Objective To investigate clinical effect of Guilongkechuanning capsules combined with antibiotic drugs in treating lung cancer patients with respiratory tract infection.Methods A total of 150 lung cancer patients with respiratory tract infection were randomly divided into treatment group and control group.Ceftizoxime 1g was given to all of the patients for anti-inflammatory.While Guilongkechuanning capsules were given to the treatment group only.Results After two weeks of different treatment options, the total effect rate of treatment group was 88.0%, it was 73.3% in control group, the total efficiency of treatment group was better than control group(P<0.05).WBC, NEUT (%) and CRP of patients in treatment group decreased significantly than control group(P<0.05).The time of fever relief, pulmonary rales disappearing, cough and sputum significant reducing in treatment group were less than the control group, the differences were all statistically significance (P<0.01).Conclusion Guilongkechuanning pill combined with antibacterial drugs in control of lung infection in the patients has obvious curative effect, can significantly reduce the symptoms of patients, improve the efficiency, reduce hospitalization time.

Objective To analyze the influence of dexamethasone in the hypotonic-induced volume-sensitive chloride currents in human trabecular meshwork cells,and to investigate the possible mechanism of volume-sensitive chloride channels(VACC)in the glucocorticoid-induced glaucoma(GIG)cases.Methods The human trabecular meshwork cells were seeded in 35 mm diameter plastic petri dishes,so that they could grow in monolayer.The cultured cells were divided into normal cell culture medium group and dexamethasone 1 d,3 d,7 d groups.The chlorine current density values of the cells in four groups were recorded respectively by the whole-cell patch-clamp technique. The differences among groups were compared.Results In normal group,after hypotonic stimulation,under+100 and-100 mV voltage clamp,the outward and inward current density values of the trabecular cells were (19.94±0.87) and (-6.53±0.41)pA/pF.In dexamethasone 1 d,3 d,and 7 d groups,under the same condition,the outward and inward current density values of the trabecular cells were (19.39 ± 1.40)and (-6.42 ± 0.28)pA/pF, (17.97±2.35)and (-5.82±0.94)pA/pF,(17.16±1.16)and (-5.65±0.43)pA/pF.The trabecular cells cultured with dexamethasone for 1 d had lower outward and inward current density values under hypotonic stimulation compared with normal group,but there was no significant difference (P>0.05).The trabecular cells cultured with dexamethasone for 3 d and 7 d,when compared with normal group,had significantly lower outward and inward current density values under hypotonic stimulation (P<0.05 ). Conclusion Dexamethasone could reduce the volume-sensitive chloride current in trabecular meshwork cells,which would affect trabecular meshwork cell volume adjustment.This would possibly cause the increase of the aqueous humor outflow resistance among GIG cases.

Objective:To investigate the alterations of cholinergic and monoamine neurotransmitters in cerebrospinal fluid in patients with postoperative delirium.Methods:Sixty-eight patients with normal preoperative cognitive functions were enrolled.They were diagnosed with spinal extramedullary intradural space-occupying lesion and underwent surgical resection.Among these patients, 18 developed postoperative delirium (delirium group), 46 had no postoperative delirium (control group), and the diagnosis of delirium was unclear in four cases (excluded). Cerebrospinal fluid (CSF) was collected before the surgical resection of lesions and on the third day postoperatively.The concentrations of acetylcholine (Ach), norepinephrine (NE), adrenaline (E), dopamine (DA) and serotonin (5-HT) were measured using the high-performance liquid chromatography/electrochemical method.Results:Prior to the surgical resection, there were no significant differences in the Ach, NE, E, DA or 5-HT baseline levels in the CSF between the delirium group and the control group (all P>0.05). After surgery, the Ach level in the delirium group ((0.63±0.26) μmol/L) was significantly lower than that in the control group ((0.77±0.19) μmol/L) ( P=0.032), and there were no significant differences in other neurotransmitter levels (all P>0.05). In the delirium group, the level of Ach in the CSF after surgery ((0.63±0.26) μmol/L) was significantly lower than the baseline level ((0.75±0.19) μmol/L) ( P=0.021). The postoperative NE level ((1.58±0.28) μmol/L) was significantly higher than the baseline level ((1.49±0.21) μmol/L) ( P=0.036). There was no significant difference in the adrenaline level ( P=0.497). The postoperative DA level ((0.86±0.18) μmol/L) was significantly higher than the baseline level ((0.82±0.15) μmol/L) ( P=0.045), and the postoperative 5-HT level ((2.94±0.28) μmol/L) was also significantly higher than the baseline level ((2.75±0.35) μmol/L) ( P=0.022). In the control group, only the postoperative 5-HT level ((2.90±0.31) μmol/L) was significantly higher than the baseline level ((2.76±0.26) μmol/L) ( P=0.016), while the postoperative levels of other neurotransmitters were not significantly changed when compared to the baseline levels (all P>0.05). Conclusion:The cholinergic neurotransmitter levels were reduced while the monoamine neurotransmitter levels were increased in the cerebrospinal fluid in patients with postoperative delirium, which suggests that cholinergic hypoactivity and monoaminergic hyperexcitability may be important pathophysiological processes in the occurrence and development of postoperative delirium.

Background and objective FK506, also named tacrolimus, a new macrolide immunosuppressive agent, has been shown to possess anti-proliferation activities in some cancer cells. The aim of this study was to investigate the effect of FK506 on the cell proliferation and migration of lung cancer cell lines and its mechanism. Methods A549 and H1299 cell lines were cultured in vitro. The effect of FK506 on cell viability and DNA synthesis ability of A549 and H1299 were measured by CCK-8 assay and EDU-labeling assay, respectively. Flow cytometry assay was used to detect the cell cycle. The in vitro mi-gration of lung cancer cells was detected by Boyden chamber assay and wound-healing assay after the treatment of FK506. The expression of p27, RB1, CDK4, CDK6 and MMP9 were detected using Western blot. Results FK506 inhibited cell growth and induced cell cycle arrest in G0/G1 phase in A549 and H1299 cells in a dose- and time-dependent manner. Compared to the control groups, the migration of A549 and H1299 cells treated with FK506 were decreased obviously. Moreover, FK506 in-creased the expression of P27 and RB1, and reduced the expression of CDK4, CDK6 and MMP9. Conclusion FK506 inhibit the cell growth and migration of lung cancer cells in vitro. The inhibitive effects may be associated with the up-regulation of p27 expression and inhibition CDK4, CDK6 and MMP9 expression.

BACKGROUND: Angiogenesis is an important process in the development of tumor. PD 0332991, a cell cycle inhibitor, can specifically inhibit CD4/6 phosphorylation and cell cycle progression. In xeongraft mice models, PD 0332991 treated mice had significantly decreased angiogenesis and vascular density compared with the control group, but the mechanism remains unknown. The purpose of this study is to investigate the role and molecular mechanism of PD 0332991 on vascular endothelial cells. METHODS: EA.hy926 cells, a kind of vascular endothelial cell, were used as the research model. The effects of PD 0332991 on the activity and proliferation of EA.hy926 cells were detected by the MTT, EdU assays. Wound-healing assays and transwell assays were used to determine the effects of PD 0332991 on the mobility of EA.hy926. The influence of PD 0332991 on cell cycle and apoptosis of endothelial cells was tested by flow cytometry, and the Western blot was applied to observe the expression of cell cycle related proteins in EA.hy926 cells treated by PD 0332991. RESULTS: PD 0332991 significantly inhibited the proliferation and mobility of EA.hy926 cells, caused cell cycle arrest and apoptosis. At the same time, PD 0332991 inhibited the expression of CDK4/6 and phosphorylation of Rb, and thus inhibited the cell cycle progression of EA.hy926 cells. CONCLUSIONS PD 0332991 can inhibit the proliferation and activity of endothelial cells and induces apoptosis.
Angiogenesis Inhibitors ; pharmacology ; Animals ; Apoptosis ; drug effects ; Cell Line, Tumor ; Cell Proliferation ; drug effects ; Cell Survival ; drug effects ; Cyclin-Dependent Kinase 4 ; genetics ; metabolism ; Cyclin-Dependent Kinase 6 ; genetics ; metabolism ; Endothelial Cells ; cytology ; drug effects ; metabolism ; Humans ; Lung Neoplasms ; drug therapy ; genetics ; metabolism ; physiopathology ; Mice ; Piperazines ; pharmacology ; Pyridines ; pharmacology