Objective To investigate the significance and mechanism of intracerebroventricular injection viper venom nerve growth factor (Vngf) in rat neural plasticity after cerebral ischemia reperfusion injury.Methods Ninety Wistar male rats were randomly assigned into Vngf-25 U group (n = 18), Vngf-50 U group (n = 18), Vngf-100 U group (n = 18), ischemia reperfusion group (n = 18) and sham operated group.The expression of candidate plasticity-related gene 15(cpg-15) Mrna and nuclear factor of kappa B ( NF-Κb ) Mrna in rat brain tissues which were collection at 2,7,14 days after surgery were evaluated by the real time PCR.Results The expression of cpg-15 Mrna and NF-Κb Mrna began to increase after surgery( the F value of cpg-15:70.43, 34.11, 31.89, the F value of NF-Κb: 27.47, 34.56, 31.89,P＜0.01).At the same time, expression of cpg-15 Mrna and NF-Κb Mrna in the Vngf groups was significantly different from the I/R group and the sham operated group (the F value of cpg-15:48.18, 55.93, 78.43, the F value of NF-Κb: 45.92, 55.72, 50.49, P ＜0.01).The more Vngf were injected, the more cpg-15 Mrna and NF-Κb Mrna were expressed in Vngf groups.Conclusions The Vngf could accelerate neural plasticity and restore neurofunctional defect through up-regulated the expression of cpg-15 and NF-Κb.

ObjectiveTo verify the reliability of the mouse model of cerebral cortical microinfarct induced by two-photon microscopy and to explore its pathological changes.MethodsSeventeen male C57BL/6J mice were randomly divided into a microinfarct group (n=11) or a sham operation group (n=6).A thinned cranial window of 3 mm diameter was performed over the cerebral cortex with a high-speed micro-drill until the small blood vessels were clearly observed under a dissecting microscope.Then, a permanent single cortical penetrating arteriole occlusion was induced with a gradually enhanced ultrashort laser irradiation through the thinned cranial window with two-photon microscopy.At 7 days after modeling, the cerebral microinfarct volume was measured with HE staining, and the neuron loss, activation of glial cells and deposition of 3-nitrotyrosine were assessed using immunohistochemistry.ResultsThe target vessels of cerebral cortex in 8 (72.7%) mice were occluded and the microinfarcts formed in the microinfarct group, and the average microinfarct volume was 317.23±20.29 μm3.There were remarkable neuron loss and microglia infiltration in the infarcted core, a large number of reactive astrocytes surrounding the infarcted lesion, and massive deposition of 3-nitrotyrosine in the peri-infarct area.No infarcts were observed in the sham operation group.The deposition of 3-nitrotyrosine in the sham operation group was significantly less than that in the microinfarct group (8.00±1.48 vs.98.38±9.10;t=23.962, P<0.001).Conclusions The mouse model of cerebral cortical microinfarct induced by two-photon microscopy is reliable, and its histopathologic changes are consistent with the pathologic features of cerebral microinfarct.

Objective To investigate the cerebral ischemia/reperfusion protection mechanism of viper venom nerve growth factor(vNGF) by the change of expression of growth associated protein-43 (GAP-43) and neurological function.Methods 45 adult male Wistar rats (weight 220～280 g) were divided randomly into 3 groups: sham group(S, n=9), balanced salt solution group (BSS, n=9) and venom nerve growth factor group (vNGF, n=27). Each group was observed for 7 days. vNGF group was divided into 25 U, 50 U and 100 U subgroups respectively. The following indexes in 3 groups were observed respectively: neurologic deficits and the expression of GAP-43 (immunohistochemistry method).Results Neurological function: The scores of neurological function was 0 in S group. The neurological deficits score was lower at the same time in vNGF group than that in BSS group (P<0.05). Immunohistochemistry: GAP-43 expressed in both BSS group and vNGF group. The expression of GAP-43 in vNGF group increased in 25 U, and to maximum in 100 U. The expression of GAP-43 in BSS group was significantly lower than in vNGF group (P<0.05). Conclusion vNGF can effectively enhance and prolong the expression of GAP-43, increase the survival rats of nerve cells, and has the protection effect on nerve cells after cerebral ischemia injured.

Objective To investigate whether the median(50%)effective effect-concentration(EC50)of propofol inducing loss of consciousness (LOC) varies. Methods 56 patients undergoing gastroscopy under general anaesthesia were enrolled on the study. Anaesthesia was conducted with a target-controlled infusion(TCI) of propofol. The initial target effect-site propofol concentration (Ceprop) was 5.00 μg/mL and was adjusted stepwise by 0.50μg/mL by an up-down sequential method to reach no-movement. Results Propofol EC50 to induce no-movement was higher in patients with anxiety than those without anxiety(6.46μg/mL vs. 5.75μg/mL,P<0.05). Conclusions During general anaesthesia ,patients with anxiety had a higher propofol EC50 for no-movement compared with those without anxiety. Differences in preoperative anxiety levels may reduce anaesthetic effects.

Objective:To explore the relationship between serum anti-Müllerian hormone (AMH) level and related clinical factors in healthy females, and establish and validate equation of correlation between age and serum AMH level for healthy females.Methods:From March 2015 to December 2016, a total of 602 females who measured serum AMH level in Department of Nuclear Medicine, the Second Affiliated Hospital of Soochow University were retrospectively enrolled. All cases had relatively complete clinical data, and were divided into healthy group (484 cases, 20-52 years) and case group (118 cases, 20-42 years; patients with menstrual disorders). Relationships between serum AMH level and estradiol (E2), tesosterone (T), follicle stimulating hormone (FSH), luetinizing hormone (LH), body mass index (BMI) of healthy group were analyzed by Spearman rank correlation. Kruskal-Wallis rank sum test was used to analyze the relationship between history of gestation and serum AMH level. Serum AMH level of health group was processed to establish predictive equation for serum AMH level. Internal ( n=27) and external ( n=37) validation group were chosen from healthy females with serum AMH level measured to validate the equation, and signed rank test was used to analyze the data. Difference between serum AMH level in case group and healthy group with corresponding age was explored by independent-sample t test. Results:Serum AMH levels were positively correlated with E2 and T ( rs values: 0.263, 0.334, both P<0.001), and negatively correlated with FSH, LH, BMI ( rs values: from -0.515 to -0.110, all P<0.005). Predictive equation was established as LogAMH=-1.208+ 0.1×age-0.000 042×age 3 ( R2=0.735, P<0.001). No statistically significant difference was found between real serum AMH levels and calculated serum AMH levels in the internal and external validation groups ( z values: -1.62 and -1.52, both P>0.05). Females in case group ( n=118) and control group ( n=446) were divided into two sub-groups respectively (<35 years and ≥35 years), and serum AMH levels of case group were lower than those of control group with corresponding age ( t values: 18.64, 11.70, both P<0.001). Conclusions:In healthy females, serum AMH level is related to some clinical data. The equation between serum AMH level and age established in the study may provide reference for clinical diagnosis and treatment.

Objective:To explore the efficacy and safety of pretreating with oral immunosuppressants alone for ABO-incompatible (ABOi) renal transplant recipients with an initial isoagglutinin titer <1: 8.Methods:From September 2014 to October 2019, 16 cases of ABOi renal transplantation pretreated with oral immunosuppressants alone and 32 cases of ABO-compatible (ABOc) renal transplantation were recruited for comparing the inter-group incidence of graft function, acute rejection, infection and recipient and allograft survival.Results:The 16 ABOi renal transplantations were AB-to-A(n=4), AB-to-B(n=3), A-to-B(n=1), B-to-A(n=4), A-to-O(n=2) and B-to-O(n=2). The initial isoagglutinin titer (IgM & IgG) and that on the date of transplantation were both ≤1∶8. The median follow-up period was 495(90-1696) days. One patient in ABOi group underwent allograft nephrectomy due to hyperacute rejection. The graft survival rates were 93.75%(15/16) and 100%(32/32) in ABOi and ABOc groups respectively. No recipient died. No significant inter-group difference existed in postoperative renal function after 6 months (serum creatinine μmol/L: 114.30±28.13 vs. 106.08±23.80, P=0.38; eGFR ml/min/1.73 m 2: 64.93±19.60 vs. 82.34±22.58, P=0.13). In ABOi group, there were 3 episodes of postoperative infection, 2 episodes of acute rejection within 2 weeks (including 1 episode of hyperacute rejection) and 1 episode of acute rejection after 2 weeks; 5 episodes of postoperative infection, no acute rejection within 2 weeks and 5 episodes of acute rejection after 2 weeks in ABOc group. No significant inter-group difference existed in the incidence of infection or rejection ( P>0.05). Conclusions:Using oral immunosuppressant alone is both safe and feasible for ABOi renal transplantation recipients with an initial isoagglutinin titer ≤1∶8. It may greatly simplify the pretreatment scheme for those with a low initial isoagglutinin titer and lower the incidence of complications.