Results 81 to 90 of about 457,015 (304)

Nuclear Factor I‐B Delays Liver Fibrosis by Inhibiting Chemokine Ligand 5 Transcription

open access: yesAdvanced Science, EarlyView.
This study identifies the transcription factor Nuclear Factor I‐B (NFIB) as a key suppressor of liver fibrosis. NFIB expression declines during hepatic stellate cell activation, and its overexpression reduces fibrosis in mice models. The mechanism involves NFIB directly repressing chemokine C─C motif ligand 5 (CCL5), thereby alleviating oxidative ...
Qianqian Chen   +14 more
wiley   +1 more source

17,β-estradiol inhibits hepatitis C virus mainly by interference with the release phase of its life cycle [PDF]

open access: yes, 2016
Rationale & Aim: Estrogen and estrogen-mediated signalling protect from hepatitis C virus through incompletely understood mechanisms. We aimed to ascertain which phase(s) of HCV life cycle is/are affected by estrogens.
Barbaglia, Matteo N.   +10 more
core   +2 more sources

PREVALENCE OF HEPATITIS D VIRUS (HDV) IN SOUTH GUJARAT

open access: yesNational Journal of Medical Research, 2012
Aim: Hepatitis D Virus (HDV) infects only patients that are already infected by hepatitis B virus (HBV).There is lack of data on the impact of Hepatitis D Virus (HDV) in patients with hepatitis B virus (HBV) in south Gujarat.
Shah Latika J, Mulla Summaiya A
doaj  

Fast Differentiation of HepaRG Cells Allowing Hepatitis B and Delta Virus Infections

open access: yesCells, 2020
HepaRG cells are liver bipotent progenitors acquiring hepatocytes features when differentiated in the presence of dimethylsulfoxide (DMSO). Differentiated HepaRG (dHepaRG) are considered the best surrogate model to primary human hepatocytes (PHH) and are
Julie Lucifora   +3 more
doaj   +1 more source

Hepatitis D virus: is it all in the family?

open access: yesGut, 2020
Hepatitis delta virus (HDV) infection is the most severe form of chronic viral hepatitis: HDV-infected individuals are more likely to die from advanced liver disease compared with hepatitis B virus (HBV)-infected without HDV and their risk of developing hepatocellular carcinoma is up to nine times higher.1 HDV is a defective virus, using the HBV ...
Anders Boyd, Gilles Wandeler
openaire   +2 more sources

Reconstitution of hepatitis B virus (HBV)-specific T cell responses with treatment of human immunodeficiency virus/HBV coinfection [PDF]

open access: yes, 2003
Liver-related mortality is an increasing problem in human immunodeficiency virus (HIV)/hepatitis B virus (HBV)-coinfected patients receiving highly active antiretroviral therapy (HAART).
Bertoletti, A   +4 more
core   +1 more source

Inhibition of SLC11A1‐Mediated Lysosomal Iron Accumulation in Microglia Promotes Repair Following White Matter Stroke

open access: yesAdvanced Science, EarlyView.
Genetic and pharmacological inhibition of SLC11A1 functioning as an H+/Fe2+ antiporter–mediated lysosomal iron accumulation in microglia promotes lysosomal lumen acidification, increases CTSD expression, enhances lysosomal myelin debris uptake and degradation, and promotes repair following white matter stroke. ABSTRACT White matter stroke (WMS) results
Lingling Qiu   +11 more
wiley   +1 more source

Prevalence and Genotyping of Hepatitis D Virus among HBs Ag Positive Patients Referred to Besat Clinic, Kerman during 2012-2013

open access: yesMajallah-i Dānishgāh-i ’Ulūm-i Pizishkī-i Shahīd Ṣadūqī Yazd, 2016
Introduction: Hepatitis D virus (HDV) is a 35 nm in diameter agent that depends on hepatitis B surface antigen in order to proliferate and accumulate. Infection with delta agent can occur spontaneously with hepatitis B virus infection and it cause acute ...
Kh Barkhordari   +5 more
doaj  

Supporting children with genetic syndromes in the classroom: the example of 22q deletion syndrome [PDF]

open access: yes, 2013
An increasing number of children are likely to have a known genetic cause for their special educational needs. One such genetic condition is 22q11.2 deletion syndrome (22qDS), a genetic syndrome associated with early speech and language difficulties ...
Reilly, C, Stedman, L
core   +1 more source

Microglial Fkbp5 Impairs Post‐Stroke Vascular Integrity and Regeneration by Promoting Yap1‐Mediated Glycolysis and Oxidative Phosphorylation

open access: yesAdvanced Science, EarlyView.
A post‐stroke perivascular niche of microglia characterized by low expression of M2 markers and elevated glycolysis, oxidative phosphorylation (OXPHOS), and phagocytic activity is identified, which is termed stroke‐activated vascular‐associated microglia (stroke‐VAM).
Yanan Li   +8 more
wiley   +1 more source

Home - About - Disclaimer - Privacy