Allotetraploidization event of Coptis chinensis shared by all Ranunculales

Coptis chinensis Franch.,also named Chinese goldthread is a member of Ranunculaceae in the order Ranunculales and represents an important lineage of early eudicots with traditional medicinal value.In our study,by using syntenic analysis combined with phylogenomic analysis of C.chinensis and four other representative genomes from basal and core eudicots,we confirmed that the WGD event in C.chinensis was shared by Aquilegia coerulea and Papaver somniferum L.and quickly occurred after Ranunculales diverged from other eudicots,likely a Ranunculales common tetraploidization(RCT).The synonymous nucleotide substitutions at synonymous sites distribution of syntenic blocks across these genomes showed that the evolutionary rate of the P.somniferum genome is faster than that of the C.chinensis genome by approximately 13.7%,possibly due to Papaveraceaes having an additional special tetraploidization event(PST).After Ks correction,the RCT dated to 115—130 million years ago(MYA),which was close to the divergence of Ranunculaceaes and Papaveraceaes approximately115.45—130.51 MYA.Moreover,we identified homologous genes related to polyploidization and speciation and constructed multiple sequence alignments with different reference genomes.Notably,the event-related subgenomes in the basal genomes all showed genomic fractionation bias,suggesting a likely allopolyploid nature of the RCT,PST and T-Alpha and T-Beta events in Tetracentron sinense.In addition,we detected that the sixteen P450 subfamilies were markedly expanded in the genomes of Ranunculales,and most of them were related to the RCT and PST events.We constructed a new platform for Early Eudicot Comparative Genomic Research(http://www.cgrpoee.top/index.html)to store more information.In summary,our findings support the WGD of C.chinensis shared by Ranunculales,which is likely an allotetraploidization event.This present effort offered new insights into the evolution of key polyploidization events and the genes related to secondary metabolites during the diversification of early eudicots.

机械振动对去卵巢大鼠骨质疏松性骨折愈合中CGRP和SP表达的影响

目的探讨机械振动对去卵巢后骨质疏松性骨折大鼠骨折端愈合过程中神经肽降钙素基因相关肽(calcitonin gene-related peptide,CGRP)和P物质(substance P,SP)表达的影响。方法选取3月龄的雌性Wistar大鼠30只,按照随机法分为对照组(Sham)、去卵巢组(OVX)、振动组(OVX-V),每组10只。摘除去卵巢组和振动组大鼠的卵巢以建立骨质疏松模型,对照组则去除同质量脂肪组织构建假去卵巢骨质疏松模型,同时对振动组大鼠进行频率35 Hz、振幅2 mm、加速度0.5 g的振动干预,持续20 min,其他组放于关闭的振动台上自由活动20 min,每周5 d。在干预2周和6周后,拍摄大鼠骨折端X线片观察对比3组的愈合情况,采用酶联免疫吸附测定(ELISA)技术来测定骨折端CGRP和SP的表达水平。结果对照组与振动组在干预2周后大鼠骨折愈合率较去卵巢组高,振动组在干预6周后大鼠骨折愈合率高于其他两组(P<0.05)。在干预2周后,振动组大鼠骨组织CGRP含量[0.464±0.018]和SP含量[0.450±0.019]均高于去卵巢组但明显低于对照组(P<0.05)。在干预6周后,振动组大鼠骨组织中CGRP含量[0.632±0.016]和SP含量[0.636±0.017]呈上升趋势且明显高于去卵巢组,但仍低于对照组(P<0.05)。结论机械振动有助于提高去卵巢骨质疏松骨折大鼠骨组织中神经肽CGRP和SP的表达水平,从而增加成骨细胞活性并抑制骨吸收,加速骨折愈合。

胃食管反流病患者血清炎症因子水平、SP及CGRP的相关性分析

目的研究胃食管反流病(gastroesophageal reflux disease,GERD)患者血清炎症因子水平、P物质(substance P,SP)及降钙素基因相关肽(calcitonin gene-related peptide,CGRP)的相关性。方法收集2018年5月至2021年5月本院128例GERD患者临床资料,根据GERD症状评分分级,将患者分为轻度、中度、重度及危重度四组。比较不同病情程度患者血清炎症因子(IL-6、IL-8及TNF-α)、SP及CGRP水平。分析GERD患者血清炎症因子与SP、CGRP的关系。采用ROC分析血清炎症因子、SP及CGRP判断GERD病情程度的价值。结果128例患者中轻度组30例,中度组42例,重度组34例,危重组22例。四组患者血清IL-6、IL-8、TNF-α、SP及CGRP水平比较,差异有统计学意义(P<0.05)。四组患者间两两比较,血清IL-6、IL-8、TNF-α、SP及CGRP水平差异有统计学意义(P<0.05)。血清IL-6、IL-8及TNF-α与SP、CGRP呈显著正相关性(P<0.05)。经多因素Logistic回归分析证实,IL-6、IL-8、TNF-α、CGRP及SP水平是影响GERD患者病情程度的危险因素(均P<0.05)。经ROC分析,血清IL-6、IL-8、TNF-α、CGRP及SP对判断GERD病情程度具有较高应用价值。CGRP和SP与血清炎症因子判断GERD患者病情程度的AUC病情程度比较,差异均无统计学意义(P>0.05)。结论GERD患者病情程度与血清炎症因子、SP及CGRP相关,且血清炎症因子与SP、CGRP间存在相关性,二者发挥协同作用,参与GERD病理进程。

Identify lymphatic metastasis-associated genes in mouse hepatocarcinoma cell lines using gene chip

AIM: In order to obtain lymphogenous metastasisassociated genes, we compared the transcriptional profiles of mouse hepatocarcinoma cell lines Hca-F with highly lymphatic metastasis potential and Hca-P with low lymphatic metastasis potential.METHODS: Total RNA was isolated from Hca-F and Hca-P cells and synthesized into double-stranded cDNA. In vitro transcription double-stranded cDNA was labeled with biotin (i.e. biotin-labeled cRNA, used as the probe). The cRNA probes hybridized with Affymetrix GeneChip() MOE430A (containing 22 690 transcripts, including 14 500 known mouse genes and 4 371 ESTs) respectively and the signals were scanned by the GeneArray Scanner. The results were then analyzed by bioinformatics.RESULTS: Out of the 14 500 known genes investigated,110 (0.8%) were up regulated at least 23 fold. Among the total 4 371 ESTs, 17 ESTs (0.4%) (data were not presented) were up regulated at least 23 fold. According to the Gene Ontology and TreeView analysis, the 110genes were further classified into two groups: differential biological process profile and molecular function profile.CONCLUSION: Using high-throughput gene chip method,a large number of genes and their cellular functions about angiogenesis, cell adhesion, signal transduction, cell motility, transport, microtubule-based process, cytoskeleton organization and biogenesis, cell cycle, transcription,chaperone activity, motor activity, protein kinase activity,receptor binding and protein binding might be involved in the process of lymphatic metastasis and deserve to be used as potential candidates for further investigation.Cyclin D1, Fosl1, Hsp47, EGFR and AR, and Cav-1 are selected as the possible candidate genes of the metastatic phenotype, which need to be validated in later experiments.ESTs (data were not presented) might indicate novel genes associated with lymphatic metastasis. Validating the function of these genes is helpful to identify the key or candidate gene/pathway responsible for lymphatic metastasis, which might be used as the diagnostic markers and the therapeutic targets for lymphatic metastasis.

Abnormal Change of p53 Gene in Gastric and PrecancerousLesions and APC Gene Deletion in Gastric Carcinoma and Near Tissues

p53 gene mutation (exon4, 5, 6, 7, 8 and intron6) in gastric cancer and precancerous lesions and p53 gene (exon4 and ontron6), APC gene deletion in gastric carcinomas were studied by PCR/SSCP and PCR/RFLP- Results showed mutation rate of p53 in metaplasia, dysplasia and gastric carcinoma was 37. 5 % (3/8), 42. 11 % (8/19), 53. 33 (16/30) respectively- There was significant dif-ference among groups of metaplasia, dysplasia, cancer and normal controls. Noexon8 mutation was found in metaplasia and dysplasia, but 4 cases were found to have exon8 mutation in cancer group. It is suggested that exon8 mutation occurs at the late stage of gastric cancer, but exon 5, 6, 7 mutation occur in the course ofprecancerous lesion to cancer. Loss of heterozygosity (LOH) of exon4, intron6,APC was 47,37 % (9/19), 8. 73% (2/23), 16. 67 % (3/18) respectively. LOH of exon4 had something to do with poor differentiation, lymph node metastasis,depth of invasion- LOH of exon4 may be one of prognostic marker of gastric cancer. We are led to conclude that p53 gene mutation is an early event and perhaps work together with ras oncogene in gastric carcinogenesis

Genetic aberration in primary hepatocellular carcinoma:correlation between p53 gene mutation and loss-of-heterozygosity on chromosome 16q21-q23 and 9p21-p23

To elucidate the molecular pathology underlying the development of hepatocellular carcinoma (HCC), we used 41 highly polymorphic microsatellite markers to examine 55 HCC and corresponding non-tumor liver tissues on chromosome 9, 16 and 17. Loss-of-heterozygosity (LOH) is observed with high frequency on chromosomal region 17p13 (36/55, 65%), 9p21-p23 (28/55, 51%), 16q21-q23 (27/55, 49%) in tumors. Meanwhile, microsatellite instability is rarely found in these microsatellite loci. Direct sequencing was performed to detect the tentative mutation of tumor suppressor genes in these regions: p53, MTS1/p16, and CDH1/E-cadherin. Within exon 5-9 of p53 gene, 14 out of 55 HCC specimens (24%) have somatic mutations, and nucleotide deletion of this gene is reported in HCC for the first time. Mutation in MTS1/pl6 is found only in one tumor case. We do not find mutations in CDH1/E-cadherin. Furthermore, a statistically significant correlation is present between p53 gene mutation and loss of chromosome region 16q21q23 and 9p21-p23, which indicates that synergism between p53 inactivation and deletion of 16q21-q23 and 9p21-p23 may play a role in the pathogenesis of HCC. Genetic aberration in hepatocellular

ADENOVIRUS-MEDIATED P53 GENE TRANSFER INCREASES THE THERMOSENSITIVITY OF HUMAN GASTRIC CARCINOMA CELL LINES(IN VITRO AND IN VIVO)

Objective: To evaluate the effect of adenovirus-mediated p53 gene (Adp53) on apoptosis andradiosensitivity of human gastric carcinoma cell lines.Methods: Recombinant adenovirus expressing wild-type p53 gene was transferred into four human gastric carcinoma cell lines with different p53 genetic status. p53 proteinexpression was detected by immunohistochemistry assayand western blot assay. Cell survival was assessed using a clonogenic assay. TUNEL assay was used in determination of apoptosis. Four human gastric carcinoma cells infectedwith Adp53 were irradiated with 4Gy and cell cycle distribution and Sub-G1 peak were assayed by flowcytometry. Results: G2/M arrest, apoptosis and inhibition of tumor cell proliferation were induced by infection atAdp53 at 100 MOI which caused high transfer rate ofwild-type p53 and strong expression of p53 protein in four human gastric carcinoma cells. The radio-enhancement ratio of Adp53 at 4Gy were 3.0 for W cell, 3.6 for M cell, 2.2 for neo cell and 2.5 for 823 cell in vitro. Conclusion: Thisstudy demonstrated that Adp53 transfer increased cellularapoptosis and radiosensitivity of human gastric carcinoma cell lines in vitro independently on cellular intrinsic p53status thus supporting the combination of p53 gene therapy with radiotherapy in clinical trials.

Comparative Study of the Effect of Shugan Shuru Granule (疏肝舒乳颗粒) on Pathology and p53 Gene Expression in Patients with Hyperplastic Disease of Breast

Objective: To study the effect of Shugan Shuru Granule (疏肝舒乳颗粒,SSG) on the p53 gene expression in patients with hyperplastic disease of breast (HDB) to indirectly explore the mechanism of SSG’s effect on HDB on the molecular pathological level. Methods: Sixty-six patients with HDB were allocated in the treated group and the control group,with the former treated with SSG and the latter not. All patients underwent breast operation and their diseased mammary tissues were cut out, sectioned, and observed under microscopy with HE staining and immunohistochemical staining, with ABC method adopted to estimate the degree of hyperplasia and p53 gene expression. The severity of HDB was classified into normal, mild, moderate and severe grades (marked as 0 to Ⅲ), according to the degree of hyperplasia in the mammary gland. Results: Hyperplasia in the control group mostly belonged to grade Ⅰ-Ⅲ before treatment, showing overgrowth of gland and proliferation of glandular epithelial cells, which were high columnar shaped, more stratified, with papillary or substantive dysplasia. While in the treated group, most belonged to grade 0-Ⅰ after SSG treatment, with proliferated gland and dysplasia recovered to normal or disappeared. The positive rate of p53 gene expression in the treated group was 9.09%, and in the control group 39.39%, comparison between the two groups showing significant difference (P<0.01), the intensity in the former was significantly weaker than that in the latter.Conclusion: SSG could not only inhibit the proliferation of mammary duct epithelia and lobuli, but also inhibit the over-expression of P53. Therefore, it could be regarded as an effective remedy for treatment of HDB and prevention of mammary cancer genesis.

Involvement of gene expressions in apoptosis of vascularendothelial cells induced by rattlesnake venom

Formation of apoptotic bodies is a typical character ofaPoptotic cell death, but how the processes are controlledis not known. In this study, we compared two apoptosisinducing systems in vascular endothelial cells (VEC). Wefound that the formation of aPoptotic bodies during apop-tosis induced by rattlesnake venom, which is an unique andspecific aPoptosis inducer to vascular endotheliaI cells, wasmuch faster than that induced by deprivation of survivalfactors (aFGF and serum). When we blocked the synthesisof mRNAs in cells treated with rattlesnake venom by DRB(5, 6- dichloro- 1 -β- D- rib ofur anosylb enzimidazole ), an in-hibitor of transcription, the formation of aPoptotic bodieswas dramatically inhibited. We examined the expressionof Psa gene and found that its expression was much higherin apoptosis induced by rattlesnake venom than that inaPoptosis induced by deprivation of aFGF and serum. Ourresults suggest that gene expression is important and P53gene may play a major role in inducing the formation ofapoptotic bodies in VEC.

Construction of retroviral vector of p^(125FAK) specific ribozyme genes and its effects on BGC-823 cells

瞄准：构造制动火箭 p (125FAK ) 的病毒的向量特定的 ribozyme 基因并且在 BGC-823 探索 ribozyme 的可行性基因治疗在试管内。方法：从 nt 的 A 撞木鲛 ribozyme DNA 指向 p (125FAK ) mRNA 1010 到 nt， 1032 被综合并且重新结合进制动火箭病毒的向量 pLXSN 形成 pLRZXSN 交换子。用调停 lipofectin 的 DNA transfection 技术， pLRZXSN 被介绍进 BGC-823 房间。BGC-823 细胞和 apoptosis 的生长上的 ribozyme 的效果被细胞殖民地试金，流动血细胞计数(FCM ) ，反向的 transcriptase 聚合酶链反应(RT-PCR ) ， DNA 破碎的察觉和电子显微镜学学习。结果：在房间为 48 h 被对待以后， BGC-823 房间殖民地的数字被 56% 禁止。房间增长被 ribozyme 和禁止的效果取决于的 p (125FAK ) 有效地禁止集中和孵化的时间。p (125FAK ) 的表示 mRNA 和蛋白质 P (125FAK ) 在与 p (125FAK ) 对待的 BGC-823 房间严厉地减少了 ribozyme。apoptosis 的特征，也就是 sub-G1 山峰， DNA 破碎和词法变化，在与 p (125FAK ) 对待的 BGC-823 房间被揭示 ribozyme。结论：p (125FAK ) ribozyme 减少 p (125FAK ) 基因表示并且导致人的胃的癌症房间的 apoptosis 在试管内。

Codon 249 mutations of p53 gene in non-neoplastic liver tissues

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RELATIONSHIP BETWEEN THE MUTATION OF P53 GENE AND INFILTRATION，METASTASIS AND PROGNOSIS OF GASTRIC CARCINOMA

gastric carcinomas were examined immunohistochemically with McAb to p53 protein in order to investigate the relationship between the expression of p53 protein and histological differentiation of gastric carcinoma, and to approach the mechanism of infiltration and metastasis of gastric carcinoma. The results showed that nuclear expression of p53 protein was significantly related to tumor size, depth of invasion, lymph node and liver metastases; but not related to histological differentiation. It is suggested that the accumulation of p53 protein was increased with the progression of gastric carcinoma, and therefore the cancer clone with p53 gene mutation may play an important role in the development of tumor invasion and metastasis.

Protective effects of proanthocyanidins on beta-amyloid peptide (25-35)-induced PC12 cell apoptosis by blocking S-phase and increasing p53 gene expression

BACKGROUND： Current studies related to the effects of proanthocyanidins on Alzheimer＇s disease have focused primarily on the signal transduction pathway of cellular apoptosis. However, the influence of p53 gene expression on cell cycle regulation, with regard to the protective mechanisms of proanthocyanidins, has not been reported. OBJECTIVE： To observe the effect of proanthocyanidins on cell cycle distribution, cellular apoptosis and p53 gene expression in β-amyloid peptide （25-35） （Aβ25-35）-induced PC12 cells cultured in serum-free media, and to investigate the molecular neuroprotective mechanisms of proanthocyanidins with regard to cell cycle regulation. DESIGN, TIME AND SETTING： A parallel, controlled, at the Institute of Biochemistry and Molecular Biology cellular, and molecular study was performed Guangdong Medical College from July 2006 to July 2008. MATERIALS： Proanthocyanidins were provided by Nanjing Xuezi Medical and Chemical Research Center, China; Aβ25-35 was provided by Sigma, USA; PC12 cells were provided by the Institute of Basic Medical Science, Academy of Military Medical Sciences; and rabbit anti-p53 polyclonal antibody was provided by Santa Cruz Biotechnology, USA. METHODS： PC12 cells were cultured in serum-free media for 24 hours. Cells from the model group were treated with 25 μmol/L Aβ25-35 for 24 hours. Cells in the drug protection group were pre-treated with 30 mg/L proanthocyanidins for 1 hour and then treated with 25 μmol/LAβ2^-35 for 24 hours. The control group was not treated. MAIN OUTCOME MEASURES： Flow cytometry was used to detect cell cycle distribution and rate of apoptosis; reverse-transcriptase polymerase chain reaction was used to detect p53 mRNA expression; and Western blot was used to detect p53 protein expression. RESULTS： After treating with 25 μmol/LAβ25-35 for 24 hours, the rate of apoptosis and the percentage of cells in S phase were significantly increased （P 〈 0.01 ）, and p53 mRNA and protein expressions were decreased. Pretreatment with proanthocyanidins for 1 hour blocked the increase in apoptosis and the percentage of cells in S phase in Aβ25-35-induced PC12 cells （P 〈 0.01 ） and increased p53 mRNA and protein expressions. CONCLUSION： Proanthocyanidins blocked apoptosis and S-phase arrest in Aβ25-35-induced PC12 cells cultured in serum-free media. The protective mechanism could be related to increased p53 mRNA and protein expressions.

PROMOTER HYPERMETHYLATION OF p16 GENE AND DAPK GENE IN SERA FROM HEPATOCELLULAR CARCINOMA (HCC) PATIENTS

Objective： To analyze the aberrant methylation of p16 gene and DAPK gene in sera from primary liver cancer patients ad to evaluate the clinical significance. Methods： A methylation-specific PCR was performed for the detection of promoter hypermethylation of p16 gene and DAPK gene in blood DNA from 64 cases of HCC patients, and to analyze the relation of the aberrant methylation of p16 gene and KAPK gene and the clinical pathological data. Results： 76.6%（49/64） of the sera from 64 cases of HCC patients showed hypermethylation for p16 promoter and 40.6% （26/64） for KAPK promoter, whereas no methylated p16 gene promoter and DAPK gene promoter were found in sera from benign liver diseases patients and normal control. Methylated p16 gene and KAPK gene promoters in sera did not strongly correlated with HBsAg, stage, metastasis and differentiation in HCC; but strongly correlated with AFP. Conclusion： Detection of the aberrant methylation of p16 gene and KAPK gene in blood DNA from HCC patients might offer an effective means for the earlier auxiliary diagnosis of the malignancy.

Quantitative Study on Expression of P16 Multiple Tumor Suppressor Gene in Salivary Gland Neoplasm

The expression of P16 gene were found in all 3 groups. The positive unit (PU) was higher in tumor group and cancer group than that in normal group ( P <0.01). Furthermore, the PU of P16 was stronger in cytoplasm than in nucleus. Malignant tumors and acini surrounding the tumor revealed strong positives and week positives respectively. The PU of P16 gene was higher in deep lobe of recurrent parotid neoplasm with incomplete capsule than that in shallow lobe of primary parotid neoplasm with complete capsule. Our findings suggests that P16 gene plays equally important role in the salivary gland tumors and tumors in other part of the body.

The Effects of Wild-type p5 3Gene Transfection on the Growth and Chemotherapeutic Sensitivity of Human Glioma Cells

To evaluate the effects of wild type p53 gene on the growth and chemotherapeutic sensitivity of human glioma cells, plasmid PC53 SN3 carrying wild type p53 gene was transfected into U251 cells. p53 gene expression in transfected cells was detected by RT PCR, the cell growth inhibition and apoptosis in either the absence or the presence of cisplatin was assessed by MTT and flow cytometry. The transfection of p53 gene into U251 cells was confirmed by RT PCR. MTT showed that p53 gene by itself induced strong inhibition effect on the growth of U251 cells [inhibition rate, IR (79.60±5.69) %]. The killing effects of cisplatin by itself on U251 cells was not strong [IR (19.40±6.69) %, (24.41±2.68) %, (51.84±13.38) %, (66.22±5.02) %] and increased with the increase of cisplatin concentration (1, 2, 4, 8 μg/ml). When combined treatment of wild type p53 gene transfection and cisplatin was used, that was significantly increased [IR (91.64±1.00) %, (94.98±1.67) %, (95.32±2.01)%, (95.65±1.00) %]. The apoptosis rate of U251 cells induced by p53 gene transfection was 17.38%. That induced by cisplatin increased (5.71 %, 5.93 %, 6.27 %, and 6.81 %) with the increase of cisplatin concentration (1, 2, 4, 8 μg/ml). The apoptosis rate was also significantly increased (23.50 %, 23.54 %, 23.89 %, and 28.88 %) after combined treatment of p53 and cisplatin with different concentration (1, 2, 4, 8 μg/ml). It is concluded that wild type p53 gene and cisplatin could result in synergistic inhibition effects on the growth of human glioma cells.

Numerical simulation of avascular tumor growth based on p27 gene regulation

A multi-scale continuous-discrete model based on the effects of the p27 gene control is built to simulate the avascular tumor growth. At the tissue level, the continuous Eulerian model is adopted to determine the distribution of the concentration of oxygen, the extracellular matrix （ECM）, and the matrix-degradative enzyme （MDE）. At the cellular level, the discrete Lagrangien model is adopted to determine the movement, the proliferation, and the death of single tumor cells （TCs）. At the genetic level, whether a cell is committed to mitosis is determined by solving a set of equations modeling the effects of the p27 gene control. The avascular morphological evolution of the solid tumor growth is simulated, including the radius the oxygen distribution over time, and the expression. of the solid tumor, the number of the TCs, inhibiting effect＇ of the up-regulating p27 gene

Genetic Diversity of Chinese Soybean mosaic virus Strains and Their Relationships with Other Plant Potyviruses Based on P3 Gene Sequences

Soybean mosaic virus （SMV）, a member of the genus Potyvirus, is a major pathogen of soybean plants in China, and 16 SMV strains have been identified nationwide based on a former detailed SMV classification system. As the P3 gene is thought to be involved in viral replication, systemic infection, pathogenicity, and overcoming resistance, knowledge of the P3 gene sequences of SMV and other potyviruses would be useful in efforts to know the genetic relationships among them and control the disease. P3 gene sequences were obtained from representative isolates of the above-mentioned 16 SMV strains and were compared with other SMV strains and 16 Potyvirus species from the National Center for Biotechnology GenBank database. The P3 genes from the 16 SMV isolates are composed of 1041 nucleotides, encoding 347 amino acids, and share 90.7-100% nucleotide （NT） sequence identities and 95.1-100% amino acid （AA） sequence identities. The P3 coding regions of the 16 SMV isolates share high identities （92.4-98.9% NT and 96.0-100% AA） with the reported Korean isolates, followed by the USA isolates （88.5-97.9% NT and 91.4-98.6% AA）, and share low identities （80.5-85.2% NT and 82.1-84.7% AA） with the reported HZ 1 and P isolates from Pinellia ternata. The sequence identities of the P3 genes between SMV and the 16 potyviruses varied from 44.4 to 81.9% in the NT sequences and from 21.4 to 85.3% in the AA sequences, respectively. Among them, SMV was closely related to Watermelon mosaic virus （WMV）, with 76.0-81.9% NT and 77.5-85.3% AA identities. In addition, the SMV isolates and potyvirus species were clustered into six distinct groups. All the SMV strains isolated from soybean were clustered in Group I, and the remaining species were clustered in other groups. A multiple sequence alignment analysis of the C-terminal regions indicated that the P3 genes within a species were highly conserved, whereas those among species were relatively variable.

Association between Maternal Drug Use and Cytochrome P450 Genetic Polymorphisms and the Risk of Congenital Heart Defects in Offspring

Objective This study aimed to assess the associations between maternal drug use,cytochrome P450(CYP450)genetic polymorphisms,and their interactions with the risk of congenital heart defects(CHDs)in offspring.Methods A case-control study involving 569 mothers of CHD cases and 652 controls was conducted from November 2017 to January 2020.Results After adjusting for potential confounding factors,the results show that mothers who used ovulatory drugs(adjusted odds ratio[a OR]=2.12;95% confidence interval[CI]:1.08-4.16),antidepressants(a OR=2.56;95%CI:1.36-4.82),antiabortifacients(a OR=1.55;95%CI:1.00-2.40),or traditional Chinese drugs(a OR=1.97;95%CI:1.26-3.09)during pregnancy were at a significantly higher risk of CHDs in offspring.Maternal CYP450 genetic polymorphisms at rs1065852(A/T vs.A/A:OR=1.53,95%CI:1.10-2.14;T/T vs.A/A:OR=1.57,95%CI:1.07-2.31)and rs16947(G/G vs.C/C:OR=3.41,95%CI:1.82-6.39)were also significantly associated with the risk of CHDs in offspring.Additionally,significant interactions were observed between the CYP450 genetic variants and drug use on the development of CHDs.Conclusions In those of Chinese descent,ovulatory drugs,antidepressants,antiabortifacients,and traditional Chinese medicines may be associated with the risk of CHDs in offspring.Maternal CYP450 genes may regulate the effects of maternal drug exposure on fetal heart development.

FREQUENT STRUCTURE ALTERATIONS OF p53 GENE IN NASOPHARYNGEAL CARCINOMA

By southern hybridization with 1. 8 kb cDNA probe,a high frequency （40. 5 % ） of structural abnor- mality of p53 gene was observed in primary nasopharyngeal carcinoma （NPC） biopsies. The regions of ex- ons 1 to 4 of the gene were examined by polymerase chain reaction-single strand con formation polymor- phism,no point mutation was found. Because very low rate of point mutation had been reported in exons 5 to 8, we considered that structural abnormality in the region of e-cons 1 to 8 of the gene might be uncom- mon in NPC. The spectrophotometer scanning analysis of autoradiograms and rehybridization investigation of nitrocellulose filter with exon 11 probe indicated that most of structure aberrations we observed might be rearrangement occurring in exon 11.