ObjectiveTo study the effect the low level laser irradiation in nostril combined with the electric stimulation of cerebellum on acute cerebral infarction.Methods88 patients with acute cerebral infarction were randomly divided into two groups, 45 cases in the study group who were accepted level laser irradiation in nostril combined with the electric stimulation of cerebellum and the normal medicine therapy, 43 cases in the control group who were accepted the normal medicine therapy only. The effects of two groups were observed.ResultsThe scores of the nervous function defect degree and the cerebrovascular dynamics indexes of study group were obviously increased (P<0.05 or P<0.01) compared with those before treatment. The indexes of blood viscosity were significantly decreased compared with those before treatment(P<0.01).However, all these indexes of the control group showed no significantly difference before and after treatment. ConclusionThe low level laser irradiation in nostril combined with the electric stimulation of cerebellum therapy is effective on acute cerebral infarction.It is helpful for early comprehensive recovery of motor function of the hemiplegic limbs.

ObjectiveTo investigate the clinical characteristics of patients,risk factors and preventive measures of nosocomial infection in diabetic cerebral infarction(DCI).MethodsThe clinical data of 124 DCI cases with nosocomial infection and 116 DCI cases without nosocomial infection were analyzed retrospectively.ResultsThe clinical characteristics of nosocomial infection in DCI patients were that large cerebral infarction and severity neurological deficits were very common.The patients always had long hospitalization days and poor prognosis.Invasive operation,antibiotic prophylaxis,severity neurological deficits,fasting plasma glucose,urinary albumin,size of cerebral infarction,albumin/globulin and hospitalization days were the risk factors for nosocomial infection in DCI.Among the patients,nosocomial lower respiratory tract infection was the highest(41.5%),the second one was urinary tract infection(28.1%).The case that both sites of infected was common(8.9%).Klebsiella pneumoniae(16.7%),Pseudomonas aeruginosa(15.9%),Candida albicans(12.1%) and Escherichia coli(12.1%) were the most frequent pathogens.ConclusionThe patient's condition of nosocomial infection in DCI is serious and has poor prognosis.Taking preventive measures according to the risk factors can reduce the infection rate.

Objective To explore the relationship of serum anti-MICA antibody and development of chronic rejection (CR) after renal transplantation. Methods The enrolled 105 patients included 43 cases of CR, and 62 cases of functioning renal allograft as controls. Data including PRA level before transplantation, HLA mismatch, cold ischemic time, SCr at discharge, immunosuppressive regimen,and months after transplantation were analyzed. Blood samples were collected immediately after grouping for anti-MICA antibodies, SCr determination. Acute rejection episodes and renal allograft function which was evaluated by △SCr/M [(SCr at present - SCr at discharge) /months after transplantation) were compared between anti-MICA-antibody positive patients and anti-MICA-antibody negative patients. Results There was no significant difference in gender, age, HLA mismatch, cold ischemic time, immunosuppressive regimen, SCr at discharge, months after transplantation between CR and control groups (P＞0.05). Serum creatinine level and number of antiMICA-antibody positive patients in CR group were significantly increased as compared with those in control group (P＜0.01 ). Acute rejection episodes during the first 3 months after transplantation in anti-MICA-antibody positive patients were significantly more than those in anti-MICA-antibody negative patients (P＜0.05),and the △SCr/M in the former was higher than that in the latter (8.3 +3.6 vs 2.4 ± 2.6, P＜0.05). Conclusion Humoral immunoreaction mediated by MICA partly participates the development of CR after renal transplantation. MICA antibody is a risk factor affecting long-term allograft function.

The aim of this study was to investigate the effects of Avastin on aquaporin4 (AQP4) expression in human retinal Müller cells in vitro under hypoxia, so as to explore the mechanism of Avastin treating retinal edema. The human Müller cells were cultured using the enzymatic digestion method. Müller cells were identified under the transmission electron microscopy and by using immunofluorescence staining. By using semi-quantitative reverse transcription polymerase chain reaction (RT-PCR), the expression of AQP4 mRNA and VEGF mRNA in Müller cells cultured with 500 μmol/L CoCl(2) for 0, 3, 6, 12 and 24 h, and with 0, 100, 300, 500 and 700 μmol/L CoCl(2) for 24 h was detected. The expression of AQP4 mRNA in Müller cells cultured with 50 ng/mL exogenous vascular endothelial growth factor (VEGF) for 0, 0.5, 1, 2 and 4 h, and with 0, 25, 50 and 75 ng/mL VEGF for 24 h was detected. Amplified cDNA products of AQP4 mRNA in Müller cells cultured with 500 μmol/L CoCl(2) and 200 μg/mL Avastin for 24 h were detected. The results showed that more than 95% cells displayed positive immunofluorescence reaction. Characteristic 8-10 nm intracellular filaments could be seen in the cytoplasm under the transmission electron microscopy. In the CoCl(2) experimental groups, the expression of AQP4 mRNA and VEGF mRNA in Müller cells was increased as compared with the control group. Alteration of AQP4 mRNA and VEGF mRNA levels showed a significantly positive correlation (r (2)=0.822, P<0.05). The expression of AQP4 mRNA in Müller cells was increased by VEGF. The expression of AQP4 mRNA was significantly decreased by Avastin as compared with the control group. It is suggested that Avastin can decrease the expression of AQP4 mRNA in human Müller cells under chemical hypoxic conditions partially via VEGF path, which may be one of the mechanisms of Avastin treating retinal edema.

The aim of this study was to investigate the effects of Avastin on aquaporin4 (AQP4) expression in human retinal Müller cells in vitro under hypoxia, so as to explore the mechanism of Avastin treating retinal edema. The human Müller cells were cultured using the enzymatic digestion method. Müller cells were identified under the transmission electron microscopy and by using immunofluorescence staining. By using semi-quantitative reverse transcription polymerase chain reaction (RT-PCR), the expression of AQP4 mRNA and VEGF mRNA in Müller cells cultured with 500 μmol/L CoCl(2) for 0, 3, 6, 12 and 24 h, and with 0, 100, 300, 500 and 700 μmol/L CoCl(2) for 24 h was detected. The expression of AQP4 mRNA in Müller cells cultured with 50 ng/mL exogenous vascular endothelial growth factor (VEGF) for 0, 0.5, 1, 2 and 4 h, and with 0, 25, 50 and 75 ng/mL VEGF for 24 h was detected. Amplified cDNA products of AQP4 mRNA in Müller cells cultured with 500 μmol/L CoCl(2) and 200 μg/mL Avastin for 24 h were detected. The results showed that more than 95% cells displayed positive immunofluorescence reaction. Characteristic 8-10 nm intracellular filaments could be seen in the cytoplasm under the transmission electron microscopy. In the CoCl(2) experimental groups, the expression of AQP4 mRNA and VEGF mRNA in Müller cells was increased as compared with the control group. Alteration of AQP4 mRNA and VEGF mRNA levels showed a significantly positive correlation (r (2)=0.822, P<0.05). The expression of AQP4 mRNA in Müller cells was increased by VEGF. The expression of AQP4 mRNA was significantly decreased by Avastin as compared with the control group. It is suggested that Avastin can decrease the expression of AQP4 mRNA in human Müller cells under chemical hypoxic conditions partially via VEGF path, which may be one of the mechanisms of Avastin treating retinal edema.
Antibodies, Monoclonal, Humanized ; pharmacology ; Aquaporin 4 ; genetics ; metabolism ; Bevacizumab ; Cells, Cultured ; Ependymoglial Cells ; metabolism ; Gene Expression ; drug effects ; genetics ; Humans ; Hypoxia ; genetics ; metabolism

Objective After hydrogen bonding between collagen ( COL) and silk fibroin ( SF ) at different concentrations, a composite scaffold with adjustable stiffness was prepared by combining with gel system, and its physical and chemical properties were characterized. Methods SF with different qualities was dissolved in sodium alginate (SA) solution, then COL solution at different concentration and calcium carbonate ( CaCO3 ) powder were added. The hydrogels of SC1, SC2, and SC3 groups were obtained by taking out the mixed solution and adding some gluconic acid lactone ( GDL) powder, and different SF scaffolds were obtained after freeze drying. Results The SF scaffolds with adjustable stiffness were successfully prepared. The compression moduli of SC1, SC2, and SC3 groups were (17. 31±2. 73), (24. 12±1. 81), (32. 54±1. 81) kPa, respectively. The innerstructure of the scaffolds was observed. From SC1 group to SC3 group, pores of the scaffolds were smaller and fewer, and hydrophilicity of the materials become better and better. Conclusions Three-dimensional ( 3D) porous scaffolds with different matrix stiffness can be prepared by changing the concentration of SF and COL solution. The concentration of SF and COL is proportional to the compression modulus, water absorption, water retention and swelling rate of SF scaffolds, while inversely proportional to porosity. The findings of this study are expected to provide theoretical guidance for construction of scaffolds with appropriate matrix stiffness for inducing osteogenic differentiation of mesenchymal stem cells