AlM: To observe the influence ofphacoemulsification on corneal endothelial cell in patients with the different level of HbA1c.METHODS:With case-control study, 164 eyes from 115 cataract patients were divided into four groups according to the preoperative HbA1c level. Control group A: 43 eyes from 30 cases without diabetes ( HbA1c≤6. 5%). Diabetes groups:group B was consisted of 38 eyes from 26 cases(HbA1c≤6. 5%), 40 eyes of 28 case was in group C (6. 5% 8. 0%). Corneal endothelial microscopy was used to detect the parameters like endothelial cell density ( CD ) , coefficient of variation ( CV ) , percentage of regular hexagonal cells (6A) between pre-operation and post-operation at 1d, 1, 2wk, 1mo. The results were analyzed.RESULTS: The endothelial cell density, CV and 6A cell had no significant difference in four groups before treatment (P>0. 05). The CD and 6A were decreased and CV was increased in all groups after operation of 1d, 1, 2wk and 1mo. The difference was statistically significant (P< 0. 05). There were statistical differences of 6A and CV in diabetes groups compared with control group ( P<0. 05). The decreasing of CD between group A and group B had no difference (P>0. 05). There were statistical differences of CD in group C and group D compared with group A (P<0. 05). There were statistical differences of CD, 6A and CV within diabetes groups (P<0. 05). CONCLUSlON: Cataract phacoemulsification had certain degree damage on corneal endothelial cell. Corneal endothelial appeared the minimal injury when the postoperative HbA1c≤6. 5%. For diabetic cataract patients, the higher HbA1c before, the heavier damaged after the surgery.

0.05).Conclusion:The diabetes itself does not affect the sulfonylurea receptor(SUR2)expression in myocardial tissues.Sulfonylureas at treatment dosage have no effect on receptor expression of SUR2.

Objective To evaluate the clinical value analysis of atorvastatin in the treatment of patients with arteriosclerotic cerebral infarction. Methods 100 patients with atherosclerotic cerebral infarction from January 2012 to October 2013 in the first people's hospital of lianyungang were researched.They were divided randomly into observation and control groups.Observation group had 50 patients,they were treated by using of conventional treatment with atorvastatin therapy.Control group had 50 patients,using conventional therapy.Two groups'Clinical outcomes,inflammatory cytokines and lipids were compared.Results There was no significant difference in the control group and the observation group in the clinical data ;Total efficiency rate in the observation group and the control group was 90.00% and 70.00%,respectly.Total efficiency rate of observation group was higher than the control group,there was a significant difference (u=2.4696,P=0.0135 );before treatment,there was no significant difference of patients in the control group and the observation group in IL-6,hs-CRP,TG,TC,LDL-C and HDL-C;after treatment,IL-6 of observation group was lower than the control group,there was a significant difference (P<0.0001);hs-CRP of observation group was lower than the control group,there was a significant difference (P<0.0001);TG,TC,LDL-C of observation group was lower than the control group,there was a significant difference (P<0.05);HDL-C of observation group was higher than the control group,there was a significant difference (P<0.05).Conclusion The clinical value analysis of atorvastatin in the treatment of patients with arteriosclerotic cerebral infarction is well.It is worthy of promotion in clinic.

Objective To investigate the changes and their relationship between cognitive function and event-related potentials(ERP)in patients with carotid atherosclerosis.Methods 65 patients with varying degrees of carotid atherosclerosis were carried out Mini-Mental State Examination(MMSE)and Frederick ERP P300 investigation and correlation analysis was done,compared with the control group.Results Compared with the control group,account ability,short-term memory and graphics portrayed score decreased in mild and moderate carotid atherosclerosis group(all P

Background The orbital fibroblasts (OFs) in thyroid associated ophthalmopathy (TAO) play important roles in the proliferative and inflammatory response.Seeking the drug which inhibit OFs growth is of a vital significance for the prevention and treatment of TAO.Research documented that colchicine has an anti-fibrosis effect.But its influence on OFs of TAO patient is few known.Objective This study was to investigate the effect of colchicine on growth and apoptosis of OFs in vitro.Methods The retroobital connective tissue was obtained form 3 TAO patients and cultured using explant method.OFs were passaged and identified by immunochemistry,and 3-8 genetaions of cells were used in the study.Colchicine at the concentrations of 1 × 10-8,1 × 10-7,1 × 10-6,1 × 10-5,1 ×10-4 mol/L was added into the RPMI 1640 with 10％ fetal bovine serum(FBS) to incubated the cells for 24,48 and 72 hours respectively,and only RPMI 1640 was used to culture the cells as the control group.Cell counting kit-8 (CCK-8)was used to detect the absorbance value (A450) of OFs for the evaluatuion of OFs and the inhibitory rate of colchicine to OFs.The colchicine of 1 ×10-6,1 ×10-5,1 × 10-4 mol/L was added into the culture medium for 48 hours,and then the apoptotic rate of the cells and the cell percentage in various cellular cycle was assayed by flow cytometry(FCM).The expression of transforming growth factor-β (TGF-β)in the cells was detected by immunochemistry to assess the influence of colchicine on the serection of the cells.Results Cultured cells showed the spindle-like in shape and the cell number was significantly increased with the incubation time.After incubated with 1 × 10-4,1 × 10 5,1 × 10-6,1 ×10-7,1 × 10-8 mol/L colchicines,the A450 values were gradually reduced with the increase of the concentrations of colchicine(F ion =62.004,P＜0.05),and significant differences were found between different contrations of colchicine groups(all P＜0.05).Aslo,gradually declined A450 values of the cells were seen with the lapse of culture time among the groups(Ftime =459.582,P＜0.05).The inbitory rate of colchicine to the cells was elevated with the increase of concentrations.The apoptotic rates of the cells were (1.73 ± 0.15) ％,(21.04 ± 4.56) ％,(31.84 ±6.21)％and(35.32±5.56)％ in the control group and 1 × 10-6,1 × 10-5,1 × 10 4 mol/L colchicine groups respectively,with statistically significant difference among the 4 groups (F =83.905,P＜0.05).With the increase of concentrations of colchicines,the cell percentage in G2 +M phase lessened gradually,showing significant difference among the control group and the 1 × 10-6,1 × 10-5,1 × 10-4 mol/L colchicine groups (F =20.443,P＜0.05).The expression of the TGF-β in the cells was (97.60± 2.09) ％ in the control group,and that in the 1 × 10-4 mol/L colchicine group was (44.43 ± 3.96) ％,presenting a significant difference between them (t =65.330,P ＜ 0.05).Conclusions Colchicine can induce apoptosis of OFs and inhibit the prolilferation of OFs in a time-and dose-dependent manner probably by decreasing the TGF-β secretion

The significant differences in prevalence rate of essential hypertension among the races in Xinjiang, i.e. in Kazakh, Han, and Uighur had been shown in 1979 screening. They were 6.6%, 3.5% and 2.6% respectively.The present investigation shows that some dietary constituents as well as the nutritional imbalance was involved in the causal effect in the development of hypertension.Three race people living in three quite different areas (geographic, climatic environmental conditions etc,) were investigated in April to July 1981. Blood pressures of 9,313 persons were measured. The dietary pattern and staple food items were studied for 491 persons within 69 families.The findings suggested that: l)the prevalence rate of hypertension was identical to the previous screening, 2) there was a positive correlation between the high consumption of protien (r= 0.974), fat(r = 0.622) and the prevalence rate of this disease, but a negative correlation in vitamin C intake (r = -0.620).The excessive intake of salt was accounted as a risk factor for poss- ible association with this disease only in Kazakh people who were living in various areas.

Objective To evaluate the effect of ameliorating the pancreatic microcirculation in the early stage on the patients with severe acute pancreatitis(SAP). Methods 84 SAP patients admitted from 1995-1998 and 1998-2001 were retrospectively analyzed. Routine united management were given to 44 SAP patients in the former period (FP)(1995-1998),and special regime aimed at improving the microcirculation and preventing cell Ca 2+ overload besides routine management were given to 40 SAP patients in the later period(LP)(1998-2001).Results Cure rate (85.0%) in FP group was significantly higher than that of LP group(68.2%)(P

Objective To investigate the anti-inflammatory effect of peroxisome proliferator-activated receptor-γ(PPAR-γ)in non-obese diabetic mice(NOD mice)with Sj(o)gren's syndrome(SS)．Methods Twenty 8-weeks-old female NOD mice were randomly divided into 2 groups．Rosiglitazone and normal saline were administered for the rosiglitazone group and control group respectively．At age of 12 weeks and 15 weeks，one mouse in the rosiglitazone group and the control group were killed respectively,and the others were sacrificed at the age of 17 weeks．Blood were obtained by cardiac puncture，and minor salivary glands (MSG) were resected．The histopathological changes waere examined by H&E staining．The level of IL-1β，IL-4，IL-6 and TNF-α in serum were measured by ELISA．Real-time PCR waft used to evaluate the mRNA expression level of IL-1β，IL-4，IL-6 and TNF-α in MSG．Student's t-test was used to assess the differences．Results Compared with the control group，the mice in the rosiglitazone group showed that：①histopatho-logical change was significantly ameliorated．②At the age of 17 weeks，IL-6[(26±7)vs(37±11)，t=-2．298] and TNF-α[(57±22)vs(79±21)，t=-2．188] were expressed significantly lower and IL-4[(26±13)vs(12±4)，t=2．438 ] was expressed significantly higher in serum(P<0．05)．③The expression of TNF-αwas significantly decreased and the expression of IL-4 was significantly increased in MSG (P<0．05)．Conclusion PPAR-γ can ameliorate SS on NOD mice effectively．The mechanism may be related to reduction of Th1 cytokines，and the Th1/Th2 balance is changed into Th2 predominant．

Objective To evaluate the effects of sevoflurane preconditioning and postconditioning on the activity of NF-κB during lung ischemia-reperfusion (I/R) in rats.Methods Fifty-four adult male Sprague-Dawley rats,weighing 300-350 g,were randomly divided into 3 groups (n =18 each) using a random number table:sham operation group (S group),I/R group and sevoflurane preconditioning and postconditioning group (SPP group).Lung I/R was induced by clamping the left pulmonary hilum for 45 min followed by 120 min reperfusion in I/R and SP groups.The left pulmonary hilum was only isolated but not ligated in group S.In group SP,2.1％ sevoflurane was inhaled for 30 min followed by 10 min washout,the left pulmonary hilum was then ligated for 45 min,and 2.1％ sevoflurane was inhaled for 30 min again starting from onset of reperfusion.Six rats were chosen at 30,60 and 120 min of reperfusion and sacrificed in each group,lungs were removed for determination of wet/dry lung weight (W/D) ratio and content of tumor necrosis factor-α (TNF-α) (by ELISA) and expression of nuclear transcription factor κB (NF-κB) p65 of nuclear protein (by Western blot) and for microscopic examination of the pathologic changes of lungs (with light microscope).Results Compared with S group,W/D ratio,TNF-α content and nuclear protein NF-κB p65 expression in lung tissues were significantly increased at each time point of reperfusion in I/R and SPP groups.Compared with I/R group,W/D ratio,TNF-α content and nuclear protein NF-κB p65 expression in lung tissues were significantly increased at each time point of reperfusion,and the pathological changes of lungs were attenuated in SPP group.Conclusion Sevoflurane preconditioning combined with postconditioning can reduce the lung I/R injury in rats through inhibiting NF-κB activity in lung tissues.

Objective To explore the molecular mechanism of inhibition of LPS-induced inflammation by fenoterol, a β2 adrenoceptor agonist in monocyte. Methods Concentrations of interleukin 1β (IL-1β), tumor necrosis factor α (TNF-α) and MCP-1 from cell supernatants from THP-1 cells and wild type or MyD88- / - mice peritoneal macrophages stimulated by LPS in the presence or absence of fenoterol were determined by use of an ELISA system. Expression of MyD88 (myeloid differentiation factor 88) stimulated by LPS in the presence or absence of fenoterol were determined by Western blot. Results Fenoterol inhibited LPS-induced activation of MyD88 and secretion of inflammatory cytokines (TNF-α, MCP-1, and IL-1β). The reaction of MyD88- / - mice peritoneal macrophages to LPS was much lower than that of the wild type mice peritoneal macrophages. Conclusions MyD88 plays an important role in inflammation induced by LPS. The inhibition of LPS-induced expression of MyD88 by fenoterol is associated with its anti-inflammatory effect.