·To improve the effect of glaucoma filtration operation in reducing intraocular pressure ( lOP ) , it’s important to prevent and inhibit fibrotic scar formation during and after operation.This paper focuses on the current and future possible means for modulation of wound healing after glaucoma filtration surgery, mainly including series of medications ( antimetabolites, anti-inflammation drugs, antigrowth factor drugs, drugs acting on cell signal pathways, etc.) , new drug delivery system and other technologies. This article also discusses the future orientation in this field.

Objective To sum up the experience of position nursing of patients with ankylosing spondylitis and severe kyphosis. Methods Eleven patients with ankylosing spondylitis and severe kyphosis underwent surgery. The patients′spine and head were kept in a line during anesthesia to avoid spinal cord injury. The eye mask was used to make sure the eyelid close, so the bulbar conjunctiva and corneal did become dry. The angle of operation bed in time during operation was adjusted. The crushed area was observed and the position was changed to avoid pressure sores and edema. After surgery, they were keep inactive to make sure the spine stable and relieve the pressure. Results The 11 patients′surgery were successful. There were no pressure ulcer, fracture, spinal cord injury or eye injury occurs. The operation time was 9.3 ± 2.9 h. Conclusion Position nursing is very important to improve the success rate of surgery and reduce complications.

Background The extraocular muscles (EOMs) Pulley is considered as the functional origins of the recti EOMs,it is determinants of ocular motility.Objective The structure of the connective tissue around EOMs in cat was studied,and the role of EOMs Pulley to ocular movement was investigated.Methods Five adult cats were involved.The gross anatomy of an orbit in each cat was observed.The other orbit was processed with paraffin imbedding and coronal serial sections.A murine monocolonal antibody to α-smooth muscle actin (α-SMA) was used to show smooth muscle,while Masson trichrome stain was used to show muscle and collagen,and Weigert stain to show elastin.Results An encircling ring of collagen circled EOM was thin and connected to the orbital layer of muscle fiber loosely.Less elastin fibers and little smooth muscle cells were embedded in the collagen ring and connective band.Collagen ring around medial rectus and the connective band between medial rectus and inferior rectus was not more significantly developed than other bands.Conclusions The connective tissue around EOMs in cat may be related to its function of ocular movement,which is not developed.

Objective To determine the median effective dose(ED50)of etomidate inhibiting responses to endotracheal intubation when combined with dexmedetomidine in the patients with obstructive jaundice. Methods American Society of Anesthesiologists physical status Ⅱ or Ⅲ patients with obstructive jaundice,aged 45-63 yr,with body mass index of 18-30kg/m2,scheduled for elective operations under general anesthesia,were divided into control group(group C)and dexmedetomidine group(group D)using a random number table. At 15min before induction of anesthesia,normal saline 0.1 ml/kg was infused intravenously in group C,and dexmedetomidine 0.4 μg/kg was infused intravenously in group D. Anesthesia was induced with midazolam 0.05 mg/kg,fentanyl 4 μg/kg,etomidate and cisatracurium 0.15 mg/kg. The ED50 of etomidate was determined using Dixon′s up-and-down method. Etomidate was injected intravenously at the initial dose of 0.2 mg/kg in the first patient in each group. Each time the dose increased/decreased in the next patient according to whether or not the increase in mean arterial pressure and/or heart rate ≥ 20% of the baseline value within 3min after endotracheal intubation. The ratio between the two successive doses was 1.1. The number of patients in whom inhibition was effective or ineffective was recorded,and the ED50 and 95% confidence interval of etomidate inhibiting responses to intubation were calculated using Probit analysis. Results The ED50 (95% confidence interval)of etomidate inhibiting responses to intubation was 0.185(0.162-0.201)mg/kg in group C,the ED50(95% confidence interval)of etomidate inhibiting responses to intubation was 0.129(0.093-0.143)mg/kg in group D,and there was significant difference between the two groups(P<0.05).Conclusion When combined with dexmedetomidine,the ED50 of etomidate inhibiting responses to endotracheal intubation is 0.129 mg/kg in the patients with obstructive jaundice.

Objective To propose an accurate method of noninvasive determination of central venous pressure(CVP ) by locating the central point of right atrium (RA ) using echocardiography .Methods Through the 3D reconstruction ,the accurate positions of RA of 30 patients who had been examined by multislice 3‐dimensional computed tomography for chest imaging were recorded .Based on solid geometric principles ,the central point in RA was located by echocardiography and then compared with CT‐location point .The accuracy and feasibility were assessed by absolute distance (Da) ,vertical distance (Dv) and the whole time of location (T) between the two points .Results Mean Da ,Dv and T of the whole subjects were 07.6cm(95% CI:06.2to08.1cm),01.6cm(95% CI:-00.2to03.4cm),and438.0s(95% CI:400.1to 47 4.0 s) ,respectively .Conclusions The echocardiographic method on the basis of solid geometry proposed in this study could be used to locate the central point in RA accurately and simply .Thus it would be helpful to improve the accuracy of noninvasive determination of central venous pressure .

Objective: To explore and evaluate the biomechanic relationships between different depth of pedicle screw penetration with the sagittal plane reconstruction in thoracolumbar fracture. Methods:Six fresh cadaveric specimens of lumbar spine from L_1 to L_3 were used to make the model of thoracolumbar fracture. The system of universal spine system( USS )pedicle screw was adopted with the 6 mm diameter of screw. Each of two Schanz screws was implanted into the pedicles of L_1 and L_3 A canulated screw was fixed into the former of vertebral body in L_1 and L_3, and the distance of the two canulated screws was taken as the normal height. The axial loads were given while the pedicle screws were implanted at the depth of D1, D2 and D3, and the distance of the two canulated screw was measured as well as the distance was reduced to the normal height by axial load. The index measured included of the depth of pedicle screw penetration, the height of fractured vertebral body and afterload. Results: Along with the increasing of afterload, the height of injured vertebral body was increased accordingly, but the extent was different at three depth of pedicle screw penetration (D1, D2, and D3). While the injured vertebral body was reduced totally (reduced distance 0.00 mm), there was (2 630±13) g of afterload needed in Dl depth, and (2 339±61) g and(2 221± 164) g of afterload in D2 and D3 depth respectively. There was significant difference in distance between D1, D2 and D3 (P< 0.01), however, no significant difference between D2 and D3 (P> 0.05). Conclusion: There is a relationship in the depth of pedicle screw penetration, the capacity of reduction and sagittal plane reconstruction. The depth of pedicle screw had a significant effect on the capacity of reduction for the injured vertebral body, which would be the best option in biomechanics when the pedicle screw was implanted more than 1/2 pedicle or all of it.

Background Arresting the overexpression of vascular endothelial growth factor (VEGF) will be a new approach to the inhibition of neovascularization.RNA interference (RNAi) can inhibit the expression of specific gene,and its application in eye has little interference to other gene expression.Objective This study was to investigate the effect of small interference RNA (siRNA) targeting VEGF on the expression of VEGF and retinal neovascularization in oxygen-induced retinopathy (OIR) model.Methods psi-HITM/enhanced green fluorescent protein (EGFP)/VEGF siRNA was designed and prepared in vitro.Mouse endothelioma (EOMA) were cultured in DMEM without antibiotic and divided into 5 groups.The cells were incubated in DMEM only in the blank control group;while 1 μl of LipofectamineTM 2000 + psi-HITM/EGFP,1 μl LipofectamineTM 2000 + 40,50 or 60 nmol/L of psi-HITM/EGFP/VEGF siRNA was added into DMEM in the negative control group and siRNA groups,respectively.The expression of VEGF mRNA and protein was detected by real time PCR (RT-PCR) and Western blot.The optimal effective concentration of VEGF siRNA was assessed.OIR models were established in 48 7-day-old C57BL/6J mice by raising them at an oxygen concentration of (75±2) ％ for 5 days and then to normal air.The mice were randomized into the model group,null vector group and VEGF siRNA group.1 μl of a mixture of psi-HITM/EGFP or VEGF siRNA (60 nmol/L) and LipofectamineTM 2000 was intravitreally injected,respectively,in the null vector group and VEGF siRNA group.The normal mice were used as the normal control group.Expression of VEGF mRNA and protein in the mouse retinas was detected by RT-PCR and Western blot,respectively,and FITC-dextran stretched retinal preparation was examined to evaluate the neovascularization,and retinal sections were examined to quantify the number of vascular endothelial cell nuclei extending beyond the internal limiting membrane (ILM).Results The in vitro transfection test showed that the expression of VEGF mRNA and protein in the EOMA cells was significantly different among the blank control group,negative control group and 40,50,60 nmol/L VEGF siRNA groups (F =148.890,P ＜ 0.001; F =306.960,P ＜ 0.001),and the expression of VEGF mRNA was lower in different concentrations of VEGF siRNA groups than that in the blank control group (t=73.950,119.890,156.480,all at P＜0.001).Also,the expression of VEGF protein was less in different concentrations of VEGF siRNA groups than that in the blank control group (t =15.452,23.344,42.119,all at P＜0.001).The optimal inhibitory concentration of VEGF siRNA was 60 nmol/L.In vivo study determined that compared to the model group and null vector group,the non-perfusion zones and neovascular net in the retina were decreased,and the number of vascular endothelial cell nuclei extending beyond the ILM was less in the VEGF siRNA group.The relative expression level of VEGF mRNA in the retinas was 1.23±0.18,4.02±0.16,3.98±0.19 and 1.98±0.12 in the normal control group,model group,null vector group and VEGF siRNA group,respectively,with a significant difference among them (F=369.780,P＜0.001),and the relative expression levels of VEGF mRNA in the model group and null vector group were higher than that in the normal control group (t=37.880,37.336,both P＜0.001),and the expression of VEGF mRNA in the VEGF siRNA group declined by 50.8％ (t=10.183,P＜0.001).The difference in the expression levels of VEGF protein also was assayed among the various groups (F=408.980,P＜0.001),and VEGF level in the retina was lowered by 68.0％ in the VEGF siRNA group compared to the model group (t =11.473,P＜0.001).However,VEGF level in the VEGF siRNA group remained at a high level in comparison with the normal control group (t =2.422,P＜0.001).Conclusions Intravitreal injection of VEGF siRNA can attenuate retinal neovascularization by effectively downregulate the expression VEGF mRNA and protein in the retina.

Objective To investigate the effect of fluvastatin (FLV) on the expression of β1 integrin in puromycin aminonucleoside (PAN)-treated podocytes and its mechanism.Methods Cultured human podocytes were divided into PAN,different concentrations of fluvastatin (1 × 10-8 to 1 × 10-5 mol/L),SOD,H2O21 groups respectively.Expressions of β1 integrin and reactive oxygen species (ROS) in podocytes were detected by Western blotting and DCFHDA (2' 7'-Dichlorofluoresecein 3' 6'-diacetate) respectively.The viability of podocyte was determined by MTT colorimetry.Results PAN and H2O2 significantly decreased the expression of β1 integrin and increased the synthesis of ROS in podocytes (P＜0.05respectively).Lower concentration fluvastatin or SOD treatment up-regulated β1 integrin and downregulated ROS of podocytes induced by PAN (P＜0.05 respectively).MTT revealed that lower podocyte viability was found in higher concentration fluvastatin,PAN and H2O2 groups.Lower concentration fluvastatin and SOD could protect podocytes against PAN.Conclusion Fluvastatin attenuates the injury of podocyte induced by PAN and increases the expression of β1 integrin,whose mechanism may be associated with the inhibition of the ROS activity.

Objective To explore the effect and mechanism of fluvastatin on the expression of fibronectin(FN) in human peritoneal mesothelial cells (HPMCs) induced by high-glucose peritoneal dialysate (HGPDS).Methods Cultured HPMCs were randomly divided into control,HGPDS,HGPDS plus GSK650394 10-5 mol/L (the competitive inhibitor of SGK1),different concentrations of fluvastatin,fluvastatin 10-6 mol/L and GSK650394 10-5 mol/L alone.The morphology change of HPMC was observed by light microscopy.The cellular viability was detected by MTT colorimetry.The mRNA and protein expressions of serum and glucocorticoid-inducible kinase 1 (SGK1) and FN were detected by RT-PCR,Western blotting or ELISA.Results After incubation with HGPDS,the cell morphology changed from typical cobblestone-like appearance to fibroblast-like appearance,and the cell viability was inhibited significantly (P＜0.05).Fluvastatin 10-6mol/L and GSK650394 could improved the cell morphology and the cell viability injured by HGPDS (P＜0.05).Compared with the normal control group,the mRNA and protein expressions of SGK1 and FN increased significantly in HPMC treated with HGPDS(P＜0.05).GSK650394 significantly decreased the high expression of SGK1 and FN (P＜0.05),also the fluvastatin had same effects as GSK650394 in dose-dependent manner (P＜0.05).Conclusions High-glucose peritoneal dialysate can increase FN expression in human peritoneal mesothelial cells,which can be attenuated by fluvastatin.The protective role of fluvastatin in HPMC may be partially achieved through the signal pathway of SGK1.