Publications by authors named "Cai-Feng Chen"

Six terpyridine ligands(L-L) with chlorophenol or bromophenol moiety were obtained to prepare metal terpyridine derivatives complexes: [Ru(L)(DMSO)Cl] (1), [Ru(L)(DMSO)Cl] (2), [Ru(L)(DMSO)Cl] (3), [Cu(L)Br]·DMSO (4), Cu(L)Br (5), and [Cu(L)Br]⋅CHOH (6). The complexes were fully characterized. Ru complexes 1-3 showed low cytotoxicity against the tested cell lines.

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Three new synthetic terpyridine copper(II) complexes were characterized. The copper(II) complexes induced apoptosis of three cancer cell lines and arrested T-24 cell cycle in G1 phase. The complexes were accumulated in mitochondria of T-24 cells and caused significant reduction of the mitochondrial membrane potential.

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Purpose: The aim of this study was to identify the correlations of IFN-γ-inducible protein-10 (IP-10) with the risk of chronic hepatitis B (CHB) and the efficacy of interferon therapy in Asians.

Method: Serum IP-10 levels were assayed using enzyme linked immunosorbent assay (ELISA) in both CHB and control group. CHB group received interferon-α2b treatment to compare the pre-treatment and post-treatment serum IP-10 levels.

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Chronic hepatitis B virus (HBV) infection is a major global health burden. Functional exhaustion and numerical reduction of HBV-specific cytotoxic T lymphocytes (CTLs) in the liver and peripheral blood limit anti-HBV CTL activity in patients with chronic HBV infection (CHB). However, the ongoing anti-HBV CD8(+) T cell responses in the lymphoid organs are largely unknown due to the infeasibility of obtaining lymphoid organs from CHB patients.

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Article Synopsis
  • JMJD6 is identified as a potential regulator of T cell proliferation during chronic hepatitis B virus (HBV) infection, showing reduced expression in T lymphocytes of chronic hepatitis B patients.
  • Lower levels of JMJD6 lead to impaired T cell proliferation, while silencing JMJD6 in human T cells further inhibits their growth.
  • Platelet-derived growth factor-BB (PDGF-BB) is found to downregulate JMJD6, affecting T cell function, and both JMJD6 and PDGF-BB levels correlate with liver damage and treatment outcomes in chronic HBV infection.
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Objective: To explore the effect of Modified Sijunzi Decoction (MSD) on the bone metabolism of prednisone intervened adriamycin-induced nephropathy rats.

Methods: The adriamycin-induced nephropathy rat model was prepared. Totally 50 SD rats were randomly divide into five groups, i.

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1-17-2 is a rat anti-human DEC-205 monoclonal antibody that induces internalization and delivers antigen to dendritic cells (DCs). The potentially clinical application of this antibody is limited by its murine origin. Traditional humanization method such as complementarity determining regions (CDRs) graft often leads to a decreased or even lost affinity.

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Although extensive studies have demonstrated the functional impairment of antigen-specific CD4(+) and CD8(+) T-cells during chronic hepatitis C virus (HCV) infection, the functional status of global CD4(+) and CD8(+) T-cells remains unclear. In this report, we recruited 42 long-term (~20 years) treatment-naïve chronic HCV (CHC) patients and 15 healthy donors (HDs) to investigate differences in global CD4(+) and CD8(+) T-cells function. We show that CD4(+) and CD8(+) T-cells from CHC patients underwent increased apoptosis after TCR stimulation.

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Inflammation caused by chronic hepatitis B virus (HBV) infection is associated with the development of cirrhosis and hepatocellular carcinoma; however, the mechanisms by which HBV infection induces inflammation and inflammatory cytokine production remain largely unknown. We analyzed the gene expression patterns of lymphocytes from chronic HBV-infected patients and found that the expression of ZFP36, an AU-rich element (ARE)-binding protein, was dramatically reduced in CD4(+) and CD8(+) T lymphocytes from chronic HBV patients. ZFP36 expression was also reduced in CD14(+) monocytes and in total PBMCs from chronic HBV patients.

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Human adenoviruses (HAdVs) are the etiologic agent of many human infectious diseases. The existence of at least 54 different serotypes of HAdVs has resulted in difficulties in clinical diagnosis. Acute respiratory tract disease (ARD) caused by some serotypes from B and C species is particularly serious.

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Objective: To investigate the structure and function of the N-terminal region (NTR) of death receptor 5 (DR5).

Methods: A series of deletions of the DR5 extracellular domain (DR5-ECD) proteins were expressed in E.coli.

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