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Objective To investigate the effect of low-dose glucocorticoid on prognosis of critical illness-related corticosteroid insufficient (CIRCI) patients with acute exacerbation of chronic obstructive pulmonary disease (AECOPD).Methods A total of 385 eligible patients met the criteria of AECOPD were admitted from January 2010 to December 2012.The AECOPD patients co-morbid with CIRCI screened by an adrenal corticotrophic hormone test within 12 hours after admission were randomly divided into treatment group (n =32) and control group (n =31) for prospective,randomized (random number) and controlled clinical study.Hydrocortison (150mg/d) for treatment group or normal saline instead for control group was injected intravenously for 7 days.The 28-day mortality,shock-free days,length of ICU stay within 28 days and ventilator-free days were evaluated.And the markers of inflammation C-reactive protein,tumor necrosis factor-α,interleukin 6 and procalcitonin were measured before and 7 days after treatment.The variables were analyzed by Student' s t-test,non-parametric statistical test,Chi-square test or KaplanMeier test with SPSS 18.0 statistic software.P ＜ 0.05 was considered statistically significant.Results A cohort of 385 patients with AECOPD was screened,and the prevalence rate of CIRCI was 16.4％.The shock rate was higher in the AECOPD patients co-morbid with CIRCI than that in the AECOPD patients without CIRCI (23.8％ vs 8.7％,P ＜0.01).Compared with the control group,the 28-day mortality was significantly lower in treatment group (2/32 vs 8/31,P ＜ 0.05),and shock-free days within 28 days longer in the treatment group (18.2 ± 9.5 vs 25.8 ± 4.1,P ＜ 0.05).However,there was no difference in the shock rate,days of ICU stay and ventilator-free days between the two groups.After treatment,the levels of infection markers were decreased and obviously lower than those in control group (P ＜ 0.01),such as Creactive protein (13.2 ± 5.5 mg/L vs 8.3 ± 3.1 mg/L for control group; 13.5 ± 5.9 mg/L vs 5.1 ± 2.3mg/L for treatment group),tumor necrosis factor-α (26.1 ± 16.2 μg/L vs 17.5 ± 11.7 μg/L for control group ; 25.0 ± 14.8 μg/L vs 10.4 ± 7.8 μg/L for treatment group) and procalcitonin [3.88 (0.25,8.5) μg/L vs 2.03 (0.15,5.1) μg/L for control group; 3.77 (0.21,8.0) μg/L vs 1.26 (0.10,3.2) μg/L for treatment group],furthermore,the levels of infection markers were decrease more obviously in the treatment group than those in the control group (P ＜ 0.01).Conclusions There was high prevalence rate of CIRCI in the patients with AECOPD in the department of critical medicine,and low-dose glucocorticoid reduced 28-day mortality,shock days and markers of infection and inflammation.
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Objective To investigate the vascular protective effect of pretreatment with candesartan on cerebral ischemia in rats.Methods Forty-eight male Sprague Dawley rats were randomly divided into sham operation,ischemia-reperfusion,low-dose candesartan group was randomly redivided into reperfusion 24 h and 72 h subgroups (n = 6).A model of middle cerebral artery occlusion was induced by intraluminal suture method after 4 weeks of drug gavage.Blood pressure was measured preoperatively.The neurological scores were performed after 24 and 72 hours of reperfusion.Then the rats were decapitated and the brains were removed.The infarct volume was measured using 2,3,5-triphenyltetrazolium chloride staining.The expression of vascular endothelial growth factor (VEGF) protein in ischemic regions was detected by immunohistochemical staining and Western blot analysis.Results The neurological scores of the low-dose and high-dose candesartan groups at 24 and 72 hours after reperfusion were significantly better than those of the ischemia-reperfusion group (P = 0.008and 0.001,respectively),and the infarct volume was reduced significantly (P=0.010 and 0.000,respectively).At the second week after medication,the blood pressure was decreased significantly in the high-dose candesartan group,and there was no significant antihypertensive effect in the low-dose candesartan group.The positive expression of VEGF mainly distributed in the vascular endothelial cells around the infarcts.Its expression was further upregulated with the time.It reached the peak after 72-hour reperfusion.The result of Western blot analysis was consistent with that of immunohistochemical staining.Conclusions Candesartan may reduce the infarct volume by upregulating the expression of VEGF in the ischemic region and improve the neurological score.
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@#ObjectiveTo investigate the in vitro effect of ghrelin on membrane membrane potentail of GH3 cells.MethodsNystatin-perforated whole-cell recording configuration was used.ResultsThe membrane potentail of GH3 was decreased from-(72±4.78) mV to(54.8±4.58) mV(P<0.01) after application of ghrelin(10-7～10-8 M)ConclusionGhrelin can transiently and significantly decreased the amplitude of membrane potentail,which may contribute to the ghrelin-stimulated GH secretion from GH3 cells.
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@#ObjectiveTo identify the influence of cholesterol on insulin-secreting cells.Methods MIN6 mouse insulin cells were cultured in vitro. After confluence of cells, on one hand, free cholesterol in series concentrations was added to cultu re medium to act for 24 hours, and on the other hand, free cholesterol in same c oncentration was added to culture medium to act for different periods. MTT test was used to evaluate the viability of MIN6 cells.Results25μmol/L free cholesterol significantly decreased the viability of MIN6 c ells after 24 hours and 100μmol/L free cholesterol significantly decreased the viability of MIN6 cells after 12 hours and induced cells death after 24 hours.Conclusions Free cholesterol decreases viability of MIN6 cells in a dose-dependent and time-dependent manner, and it is indicated that elevated free cholesterol concentration in blood may be one factor involved in the dysfunction of pancreatic β-cells.
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Objective:To investigate the vasodilatative roles and mechanisms of 17 ? estradiol(E 2) on rat thoracic aortas (TA). Methods:Rings cut from thoracic aortas of female rats were used by in vitro perfusion. The endothelium dependent and endothelium independent vasorelaxing effects of E 2 were measured. Furthermore, it was also observed whether the relaxing effects of E 2 were modulated by tamoxifen, N ? nitro L arginine methyl ester(L NAME),TEA, methylene blue(MB) or Methylene Blue(MB).Results:E 2 caused acute concentration dependent relaxation in TA with endothelium, but not significant without endothelium( P
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@#ObjectiveTo identify the differences between acetylcholine(Ach)-induced increase and adenosine triphosphate(ATP)-induced increase in cytosolic free Ca2+ concentration ([Ca2+]c) in mouse pancreatic β-cells. MethodsMouse pancreatic β-cells were primarily cultured and divided into two groups,one group was stimulated by Ach and another by ATP.[Ca2+]c was recorded with Fura-2 in normal condition, chelation of extracellular Ca2+ by EGTA and depletion of intracellular Ca2+ stores by Thapsigargin.ResultsAch induced a transient peak increase and sustained increase in [Ca2+]c. ATP induced a transient peak increase and no sustained increase. Chelation of extracellular Ca2+ by EGTA eliminated the sustained increase induced by Ach, and did not eliminate the transient peak increase induced by Ach and ATP. Depletion of intracellular Ca2+ stores by Thapsigargin eliminated the transient peak increase induced by Ach and ATP and the sustained increase induced by Ach. ConclusionsAch induces intracellular Ca2+ release and the following Ca2+ release-activated Ca2+ influx, and ATP induces intracellular Ca2+ release, but blocks the following Ca2+ release-activated Ca2+ influx.
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AIM To investigate the effect of tamoxifen on the proliferation of the anterior pituitary cell of rats and its mechanism. METHODS Primary culture of the anterior pituitary cell of rats and 3H TdR incorporation method were applied. The changes of cell morphology were observed directly by electric microscope. RESULTS Tamoxifen could inhibit the proliferation of the anterior pituitary cell of rats. The inhibitory effect of tamoxifen (0 1 ?mol?L -1 ) could be reversed by estrogen.The classical apoptotic changes appeared in the cells after tamoxifen incubation for 48 h. CONCLUSION Tamoxifen can inhibit the proliferation of the anterior pituitary cell of rats and resultin the cell apoptosis.