Animals ; Epilepsy ; immunology ; metabolism ; Hippocampus ; metabolism ; Male ; Rats ; Rats, Sprague-Dawley ; gamma-Aminobutyric Acid ; immunology ; metabolism

Objective To investigate the molecular mechanism of calreticulin ( CRT) transcription induced by HBV and its viral proteins. Methods The human hepatocellular cell line, HepG2, was trans-fected with pHBV1. 3 and eukaryotic expression plasmids of HBV viral proteins, respectively. The expres-sion of CRT was measured after transfection. A reporter plasmid of CRT promoter was constructed to analyze the induction of CRT promoter by pHBV1. 3 and HBV viral proteins. Furthermore, two truncated and one C/EBPα site deficient mutants were constructed to evaluate the regulatory effects of HBx on CRT promoter. Fi-nally, HepG2 cells were transfected with HBx expression plasmids and the cellular localization of C/EBPαwas analyzed. Results In this study, pHBV1. 3 could significantly up-regulate the expression of CRT at mRNA and protein levels as well as enhancing the activity of CRT promoter. Among the seven HBV viral proteins, HBx could enhance the activity of CRT promoter and the expression of CRT at mRNA and protein levels. HBx could not induce the transcription of CRT when the C/EBPα binding site was deleted from the CRT promoter. The expression of HBx could promote the nuclear translocation of C/EBPα. Conclusion HBV and its viral protein HBx could up-regulate the CRT expression at transcriptional level. The transcrip-tional factor C/EBPα played a critical role in HBx-induced transcriptional activation of CRT.

Objectives To explore the clinical features and diagnosis of LMNA-associated congenital muscular dystrophy. Methods The clinical data from a case of muscular dystrophy caused by LMNA gene mutation were retrospectively analyzed. The related literatures were reviewed. Results A 8-month-old female infant suffered from weakness of raising head, eyelid droop, and motor development retardtion. LMNA gene was sequenced for the infant, her parents and the older sister. Heterozygous mutation of c. 94_96 del AAG (p. K 32 del) was found in the infant leading to the diagnosis of LMNA- associated congenital muscular dystrophy. No mutation was found in the infant’s parents and her older sister. The literature review showed that all ofLMNA- associated congenital muscular dystrophy patients had LMNA gene mutation, more than 80% patients mainly presented with weakness of raising head and may accompany with weakness of proximal limb, motor development retardation, and weakness of axial muscle. Conclusions Mutation analysis of LMNA gene is conducive to the diagnosis of congenital muscular dystrophy.

To identify the species of Mycobacterium clinical isolates by molecular biology techniques,six clinical isolates which were preliminarily recognized as Mycobacterium tuberculosis by the TCH and PNB culture methods were selected in this study.PCR was applied to amplify the oxyR-ahpC interval resistant-zone(intergenic region) and the length of PCR product in four strains was the same as that of H37Rv,while the length in the other two strains was different from that of H37Rv but same as Mycobacterium intracellulare 95002.With sequencing and on-line homology comparison with H37Rv,U18263 and U71061,the DNA sequence of oxyR-ahpC intergenic region displayed a 99% homology with Mycobacterium intracellulare U71061 and an 84% homology with Mycobacterium tuberculosis H37Rv.In addition,the results of hsp65 PCR-restriction fragment length polymorphism analysis and multi-locus PCR amplification in the two strains were identical with those of Mycobacterium intracellulare 95002.These two clinical isolates which were preliminarily recognized as Mycobacterium tuberculosis by PNB and TCH culture methods were finally identified as Mycobacterium intracellulare.Results predicted that the application associated with various techniques of molecular biology would provide a faster,easier and more correct way for the species identification of Mycobacterium.

Objective To understand the achievements of clonorchiasis sinensis control in Shandong Province during the past forty years. Methods The data of the previous annual clonorchiasis sinensis investigation in Shandong Province were collected and analyzed. Results From 1960s to 1970s, there were 107 counties existing the prevalence of clonorchiasis sinensis in Shandong Province. The infection rate of population was 1.51%, and 85.70% of the infected people were children below fifteen years old. Through the forty years' control, the decreasing of intermediate hosts such as various kinds of fishes and water-snails due to 85. 00% of ditches and ponds dried up by the lasting drying weather after 1980s, and 90. 00% of rivers polluted by increasing liquid waste, as well as the decreasing of infective chances due to 97. 90% of people breaking off the habit of eating not-well-cooked fishes by popularizing health knowledge, to 2003, the population infection rate dropped to 0.04%, 95.60% of the village where residents had the infection dropped to below 1. 00% , and 60. 00% of counties where no Clonorchis sinensis infection was found. Conclusion The clonorchiasis sinensis transmission areas reduce gradually, the infection rate of population decreases to the lowest in the history and the transmission has been controlled in Shandong Province.

Objective To explore the effect of intravenous immunoglobulin (IVIG) on immunity and outcome for sepsis in children.Methods Eighty-four children who met the diagnosis of sepsis were included in study and divided into treatment group (36 cases) and control group (48 cases ).The patients in teatment group were administered IVIG with the dose of 1 g/kg.Peripheral venous blood samples of patients in both groups were collected before (0 h),24 h,72 h and 5 d after administration to detect the numbers of immunocyte including CD3 +,CD4 +,CD56 +,CD19 +,CD8 +cells by flow cytometry and the levels of cytokines including tumor necrosis factor (TNF)-at,interleukin (IL)-10,IL-1 7 by enzyme linked immunosorbent assay.The numbers of immunocyte and levels of cytokines and TNF-a/IL-10 were compared and the mortality at 28 days was assessed between two groups.Results The numbers of CD3 +,CD4 +,CD56 +,CD19 +cells and the levels of TNF-a,IL-17 and TNF-α/IL-10 of patients in teatment group were significantly decreased than those in control group at 24 h,72 h and 5 d afte administration ( P ＜0.05 ) and showed downtrend.However,the level of IL-10 increased significantly (P ＜ 0.05 ) and showed uptrend in treatment group.The number of CD8+ cells had no change.No difference of mortality was observed between two groups (27.7％,10/36 vs 16.6％,8/48,x2 =1.50,P =0.169,OR =1.92,95％ CI:0.671 ～5.510).Conclusion IVIG can suppress the immunity of children with sepsis and has no survival benefit.

Fatigue is an exhaustion state caused by prolonged physical work and mental work, which can reduce working efficiency and even cause industrial accidents. Fatigue is a complex concept involving both physiological and psychological factors. Fatigue can cause a decline of concentration and work performance and induce chronic diseases. Prolonged fatigue may endanger life safety. In most of the scenarios, physical and mental workloads co-lead operator into fatigue state. Thus, it is very important to study the interaction influence and its neural mechanisms between physical and mental fatigues. This paper introduces recent progresses on the interaction effects and discusses some research challenges and future development directions. It is believed that mutual influence between physical fatigue and mental fatigue may occur in the central nervous system. Revealing the basal ganglia function and dopamine release may be important to explore the neural mechanisms between physical fatigue and mental fatigue. Future effort is to optimize fatigue models, to evaluate parameters and to explore the neural mechanisms so as to provide scientific basis and theoretical guidance for complex task designs and fatigue monitoring.
Attention ; Brain ; physiology ; Fatigue ; Humans ; Mental Fatigue ; Workload

Objective:To study the mechanisms of immune suppression mediated by Gr-1+CDllb+ myeloid derived suppressor cells (Gr-1~+CDllb~+MDSC)from tumor-bearing mice.Methods:Gr-1~+CDllb~+MDSC recruited into spleen and bone marrow of tumor-bearing mice were purified by Percoll,and suppression mediated by MDSC on T cell proliferation from spleen of naive mice was detected by flow cytometry with CSFE and FTTC-anti CD3 staining,and NO,ROS,IL-10 and TGF-β in the supematant of MDSC were detected by Griess and ELISA.Results:There were much more Gr-1~+CDllb~+MDSCs in spleen and bone marrow from tumor-bearing mouse than those of naive mouse,and suppression on T cell proliferation mediated by MDSC from tumor beating mouse was significantly increased,and there were much more NO,ROS,IL-10 and TGF-βin the supematant of these MDSC than that from naive mouse.Conclusion:MDSC from tumor-bearing mice secreted hish level of NO,ROS,IL-10 and TGF-βto induce immune suppression,and inhibite the proliferation of T cells.

Aged ; Diagnosis, Differential ; Fibronectins ; metabolism ; Glomerulonephritis, Membranoproliferative ; pathology ; Humans ; Immunohistochemistry ; Kidney Diseases ; metabolism ; pathology ; Kidney Glomerulus ; metabolism ; pathology ; ultrastructure ; Male ; Microscopy, Electron

AIM AND METHODSThe relation between AT sclerosis (loss of neurons and proliferation of astrocytes) and long-lasting epileptic susceptibility was investigated by thionine staining, GFAP immunohistochemistry and observing the behavior of rats, after scorpion venom (SV) or normal saline (NS) administrated for three week.

RESULTSCompared with NS+ NS group, both the loss of neurons and proliferation of astrocytes were very marked in KA+ NS group (epileptic susceptible rats) (P < 0.05), but those changes were not visible in KA+ NS group (epileptic nonsusceptible rats).

CONCLUSIONSIt suggested that AT sclerosis may be one of important reasons of the long-lasting epileptic susceptibility.

Animals ; Astrocytes ; pathology ; Epilepsy ; pathology ; Glial Fibrillary Acidic Protein ; metabolism ; Male ; Neurons ; metabolism ; pathology ; Rats ; Rats, Sprague-Dawley