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  1 / 221995 MEDLINE  
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[PMID]: 29524828
[Au] Autor:Witt-Kehati D; Fridkin A; Alaluf MB; Zemel R; Shlomai A
[Ad] Address:Felsenstein Medical Research Center and the Sackler Faculty of Medicine, Tel-Aviv University, Tel-Aviv, Israel.
[Ti] Title:Inhibition of pMAPK14 Overcomes Resistance to Sorafenib in Hepatoma Cells with Hepatitis B Virus.
[So] Source:Transl Oncol;11(2):511-517, 2018 Mar 07.
[Is] ISSN:1936-5233
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Hepatitis B virus (HBV) targets the liver and is a major driver for liver cancer. Clinical data suggest that HBV infection is associated with reduced response to treatment with the multi-kinase inhibitor sorafenib, the first available molecularly targeted anti-hepatocellular carcinoma (HCC) drug. Given that Raf is one of the major targets of sorafenib, we investigated the activation state of the Raf-Mek-Erk pathway in the presence of HBV and in response to sorafenib. Here we show that hepatoma cells with replicating HBV are less susceptible to sorafenib inhibitory effect as compared to cells in which HBV expression is suppressed. However, although HBV replication is associated with increased level of pErk, its blockade only modestly augments sorafenib effect. In contrast, the phosphorylated form of the pro-oncogenic Mitogen-Activated Protein Kinase 14 (pMAPK14), a protein kinase that was recently linked to sorafenib resistance, is induced in sorafenib-treated hepatoma cells in association with HBV X protein expression. Knocking down pMAPK14 results in augmentation of the therapeutic efficacy of sorafenib and largely alleviates resistance to sorafenib in the presence of HBV. Thus, this study suggests that HBV promotes HCC resistance to sorafenib. Combining pMAPK14 inhibitors with sorafenib may be beneficial in patients with HBV-associated HCC.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  2 / 221995 MEDLINE  
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[PMID]: 29524758
[Au] Autor:Shahmohammadi S; Sahraian MA; Shahmohammadi A; Doosti R; Zare-Mirzaie A; Naser Moghadasi A
[Ad] Address:MS Research Center, Neuroscience Institute, Tehran University of Medical Sciences, Tehran, Iran.
[Ti] Title:A presentation of ulcerative colitis after rituximab therapy in a patient with multiple sclerosis and literature review.
[So] Source:Mult Scler Relat Disord;22:22-26, 2018 Mar 01.
[Is] ISSN:2211-0356
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:Multiple sclerosis (MS) is one of the most important demyelinating diseases that affects the central nervous system. Its treatment often involves a long-term disease modifying therapy. According to some studies, the prevalence of autoimmune disorders, such as autoimmune hepatitis (AIH) and ulcerative colitis (UC) is higher in MS patients than in the normal population. There are also few studies that have reported the onset of UC after rituximab therapy. The present study presents a report of a 31-years old female patient suffering from aggressive multiple sclerosis, which developed into autoimmune hepatitis during the MS therapy. Thereafter, she received rituximab for the treating both MS and AIH. One week after the third cycle of rituximab (6 doses of 1000 mg), she experienced abdominal pain, fever, and severe bloody diarrhea; finally, she was diagnosed with ulcerative colitis (UC). It seems that the administration of certain immunomodulators or immunosuppressive drugs may have a main role in the exacerbation of some autoimmune diseases.
[Pt] Publication type:JOURNAL ARTICLE; REVIEW
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  3 / 221995 MEDLINE  
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[PMID]: 29524530
[Au] Autor:Zhang Z; Filzmayer C; Ni Y; Sültmann H; Mutz P; Hiet MS; Vondran FWR; Bartenschlager R; Urban S
[Ad] Address:Department of Infectious Diseases, Molecular Virology, University Hospital Heidelberg, Heidelberg, Germany.
[Ti] Title:Hepatitis D Virus replication is sensed by MDA5 and induces IFN-ß/λ responses in hepatocytes.
[So] Source:J Hepatol;, 2018 Mar 07.
[Is] ISSN:1600-0641
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:BACKGROUND & AIMS: Hepatitis B virus (HBV) and D virus (HDV) co-infections cause the most severe form of viral hepatitis. HDV induces an innate immune response, but it is unknown how the host cell senses HDV and if this defense affects HDV replication. We aim to characterize interferon (IFN) activation by HDV, identify the responsible sensor and evaluate the effect of IFN on HDV replication. METHODS: HDV and HBV susceptible hepatoma cell lines and primary human hepatocytes (PHH) were used for infection studies. Viral markers and cellular gene expression were analyzed at different time points after infection. Pattern recognition receptors (PRRs) required for HDV-mediated IFN activation and the impact on HDV replication were studied using stable knock-down or overexpression of the PRRs. RESULTS: Microarray analysis revealed that HDV but not HBV infection activated a broad range of interferon stimulated genes (ISGs) in HepG2 cells. HDV strongly activated IFN-ß and IFN-λ in cell lines and PHH. HDV induced IFN levels remained unaltered upon RIG-I or TLR3 knock-down, but were almost completely abolished upon MDA5 depletion. Conversely, overexpression of MDA5 but not RIG-I and TLR3 in Huh7.5 cells partially restored ISG induction. During long-term infection, IFN levels gradually diminished in both HepG2 and HepaRG cell lines. MDA5 depletion had little effect on HDV replication despite dampening HDV-induced IFN response. Moreover, treatment with type I or type III IFNs did not abolish HDV replication. CONCLUSIONS: Active replication of HDV induces an IFN-ß/λ response, which is predominantly mediated by MDA5. This IFN response and exogenous IFN treatment have only a moderate effect on HDV replication in vitro indicating the adaption of HDV replication to an IFN activated state. LAY SUMMARY: In contrast to HBV, infection with HDV induces a strong IFN-ß/λ response in innate immune competent cell lines. MDA5 is the key sensor for the recognition of HDV replicative intermediates. An IFN-activated state did not abrogate HDV replication in vitro indicating resistance to self-induced innate immune responses and therapeutic IFN treatment.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  4 / 221995 MEDLINE  
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[PMID]: 29524528
[Au] Autor:Sersté T; Cornillie A; Njimi H; Pavesi M; Arroyo V; Putignano A; Weichselbaum L; Deltenre P; Degré D; Trépo E; Moreno C; Gustot T
[Ad] Address:Liver Unit, Department of Gastroenterology and Hepatopancreatology and Digestive Oncology, CUB Hôpital Erasme, Université Libre de Bruxelles, Bruxelles, Belgium; Department of Hepatogastroenterology, CHU Saint-Pierre, Bruxelles, Belgium. Electronic address: thomas.serste@skynet.be.
[Ti] Title:The prognostic value of Acute-on-Chronic Liver Failure during the course of severe alcoholic hepatitis.
[So] Source:J Hepatol;, 2018 Mar 07.
[Is] ISSN:1600-0641
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:BACKGROUND & AIMS: A better identification of factors predicting death is needed in alcoholic hepatitis. Acute-on-chronic liver failure (ACLF) occurs during the course of liver disease and can be identified when AH is diagnosed (prevalent ACLF, pACLF) or during follow-up (incidental ACLF, iACLF). This study analyzed the impact of ACLF on outcomes in AH and the role of infection in the onset of ACLF and death. METHODS: Patients admitted from July, 2006 to July, 2015 suffering from biopsy-proven severe (s)AH with a Maddrey discriminant function (mDF) ≥32 were included. Infectious episodes, ACLF, and mortality were assessed during a 168-day follow-up period. Results were validated on an independent cohort. RESULTS: One hundred sixty-five patients were included. Mean mDF was 66.3±20.7 and mean MELD score was 26.8±7.4. The 28-day cumulative incidence of death (CID) was 31% (95%CI, 24-39%). Seventy-nine patients (47.9%) had pACLF. The 28-day CID without pACLF and with pACLF-1, pACLF-2, and pACLF-3 were 10.4% (95%CI, 5.1-18.0), 30.8% (95%CI, 14.3-49.0), 58.3% (95%CI, 35.6-75.5), and 72.4% (95%CI, 51.3-85.5), respectively, p <0.0001. Twenty-nine patients (17.5%) developed iACLF. The 28-day relative risk of death in patients developing iACLF was 41.87 (95%CI, 5.2-335.1, p< 0.001). A previous infection was the only independent risk factor for developing iACLF during the follow-up. Prevalence, incidence, and impact on prognosis of ACLF were confirmed in a validation cohort of 97 patients with probable sAH. CONCLUSIONS: ACLF is frequent during the course of sAH and is associated with high mortality. Infection strongly predicts the development of ACLF in this setting. LAY SUMMARY: In patients with chronic liver disease, an acute deterioration of liver function combined with single or multiple organ failures is known as acute-on-chronic liver failure (ACLF). This study shows that ACLF is frequent during the course of severe alcoholic hepatitis (sAH). In sAH, ACLF is associated with high mortality and frequently occurs secondary to a previous infection.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  5 / 221995 MEDLINE  
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[PMID]: 29515745
[Au] Autor:Diop M; Cisse-Diallo VMP; Ka D; Lakhe NA; Diallo-Mbaye K; Massaly A; Dièye A; Fall NM; Badiane AS; Thioub D; Fortes-Déguénonvo L; Lo G; Diop CT; Ndour CT; Soumaré M; Seydi M
[Ad] Address:Service des Maladies Infectieuses et Tropicales, CHNU de Fann, Dakar, Sénégal.
[Ti] Title:Réactivation d'une hépatite B occulte chez un patient drépanocytaire homozygote: cas clinique et revue de la litérature. [Occult hepatitis B reactivation in a patient with homozygous sickle cell disease: clinical case and literature review].
[So] Source:Pan Afr Med J;28:127, 2017.
[Is] ISSN:1937-8688
[Cp] Country of publication:Uganda
[La] Language:fre
[Ab] Abstract:Occult Hepatitis B corresponds to the presence of hepatitis B virus-deoxyribonucleic acid (HBV-DNA) in serum and/or in liver of a patient despite HBsAg negativity. Clinically, it is usually asymptomatic. Its reactivation is rare and commonly occurs in immunosuppressed individuals. We report the case of a 21-year old patient from Senegal, with homozygous sickle cell disease, presenting with cholestatic jaundice. Laboratory tests showed reactivation of occult Hepatitis B. This study emphasizes the need to systematically investigate the presence of occult Hepatitis B in patients with sickle cell disease suffering from acute liver disease.
[Pt] Publication type:ENGLISH ABSTRACT; JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180311
[Lr] Last revision date:180311
[St] Status:In-Process
[do] DOI:10.11604/pamj.2017.28.127.13640

  6 / 221995 MEDLINE  
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[PMID]: 29515736
[Au] Autor:Boushab BM; Mohamed Limame OCM; Fatim Zahra FM; Mamoudou S; Roseline Darnycka BM; Saliou SM
[Ad] Address:Department of Internal Medicine, Aïoun Regional Hospital, Hodh El Gharbi, Mauritania.
[Ti] Title:Estimation of seroprevalence of HIV, hepatitis B and C virus and syphilis among blood donors in the hospital of Aïoun, Mauritania.
[So] Source:Pan Afr Med J;28:118, 2017.
[Is] ISSN:1937-8688
[Cp] Country of publication:Uganda
[La] Language:eng
[Ab] Abstract:Introduction: To estimating the seroprevalence of HIV, hepatitis B, hepatitis C and syphilis among blood donors in the Aïoun hospital. Methods: This is a retrospective study from 1 January 2010 to 31 December 2015. Results: On the five-year study period, 1,123 donors were collected. Of these, 182 were HIV-positive, an overall prevalence of 16.2% with predominance in male with a sex ratio Man/Woman of 5.2. The average age of donors was 32.7 ± 10 years (range 17-73 years). The most represented that age group 21-30 years (40.5%). The seroprevalence found were 1.2% for HIV, 11.8% for HBV, HCV 0.2% and 3% for syphilis. Co-infection was found in 0.7% of which 0.5% of dual HIV HBV/Syphilis and 0.2% in HBV/HIV. Conclusion: The transmission of infectious agents related to transfusion represents the greatest threat to transfusion safety of the recipient. Therefore, a rigorous selection and screening of blood donors are highly recommended to ensure blood safety for the recipient.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180311
[Lr] Last revision date:180311
[St] Status:In-Process
[do] DOI:10.11604/pamj.2017.28.118.12465

  7 / 221995 MEDLINE  
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[PMID]: 29506502
[Au] Autor:Romiszewski P; Kostro K; Lisiecka U
[Ad] Address:Animal Medical Center, 5255 York Rd, P.O. Box. 324, Holicong, PA, 18928, USA.
[Ti] Title:Effects of subclinical inflammation on C-reactive protein and haptoglobin levels as well as specific humoral immunity in dogs vaccinated against canine distemper and parvovirus.
[So] Source:BMC Vet Res;14(1):70, 2018 Mar 05.
[Is] ISSN:1746-6148
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:BACKGROUND: The aim of the present study was to assess the effects of subclinical inflammation on specific humoral immunity in dogs vaccinated with Nobivac® DHP based on serum levels of CRP and Hp. Dogs from the group I were administered Nobivac® DHP, the vaccine against distemper, infectious hepatitis and parvovirus whereas group II animals received subcutaneous turpentine oil to induce subclinical inflammation, followed by Nobivac® DHP after 24 h. Animals in group III received only turpentine oil in the way and amount identical to that as in group II. RESULTS: Nobivac DHP relatively poorly induced the immune inflammatory response showing good immunogenic properties, which was evidenced by only a double increase in mean CRP and Hp levels associated with antigenic stimulation in group I. In group II, serum neutralization (SN) and haemagglutination inhibition (HI) results were quite closely correlated with serum levels of CPR and Hp. CONCLUSIONS: Our findings suggest that the efficacy of vaccinations in dogs can be significantly affected by subclinical inflammations, which is indicated by a correlation between serum CRP and Hp levels versus antibody titres for canine distemper and parvovirus in both experimental groups of dogs (group I and II). The correlation of mean CRP and Hp values in dogs with subclinical inflammation and after vaccination with the kinetics of increasing antibody titres against distemper and parvovirus in group II dogs reflects the severity of inflammatory response and the extent of specific humoral immunity. Routine determinations of serum CRP and Hp levels as the indices of inflammation severity can be the essential biochemical markers for assessment of dogs' health in the period preceding specific immunoprophylaxis and efficacy of the vaccine.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180311
[Lr] Last revision date:180311
[St] Status:In-Process
[do] DOI:10.1186/s12917-018-1383-6

  8 / 221995 MEDLINE  
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[PMID]: 29501636
[Au] Autor:Suhail M; Sohrab SS; Qureshi A; Tarique M; Abdel-Hafiz H; Al-Ghamdi K; Qadri I
[Ad] Address:King Fahd Medical Research Center, King Abdulaziz University, PO Box 80216, Jeddah 21589, Saudi Arabia.
[Ti] Title:Association of HCV mutated proteins and host SNPs in the development of hepatocellular carcinoma.
[So] Source:Infect Genet Evol;60:160-172, 2018 Mar 01.
[Is] ISSN:1567-7257
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:Hepatitis C virus plays a significant role in the development of hepatocellular carcinoma (HCC) globally. The pathogenic mechanisms of hepatocellular carcinoma with HCV infection are generally linked with inflammation, cytokines, fibrosis, cellular signaling pathways, and liver cell proliferation modulating pathways. HCV encoded proteins (Core, NS3, NS4, NS5A) interact with a broad range of hepatocytes derived factors to modulate an array of activities such as cell signaling, DNA repair, transcription and translational regulation, cell propagation, apoptosis, membrane topology. These four viral proteins are also implicated to show a strong conversion potential in tissue culture. Furthermore, Core and NS5A also trigger the accretion of the ß-catenin pathway as a common target to contribute viral induced transformation. There is a strong association between HCV variants within Core, NS4, and NS5A and host single nucleotide polymorphisms (SNPs) with the HCC pathogenesis. Identification of such viral mutants and host SNPs is very critical to determine the risk of HCC and response to antiviral therapy. In this review, we highlight the association of key variants, mutated proteins, and host SNPs in development of HCV induced HCC. How such viral mutants may modulate the interaction with cellular host machinery is also discussed.
[Pt] Publication type:JOURNAL ARTICLE; REVIEW
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  9 / 221995 MEDLINE  
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[PMID]: 29453971
[Au] Autor:Liu C; Wu W; Shang H; Lin S; Xun Z; Huang E; Lin J; Yang B; Ou Q
[Ad] Address:Department of Laboratory Medicine, The First Affiliated Hospital of Fujian Medical University, Fuzhou, Fujian Province, China; Gene Diagnostic Laboratory, The First Affiliated Hospital of Fujian Medical University, Fuzhou, Fujian Province, China.
[Ti] Title:Prediction value of serum HBV large surface protein in different phases of HBV infection and virological response of chronic hepatitis B patients.
[So] Source:Clin Chim Acta;481:12-19, 2018 Feb 14.
[Is] ISSN:1873-3492
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:BACKGROUND: Serum HBV large surface protein (HBV-LP) is an envelope protein that has a close relationship with HBV DNA level. This study is to explore the prediction value of HBV-LP in different phase of HBV infection and during antiviral therapy in chronic hepatitis B (CHB) patients. METHODS: A retrospective study was conducted in 2033 individuals, which included 1677 HBV infected patients in different phases and 356 healthy controls. HBV-LP, HBV serum markers and HBV DNA were detected by ELISA, CMIA and qRT-PCR, respectively. 85 CHB patients receiving PegIFNα or ETV were divided into virological response (VR) and partial virological response (PVR). The dynamic changes of HBV DNA and HBV-LP were observed. RESULTS: The level of HBV-LP in 2033 individuals was shown as: HBeAg-positive hepatitis > HBeAg-positive infection > HBeAg-negative hepatitis > HBeAg-negative infection > healthy controls. HBV-LP was positive in all patients whose HBV DNA > 1.0E + 06 IU/ml. When HBsAg was <0.05 IU/ml or >1000 IU/ml, HBV DNAs were all negative if HBV-LP < 1.0 S/CO. When HBsAg was between 0.05 IU/ml and 1000 IU/ml, the consistency of HBV-LP with HBV DNA was 100% in case of HBV-LP > 4.0 S/CO in HBeAg-positive patients and HBV-LP > 2.0 S/CO in HBeAg-negative ones. During antiviral therapy, baseline HBV-LP was lower in VR patients than that in PVR patients. The optimal cut-off points to predict VR by baseline HBV-LP were 32.4 and 28.6 S/CO for HBeAg-positive and HBeAg-negative hepatitis patients, respectively. CONCLUSIONS: HBV-LP may be a useful marker for distinguishing the different phases of HBV infection. Moreover, baseline HBV-LP level can be used for predicting VR of CHB patients.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  10 / 221995 MEDLINE  
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[PMID]: 29452294
[Au] Autor:Cusato J; De Nicolò A; Boglione L; Favata F; Ariaudo A; Mornese Pinna S; Carcieri C; Guido F; Avataneo V; Cariti G; Di Perri G; D'Avolio A
[Ad] Address:Department of Medical Sciences, University of Turin, Amedeo di Savoia Hospital, Turin, Italy. Electronic address: jessica.cusato@unito.it.
[Ti] Title:Vitamin D pathway genetic variants are able to influence sofosbuvir and its main metabolite pharmacokinetics in HCV mono-infected patients.
[So] Source:Infect Genet Evol;60:42-47, 2018 Feb 13.
[Is] ISSN:1567-7257
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:Vitamin D levels and genetic variants were associated with drug outcome/toxicity and concentrations. The plasma exposure of GS-331007, the main sofosbuvir metabolite, has been related to SVR. We evaluated the impact of polymorphisms in genes (CYP27B1, CYP24A1, VDBP and VDR) related to vitamin D pathway on sofosbuvir and GS-331007 plasma levels in HCV mono-infected patients at one month of treatment. Polymorphisms were investigated through real-time PCR; drug plasma quantification was performed through a UHPLC-MS/MS method. GS-331007 levels were associated with CYP24A1rs2248359 and VDRCdx2 variants in all the analyzed patients and linear regression analysis showed that sex, body mass index, HCV genotype, baseline estimated glomerular filtration rate, VDRCdx2AG/GG and CYP27B1-1260TT genotypes significantly predict concentrations. We performed sub-analyses considering the HCV genotype and the concomitant drug, identifying polymorphisms associated with GS-331007 concentrations. This is the first study focusing on vitamin D pathway gene variants and DAAs concentrations, but further studies are required.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher


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