ABSTRACT
Hepatic encephalopathy (HE) is a serious neuropsychological complication in advanced liver disease, and is a major cause of death in patients with liver disease. The paper briefly introduces the advances in application of HE grading, examination methods, and electroencephalography (EEG) in the diagnosis of HE, and points out that EEG has been developed greatly in the field of HE, with huge potentials for the diagnosis, evaluation, prognosis, and guidance for treatment of HE. However, the clinical value of EEG monitoring in HE has not been widely acknowledged in the medical world, and further investigation is still needed in the future.
ABSTRACT
Hepatitis B virus-associated glomerulonephritis (HBV-GN) is the most common extrahepatic injury induced by chronic hepatitis B virus (HBV) infection, which has been taken seriously by scholars in recent years. This article summarizes the research advances in related risk factors for HBV-GN, pathogenesis, and treatment. Since the diagnostic rate of HBV-GN is low and the sample size is small at present, there is still much space for research in this field. More clinical trials with good quality are needed in the future to investigate the therapeutic regimens for this disease.
ABSTRACT
Drug-induced liver injury (DILI) is a major reason for the recall of marketed drugs and the failure of clinical trials. Detection of potential liver injury remains a challenge for clinical management and preclinical drug safety studies. Currently, serum levels of alanine aminotransferase and aspartate aminotransferase are the gold standards for evaluating liver injury. However, these biomarkers are nonspecific and insensitive, and often result in false-positive results. Therefore, researchers have never stopped searching for the biomarkers of DILI with high sensitivity and specificity. This review summarizes recent research progress in the biomarkers of DILI to better predict and diagnose DILI.
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Objective To investigate the effects of Plasmodium vivax merozoite surface protein 1(PvMSP1)on differentia-tion,maturation and function of dendritic cells(DC)and the mechanisms of PvMSP1 on the activation of DC via toll like receptors (TLR). Methods DCs were incubated with different doses of PvMSP1(1.0,10.0,100.0μg/ml)in vitro. The changes of CD83, CD86,and HLA-DR on DC were detected by flow cytometry(FCM);the expressions of cytokine IL-10 and IL-12 of DC were mea-sured by ELISA;the expressions of TLR4 and TLR9 mRNA of DC were measured by RT-PCR;the proliferation induction to autol-ogous lymphocytes of DC was measured by MTT. Meanwhile,the untreated DC and LPS inducing DC were as the negative control and positive control,respectively. All the data were analyzed statistically. Results Compared with the untreated DC,the propor-tions of CD83,CD86 and HLA-DR on DC induced by LPS and PvMSP1 increased significantly(all P0.05). In the PvMSP1-treated group,the DC TLR4 mRNA production increased(P0.05);DC stimulated the proliferation of autologous lympho-cytes. Conclusion PvMSP1 enhances DC differentiation and maturation,and the mature DC induced by PvMSP1 has the ability of antigen presenting. The route for PvMSP1 inducing DC maturation might be TLR4 pathway rather than TLR9 pathway.
ABSTRACT
<p><b>OBJECTIVE</b>To investigate α-toxin-induced apoptosis of umbilical vein endothelial cells and explore its role in vertical infection of Staphylococcus aureus L-form.</p><p><b>METHODS</b>HUV-EC-C cells exposed to different concentrations (0, 10, 30, 90, and 270 ng/ml) of α-toxin for different time lengths (0, 2, 4, 6, and 8 h) were examined for apoptosis using flow cytometry with Annexin V-PI staining. The levels of tumor necrosis factor-α (TNF-α) and the activities of, caspase-3 and caspase-8 in the cell culture were detected by ELISA and colorimetric method, respectively. α-Toxin-induced cell apoptosis was also analyzed in HUV-EC-C cells treated with a neutralizing antibody of TNF-α or with the inhibitory peptides of caspase-3 (zDEVD-FMK) and caspase-8 (zIETD-fmk).</p><p><b>RESULTS</b>α-Toxin induced apoptosis of HUV-EC-C cells in a dose- and time-dependent manner and caused significantly enhanced expression of TNF-α and the activation of both caspase-3 and caspase-8. Inhibition of TNF-α with its neutralizing antibody and the inhibitory peptides of caspase-3 or -8 all significantly decreased α-toxin-induced cell apoptosis, and the caspase-3 inhibitor completely blocked α-toxin-induced cell apoptosis.</p><p><b>CONCLUSION</b>α-Toxin-induced apoptosis is partially mediated by the extrinsic cell death pathway of TNF-α and caspase-8 and plays an important role in the vertical infection of S. aureus L-form to affect fetal growth and development.</p>