Disc displacement with reduction treated by modified Twin-block / 口腔疾病防治

Objective@# To investigate the morphology and position changes of displaced disk with reduction after treatment by modified Twin-block. @*Methods @#19 patients were diagnosed as displaced disk with reduction and they were treated with modified Twin-block from July 2015 to June 2016. 28 temporomandibular joints (TMJ) of these patients were included in the analysis. The disk length, disk-condylar distance, and disk-condylar angle were measured with MRI before and after treatment. Paired t-test was used. Disk morphology before and after treatment was also documented and analyzed by Wilcoxon signed rank test. The statistical significance was set at P<0.01.@*Results @# 28 TMJ disks were anteriorly displaced with reduction. 24 of them were repositioned while the other 4 were still anteriorly positioned after treatment. The disk length was increased significantly (P<0.01) while the disk-condylar distance and disk-condylar angle were decreased significantly after treatment (P<0.01). The disk morphology as hemiconvex (16) and bi planar (9) were the majority before treatment, while biconcave (16) and biplanar (10) were changed to the larger part after treatment. There was improvement on the disk deformation with a statistical significance (P<0.01). Larger disk-condylar distance, disk-condylar angle and severer deformation of disks were observed in the 4 disks without reposition.@*Conclusion @# Modified twin-block is an effective appliance for disk displacement with reduction by repositioning the disk and modifying the disk deformation. However the effect is not good for disks with severer deformation and displacement. Further studies with larger sample and stratified group are still needed.

Heat shock protein 90-mediated inhibition of hepatitis B virus replication in hepatic cells / 中华肝脏病杂志

<p><b>OBJECTIVE</b>To evaluate the effect of heat shock protein 90 (HSP90) on hepatitis B virus (HBV) replication in hepatocytes and to investigate the related molecular mechanism.</p><p><b>METHODS</b>A eukaryotic plasmid expressing human HSP90 was constructed (designated as HA-HSP90). HepG2 cells were co-transfected with HA-HSP90 and the HBV replicative plasmid HBV1.3. Expression of the exogenous HSP90 was assessed by Western blotting. Expression of the HBV surface antigen (HBsAg) was determined by enzyme-linked immunosorbent assay, and HBV replicative intermediates were detected by Southern blotting. Small interfering (si)RNAs were designed against HSP90 and TBK1 and transfected into the HepG2 cells to further assess the effects of HSP90 and its underlying mechanism. HSP90-mediated effects on the expression of interleukins IL-1b and IL-6 and the interferon response gene IFIT1 were assessed by quantitating mRNA levels with real time RT-PCR.</p><p><b>RESULTS</b>The HA-HSP90 plasmid successfully expressed exogenous HSP90 protein in HepG2 cells. The exogenous HSP90 was able to inhibit HBV replication and HBsAg expression. IFIT1 expression was up-regulated after HA-HSP90 transfection, but neither IL-1b nor IL-6 were affected. The siRNA-mediated TBK1 down-regulation had no effect on the HSP90-inhibited HBV replication.</p><p><b>CONCLUSION</b>HSP90 can inhibit HBV replication and TBK1 is not involved in this process.</p>

Bioinformatics analysis on ORF1 protein of Torque teno virus (SANBAN isolate)

OBJECTIVE@#To analyze the sequence of ORF1 protein of Torque teno virus to prepare for the future hybrid experiments.@*METHODS@#The sequence of ORF1 protein of Torque teno virus was analyzed by bioinformatics using some web tools.@*RESULTS@#The most likely cleavage site was between position 14aa and 15aa and signal peptide may be position 1aa-14aa. Two possible transmembrane helices from inside to outside and three possible transmembrane helices from outside to inside were found. The position 509 (NKTN) was the potential N-glycosylation site. The speculative molecular weight of TTV ORF1 protein, which may be a kind of unstable protein was 88 705.7 Da. 1aa-91aa and 278aa-361aa were localized in non-regular secondary structure region.@*CONCLUSIONS@#TTV ORF1 protein may be a nuclear protein which contains two non-regular secondary structure region. 265aa to 486aa and 510aa to 679aa may be the two approciate fragments to construct the plasmids, which would be prepared for the future hybrid experiments to study the functional positions of the protein and the interactions between TTV and its hosts. Bioinformatics analysis would possibly make it easier to study the protein's function.

Toll-like receptor dependent innate immune responses by primary mouse hepatocytes and its control of HBV replication / 中华肝脏病杂志

<p><b>OBJECTIVE</b>This report aims to investigate the Toll-like receptor (TLR) signaling pathways and induced antiviral activity in hepatocytes.</p><p><b>METHODS</b>We isolated primary hepatocytes from wild-type C57BL/6 mice and examined the expression of TLR by realtime RT-PCR. Hepatocytes were stimulated with TLR 1-9 agonists and the supernatants were harvested. The secretion of cytokines were tested by ELISA. The antiviral effectors in supernatants were assayed via virus protection assay (in EMCV system) and the control of HBV replication were assessed via Southern blotting (in HBV system).</p><p><b>RESULTS</b>We demonstrated that hepatocytes expressed TLR1-9. In accordance with these TLR expression profiles, hepatocytes responded to all TLR ligands by producing inflammatory cytokines (TNF-α or IL-6), to TLR -1,-3,-7 and -9 ligands by producing type I IFN (IFN-α or IFN-β). Only TLR 3 and TLR 7 agonists could stimulate the production of high amounts of antiviral mediators by hepatocytes in virus protection assay. By contrast, supernatants from TLR1, -3 and -4 directly stimulated hepatocytes and TLR 3, -7 and -9 transfected hepatocytes were able to potently suppress HBV replication.</p><p><b>CONCLUSION</b>Primary hepatocytes display a unique TLR signaling pathway and can control HBV replication after stimulation by TLR agonists in mice. It may be helpful for the development of TLR-based therapeutic approaches against hepatotropic virus.</p>

Antigenicity of major hydrophilic region II of hepatitis B virus surface antigen / 中华肝脏病杂志

<p><b>OBJECTIVE</b>To study whether the substitutions at the major hydrophilic region II (MHRII) of hepatitis B surface antigen (HBsAg) will impair the antigenicity of HBsAg.</p><p><b>METHODS</b>Four recombinant plasmids expressing mutant HBsAg (mtHBsAg) P1120T, C121S, K122I and T123N were constructed. HepG2 cells were transfected with the four plasmids and a plasmid expressing G145R HBsAg. The immunoreactivity of the cells expressing mtHBsAg with P1120T, C121S, K122I, T123N and G145R were detected by immunofluorescence (IF) staining and ELISA with 4 antibodies and 7 HBsAg diagnostic kits respectively.</p><p><b>RESULTS</b>mtHBsAg with P120T was recognized by mAb1 and mAb2. mtHBsAg with C121S and K122I was not recognized by any mAbs. mtHBsAg with T123N in lysates was recognized by mAb2, but not recognized in the supernatants.</p><p><b>CONCLUSION</b>Substitutions at amino acid positions 120-123 of HBsAg strongly impaired the antigenicity of HBsAg, a fact that was not appreciated previously.</p>