The screw holes of anatomic plate are oval, and longitudinal axis of the screw hole is parallel to the axis of the plate. The plate surrounding the screw hole is smooth, parallel to the longitudinal axis of the long bone. Under outside force or inside force, the top of screw can move on the smooth surface surrounding the screw hole; the movement is a reversible one. Domestic plate can fix bone fracture stably, and the outside force and inside force can result in micromovement of the fracture ends, stimulating the fracture ends and bone callus formation. Repetitive force is beneficial to bone callus response, protect fragile new vessels and bone trabecula from damage, and promote fracture healing.

Objective To determine the effects of valsartan, a specific angiotensin Ⅱ type 1 receptor blockade, on arrhythmia in rabbits after myocardial infarction and to discuss the mechanism. Method Twentyfour rabbits were randomly (random number) divided into sham operated (SO) group ( n = 8), myocardial infarction (MI) group ( n = 8) and valsartan (VAL) group ( n = 8). The rabbits of SO group were operated upon with median stemotomy without left ventricular coronary artery hgature. The rabbits of MI group and VAL group had median stemotomy with left ventricular coronary artery ligature. After MI, the rabbits of VAL group were fed with border zone of infracted left ventricular wall and the L-type calcium current was recorded by whole-cell patch clamp technique. Results Ventricular tachycardia or fibrillation (VT/VF) episodes were markedly decreased in VAL group than that in MI group [(3.2 ± 0. 6) vs. ( 11.7 ± 1.8)] after 12 weeks. The density of Ica-L current was higher in MI group than that in SO group and VAL group [( - 9.12 ± 0.73) pA/pF vs. ( - 6.29 ± 0.65) pA/pF and ( - 6.75 ± 0.64) pA/pF], ( P ＜ 0.05), however, there were no significant differences in Ica-L current between So group and VAL group ( P ＞ 0.05). Conclusions Valsartan reduces the VT/VF episodes in rabbits after MI. The effects of valsartan may be attributed to the inhibited electrical remodeling after MI.

With the continuous development of precision targeting medicine, antiangiogenic drugs have achieved good therapeutic effects in the treatment of advanced cancer, but renal injury and other adverse reactions often occur during the use, which reduce the quality of life of patients. This article reviews the mechanism of renal injury induced by antiangiogenic drugs and the potential relation between renal injury and prognosis.

Objective To explore the potential mechanisms of low density lipoprotein receptor (LDLr) in high glucose peritoneal dialysis solution (PDS)-induced peritoneal fibrosis.Methods Human peritoneal mesothelial cells (PMCs) were applied.In pre-experiment,human PMCs were cultured with 1.5％ PDS,2.5％ PDS and 4.25％ PDS for 6 h,12 h and 24 h.4.25％ mannitol was used as high osmotic pressure control.In formal experiment,PMCs were divided into the control group (treated with phosphate buffer saline) and the high glucose PDS group (treated with 4.25％ PDS for 24 h).Morphological change of PMCs was observed by inverted microscope.The mRNA and protein expressions of extracellular matrix proteins such as α-smooth muscle actin (α-SMA),fibroblast specific protein-1 (FSP-1) and collagen Ⅰ in PMCs were respectively measured by real-time PCR and Western blotting.The lipid accumulation was observed by oil red O staining and filipin staining,and the content of intracellular cholesterol ester was detected by high-performance liquid chromatography.The co-expression of the sterol regulatory element-binding protein (SREBP) cleavage-activating protein (SCAP) with golgin was observed with immunofluorescent staining.The mRNA and protein expressions of LDLr,SREBP-2 and SCAP were respectively detected by real-time PCR and Western blotting.The mRNA and protein expressions of mammalian target of rapamycin (mTOR),eukaryotic initiation factor 4E-binding protein 1 (4EBP1),and p70 S6 kinase (S6K1) were respectively detected by real-time PCR and Western blotting.Results (1) Compared with the 1.50％ PDS stimulation,4.25％ PDS for 24 h intervention significantly increased the expression of LDLr in PMCs (P ＜ 0.05),and high osmotic pressure control at 6 h,12 h and 24 h had no statistical difference (P ＞ 0.05).(2) Compared with those in the control group,in high glucose PDS group PMCs showed notable elongation consistent with the morphology of myofibroblasts,the expressions of α-SMA,FSP-1 and collagen Ⅰ were increased (all P ＜ 0.05),and the intracellular cholesterol were enhanced (P ＜ 0.05).Meanwhile,the co-expression of SCAP with golgin was enhanced,and the mRNA and protein expressions of LDLr,SREBP-2 and SCAP were up-regulated in high glucose PDS group (all P ＜ 0.05).Further,the mRNA and protein phosphorylation of mTOR,4EBP1 and S6K1 were increased (all P ＜ 0.05).Conclusions The disruption of LDLr feedback regulation is involved in high glucose PDS-mediated cholesterol accumulation in PMCs by mammalian target of rapamycin complex 1 (mTORC1) pathway,which promotes the accumulation of extracellular matrix and peritoneal fibrosis.

Objective To investigate the effect of 1α, 25-dihydroxyvitamin D3 [1α,25-(OH)2 D3] on tumor necrosis factor-α ( TNF-α) induced activation of human umbilical vein endothelial cells ( HUVECs ) . The mechanism involved in this process was also studied. Methods HUVECs were cultured and treated with TNF-α( 40 ng/ml), 1α,25-(OH)2D3(10-8 mol/L), and SN50 as indicated. Vascular cell adhesion molecule (VCAM) and E-selectin were used as markers of endothelial activation, which were detected by Western blotting and realtime PCR (RT-PCR). NF-κB signaling pathway was investigated to study the mechanism. Western blotting, RT-PCR, immunofluorescence assay, and chromatin immunoprecipitation ( ChIP ) method were used to evaluate the effects of 1α,25-( OH) 2 D3 on its early activation, nuclear transport, and binding to VCAM and E-selectin promoters. Results (1) Western blotting and RT-PCR showed that TNF-α could significantly up-regulate the expression of VCAM and E-selectin in HUVECs, which can be inhibited by specific NF-κB blocker SN50. 1α,25-( OH) 2 D3 down-regulated the expression of VCAM and E-selectin induced by TNF-α. ( 2 ) Western blotting showed that TNF-α induces I-κBαphosphorylation, thereby activating NF-κB p65 subunit. Immunofluorescence showed that 1α, 25-( OH ) 2 D3 significantly inhibited the nuclear translocation of NF-κB p65 subunit. ChIP analysis revealed that 1α,25-( OH) 2 D3 inhibited the binding of NF-κB p65 to VCAM and E-selectin promoters and thus affected gene expression. Conclusions TNF-αenhanced the expression of E-selectin and VCAM in HUVECs via NF-κB signaling pathway. 1α,25-( OH) 2 D3 may inhibit NF-κB early activation, nuclear transport and the binding of NF-κB p65 to VCAM and E-selectin promoters, thereby inhibiting TNF-α-induced endothelial cell activation.

【Objective】 To study the correlation of clinical symptoms and cognitive functions with serum inflammatory factors in schizophrenia. 【Methods】 A total of 42 SCz patients (case group) and 47 healthy controls (control group) were enrolled in this study. We used enzyme-linked immunosorbent assay (ELSA) to determine six inflammatory factors in serum. PANSS was used to assess clinical symptoms and MCCB was used to assess the patients’ cognitive functions. 【Results】 ① Inflammatory factors: The serum levels of IL-1β, IL-4, IL-6 and IL-8 were significantly higher in case group than in control group (P<0.01). ② Cognitive functions: The scores of Trail Making Test, Hopkins Verbal Learning Test, Symbol Coding, Spatial Span, Brief Visuospatial Memory Test, Assessment Battery-Mazes, Category Fluency and Test-Managing Emotions of case group were significantly lower than those of control group (P<0.05). ③ Correlation between serum inflammatory factors and clinical symptoms: There was no correlation between serum inflammatory factors and psychiatric symptoms in schizophrenia. ④ Correlation between serum inflammatory factors and cognitive functions: The levels of IL-6 (rs=-0.33, P<0.05) and IL-8 (rs=-0.50, P<0.01) in case group were significantly negatively correlated with the scores of Space Scan test. 【Conclusion】 Patients with schizophrenia are presented with immune dysfunction, and the latter is correlated with cognitive impairments.

【Objective】 To explore the effect of childhood maltreatment on clinical symptoms and early efficacy of antipsychotics in patients with schizophrenia. 【Methods】 Totally 73 schizophrenic patients were divided into mild maltreatment group(n=42) and severe maltreatment group(n=31) according to the Child Trauma Questionnaire(CTQ). The Positive and Negative Symptom Scale(PANSS) and Clinical Global Impression(CGI) were measured and compared between the two groups at baseline and 3 weeks after antipsychotic treatment to analyze the correlation between child maltreatment experience and mental symptoms and the response to early treatment of antipsychotics. 【Results】 PANSS positive factor score(P=0.026) and cognitive deficit factor score (P=0.042) were significantly higher in severe abuse group than in mild abuse group. The positive factor was significantly positively correlated with emotional abuse factor in CTQ score(r=0.257, P=0.028), and the cognitive deficit factor was significantly positively correlated with emotional neglect factor(r=0.283, P=0.015). After antipsychotic treatment, the reduction rate of PANSS negative factor in severe abuse group was significantly lower than that in mild abuse group(P=0.035), and had the highest correlation with CTQ physical abuse factor(r=-0.302, P=0.011). 【Conclusion】 The severity of childhood maltreatment experienced by schizophrenic patients is more related to positive symptoms and cognitive deficits, and more childhood maltreatment experience will affect the improvement of negative symptoms by antipsychotics, suggesting a poor prognosis.