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  1. Article ; Online: HSD17B13 and other liver fat-modulating genes predict development of hepatocellular carcinoma among HCV-positive cirrhotics with and without viral clearance after DAA treatment.

    Burlone, Michela E / Bellan, Mattia / Barbaglia, Matteo N / Mocchetti, Ginevra / Mallela, Venkata R / Minisini, Rosalba / Rigamonti, Cristina / Pirisi, Mario

    Clinical journal of gastroenterology

    2022  Volume 15, Issue 2, Page(s) 301–309

    Abstract: Background: Genetic predisposition to accumulate liver fat (expressed by a polygenic risk score, GRS, based on the number of at-risk alleles of PNPLA3, TM6SF2, MBOAT7 and GCKR) may influence the probability of developing hepatocellular carcinoma (HCC) ... ...

    Abstract Background: Genetic predisposition to accumulate liver fat (expressed by a polygenic risk score, GRS, based on the number of at-risk alleles of PNPLA3, TM6SF2, MBOAT7 and GCKR) may influence the probability of developing hepatocellular carcinoma (HCC) after hepatitis C treatment. Whether this holds true taking into account carriage of the HSD17B13:TA splice variant, also affecting lipogenesis, and achievement of viral clearance (SVR), is unknown.
    Methods: PNPLA3, TM6SF2, MBOAT7, GCKR and HSD17B13 variants were determined in a cohort of 328 cirrhotic patients free of HCC before starting treatment with direct acting antivirals (DAA).
    Results: SVR in the study cohort was 96%. At the end of follow-up, N = 21 patients had been diagnosed an HCC; none of the genes included in the GRS was individually associated with HCC development. However, in a Cox proportional hazards model, a GRS > 0.457 predicted HCC independently of sex, diabetes, albumin, INR and FIB4. The fit of the model improved adding treatment outcome and carriage of the HSD17B13:TA splice variant, with sex, GRS > 0.457, HSD17B13:TA splice variant and failure to achieve an SVR (hazard ratio = 6.75, 4.24, 0.24 and 7.7, respectively) being independent predictors of HCC.
    Conclusion: Our findings confirm that genes modulating liver fat and lipogenesis are important risk factors for HCC development among cirrhotics C treated with DAA.
    MeSH term(s) 17-Hydroxysteroid Dehydrogenases/genetics ; Antiviral Agents/therapeutic use ; Carcinoma, Hepatocellular/genetics ; Carcinoma, Hepatocellular/pathology ; Hepatitis C, Chronic/complications ; Hepatitis C, Chronic/drug therapy ; Humans ; Liver Cirrhosis/complications ; Liver Cirrhosis/drug therapy ; Liver Neoplasms/complications ; Liver Neoplasms/genetics
    Chemical Substances Antiviral Agents ; 17-Hydroxysteroid Dehydrogenases (EC 1.1.-) ; HSD17B13 protein, human (EC 1.1.-.-)
    Language English
    Publishing date 2022-01-31
    Publishing country Japan
    Document type Journal Article
    ZDB-ID 2429411-1
    ISSN 1865-7265 ; 1865-7257
    ISSN (online) 1865-7265
    ISSN 1865-7257
    DOI 10.1007/s12328-021-01578-1
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Direct antivirals and cognitive impairment in hepatitis C: a clinical-neurophysiologic study.

    Vaghi, Gloria / Gori, Benedetta / Strigaro, Gionata / Burlone, Michela / Minisini, Rosalba / Barbaglia, Matteo N / Brigatti, Elena / Varrasi, Claudia / Pirisi, Mario / Cantello, Roberto

    Journal of neurovirology

    2020  Volume 26, Issue 6, Page(s) 870–879

    Abstract: Cognition was assessed in hepatitis C virus (HCV) patients, who did not meet the criteria for a minimal hepatic encephalopathy. Their liver function was compensated. We then disentangled potential cognitive changes associated with a sustained virologic ... ...

    Abstract Cognition was assessed in hepatitis C virus (HCV) patients, who did not meet the criteria for a minimal hepatic encephalopathy. Their liver function was compensated. We then disentangled potential cognitive changes associated with a sustained virologic response at 12 weeks (SVR-12), following treatment with direct antiviral agents (DAAs). We studied 23 selected HCV patients with a battery of standard neuropsychological tests, and with recordings of the P300 wave, a cerebral potential of "cognitive" significance. There was a baseline evaluation (T0) and a second one 6 months later (T1). We had 2 control groups of comparable age and sex, i.e., 15 patients suffering from non-alcoholic fatty liver disease (NAFLD) and 15 healthy subjects. At T0, we detected a significant (p < 0.05) cognitive impairment in the HCV group, which involved episodic and working memory, attention, visuospatial and verbal abilities, executive functions, and logic reasoning. The P300 latency was significantly (p < 0.05) delayed in the group. At T1, we observed some significant (p < 0.05) HCV recovery in given test domains, e.g., memory, executive functions, and reasoning. Accordingly, the P300 latency shortened significantly (p < 0.05). HCV patients exhibited subtle cognitive defects, somehow independent of their liver condition, possibly linked to direct or indirect brain involvement by the virus. These defects partly recovered following the SVR-12, as achieved through DAAs. The P300 wave was a valid neurophysiologic counterpart of these changes. DAAs can have a role in the early preservation of cognition in HCVs.
    MeSH term(s) Aged ; Antiviral Agents/therapeutic use ; Attention/drug effects ; Attention/physiology ; Brain/drug effects ; Brain/virology ; Case-Control Studies ; Cognition/drug effects ; Cognition/physiology ; Cognitive Dysfunction/diagnosis ; Cognitive Dysfunction/drug therapy ; Cognitive Dysfunction/psychology ; Cognitive Dysfunction/virology ; Event-Related Potentials, P300/drug effects ; Event-Related Potentials, P300/physiology ; Executive Function/drug effects ; Executive Function/physiology ; Female ; Hepacivirus/drug effects ; Hepacivirus/pathogenicity ; Hepatitis C, Chronic/diagnosis ; Hepatitis C, Chronic/drug therapy ; Hepatitis C, Chronic/psychology ; Hepatitis C, Chronic/virology ; Humans ; Liver/drug effects ; Liver/virology ; Male ; Memory, Short-Term/drug effects ; Memory, Short-Term/physiology ; Middle Aged ; Neuropsychological Tests ; Non-alcoholic Fatty Liver Disease/diagnosis ; Non-alcoholic Fatty Liver Disease/psychology ; Non-alcoholic Fatty Liver Disease/virology ; Sustained Virologic Response
    Chemical Substances Antiviral Agents
    Language English
    Publishing date 2020-09-10
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 1283265-0
    ISSN 1538-2443 ; 1355-0284
    ISSN (online) 1538-2443
    ISSN 1355-0284
    DOI 10.1007/s13365-020-00904-6
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 4426: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (2.OG)
    ab Jg. 2022: Lesesaal (EG)

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  3. Article ; Online: 17,β-estradiol inhibits hepatitis C virus mainly by interference with the release phase of its life cycle.

    Magri, Andrea / Barbaglia, Matteo N / Foglia, Chiara Z / Boccato, Elisa / Burlone, Michela E / Cole, Sarah / Giarda, Paola / Grossini, Elena / Patel, Arvind H / Minisini, Rosalba / Pirisi, Mario

    Liver international : official journal of the International Association for the Study of the Liver

    2017  Volume 37, Issue 5, Page(s) 669–677

    Abstract: Background & aims: Oestrogen and oestrogen-mediated signalling protect from hepatitis C virus through incompletely understood mechanisms. We aimed to ascertain which phase(s) of hepatitis C virus life cycle is/are affected by oestrogens.: Methods: ... ...

    Abstract Background & aims: Oestrogen and oestrogen-mediated signalling protect from hepatitis C virus through incompletely understood mechanisms. We aimed to ascertain which phase(s) of hepatitis C virus life cycle is/are affected by oestrogens.
    Methods: Huh7 cells infected with the JFH1 virus (genotype 2a) were exposed to dehydroepiandrosterone, testosterone, progesterone and 17β-estradiol (tested with/without its receptor antagonist fulvestrant). Dose-response curves were established to calculate half maximal inhibitory concentration values. To dissect how 17β-estradiol interferes with phases of hepatitis C virus life cycle, its effects were measured on the hepatitis C virus pseudo-particle system (viral entry), the subgenomic replicon N17/JFH1 and the replicon cell line Huh7-J17 (viral replication). Finally, in a dual-step infection model, infectious supernatants, collected from infected cells exposed to hormones, were used to infect naïve cells.
    Results: Progesterone and testosterone showed no inhibitory effect on hepatitis C virus; dehydroepiandrosterone was only mildly inhibitory. In contrast, 17β-estradiol inhibited infection by 64%-67% (IC
    Conclusions: 17β-estradiol inhibits hepatitis C virus acting through its intracellular receptors, mainly interfering with late phases (assembly/release) of the hepatitis C virus life cycle.
    Language English
    Publishing date 2017-05
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2102783-3
    ISSN 1478-3231 ; 1478-3223
    ISSN (online) 1478-3231
    ISSN 1478-3223
    DOI 10.1111/liv.13303
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 1632: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (1.OG)
    ab Jg. 2022: Lesesaal (EG)

    Order via subito

    This service is chargeable due to the Delivery terms set by subito. Orders including an article and supplementary material will be classified as separate orders. In these cases, fees will be demanded for each order.

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