Proliferative diabetic retinopathy (PDR) is one of the most common cause of severe sight impairment in people with diabetes. When PDR develops to a severe stage, vitreoretinal surgery is needed to prevent its aggravation. The surgery for PDR is complicated and difficult. By deeply understanding the pathological mechanism and development law of PDR, and reasonably using various surgical techniques, assisted by emerging surgical equipment and drugs, the surgical efficacy of PDR can be continuously improved, so as to help patients improve or even restore visual function to a greater extent.

Objective To observe the proportion changes of CD4+CD25+FOXP3+ T cells in peripheral blood of patients with Vogt-Koyanagi-Harada disease(VKH)before and after one month of treatment. Methods The peripheral blood samples from 15 patients with VKH disease before and after one month of treatment by glucocorticoid,and from 15 healthy volunteers were collected,and lymphoeytes were separated from them.CD4+CD25+regulatory T cells were Iabeled by antibodies of cell surface marker CD4、CD25 and transcription factor FOXP3.The proportion of CD4+CD25+FOXP3+ T cells were detected by flow cytometry. Results Before the treatment,the percentage of CD4+ CD25+FOXP3+ T cells in periphery blood was(0.30±0.19)%of CD4+ cell in VKH patients,and(1.41±0.52)%in control group,the difference was statistically significant(t=7.665,P＜0.01);after one month of treatment,the VKH patients group was(1.28±0.54)%which close to the control group.However there were two patients whose CD4+ CD25+ T cells inereased extraordinarily after one month of treatment. Conclusions The proportion of CD4+ CD25+ FOCP3+ T cells in periphery blood in VKH patients were lower than control group obviously before treatment,but were close to eontrol group after treatment.Those results indicated that VKH diseases may be associated with the decreased proportion of CD4+ CD25+ regulatory T cells.

Objective To investigate the correlation between middle cerebral artery (MCA) atherosclerotic plaques and single subcortical infarction (SSI) using high-resolution magnetic resonance imaging (HR-MRI).Methods The patients with SSI received HR-MRI examinations at the ipsilateral MCA horizontal segment stenosis from January 2012 to November 2014 were analyzed prospectively.They were divided into proximal SSI (pSSI) and distal SSI (dSSI).The longitudinal and transverse diameters and volume of different types of infarction pattern as well as the degree of luminal stenosis of MCA deep perforating parent artery,plaque distribution,plaque enhancement or not,white matter lesions,and general information of both groups were documented respectively.Results A total of 78 patients with SSI were enrolled,including 40 (51％) in the pSSI group and 38 (49％) in the dSSI group.The proportions of Fazekas scale grade 3 white matter lesions (63.5％vs.40.0％;x2 =4.183,P=0.041) and deep white matter lesions (50.0％ vs.15.0％;x2 =10.961,P =0.001) in the dSSI group were significantly higher than those in the pSSI group.The proportions of MCA plaque in the opening (35.0％ vs.13.2％;x2=3.930,P=0.047),plaque enhancement (87.5％ vs.30.0％;x2 =25.447,P ＜ 0.001) and posterosuperior wall plaques (42.5％ vs.21.4％;x2 =9.491,P ＜ 0.001) and the degree of luminal stenosis (60.38％ ± 10.20％ vs.45.00％ ±6.44％;t =3.625,P =0.031) in the pSSI group were all significantly higher than those in the dSSI group.In addition,the longitudinal and transverse diameters and volume of the infarcts in the pSSI group were significantly larger than those in the dSSI group (all P ＜ 0.001).Multivariate logistic regression analysis showed that MCA enhanced plaques on the lesionipsilateral sides (odds ratio[OR] 11.764,95％ confidence interval[CI] 2.081-66.511;P =0.005) and posterosuperior wall plaques (OR 6.131,95％ CI 1.012-23.339;P =0.037) were independently associated with pSSI,while deep white matter lesions (OR 0.280,95％ CI 0.203-0.648;P=0.012) was independently associated with dSSI.Conclusions The atherosclerotic plaques of MCA deep perforating parent artery are common in both the pSSI group and the dSSI group.pSSI is mainly associated with the location of atherosclerotic plaques of deep perforating parent artery and enhanced plaques,while dSSI is mainly associated with deep perforating artery vasculopathy.

Aim To study effects of pioglitazone on cardiac fibroblast proliferation induced with high glucose and high insulin.Methods The neonatal rat cardiac fibroblasts were cultured and treated with different factors.The cellular number was determined by crystal violet uptake;the DNA synthesis was assayed with thymidine intake method;the percentage of S+G_2+M in the cell cycle was determined by flow cytometry.Results Pioglitazone inhibited the cell number、DNA synthesis and the percentage of S+G_2+M in the cell cycle of cultured cardiac fibroblasts induced with high glucose and high insulin.Conclusion Pioglitazone inhibits cardiac fibroblast proliferation induced with high glucose and high insulin and the effective mechanism of pioglitazone on cardiac fibroblast proliferation needs further study.

Objective To explore the value of high-resolution MRI(HR-MRI) on clinical application in the differential diagnosis between Moyamoya disease(MMD) and atherosclerosis-related Moyamoya syndrome (A-MMS). Methods Seventeen cases of patients with MMD and 18 cases of patients with A-MMS in our hospital from January 2014 to September 2015 were prospectively enrolled in the study. Record the clinical data and the proximal middle cerebral artery (M1 portion) performance on HR-MRI, the max-vessel area, the min-vessel area, the max-lumen area, the min-lumen area, the wall max-thickness, the styles of M1 portion thickening (eccentric or concentric), whether the wall was enhanced or not, and analysis the recorded data statistically, t test and χ2 test were used for the statistical analysis. Results The wall max-thickness of MMD group was (0.94 ± 0.17) mm, which was smaller than that in A-MMS group (1.23 ± 0.42) mm, there was statistic significance (t=-2.977, P=0.006). The cases of M1 portion non-enhancement was 15, slight enhancement 2, strong enhancement 0 in MMD group, and non-enhancement 5, slight enhancement 5, strong enhancement 8 in the A-MMS group, the difference was significant statistically (χ2=9.794, P=0.001). The cases of M1 portion concentric thickening was 16, 9 cases in the A-MMS group, there was statistic difference between them (χ2=6.317, P=0.012). Wall concentric thickening diagnose the MMD with a sensitivity of 94.1% (16/17), specificity of 50.0% (9/18), accuracy of 71.4%(25/35). Wall strong enhancement appear in the A-MMS with a sensitivity of 44.4%(8/18), specificity of 100%(17/17), accuracy of 71.4%(25/35).With a cut-off the maximum wall thickness of 1.2 mm could be used to noninvasively differential diagnose the MMD and A-MMS with a sensitivity of 55.6%(10/18), specificity of 88.2%(15/17), accuracy of 71.4%(25/35). Conclusion HR-MRI is a good tool for the differential diagnosis between MMD and A-MMS.

BACKGROUND: Ahmed glaucoma valve (AGV) is usually implanted at the superotemporal area of eyes. Comeal endothelial calls cannot regenerate,.so the repair of the endothelial cells mainly depend on the extension and progradation of the healthy cells in other area. Therefore, changes of density and shape are observed in the corneal endothelial cells after AGV implantation. OBJECTIVE: To observe the changes of density and morphology of corneal endothelial cells after AGV implantation. METHODS: Ahmed glaucoma valves were implanted in 34 eyes of 34 patients with refractory glaucoma. Density and morphology of corneal endothelial calls were evaluated in the superotemporal, superonasal, infratemporal, infranasal, and central corneal areas to calculate mean value of total comea before and at 3 and 6 months after surgery. Percentage of hexagonal cells was statistically summarized.RESULTS AND CONCLUSION: Mean density of corneal endothelial calls was statistically decreased following AGV implantation (P < 0.05), In particular, the decrease was obvious in the superetemporal area. Density of corneal endothelial cells was not changed in central area before and after AGV implantation. Morphological changes demonstrated that hexagonal cells were increased, but polygon cells were increased (P< 0.05). Density of corneal endothelial cells was gradually decreased, and morphology was also changed at 6 months after AGV implantation, suggesting that more care should be taken during intra-operation in order to minimize damage td the endothelium and prolong monitoring time of corneal endothelial cells following AGV implantation.

Objective To evaluate the effect of sevoflurane on brain injury in pigs with hemorrhagic shock (HS).Methods Twenty-four adult male Bama miniature pigs, aged 6 months, weighing 22-25 kg, were equally and randomly divided into 3 groups using a random number table: sham operation group (group Sham) , group HS, and sevoflurane group (S group).In group Sham, the bilateral femoral arteries and internal jugular vein were only punctured.The animals were anesthetized with iv propofol 3.0 mg/kg, tracheostomized and mechanically ventilated.The right femoral artery was cannulated for blood-letting.HS was induced by blood-letting (40％ blood volume within 15 min), and it was then maintained for 1 h after the end of blood-letting to induce brain injury.In group S, 2％ sevoflurane was inhaled for 30 min after successful establishment of the model.Immediately before establishment of the model (T0) , and at 30, 60,90, 120, 180 and 240 min after HS (T1-6) , blood samples were collected from the internal jugular vein for determination of interleukin-1beta (IL-1β) and tumor necrosis factor-alpha (TNF-α) concentrations in serum (by enzyme-linked immunosorbent assay), and neuron-specific enolase (NSE) and S-100β protein concentrations in serum (using double antibody sandwich method).Results Compared with group Sham, the serum IL-1β, TNF-α, NSE and S-100β protein concentrations were significantly increased at T2-6 in HS and S groups (P＜0.05).Compared with group HS, the serum IL-1β, TNF-α, NSE and S-100β protein concentrations were significantly decreased at T3-6 in group S (P＜ 0.05).Conclusion Sevoflurane can mitigate brain injury in pigs with HS, and the mechanism is associated with inhibition of inflammatory responses.

Objective To evaluate the effect of sevoflurane on myocardial injury induced by hemorrhagic shock and resuscitation (HS/R) in pigs.Methods Twenty-four Bama miniature pigs (12 males, 12 females) , weighing 20-25 kg, aged 3-5 months, were randomly divided into 3 groups (n=8 each) using a random number table: sham operation group (group S) , HS/R group and sevoflurane group (group Sev).The left and right femoral arteries and right femoral vein were cannulated for blood pressure monitoring, blood-letting, blood sampling and fluid infusion.HS/R was induced by blood-letting maintaining for 1 h, followed by resuscitation with autologous blood reinfusion and infusion of lactated Ringer's solution 2 times the volume of the blood withdrawn.The pigs in group Sev were exposed to 2％ sevoflurane for 30 min before resuscitation.After cannulation, at 30 min after hemorrhagic shock, before resuscitation, and at 30 min, and 1.5, 2.5 and 3.5 h after resuscitation, blood samples were collected from the femoral artery for determination of creatine kinase-MB (CK-MB) activity and cardiac troponin Ⅰ (cTnI) concentration in serum using an automatic biochemical analyzer.Myocardial specimens were obtained at 3.5 h after resuscitation for detection of tumor necrosis factor-alpha (TNF-ot) and interleukin-6 (IL-6) contents (by ELISA) , and phosphor-signal transducer and activator of transcription 1 (p-STAT1) expression (by Western blot), and for examination of the pathological changes (with light microscope).Results Compared with S group , the CK-MB activity and cTnI concentration in serum and contents of TNF-α and IL-6 were significantly increased, and the expression of p-STAT1 was up-regulated in HS/R and Sev groups (P＜0.05).Compared with HS/R group, the CK-MB activity and cTnI concentration in serum and contents of TNF-α and IL-6 were significantly decreased, and the expression of p-STAT1 was downregulated (P＜0.05) , and the pathological changes of myocardia were alleviated in Sev group.Conclusion Sevoflurane can alleviate HS/R-induced damage to myocardia of pigs, and inhibited STAT1 activity and attenuated inflammatory responses in the myocardium are involved in the mechanism.

Objective To evaluate the changes in the expression of aquaporin-8 (AQP8) in intestinal mucosa in pigs with hemorrhagic shock.Methods Sixteen Bama miniature pigs,weighing 22-25 kg,were equally and randomly divided into sham operation group (group S) and hemorrhagic shock group (group HS).The animals were fasted for 8 h before operation.The animals were anesthetized with propofol 3 mg/kg injected via the auricular vein,and tracheostomized and mechanically ventilated.In group S,the femoral artery and internal jugular vein were only cannulated.In group HS,the femoral artery and internal jugular vein were cannulated for blood pressure and mean arterial pressure monitoring and blood sampling.Hemorrhagic shock was then induced by removing 40 percent of blood volume over 15 min.Before anesthesia (T0),and at 30 min and 1.0,1.5,2.0,3.0 and 4.0 h after the end of blood-letting (T1.6),blood samples were collected for determination of serum D-lactate and intestinal fatty acid binding protein (I-FABP) concentrations.After blood sampling at T6,the pigs were sacrificed,and intestinal specimens were obtained for microscopic examination and for determination of AQP8 cotent in intestinal mucosa (by ELISA).The water content of intestines was calculated by wet/dry weight ratio.Results Compared with group S,the serum D-lactate concentrations at T2-6,I-FABP concentrations at T1-6,and water content of intestines were significantly increased,and the cotent of AQP8 was up-regulated at T6 in group HS.No changes were found in the intestinal mucosa in group S.In group HS,severe damage to the intestinal mucosa was found,and bleeding,inflammatory cell infiltration,and epithelial cell necrosis were observed.Conclusion The mechanism of hemorrhagic shock-caused damage to intestines is related to up-regulated expression of AQP8 in intestinal mucosa in pigs.

Objective To evaluate the effect of sevoflurane on activation of nuclear factor kappa B (NF-κB) during brain injury induced by hemorrhagic shock (HS) in pigs.Methods Thirty-two adult male Bama miniature pigs,aged 6 months,weighing 22-25 kg,were divided into 4 groups (n=8 each) using a random number table:sham operation group (group Sham),HS group,sevoflurane preconditioning group (group Sev-Pre) and sevoflurane postconditioning group (group Sev-Post).The animals were anesthetized,and tracheostomized and mechanically ventilated.In group Sham,the bilateral femoral arteries and internal jugular veins were only cannulated.HS was induced by removing 40％ of blood volume within 15 min (30 ml/kg) via the right femoral artery and maintaining at this level for 1 h before resuscitation in HS,Sev-Pre and Sev-Post groups.In group Sev-Pre,2％ sevoflurane was inhaled for 30 min,and then HS was induced.In group Sev-Post,2％ sevoflurane was inhaled for 30 min starting from the time point immediately after HS was induced.Immediately before establishment of the model and at 30,60,90,120,180 and 240 min of HS (T1-6),blood samples from the jugular vein were collected for determination of serum interleukin-1beta (IL-1β) and tumor necrosis factor-alpha (TNF-α) concentrations by enzymelinked immunosorbent assay.At 4 h of HS,the rats were sacrificed,and brains were removed for microscopic examination of hippocampal CA1 region (using haematoxylin and eosin staining) and for determination of the expression of NF-κB in nucleoprotein (by Western blot).Results Compared with group Sham,the concentrations of serum IL-1β and TNF-α were significantly increased at T2-6,and the expression of NF-κB in nucleoprotein in hippocampal CA1 region was up-regulated in HS,Sev-Pre and Sev-Post groups (P＜0.05).Compared with group HS,the concentrations of serum IL-1β and TNF-α were significantly decreased at T3-6,and the expression of NF-κB in nucleoprotein in hippocampal CA1 region was down-regulated in Sev-Pre and Sev-Post groups (P＜0.05).There were no significant differences between group SevPre and group Sev-Post in concentrations of serum IL-1β and TNF-α and expression of NF-κB in nucleoprotein in hippocampal CA1 region (P＞0.05).The pathologic changes were significantly attenuated in SevPre and Sev-Post groups as compared with group HS.Conclusion The mechanism by which sevoflurane attenuates brain injury induced by HS may be related to inhibition of NF-κB activation and reduction of inflammatory responses in pigs.