ABSTRACT
Objective To explore the effect of hepatitis B virus(HBV) on the expression of complement 3 (C3) and complement 4 (C4) and its regulatory mechanism.Methods Differentially expressed genes between HepG2 and HepG2.2.15 cells was screened by gene chip,serum complement component 3 (C3) and 4 (C4) levels in patients with HBV infection and in healthy individuals were measured by Immunoturbidimetry,HBV infectious clone pHBV1.3 was transfected into HepG2 cells,and expression of C3 and C4 was measured by RT-PCR and Western blot.Results Expression of C3 and C4 mRNA was lower in HepG2.2.15 cells than in HepG2 cells,serum C3 and C4 levels was much lower in patients with chronic hepatitis B and hepatic carcinoma as compared to healthy individuals (P＜0.05 ).HBV could downregulate the expression of C3 and C4 at mRNA and protein levels.Conclusion HBV may inhibit the expression both in vivo and in vitro.
ABSTRACT
Objective Alzheimer's disease(AD) is a common and devastating disease and there is no readily available biomarker to aid diagnosis or to monitor disease progression. This study is to further understand the pathogenesis of Alzheimer's disease and seek new biomarkers for AD. Methods AD rats made by Aβ1-40 were assessed using the Morris water maze method. Sera of two groups were collected and albumin, IgG and sodium chloride were removed from the serum before concentration. Two-dimensional electrophoresis(2-DE) was performed on serum protein. Altered proteins were identified by matrix assisted laser desorption/ionization time of flight mass spectrometry(MALDI-TOF-MS). Results Compared with untreated samples, 10 altered proteins were found through 2-DE and all of them were down-regulated of which 2 were identified by MALDI-TOF-MS to be plasma retinol-binding protein precursor and complement component 4, gene 2 (C4b). Conclusion C4b may be the biomarker of AD and it may be helpful to understand the pathogenesis of AD.
ABSTRACT
A 66-year-old male was admitted for increasing azotemia. He was diagnosed with chronic antibody- mediated rejection and had received a livingdonor renal transplant from his 32-year-old son prior to his admission. The peritubular capillaries of his kidney were diffusely positive on C4d immunostaining. It is known that there is an agreement between C4d staining and serological and histopathological data during rejection that is thought to have a humoral component. The role of alloantibodies in chronic renal allograft deterioration and the corresponding morphologic changes have been increasingly recognized during the recent years. However the treatment guidelines for chronic antibody-mediated rejection have not yet been established. Intravenous immunoglobulin (IVIG) has been shown to decrease the titers of anti-HLA antibodies in highly sensitized patients awaiting transplant. There are also numerous proposed mechanisms regarding how IVIG exerts its immunomodulatory action. As we have experienced chronic antibody-mediated rejection and how IVIG treatment improves renal function, we recognize that IVIG has the potential to be used for treating certain subgroups of chronic allograft nephropathy patients with positive C4d staining and anti-HLA antibodies.