The international road of Chinese medicine can be comparable to the Long March of the Red Army. The article reviews the history, global impact and achievements of the World Congress of Chinese Medicine (WCCM) on its way to the TCM's globalization in the past decade. It also discusses the great significance of WCCM's effort. The article concludes by bringing up a scheme for further developing the WCCM and envisioning its promising future.

Objective To review the effect of endothelial cells in the tumoral invasion miroecosystem(TIMES) and the progress of recent research in this field. Methods The relative references of TIMES, including investigative background, main components, differences compared with the tumor microenvironment, and effect of endothelial cell are studied systematically. Results The TIMES is considered as a naturally integreted functional unit which is composed of cell communities and host environment during the process of tumoral cells invading, it is an ecosystem at both cellular and molecular level. Being different from TIMES, the term of tumoral microenvironment means the environment conditions for the existence of tumor cells, it is a kind of constructive system, not including tumor cell itself, and not possessing the regulation of ecosystem. The main elements of TIMES include tumor cell communities, host cell communities, and their enviroment(extracellular matrix), among them the endothelial cell communities are the most important host communities. The main effect of endothelial cells on the TIMES is the trophic links between tumor cell communities and endothelial communities, which froms a material cycle, including nutritional and matrix cycyles. The tumoral invasion and metastasis result from the continuous rebuilding of trophic links between tumor cell communities and endthelial cell communities.Conclusions The endothelial cell regulates TIMES by its trophic links with tumor cell communities. To block the links between tumor cell communities and endothelial cell communities might be the one of the key factors in tumoral treatment.

Objective To investigate the effect of Alzheimer' s beta-amyloid (Aβ) on the production and the translocation in cytoplasm of retinoid receptor-α (RXRα). MethodsN2awt cells were treated with Aβ peptide or amyloid protein precursor(APP695) transfection. The nucleus were separated from the cytoplasm by kit. The quantity of RXRα in the nucleus and cytoplasm was detected by Westernblot. The translocation of RXRα in the nucleus and cytoplasm of above N2awt cells or of the cortex cells in the brains of Alzheimer' s disease (AD) patients and their normal control groups was observed by immune fluorescence. ResultsIn N2awt cells, the increasing APP or Aβ had no significant effect on the production of RXRα but resulted in RXRα exporting into cytoplasm, the ratio of RXRα in cytoplasm increased from 3.2％ (in control group) to 17.6％ (in APP+ group) and from 3.8％ (in control group) to 14.3％ (in Aβ + group) respectively; compared with normal cortex cells, the translocation of RXRα in the cytoplasm of the cortex cells in the brains of AD increased significantly. ConclusionAβ may affect RXRα exporting into cytoplasm.

Objective To screen the liver cell proteins interacting with the novel protein encoded by the 2.2 kb singly spliced variant of hepatitis B virus genome. Methods The splicing-specific gene TPss generated by the 2.2 kb singly spliced variant of HBV genome was amplified by PCR and cloned into the bait vector pGBKT7. After exclusion of self-activatian capacities of TPss protein, a two-hybrid library screening was performed using a pre-transformed human liver cDNA library to screen the liver cell proteins interacting with TPss. Mammalian two-hybrid assay was also done to further confirm the interactions between the bait and prey proteins in Huh7 and HepG2 hepatacytes. Results TPss gene with the size of 336 bp was successfully amplified and cloned, and the TPss protein expressed well in AHI09 yeast cells. Four liver cell proteins interacting with TPss, i. e. , cathepsin B, epoxide hydrolase 1, cathepsin D and fibrinogen gamma chain, were screened by yeast two-hybrid assay and further confirmed by mammalian two-hybrid assay. Conclusion TPss could interact with liver cell proteins.

Objective To obtain protein of the major surface antigen P30 of Toxoplasma gondii by molecularcloning. Methods The gene of P30 (containing the whole P30 gene sequence, without the gene encoding signalpeptide) was obtained by polymerase chain reaction (PCR) using the primer designed according to the DNA sequence ofP30. The recombinant plasmid was constructed using EcoR Ⅰ, Xho Ⅰ and was then transformed into E. coli Top10. Thepositive clones were identified by restriction enzymes and DNA sequence analysis. The fusion protein was induced by IPTGand purified by affinity chromatography using ProBond~(TM) Resin (a kind of nickel-charged sepharose resin) and was identi-fied by SDS-PAGE and Western blotting. Results The products of PCR, cleavage and link reaction were same as ex-pected and the sequence of inserted fragment in the recombinant plasmid was same as reported except one synonymy muta-tion. A 58 kDa fusion protein was induced by IPTG and was purified by chromatography. Conclusion Fusion proteincontaining Toxoplasma gondii P30 was achieved and was provided as experiment material for further research.

Objective To investigate the signaling role of arachidonic acid in the invasion of RAW264.7 macrophage by Toxoplasma gondii . Methods Rate of infection was calculated by both light microscope and flow cytometer. Fluorescent emission spectra were recorded using a microspectrofluometer for the concentration of cytoplasmic free calcium. Results Calcium concentration in macrophages and rate of infection increased with a higher concentration of exogenous arachidonic acid in a dose-dependent manner. The invasion was dependent on the mobilization of calcium from the extracellular medium and from intracellular stores and followed the influx of calcium into the parasitized cell. Conclusion Arachidonic acid may enhance the rate of infection via calcium transduction pathway.

Objective To compared different fixation methods for acetabular fractures involving the quadrilateral plate using a finite element model of the acetabulum.Methods A model of acetabular fractures with quadrilateral plate involved was developed in the finite element software and processed in Hypermesh V10.0 to generate internal fixation with dual-column titanium plate (Group A),anterior special titanium moulding plate plus quadrilateral screws (Group B),and anterior special titanium moulding plate plus quadrilateral screws combined with posterior column screws (Group C).Pelvic stress in sitting and standing positions were simulated in sequence with constraint of tuber nodes and inferior femur.Maximum stress and displacement of the acetabulum and displacement of nodes on fracture lines were measured after a force of 600 N was applied to S1 verterbrae in line with the direction of gravity in sitting and standing positions.Results In sitting position,the maximum stress and displacement of the acetabulum exhibited a sequence of Group C (9.47,1.08) ＜ Group B (19.84,1.11) ＜ Group A (29.73,1.14).Moreover,the same result was found in standing position with Group C (9.62,1.09) ＜ Group B (12.18,1.10) ＜ Group A (13.28,1.13).Mean displacement of nodes on fracture lines ranked in order of Group C ＜ Group B ＜ Group A (P ＞ 0.05).Conclusions The finite element model can reflect the distribution of pelvic stress effectively.Anterior special titanium moulding plate plus quadrilateral screws combined with posterior column screws provide favorable biomechanical stability in treatment of acetabular fractures involving the quadrilateral area.

Objective To investigate the anti-IFN-α effects of the novel protein TSR'r' encodedby the 458 nt-1308 nt spliced variant of hepatitis B virus genome,and to determine its functional domaias.Methods the TSR'r' gene(originated from open reading frame of HBV DNA polymerase,T represents terminal protein region,S represents the Spacer region,R'represents the truncated reverse transcriptase region,and r'represents the truncated RNaseH region)of the 458 nt-1308 nt spliced variant of HBV genome and its deletants were amplified by PCR and were cloned into the pcDNA3.1/HisC vector.The recombinant vector was transfected into Huh7 hepatocytes individually by FuGENE6 transfection reagent,and the expression of the fusion protein was detected by Western blot.Huh7 hepatocytes were co-transfected with p6 16CAT and the recombinant vector harboring either TSR'r'or the related deletant,and treated with IFN-α 2a 48 h post transfection.After 24 h stimulating.the cells were lysed and the intracellular CAT value was calculated.All data were processed with One-way analysis of variance(ANOVA).Resuits Recombinant vectors harboring either the TSR'r'gene or related deletant were constructed successfully,and the fusion proteins were expressed well in Huh7 cells.When Huh7 hepatocytes were co-transfected with p6-16CAT and TSR'r' recombinant.the intracellular CAT values reduced gradually as paralleled with the increasing amount of TSR'r'recombinant.Furthermore,as compared with the empty vector,intracellular CAT values also decreased significantly when the Huh7 cells co-transfected with recombinant harboring TP plus Spacer regions,while any of the other deletants(harboring either TP or Spacer region or neither)showed no significant difference.Conclusion The novel protein encoded by the 458 nt-1308 nt spliced variant of hepatitis B virns genome suppressed the response of Huh7 hepatocytes to IFN-α.and the N-terminal TP plus Spacer region was the functional domain of the protein for anti-IFN-α effects.

OBJECTIVE To investigate the correlated resistant genes encoding ?-lactamases,aminoglycoside and genetic marker of integron and transposon in multi-resistant Pseudomonas aeruginosa(MRPA) isolated from clinical specimens and study their relationship by phylogenetic analysis.METHODS Twenty-one resistant genes,two integron-Ⅰ genes and one transposon genetic gene were analyzed by PCR and verified by DNA sequencing.Multi-resistant genes cluster analysis was performed by UPGMA.RESULTS The positive rates of CARB,oprD2,aac(3)-Ⅱ,aac(6′)-Ⅱ,ant(2″)-Ⅰ,intⅠ1,qacE△1-sul1 and merA in 20 strains of MRPA were 15%,100%,70%,15%,15%,85%,85% and 85%,respectively,and other genes were negative.It was classfied to three subgroup,by the multi-resistant genes cluster analysis.CONCLUSIONS MRPA isolated from clinical specimens has carried many resistant genes.The deficiency rate of oprD2 gene is very high.The positive rate of genetic mark genes about integron and transposon is very high.It may be the main multi-resistant mechanism of MRPA.Multi-resistant genes cluster analysis shows that there is clone transmission in MRPA and it can induce nosocomial infection prevalence.

Objective: To assess the diagnosis of thrombelastography (TEG) for trauma-induced coagulopathy (TIC) and explore whether TEG could guide transfusion for TIC patients. Methods: We retrospectively analyzed all trauma patients who underwent the TEG and conventional coagulation tests (CCTs) admission in the emergency intensive care unit from February to December 2018. The definition of TIC is prothrombin time (PT) 18 s, international normalized ratio (INR) 1.5, activated partial thromboplastin time (APTT) 60 s or platelet count (PLT) 100×10⁹/L. The diagnostic value of TEG for TIC was evaluated by receiver operating characteristic curve, area under the curve (AUC), sensitivity, specificity, positive predictive value (PPV) and negative predictive value (NPV), and the transfusion guidance of TEG for TIC patients was assessed by multivariate regression analyses. Results: A total of 242 patients were included, including 62 patients in the TIC group and 180 patients in the non-TIC group. The differences in TEG between the two groups were statistically significant. The AUCs of TIC assessed by maximum amplitude (MA) and coagulation index (CI) were the largest, 0.779 and 0.786 respectively, and the sensitivity were greater than 80% and NPV were greater than 90%. The sensitivity, PPV and NPV of reaction time (R) were minimal. After confounders were controlled, all TEG values were correlated with blood volumes within the first 24 h and massive transfusion, of which R had the highest odds ratio and regression coefficient. Conclusions MA and CI have the highest diagnostic value, while R has little diagnostic value but a relatively large blood therapeutic significance of TIC. MA < 52.9 mm or CI < -1.0 can be used as a threshold for identifying TIC. The diagnosis of TIC and the guidance transfusion for TIC patients by TEG is beneficial.