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| 1 | Thrombin activation and liver inflammation in advanced hepatitis C virus infection显示文摘Hepatitis C virus(HCV) infection is associated with increased thrombotic risk. Several mechanisms are involved including direct endothelial damage by the HCV virus, with activation of tissue factor, altered fibrinolysis and increased platelet aggregation and activation. In advanced stages, chronic HCV infection may evolve to liver cirrhosis, a condition in which alterations in the portal microcirculation may also ultimately lead to thrombin activation, platelet aggregation, and clot formation. Therefore in advanced HCV liver disease there is an increased prevalence of thrombotic phenomena in portal vein radicles. Increased thrombin formation may activate hepatic stellate cells and promote liver fibrosis. In addition, ischemic changes derived from vascular occlusion by microthrombi favor the so called parenchymal extinction, a process that promotes collapse of hepatocytes and the formation of gross fibrous tracts. These reasons may explain why advanced HCV infection may evolve more rapidly to end-stage liver disease than other forms of cirrhosis. | Emilio González-Reimers Geraldine Quintero-Platt Candelaria Martín-González Onán Pérez-Hernández Lucía Romero-Acevedo Francisco Santolaria-Fernández | 2016 | World Journal of Gastroenterology2016，22，18： | 5 |
| 2 | Liver steatosis in hepatitis C patients显示文摘There is controversy regarding some aspects of hepatitis C virus(HCV) infection-associated liver steatosis,and their relationship with body fat stores. It has classically been found that HCV,especially genotype 3,exerts direct metabolic effects which lead to liver steatosis. This supports the existence of a so called viral steatosis and a metabolic steatosis,whichwould affect HCV patients who are also obese or diabetics. In fact,several genotypes exert metabolic effects which overlap with some of those observed in the metabolic syndrome. In this review we will analyse the pathogenic pathways involved in the development of steatosis in HCV patients. Several cytokines and adipokines also become activated and are involved in 'pure' steatosic effects,in addition to inflammation. They are probably responsible for the evolution of simple steatosis to steatohepatitis,making it difficult to explain why such alterations only affect a proportion of steatosic patients. | Emilio González-Reimers Geraldine Quintero-Platt Melchor Rodríguez-Gaspar Remedios Alemán-Valls Onán Pérez-Hernández Francisco Santolaria-Fernández | 2015 | World Journal of Hepatology2015，7，10： | 3 |
| 3 | Adipokines,cytokines and body fat stores in hepatitis Cvirus liver steatosis显示文摘AIM: To identify patients with or without liver steatosis and its severity in treatment-na?ve patients affected by hepatitis C virus(HCV) infection.METHODS: We included 56 HCV infected patients, and assessed the amount of liver fat by histomorphometry, and its relationships with fat and lean mass at different parts of the body(by densitometry), hormones [insulin, homeostatic model assessment(HOMA)], adipokines(resistin, adiponectin, leptin), and cytokines(tumor necrosis factor α, interleukin-6).RESULTS: Although the intensity of liver steatosis is related to trunk fat mass and HOMA, 33% of patients showed no liver steatosis, and this finding was not related to body mass index or genotype. Besides trunkfat mass, no other factor was related to the presence or not of liver steatosis, or to the intensity of it, by multivariate analysis. Lean mass was not related to liver steatosis. Adiponectin levels were lower among patients. No differences were observed in leptin and resistin.CONCLUSION: Steatosis in HCV infection is common(67.2%), and closely related to trunk fat, and insulin resistance, but not with leg fat mass or adipokines. | emilio gonzález-reimers javier lópez-prieto geraldine quintero-platt ricardo pelazas-gonzález m remedios alemán-valls onán pérez-hernández m joséde-la-vega-prieto m angeles gómez-rodríguez candelaria martín-gonzález francisco santolaria-fernández | 2016 | World Journal of Hepatology2016，8，1： | 2 |
| 4 | Stress-induced fcc-hcp martensitic transformation in CoNi显示文摘 | Liu Y N Yang H Geraldine Tan | 2004 | Journal of Alloys and Compounds2004，368，12： | 1 |
| 5 | Bone changes in alcoholic liver disease显示文摘Alcoholism has been associated with growth impairment, osteomalacia, delayed fracture healing, and aseptic necrosis(primarily necrosis of the femoral head), but the main alterations observed in the bones of alcoholic patients are osteoporosis and an increased risk of fractures. Decreased bone mass is a hallmark of osteoporosis, and it may be due either to decreased bone synthesis and/or to increased bone breakdown. Ethanol may affect both mechanisms. It is generally accepted that ethanol decreases bone synthesis, and most authors have reported decreased osteocalcin levels(a 'marker' of bone synthesis), but some controversy exists regarding the effect of alcohol on bone breakdown, and, indeed, disparate results have been reported for telopeptide and other biochemical markers of bone resorption. In addition to the direct effect of ethanol, systemic alterations such as malnutrition, malabsorption, liver disease, increased levels of proinflammatory cytokines, alcoholic myopathy and neuropathy, low testosterone levels, and an increased risk of trauma, play contributory roles. The treatment of alcoholic bone disease should be aimed towards increasing bone formation and decreasing bone degradation. In this sense, vitamin D and calcium supplementation, together with biphosphonates are essential, but alcohol abstinence and nutritional improvement are equally important. In this review we study the pathogenesis of bone changes in alcoholic liver disease and discuss potential therapies. | Emilio González-Reimers Geraldine Quintero-Platt Eva Rodríguez-Rodríguez Antonio Martínez-Riera Julio Alvisa-Negrín Francisco Santolaria-Fernández | 2015 | World Journal of Hepatology2015，7，9： | 1 |
| 6 | Noise susceptibility of cochlear implant users: the role of spectral resolution and smearing显示文摘 | Fu Q Geraldine N | 2004 | JARO2004，6，： | 1 |
| 7 | Invertebrate bioturbation can reduce the clogging of sediment:an experimental study using infiltration sediment columns显示文摘 | Geraldine N Mermillod-Blondin F Cois-Carcaillet F | 2006 | Freshwater Biology2006，，51： | 1 |
| 8 | Expression, Regulation, and Function of αv integrins in hepatocellular carcinoma:An in vivo and in vitro study显示文摘 | Mimoun N Zakia H Geraldine G | 2002 | Hepatology2002，36，2： | 1 |
| 9 | Potential sources of methyl mercury in tree foliage 显示文摘 | Melissa T D Geraldine N Chad H R | 2012 | Environ Pollut2012，160，： | 1 |
| 10 | αβ T-cell receptors from multiple sclerosis brain lesions show MAIT cell–related features显示文摘 | Kathrin Held Latika Bhonsle-Deeng Katherina Siewert Wakiro Sato Eduardo Beltrán Stephan Schmidt Geraldine Rühl Judy K.M. Ng Peter Engerer Markus Moser Wolfgang E.F. Klinkert Holger Babbe Thomas Misgeld Hartmut Wekerle David-Axel Laplaud Reinhard Hohlfeld | 2015 | Neurology: Neuroimmunology & Neuroinflammation2015，，4： | 1 |
| 11 | House of risk: a model for proactive supply chain risk management 显示文摘 | PUJAWAN I N GERALDIN L H | 2009 | Business Process Management Journal2009，15，6： | 1 |
| 12 | Effects of In fusion Time and Addition of Milk on Content and Absorption of Polyphenols from Black tea显示文摘 | Janet A K Philip C M Geraldine M N | | 0，，55： | 1 |
| 13 | Cell cycle basis for the onset and progression c-Myc-induced,TGFαenhanced mousee mammary gland carcinogenesis显示文摘 | DEZHONG J L GERALDINE N SANDRA L D | 2000 | Oncogene2000，19，： | 1 |
| 14 | Effects of Infusion Time and Addition of Milk on Content and Absorption of Polyphenols Jrom Black tea 显示文摘 | JANET A K PHILIP C M GERALDINE M N | 2007 | J Agric Food Chem2007，，55： | 1 |
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