Here we report that protein arginine methyltransferase 6 (PRMT6) is highly expressed in lung cancer and is required for cell metabolism, tumorigenicity, and cisplatin response of lung cancer. PRMT6 regulated the oxidative pentose phosphate pathway (PPP) flux and glycolysis pathway in human lung cancer by increasing the activity of 6-phospho-gluconate dehydrogenase (6PGD) and α-enolase (ENO1). Furthermore, PRMT6 methylated R324 of 6PGD to enhancing its activity; while methylation at R9 and R372 of ENO1 promotes formation of active ENO1 dimers and 2-phosphoglycerate (2-PG) binding to ENO1, respectively. Lastly, targeting PRMT6 blocked the oxidative PPP flux, glycolysis pathway, and tumor growth, as well as enhanced the anti-tumor effects of cisplatin in lung cancer. Together, this study demonstrates that PRMT6 acts as a post-translational modification (PTM) regulator of glucose metabolism, which leads to the pathogenesis of lung cancer. It was proven that the PRMT6-6PGD/ENO1 regulatory axis is an important determinant of carcinogenesis and may become a promising cancer therapeutic strategy.