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| 1 | 肝脏富血供肿瘤:低管电压、高管电流多层CT扫描在肝动脉晚期对肿瘤检出的初步临床经验显示文摘目的在个体内比较低管电压(80kV)、高管电流CT检查技术与标准CT扫描方案(140kV)检查时,在影像质量、辐射剂量及动脉晚期发现富血供恶性肝脏肿瘤等方面的不同。方法本项前瞻性符合HIPAA法案,单中心研究获机构伦理审查委员会批准,并签署知情同意书。48例(男性31例.女性17例,平均年龄35~77岁)病人的60个恶性富血供肝脏肿瘤病灶[平均直径(20.1±16.4)mm]人组。33个结节通过局部病灶的组织病理学分析获得证实,27个结节影像学随访至少12个月。病人接受双能64层螺旋CT检查。 | D. Marin R.C. Nelson E. Samei E.K. Paulson L.M. Ho D.T. Boll 何岸苇(译) 万业达(校) | 2009 | 国际医学放射学杂志2009，32，4： | 49 |
| 2 | Early-Life Sodium Exposure Unmasks Susceptibility to Stroke in Hyperlipidemic, Hypertensive Heterozygous Tg25 Rats Transgenic for Human Cholesteryl Ester Transfer Protein显示文摘 | Julius L. Decano Jason C. Viereck Ann C. McKee James A. Hamilton Nelson Ruiz-Opazo Victoria L.M. Herrera | 2009 | Circulation2009，，11： | 1 |
| 3 | Effectiveness of Simeprevir plus Sofosbuvir, With or Without Ribavirin, in Real-World Patients with HCV Genotype 1 Infection显示文摘 | M.S. Sulkowski H.E. Vargas A.M. Di Bisceglie P.A. Kuo K.R. Reddy J.K. Lim G. Morelli J.M. Darling J.J. Feld R.S. Brown L.M. Frazier T.G. Stewart M.W. Fried D.R. Nelson I.M. Jacobson | 2015 | Gastroenterology2015，，： | 1 |
| 4 | 自发性卵巢早衰女性生育脆性X染色体综合征儿显示文摘Objective: To inform clinicians about a reproductive risk associated with spontaneous premature ovarian failure and the fragile X mental retardation 1 gene (FMR1). Design: Case report. Setting: National Institutes of Health Clinical Center. Patient(s): A 35-year-old woman with confirmed spontaneous premature ovarian failure. Intervention(s): FMR1 genetic testing. Main Outcome Measure(s): Number of CGG trinucleotide repeats in the 5′untranslated region of FMR1. Result(s): Despite having ovarian failure the woman subsequently conceived and delivered a son with fragile X syndrome (>200 CGG repeats). She was then found to carry an FMR1 premutation (85 CGG repeats). Conclusion(s): This is a real-life manifestation of a theoretical risk; a woman conceived subsequent to the diagnosis of spontaneous premature ovarian failure and has a child who manifests mental retardation due to fragile X syndrome. Women with spontaneous premature ovarian failure are at increased risk of having an FMR1 premutation and should be informed of the availability of fragile X testing. Should an FMR1 premutation be uncovered, this will allow patients to make informed reproductive decisions and help clinicians to properly diagnose family members who may have menstrual irregularity, developmental delay, or neurologic symptoms. | Corrigan E.C. Raygada M.J. Vanderhoof V.H. Nelson L.M. 李跃萍 | 2006 | 世界核心医学期刊文摘(妇产科学分册)2006，0，3： | 0 |
| 5 | 自身免疫性卵巢炎是染色体核型为46XX的自发性卵巢功能早衰患者卵泡功能障碍的原因显示文摘Objective: To assess the association between serum adrenal cortex autoantibodies and histologically confirmed autoimmune lymphocytic oophoritis. Design: Controlled, prospective. Setting: Tertiary research center. Patient(s): Two hundred sixty-six women with 46,XX spontaneous premature ovarian failure. Intervention(s): Ovarian biopsy in 10 women. Main Outcome Measure(s): Serum adrenal cortex autoantibodies assessed by indirect immunofluorescence and autoimmune oophoritis assessed by immunohistochemical lymphocyte markers. Result(s): We obtained a histologic diagnosis of autoimmune oophoritis in four women who tested positive for adrenal cortex autoantibodies and excluded this diagnosis in ovarian biopsies from six women who tested negative for adrenal cortex autoantibodies (4/4 vs 0/6). Women with histologically confirmed autoimmune oophoritis had a greater total ovarian volume as assessed by transvaginal sonography (11.4 ±5.6 mL vs 1.5 ±0.4 mL) (mean ±SEM). They were also more likely to have subclinical adrenal insufficiency and clinical signs of androgen deficiency (3/4 vs 0/6). Overall, 10/266 women tested positive for adrenal cortex autoantibodies (3.8%, 95%confidence interval: 1.8%-6.5%). Conclusion(s): In women who present with 46,XX spontaneous premature ovarian failure as their primary concern there is a clear association between serum adrenal cortex autoantibodies and the presence of histologically confirmed autoimmune oophoritis. | Bakalov V.K. Anasti J.N. Calis K.A. L.M. Nelson 张剑萍 | 2006 | 世界核心医学期刊文摘(妇产科学分册)2006，0，2： | 0 |
| 6 | 核型为46,XX的自发卵巢早衰患者干细胞因子KIT配位子基因(KITLG)的研究显示文摘Objective: To investigate mutations in the human KIT ligand gene (KITLG) gene as a mechanism of 46,XX spontaneous premature ovarian failure. The human KIT ligand gene, known also as human stem cell factor, is the ligand of the c-kit transmembrane tyrosine kinase receptor (KIT). This ligand-receptor interaction is known to play important roles in mouse germ cell migration and proliferation. Design: Cross-sectional study. Setting: Clinical research center. Patient(s): Forty women with 46,XX spontaneous premature ovarian failure. Intervention(s): None. Main Outcome Measure(s): Single-stranded conformational poly-morphism analysis and DNA sequencing. Result(s): We found one nucleotide change of the KITLG coding region (811G→ T) that led to an alteration of the amino acid composition of the KITLG protein in one Caucasian patient (Asp210Tyr). However, we found the same alteration in two normal control Caucasian samples. Three nucleotide substitutions were found in the noncoding exon of KITLG (exon 10). We also identified two intronic polymorphisms. Thus, we did not identify a single significant mutation in the coding region of the KITLG gene in any of 40 patients (upper 95% confidence limit is 7.2% ). Conclusion(s): Mutations in the coding regions of the KITLG gene appear not to be a common cause of 46,XX spontaneous premature ovarian failure in North American women. | Udofa E.A. Soto J. L.M. Nelson 朱亮 | 2006 | 世界核心医学期刊文摘(妇产科学分册)2006，0，11： | 0 |
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