Regional Assessment of Liver Disease Progression and Response to Therapy by Multi-time Point m-SLIC Correspondence

2018 ◽  
pp. 44-50
Author(s):  
Benjamin Irving ◽  
Chloe Hutton ◽  
Katherine Arndtz ◽  
Naomi Jayaratne ◽  
Matt Kelly ◽  
...  
Keyword(s):  
Liver Disease ◽  
Disease Progression ◽  
Response To Therapy ◽  
Regional Assessment ◽  
Liver Disease Progression ◽  
Time Point

1894-P: HIF-2α Induced by Hypoxia Exacerbates Nonalcoholic Fatty Liver Disease Progression via Suppressing PPARα

Diabetes ◽  
2019 ◽  
Vol 68 (Supplement 1) ◽  
pp. 1894-P
Author(s):  
JIANDI CHEN ◽  
JIANXU CHEN ◽  
HUIRONG FU ◽  
YUN LI ◽  
SHUNKUI LUO ◽  
...  
Keyword(s):  
Liver Disease ◽  
Fatty Liver ◽  
Nonalcoholic Fatty Liver Disease ◽  
Disease Progression ◽  
Fatty Liver Disease ◽  
Nonalcoholic Fatty Liver ◽  
Liver Disease Progression

scholarly journals Genetic variants of programmed cell death 1 are associated with HBV infection and liver disease progression

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Nghiem Xuan Hoan ◽  
Pham Thi Minh Huyen ◽  
Mai Thanh Binh ◽  
Ngo Tat Trung ◽  
Dao Phuong Giang ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Cell Death ◽  
Liver Disease ◽  
Programmed Cell Death ◽  
Disease Progression ◽  
Infection Risk ◽  
Hbv Infection ◽  
Liver Disease Progression ◽  
Increased Risk ◽  
Programmed Cell Death 1

AbstractThe inhibitory effects of programmed cell death 1/programmed cell death ligand 1 (PD-1/PD-L1) modulates T-cell depletion. T-cell depletion is one of the key mechanisms of hepatitis B virus (HBV) persistence, in particular liver disease progression and the development of hepatocellular carcinoma (HCC). This case–control study aimed to understand the significance of PD-1 polymorphisms (PD-1.5 and PD-1.9) association with HBV infection risk and HBV-induced liver disease progression. Genotyping of PD-1.5 and PD-1.9 variants was performed by direct Sanger sequencing in 682 HBV-infected patients including chronic hepatitis (CHB, n = 193), liver cirrhosis (LC, n = 183), hepatocellular carcinoma (HCC, n = 306) and 283 healthy controls (HC). To analyze the association of PD-1 variants with liver disease progression, a binary logistic regression, adjusted for age and gender, was performed using different genetic models. The PD-1.9 T allele and PD-1.9 TT genotype are significantly associated with increased risk of LC, HCC, and LC + HCC. The frequencies of PD-1.5 TT genotype and PD-1.5 T allele are significantly higher in HCC compared to LC patients. The haplotype CT (PD-1.5 C and PD-1.9 T) was significantly associated with increased risk of LC, HCC, and LC + HCC. In addition, the TC (PD-1.5 T and PD-1.9 C) haplotype was associated with the risk of HCC compared to non-HCC. The PD-1.5 CC, PD-1.9 TT, genotype, and the CC (PD-1.5 C and PD-1.9) haplotype are associated with unfavorable laboratory parameters in chronic hepatitis B patients. PD-1.5 and PD1.9 are useful prognostic predictors for HBV infection risk and liver disease progression.

Impact of genotype 3 on clinical outcome in patients with hepatitis C: both diabetes meliitus and liver disease progression

2017 ◽  
Vol 66 (1) ◽  
pp. S711-S712
Author(s):  
W. Zanjir ◽  
R. Maan ◽  
B. Hansen ◽  
O. Cerocchi ◽  
H. Janssen ◽  
...  
Keyword(s):  
Liver Disease ◽  
Hepatitis C ◽  
Clinical Outcome ◽  
Disease Progression ◽  
Genotype 3 ◽  
Liver Disease Progression

scholarly journals Dynamin-related protein 1 deficiency accelerates lipopolysaccharide-induced acute liver injury and inflammation in mice

2021 ◽  
Vol 4 (1) ◽  
Author(s):  
Lixiang Wang ◽  
Xin Li ◽  
Yuki Hanada ◽  
Nao Hasuzawa ◽  
Yoshinori Moriyama ◽  
...  
Keyword(s):  
Liver Disease ◽  
Liver Injury ◽  
Er Stress ◽  
Disease Progression ◽  
Acute Liver Injury ◽  
Mitochondrial Dynamics ◽  
Mitochondrial Fission ◽  
Mitochondrial Fusion ◽  
Related Protein ◽  
Liver Disease Progression

AbstractMitochondrial fusion and fission, which are strongly related to normal mitochondrial function, are referred to as mitochondrial dynamics. Mitochondrial fusion defects in the liver cause a non-alcoholic steatohepatitis-like phenotype and liver cancer. However, whether mitochondrial fission defect directly impair liver function and stimulate liver disease progression, too, is unclear. Dynamin-related protein 1 (DRP1) is a key factor controlling mitochondrial fission. We hypothesized that DRP1 defects are a causal factor directly involved in liver disease development and stimulate liver disease progression. Drp1 defects directly promoted endoplasmic reticulum (ER) stress, hepatocyte death, and subsequently induced infiltration of inflammatory macrophages. Drp1 deletion increased the expression of numerous genes involved in the immune response and DNA damage in Drp1LiKO mouse primary hepatocytes. We administered lipopolysaccharide (LPS) to liver-specific Drp1-knockout (Drp1LiKO) mice and observed an increased inflammatory cytokine expression in the liver and serum caused by exaggerated ER stress and enhanced inflammasome activation. This study indicates that Drp1 defect-induced mitochondrial dynamics dysfunction directly regulates the fate and function of hepatocytes and enhances LPS-induced acute liver injury in vivo.

scholarly journals Statins Are Associated With Decreased Liver Disease Progression in HIV/HCV Co-Infected Adults

2015 ◽  
Vol 2 (suppl_1) ◽  
Author(s):  
Nouf Almaghlouth ◽  
Catherine Sutcliffe ◽  
Shruti Mehta ◽  
Richard Moore ◽  
Mark Sulkowski
Keyword(s):  
Liver Disease ◽  
Disease Progression ◽  
Liver Disease Progression

scholarly journals Non-alcoholic fatty liver disease progression and current research

2019 ◽  
Vol 6 (1) ◽  
pp. 189-198
Author(s):  
Smriti Narayan ◽  
Sonu Kumar Gupta ◽  
Priyanka Singh ◽  
Villayat Ali ◽  
Malkhey Verma
Keyword(s):  
Liver Disease ◽  
Fatty Liver ◽  
Disease Progression ◽  
Fatty Liver Disease ◽  
Alcoholic Fatty Liver ◽  
Liver Disease Progression ◽  
Alcoholic Fatty Liver Disease

scholarly journals Analysis of site and structure specific core fucosylation in liver disease progression using exoglycosidase-assisted data-independent LC-MS/MS

2020 ◽  
Author(s):  
Miloslav Sanda ◽  
Jaeil Ahn ◽  
Petr Kozlik ◽  
Radoslav Goldman
Keyword(s):  
Liver Disease ◽  
Disease Progression ◽  
Serum Proteins ◽  
Receptor Activation ◽  
Biological Macromolecules ◽  
The Core ◽  
Liver Disease Progression ◽  
Living Organisms ◽  
Protein Attachment ◽  
Core Fucosylation

ABSTRACTCarbohydrates form one of the major groups of biological macromolecules in living organisms. Many biological processes including protein folding, stability, immune response, and receptor activation are regulated by glycosylation. Fucosylation of proteins regulates such processes and is associated with various diseases including autoimmunity and cancer. Mass spectrometry efficiently identifies structures of fucosylated glycans or sites of core fucosylated N-glycopeptides but quantification of the glycopeptides remains less explored. We performed experiments that facilitate quantitative analysis of the core fucosylation of proteins with partial structural resolution of the glycans and we present results of the mass spectrometric SWATH-type DIA analysis of relative abundances of the core fucosylated glycoforms of 45 glycopeptides derived from 18 serum proteins in liver disease of different etiologies. Our results show that a combination of soft fragmentation with exoglycosidases is efficient at the assignment and quantification of the core fucosylated N-glycoforms at specific sites of protein attachment. In addition, our results show that disease-associated changes in core fucosylation are peptide-dependent and further differ by branching of the core fucosylated glycans. Further studies are needed to verify whether tri- and tetra-antennary core fucosylated glycopeptides could be used as markers of liver disease progression.

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