Objective:To investigate the effects of hemodialysis f on immune function of patients with end-stage nephropathy associated HBV virus infection.Methods:50 cases of patients with end-stage nephropathy associated HBV virus infection from June 2011 to June 2013 were randomly selected as observation group.50 cases of patients with end-stage renal disease as the control group.Patients in control group and observation group were treated with continuous hemodialysis therapy .24 h urinary protein ,serum al-bumin,blood urea nitrogen and creatinine in control group and observation group before and after treatment were analyzed .The regulatory T lymphocyte ,the CD8+T lymphocytes,perforin and granzyme B in peripheral blood in control group and observation group before and after treatment were analyzed by flow cytometry.Results:After dialysis treatment ,clinical symptoms and laboratory indexes of the two groups were significantly improved ( P<0.05 ).Clinical symptoms and laboratory indexes in control group and observation group after treatment had no statistical difference ( P>0.05 ).There was no significant change of immune function in the control group before and after treatment ( P>0.05 ).But the ratio of Treg cells and CD 8+T lymphocyte in observation group after treatment were sig-nificantly increased than that of before treatment ( P<0.05 ).Before treatment ,the active molecule perforin and granzyme B expression rate of T cells in the peripheral blood of observation group were higher than the control group ( P<0.05 ).After treatment ,Treg cell and CD8+T lymphocyte ratio were significantly decreased as well as perforin and granzyme B expression rate ( P<0.05 ).Conclusion:Compared with control group ,hemodialysis can significantly improve the immune function of the patients with end -stage nephropathy as-sociated HBV virus infection.

Anaplasma phagocytophilum ( A. phagocytophilum) is tick-borne obligate pathogen that parasitizes rodents, ruminants, deer, horses and human. Ticks can transmit A. phagocytophilum to human resulting in a disease called anaplasmosis. With the increase in outdoor activities, the chances of exposing to ticks increase in human and the probability of suffering from anaplasmosis increases correspondingly. Most patients can recover from anaplasmosis after doxycycline therapy, but immunocompromised patients are at risk of seizure, renal failure and even death. A comprehensive understanding of A. phagocytophilum pathogenic mechanisms can provide new therapeutic strategies for the treatment of critically ill patients. Therefore, this review first gave examples of pathogenesis-related proteins of A. phagocytophilum, and then summarized the current research status of the pathogenic mechanism of this pathogen from three aspects of interference with cytoskeletal remodeling, inhibition of host cell apoptosis and dysfunction of the innate immune response, and proposed main issues to be addressed.

Hepatocellular carcinoma (HCC) is highly heterogeneous in nature and has been one of the most common cancer types worldwide. To ensure repeatability of identified gene expression patterns and comprehensively annotate the transcriptomes of HCC, we carefully curated 15 public HCC expression datasets that cover around 4000 clinical samples and developed the database HCCDB to serve as a one-stop online resource for exploring HCC gene expression with user-friendly interfaces. The global differential gene expression landscape of HCC was established by analyzing the consistently differentially expressed genes across multiple datasets. Moreover, a 4D metric was proposed to fully characterize the expression pattern of each gene by integrating data from The Cancer Genome Atlas (TCGA) and Genotype-Tissue Expression (GTEx). To facilitate a comprehensive understanding of gene expression patterns in HCC, HCCDB also provides links to third-party databases on drug, proteomics, and literatures, and graphically displays the results from computational analyses, including differential expression analysis, tissue-specific and tumor-specific expression analysis, survival analysis, and co-expression analysis. HCCDB is freely accessible at http://lifeome.net/database/hccdb.
Carcinoma, Hepatocellular ; genetics ; Databases, Genetic ; Gene Expression Profiling ; Gene Expression Regulation, Neoplastic ; Humans ; Liver Neoplasms ; genetics

Amyotrophic lateral sclerosis (ALS) is a progressive neurodegenerative disease affecting both upper and lower motor neurons (MNs) with large unmet medical needs. Multiple pathological mechanisms are considered to contribute to the progression of ALS, including neuronal oxidative stress and mitochondrial dysfunction. Honokiol (HNK) has been reported to exert therapeutic effects in several neurologic disease models including ischemia stroke, Alzheimer's disease and Parkinson's disease. Here we found that honokiol also exhibited protective effects in ALS disease models both in vitro and in vivo. Honokiol improved the viability of NSC-34 motor neuron-like cells that expressed the mutant G93A SOD1 proteins (SOD1-G93A cells for short). Mechanistical studies revealed that honokiol alleviated cellular oxidative stress by enhancing glutathione (GSH) synthesis and activating the nuclear factor erythroid 2-related factor 2 (NRF2)-antioxidant response element (ARE) pathway. Also, honokiol improved both mitochondrial function and morphology via fine-tuning mitochondrial dynamics in SOD1-G93A cells. Importantly, honokiol extended the lifespan of the SOD1-G93A transgenic mice and improved the motor function. The improvement of antioxidant capacity and mitochondrial function was further confirmed in the spinal cord and gastrocnemius muscle in mice. Overall, honokiol showed promising preclinical potential as a multiple target drug for ALS treatment.