Codon is an important carrier of genetic information in organisms. In evolution, codon bias is formed in many organisms. In this study, the analysis of expressed genes in Lonicera japonica Thunb. is presented. The codon bias of genes with complete coding region is analyzed through CodonW. And we calculated the codon usage bias of hydroxycinnamoyl-CoA: quinate hydroxycinnamoyl transferase (HQT) genes. The results showed that L. japonica were bias toward the synonymous codons with A and T at the third codon position.

Objective To explore the effects of upper limb robot-assisted therapy on motor recovery in acute stroke patients. Methods From August, 2013 to September, 2014, 46 acute stroke patients at their first-ever stroke were enrolled and randomized into experimental group and control group with 23 cases in each group. Both groups received routine therapy. Additional robot-assisted therapy was provided to the experimental group, and additional repetitive movement training was provided to the control group, 30 minutes a day, 5 days a week for 12 weeks. Fugl-Meyer Assessment-Upper Limb (FM-UL), modified Ashworth Scale (MAS) and modified Barthel index (MBI) were used to assess the motor function of the upper limbs and hands, the muscular tension of elbow, and activities of daily living (ADL) before and after treatment. Results After treatment, the scores of FM-UA, MAS and MBI improved in both groups (t>3.856, Z>1.889, P<0.05), and the scores of FM-UA and MAS were better in the experiment group than in the control group (t=-2.386, Z=-2.625, P<0.05), however, there was no significant difference in the score of MBI between two groups (t=-1.326, P=0.098). Conclusion Upper limb robot-assisted therapy can facilitate the recovery of the motor function of upper limbs in acute stroke patient.

AIM　To investigate protective effects and mechanism of tanshinones on ischemia-like injury models. METHODS　Six ischemia models including hypoxia, hypoglucose, oxidant injury, caffeine injury, nitric oxide neurotoxicity and excitatory amino acid injury were used to assay the anti-ischemic roles of tanshinones in cultured primary cortex neurons. The changes of injuried cortex neurons were observed by the way of morphological examination, and live neurons of crystal violet staining were measured according to absorbent index. RESULTS　It was found that tanshinones possessed obvious protective effects on primary neurons in injury models by the way of morphological examination. Crystal violet staining also indicated that tanshinones increased number of live neurons in injury models significantly. The protective effects of tanshinones on models of oxidant injury, caffeine injury and NMDA injury were superior to other injury models. CONCLUSIONS　83.0 μmol*L-1 tanshinones protected rat cortex cells from all injury models effectively in vitro.

AIM To investigate protective effects and mechanism of tanshinones on ischemia-like injury models. METHODS Six ischemia models including hypoxia, hypoglucose, oxidant injury, caffeine injury, nitric oxide neurotoxicity and excitatory amino acid injury were used to assay the anti-ischemic roles of tanshinones in cultured primary cortex neurons. The changes of injuried cortex neurons were observed by the way of morphological examination, and live neurons of crystal violet staining were measured according to absorbent index. RESULTS it was found that tanshinones possessed obvious protective effects on primary neurons in injury models by the way of morphological e~nation. Crystal violet staining also indicated that tanshinones increased number of live neurons in injury models significantly. The protective effects of tanshinones on models of oxidant injury, caffeine injury and NMDA injury were superior to other injury models. CONCLUSIONS 83.0 ?mol? L- 1 tanshinones protected rat cortex cells fm all injury models effectively in vitro.

Aim To investigate protective effects and mechanism of TPG on ischemia_like injury models. Methods Six ischemia models including hypoxia, hypoglucose, oxidant injury, calcium overload, nitric oxide neurotoxicity and excitatory amino acid injury were used to assay the anti_ischemic roles of TPG in cultured primary cortex neurons. Results It was found that TPG possessed obvious protective effects on primary neurons in injury models by the way of morphological examination. Crystal violet staining also indicated that TPG increased number of life neurons in injury models significantly. Couclusions 50～200 ?g?ml-1 TPG protected rat cortex cells from all injury models effectively in vitro.

BACKGROUND:After acute myocardial infarction(AMI),there is still surviving myocardium in and around the infarcted area,which plays an important role in the occurrence of arrhythmia. OBJECTIVE:To study the alterations of the activities of Na+ channel current(INa),L-calcium current(ICa-L),transient outward K+ current(Ito) and inward rectifying K+ current(IK1) in the cardiomyocytes in the infarcted area after AMI. DESIGN: A randomized controlled study. SETTING:Department of Cardiology,Bethune International Peace Hospital. PARTICIPANTS:The experiment was finished in the Central Laboratory of the Department of Cardiology,Bethune International Peace Hospital from January to June 2003.Twenty New Zealand pure big-ear rabbits were randomly divided into AMI group(n=10) and control group(n=10). INTERVENTIONS:Rabbit AMI models were established by ligation of the left anterior descending coronary artery.The ventricular myocytes were separated with the method of enzymatic dissociation technique,and the changes of the ion currents were recorded with the whole cell patch-clamp techniques. MAIN OUTCOME MEASURES:The changes of INa,ICa-L,Ito and IK1 in the cardiomyocytes taken from the infarcted area of epicardium 24 hours after AMI in both the AMI and control groups. RESULTS:Twenty-four hours after AMI,the peak current densities of INa,ICa-L and IK1 in the AMI group [(28.48± 3.53) pA/pF,n=16;(3.91± 0.95) pA/pF,n=12;(26.93 ± 3.48) pA/pF,n=16]were all significantly reduced as compared with those in the control group [(45.50± 5.33) pA/pF,n=12;(5.58± 1.53) pA/pF,n=10;(34.12± 4.21) pA/pF,n=10] (t=3.026,P< 0.01;t=2.985,P< 0.01;t=2.706,P< 0.05).There was no significant difference in the Ito density between the AMI group and control group (P >0.05). CONCLUSION:The reduce of INa,ICa-L and IK1 caused by AMI can result in the decrease of myocardial conduction velocity,the shortening of action potential-time,abnormal repolarization,which is possibly the ionic mechanism for the reentrant ventricular arrhythmia after AMI.

Objective To determine the incidence of lung infection and associated factors in patients with traumatic brain injury for the sake of improving the clinical outcomes.Methods A retrospective analysis was made on records of 325 patients who hospitalized between January 2014 and June 2014.There were 198 male and 127 female patients,aged 11-78 years [(38.4 ±8.3) years].A total of 172 patients were injured in traffic accidents,80 in high falls,56 in blow accidents,and 17 in others.Lung infection status was documented and related risk factors were analyzed.Results Thirty-two patients (9.8％) had lung infection.Pseudomonas aeruginosa amounting to 12 strains was the most common pathogenic bacteria.Univariate analysis showed mechanical ventilation,airway open,and aspiration were significantly related to lung infection.Logistic regression identified aspiration (OR =2.891,P ＜ 0.05) and mechanical ventilation (OR =1.323,P ＜ 0.05) as the independent risk factors for lung infection.Conclusions Lung infection is a serious complication of traumatic brain injury,affected largely by aspiration and mechanical ventilation.Active preventions,reductions of risk factors,and early treatments should be done to get the best efficacy.

Some grain sprouts herbs recorded in Chinese Pharmacopoeia 2010, including Oryzae Fructus Germinatus, Setariae Fructus Germinatus and Hordei Fructus Germinatus, together with their adulterants, were identified by ITS2 sequences. The genomic DNA were extracted, their ITS2 sequences were amplified, and purified PCR products were
sequenced. Sequences were assembled using the CodonCode Aligner. The genetic distances, variable sites and the neighbor-joining (NJ) phylogenetic tree were computed by MEGA 6.0 in accordance with the Kimura 2-Parameter (K2P) model. The results showed that their intraspecific genetic distances were all much lower than the interspecific ones of themselves and their adulterants. The NJ tree based on ITS2 sequence indicated that Oryza sativa, Setariaitalica, and Hordeum vulgar formed one monophyletic clade respectively, in addition any one of the grain sprouts herbs and its adulterants could be distinguished clearly. Therefore, ITS2 sequence is suitable to be as a barcode to identify the grain sprouts herbs and their adulterants.

Objective To evaluate the effects of recombinant human neuregulin-1? on a rat model of adriamycin-induced dilated cardiomyopathy(ADR-DCM).MethodsMatched adult male Sprague-Dawley rats were administered with 2.5 mg/kg adriamycin intravenously once a week for 10 weeks to establish models of ADR-DCM.The ADR-DCM rats were randomly divided into 3 groups as follows: the rhNRG-1? group(rhNRG-1?,20 ?g/kg,i.v.,once a day for 10 d,n=8),the negative control group(excipient,n=8),and the positive control group(digoxin,0.062 5 mg/kg,i.v.,once a day for 10 d,n=7).Another 8 normal SD rats in the same situation served as normal control group(control,n=8).Their heart function and hemodynamics were evaluate after the treatment.The ratio of heart weight/body weight was calculated and the thickness of LV parietes was measured.The pathological lesions of cardiac muscle tissues were evaluated after HE staining.Brain contents of natriuretic peptide(BNP) and troponin T(TnT) were determined.The animal treatment was all accorded to the ethical standards.ResultsCompare with the normal control group,the LVESD and LVEDD of ADR-DCM rats were increased(P

Objective Protein N-SRCR derived from salivary agglutinin (SAG) inhibits HIV-1 infection.An N-SRCR monoclonal antibody was prepared for the study of the interaction between N-SRCR and HIV-1 envelop glycoprotein (gp120).Methods The purified recombinant N-SRCR expressed by 293 cells was used to immunize four weeks old BALB/c mice.After the final boost,the mouse spleen cells were isolated and fused with mouse myeloma cell line SP2/0-Ag-14,and the resulting hybridomas were screened for the production of N-SRCR-specific antibodies by ELISA assay.The monoclonal antibody against N-SRCR was purified by HiTrap Protein G kit,the purity determined by SDS-PAGE and the antibody titers by ELISA.The antibody specificity.was charqacterized by western blotting.Results A strain of hybridoma cell clones stably secreting N-SRCR antibody,named 1D6,was obtained.The high purity of the IgG was demonstrated by SDS-PAGE,and the ELISA titers of 1D6 was more than 100?25.Conclusion A monoclonal antibody against N-SRCR was successfully prepared,which laid the ground for further studies on the biological function of N-SRCR and the interactions between SRCR domains and HIV-1 Env gp120.