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51.
Mohammad Asim Abdul Malik Manash P. Sarma Sunil K. Polipalli Nargis Begum Istaq Ahmad Luqman A. Khan S.A. Husain Naseem Akhtar Sajid Husain L. Thayumanavan Rajiv Singla P. Kar 《Journal of medical virology》2010,82(7):1115-1125
The study aims to characterize mutations of the HBV genome involving BCP, Precore/core and X regions and also defines HBV genotypes in patients of hepatocellular carcinoma (HCC). The study involved 150 HBV‐related HCC cases and 136 HBV‐related chronic liver disease patients without HCC as controls. HBV DNA was subjected to mutational analysis using SSCP technique, genotyping by RFLP, and direct nucleotide sequencing. HBV DNA was found in 58.7% (88/150) of the HCC cases and 74.3% (101/136) of controls. HBV mutants were observed in 44.3% of HCC cases and 43.2% of controls. HBV/D was prevalent amongst the patients and controls, followed by HBV/A. The prevalence of the TT1504 mutation in the X gene, the V1753 and T1762/A1764 mutations in the BCP region, and G1914 mutation in the core gene were significantly higher in the HCC group than in the non‐HCC group. Multivariate analyses showed that the TT1504, V1753, A1762T/G1764A, and the G1914 mutations and the patient's age, sex, and HBeAg status increased the risk of HCC development significantly. Also, patients with HCC had lower levels of serum albumin, viral load, and platelet counts but higher values of alkaline phosphatase, alanine aminotransferase, aspartate aminotransferase, bilirubin, and Alpha feto‐protein than those of controls (P < 0.001 for all comparisons). HBV/D was the predominant genotype associated with HCC cases seen in India. The presence of different types of HBV mutations, age, sex, HBeAg status, and viral load was found to increase significantly the risk of HCC development in India. J. Med. Virol. 82: 1115–1125, 2010. © 2010 Wiley‐Liss, Inc. 相似文献
52.
Gao HZ Kobayashi K Tabata A Tsuge H Iijima M Yasuda T Kalkanoglu HS Dursun A Tokatli A Coskun T Trefz FK Skladal D Mandel H Seidel J Kodama S Shirane S Ichida T Makino S Yoshino M Kang JH Mizuguchi M Barshop BA Fuchinoue S Seneca S Zeesman S Knerr I Rodés M Wasant P Yoshida I De Meirleir L Abdul Jalil M Begum L Horiuchi M Katunuma N Nakagawa S Saheki T 《Human mutation》2003,22(1):24-34
Classical citrullinemia (CTLN1), a rare autosomal recessive disorder, is caused by mutations of the argininosuccinate synthetase (ASS) gene, localized on chromosome 9q34.1. ASS functions as a rate-limiting enzyme in the urea cycle. Previously, we identified 32 mutations in the ASS gene of CTLN1 patients mainly in Japan and the United States, and to date 34 different mutations have been described in 50 families worldwide. In the present study, we report ASS mutations detected in 35 additional CTLN1 families from 11 countries. By analyzing the entire coding sequence and the intron-exon boundaries of the ASS gene using RT-PCR and/or genomic DNA-PCR, we have identified 16 novel mutations (two different 1-bp deletions, a 67-bp insertion, and 13 missense) and have detected 12 known mutations. Altogether, 50 different mutations (seven deletion, three splice site, one duplication, two nonsense, and 37 missense) in 85 CTLN1 families were identified. On the basis of primary sequence comparisons with the crystal structure of E. coli ASS protein, it may be concluded that any of the 37 missense mutations found at 30 different positions led to structural and functional impairments of the human ASS protein. It has been found that three mutations are particularly frequent: IVS6-2A>G in 23 families (Japan: 20 and Korea: three), G390R in 18 families (Turkey: six, U.S.: five, Spain: three, Israel: one, Austria: one, Canada: one, and Bolivia: one), and R304W in 10 families (Japan: nine and Turkey: one). Most mutations of the ASS gene are "private" and are distributed throughout the gene, except for exons 5 and 12-14. It seems that the clinical course of the patients with truncated mutations or the G390R mutation is early-onset/severe. The phenotype of the patients with certain missense mutations (G362V or W179R) is more late-onset/mild. Eight patients with R86H, A118T, R265H, or K310R mutations were adult/late-onset and four of them showed severe symptoms during pregnancy or postpartum. However, it is still difficult to prove the genotype-phenotype correlation, because many patients were compound heterozygotes (with two different mutations), lived in different environments at the time of diagnosis, and/or had several treatment regimes or various knowledge of the disease. 相似文献
53.
Begum M Tashiro H Katabuchi H Suzuki A Kurman RJ Okamura H 《Laboratory investigation; a journal of technical methods and pathology》2006,86(3):286-296
Human endometrial carcinomas, as well as complex atypical hyperplasias (CAH), are estrogen related and frequently have mutations in the PTEN gene. However, the mutual contribution of estrogen and PTEN mutations to endometrial carcinogenesis in vivo is unknown. To address this issue, we investigated whether neonatal estrogenic treatments augment the incidence of CAH and carcinomas in murine PTEN (mPTEN) heterozygous (+/-) mutant mice, an animal model for endometrial carcinoma. Low doses of diethylstilbestrol (1 ng/g/day), genistein (50 microg/g/day) in phytoestrogens, estriol (E(3)) (4 microg/g/day), and vehicle (ethanol and corn oil) were administered subcutaneously daily to neonatal pups from the 1st to 5th day after birth. At 52 weeks of age, the morphological changes in the endometrium, and uterine expression of Hoxa 10 and Hoxa 11, were evaluated. These Hoxa genes are abdominal B-type homeobox genes, which normally regulate differentiation of the Müllerian duct. The incidence of CAH and adenocarcinomas of the endometrium was significantly decreased by the neonatal estrogenic treatments in the mPTEN+/- mice. Coincidentally, all treatments significantly decreased the stromal cell density, and CAH and adenocarcinomas rarely developed in the epithelium adjacent to the affected endometrial stroma. Moreover, the uterine expression of Hoxa 10 in mice with neonatal genistein and E(3) treatments, and that of Hoxa 11 in mice with all treatments, was significantly lower when compared with vehicle alone. Taken together, neonatal estrogenic exposure induced stromal atrophy and/or hyalinization accompanied by repressed expression of Hoxa 10 and Hoxa 11, and exerted an inhibitory effect on PTEN-related tumorigenesis. These findings provide new insight into the interaction between endometrial epithelium and stroma in endometrial carcinogenesis in vivo. 相似文献
54.
SHAN SHAN GUO YI ZHONG WANG XIU KUN WANG YING JIE GAO YA HONG JIN DE FENG LI GUI DONG YUAN YI ZHANG GUI ZHEN ZONG YE ZHAO XIAO LAN CUI Institute of Chinese Meteria Medica China Academy of Chinese Medical Sciences Beijing P. R. China Aerospace Central Hospital Beijing P. R. China 《中华微生物学和免疫学杂志(英文版)》2006,4(4):272-277
To observe the effect of Gardenia extract ZG on the adsorption quantity of herpes simplex virus type 1 (HSV-1) so as to explore the mechanism of its antiviral activity, fluorescein isothiocyanate (FITC) was used as the fluorescent probe to label viruses and heparin sodium was used as control. Meanwhile , the effect of Gardenia extract ZG on the adsorption quantity on the surface of Hep-2 cells was determined by flow cytometry. It was demonstrated that adsorption of HSV-1 on the surface of Hep-2 cells exhibited the character of saturation and specificity and heparin sodium could prevent attachment of viruses on these cells. These results are in accord with those reported previously. It was also proved that the manner of drug-use prior to adsorption or simultaneous use of drug and adsorption was better than adsorption prior to drug-use, and the inhibition rates of the former and latter manner were 84. 76% and 82.92% respectively. Three manners of drug-use with Gardenia extract ZG were all effective to reduce the adsorption quantity of viruses, especially the manner of simultaneous use of drug and adsorption with an adsorption inhibition rate of 68.46% . From the above observation, it is apparent that the mechanism of anti-viral activity of Gardenia extract ZG may be via several steps involved in the HSV-1 adsorption. 相似文献
55.
目的:对耳大神经及腮腺筋膜解剖进行再认识,由此改良腮腺切除手术方法。方法:解剖成人尸体10侧,术中活体解剖20侧,对耳大神经和腮腺筋膜的解剖要素进行观察。根据观察结果进行改良腮腺切除术14例,即在腮腺筋膜表面翻瓣后,由前向后另翻腮腺筋膜瓣,切除腮腺后将筋膜瓣复位缝合,完整保留耳大神经和腮腺筋膜。结果:耳大神经在下颌角水平之上0-2cm依次分耳后、耳垂、耳前支,神经主干末段和分支起始段均分布于腮腺筋膜浅层表面,后者致密,其致密纤维包裹在神经周围。改良手术后2例(14.3%)发生轻度Frey’s综合征,无1例发生术区皮肤长期麻木、长期面瘫、涎瘘及肿瘤复发。结论:耳大神经各分支和腮腺筋膜具有不可代替的解剖生理功能,改良术式能将两者完好保留,显著降低术后并发症。 相似文献
56.
Sezai Sahmay Yavuz Aydın Nil Atakul Begum Aydogan Semih Kaleli 《Gynecological endocrinology》2014,30(2):130-134
The relation of antimullerian hormone (AMH) levels with the clinical and biochemical markers of polycystic ovary syndrome (PCOS) could be different. A total of 463 PCOS patients were evaluated in this cross-sectional study. Groups were constructed according to polycystic ovarian morphology (PCOM) and menstrual cycle-length. The relation of serum AMH with androgenic hormones, menstrual cycle-length and clinical signs of PCOS were investigated. A powerful positive relation was found between the PCOM and AMH levels (odds ratio?=?2.49). There was a negative correlation between age and AMH level (p?0.001, r[correlation coefficent]?=??0.155). Positive correlations were found between luteinizing hormone (LH) and AMH (p?0.001, r?=?0.25) and also between cycle length and AMH (p?0.01, r?=?0.27). We found a negative week correlation between AMH and follicle-stimulating hormone (FSH) (p?=?0.01, r?=??0.19). After controlling main androgenic hormones, AMH was found to be correlated with the Ferriman–Gallway score (p?=?0.03, r?=?0.18). There was a positive relationship between hirsutism and AMH (odds ratio?=?1.43), but no correlation between AMH and other parameters of clinical hyperandrogenism like hair-loss, acne and seborrhea were identified. The strongest relation was presented between the AMH levels and PCOM. Also, cycle-length correlated well with the AMH levels. The relationship between hirsutism and AMH is found to be independent from androgenic hormones. 相似文献
57.
对中国汉族年轻成人正常(牙合)牙齿的舌侧形态进行三维测量,为研发基于中国人牙体舌侧形态的舌侧直丝弓托槽提供数据参考。方法:采用上海正雅齿科科技有限公司开发的数字化正畸设计系统软件,对普查获得的64副中国汉族正常(牙合)个体的牙齿模型进行三维扫描,并对三维数字模型舌侧面进行计算机定点及测量分析。结果:获得正常(牙合)人群牙齿舌侧的轴倾度、转矩角、冠凸距和尖牙与磨牙补偿角指标的参考值,与国内相关研究结果相近。结论:本研究的测量结果可用于研发中国人舌侧直丝弓托槽标准型。 相似文献
58.
目的:探讨survivin基因启动子-31G/C多态性与中国人群肿瘤易感性的关系。方法:在Pubmed、Medline和中国期刊网全文数据库等数据库中检索相关中外文文献,制定文献纳入及排除标准,运用statal1.0软件进行Meta分析,计算合并的比值比(0R)及95%可信区间(CI)。结果:在中国人群中,survivin基因启动子-31G/C位点携带C碱基的肿瘤易感性是携带G碱基的1.30倍(OR=1.30,95%CI:1.08~1.56),且携带C/C基因型比携带其他基因型更容易导致肿瘤的发生。结论:survivin基因启动子-31G/C位点可能是中国人群肿瘤的一个重要分子标记物。 相似文献
59.
Berna Aslan Çetin Begum Aydogan Mathyk Nadiye Koroglu Ilkbal Temel Yuksel Merve Konal Hakan Erenel 《The journal of maternal-fetal & neonatal medicine》2013,26(24):4108-4113
AbstractPurpose: Surgical site infections (SSIs) after cesarean section cause maternal morbidity and economic and emotional burdens on society. Our aim is to measure procalcitonin (PCT) levels in patients who developed incisional SSIs after cesarean section while also comparing PCT concentrations between patients who underwent a secondary suture and who did not require a secondary suture.Methods: Ninety-four patients who developed incisional SSI after cesarean section were enrolled in our study. At the time of admission, serum PCT, C-reactive protein (CRP), and white blood cell (WBC) counts were measured. The study population was grouped into two, based on the need of a secondary suture and the patients baseline blood tests were compared.Results: The mean serum CRP level was not significant among the groups; however, the median serum PCT level was significantly higher in patients who required a secondary suture (0.21 vs. 0.05?ng/ml, p?≤?.0001). Serum PCT levels were positively correlated with the length of hospital stay (r?=?0.72, p?=?.0001). Area under the curve (AUC) for PCT in predicting the need of a secondary suture was 0.85 (95% CI: 0.772–0.922) and the cutoff point was 0.142?ng/ml with a sensitivity of 75% and specificity of 97.8% (p?=?.0001).Conclusion: Serum PCT is a promising marker for both diagnosing and predicting the severity of SSIs after cesarean sections.Trial registration: ClinicalTrials.gov identifier: NCT03223233. 相似文献
60.
Alan J. Nixon Laila Begum Hussni O. Mohammed Barbara Huibregtse Michael M. O'Callaghan Gloria L. Matthews 《Journal of orthopaedic research》2011,29(7):1121-1130
Autologous chondrocyte implantation (ACI) has been used clinically for over 15 years and yet definitive evidence of chondrocyte persistence and direct impact on cartilage repair in full‐thickness lesions is scant and no data are available on ACI in partial‐thickness defects in any animal model. This study assessed the effect of chondrocytes secured using periosteal overlay in partial‐ and full‐thickness cartilage defects in the equine model. Paired cartilage defects 15 mm in diameter were made in the patellofemoral joint of 16 horse and repaired with ACI or periosteal flap alone. Response was assessed at 8 weeks by clinical, microradiographic, and histologic appearance, and by collagen type II immunohistochemistry, and proteoglycan and DNA quantification. ACI improved histologic scores in partial‐ and full‐thickness cartilage defects, including defect filling, attachment to the underlying subchondral bone, and presence of residual chondrocyte accumulations. For partial‐thickness defects chondrocyte predominance, collagen type II content, and toluidine stained matrix were enhanced, and attachment to the surrounding cartilage improved. DNA and PG content of grafted partial‐thickness defects was improved by chondrocyte implantation. Periosteal patches alone did not induce cartilage repair. This study indicated implantation of chondrocytes to cartilage defects improved healing with a combination of persisting chondrocyte regions, enhanced collagen type II formation, and better overall cartilage healing scores. Use of ACI in the more challenging partial‐thickness defects also improved histologic indices and biochemical content. The equine model of cartilage healing closely resembles cartilage repair in man, and results of this study confirm cell persistence and improved early cartilage healing events after ACI. © 2011 Orthopaedic Research Society Published by Wiley Periodicals, Inc. J Orthop Res 29: 1121–1130, 2011 相似文献