Objective To study effect of Tanshinone ⅡA (Tan ⅡA) on the content of NO and the activities of NOS and iNOS in cerebral ischemia reperfusion (I/R) injury rats,and explore its protective mechanism. Methods Rats were randomly divided into 4 groups,which were sham operated group,I/R group,low dose Tan ⅡA treated group and high dose Tan ⅡA treated group. The focal middle cerebral arterymocclusion (MCAO) model was made by suture-occluded method. Rats were pretreated with Tan ⅡA,ig for 3 d before MCAO. After 90 min MCAO following 24 h of reperfusion,pathomorphologic changes was investigated with HE staining. The content of NO and the activities of NOS and iNOS was also determined. Result The change of ischemic impairment in low or high dose Tan ⅡA treated group was lighter than that of I/R group,and high dose Tan ⅡA treated group was lighter than that of low dose Tan ⅡA treated group. Compared with sham operated group,the content of NO and the activities of NOS and iNOS increased at 24 h of reperfusion in the ischemic territory (P

0 05) Conclusion There is significant increase in the levels of serum myocardial enzyme and CSF LDH of adult patients with acute intracranial infection The levels of serum myocardial enzyme and CSF LDH is helpful to the diagnosis and the differential diagnosis of intracranial infection in early stage

Objective To approach the effects of Gingkgo biloba extra(GBE)on expression of P-selectin and myeloperoxidase(MPO)activity of cerebral ischemia-reperfusion injury in rats.Methods The rats were randomly divided into sham operated group,ischemia-reperfusion group,low dose GBE group and high dose GBE group.The models of ischemia-reperfusion were established by focal middle cerebral artery occlusion(MCAO)method.Rats were given high or low dose GBE intraperitoneally,30 min before MCAO.The expression of P-selectin was tested by immunohistochemistry and the MPO activity by chromatometry in the rat brain.The volume of cerebral infarction and the pathologic changes were observed by HE staining and TTC staining.Results(1)Compared with sham operated group,the expression of P-selectin and MPO activity were increased in models of ischemia-reperfusion(allP

Objective To study the effect of Tanshinone ⅡA(Tan ⅡA) on the contents of nitrous oxide(NO) and the activities of nitric oxide synthase(NOS) and immunologic NOS(iNOS) following cerebral ischemia reperfusion(I/R)injury in rats.Methods 40 Wistar rats were randomly divided into 4 groups,which were sham group,I/R group,low dosage Tan ⅡA treated group and high dosage Tan ⅡA treated group.The focal middle cerebral artery occlusion(MCAO) model was made.Rats were pretreated with Tan ⅡA for 3 d respectively before MCAO.After 90 min MCAO following 24 h of reperfusion,HE staining was investigated.The contents of NO and the activities of NOS and iNOS were also investigated.Results The change of ischemic impairment in low or high dosage Tan ⅡA treated group was lighter than that of I/R group,and high dosage Tan ⅡA treated group was lighter than that of low dosage Tan ⅡA treated group.Compared with the sham group,the contents of NO and the activities of NOS and iNOS increased in the ischemic territory(P<0.05).Compared with I/R group,low and high dose Tan ⅡA treated group reduced the contents of NO and the activities of NOS and iNOS dose-dependently(P<0.05).Conclusion Tan ⅡA may reduced cerebral ischemia-reperfusion injure by reducing the contents of NO and the activities of NOS and iNOS dose-dependently.

Objective To study the effect of tanshinone ⅡA on the expression of P-selectin and ICAM-1 after cerebral ischemia reperfusion (I/R)injury in rats. Methods Rats were randomly divided into 4 groups: Sham operated group, I/R group, low dose Tan ⅡA treated group and high dose Tan ⅡA treated group. The focal middle cerebral artery occlusion (MCAO) model was made by suture-occluded method. Rats were pretreated with Tan ⅡA, ig for 3d,respectively before MCAO. After 90min MCAO following 24 hours of reperfusion, the expression of P-selectin and ICAM-1 was detected with using immunohistochemistry method. Result Compared with sham operated group, the expression of P-selectin and ICAM-1 increased after reperfusion for 24 hours in the ischemic territory(all P＜0.01).Compared with I/R group, the expression of P-selectin and ICAM-1 decreased in a dose dependent manner in low and high dose Tan ⅡA treated group(P＜0.01).Compared with that of I/R group, cerebral infarction volume was decreased in a dose dependent manner in low dose Tan ⅡA treated group and high dose Tan ⅡA treated group(all P＜0.01).The change of ischemic impairment in low or high dose Tan ⅡA treated group was less than that in IR group, and the change of ischemic impairment in high dose Tan ⅡA treated group was less than that in low dose Tan ⅡA treated group. Conclusion Tan ⅡA may reduce cerebral ischemia-reperfusion inflammation injure by decreasing the expression of p-selectin and ICAM-1.Tan ⅡA plays protective effect on cerebral ischemia injury, especially when high dose of Tan ⅡA(30mg/kg)was used.

Objective To study the effect of procyanidin on neural cell apoptosis and the expression of Caspase-3 of cerebral ische-mia reperfusion(I/R) injury in rats. Methods 40 rats were randomly divided into 4 groups, which were sham operated group, I/R group, low dose procyanidin treated group and high dose procyanidin treated group. The focal middle cerebral artery occlusion (MCAO) model was made by suture-occluded method. After MCAO for 90min following 24h of reperfusion, neural cell apoptosis and the expression of caspase-3 was investigated with TUNEL and immunohistochemistry. HE staining and Trc staining was also used. Result Compared with sham opera-ted group, neural cell apoptosis rate and the expression of caspase-3 were increased at the 24th hour of reperfusion in the ischemic territory(P < 0.05) . Compared with I/R group, low and high dose procyanidin treated group reduced expression of caspase-3 and neural cell apopto-sis rate in a dose-dependent manor (P <0.05). The change of ischemic impairment in procyanidin treated group was less than that of I/R group, and the change of high dose procyanidin treated group was less than that of low dose procyanidin treated group. Compared with that of I/R group, cerebral infarction volume of procyanidin treated group was decreased in a dose-dependent manor (P < 0.05). Conclusion Procyanidin may reduce cerebral ischemia-reperfusion injure by reducing expression of caspase-3 and neural cell apoptosis.

Objective It is to observe the influence of atorvastat on the clinical therapeutic effect in the patients with cerebral infarction and lipid lowering, C-reactive protein level. Methods 60 patients with cerebral infarction are admined by atorvastatin 20mg,orally taking, 1 time per day,course of treatment for 4 weeks. Observing the variation of the high sensitivity C-reactive protein(hs-CRP) and concentration of blood fat in the circa about treatment. Results Treatment group's excellence rate is 70.0 %, total effective rate is 86.7 % after 4 weeks' atorvastatin treatment. It obviously outweighs the control group(43.3 % and 66.7 % ) ( P＜0.05 ) without evident adverse effect; TC, LDL-C significantly step clown and HDL-C(P＜0.05 ) significantly steps up comparing pretherapy. They also obviously outweigh the control group(P＜0.05 and P＜0.01 ). The blood serum hs-CRP level obviously decreases( P＜0.01 ). Conclusion Atorvastat can not only lower the lipid, but also degrade the concentration of CRP.It has significant clinical therapeutic effect while without evident adverse effect. The early use of atorvastatin can prevent and control ischemic cerebrovascular disease preferably. It can also reduce the genesis of cerebrovascular disease and improve the prognosis of cerebrovascular disease.

Foot-and-mouth disease virus (FMDV) is a positive-sense RNA virus which has caused severe damage to world-wide livestock industry. The extensive genetic and antigenic diversity observed in the evolution of FMDV is generally the obstacle for controlling the disease. The homologous recombination, as a significant force driving the evolution of virus, has also effect on the epidemiological trait of FMDV. However,the role of homologous recombination in the diversification of FMDV in China has not investigated. So it is necessary to study the homologous recombination underlying the evolution of FMDV to control FMD. Based on a sound evolutionary framework, molecular evolutionary analysis was used to identify the putative recombinants. All complete FMDV genomes from China were respectively retrieved from GenBank. Homologous recombination was identified using Simplot program. Phylogenetic relations were analyzed to determine the recombination events among these FMDV isolates by using MEGA 4. The isolates O/NY00, O/China/1/99Tibet, O/Tibet/CHA/99, O/OMIII and O/ES/2001 among 16 FMDVs were identified as putative recombinants by analyzing the FMDV genomic sequences extracted from GenBank. The recombination events frequently happen between serological type Asia1 and O which are endemic FMDV circulating in China, suggesting frequent cross infection of FMDV in China. This situation further makes controlling FMDV in China more difficult. Moreover, serotypic conversion of FMDV between Asia1 and O was detected to be due to homologous recombination. These results provided clues for understanding the antigenic and genetic diversification in FMDV, and shed lights on the potential vaccination and treatment of FMD.

Nonalcoholic fatty liver disease (NAFLD) has become the most important chronic liver disease in the world, but there is still no approved drug for clinical practice. Due to the heterogeneity of NAFLD itself, although drug therapy is being developed, the response rate seems to remain low. In order to meet the needs of clinical trial design and provide accurate information for drug developers, relevant scholars have proposed to change the name of NAFLD to metabolic associated fatty liver disease This article summarizes the origin of NAFLD heterogeneity and the background of NAFLD renaming, so as to provide new ideas for accelerating the development of new therapies.

Objective To analyze the efficacy and safety of hypofractionated stereotactic radiotherapy ( FSRT ) combined with temozolomide ( TMZ ) for large brain metastases ( BMs ) in a prospective phaseⅡclinical trial.Methods From 2010 to 2015, a total of 33 patients were enrolled as subjects.The median Karnofsky Performance Status scores before and after treatment were 70 and 80, respectively.The major primary tumor was non-small cell lung cancer (57.6%).The brain metastasis had a diameter of≥3 cm or a volume of ≥6 cm3 .The radiation dose was 52 Gy in 13 fractions or 52.2 Gy in 15 fractions.Patients received TMZ at a dose of 75 mg/m2 per day concurrently.The radiotherapy was followed by 6 cycles of adjuvant treatment with TMZ (150 mg/m2, days 1-5, 28 days per cycle).Patients were reexamined by magnetic resonance imaging ( MRI) during the treatment.The radiation field would be shrunk if the gross target volume ( GTV) was reduced by≥20%.The treatment outcomes were evaluated by MRI at 2-3 months after treatment.Results The total numbers of tumors and GTVs were 95 and 38, respectively. Twenty-four (63%) out of the 38 GTVs had a volume larger than 10 cm3 and the median GTV was 15.3 cm3 (5.7-142.8 cm3).Twenty-two (67%) out of the 33 patients achieved field shrinking during the treatment, and the median reduction rate of GTV was 44%( 21%-88%) .The median total dose was 59.5 Gy, and 100%and 21.2%of patients completed the concurrent and adjuvant treatment with TMZ, respectively.In all patients, the overall response rate was 97.0%;the 1-year local control, intracranial progression-free
survival, and overall survival rates were 97%, 70%, and 62%, respectively;the median survival time was 15.3 months.The main adverse reactions were grade 1-2 nausea and vomiting.One patient got grade 3 liver function impairment.Conclusions FSRT combined with TMZ is a safe and effective approach for treating large BMs.More than 50%of patients can achieve field shrinking to shorten treatment duration and reduce toxicity.Clinical Trial Registry ClinicalTrials.gov,registration number:NCT02654106.