Literatura científica selecionada sobre o tema "Hepatitis C"
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Artigos de revistas sobre o assunto "Hepatitis C"
Nouman, Muhammad Khuram, Bushra Zaidi, Ghulam Mohiuddin, Faryal Asif e Muhammad Khan Malik. "HEPATITIS C". Professional Medical Journal 25, n.º 03 (10 de março de 2018): 387–91. http://dx.doi.org/10.29309/tpmj/2018.25.03.381.
Texto completo da fonteJamali, Ghulam Mustafa, Anwar Ali Jamali e Habibullah Shaikh. "HEPATITIS C VIRUS;". Professional Medical Journal 24, n.º 11 (3 de novembro de 2017): 1621–29. http://dx.doi.org/10.29309/tpmj/2017.24.11.646.
Texto completo da fonteJain, Ravi, e Ashok Yadav. "Hepatitis B Versus Hepatitis C in Blood Donors". Annals of Applied Bio-Sciences 4, n.º 1 (janeiro de 2017): A8—A13. http://dx.doi.org/10.21276/aabs.2017.1306.
Texto completo da fonteBillah, Mustansar, Syed Muhammad Raza Shah e Muhammad Mujtaba Hashir. "HEPATITIS B AND HEPATITIS C". Professional Medical Journal 25, n.º 08 (9 de agosto de 2018): 1245–51. http://dx.doi.org/10.29309/tpmj/18.4766.
Texto completo da fonteTARIQ, FAQIR MUHAMMAD, IRSHAD AHMAD, HABIB SUBHANI e Irshad Ul Haq. "HEPATITIS C". Professional Medical Journal 16, n.º 02 (10 de junho de 2009): 169–72. http://dx.doi.org/10.29309/tpmj/2009.16.02.2890.
Texto completo da fonteSalam, Abdul, Bilqis Aslam Baloch, Naseer Khan, Ghulam Sarwar e Masoom ,. "SEROPREVALENCE OF HBsAg (HBS) AND ANTI-HCV". Professional Medical Journal 21, n.º 04 (7 de dezembro de 2018): 766–70. http://dx.doi.org/10.29309/tpmj/2014.21.04.2424.
Texto completo da fonteAndrade, Luís Jesuino, Paulo Melo, Isabel Lins, Raymundo Paraná e Augusto Lins. "HEPATITIS C VIRUS AND HEPATITIS C-INFECTION". Brazilian Journal of Medicine and Human Health 3, n.º 1 (31 de maio de 2015): 19–28. http://dx.doi.org/10.17267/2317-3386bjmhh.v3i1.453.
Texto completo da fonteViana, Daniel Rodrigues, Nathalia Mundoco Veloso, Osvaldo Carvalho Neto, Nicolas Garcia Papacosta, Gabriel Martins Nunes e Virgílio Ribeiro Guedes. "Hepatite B e C: diagnóstico e tratamento". Revista de Patologia do Tocantins 4, n.º 3 (26 de setembro de 2017): 73. http://dx.doi.org/10.20873/uft.2446-6492.2017v4n3p73.
Texto completo da fonteMoradpour e Blum. "Hepatitis C". Therapeutische Umschau 61, n.º 8 (1 de agosto de 2004): 493–98. http://dx.doi.org/10.1024/0040-5930.61.8.493.
Texto completo da fonteKhan, Momin, Abdul Jabbar, Bacha Amin Khan, Abdul Ahad e Fazal Akbar. "HEPATITIS C". Professional Medical Journal 25, n.º 04 (10 de abril de 2018): 484–88. http://dx.doi.org/10.29309/tpmj/2018.25.04.332.
Texto completo da fonteTeses / dissertações sobre o assunto "Hepatitis C"
Pajenčkovskytė, Karolina. "Sergančiųjų lėtiniu virusiniu C hepatitu genotipai". Master's thesis, Lithuanian Academic Libraries Network (LABT), 2004. http://vddb.library.lt/obj/LT-eLABa-0001:E.02~2004~D_20040608_165139-44050.
Texto completo da fonteBerg, Thomas. "Chronische Hepatitis C". Doctoral thesis, Humboldt-Universität zu Berlin, Medizinische Fakultät - Universitätsklinikum Charité, 2002. http://dx.doi.org/10.18452/13812.
Texto completo da fonteThe major goal of this thesis is the analysis of the clinical outcome of patients with Hepatitis C virus (HCV) infection and the response to therapy. Analysed were 1. different types of therapeutic strategies 2. causes responsible for ineffective antiviral therapy (non-response) 3. clinical relevance of the newly discovered hepatitis-associated viruses and 4. the role of these viruses in patients with acute or chronic hepatitis of unknown causes and in those receiving liver grafts. Ad 1. Compared were different therapeutic concepts such as short-term combination therapy, triple-therapy, high dose IFN?-therapy and the use of antiviral substances such as ribavirin and amantadine. It emerged that relevant prognostic parameters can be deduced with respect to the therapeutic response rate. Ad 2. Analysed were possible molecular mechanisms, which may interfere with response or non-response to antiviral therapy. In this respect, we focussed on the interaction of certain HCV-proteins as NS5A, E2, so-called PKR-eIF2a phosphorylisation-homology-domain (PePHD). with the interferon-?-induced effector proteins. There is evidence, that number of mutations within the NS5A proteins are of prognostic relevance with respect to the response to interferon?-therapy. In contrast, mutations within the PePHD-region do not play any role in this respect. Ad 3. We also studied the clinical relevance of the newly discovered viruses GBV-C/HGV and TTV, and found, that they have no impact concerning the course of chronic hepatitis C. These viruses are interferon-sensitive and do not influence the IFNa-response as it could be documented by following the course of co-infected patients. Ad 4. Our studies also focused on the prevalence, transmission and relevance of GBV-C/HGV and TTV infections with respect to their role as hepatitis-inducing agents. We can show that both virus types are parenterally transmitted. There is a high prevalence for both types in patients confronted with risk factors for parenteral factors. From analysis of many patients being chronically infected with these viruses it became quite clear that they lack any important potency to provoke chronic liver disease.
Silva, Filho Hermes Pedreira da. "Estudo Molecular dos Vírus B e C das Hepatites nas Regiões Norte e Nordeste do Brasil". reponame:Repositório Institucional da FIOCRUZ, 2010. https://www.arca.fiocruz.br/handle/icict/4219.
Texto completo da fonteMade available in DSpace on 2012-07-19T21:21:54Z (GMT). No. of bitstreams: 1 Hermes Pedreira EStudo molecular dos vírus B e C...2010.pdf: 5589974 bytes, checksum: b86706272dbb22d0d349edae7d641ce1 (MD5) Previous issue date: 2010
Fundação Oswaldo Cruz. Centro de Pesquisas Gonçalo Moniz. Salvador, Bahia, Brasil
Infecções pelos vírus B e C das hepatites constituem um significante problema de saúde pública em todo mundo. Mais de 350 milhões de pessoas estão cronicamente infectadas pelo VHB e 170 milhões pelo VHC. No Brasil, a prevalência de pessoas infectadas pelo VHB varia de baixa endemicidade (<2%) até alta, (>7%), e estima-se que 1,5% da população esteja infectada pelo VHC (WHO). Estudos recentes tem demonstrado consideráveis variações entre os isolados do VHB, confirmando a diversidade de genótipos do vírus circulantes e o surgimento de mutações no genoma viral que podem ter impacto na resposta terapêutica e imune. Informações sobre a diversidade genética do VHB serão de grande valor para determinar fatores de risco associados a disseminação do vírus e auxiliar na adoção de medidas de prevenção e terapêutica. A infecção pelo VHC tornou-se um sério problema de saude pública desde que não existe uma vacina disponível e o tratamento é extremamente caro para os órgãos públicos como desgastante para o paciente. Este trabalho utilizou as ferramentas moleculares e de epidemiologia no estudo destes vírus para caracterizar molecularmente os vírus B e C das hepatites nas Regiões Norte e Nordeste, particularmente na Bahia, através de sequenciamento de DNA e análises filogenéticas. Amostras de pacientes provenientes da Bahia, Acre, Rondonia, Amazonas, Maranhão e Tocantins foram analisadas. As amostras foram oriundas de outros estudos e de centros de referência para tratamento das hepatites, sendo avaliadas 635 amostras para o VHC e 335 de VHB. Sequencias das regiões pré-S/S e pré- Core/Core do VHB e NS5b, 5UTR, E1 e Core do VHC foram utilizadas para classificação genotípica e análise filogenetica. Os genótipos mais frequentes para o VHB foram A (57%), D (10%) e F(33%) na Bahia e nas amostras da região Norte. Nós encontramos em nosso estudo 55,6% de pacientes co-infectados com VHB/Delta. Não foi possível estabelecer uma ligação genótipo específico com a evolução da infecção, e determinar a presença de mutantes relacionados à resposta terapêutica e ao escape imunológico. Com relação ao VHC, a subtipagem dos isolados foi realizada através do sequenciamento da região NS5b e 5UTR (n=230). Os sub-genótipos mais frequentes foram 1a(45,6%), 1b (46,9%), 3a (6,5%) e 2a/b(0,8%). As regiões E1 e Core também foram sequenciadas e no futuro serão utilizadas para avaliar possiveis mutações. O presente estudo mostra que a aplicação de protocolos de sequenciamento, bioinformática e filogenia são indispensáveis para a compreensão da epidemiologia molecular dos vírus das hepatites.
Infections with hepatitis B and C viruses constitute a significant public health problem worldwide. More than 350 million people are chronically infected with HBV and 170 million by HCV. In Brazil, HBV remains endemic despite widespread vaccination with prevalence of infection ranging from (<2%) low endemicity, until high (>7%) in different regions. Prevalence of HCV infection in Brazil has been estimated at 1.5%. Recent studies have shown considerable genetic variation among HBV isolates, confirming the diversity of circulating genotypes of the virus and the emergence of mutations in the viral genome that may impact on therapeutic and immune response. Information on the genetic diversity of HBV is useful for molecular epidemiology to determine risk factors associated with the spread of the virus and to inform prevention strategies and for monitoring therapy. Because there is no vaccine available to prevent HCV infection and treatment is extremely expensive for public agencies, HCV is an emerging public health problem. The treatment efficiency is directly related to viral genotype. In this study molecular epidemiology tools were used to characterize HBV and HCV in the North and Northeast, particularly in Bahia, through DNA sequencing and phylogenetic analysis. Samples from Bahia, Acre, Rondônia, Amazonas, Maranhão and Tocantins were analyzed. The samples were collected in collaboration with other studies and centers of references for hepatitis treatments. 635 samples from HCV infected patients and 335 samples from HBV infected were evaluated. Sequences of the regions pre-S / S, HBV core / pre-core, NS5B, 5UTR, HCV Core and E1 were used for genotypic classification and phylogenetic analysis. The most frequent HBV genotypes were A (57%), D (10%) and F (33%) in Bahia and in the samples from the North region. Fifty five percent of the patients from Rondônia were coinfected with HBV and HDV. In this study, we were unable to establish a connection with the particular genotype evolution of the infection and determine the presence of mutants related to therapeutic response and immune escape. In the North region co-infection with HBV genotype F and D virus is strongly associated with poor outcome of the disease as informed by the physicians and literature. Regarding HCV, the subtyping of isolates was performed by sequencing the NS5B region and 5UTR (n=230). The sub-genotypes more frequent were 1a (45.6%), 1b (46.9%), 3a (6.5%) and 2a / b (0.8%). The Core and E1 regions were also sequenced and in the future could be used to evaluate possible mutations. This study shows that the implementation of protocols for sequencing, bioinformatics and phylogenetic are essential for understanding the molecular epidemiology of hepatitis.
Valente, Vanderleia Barbaro. "Estudo da distribuição dos marcadores sorológicos das hepatites B e C entre doadores de sangue do Hemocentro de Ribeirão Preto, SP". Universidade de São Paulo, 2002. http://www.teses.usp.br/teses/disponiveis/17/17139/tde-29052003-193717/.
Texto completo da fonteThis study, which involved all blood donors (25.891) that attended the Blood Center of Ribeirão Preto for the first time from June 1996 to June 2001 had the following objectives: 1) To study the positiveness for hepatitis B and C serologic markers in donors screening tests. 2) To analyze the flow of positive donors for hepatitis B and C markers to the Hepatitis Ambulatory (HA) in the Clinical Hospital of the Faculty of Medicine of Ribeirão Preto of the University of São Paulo. 3) To estimate the predominance of present or former infection by hepatitis B and C viruses among donors, by analyzing results of screening tests that confirm these diseases. 4) To evaluate the importance of determining the glutamic-piruvic transaminase (GTP) as an indirect marker of infection by hepatitis B and C viruses. Registered data from the Blood Center as well as from the Epidemiological Surveillance Nucleus (ESN) and HA were used with the purpose of collecting information about donors, type of donation and results in serologic screening tests (HBsAg, anti-HBc, anti-HCV, GTP, anti-HIV, anti-HTLV, Chagas disease and syphilis). In addition, a study was performed on the results in repetition tests that took place in the Blood Center of positive donors for hepatitis B and C markers in serologic tests as well as on their attendance at the ESN and the confirmation in the HA of the results for these markers. The population of donors was composed in its majority by men (83,6%) and individuals from 26 to 45 year-old (64,0%). Linked donations predominated (85,4%), and the greatest reasons for donation arose from solicitation and stimulus coming from family and friends. The value of prevalence in serologic screening tests was 0,63% (IC95%: 0,54 0,72) for HBsAg and 1,15% (IC95%: 1,02 1,28) for anti-HCV. The total of positive donors that should have been evaluated in the HA suffered a loss of 55,5% among the suspects of having hepatitis B and of 58,7% among the suspects of having hepatitis C, reaching a total of 266 donors lost during follow-up. The value of prevalence in confirmatory tests was 0,22% (IC95%: 0,16 0,28) for hepatitis B and 0,31% (IC95%: 0,24 0,38) for hepatitis C. The copositiveness between GPT and hepatitis markers in serologic screening tests was 8.8% for hepatitis C virus and 0.5% for hepatitis B virus, indicating that determination of this enzyme is not helpful in selection of donors in blood banks.
Silva, Edvaldo Ferreira da. "Prevalência de marcadores sorológicos das hepatites A e B em pacientes com hepatite C crônica atendidos no ambulatório de hepatites do serviço de Gastroenterologia Clínica do Hospital das Clínicas da Faculdade de Medicina da Universidade". Universidade de São Paulo, 2014. http://www.teses.usp.br/teses/disponiveis/5/5168/tde-04022015-153903/.
Texto completo da fonteBackground and Aims: Patients with chronic HCV and superinfection by hepatitis A virus (HAV) or hepatitis B virus (HBV) have higher morbidity and mortality when compared with those without HCV. For this reason, HAV and HBV active immunization has become mandatory in this population and hence their serological markers must be determined. The aim of this study was to evaluate the prevalence of serological markers of HAV and HBV infection in patients with chronic HCV. Methods: 1.000 chronic HCV infected patients at the University of Sao Paulo School of Medicine outpatient Liver Clinic were evaluated for the prevalence of serological markers of HAV and HBV infection. Results: Anti-HAV IgG was positive in 923 of 1000 patients (92.3%). When stratified by age, the anti-HAV IgG was found in 61% of patients between 20-29 years, 70% between 30-39 years, 85% between 40-49 years, 94% between 50-59 years, and 99% over 60 years of age. Anti-HBc IgG was positive in 244 patients (24%). Stratified by age, anti-HBc IgG was found in 4.3% of patients between 20-29 years, 17% between 30-39 years, 21% between 40 -49 years, 24% between 50-59 years, and 28% of patients over 60 years of age. Of the 244 anti-HBc IgG positive patients, 0.8% were also HBsAg positive, 8.5% were anti-HBc IgG isolated and 16% were also anti-HBs positive. Conclusions: The prevalence of anti-HAV IgG was similar to the general population in the city of São Paulo. However, anti-HBc IgG was higher in our chronic HCV patients, when compared historically to the general population of western countries, suggesting similar risk factors for HBV and HCV acquisition, so emphasizing the importance of immunization programs in this population. Keywords: Hepatitis C, Chronic; Hepatitis C; Hepacivirus, Prevalence; Hepatitis A; Hepatitis B Título: Prevalência de Marcadores Sorológicos das Hepatites A e B em Pacientes com Hepatite C Crônica atendidos no Ambulatório de Hepatites do Serviço de Gastroenterologia Clínica do Hospital das Clínicas da Faculdade de Medicina da Universidade de São Paulo - HCFMUSP Background and Aims: Patients with chronic HCV and superinfection by hepatitis A virus (HAV) or hepatitis B virus (HBV) have higher morbidity and mortality when compared with those without HCV. For this reason, HAV and HBV active immunization has become mandatory in this population and hence their serological markers must be determined. The aim of this study was to evaluate the prevalence of serological markers of HAV and HBV infection in patients with chronic HCV. Methods: 1.000 chronic HCV infected patients at the University of Sao Paulo School of Medicine outpatient Liver Clinic were evaluated for the prevalence of serological markers of HAV and HBV infection. Results: Anti-HAV IgG was positive in 923 of 1000 patients (92.3%). When stratified by age, the anti-HAV IgG was found in 61% of patients between 20-29 years, 70% between 30-39 years, 85% between 40-49 years, 94% between 50-59 years, and 99% over 60 years of age. Anti-HBc IgG was positive in 244 patients (24%). Stratified by age, anti-HBc IgG was found in 4.3% of patients between 20-29 years, 17% between 30-39 years, 21% between 40 -49 years, 24% between 50-59 years, and 28% of patients over 60 years of age. Of the 244 anti-HBc IgG positive patients, 0.8% were also HBsAg positive, 8.5% were anti-HBc IgG isolated and 16% were also anti-HBs positive. Conclusions: The prevalence of anti-HAV IgG was similar to the general population in the city of São Paulo. However, anti-HBc IgG was higher in our chronic HCV patients, when compared historically to the general population of western countries, suggesting similar risk factors for HBV and HCV acquisition, so emphasizing the importance of immunization programs in this population
Thiel, Jens. "Einfluss von Immunsuppression auf Hepatitis-C-assoziierte Immunphänomene und Hepatitis-C-Quasispezies". [S.l.] : [s.n.], 2003. http://deposit.ddb.de/cgi-bin/dokserv?idn=969417918.
Texto completo da fonteShen, Hong. "Hepatitis C infection models". Thesis, Paris 5, 2012. http://www.theses.fr/2012PA05T016.
Texto completo da fonteHepatitis C virus (HCV) is one of the major causes of liver disease all over the world which has a high risk to progress to cirrhosis and hepatocellular carcinoma. Currently, the licensed standard treatment of HCV infection is Pegylated-interferon (peg-IFN) and ribavirin. Although the sustained viral response (SVR) rate of treatment has improved during these years, this therapy is not effective in all patients. In addition, several toxic side effects, complication and high cost limit the patient compliance and the efficacy of the treatment. There is no easy model of HCV infection and it is necessary to develop useful in vitro and in vivo models to study the pathobiology of HCV infection, including early events of acute infection (viral entry, immunological mechanisms, and genetic predictors) as well as the evaluation of the potency of the HCV antiviral drugs. We report here in our efforts in developing suitable models of HCV infection. In a first step, we preliminary established a small animal model to study HCV infection. Tupaia is a small, closed related to primate and cost-effective animal. In our work, we investigated the susceptibly of tupaia to HCV infection. Twelve adult tupaias were inoculated with native HCV from patient serum and full-length HCV RNA (Genotype 1a). Three young tupaias were artificially breeded for a month and then inoculated by native HCV from patient serum. HCV RNA, anti-HCV and HCV quasi species evolution were determined in the animal before and after inoculation. Transient and intermittent infection occurred in two among 3 young tupaias and HCV chronic infection occurred in four among 12 adult tupaias. Tupaia should represent a useful model for study HCV chronic infection. In a second step, an in vitro culture system of primary tupaia hepatocytes has been established in which HCV infection could be blocked neither by the soluble CD81 nor by antibodies against CD81. To understand these results, we cloned, sequenced the large extracellular loop (LEL) of tupaia CD81 and analyzed the interaction of HCV E2 with the tupaia CD81 LEL by enzyme-linked immunosorbent assay (EIA). We found that in the tupaia the amino acids sequence of HCV CD81 LEL presented in 6 different amino acid residues compared with human CD81 LEL sequence and the CD81 LEL ability to bind to HCV E2 was also decreased. The different structure of CD81 between human and tupaia could explain the alteration of the interaction between HCV E2 and CD81. This result demonstrated an important role of CD81 LEL for HCV entry. In a third step, we developed an ex vivo model of human liver slices culture and their infection with HCV. The development of human cultured HCV-replication-permissive hepatocarcinoma cell lines has provided important new virological tools to study the mechanisms of HCV infection; however this experimental model remains distantly related to physiological and pathological conditions. Here, we report the development of a new ex vivo model using human adult liver slices culture, demonstrating, for the first time, the ability of primary isolates to undergo de novo viral replication with the production of high titer infectious virus, as well as JFH-1, H77/C3, Con1/C3 (HCVcc). This experimental model was validated by demonstrating the HCV neutralization or HCV inhibition, in a dose-dependent manner, either by CD81 or E2 specific antibodies or convalescent serum from a recovered HCV patient, or by anti-viral drugs. This new ex vivo model represents a powerful tool for studying the viral life cycle, dynamics of virus spread in the liver and also for evaluating the efficacy of the new antiviral drugs. In the last step, we evaluated the efficacy of the new antiviral drugs with our ex vivo model of human adult liver slices. HCV NS3/4A protease is essential for viral replication and has been one of the most important target for developing specific antiviral drug
Hopwood, Maxwell Norman. "Living with Hepatitis C". Maastricht : Maastricht : Universiteit Maastricht ; University Library, Universiteit Maastricht [host], 2007. http://arno.unimaas.nl/show.cgi?fid=9171.
Texto completo da fonteMontes, Teves Pedro. "Hepatitis C: retos pendientes". Sociedad de Gastroenterología del Perú, 2014. http://hdl.handle.net/10757/331937.
Texto completo da fonteWinckler, Fernanda Cristina. "Influência da Resposta inflamatória na resposta virológica sustentada em pacientes com hepatite C crônica genótipo 1 durante o tratamento antiviral com terapia tripla". Botucatu, 2016. http://hdl.handle.net/11449/144991.
Texto completo da fonteCoorientador: Marjorie de Assis Golim
Resumo: A hepatite C é uma doença infecciosa que torna-se crônica em cerca de 85% dos infectadosque poderão desenvolver cirrose e carcinoma hepato celular. O tratamento antiviral em muitosdos pacientes não é eficaz, principalmente quando estes portam o genótipo 1 e fibroseavançada, a resposta inflamatória também desempenha seu papel sobre a resposta virológicasustentada (RVS) durante o tratamento com Interferon Peguilado (PegIFN) associado aRibavirina (RBV). Nesse estudo nosso objetivo principal foi avaliar a influência da respostainflamatória através de células e citocinas/quimiocinas sobre a resposta virológica do pacienteem tratamento antiviral com terapia tripla. Incluimos pacientes com RNA VHC+, nuncatratados (naive), portadores do genótipo 1, ambos os sexos e com fibrose avançada F3 (n=6);F4 (n=21) candidatos ao tratamento em regime triplo. Os pacientes tiveram suas amostrascoletadas e analizadas nas semanas 0 e 12 do tratamento e os seguintes parâmetros foramanalisados: IL-2, IL-4, IL-6, IL-8, IL-10, IL-17A, TNF-α, IFN-γ, RANTES, MCP-1, MIG, IP-10, através de citometria de fluxo (método CBA). Foram incluídos 15 voluntários saudáveis(grupo controle) e 27 pacientes que foram separados em G1(RVS) e G2 (não RVS), a taxa deRVS foi de 63%. Os pacientes com hepatite C crônica tiveram os níveis circulantes de IP10,MCP-1, MIG, RANTES, IL-8 e IL-6 mais elevados quando comparados com voluntáriossaudáveis, quando comparados G1xG2 os níveis de RANTES (p=0,04... (Resumo completo, clicar acesso eletrônico abaixo)
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Livros sobre o assunto "Hepatitis C"
Askari, Fred K. Hepatitis C, the silent epidemic: The authoritative guide. Cambridge, Mass: Perseus, 2001.
Encontre o texto completo da fonteAskari, Fred K. Hepatitis C, the silent epidemic: The authoritative guide. New York: Plenum Trade, 1999.
Encontre o texto completo da fonteSawyer, Forrest. Hepatitis C. Princeton, N.J: Films for the Humanities & Sciences, 2003.
Encontre o texto completo da fonteEngland, Health Promotion, ed. Hepatitis C. London: Health Promotion England, 2000.
Encontre o texto completo da fonteR, Foster G., ed. Hepatitis C. London: Baillière Tindall, 2000.
Encontre o texto completo da fonteNational Institute on Drug Abuse, ed. Hepatitis C. Bethesda, MD (6001 Executive Blvd., Bethesda 20892): National Institute on Drug Abuse, U.S. Dept. of Health and Human Services, National Institutes of Health, 2000.
Encontre o texto completo da fonteCanada. Library of Parliament. Parliamentary Research Branch. Hepatitis C. Ottawa: Library of Parliament, 1999.
Encontre o texto completo da fonteOzaras, Resat, e Dominique Salmon-Ceron, eds. Viral Hepatitis: Chronic Hepatitis C. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-03757-4.
Texto completo da fonteN, Lau Johnson Y., ed. Hepatitis C protocols. Totowa, N.J: Humana Press, 1998.
Encontre o texto completo da fonteW, Reesink H., ed. Hepatitis C virus. 2a ed. Basel: Karger, 1998.
Encontre o texto completo da fonteCapítulos de livros sobre o assunto "Hepatitis C"
Arends, Joop E., Maria Cristina Leoni e Dominique Salmon. "Acute Hepatitis C". In Viral Hepatitis: Acute Hepatitis, 45–65. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-03535-8_4.
Texto completo da fonteArends, Joop E., Maria Cristina Leoni e Dominique Salmon-Ceron. "Acute Hepatitis C". In Viral Hepatitis: Chronic Hepatitis C, 197–217. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-03757-4_11.
Texto completo da fonteKorn, Klaus. "Hepatitis C". In S2k-Leitlinie - Labordiagnostik schwangerschaftsrelevanter Virusinfektionen, 133–43. Berlin, Heidelberg: Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/978-3-662-43481-9_13.
Texto completo da fonteDusheiko, Geoffrey. "Hepatitis C". In Sherlock's Diseases of the Liver and Biliary System, 436–67. Chichester, UK: John Wiley & Sons, Ltd, 2018. http://dx.doi.org/10.1002/9781119237662.ch23.
Texto completo da fonteFried, Michael W., Jama M. Darling e Stanley M. Lemon. "Hepatitis C". In Schiff's Diseases of the Liver, 628–98. Oxford, UK: John Wiley & Sons, Ltd, 2017. http://dx.doi.org/10.1002/9781119251316.ch25.
Texto completo da fonteKanto, Tatsuya, e Sachiyo Yoshio. "Hepatitis C". In Liver Immunology, 273–86. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-51709-0_17.
Texto completo da fonteDusheiko, Geoffrey. "Hepatitis C". In Sherlock's Diseases of the Liver and Biliary System, 406–26. Oxford, UK: Wiley-Blackwell, 2011. http://dx.doi.org/10.1002/9781444341294.ch20.
Texto completo da fonteCharlton, Michael, e Travis Dick. "Hepatitis C". In Practical Gastroenterology and Hepatology Board Review Toolkit, 480–86. Oxford, UK: John Wiley & Sons, Ltd, 2016. http://dx.doi.org/10.1002/9781119127437.ch77.
Texto completo da fonteSainburg, Robert L., Andrew L. Clark, George E. Billman, Zachary J. Schlader, Toby Mündel, Kevin Milne, Earl G. Noble et al. "Hepatitis C". In Encyclopedia of Exercise Medicine in Health and Disease, 408. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-540-29807-6_2485.
Texto completo da fonteDarling, Jama M., Stanley M. Lemon e Michael W. Fried. "Hepatitis C". In Schiff's Diseases of the Liver, 582–652. Oxford, UK: Wiley-Blackwell, 2011. http://dx.doi.org/10.1002/9781119950509.ch25.
Texto completo da fonteTrabalhos de conferências sobre o assunto "Hepatitis C"
Ekmen, Onder. "A Case of Fulminant Hepatitis B Reactivation After Hepatitis C Treatment in Hepatitis B+C Co-infection". In 39. Jahrestagung der Deutschen Arbeitsgemeinschaft zum Studium der Leber. Georg Thieme Verlag, 2023. http://dx.doi.org/10.1055/s-0042-1760078.
Texto completo da fontePrasetia Nurwidda, Arvi Dian, Poernomo Boedi Setiawan, Iswan Abbas Nusi, Herry Purbayu, Titong Sugihartono, Ummi Maimunah, Ulfa Kholili et al. "Thrombocytopenia in Chronic Hepatitis C". In Surabaya International Physiology Seminar. SCITEPRESS - Science and Technology Publications, 2017. http://dx.doi.org/10.5220/0007340404460452.
Texto completo da fonteLópez, Sandra, Itxaso Respaldiza e Ander Portugal. "Hepatitis C, el enemigo silencioso". In XXIX Congreso Nacional de Medicina General y de Familia y V Jornadas SEMG Andalucía. Grupo Pacífico, 2023. http://dx.doi.org/10.48158/semg23-611.
Texto completo da fonteChawathe, Sudarshan S. "Diagnostic Classification Using Hepatitis C Tests". In 2020 IEEE International IOT, Electronics and Mechatronics Conference (IEMTRONICS). IEEE, 2020. http://dx.doi.org/10.1109/iemtronics51293.2020.9216446.
Texto completo da fonteShahzadi, Mehreen, Faisal Bukhari e Numan Shafi. "Intelligent Predictive Model for Hepatitis C". In 2023 3rd International Conference on Artificial Intelligence (ICAI). IEEE, 2023. http://dx.doi.org/10.1109/icai58407.2023.10136685.
Texto completo da fontePaschoini, MC, LN Resende, MM Mendonça, GPM Gomide e JU Ribeiro. "P3.181 Hepatitis c: challenging modern obstetrics". In STI and HIV World Congress Abstracts, July 9–12 2017, Rio de Janeiro, Brazil. BMJ Publishing Group Ltd, 2017. http://dx.doi.org/10.1136/sextrans-2017-053264.416.
Texto completo da fonteEid, Fatma Elzahraa, Haitham Elmarakeby, Lenwood Heath e Mahmoud ElHefnawi. "Human microRNAs targeting hepatitis C virus". In 2014 Middle East Conference on Biomedical Engineering (MECBME). IEEE, 2014. http://dx.doi.org/10.1109/mecbme.2014.6783236.
Texto completo da fonteNandian Saputra, Trimardi Aditya, Ken Indiana Arizona, Muhammad Rizky Andrian, Felix Indra Kurniadi e Budi Juarto. "Random Forest in Detecting Hepatitis C". In 2022 9th International Conference on Information Technology, Computer, and Electrical Engineering (ICITACEE). IEEE, 2022. http://dx.doi.org/10.1109/icitacee55701.2022.9924074.
Texto completo da fonteKchir, H., D. KAFFEL, H. Dabbebi, D. ISSAOUI, H. Sahli, W. Hamdi, M. Elleuch, M. M. Kchir, R. Debbeche e N. Maamouri. "AB1049 Rheumatological manifestations during chronic hepatitis c". In Annual European Congress of Rheumatology, EULAR 2018, Amsterdam, 13–16 June 2018. BMJ Publishing Group Ltd and European League Against Rheumatism, 2018. http://dx.doi.org/10.1136/annrheumdis-2018-eular.5886.
Texto completo da fonteMatthews, Charmaine, Helen Caldwell, Eimear Kealey, Elliot Graves, Michael Jones, David Byrne e Paul Richardson. "OP28 Hepatitis C – the male prisoner’s perspective". In Abstracts of the British Association for the Study of the Liver Annual Meeting, 20–23 September 2022. BMJ Publishing Group Ltd and British Society of Gastroenterology, 2022. http://dx.doi.org/10.1136/gutjnl-2022-basl.41.
Texto completo da fonteRelatórios de organizações sobre o assunto "Hepatitis C"
Kuypers, Marshall A., Gregory Joseph Lambert, Thomas W. Moore, Glass, Robert John,, Patrick D. Finley, David Ross e Maggie Chartier. Modeling Hepatitis C treatment policy. Office of Scientific and Technical Information (OSTI), setembro de 2013. http://dx.doi.org/10.2172/1096266.
Texto completo da fonteSjogren, Maria H., e Kent Holtzmuller. Hepatitis C Virus Infection: Mechanism of Disease Progression. Fort Belvoir, VA: Defense Technical Information Center, outubro de 2001. http://dx.doi.org/10.21236/ada406083.
Texto completo da fonteSjogren, Maria H. Hepatitis C. Virus Infection: Mechanism of Disease Progression. Fort Belvoir, VA: Defense Technical Information Center, outubro de 2004. http://dx.doi.org/10.21236/ada433067.
Texto completo da fonteSjogren, Maria H., e Brooke Huntley. Hepatitis C. Virus Infection: Mechanisms of Disease Progression. Fort Belvoir, VA: Defense Technical Information Center, outubro de 2007. http://dx.doi.org/10.21236/ada477987.
Texto completo da fonteAdebiyi, Sadiat, Sakinah Shaw e Tracy McClinton. Annual Hepatitis C Screening QI: A Scoping Review. University of Tennessee Health Science Center, abril de 2022. http://dx.doi.org/10.21007/con.dnp.2022.0026.
Texto completo da fonteAdebiyi, Sadiat, Sakinah Shaw e Tracy McClinton. Annual Hepatitis C Screening QI: A Scoping Review. University of Tennessee Health Science Center, abril de 2022. http://dx.doi.org/10.21007/con.dnp.2022.0026.
Texto completo da fonteKoizumi, Yoshiki, Syo Nakajim, Hirofumi Ohash, Yasuhito Tanaka, Takaji Wakita, Alan S. Perelson, Shingo Iwami e Koichi Watashi. Quantifying antiviral activity optimizes drug combinations against hepatitis C virus infection. Office of Scientific and Technical Information (OSTI), março de 2016. http://dx.doi.org/10.2172/1242919.
Texto completo da fonteNelson, David, Michael Fried, Mark Sulkowski, Donna Evon, Jodi Segal, Anna Lok, Paul Stewart_ Stewart et al. Comparing Oral Medicines to Treat Hepatitis C Virus -- The PRIORITIZE Study. Patient-Centered Outcomes Research Institute® (PCORI), março de 2022. http://dx.doi.org/10.25302/03.2022.hpc.150327891.
Texto completo da fonteHung, Hsuan-Yu, Hui-Hsiung Lai, Hui-Chuan Lin e Chung-Yu Chen. Impact of interferon-free antivirus therapy on lipid profiles in patients with chronic hepatitis C: A network meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, julho de 2022. http://dx.doi.org/10.37766/inplasy2022.7.0055.
Texto completo da fonteNguyen, Tung, Mandana Khalili, Janice Tsoh, Judith Walsh, Elizabeth Goldman, Arcadi Kolchak, Ginny Gildengorin, Ching Wong e Ivy Lau. Comparing Ways to Increase Hepatitis B and C Screening Among Asian Americans. Patient-Centered Outcomes Research Institute® (PCORI), março de 2020. http://dx.doi.org/10.25302/02.2020.ad.12114615.
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