植物叶片衰老研究进展

叶片衰老是植物叶片生长发育过程中衰变的重要信号，在此综述了植物叶片衰老的特性、机理、与叶片衰老相关的基因、影响叶片衰老的因子（即器官、植物激素、氧化胁迫等），同时又介绍了叶片衰老相关基因表达的调控，并对开展植物叶片衰老研究的综合发展趋势作了分析。     

Association analysis between two SNPs in SNCA and PARK16 genes and Parkinson disease in a Han Chinese population in Liaoning area

AIM: To investigate the genotypic frequency of rs3857059 in SNCA gene and rs16856139 in PARK16 gene for determining the potential genetic risk factors of Parkinson disease (PD) in a Han Chinese population in Liaoning area of China. METHODS: The genomic DNA from 213 PD patients and 214 matched controls was amplified in the multiplex PCR system and subsequently genotyped by digestion with endonuclease Pvu II. Genetic parameter and association studies were carried out with SPSS 13.0 and PLINK 1.07 software. RESULTS: We accurately detected all genotypes in the 2 loci with PCR-restriction fragment length polymorphism (RFLP) techniques. The gene frequency of G allele in the rs3857059 locus was higher in PD group than that in control group with statistical significance (χ²= 7.592,P<0.01, OR=0.677, 95% CI=0.517~0.888). The T allele frequency in the rs16856139 locus was lower in PD group than that in control group and statistical result revealed a significant difference (χ²=11.511, P<0.01, OR=0.390, 95% CI=0.227~0.669). CONCLUSION: The 2 SNPs investigated in SNCA and PARK16 genes are likely to play roles as common risk factors for PD disease in the Han Chinese population.     

TMV侵染烟草基因差异表达的cDNA-AFLP分析

以烤烟品种龙江925 [高抗烟草普通花叶病(TMV)]接种TMV的叶片为材料,选用240对引物组合的扩增, 获得约 9 500个转录基因片段, 经过克隆测序最终获得了12个诱导表达片段, 它们与核酸代谢、蛋白质合成与修饰、能量代谢、胁迫响应、细胞内运输、糖代谢等相关, 并利用荧光定量PCR分析一个诱导表达片段TIF2在0~72 h之间5个时间点(0、12、24、48和72 h)的基因差异表达, 证实了所获得的基因序列为真实诱导的表达序列。对此序列进行RACE, 最终获得全长cDNA序列, 全序列857 bp, 预测的编码区在101~613 bp之间, 共编码170个氨基酸。经Blastn、Blastp比对分析, 在烟草中没有获得其同源序列, 确定该基因是在烟草中发现的与抗TMV相关的新基因。     

Progress on DAB2IP gene

Human DAB2 interaction protein (DAB2IP) is a novel member of Ras GTPase-activating protein family. It interacts directly with disabled-2 protein (DAB2/DOC2) which suppresses growth of cancers derived from different tissues, including mammary, prostate and ovarian cancers. DAB2IP was identified as an immediate downstream effector mediated by DAB2/DOC2. DAB2IP and DAB2/DOC2 form a unique protein complex that has a negative regulatory effect on the Ras-mediated signal pathway. It is demonstrated that DAB2IP is a tumor suppressor gene inactivated by methylation in several cancers. This article reviews the structure and biological functions of DAB2IP gene as well as its potential roles in carcinogenesis and evolution.     

Association analysis between ZNF804A rs1344706 polymorphism and therapeutic response to atypical antipsychotics in first-episode Chinese schizophrenia patients

AIM: To investigate the potential association between ZNF804A rs1344706 polymorphism and therapeutic response to atypical antipsychotics in first-episode Chinese schizophrenia patients.METHODS: Seventy-one first-episode schizophrenia inpatients receiving olanzapine, aripiprazole or quetiapine monotherapy were enrolled.Symptom responses to the treatment were assessed using the positive and negative symptom scale (PANSS) at the time of admission and re-assessed after 4 weeks of treatment.The single nucleotide polymorphism (SNP) rs1344706 was genotyped by direct sequencing.RESULTS: There was substantial difference of treatment response among the patients with 3 different genotypes regarding total PANSS score and positive subscore (for total PANSS score, F=4.608, df=2, P<0.05; for positive subscore, F=4.183, df=2, P<0.05).Compared with G homozygotes, T carriers showed significantly less improvement in total PANSS score as well as positive subscore (for total PANSS score, F=8.724, df=1, P<0.01, for positive subscore, F=9.392, df=1, P<0.01).CONCLUSION: Our results suggest that significant correlation exists between ZNF804A rs1344706 polymorphism and therapeutic response to atypical antipsychotics among the first-episode of schizophrenia, although replication is required to confirm this finding.     

Effect of CLCN2 antisense oligonucleotide on U251 cells injury by cisplatin

AIM: To investigate the effect of chloride channel CLCN2 antisense oligonucleotide on the cell injury of malignant U251 glioma cells induced by cisplatin (DDP). METHODS: The experiment was divided into 4 groups: control group (nonsense oligonucleotide), CLCN2 antisense oligonucleotide group, DDP group (DDP＋nonsense oligonucleotide), DDP＋CLCN2 antisense oligonucleotide group. The viability of U251 cells was measured by MTT assay, CLCN2 mRNA level was determined by RT-PCR, cell apoptosis was measured by TUNEL assay. RESULTS: Compared to the control group, the cell viability, CLCN2 and cyclinD1 mRNA decreased in CLCN2 antisense oligonucleotide group, DDP treated group and CLCN2 antisense oligonucleotide with DDP treated group, cells apoptosis increased. Compared to DDP group, the cell viability (P<0.05) and CLCN2 mRNA decreased in CLCN2 antisense oligonucleotide with DDP treated group, and cells apoptosis increased (P<0.01). Compared to CLCN2 antisense oligonucleotide group, CLCN2 mRNA significantly decreased (P<0.01) in CLCN2 antisense oligonucleotide with DDP treated group. CONCLUSION: CLCN2 antisense oligonucleotide inhibits the expression of CLCN2 mRNA in U251 cells. Inhibition of CLCN2 mRNA facilitates the cell injury of U251 cells induced by DDP. The decrease in CLCN2 mRNA is involved in the mechanism of cell injury by DDP.     

Effect of hTERT antisense oligodeoxynucleotide on Cis-diamminedichicloroplatinum-induced apoptosis in Jurkat cells

AIM:To explore the effect of hTERT antisense phosphorothioate oligodeoxynucleotide (ASODN) on apoptosis induced by chemotherapeutic drugs in Jurkat cell lines. METHODS:Cell viability was determined using the trypan blue dye exclusion assay. Apoptosis was detected by morphological observation, DNA gel electrophoresis and flow cytometry analysis. RESULTS:The survival rates of Jurkat cells cultured with daunorubicin, vincristin, and etoposide, respectively were similar with that cultured with those chemotherapic drugs plus hTERT ASODN. The survival rates of Jurkat cells cultured with cis-diamminedichicloroplatinum(DDP) added 24 hours later were higher than that cultured with hTERT ASODN and DDP added 24 hours later. The survival rates of Jurkat cells cultured with DDP were similar with that cultured with hTERT SODN and DDP. In morphological observation of apoptotic cells using Giemsa staining, cells displayed classic apoptotic changes treated with DDP or DDP combined with hTERT ASODN or SODN at 48 hours. Agarose gel electrophoresis of genomic DNA from Jurkat cells treated with ASODN and DDP combination for 48 hours showed typical DNA "ladder". Neither the DNA from Jurkat cells treated with SODN plus DDP nor the DNA from the cells treated with DDP alone showed ladder pattern. Apoptosis rates of Jurkat cells treated with DDP for 48 hours after 24 hours of exposure to ASODN significantly increased. There was significant difference in the percentage of apoptotic Jurkat cells between hTERT ASODN plus DDP and SODN plus DDP or DDP alone, respectively. CONCLUSION:The hTERT ASODN complementary to the translation initiation region of hTERT mRNA enhanced DDP-induced apoptosis in Jurkat cells.     

Effects of p27kip1 gene on DNA and protein synthesis in esophageal carcinoma cells

AIM: To investigate the effects of p27kip1 gene on DNA replication and protein synthesis in esophageal carcinoma cells. METHODS: Recombinant adenovirus Ad-p27kip1 was constructed and transfected into esophageal carcinoma cell EC-9706, and its effects on DNA replication, protein synthesis and the growth of esophageal carcinoma cells were explored by means of cell growth count, [3H]-TdR, [3H]-Leucine incorporation method and flow cytometry. RESULTS: The growth of esophageal carcinoma cells was inhibited obviously. The radioactive intensity of -TdR and -Leucine in Ad-p27kip1 group decreased significantly than that in control group after EC-9706 transfection (P<0.01), while the multiplication of esophageal carcinoma cell was inhibited obviously. CONCLUSION: Ad-p27kip1 inhibited the multiplication of the esophageal carcinoma cells, which may be related to its suppressive function for DNA replication and protein synthesis.     

Mechanisms of heart failure induced by adriamycin

AIM: To investigate the changes of cardiac function, oxidative stress and apoptosis in myocardium of rat model of heart failure induced by adriamycin (ADR). METHODS: At the end of the study, we observed content of malondialdehyde (MDA), activity of superoxide dismutase (SOD) and apoptosis. Expression of P53 protein and p53 mRNA were measured with immunohistochemical method and RT-PCR, respectively. RESULTS: Our data showed that content of MDA increased, activity of SOD decreased and apoptosis in myocardium happened while cardiac function decreased after ADR treatment. p53 gene expression and P53 protein obviously increased in heart failure group. CONCLUSION: There were oxidative stress and apoptosis occurred significantly in a model of heart failureinduced by ADR. p53 gene might play an important role in the apoptosis. Correlation analyses suggested that apoptosis in myocardium was related to oxidative stress in ADR-induced heart failure model.