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163篇 您的检索式:作者名="Calvino"
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1Role 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 2008World Journal of Gastroenterology2008,14,47:13
2Pathogenesis of H elicobacter pylori Infection显示文摘Trinidad Parra Cid Miryam Calvino Fernández Selma Benito Martínez Nicola L. Jones 2013Helicobacter2013,,:4
3Costimulatory 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 2009World Journal of Gastroenterology2009,15,41:3
4Diagnostic delay in oral squamous cell carcinoma: the role of cognitive and psychological variables显示文摘This retrospective study investigated, in two cohorts of subjects living in Southern Italy and awaiting treatment for oral squamous cell carcinoma(OSCC), the variables related to diagnostic delay ascribable to the patient, with particular reference to the cognitive and psychological ones. A total of 156 patients with OSCC(mean age: 62 years, M/F: 2.39 : 1) were recruited at the Universities of Palermo and Naples. Risk factors related to patient delay included: sociodemographic, health-related, cognitive and psychological variables. The analysis was conducted by considering two different delay ranges: dichotomous(f1 month vs..1 month) and polytomous(,1 month, 1–3 months,.3 months) delay. Data were investigated by univariate and multivariate analyses and a P value f0.05 was considered statistically significant. For both delay measurements, the most relevant variables were: ‘Personal experience of cancer'(dichotomous delay: P50.05, odds ratio(OR)50.33, 95% confidence interval(CI)50.11–0.99; polytomous delay: P50.006, Chi-square510.224) and ‘Unawareness'(dichotomous delay: P,0.01, OR54.96, 95% CI52.16–11.37; polytomous delay: P50.087, Chi-square54.77). Also ‘Denial'(P,0.01, OR56.84, 95% CI52.31–20.24) and ‘Knowledge of cancer'(P50.079, Chi-square58.359) were found to be statistically significant both for dichotomous and for polytomous categorization of delay, respectively. The findings of this study indicated that, in the investigated cohorts, the knowledge about cancer issues is strongly linked to the patient delay. Educational interventions on the Mediterranean population are necessary in order to increase the patient awareness and to emphasize his/her key role in early diagnosis of OSCC.Vera Panzarella Giuseppe Pizzo Francesco Calvino Domenico Compilato Giuseppe Colella Giuseppina Campisi 2014International Journal of Oral Science2014,6,1:2
5Lanthanide eompounds as environmentally - friendly corrosion inhibitors of alu minium alloys : a review 显示文摘Bethencourt M Botana F J Calvino J J 1998Corrosion Science1998,40,11:1
6Henoch- Schonlein purpura in children from northwestern Spain: a 20 year epidemiologic and clinical study显示文摘Calvino MC Llorca J Garcia Porrua C 2001Medicine2001,80,5:1
7Comparing differ- ent control strategies for indoor thermal comfort aimed at the evaluation of the energy cost of quality of building 显示文摘Calvino F Maria L G Massimo M 2010Applied Thermal Engineering2010,30,:1
8Herloch-Schonlein purpura in children from northwestern Spain:a 20-year epidemiologic and clinical study显示文摘Calvino MC Llorca J Garcfa Porraa C 2001Medicine2001,80,5:1
9Oxidative stress by Helicobacter pylofi causes apoptosis through mitochondrial pathway in gastric epithelial cells显示文摘Calvino - FernOndez M Benito - Martinez S Parra - Cid T 2008Apoptosis2008,13,10:1
10Comparison of ischemia - modified albumin levels in patients undergoing percutaneous coronary interven- tion for unstable angina pectoris with versus without coronary collater- als显示文摘Garrido IP Roy D Calvino R 2004Am J Cardiol2004,93,1:1
11Yield responses to narrow rows depend on increased radiation interception显示文摘Andrade F H Calvino P Cirilo A 2002Agronomy Journal2002,94,:1
12Comparison of ischemia-modified albumin levels in patients undergoing precutaneous coronary interven- tion for unstable angina pectoris with versus without coronary collater- als 显示文摘Garrido IP Roy K Calvino R 2004Am J Cardiol2004,93,1:1
13Multilevel current-source inverter with FPGA control显示文摘Aguirre M P Calvino L Valla M I 2013IEEE Transactions on Industrial Electronics2013,60,1:1
14Effects of balloon occlusion during percutaneous coronary intervention on circulating ischemia modified albumin and transmyocardial lactate extraction 显示文摘Sinha MK Vazquez JM Calvino R 2006Heart2006,92,12:1
15Bim-mediated apoptosis and PD-1/PD-L1 pathway impair reactivity of PD1 + /CD127 ? HCV-specific CD8 + cells targeting the virus in chronic hepatitis C virus infection显示文摘Juan R. Larrubia Selma Benito-Martínez Joaquín Miquel Miryam Calvino Eduardo Sanz-de-Villalobos Alejandro González-Praetorius Sonia Albertos Silvia García-Garzón Megha Lokhande Trinidad Parra-Cid 2011Cellular Immunology2011,,2:1
16Yield responses to narrow rows depend on increased radiation interception显示文摘Andrade F H Calvino P Cirilo A 2002Agronomy Journal2002,94,5:1
17Endogenous modulators of brain Na^+, K^+-atpase at early postnatal stages of rat development 显示文摘CALVINO M A PENA C ARNAIZ G 1998Int J Dev Neurosci1998,16,2:1
18Some major aspects of the chemical behavior of rare earth oxides:An overview显示文摘Bernal S Blanco G Calvino J J 2006Journal of Alloys and Compounds2006,,408412:1
19Comparison of ischemia modified albumin levels in patients undergoing percutaneons coronany intervention for unstable angina pectoris with versus coronary collaterals显示文摘GARRIDO I P ROY D CALVINO R 2004Am J Cardiol2004,93,:1
20The role of CCR5/ CXCR3 expressing CD8^+ cells in liver damage and viral control during persistent hepatitis C virus infection显示文摘Larruhia J R Calvino M Benito S 2007J Hepatol2007,47,:1
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