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| 1 | Vleiotic recombination and male infertility: from basic science to clinical reality?显示文摘 | Michael Chann Patricio E Lau Helen G Tempest | 2011 | Asian Journal of Andrology2011，13，2： | 6 |
| 2 | Favorable response to subcutaneous administration of infliximab in rats with experimental colitis显示文摘AIM: To investigate the influence of infliximab (Remicade)on experimental colitis produced by 2,4,6,trinitrobenzene sulfonic acid (TNBS) in rats.METHODS: Thirty-six Wistar rats were allocated into four groups (three groups of six animals each and a fourth of 12 animals). Six more healthy animals served as normal controls (Group 5). Group 1:colitis was induced by intracolonic installation of 25 mg of TNBS dissolved in 0.25 mL of 50% ethanol and infliximab was subcutaneously administered at a dose of 5 mg/kg BW; Group 2: colitis was induced and infliximab was subcutaneously administered at a dose of 10 mg/kg BW; Group 3: colitis was induced and infliximab was subcutaneously administered at a dose of 15 mg/kg BW; Group 4: colitis was induced without treatment with infliximab. Infliximab was administered on d 2-6. On the 7th d, all animals were killed. The colon was fixed in 10%buffered formalin and examined by light microscopy for the presence and activity of colitis and the extent of tissue damage. Tumor necrosis factor-alpha (TNF-α) and malondialdehyde (MDA) were also measured.RESULTS: Significant differences concerning the presence of reparable lesions and the extent of bowel mucosa without active inflammation in all groups of animals treated with infliximab compared with controls were found. Significant reduction of the tissue levels of TNF-α in all groups of treated animals as compared withthe untreated ones was found (0.47±0.44, 1.09±0.86,0.43±0.31 vs 18.73±10.53 respectively). Significant reduction in the tissue levels of MDA was noticed in group 1 as compared to group 4, as well as between groups 2 and 4.CONCLUSION: Subcutaneous administration of infliximab reduces the inflammatory activity as well as tissue TNF-α and MDA levels in chemical colitis in rats.Infliximab at a dose of 5 mg/kg BW achieves better histological results and produces higher reduction of the levels of TNF-α than at a dose of 10 mg/kg BW.Infliximab at a dose of 5 mg/kg BW produces higher reduction of tissue MDA levels than at a dose of 15 mg/kg BW. | John K Triantafillidis Apostolos E Papalois Aikaterini Parasi Emmanuel Anagnostakis Stavros Burnazos Aristofanis Gikas Emmanuel G Merikas Emmanuel Douzinas Maria Karagianni Helen Sotiriou | 2005 | World Journal of Gastroenterology2005，11，43： | 5 |
| 3 | Counter-regulatory phosphatases TNAP and NPP1 temporally regulate tooth root cementogenesis显示文摘Cementum is critical for anchoring the insertion of periodontal ligament fibers to the tooth root. Several aspects of cementogenesis remain unclear, including differences between acellular cementum and cellular cementum, and between cementum and bone.Biomineralization is regulated by the ratio of inorganic phosphate(Pi) to mineral inhibitor pyrophosphate(PPi), where local Piand PPi concentrations are controlled by phosphatases including tissue-nonspecific alkaline phosphatase(TNAP) and ectonucleotide pyrophosphatase/phosphodiesterase 1(NPP1). The focus of this study was to define the roles of these phosphatases in cementogenesis. TNAP was associated with earliest cementoblasts near forming acellular and cellular cementum. With loss of TNAP in the Alpl null mouse, acellular cementum was inhibited, while cellular cementum production increased, albeit as hypomineralized cementoid. In contrast, NPP1 was detected in cementoblasts after acellular cementum formation, and at low levels around cellular cementum. Loss of NPP1 in the Enpp1 null mouse increased acellular cementum, with little effect on cellular cementum.Developmental patterns were recapitulated in a mouse model for acellular cementum regeneration, with early TNAP expression and later NPP1 expression. In vitro, cementoblasts expressed Alpl gene/protein early, whereas Enpp1 gene/protein expression was significantly induced only under mineralization conditions. These patterns were confirmed in human teeth, including widespread TNAP, and NPP1 restricted to cementoblasts lining acellular cementum. These studies suggest that early TNAP expression creates a low PPienvironment promoting acellular cementum initiation, while later NPP1 expression increases PPi, restricting acellular cementum apposition. Alterations in PPihave little effect on cellular cementum formation, though matrix mineralization is affected. | Laura E Zweifler Mudita K Patel Francisco H Nociti Jr Helen F Wimer Jose L Milln Martha J Somerman Brian L Foster | 2015 | International Journal of Oral Science2015，7，1： | 5 |
| 4 | Oral treatment with plecanatide or dolcanatide attenuates visceral hypersensitivity via activation of guanylate cyclase-C in rat models显示文摘AIM To investigate the effects of plecanatide and dolcanatide on maintenance of paracellular permeability, integrity of tight junctions and on suppression of visceral hypersensitivity. METHODS Transport of fluorescein isothiocyanate(FITC)-dextran was measured to assess permeability across cell monolayers and rat colon tissues. Effects of plecanatide and dolcanatide on the integrity of tight junctions in Caco-2 and T84 monolayers and on the expression and localization of occludin and zonula occludens-1(ZO-1) were examined by immunofluorescence microscopy. Anti-nociceptive activity of these agonists was evaluated in trinitrobenzene sulfonic acid(TNBS)-induced inflammatory as well as in non-inflammatory partial restraint stress(PRS) rat models. Statistical significance between the treatment groups in the permeability studies were evaluated using unpaired t-tests.RESULTS Treatment of T84 and Caco-2 monolayers with lipopolysaccharide(LPS) rapidly increased permeability, which was effectively suppressed when monolayers were also treated with plecanatide or dolcanatide. Similarly, when T84 and Caco-2 monolayers were treated with LPS, cell surface localization of tight junction proteins occludin and ZO-1 was severely disrupted. When cell monolayers were treated with LPS in the presence of plecanatide or dolcanatide, occludin and ZO-1 were localized at the cell surface of adjoining cells, similar to that observed for vehicle treated cells. Treatment of cell monolayers with plecanatide or dolcanatide without LPS did not alter permeability, integrity of tight junctions and cell surface localization of either of the tight junction proteins. In rat visceral hypersensitivity models, both agonists suppressed the TNBS-induced increase in abdominal contractions in response to colorectal distension without affecting the colonic wall elasticity, and both agonists also reduced colonic hypersensitivity in the PRS model. CONCLUSION Our results suggest that activation of GC-C signaling might be involved in maintenance of barrier function, possibly through regulating normal localization of tight junction proteins. Consistent with these findings, plecanatide and dolcanatide showed potent antinociceptive activity in rat visceral hypersensitivity models. These results imply that activation of GC-C signaling may be an attractive therapeutic approach to treat functional constipation disorders and inflammatory gastrointestinal conditions. | Illona-Marie Boulete Anusha Thadi Catherine Beaufrand Viren Patwa Apoorva Joshi John A Foss E Priya Eddy Helene Eutamene Vaseem A Palejwala Vassilia Theodorou Kunwar Shailubhai | 2018 | World Journal of Gastroenterology2018，24，17： | 5 |
| 5 | Costimulation of resting B lymphocytes alters the IL-4-activated IRS2 signaling pathway in a STAT6 independent manner: implications for cell survival and proliferation显示文摘IL-4 is an important B cell survival and growth factor. IL-4 induced the tyrosine phosphorylation of IRS2 in resting B lymphocytes and in LPS- or CD40L-activated blasts. Phosphorylated IRS2 coprecipitated with the p85 subunit of PI 3’ kinase in both resting and activated cells. By contrast, association of phosphorylated IRS2 with GRB2 was not detected in resting B cells after IL-4 treatment although both proteins were expressed. However, IL-4 induced association of IRS2 with GRB2 in B cell blasts. The pattern of IL-4- induced recruitment of p85 and GRB2 to IRS2 observed in B cells derived from STAT6 null mice was identical to that observed for normal mice. While IL-4 alone does not induce activation of MEK, a MEKI inhibitor suppressed the IL-4-induced proliferative response of LPS-activated B cell blasts. These results demonstrate that costimulation of splenic B cells alters IL-4-induced signal transduction independent of STAT6 leading to proliferation. Furthermore, proliferation induced by IL-4 in LPS-activated blasts is dependent upon the MAP kinase pathway. | ZAMORANO JOSE,Unidad de Investigacion, Hospital San Pedro de Alcantara, Avda Millan Astray, 10003 Caceres ANN E KELLY, JONATHAN AUSTRIAN, HELEN Y WANG, ACHSAH D KEEGAN (Department of Immunology, Jerome Holland Labs, American Red Cross, Rockville, MD, USA | 2001 | Cell Research2001，11，1： | 4 |
| 6 | Macrophage secretory products induce an inflammatory phenotype in hepatocytes显示文摘AIM:To investigate the influence of macrophages on hepatocyte phenotype and function.METHODS:Macrophages were differentiated from THP-1 monocytes via phorbol myristate acetate stimulation and the effects of monocyte or macrophageconditioned medium on HepG2 mRNA and protein expression determined.The in vivo relevance of these findings was confirmed using liver biopsies from 147 patients with hepatitis C virus(HCV)infection.RESULTS:Conditioned media from macrophages,but not monocytes,induced a transient morphological change in hepatocytes associated with upregulation of vimentin(7.8±2.5-fold,P=0.045)and transforming growth factor(TGF)-β1(2.6±0.2-fold,P<0.001)and downregulation of epithelial cadherin(1.7±0.02-fold,P=0.017)mRNA expression.Microarray analysis revealed significant upregulation of lipocalin-2(17-fold,P <0.001)and pathways associated with inflammation,and substantial downregulation of pathways related to hepatocyte function.In patients with chronic HCV,realtime polymerase chain reaction and immunohistochemistry confirmed an increase in lipocalin-2 mRNA(F0 1.0 ±0.3,F1 2.2±0.2,F2 3.0±9.3,F3/4 4.0±0.8,P= 0.003)and protein expression(F1 1.0±0.5,F2 1.3± 0.4,F3/4 3.6±0.4,P=0.014)with increasing liver injury.High performance liquid chromatography-tandem mass spectrometry analysis identified elevated levels of matrix metalloproteinase(MMP)-9 in macrophageconditioned medium,and a chemical inhibitor of MMP-9 attenuated the change in morphology and mRNA expression of TGF-β1(2.9±0.2 vs 1.04±0.1,P<0.001) in macrophage-conditioned media treated HepG2 cells.In patients with chronic HCV infection,hepatic mRNA expression of CD163(F0 1.0±0.2,F1/2 2.8±0.3,F3/4 5.3±1.0,P=0.001)and MMP-9(F0 1.0±0.4,F1/2 2.8±0.3,F3/4 4.1±0.8,P=0.011)was significantly associated with increasing stage of fibrosis.CONCLUSION:Secreted macrophage products alter the phenotype and function of hepatocytes,with increased expression of inflammatory mediators,suggesting that hepatocytes actively participate in liver injury. | Michelle Melino Victoria L Gadd Gene V Walker Richard Skoien Helen D Barrie Dinesh Jothimani Leigh Horsfall Alun Jones Matthew J Sweet Gethin P Thomas Andrew D Clouston Julie R Jonsson Elizabeth E Powell | 2012 | World Journal of Gastroenterology2012，18，15： | 3 |
| 7 | 雄激素受体的目标基因在骨骼肌的表达显示文摘本文通过研究体外和体内模型中潜在的雄激素受体调节基因来确定骨骼肌中雄激素的合成代谢作用机制。睾酮治疗组的去势雄性小鼠与对照组去势雄性小鼠比较,其骨骼肌中肌源性调节因子肌细胞生成素的表达显著下降,而缺乏DNA结合活性的雄性雄激素受体敲除小鼠(AR^△ZF2)与野生型小鼠比较,其骨骼肌中肌源性调节因子肌细胞生成素的表达显著升高,证明了肌细胞生成素是通过雄激素/雄激素受体通路被抑制。通过12小时的骨骼肌细胞(SkMC)的成肌细胞联合双氢睾酮治疗,睾酮治疗组的去势雄性小鼠肌肉中的泛素连接酶Fbxo32被抑制,而肌肉中c—Myc表达较对照组去势雄性小鼠降低,在△R^△ZF2组小鼠肌肉中c-Myc表达升高。调节成肌细胞由增殖向分化转变的一组基因如Tceal7,p57^Kip2,Igf2和钙调磷酸酶Aa的表达在AR^△ZF2组小鼠肌肉中升高,除p57^Kip2外的上述所有基因在睾酮治疗组去势雄性小鼠肌肉中的表达均较对照组降低。因此得出结论,雄激素通过雄激素受体在雄性小鼠体内发挥作用,它在肌肉生长和发展过程中可维持成肌细胞处于增殖状态并推迟成肌细胞向分化状态转变,另外还可抑制泛素连接酶介导的导致肌肉萎缩的通路来保持小鼠肌肉质量,从而一定程度上促进肌肉不断生长达到顶峰。 | Kesha Rana Nicole KL Lee Jeffrey D Zajac Helen E MacLean | 2014 | Asian Journal of Andrology2014，16，5： | 3 |
| 8 | Regulation of cell adhesion in the testis: a new role for p73显示文摘在成年睾丸的男细菌房间在他们从 spermatogonial 干细胞转移到直的基因表示侧面和形态学经历的戏剧的变化成熟精子依赖于他们有 Sertoli 房间的协会。Sertoli 房间为男细菌房间的幸存和成熟是关键的。二份最近的报纸, Holembowski et al.1 和 Inoue et al.2 为 p53 家庭成员,描述了一个令人吃惊的角色 p73,在细菌 cell-Sertoli 的规定房间粘附。 | Helen E Abud Gary R Hime | 2014 | Asian Journal of Andrology2014，16，6： | 2 |
| 9 | Causes of encephalitis and differences in their clinical presentations in England: a multicentre, population-based prospective study显示文摘 | Julia Granerod Helen E Ambrose Nicholas WS Davies Jonathan P Clewley Amanda L Walsh Dilys Morgan Richard Cunningham Mark Zuckerman Ken J Mutton Tom Solomon Katherine N Ward Michael PT Lunn Sarosh R Irani Angela Vincent David WG Brown Natasha S Crowcroft | 2010 | The Lancet Infectious Diseases2010，，12： | 2 |
| 10 | Interactions among age, adiposity, bodyweight, lifestyle factors and sex steroid hormones in healthy Singaporean Chinese men显示文摘瞄准:为了在年龄,生活方式因素,人体测量的参数,百分比身体脂肪和类固醇之中检验相互关系,在 531 个健康新加坡人中国人的荷尔蒙参数在 29 和 72 岁之间变老。方法:各种各样的生活方式参数通过调查,和睾丸激素被确定(T) , estradiol (E2 ) , dehydroepi 雄甾酮硫酸盐(DHEAS ) 和性别荷尔蒙绑定血球素(SHBG ) 用确定的方法被测量。人体测量的参数镇定、计算,并且百分比身体脂肪(Siri ) 用 DEXA 扫描仪被测量。结果:SHBG, DHEAS, bioavailable-T (Bio-T ) , E2, Siri, Ht, W/H, W/Ht 和工作应力独立地与年龄被相关。多使用变量分析并且好久调整,吸烟并且另外的相关因素,锻练并且白酒消费在雄激素层次和身体作文上有积极影响。然而,黑色和绿茶消费在身体作文上并且与 E2 和免费 Estradiol 索引(FEI ) 的高水平与否定效果被联系。有更短的睡觉持续时间的人与夜里的睡觉的 6 h 或更多作为与那些相比有显著地更低的 T 层次。更高的 T 层次与脂肪过多的底层和脂肪过多的另外的索引被联系,而更高的 E2 层次与脂肪过多的高水平有关。有更高的 DHEAS 的人比有低 DHEAS 层次的那些显著地更高、重。结论:学习在 gonadal/adrenal 和新陈代谢的分隔空间之中显示出靠近的相互作用,与是的年龄在他们的相互作用的一个关键决定因素。生活方式因素象锻练那样,吸烟,睡觉并且酒精和茶消费可能显著地在在人决定健康的地位起作用。 | Victor H. H. Goh Terry Y. Y. Tong Helen E E Mok Baharudin Said | 2007 | Asian Journal of Andrology2007，9，5： | 2 |
| 11 | From the archives of the AFIP gastrointestinal stromal tumors: radiologic features with pathologic correlation 显示文摘 | Angela D Helen E William M | 2003 | Radio Graphics2003，23，： | 1 |
| 12 | Scharfman,brain-derived neurotrophic factor显示文摘 | Devin K Binder Helen E | 2004 | Growth Factors2004，3，： | 1 |
| 13 | CD28 costimulation improves expansion and persistence of chimeric antigen receptor-modified T cells in lymphoma patients显示文摘 | Savoldo Barbara Ramos Carlos Almeida Liu Enli Mims Martha P Keating Michael J Carrum George Kamble Rammurti T Bollard Catherine M Gee Adrian P Mei Zhuyong Liu Hao Grilley Bambi Rooney Cliona M Heslop Helen E Brenner Malcolm K Dotti Gianpie | 2011 | Journal of Clinical Investigation2011，，5： | 1 |
| 14 | Fertility after Ec topic Pregnancy 显示文摘 | Dorothy E Helen F Herbet B | 1989 | Am J ObstetGynecol1989，161，： | 1 |
| 15 | Primary Percutaneous Coronary Intervention in Patients With Acute Myocardial Infarction, Resuscitated Cardiac Arrest, and Cardiogenic Shock显示文摘 | Darren M Marie-Claude M Helene E | 2013 | Jacc Car- diovascular Interventions2013，6，2： | 1 |
| 16 | Adoptive cellular therapy with T cells specific for EBV-derived tumor antigens 显示文摘 | John Craddock Helen E Heslop | 2008 | Update Cancer Ther2008，3，1： | 1 |
| 17 | 查看详情显示文摘 | Anastasios E Helen B Spyros A Despina T | | 0，，31： | 1 |
| 18 | Brain derived neurotrophic factor and epilepsy-a missing link显示文摘 | Helen E Scharfman | 2005 | Epilepsy Curr2005，3，： | 1 |
| 19 | High solid simultaneous saccharification and fermentation of wet oxidized corn straw to ethanol显示文摘 | Eniko Varga Helene B Klinke Kati R e ciey | 2004 | Biotechnology and Bioengineering2004，88，5： | 1 |
| 20 | Objective structured clinical examination (OSCE) : review of literature and imphcations for nursing education 显示文摘 | Helen E | 2007 | Nurse Educ Today2007，27，5： | 1 |
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