B7H1 is a recently described B7 family member.Ligation of PD-1 receptors with B7hl on the surface of activated T cell inhibits T cell proliferation and cytokine production. B7H1 plays a negative regulatory role in peripheral tolerance, autoimmune diseases and chronic infections.B7H1 also has been found to be largely expressed on a broad range of cancers and is thought to contribute to immune evasion by cancers. Blockade of B7H1/PD-1 pathway may contribute to the treatment of autoimmune diseases and maligant tumors.

Objective To summarize the methods of multiple digital replantation in different stages and improve the survival rate of replanted digits Methods In the procedure of replantation for fingertip one artery and one vein were anastomosoed, or one atrery was anastomosed accompanied with pulling out the nail and cutting small incision For middle of digit one artery and one vein were anastomosed For the proximal digit the ratio of anastomose for arteries and veins was 1 to 2 or 2 to 2 Superficial vein from arm or artery from the other finger was used if defection of vessel occur Results One hundred and twenty nine digits survived among the 142 replanted digits from 58 cases (survival rate was 90 8%),among which 113 fingers from 46 cases were subjected to following up form 3 months to 3 years, the rate of excellent and good was 85 8% Conclusion It takes more time and higher techniques to replant multiple digits To improve the survival rate, it is important to anastomose vessel excellently, deal with the defection of vessel correctly, and treat postoperative vessel crisis properly In addition, training exercise plays an important role in fnnctional recovery

Aim To study the role of calcineurin signal transduction pathway in the anti-hypertrophic effect of L-arginine in vivo and in vitro.Methods The hypertrophic effects was assayed by calculating the right ventricular hypertrophy index(RVHI=right ventricle weight/left ventricle and septum weight),and atrial natriuretic peptide(ANP)mRNA expression in rat right ventricle hypertrophy model induced by monocrotaline(MCT) or by measuring the cell diameter,protein content,and ANP mRNA expression in hypertrophic cardiomyocyte induced by prostaglandin F2?(PGF2?).For mechanism studies,the intracellular free calcium concentration([Ca2+]i) in cultured cardiomyocytes was measured by using Fura 2/AM as a fluorescent indicator.ANP and CaN mRNA expressions,and expressions of CaN and its downstream effectors,NFAT3 and GATA4 proteins were assayed by RT-PCR and Western blot,respectively,in vivo and in vitro.Results In MCT-hypertrophic model,prevention-and treatment-administration of L-arginine,a nitric oxide(NO) precursor,200 mg?kg-1?d-1,could obviously inhibit the elevated RVHI and ANP mRNA expression;similar to that found in vivo.Addition of L-arginine 1 mmol?L-1 could markedly inhibit the increased cell diameter,protein content and the expression of ANP mRNA in the hypertrophic cardiomyocyte induced by PGF2? 100 nmol?L-1,and it could also decrease the elevated [Ca2+]i in vitro;notably,the above dose or concentration of L-arginine could blunt the elevated expressions of calcineurin mRNA and the calcineurin-,NFAT3-,GATA4-proteins induced by MCT or by PGF2?.These effects of L-arginine were blocked by NG-nitro-L-arginine-methyl ester,a NO synthase inhibitor,in vivo and in vitro.Conclusion These results suggest that calcineurin signal transduction pathway may play an important role in the NO-induced inhibition of cardiac hypertrophy.The anti-hypertrophic effects of L-arginine may involve the decrease of [Ca2+]i,and then inhibit the activated calcineurin pathway,through the release of NO.

By inflicting the hindlimbs of dogs with steel bullets in different velocities, a model of traumatic stress was reproduced. The contents of myelin basic protein (MBP) and endothelin 1 (ET1) in cerebrospinal fluid (CSF) were determined with ELISA and radioimmunoassay methods, and the wltrastructural changes in limbic system were studied with neuropathological techniques. The MBP level and ET1 contents increased markedly in CSF, and neuronal degeneration and nerve fiber demyelination were seen in the hypothalamus and hippocampus in high speed missile group. The results indicate that the hypothalamus and hippocampus were vulnerable in severe injury of remote tissues,and it might be one of the important neuropathological basis for changes in the early stage of posttraumatic stress disorder (PTSD). The results also suggested that the CSF MBP and CSF ET1 determinations might serve as sensitive indicators for central nervous system damage in stress disorder following severe injury.

Objectlve To study the significance of injury and posthumous changes to the axonal in brain stem and provide evidence to the forensic discrimination of brainstem injury. Methods Select the cases that died of the primary brainstem injury or other disease randomly, All cases were divided into control group and experimental group, control group and experimental group that were autopsied at the postmortem interval less than 24h or 48h, or longer than 24h or 48h. The brainstem tissue were cut and stained by silver; Two hundred four samples were observed in microscope and selected 9～10 widest axonal to measure its diameter, then analysis the data. Results There is significant difference in axonal diameter of midbrain and mudella between control group (not including those cases died of cardiovascular diseases) and experiment group (P0.05). Conclusion The axonal swelling of the brainstem is closely related with the traumatic injury, so axonal swelling is a finding useful for identification of traumatic brainstem lesions, but death from cardiovascular diseases should be excluded.

Aim To investigate the effect of GW0742 on the endothelial dysfunction induced by high glucose
(glucose at 55 mmol · L -1 )in isolated rat thoracic aorta and its related mechanisms.Methods The end
othelium-dependent relaxation of acetylcholine was per-formed in the absence or presence of GW0742 at differ-ent concentrations under high glucose condition.The structure of aorta was observed by HE staining.Moreo-ver,the content of NO was also measured by nitrate re-duction method.The mRNA and protein expression were detected by quantitative real-time PCR and West-ern blot,respectively.Results Compared with the control group,acetylcholine-induced vasodilatation was impaired by high glucose.Meanwhile,the structures of endothelial cells and smooth muscle cells were also in-terrupted.Furthermore, the expressions of PPARβmRNA and protein reduced while the NF-κB p65 ex-pression increased significantly which occurred in par-
allel with decreasing eNOS expression and NO concen-tration (P <0.01 ).GW0742 (0.01 ,0.1 ,1 μmol· L -1 )restored the relaxation of acetylcholine in a dose-dependent manner,and reversed the mRNA and pro-tein expression of PPARβ,NF-κB p65 and eNOS,as well as NO content (P <0.01 ).Conclusion GW0742 attenuates the injury of endothelial dysfunc-tion induced by high glucose,which may be,at least partly,mediated by the up-regulation of PPARβ,then the down-regulation of NF-κB,and the activation of eNOS-NO signal pathway.

Objective To investigate the correlation between cognitive function and cerebral microbleeds (CMBs) in patients with small artery occlusive stroke (SAO).Methods The patients with SAO in Nanjing Stroke Registration Program were recruited from January 2011 to May 2011.The Montreal Cognitive Assessment (MoCA) was used to conduct the cognitive evaluation.At the same time,conventional MRI sequences and susceptibility-weighted imaging (SWI) were used to detect CMBs.Results A total of 70 patients with SAO were included in the study,48 of them had abnormal MoCA scores ( ＜26 points) and 22 of them had normal MoCA scores (≥26).The age of patients (t =-2.237,P =0.023),years of education (t =2.297,P =0.029),history of hypertension (x2 =2.297,P =0.025 ),severity of white matter hyperintensities (Z =-3.263,P =0.001) and presence of CMBs (P =0.001) were associated with the abnormal MoCA scores in patients with SAO.Logistic regression analysis showed that after adjusting for age,sex,white matter lesions,hypertension,diabetes and coronary heart disease,the presence of CMBs (odds ratio 5.648,95％ confidence interval 1.105-28.869; P =0.038) was still an independent risk factor for abnormal MoCA scores.The more serious of CMBs,the lower the MoCA scores (r =- 0.532,P ＜ 0.001 ).In patients with CMBs,the cognitive domain,such as the total MoCA score (t =5.180,P ＜ 0.001 ),visuospatial/executive function (t =3.924,P ＜ 0.001 ) and attention (t =4.309,P ＜ 0.001 ) were impaired significantly.The CMBs at different parts resulted in cognitive impairment in the related fields.Conclusions The numbers of CMBs and their locations were closely associated with cognitive impairment in patients with SAO.

Objective To investigate the related risk factors for small artery occlusion (SAO) and its 2 subtypes. Methods The clinical and imaging data in 291 patients with first-ever stroke who met the TOAST criteria of large artery atherosclerotic stroke (LAA) or SAO were collected from the Nanjing Stroke Registry Prog-am from December 2009 to November 2010. All the patients were divided into a LAA group (n = 120) and a SAO group (n = 171). The latter was redivided into either a lacunar infarction with ischemic leukoaraiosis (ILA) subgroup (n = 84)or an isolated lacunar infarction (ILI) subgroup (n = 87). The risk factors of the LAA group and SAO group and its subgroups were compared. Multivariate logistic regression analysis was conducted and the independent risk factors were screened. Results The mean age in the SAO group was larger than that in the LAA group. The proportion of the patients with hypertension and the serum homocysteine (Hcy) level were significantly higher than those in the LAA group (all P ＜0. 05). Multivariate logistic analysis showed that the advanced age (odds ratio, [OR] = 1.041,95% confidence interval [CI] 1.02-1.06, P = 0.045), hypertension (OR = 2. 912,95% CI 1. 11-6. 46, P =0. 031) and increased plasma Hcy (OR = 1. 109, 95% CI 1. 11-1. 32, P =0. 001) were the independent risk factors for SAO. The advanced age (OR = 1. 047,95% CI 1.00-1.09, P = 0.043), hypertension (OR = 2. 632, 95% CI 1.08-6.41, P= 0.033) and increased plasma Hcy (OR = 1. 211, 95% CI 1. 11-1. 32, P ＜0. 001) were the independent risk factors for ILA, while the hypercholesterolemia (OR =0. 136, 95% CI 0. 05-0. 37, P ＜0. 001) was the independent risk factor for ILI. Conclusions The advanced age, hypertension and increased plasma Hcy level may play important roles in the pathogenesis of SAO. The hypercholesterolemia is an independent risk factor for ILI, while advanced age, hypertension and increased plasma Hcy level are the independent risk factors for ILA.

Aim To investigate the effect of polydatin on cardiomyocyte hypertrophy induced by high glucose (25.5 mmol·L -1 )and insulin (0.1 μmol ·L -1 ) (HGI)and its possible influence on peroxisome prolif-erator-activated receptor-β (PPARβ)/nuclear tran-scription factor-κB (NF-κB)/nitric oxide (NO)signa-ling pathway.Methods The cardiomyocyte hypertro-phy was characterized in rat primary cardiomyocytes by measuring the cell surface area,protein content,and atrial natriuretic factor (ANF)mRNA expression.The mRNA and protein expressions were measured by qRT-PCR and Western blotting,respectively.The activity of NO synthase (NOS)and NO content were measured by reagent kit through ultraviolet spectroscopy.Results HGI significantly induced cardiomyocyte hypertrophy which increased the cell surface area,protein content and ANF mRNA expression (P <0.01 ).Meanwhile, the expressions of PPARβmRNA and protein reduced while the NF-κB p65 and iNOS expressions increased significantly which occurred in parallel with rising NOS activity and NO concentration (P <0.01 ).Polydatin (0.1,1,10 μmol·L -1 )inhibited the cardiomyocyte hypertrophy induced by HGI (P <0.01 ),and re-versed the mRNA and protein expressions of PPARβ, NF-κB p65 and iNOS,and NOS activity,as well as NO content.These effects of polydatin were abolished by GSK0660 (1 μmol·L -1 ),a selective PPARβan-tagonist (P <0.05 ).Conclusion Polydatin resists HGI-induced cardiomyocyte hypertrophy,which may be mediated by PPARβup-regulation,and then NF-κB-iNOS-NO pathway inactivation.

AIM:To study the role of prostaglandin F2?(PGF2?) in cardiac hypertrophy and its relation with calcineurin(CaN) signal transduction pathway in vitro.METHODS:The cultured neonatal rat cardiomyocyte was used to observe the hypertrophic effect of PGF2?,and the hypertrophic response was assayed by measuring the cell diameter,protein content and atrial natriuretic factor(ANF) mRNA expression.For mechanism studies,the intracellular free calcium concentration([Ca2+]i) in cultured cardiomyocytes was measured by using Fura-2/AM as a fluorescent indicator.ANF and CaN mRNA expressions,and the expressions of CaN and its downstream effectors,NFAT3 and GATA4 proteins were assayed by RT-PCR and Western blotting,respectively.RESULTS:In cultured cardiomyocytes,PGF2? induced profound hypertrophic morphology change and the significant increase in cell diameter,and protein content in a concentration-dependent manner compared with those in vehicle control(P