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| 1 | Role of chemokines and their receptors in viral persistence and liver damage during chronic hepatitis C virus infection显示文摘Chemokines produced in the liver during hepatitis C virus(HCV) infection induce migration of activated T cells from the periphery to infected parenchyma.The milieu of chemokines secreted by infected hepatocytes is predominantly associated with the T-helper cell/Tc1 T cell(Th1/Tc1) response.These chemokines consist of CCL3(macrophage inflammatory protein-1α;MIP-1α),CCL4(MIP-1β),CCL5(regulated on activation normal T cell expressed and secreted;RANTES),CXCL10(interferon-γ-inducible protein-10;IP-10),CXCL11(interferon-inducible T-cell α chemoattractant;I-TAC),and CXCL9(monokine induced by interferon γ;Mig) and they recruit T cells expressing either CCR5 or CXCR3 chemokine receptors.Intrahepatic and peripheral blood levels of these chemokines are increased during chronic hepatitis C.The interaction between chemokines and their receptors is essential in recruiting HCV-specific T cells to control the infection.When the adaptive immune response fails in this task,non-specific T cells without the capacity to control the infection are also recruited to the liver,and these are ultimately responsible for the persistent hepatic damage.The modulation of chemokine receptor expression and chemokine secretion could be a viral escape mechanism to avoid specific T cell migration to the liver during the early phase of infection,and to maintain liver viability during the chronic phase,by impairing non-specific T cell migration.Some chemokines and their receptors correlate with liver damage,and CXCL10(IP-10) and CXCR3 levels have shown a clinical utility as predictors of treatment response outcome.The regulation of chemokines and their receptors could be a future potential therapeutic target to decrease liver inflammation and to increase specific T cell migration to the infected liver. | Juan R Larrubia Selma Benito-Martínez Miryam Calvino Eduardo Sanz-de-Villalobos Trinidad Parra-Cid | 2008 | World Journal of Gastroenterology2008，14，47： | 13 |
| 2 | How important is donor age in liver transplantation?显示文摘The age of liver donors has been increasing in the past several years because of a donor shortage. In the United States, 33% of donors are age 50 years or older, as are more than 50% in some European countries. The impact of donor age on liver transplantation(LT) has been analyzed in several studies with contradictory conclusions. Nevertheless, recent analyses of the largest databases demonstrate that having an older donor is a risk factor for graft failure. Donor age is included as a risk factor in the more relevant graft survival scores, such as the Donor Risk Index, donor age and Model for End-stage Liver Disease, Survival Outcomes Following Liver Transplantation, and the Balance of Risk. The use of old donors is related to an increased rate of biliary complications and hepatitis C virus-related graft failure. Although liver function does not seem to be significantly affected by age, the incidence of several liver diseases increases with age, and the capacity of the liver to manage or overcome liver diseases or external injuries decreases. In this paper, the importance of age in LT outcomes, the role of donor age as a risk factor, and the influence of aging on liver regeneration are reviewed. | Alberto Lué Estela Solanas Pedro Baptista Sara Lorente Juan J Araiz Agustin Garcia-Gil M Trinidad Serrano | 2016 | World Journal of Gastroenterology2016，22，21： | 10 |
| 3 | Pathogenesis of H elicobacter pylori Infection显示文摘 | Trinidad Parra Cid Miryam Calvino Fernández Selma Benito Martínez Nicola L. Jones | 2013 | Helicobacter2013，，： | 4 |
| 4 | YKL40 expression in CD14^+ liver cells in acute and chronic injury显示文摘AIM:To demonstrate that CD14 + cells are an important source of the growth factor YKL40 in acute and chronic liver damage.METHODS:Rats were inoculated with one dose of CCl4 to induce acute damage.Liver biopsies were obtained at 0,6,12,24,48 and 72 h.For chronic damage,CCl4 was administered three days per week for 6 or 8 wk.Tissue samples were collected,and cellular populations were isolated by liver digestion and purified by cell sorting.YKL40 mRNA and protein expression were evaluated by realtime polymerase chain reaction and western blot.RESULTS:Acute liver damage induced a rapid increase of YKL40 mRNA beginning at 12 h.Expression peaked at 24 h,with a 26fold increase over basal levels.By 72 h however,YKL40 expression levels had nearly returned to control levels.On the other hand,chronic damage induced a sustained increase in YKL40 expression,with 7and 9fold higher levels at 6 and 8 wk,respectively.The pattern of YKL40 expression in different subpopulations showed that CD14+cells,which include Kupffer cells,are a source of YKL40 after acute damage at 72 h[0.09 relative expression units(REU)]as well as after chronic injury at 6 wk(0.11 REU).Hepatocytes,in turn,accounted for 0.06 and 0.01 REU after 72 h(acute)or 6 wk(chronic),respectively.The rest of the CD14cells(including T lymphocytes,B lymphocytes,natural killer and natural killer T cells) yielded 0.07 and 0.15 REU at 72 h and 6 wk,respectively.YKL40 protein expression in liver was detected at 72 h as well as 6 and 8 wk,with the highest expression relative to controls(11fold;P≤0.05)seen at 6 wk.Macrophages were stimulated by lipopolysaccharide.We demonstrate that under these conditions,these cells showed maximum expression of YKL40 at 12 h,with P<0.05 compared with controls.CONCLUSION:Hepatic CD14 + cells are an YKL40 mRNA and protein source in acute and chronic liver injury,with expression patterns similar to growth factors implicated in inflammationfibrogenesis. | Oscar Pizano-Martínez Irinea Yaez-Sánchez Pilar Alatorre-Carranza Alejandra Miranda-Díaz Pablo C Ortiz-Lazareno Trinidad García-Iglesias Adrian Daneri-Navarro Mónica Vázquez-Del Mercado Mary Fafutis-Morris Vidal Delgado-Rizo | 2011 | World Journal of Gastroenterology2011，17，33： | 3 |
| 5 | New genes emerging for colorectal cancer predisposition显示文摘Colorectal cancer(CRC)is one of the most frequent neoplasms and an important cause of mortality in the developed world.This cancer is caused by both genetic and environmental factors although 35%of the variation in CRC susceptibility involves inherited genetic differences.Mendelian syndromes account for about5%of the total burden of CRC,with Lynch syndrome and familial adenomatous polyposis the most common forms.Excluding hereditary forms,there is an important fraction of CRC cases that present familial aggregation for the disease with an unknown germline genetic cause.CRC can be also considered as a complex disease taking into account the common diseasecommom variant hypothesis with a polygenic model of inheritance where the genetic components of common complex diseases correspond mostly to variants of low/moderate effect.So far,30 common,low-penetrance susceptibility variants have been identified for CRC.Recently,new sequencing technologies including exomeand whole-genome sequencing have permitted to add a new approach to facilitate the identification of new genes responsible for human disease predisposition.By using whole-genome sequencing,germline mutations in the POLE and POLD1 genes have been found to be responsible for a new form of CRC genetic predisposition called polymerase proofreading-associated polyposis. | Clara Esteban-Jurado Pilar Garre Maria Vila Juan José Lozano Anna Pristoupilova Sergi Beltrán Anna Abulí Jenifer Muoz Francesc Balaguer Teresa Ocaa Antoni Castells Josep M Piqué Angel Carracedo Clara Ruiz-Ponte Xavier Bessa Montserrat Andreu Luis Bujanda Trinidad Caldés Sergi Castellví-Bel | 2014 | World Journal of Gastroenterology2014，20，8： | 3 |
| 6 | Costimulatory molecule programmed death-1 in the cytotoxic response during chronic hepatitis C显示文摘Hepatitis C virus (HCV)-specific CD8+ T cells play an important role in the resolution of HCV infection. Nevertheless, during chronic hepatitis C these cells lack their effector functions and fail to control the virus. HCV has developed several mechanisms to escape immune control. One of these strategies is the upregulation of negative co-stimulatory molecules such us programmed death-1 (PD-1). This molecule is upregulated on intrahepatic and peripheral HCV-specific cytotoxic T cells during acute and chronic phases of the disease, whereas PD-1 expression is low in resolved infection. PD-1 expressing HCV-specific CD8+ T cells are exhausted with impairment of several effector mechanisms, such as: type-1 cytokine production, expansion ability after antigen encounter and cytotoxic ability. However, PD-1 associated exhaustion can be restored by blocking the interaction between PD-1 and its ligand (PD-L1). After this blockade, HCV-specificCD8+ T cells reacquire their functionality. Nevertheless, functional restoration depends on PD-1 expression level. High PD-1-expressing intrahepatic HCV-specific CD8+ T cells do not restore their effector abilities after PD-1/PD-L1 blockade. The mechanisms by which HCV is able to induce PD-1 up-regulation to escape immune control are unknown. Persistent TCR stimulation by a high level of HCV antigens could favour early PD-1 induction, but the interaction between HCV core protein and gC1q receptor could also participate in this process. The PD-1/PD-L1 pathway modulation could be a therapeutic strategy, in conjunction with the regulation of others co-stimulatory pathways, in order to restore immune response against HCV to succeed in clearing the infection. | Juan Ramón Larrubia Selma Benito-Martínez Joaquín Miquel Miryam Calvino Eduardo Sanz-de-Villalobos Trinidad Parra-Cid | 2009 | World Journal of Gastroenterology2009，15，41： | 3 |
| 7 | 中医药在菲律宾的发展现状与分析显示文摘菲律宾国内医疗方面主要实行省区责任制及有限制的分级转诊制度,政府推行菲律宾健康(Philhealth)计划,可为大部分民众提供小额医疗保险金。导致该国居民死亡的十大疾病包括缺血性心脏病、脑卒中及下呼吸道感染等,其中高血压性心脏病、慢性肾病和糖尿病等的增长趋势较快。菲律宾国内传统医学以正骨、按摩和草药学为主,当地政府及民众对针灸接受度较好,针灸疗法已纳入菲律宾医保范围。但中医理论及中药在当地的发展仍有较多限制,且针灸与中草药的临床应用也较为有限。菲律宾国内中医药教育亦不够系统。因此建议完善中医药教育体系、扩大针灸应用范围,并针对该国高发病种发挥中药特色,进行有针对性的推广,同时借助远程医疗等现代技术促进两国在中医药领域的合作。 | 覃叶萍 梁宁 Harold Louis Trinidad 石晗 赵静 宋坪 许家杰 曹洪欣 | 2021 | 国际中医中药杂志2021，43，6： | 3 |
| 8 | IL-6 and IGF-1 are Independent Prognostic Factors of Liver Steatosis and Non-Alcoholic Steatohepatitis in Morbidly Obese Patients显示文摘 | David García-Galiano Miguel A. Sánchez-Garrido Isabel Espejo José Luis Montero Guadalupe Costán Trinidad Marchal Antonio Membrives José M. Gallardo-Valverde Juan R. Mu?oz-Casta?eda Eugenio Arévalo Manuel Mata Jordi Muntané | 2007 | Obesity Surgery2007，，： | 2 |
| 9 | Local immunostimulation of the bovine mammary gland with interleukin-2显示文摘 | Nickerson S C Baker P A Trinidad P | 1989 | J Dairy Sci1989，72，7： | 2 |
| 10 | Preparation of Rod-like Aluminum Doped Zinc Oxide Powders by Sol-gel Technique Using Metal Chlorides and Acetylacetone Precursors显示文摘Al-doped ZnO(AZO) powders were prepared by using metal chloride precursors and the sol-gel technique. IR peaks observed at 1590 cm-1 and 1620 cm^(-1) indicated the formation of metal chelate as a consequence of the addition of acetylacetone to the metal chloride solution. TG-DSC analysis of the AZO gels confirmed the formation of metal chelate as evidenced by the development of several weight loss peaks accompanied by the introduction of new endothermic peaks. The resulting AZO gels were annealed at 500, 600, and 800 ℃ to study the effect of annealing temperature. XRD and SEM results showed that crystallization of AZO gels takes place around 600 ℃. Hexagonal wurtzite structure was identified as the main phase for all the samples. In addition, small shift of the XRD(002) peak coupled with XPS results from the AZO powders confirmed the successful doping of the ZnO powders. Micron sized rod-like AZO powders were uniform in dimension and morphology and remained stable even at 800 ℃. | KESHTKAR Javad VARGAS GARCIA Jorge Roberto GALAVIZ PEREZ Jorge MARTINEZ TRINIDAD José | 2018 | Journal of Wuhan University of Technology(Materials Science)2018，33，6： | 2 |
| 11 | Follow-up in head and neck cancer: patients perspective 显示文摘 | Trinidade A Kothari P Andreou Z | 2012 | Int J Health Care Qual Assur2012，25，2： | 1 |
| 12 | Silicosis: computed tomography findings 显示文摘 | GonzOlez V(Lzquez M Trinidad L6pez C Castell6n Plaza D | 2013 | Radiologia2013，55，6： | 1 |
| 13 | Chiari malformation:clinical and radiographic findings for 364 symptomatic patients显示文摘 | Mihorat TH Chou MW Trinidad EM | 1999 | Neurosurgery1999，44，5： | 1 |
| 14 | Dietary fiber from coconut flour: a functional food显示文摘 | TRINIDAD T P MALLILLIN A C VALDEZ D H | 2006 | Innovative Food Science and Emerging Technologies2006，7，4： | 1 |
| 15 | Synovial sarcoma of the nasal cavity显示文摘 | Acosta Diaz H1 Trinidad Ruiz G Rejas E | 2011 | Acta Otorrinolaringol Esp2011，62，： | 1 |
| 16 | Glycaemic index of different coconut(Cocos nucifera)-flour products in normal and diabetic subjects显示文摘 | Trinidad T P Valdez D H Loyola A S | | 0，，03： | 1 |
| 17 | Compliance and support for smokefree school policies显示文摘 | Trinidad DR Gilpin EA Pierce JP | 2005 | Health Educ Res2005，20，： | 1 |
| 18 | Chiari malformation: clinical and radiographic findings for 364 symptomaticpatients 显示文摘 | Mihorat TH Chou MW Trinidad EM | 1999 | J Neurosurg1999，44，5： | 1 |
| 19 | Helieobaeter pylori stimulates pepsinogens secretion from isolated human peptic cells显示文摘 | Lorente S Doiz O Trinidad Serrano M | 2002 | Gut2002，50，： | 1 |
| 20 | Chiari Ⅰ malformation redefinded: clinical and radiographic findings for 364 symptomatic patients 显示文摘 | Milhorat TH Chou MW Trinidad EM | 1999 | Neurosurery1999，44，： | 1 |
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