Brain-derived neurotrophic factor (BDNF) is one of the most prevalent growth factors in the central nervous system (CNS).In the development and maturation processes of the nervous system,BDNF plays an important role in maintaining neuronal function,promoting neuronal regeneration after injury,and preventing neuronal degeneration,etc.At present,many researchers are being dedicated to the research of BDNF for treatment of brain ischemia and have achieved some progress.This article reviews the molecular biological characteristics and biological function of BDNF,roles and mechanisms in cerebral ischemia,and the possibility as an intervention target of cerebral ischemia.

As a direct vascular recanalization method, safety and efficacy of mechanical embolectomy in acute ischemic stroke have been controversial. This article reviews the safety and efficacy of mechanical embolectomy in acute ischemic stroke via summarizing the development process of mechanical devices and the latest clinical trial results of mechanical embolectomy.

Objective:To investigate memory disorder in hippocampal infarction patient. Methods: A hippocampal infarction patient was examined by the MMSE and the WMS-RC. Results: Patient's performance on MMSE was within the normal range, but the short-term memory was impaired. Conclusion: Hippocampal plays an important role in encoding and storing new information.

Objective To investigate the effects of early physiotherapy in combination with atorvastatin on the levels of serum brain-derived neurotrophic factor (BDNF) and neurological function in patients with acute ischemic stroke.Methods Fifty patients with acute ischemic stroke were randomly divided into either an atorvastatin group (monotherapy group,n =25) or a early physiotherapy + atorvastatin group (combination treatment group,n =25).All patients received the prescribed drugs according to the diagnosis and treatment guidelines for ischemic stroke.The monotherapy group added atorvastatin calcium (20 mg,1 tablet every night orally).On the basis of the monotherapy group,the combination treatment group also conducted early physical therapy.At 2 and 6 weeks before and after treatment,a double-antboody sandwich enzyme-linked immunosorbent assay was used to detect the serum BDNF levels.The National Institutes of Health Stroke Scale (NIHSS) was used to evaluate the degree of neurological deficit.Barthel index (BI) was used to evaluate the activities of daily living.The modified Rankin scale (mRS) was used to assess the degree of disability.Results There was no significant difference in demographics and baseline data between the monotherapy group and the combination treatment group.The scores of NIHSS,BI,and mRS in both groups after treatment were significantly better than those before treatment (all P ＜ 0.001).There were no difference in the scores of NIHSS,BI and mRS at 2 weeks before and after treatment,but at 6 weeks after treatment,the scores of NIHSS (2.40 ± 1.38 vs.3.36 ± 1.73; P =0.035) and mRS (1.40 ± 0.87 vs.1.96 ±0.94; P =0.047) of the combination treatment group were significantly lower than those of the monotherapy group,and the BI scores (92.60 ±7.50 vs.85.20 ± 11.68; P=0.011) were significantly higher than those of the monotherapy group.After treatment,the serum BDNF levels were increased significantly in both groups.There were significant differences among all the time points (all P＜0.001).At 2 weeks after treatment,the serum BDNF levels (3.07 ±0.93 ng/ml vs.2.45 ±0.76 ng/ml; t =2.559,P =0.014) and at 6 weeks after treatment,those (2.90 ± 0.93 ng/ml vs.2.31 ± 0.77 ng/ml; t =2.433,P =0.019) in the combination treatment group were significantly higher than those in the monotherapy group.Spearman correlation analysis showed that the serum BDNF levels were significantly negatively correlated with the scores of NIHSS (r =-0.738,P ＜ 0.001) and mRS (r =-0.654,P ＜ 0.001),but they were significantly positively correlated with the BI scores (r =0.716,P ＜ 0.001).No serious adverse reaction occurred in both groups.Conclusions Early physiotherapy in combination with atorvastatin for the treatment of acute ischemic stroke can more effectively promote the recovery of neurological function,and its mechanism may be associated with the increased serum BDNF levels.

Objective:To construct the Escherichia coli (E. coli)expression system for preparation of the bone morphogenetic protein-2 (BMP2)with collagen-binding domain (CBD),and to study the methods and conditions for expression, purification and renaturation of CBD-BMP2.Methods:CBD sequence was cloned into the N-terminal of BMP2 sequence, the recombinant vector pet21b/CBD-BMP2 was constructed and transformed into E.coli BL21.The expression of recombinant protein was induced using isopropylβ-D-thiogalactopyranoside (IPTG) at 37 ℃.Ni-NTA chelate chromatography was used to purify CBD-BMP-2.Denaturing CBD-BMP2 was refolded by dilution method using ultrapure water.The refolding CBD-BMP2 was filtered through a 0.22μm microfiltration membrane for degermation.The recovery rate was calculated by the ratio of the protein concentration before and after degermation. The expression, purification, and renaturation of recombinant protein were detected by SDS-PAGE method.The concentration of CBD-BMP2 was detected by BCA assay.Results:The recombinant vector pet21b/CBD-BMP2 was successfully transformed into E.coli BL21,and the recombinant protein was expressed as inclusion bodies in E.coli.The SDS-PAGE results showed denaturing protein was dissolved in supernatant of lysis buffer with 8 mol·L-1 urea and the purified recombinant protein existed in elution buffer B with relative molecular mass about 14 000.Two bands (14 000 and 28 000)were seen in the SDS-PAGE picture,which indicated that the monomer was successfully refolded into dimer by dilution method.The concentrations of recombinant protein before and after degermation were 110 and 80 mg · L-1 , respectively, and the recovery rate was about 73%. Conclusion:The recombinant vector pet21b/CBD-BMP2 is transformed into E.coli BL21 successfully,and the recombinant CBD-BMP2 is expressed and refolded efficiently. The methods of prokaryotic expression system for preparing recombinant CBD-BMP2 protein are established.

Objective To evaluate the clinical efficacy and safety of akatinol memantine in the treatment of Alzheimer's disease (AD).Methods Two hundred and forty-one patients with AD were randomly assigned to receive 10 mg of donepezil daily or 20 mg of memantine daily for 24 weeks.The primary efficacy variables were the Clinician' s Interview-Based Impression of Change Plus (CIBIC-Plus),the Alzheimer Disease Assessment Scale-cognition (ADAS-cog) and the Activities of Daily Living (ADL).The secondary efficacy variables were the Neuropsychiatric Inventory (NPI) and the Mini-Mental Status Examination (MMSE).Results Two hundred and seven patients completed the study and were evaluated at week 24.Both memantine and donepezil had significant efficacies at the end point, according to the ADAS-cog, the ADL, the NPI and the MMSE.Patients receiving memantine had a similar outcome as those receiving donepezil, according to the results of all the variables changes (CIBIC-Plus: memantine 3.4±0.8vs donepezil 3.5±0.8; ADAS-cog: memantine-4.7±5.8 vs donepezil-4.6±6.5; ADL: memantine -2.4±6.7 vs donepezil-2.2±5.3 ; NP1: memantine-5.8±9.0 vs donepezil-3.1±8.5 ; MMSE:memantine 1.7±3.1 vs donepezil 1.8±2.8, all P >0.05).The adverse events were as following: donepezil group 41.88% and memanintine group 30.58%.Conclusion The memantine as a new drug for AD, has the similar efficacy as donepezil, and it is safe.