We report a gene expression study aimed at the identification of genes differentially expressed in the livers of Hispanic patients infected with hepatitis C virus (HCV). Six uninfected controls were compared with 14 HCV(+) patients in which the liver biopsies were obtained at the time of diagnosis. Among the latter, five patients were also analyzed 4 weeks after the onset of standard anti-HCV therapy (pegylated interferon-α + ribavirin). We identified many genes up- or down-regulated by the infection with HCV in the human livers. When these genes were subjected to pathway analysis, several prominent pathways were revealed including many interferon (IFN)-inducible pathways as well as immune cell trafficking, inflammation, anti-microbial responses, and even cancer. We detected expression of many genes that have previously been associated with HCV infection, as well as several novel genes including CD47. The genes induced by HCV infection showed large expression changes, whereas the genes induced by the IFN-α combination therapy were relatively few (including MX2, ORMDL3, GPAM, KOPX18, TMEM56, and HBP1) and they reflected relatively small expression changes. This is the first study to identify changes in gene expression in livers of HCV(+) Hispanic patients and the first to identify genes induced by anti-HCV combination therapy in the human liver.
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http://dx.doi.org/10.3109/08916934.2011.592881 | DOI Listing |
Hematology
December 2025
Department of Hematology, XuChang Central Hospital, XuChang, People's Republic of China.
Introduction: Mitochondria and angiogenesis play key roles in multiple myeloma (MM) development, but their interrelated genes affecting MM prognosis are under-studied.
Methods: We analyzed TCGA_MMRF and GSE4581 datasets to identify four genes - CCNB1, CDC25C, HSP90AA1, and PARP1 - that significantly correlate with MM prognosis, with high expression indicating poor outcomes.
Results: A prognostic signature based on these genes stratified patients into high- and low-risk groups, with the latter showing better survival.
J Cachexia Sarcopenia Muscle
February 2025
Department of Bioactive Material Sciences, Research Center of Bioactive Materials, Jeonbuk National University, Jeonju, Republic of Korea.
Background: The cellular prion protein (PrP), a glycoprotein encoded by the PRNP gene, is known to modulate muscle mass and exercise capacity. However, the role of PrP in the maintenance and regeneration of skeletal muscle during ageing remains unclear.
Methods: This study investigated the change in PrP expression during muscle formation using C2C12 cells and evaluated muscle function in Prnp wild-type (WT) and knock-out (KO) mice at different ages (1, 9 and 15 months).
J Dent Sci
January 2025
Department of Oral Medicine, Shanghai Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Background/purpose: Oral lichen planus (OLP) is a chronic inflammatory disorder characterized by basement membrane disruption, which plays a crucial role in its pathogenesis. Matrix metalloproteinases (MMPs), a group of proteolytic enzymes, contribute to the degradation of the basement membrane. The specific MMPs secreted by keratinocytes in OLP lesions and relevant regulatory mechanisms are not fully understood.
View Article and Find Full Text PDFJ Dent Sci
January 2025
Department of Periodontology and Endodontology, Tohoku University Graduate School of Dentistry, Sendai, Japan.
Background/purpose: Peroxisome proliferator-activated receptor γ (PPARγ) is a major transcription factor of energy metabolism-associated genes, and three PPARγ isoforms have been identified in periodontal tissues and cells. When energy metabolism homeostasis is affected by PPARγ downregulation in periodontal ligament fibroblasts (PDLFs), osteo/cementogenic abilities are markedly lost. Herein, we investigated whether PPARγ agonists promote periodontal tissue regeneration, and which PPARγ isoforms and metabolic pathways are indispensable for osteo/cementogenic abilities.
View Article and Find Full Text PDFFront Neurosci
January 2025
Translational Neuroscience Program, Department of Psychiatry, University of Pittsburgh School of Medicine, Pittsburgh, PA, United States.
Introduction: Alterations in multiple subregions of the human prefrontal cortex (PFC) have been heavily implicated in psychiatric diseases. Moreover, emerging evidence suggests that circadian rhythms in gene expression are present across the brain, including in the PFC, and that these rhythms are altered in disease. However, investigation into the potential circadian mechanisms underlying these diseases in animal models must contend with the fact that the human PFC is highly evolved and specialized relative to that of rodents.
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