ISO 300 mg/kg ip markedly inhibited the corton oil induced ear inflammation in mice. Same dose ip showed significant inhibition on the hind-paw edema in rats induced by carragreenin. All these actions of ISO were similar to sod .salicy late.ISO 300 mg/kg im markedly inhibited the immunolpgical function in mice, but the potency was lower than prednisolone.

Objective: To analyze the effect of different treating factors on cure depths of light curing composite resin, and discuss the relationship between different treating factors and cure depths. Methods:192 samples were designed with factorial experiment. The whole samples were scanned by Planmeca ProMax panoramic X-ray unit and cure depths were measured. The data was statistically analyzed by SPSS 11.5 software package for t test and stepwise regression analysis. Results:There were significant differences among different light curing units, irradiation distances and cure time(P

It is very necessary to apply case-teaching method to Emergency Medicine in Universities of TCM. To establish the case-teaching system,we ourselves have written teaching materials,trained teachers, and designed all sorts of the medical records. Moreover, we have deployed other methods and principles to put this teaching into practice, used clinical skill practising as a essential supplement of teaching effect. Comparing with the traditional teaching method, it is clear that case-teaching method could make students' learning initiative and positivity improved significantly, their test scores promoted obviously. Thus, carrying out case-teaching method in Emergency Medicine could advance students capability of acquisition of knowledge and their clinical thinking .

BACKGROUND:The linkage and synergistic effect of adaptor proteins can effectively regulate signal transduction of T cel s, which can form a limit or amplification cascade to realize the complex immune function of T cel s. C-terminal Src kinase (Csk)-binding protein (Cbp) is an adaptor protein, which mainly exert the negative feedback regulation of Src kinase activity. This negative feedback effect depends on Y317 of Cbp, which may be involved in the SH2 domain of Csk. OBJECTIVE:To explore the effects of high expression of Cbp on ultrastructure and related biological function of Jurkat cel s. METHODS:The virus particles were constructed with expressing enhanced green fluorescent protein (EGFP) only and Cbp-EGFP fusion protein to transfect Jurkat cel s. There were untransfected group (Jurkat group), negative control group (transfected with expression of EGFP virus only), and Cbp group (transfected with Cbp-EGFP virus). RESULTS AND CONCLUSION:Confocal microscope showed that cel transfection efficiency was more than 95%and Cbp was located on the cel membrane. Optical microscope showed after transfection with Cbp-EGFP virus, more Jurkat cel s shrunk, with poor size uniformity. Apoptosis detection showed that after transfection with Cbp-EGFP virus, the number of apoptotic and necrotic cel s was greatly increased. Cbp mRNA expression was increased, Csk expression was decreased obviously and lymphocyte-specific protein tyrosine kinase expression was increased. So, in Jurkat cel s, the high expression of Cbp can decrease the uniformity of cel s and increase the necrosis cel s, thus inhibiting the signal transduction.

Objective:To construct a recombinant eukaryotic expressive vector of pEGFP-N3-M-IL-2(88 Arg,125 Ala),and to study the expression of this gene in the Glioma cell line U 87,and to detect its antitumor activities of the fusion protein M-IL-2(88 Arg,125 Ala).Methods:The target fusion gene M-IL-2 (88 Arg,125 Ala) was amplified by PCR from pPICZαA/M-IL-2 (88 Arg,125 Ala) and cloned into pEGFP-N3 vector after digestion to construct recombinant eukaryotic expressive vector pEGFP -N3-M-IL-2( 88 Arg,125 Ala).And then recombinant plasmid pEGFP-N3-M-IL-2(88Arg,125Ala) was transfected into Glioma cell U87 by LipofectamineTM2000 immediately after it was confirmed by restrictive enzyme analysis and sequencing .RT-PCR and Western blot were used to confirm expression of the fusion gene in the U87.Prohibitory effect of recombinant M-IL-2(88Arg,125Ala) protein on U87 was assessed by CCK-8 assay.Results:Restrictive analysis and sequence analysis revealed that M-IL-2(88Arg,125Ala) fusion gene was cloned into the vector pEGFP-N3 suc-cessfully,fusion gene M-IL-2(88Arg,125Ala) could express in U87 cells and could inhibit the growth of U87 cells.Conclusion:The eu-karyotic expression plasmid pEGFP-N3-M-IL-2( 88 Arg,125 Ala) was constructed and expressed in U 87 cells successfully ,the fusion protein could inhibit the growth of U87 cells.We laid a foundation for further research of gene M-IL-2(88 Arg,125 Ala).

Objective To test the in vitro susceptibility to macrolides of urogenital Chlamydia trachomatis (Ct) isolates, screen resistant Ct strains, and to explore resistance mechanism at the molecular level. Methods A total of 42 Ct strains were isolated from cervical or urethral swab samples and propagated in McCoy cells until the infection rate reached more than 90%. Then, susceptibility test was performed to evaluate the activity of three macrolides. Reverse transcription PCR and PCR were used to amplify two macrolide-resistance related genes, i.e., 23S rRNA gene and L4 gene, respectively in 2 erythromycin-resistant Ct strains and 4 erythromycin-sensitive strains followed by direct sequencing. Results The minimal inhibitory concentration (MIC) varied from 0.5 to 2 mg/L for erythromycin, 0.008 to 0.032 mg/L for clarithromycin, 0.125 to 0.5 mg/Lfor azithromycin. Erythromycin resistance was found in 2 isolates with the MIC value being 2 mg/L. Two mutations, C2452A and T2611A/C (Escherichia coli numbering) in the 23S rRNA gene, were detected in the resistant strains only, while the other 2 mutations, Pro113Leu and Pro156 Ala in L4 gene, were observed in all the tested strains. Conclusions Erythromycin-resistant Ct strains have emerged in clinical settings. The low-level erythromycin resistance may be associated with C2452A and T261 1C mutations in the 23S rRNA gene, whereas the point mutations in L4 gene is unlikely related to erythromycin resistance.

Based on the relevant literature, the review summarizes the etiology, pathogenesis and treatment of irritable bowel syndrome in TCM. TCM regaredsthe affected viscerals are large intestine, related to liver, spleen and kidney. The internal medicine, external treatment, and combined therapy are generally applied in clinics.

OBJECTIVETo discover and identify differentially expressed genes associated with colorectal adenoma formation and the role of RegIV in colorectal adenoma differentiation.

METHODSA subtracted cDNA library was constructed with cDNAs that were isolated from either the normal mucosa or adenoma tissue of a single patient. Suppressive subtractive hybridization (SSH) combined with virtual northern blotting was used to characterize differentially expressed genes and contigs were assembled by electronic cloning (in silico cloning) with the EST database. Semi-quantitative RT-PCR was performed in 9 colorectal adenomas.

RESULTSThe amino acid sequence was determined with open reading frame (ORF) prediction software and was found to be 100% homologous to the protein product of RegIV (a novel gene isolated from a large inflammatory bowel disease library). RegIV was found to be highly expressed in all of the adenoma samples (9/9) compared with the normal mucosa samples, while 5/6 cases showed RegIV to be more strongly expressed in adenocarcinoma.

CONCLUSIONRegIV may play an important role in the initiation of colorectal adenoma differentiation, and its detection may be useful in the early diagnosis of colorectal adenoma formation.

Adenoma ; genetics ; metabolism ; Blotting, Northern ; Colorectal Neoplasms ; genetics ; metabolism ; Humans ; Lectins, C-Type ; biosynthesis ; genetics ; Nucleic Acid Hybridization ; Pancreatitis-Associated Proteins ; Prognosis ; Reverse Transcriptase Polymerase Chain Reaction

Objective:To investigate the effects of ursolic acid (UA) on proliferation, migration and iron death of ectopic endometrial stromal cells (EESCs) and its mechanism.Methods:Mouse model of endometriosis was established and the primary EESCs were isolated. The cells were treated with UA at different concentrations (0, 2.5, 5, 10, 20, 40, 50, 80, 100, 200 μmol/L). The cells were divided into Control group (normal culture), 2.5 μmol/L UA group (2.5 μmol/L UA treatment), 5.0 μmol/L UA group (5.0 μmol/L UA treatment), 10.0 μmol/L UA group (10 μmol/L UA treatment), and UA+DUSP19 group (10 μmol/L UA+50 μmol/L JAK2/STAT3 signal pathway activator DUSP19 treatment). Cell survival rate was detected by CCK-8 method. Cell proliferation was detected by plate cloning method. Transwell chamber assay was used to detect cell migration. The levels of Fe 2+ and the contents of malondialdehyde (MDA), reactive oxygen species (ROS) and superoxide dismutase (SOD) were detected by kit. Protein expression levels of Ki67, PCNA, CyclinD1, p-JAK2, p-STAT3, JAK2 and STAT3 were detected by western blot. Results:The number of clones in Control, 2.5 μmol/L UA, 5.0 μmol/L UA and 10.0 μmol/L UA groups were as follows: 152.22±15.47, 121.22±11.54, 92.00±5.54, 66.44±6.88; Ki67 protein expression was 1.08±0.10, 0.73±0.07, 0.61±0.06, 0.45±0.02, respectively; The expression of PCNA protein was 0.85±0.07, 0.64±0.05, 0.41±0.03, 0.31±0.05, respectively; CyclinD1 protein expression levels were 0.98±0.11, 0.65±0.06, 0.51±0.05, 0.42±0.07, respectively. The migration numbers were 92.78±6.27, 62.22±2.20, 50.22±4.59 and 39.11±4.33, respectively; Fe 2+ levels were (1.06±0.07) μmol/g, (1.21±0.11) μmol/g, (1.33±0.08) μmol/g, (1.47±0.09) μmol/g, respectively; MDA content was (0.48±0.06) μmol/g, (0.65±0.07) μmol/g, (0.85±0.08) μmol/g, (1.03±0.11) μmol/g, respectively; ROS contents were (19.85±1.21) %, (24.83±2.79) %, (29.04±1.86) %, (33.87±2.45) %, respectively; SOD content were (36.41±3.56) U/mg, (31.03±2.81) U/mg, (25.63±2.84) U/mg, (19.62±1.67) U/mg, respectively; p-JAK2 protein expression was 0.85±0.10, 0.75±0.06, 0.53±0.05, 0.31±0.03, respectively; p-STAT3 protein expression was 1.08±0.11, 0.79±0.06, 0.63±0.07, 0.42±0.03, respectively. The p-JAK2 protein content in UA group and UA+DUSP19 group was 0.38±0.05 and 0.75±0.08, respectively; p-STAT3 protein expression was 0.46±0.04 and 0.80±0.03, respectively; The cell survival rates were (52.55±2.44) % and (82.18±4.72) %, respectively; Fe 2+ levels were (1.57±0.06) μmol/g and (1.21±0.13) μmol/g, respectively. The differences in the above indicators between the Control group and the 2.5 μmol/L UA group, 5.0 μmol/L UA group and 10.0 μmol/L UA group were statistically significant ( P<0.05). There were statistically significant differences among 2.5 μmol/L UA group, 5.0 μmol/L UA group and 10.0 μmol/L UA group ( P<0.05). There were statistically significant differences in p-JAK2, p-STAT3, cell survival rate and Fe 2+ levels between UA group and UA+DUSP19 group ( P<0.05) . Conclusion:Ursolic acid can inhibit the proliferation and migration of EESCs cells and induce iron death by regulating JAK2/STAT3 signaling pathway, thus playing a protective role in endometriosis.

Objective To observe the effect of miR-369-3p on vascular endothelial growth factor C (VEGFC) gene in bladder cancer cells EJ and 5637 and observe its effect on cell proliferation and apoptosis.Methods Bladder cancer cell lines EJ and 5637 were transfected with miR-NC (control group) or transfected with miR-369-3p (experimental group).The target gene of miR-369-3p was predicted by Targets can target gene prediction software.Fluorescence real-time quantitative polymerase chain reaction (qPCR) was used to detect the changes of VEGFC at mRNA level.The changes of VEGFC,p-Raf-1 and phosphorylated extracellular signal-regulated kinase 1/2 (p-ERK1/2) at the protein level were detected by Western blotting.The effect of miR-369-3p on the proliferation of bladder cancer cells was detected by cell counting kit (CCK-8) and clone formation experiment.The effect of miR-369-3p on apoptosis was detected by flow cytometry.Results After transfection with miR-369-3p,the expression of VEGFC at mRNA and protein levels was significantly decreased (P ＜ 0.05),the expression of p-Raf-1 and p-ERK1/2 protein was significantly decreased,the cell proliferation ability was significantly decreased (P ＜ 0.05),the number of clones formed was significantly decreased (P ＜ 0.05) and the apoptosis was significantly increased (P ＜ 0.01).Conclusions miR-369-3p can inhibit the proliferation and promote the apoptosis of bladder cancer cells by interfering with the expression of VEGFC gene,which may provide a new target for the biological therapy of bladder cancer.