Objective To determine the appropriate concentration of ropivacaine for differential sensory and motor block of brachial plexus.Methods Ninety ASA Ⅰ - Ⅲ patients aged 16-75 yr weighing 40-85 kg undergoing upper extremity operation under axillary brachial plexus block were randomly divided into 3 groups according to the concentration of ropivacaine used for the block(n = 30 each): group A 0.15% ropivacaine;group B 0.10% ropivacaine and group C 0.05% ropivacaine.Axillary brachial plexus block was performed using ultrasound guidance and electric nerve stimulation.Sensory and motor block were assessed and recorded at 10,30,60and 240 min after local anesthetic injection(T1-4).The rate of adequate sensory block,the rate of differential sensory and motor block(the areas innervated by radial,median and ulnar nerves were numb but the patients could still move their elbow,wrist and fingers)and effectiveness of the block(excellent - completely no pain;good slight pain,iv fentanyl was needed;poor -rescue brachial plexus block was needed or general anesthesia was induced).Operation time and duration of analgesia and success rate of the block were recorded.Results 0.15%ropivacaine produced excellent or good block and no failure in group A.The rate of differential sensory and motor block was significantly higher in group B(0.10% ropivacaine)than in group A.The effect of block with 0.05% ropivacaine was unsatisfactory in group C.Conclusion Axillary brachial plexus block with 0.10% ropivacaine can induce differential sensory and motor block in the majority of patients.

Objective To investigate the relationship between single nucleotide polymorphisms (SNPs) of UGT1 A6 and aspirin response in a cohort of Chinese Han population.Methods A total of 323 ischemic stroke patients consecutively registered in Nanjing Stroke Registry Program from September 2011 to October 2014 were enrolled.Three SNPs (rs6759892,rs2070959 and rs1105879) of UGT1A6 were genotyped in these ischemic stroke patients.Association of genotypes and aspirin response was evaluated by generalized linear model.Indicated with the inhibition rate of platelets,aspirin response was assessed by thromboelastograph.Results The mutation allele (G) of rs2070959 was positively related to platelets inhibition (β =0.084,P =0.010,Pcorrected =0.029),especially in male (β =0.098,P =0.006,Pcorrected =O.019).The dominant models of rs6759892,rs1105879 were also modestly related to aspirin response (P=0.015,Pcorrected=0.046 in both SNPs) in male.Thus the polymorphisms of UGT1A6 showed a relationship with aspirin response,especially in males.Conclusions The results indicated that genetic polymorphism of UGT1A6 might have an effect on individuals' aspirin response,especially in males.These findings can help clinicians to optimize the antiplatelet therapy for ischemic stroke patients.

Stroke has become the leading cause of death in Chinese residents. As the cornerstone of the primary and secondary prevention of ischemic stroke, aspirin can prevent the occurrence and recurrence of ischemic stroke in a certain extent. However, some patients stil have vascular events after taking aspirin regularly or higher platelet aggregation rate. This phenomenon is caled aspirin resistance or aspirin low reactivity. This article reviews the occurrence, detection methods, and treatment measures of aspirin resistance in patients with ischemic stroke.

Objective Meningovascular syphilis is the intima inflammation of blood vessels caused by the syphilitic infec-tion, which is associated with the occurrence of ischemic stroke.The study analyzed the clinical, imaging features and prognosis for meningovascular syphilis so as to improve its diagnosis and treatment. Methods 14 patients diagnosed with meningovascular syphilis were collected prospectively from December 2007 to March 2015 in the neurological department of Jinling Hospital.The patients were followed for a period of 21.5(range 10.2~37.9)months,and the prognosis were evaluated. Results Patients with meningovascular syphilis presented with dizziness, hemiplegia, hemidysesthesia and cognitive decline.Lesions showed multiple, scattered on MR ima-ging, intracranial vascular stenosis was seen in the CTA/MRA, and the laboratory examination had characteristic changes.With a large dose and sufficient courses of penicillin treatment, meningovascular syphilis may hopefully get predominant effects.78.57%patients got good prognosis(modified Rankin Scale ,mRS≤2)at 3 months and 85.71% patients got goodlong-term prognosis(mRS≤2). Conclusion Meningovascular syphilis was usually presented as acute onset, lacks the specific clinical and neuroimaging manifesta-tions.Most patients has favourable prognosis after treatment of syphilis with full course of penicillin.

Objective It remains to be confirmed whether tissue kallikrein has neuroprotective effect in diabetes-induced stroke.This study was to investigate the neuroprotection of tissue kallikrein against cerebral ischemia-reperfusion injury in diabetic rats. Methods Healthy male SD rats were randomly divided into a sham operation, a saline control, and a tissue kallikrein group.Diabetes mellitus was induced in the animals by intraperitoneal injection of streptozotocin and the model of focal cerebral ischemia-reperfusion was made with an intraluminal vascular occlusion method. At 24 hours after modeling, we obtained the neurological deficit score, in-farct size, and brain water content, counted Iba1-and MPO-positive cells by immunohistochemistry, and determined the expressions of ICAM-1 and VCAM-1 by real-time PCR. Results In comparison with the saline controls, the rats treated with tissue kallirein showed significant decreases in the neurological deficit score (P<0.01), the infarct size ([23.57 ±5.79] vs [47.97 ±1.19]%, P<0.01), brain edema ([81.73 ±2.10] vs [84.94 ±2.34]%, P<0.05), the counts of Iba1-and MPO-positive cells (12.33 ±4.46 vs 31.83 ±8.13 and 13.83 ±4.49 vs 37.50 ±7.64, both P<0.01), and the expressions of ICAM-1 and VCAM-1 (both P<0.05). Conclusion Tissue kallikrein has a neuroprotective effect against cerebral ischemia-reperfusion injury in diabetic rats, which may be associated with its anti-inflammation property.

Objective Hypertension is a leading modifiable risk factor for cardiovascular disease .However , a lot of hyper-tension patients hold inactive attitudes to hypertension treatment .The purpose of this study was to investigate the relationship between previous treatment of hypertension and stroke severity in acute ischemic stroke . Methods We retrospectively analyzed the clinical data of 653 in-hospital ischemic stroke patients with hypertension between January 2011 and December 2014 .According to the National Institutes of Health Stroke Scale (NIHSS) at admission, the stroke patients were divided into a mild group (NIHSS≤3) and a severe group (NIHSS >3) and, based on their history of hypertension treatment , allocated to a regular treatment, an irregular treatment, a non-treatment , and an unawareness group .We studied the relationship of previous hypertension treatment with stroke severity by Spearman correlation analysis and identified the potential factors associated with stroke severity by multivariate logistic regression anal-ysis. Results Previous treatment of hypertension was positively correlated with stroke severity (r=0.146, P=0.000 2).Compared with the patients of the regular treatment group , those in the irregular treatment group (OR: 2.21; 95%CI:1.39 -3.52; P =0.001), non-treatment group ( OR: 2.18; 95%CI: 1.41 -3.36; P =0.0004) and unawareness group (OR:1.80;95%CI:1.12-2.88; P=0.015) tended to have more severe stroke. Conclusion Previous treatment of hypertension is closely related to the severity of ischemic stroke .

Objective To study the changes in interleukin-32 (IL-32) in rats with Klebsiella bacillus pneumonia and approach its significance. Methods Seventy-two Sprague-Dawley(SD)rats were divide into control group,model group and experimental group by the method of random digits table,then the experimental group was subdivided into 4 hours and 1,3 and 5 days experimental subgroups(each n=6). The rat model of Klebsiella bacillus pneumonia was established by injection of 0.3 mL Klebsiella bacterial suspension into the trachea. Before the establishment of the model in the experimental group,IL-32 inhibitory agent,protease activated receptor-2(PAR2) was injected into the abdominal cavity. After model establishment,at different time points,blood was collected via tail vein to observe the changes in serum levels of IL-32,tumor necrosis factor-α(TNF-α),IL-6 and IL-8 in all the groups. The lungs were removed and stained with hematoxylin-eosin(HE)method to investigate the histopathological changes of the lung tissues under the light microscope. Results Compared to the control group, with the prolongation of time the levels of IL-32,TNF-α,IL-8 and IL-6 were increased gradually in the model group,and reached their peaks at 3 days〔IL-32(ng/L):84.40±28.24 vs. 18.57±3.86,t=5.544,P=0.002;TNF-α(ng/L):79.27±14.64 vs. 17.82±3.86, t=9.994, P=0.000;IL-8(ng/L):55.85±10.90 vs. 16.66±3.76,t=8.544, P=0.000;IL-6(ng/L):56.65±2.57 vs. 28.48±2.11,t=19.693,P=0.000〕;PAR2 could inhibit above indexes significantly,there was statistical difference at 3 days compared with the model group〔IL-32(ng/L):54.13±6.68 vs. 84.40±28.24,t=2.560,P=0.046;TNF-α(ng/L):49.12±3.56 vs. 79.27±14.64,t=4.901,P=0.003;IL-8 (ng/L):22.95±2.52 vs. 55.85±10.90,t=7.204,P=0.000;IL-6(ng/L):36.49±2.63 vs. 56.65±2.57,t=13.443, P=0.000〕. Under the light microscope,the inflammatory changes in the lung tissue in experimental group were milder than those in the model group. Conclusion As a pro-inflammatory cytokine,IL-32 can induce the production of TNF-α,IL-6 and IL-8,and the inhibition of IL-32 production may play a role in suppression of the development of Klebsiella bacillus pneumonia.

Objective To analyze the content of clinical practice guidelines and provide references for developing Chinese clinical practice guideline of dysphagia with stroke. Methods Content analysis was used to analyze the contents of clinical practice guideline related to dysphagia with stroke which were searched from Internet. Results Ten guidelines were included which were consisted of 2 Chinese guidelines and 8 English guidelines. These guidelines' themes were stroke involving dysphagia, and only two of them were targeted on dysphagia. And one of them was targeted on dyshagia with stroke. Only one guideline hadn't been revised yet, and the rest had been updated. Twenty items were identified from 10 guidelines as been concerning to dysphagia with stroke. Conclusions Current clinical practice guideline about dysphagia with stroke can be used to guide clinical practice. However, some recommendations of guidelines are not clear and not updated in time which can't provide specific references for dysphagia. A clinical practice guideline which is suitable for dysphagia with stroke in China should be developed based on best evidece and Chinese actual conditions.

Objective: To investigate the effect of thapsigargin (TG) which can induce endoplasmic reticulum stress (ERS) on the replication of coxsackievirus B 3 (CV-B3). Methods: After 10 MOI CV-B3 infected HeLa cells were exposed 0.25 μmol/L TG for 3 h, 6 h and 9 h, virus RNA of HeLa cells were extracted and viral replication was evaluated by real time PCR. After 0.25 μmol/L、0.08 μmol/L and 0.025 μmol/L TG exposed, the plaque of CV-B3 was used to confirm further replication of CV-B3. To verify TG induced ERS through three signal pathway, one of among PERK, ATF6 and IRE1 inhibitors GSK2656157, AEBSF and STF-083010, and 0.25 μmol/L TG were used in HeLa cells infected with 10 MOI CV-B3, replication of CV-B3 was evaluated by qRT-PCR. Results: The stimulation of TG did not induce increase of virus replication after post-infection 3 h. However, TG induced replication of virus to increase 2.5 times after post-infection 6 h and 158.6 times after post-infection 9 h. And, the area of viral plaque was significantly increased. ATF6 inhibitors AEBSF significantly inhibited promotion of virus replication from TG. Conclusions TG can promote the replication of CV-B3 through ATF6 signal pathway.

Objective: To observe the changes of endogenous small interfering RNA (siRNA) in H1-Hela cells infected with human rhinovirus 16 (HRV 16). Methods: To determine whether HRV16 infection induced the changes of siRNA, H1-HeLa cells were infected with HRV16 for 12 h, 24 h and 36 h, siRNAs were detected by high-throughput sequencing, second-generation sequencing) and qRT-PCR. Results: The result showed that siRNA was generated differently at different time points post-infection, among which novel_sir907 and novel_sir1950 decreased at three time points. Further validation by qRT-PCR showed that novel_sir907 decreased at 12 h, 24 h and 36 h post-infection compared with the cell control, but novel_sir1950 increased at 12 h then decreased at 24 h and 36 h. Conclusions HRV16 infection induces changes endogenous siRNAs.