Objective To evaluate the clinical effect of group cognitive behavioral therapy on blood glucose levels,anxiety and depression in patients with type2 diabetes mellitus.Methods Ninety three patients with type 2 diabetes mellitus were recruited and randomly divided into intervention group (n =48) and control group (n =45).Both groups received diabetes health education,patients in intervention group received additional group cognitive behavioral therapy.The glucose tolerance,glycosylated hemoglobin A1c were measured; the HAMA(Hamilton Anxiety Scale)scores,HAMD(Hamilton Depression Scale)scores and CSQ (Coping Styles Questionnaire) scores in patients were analyzed before and 6 months after treatment.Results After 6-month treatment the fasting blood glucose (6.33 mmol/L vs.5.94 mmol/L),1 h postprandial plasma glucose(12.40 mmol/L vs.11.46 rmool/L),2 h postprandial plasma glucose (10.24 mmol/L vs.9.13 mmol/L),A1 c (6.31％ vs.6.07％) in intervention group were decreased significantly,compared to baseline values (all P ＜ 0.05).The HAMA total score (9.98 vs.8.14),somatic anxiety (3.98 vs.3.48),psychic anxiety(6.00 vs.4.67),HAMD total score(10.74 vs.6.93),anxiety somatic(5.02 vs.3.26),block(2.24 vs.1.38)and sleep disorders(2.40 vs.1.40)in intervention group were all decreased significantly(P ＜ 0.01 or 0.05).There were significant differences in HAMA total score (8.14 vs.9.15),HAMD total score(6.93 vs.9.33),anxiety somatic(3.26 vs.4.38),block(1.38 vs.1.98)and sleep disorders(1.40 vs.2.03)between the intervention group and control group(P ＜ 0.01 or 0.05).And the negative coping style scores in intervention group was also lower than that of the baseline (26.74 vs..29.43).Conclusion The group cognitive behavioral therapy combined with diabetes health education for patients with type 2 diabetes mellitus may improve the glucose metabolism and depression and anxiety status of patients.

Objective: To observe the effect of the administration temperature of GQD on the efficacy to ulcerative colitis (UC) of rats. Methods: The GQD was given to dextran sulfate sodium (DSS)-induced UC rats at different temperature (10℃/42℃) for 7 d. The disease activity index (DAI), histopathological score of colon, superoxide dismutase (SOD), malondialdehyde (MDA), GHS-Px, myeloperoxidase (MPO) of serum and colon tissue, and the tumor necrosis factor (TNF-α) of serum were measured and observed. Results: Compared with the control group, the UC relative symptom and index changes of rats in the model group appeared obviously. GQD showed the significant therapeutic effects in both 10℃ and 42℃ groups. The lower temperature administration achieved significantly better results than the higher one on the histopathological score, colon wall thickness, and biochemical indices. Conclusion: The cold GQD shows higher efficacy than the hot GQD when treating UC, which may be attributed to the immune response of intestinal mucosal mast cells to temperature-induced stress.

In this paper, the RP-HPLC specific chromatography was adopted, with DIKMA-C18 (4.6 mm x 250 mm, 5 µm) as the chromatographic column, with a gradient elution compose of acetonitrile and 0.1% phosphoric acid at flow rate of 0.8 mL · min(-1), the detection wavelength was 220 nm. The difference of the HPLC specific chromatograms between the Lu Dangshen and other different base sources and different producing area of Codonopsis Radix was compared, involved in the similarities and differences of the number and the relative peak area of characteristic peaks in the HPLC specific chromatograms. The HPLC specific chromatograms of Lu Dangshen was established and the relative retention times of seven peaks was determined, and the peaks of codonopyrrolidium B, syringin, lobetyolin, tangshenoside I and atractylenoide III were identified; The HPLC specific chromatograms of Lu Dangshen provided a method for scientific evaluation and effective control the quality of Lu Dangshen from Shanxi famous-region.
Chromatography, High Pressure Liquid ; methods ; Codonopsis ; chemistry ; Drugs, Chinese Herbal ; analysis ; Glucosides ; analysis ; Phenylpropionates ; analysis ; Plant Roots ; chemistry ; Quality Control

The combination of Glycyrrhizae Radix et Rhizoma and Aconiti Lateralis Radix Preparata can increase efficacy and decrease toxicity. This study started from the phenomena of protein self-assembly in the mixed decoction of Glycyrrhizae Radix et Rhizoma with Aconiti Lateralis Radix Preparata. The attenuated mechanism was explored between the combination of Glycyrrhizae Radix et Rhizoma and Aconiti Lateralis Radix Preparata by using the protein of Glycyrrhizae Radix et Rhizoma and aconitine which was the major toxic component of Aconiti Lateralis Radix Preparata. Glycyrrhizae Radix et Rhizoma protein with aconitine could form stable particles which particle mean diameter was (206.2 ± 2.02) nm and (238.20 ± 1.23) nm at pH 5.0 in normal temperature. Through the mouse acute toxicity experiment found that injection of aconitine monomer all mice were killed, and injection of Glycyrrhizae Radix et Rhizoma protein-aconitine particles with the same content of aconitine all mice survived. Survey the stability of Glycyrrhizae Radix et Rhizoma protein-aconitine shows that the colloid particles is stable at room temperature, and it has the possibility to candidate drug carrier. Glycyrrhizae Radix et Rhizoma protein can reduce the toxicity of aconitine through self-assembly.
Aconitum ; chemistry ; toxicity ; Animals ; Drugs, Chinese Herbal ; toxicity ; Female ; Glycyrrhiza ; chemistry ; toxicity ; Male ; Mice ; Mice, Inbred ICR ; Plant Proteins ; chemistry ; isolation & purification ; toxicity ; Rhizome ; chemistry ; toxicity

OBJECTIVETo investigate the mechanism of how vacuum sealing drainage (VSD) ameliorating ischemia reperfusion (I/R) injury in skeletal muscle I/R model.

METHODSThirty New Zealand white rabbits were divided into three groups: control (sham operation) group, I/R group, VSD+ I/R group.The ischemia of the left hind limb of the animal was induced by clamping the common femoral artery and vein. After 4 hours of ischemia, the clamp was removed and the hind limp underwent 6 hours reperfusion. VSD treated animals received the treatment at the beginning of reperfusion. The concentrations of myeloperoxidase (MPO), malondialdehyde (MDA), superoxide dismutase (SOD), catalase (CAT) and glutathione (GSH) in muscular tissues were assayed. HE stained pathological section was used to evaluate the degree of edema of muscular tissues, and the immunohistochemistry was used to detect the percentage of positive cells expressing high mobility group protein B1 (HMGB1). Q-RT-PCR and Western Blot were used to detect the mRNA levels and protein expression of HMGB1 in myocyte respectively. The experimental data was tested using variance analysis.

RESULTSThe levels of inflammatory factors and antioxidant factors in muscular tissues were significantly different in the I/R group compared to the VSD group and control group (the levels of MPO in I/R group, I/R+ VSD group and control group were 0.91±0.22, 0.53±0.08, 0.31±0.10, respectively, F=26.48, P=0.000; MDA were 2.04±0.92, 1.65±1.02, 1.01±0.12, F=4.250, P=0.040; SOD were 35.97±9.23, 55.99±18.97, 61.83±14.91, F=5.240, P=0.020; CAT were 31.42±16.27, 48.50±17.86, 75.95±13.09, F=9.720, P=0.002; GSH were 1.48±0.90, 3.54±1.88, 3.84±2.08, F=5.240, P=0.020). HE staining showed an increased intercellular space ratio in the I/R group (F=16.47, P<0.05). Immunohistochemistry staining showed that percentage of HMGB1 positive myocytes in control, I/R and I/R+ VSD group are 1.94%, 18.63% and 61.36%, respectively. There was significant difference among groups (F=853.886, P<0.01). A significantly inhibited HMGB1 expression by VSD therapy was also validated by the results of Q-RT-PCR (F=50.653, P<0.01) and Western blot (F=963.489, P<0.01).

CONCLUSIONThe results from the present research suggest that VSD may attenuate skeletal muscles I/R injury by increasing the cellular antioxidative stress reaction and inhibiting the reactive oxygen species as well as the inflammatory mediators.

Animals ; Antioxidants ; metabolism ; Catalase ; metabolism ; Drainage ; methods ; HMGB1 Protein ; metabolism ; Malondialdehyde ; metabolism ; Muscle, Skeletal ; physiopathology ; Oxidative Stress ; Peroxidase ; metabolism ; Rabbits ; Reperfusion Injury ; therapy ; Superoxide Dismutase ; metabolism ; Vacuum

OBJECTIVETo study the morphologic and growing alterations of oral cancer cell line Tca8113 before and after cocultured with tumor stromal fibroblasts (TSF) and normal stromal fibroblasts (NSF) respectively, and evaluate the influence of mesenchymal cells on tumor cells.

METHODSTSF and NSF were isolated and cultured. To observe the morphologic change of Tca8113 cells after cocultured with TSF and NSF respectively.

RESULTSWhen cocultured with NSF, the Tca8113 cells proliferated as rapidly as monocultured to form colonies, while the NSF proliferated slowly to form pieces and then joined each other to form network. The NSF network segmented and surrounded the colonies of cancer cells so that the cancer cells shrank, turn round, broke away from the bottom and floated into the medium. The cancer cells proliferated actively but they were elbow out entirely in the end. TSF proliferated slowly when cocultured with cancer cells, projected several branched protrusions. The cancer cells proliferated along the two sides of protrusions of TSF, or projected short protrusions to connect the body or protrusions of TSF, and overlaid the protrusions gradually, finally, cover the body. In the end, TSF melt away, and the cancer cells took on the figure of TSF.

CONCLUSIONThe results do suggest that, oral cancer cell line Tca8113 are restrained when coculture with NSF, but are promoted when with TSF.

Cell Line ; Coculture Techniques ; Fibroblasts ; Humans ; In Vitro Techniques ; Mesenchymal Stromal Cells ; Mouth Neoplasms

OBJECTIVETo investigate SiO2-induced EMT in human bronchial epithelial cells HBE in vitro.

METHODSHBE cells were cultured and then stimulated with indicated doses of SiO2 (0, 50, 100, 200, 300 µg/ml). The morphological changes were observed by microscope. In addition, Western blot was per-formed to detect the expression of E-cad, α-SMA and Vim. The changes of migration ability were examined by wound-healing assay in vitro.

RESULTS(1) After exposure to SiO2, HBE cells lost contact with their neighbor and displayed a spindle-shape, fibroblast-like morphology. (2) Compared with the control, the E-cad (300 µg/ml group) expression downregulated 2.98 fold (P < 0.05), and the Vim (300 µg/ml group) and α-SMA (200 µg/ml group) expression upregulated 4.46 fold and 3.55 fold (P < 0.05). There were significant differences between 100, 200, 300 µg/ml groups and the control group (P < 0.05). (3) In the test group, the percentage of wound-healing areas/wound areas were larger than those in control group (P < 0.05).

CONCLUSIONSSiO2 could induce EMT in human bronchial epithelial cells.

Bronchi ; cytology ; Cells, Cultured ; Epithelial Cells ; cytology ; drug effects ; Epithelial-Mesenchymal Transition ; drug effects ; Humans ; Silicon Dioxide ; adverse effects ; Stromal Cells ; cytology ; drug effects

Objective To investigate the levels and significance of Th17 cells and regulatory T cells (Treg) in peripheral blood of children with allergic rhinitis during pollen and non-pollen seasons.Methods Thirteen children with hay fever, 10 children with house dust mite(HDM)-allergic asthma and 10 healthy children were recruited into this study.Percentages of Th17 and Treg cells were detected by flow cytometry.Levels of IL-17, IL-10 and TGF-β in cell culture supernatants were measured by ELISA.Results (1) The percentages of Th17 cells in children with allergic rhinitis [(3.4±2.4)%] were significantly higher than those in HDM-allergic asthmatics [(2.1±1.6)%] and those in healthy children [(0.5±0.3)%] during pollen season (both P<0.05).The levels of Treg cells in allergic rhinitis group [(2.1±1.3)%] and in HDM-allergic asthma group [(3.6±1.9)%] were significantly lower than those in healthy control group [(5.5±2.8)%] (both P<0.05).The levels of Th17 cells [(3.0±1.9)% vs (3.4±2.4)%, P<0.05] and ratios of Th17/Treg cells [(1.4±1.0)% vs (1.7±1.5)%, P<0.05] in children with allergic rhinitis were significantly decreased during non-pollen season as compared with those during pollen season, but the levels of Treg cells were up-regulated [(2.4±1.6)% vs (2.1±1.3)%, P<0.05].(2) Correlation analysis revealed that the ratios of Th17/Treg cells were positively correlated with the concentrations of FeNO (fractional concentration of exhaled NO) (r=0.321, P<0.05) and the counts of circulating eosinophils (r=0.198, P<0.05) in children with allergic rhinitis during pollen season.Conclusion The imbalanced Th17 and Treg cells in children with allergic rhinitis during pollen season might play a vital role in the regulation of allergic airway inflammation.

TNF-related apoptosis-inducing ligand (TRAIL) has been proposed as a promising cancer therapy that preferentially induces apoptosis in cancer cells, but not most normal tissues. However, many cancers are resistant to TRAIL by mechanisms that are poorly understood. In this study, we showed that tunicamycin, a naturally occurring antibiotic, was a potent enhancer of TRAIL-induced apoptosis through downregulation of survivin. The tunicamycin-mediated sensitization to TRAIL was efficiently reduced by forced expression of survivin, suggesting that the sensitization was mediated at least in part through inhibition of survivin expression. Tunicamycin also repressed expression of cyclin D1, a cell cycle regulator commonly overexpressed in thyroid carcinoma. Furthermore, silencing cyclin D1 by RNA interference reduced survivin expression and sensitized thyroid cancer cells to TRAIL; in contrast, forced expression of cyclin D1 attenuated tunicamycin-potentiated TRAIL-induced apoptosis via over-riding downregulation of survivin. Collectively, our results demonstrated that tunicamycin promoted TRAIL-induced apoptosis, at least in part, by inhibiting the expression of cyclin D1 and subsequent survivin. Of note, tunicamycin did not sensitize the differentiated thyroid epithelial cells to TRAIL-induced apoptosis. Thus, combined treatment with tunicamycin and TRAIL may offer an attractive strategy for safely treating resistant thyroid cancers.
Anti-Bacterial Agents/*pharmacology ; *Apoptosis ; Cell Line, Tumor ; Cyclin D1/*antagonists & inhibitors/metabolism ; *Down-Regulation ; Humans ; Microtubule-Associated Proteins/*genetics/metabolism ; TNF-Related Apoptosis-Inducing Ligand/*metabolism ; Tunicamycin/*pharmacology

TNF-related apoptosis-inducing ligand (TRAIL) has been proposed as a promising cancer therapy that preferentially induces apoptosis in cancer cells, but not most normal tissues. However, many cancers are resistant to TRAIL by mechanisms that are poorly understood. In this study, we showed that tunicamycin, a naturally occurring antibiotic, was a potent enhancer of TRAIL-induced apoptosis through downregulation of survivin. The tunicamycin-mediated sensitization to TRAIL was efficiently reduced by forced expression of survivin, suggesting that the sensitization was mediated at least in part through inhibition of survivin expression. Tunicamycin also repressed expression of cyclin D1, a cell cycle regulator commonly overexpressed in thyroid carcinoma. Furthermore, silencing cyclin D1 by RNA interference reduced survivin expression and sensitized thyroid cancer cells to TRAIL; in contrast, forced expression of cyclin D1 attenuated tunicamycin-potentiated TRAIL-induced apoptosis via over-riding downregulation of survivin. Collectively, our results demonstrated that tunicamycin promoted TRAIL-induced apoptosis, at least in part, by inhibiting the expression of cyclin D1 and subsequent survivin. Of note, tunicamycin did not sensitize the differentiated thyroid epithelial cells to TRAIL-induced apoptosis. Thus, combined treatment with tunicamycin and TRAIL may offer an attractive strategy for safely treating resistant thyroid cancers.
Anti-Bacterial Agents/*pharmacology ; *Apoptosis ; Cell Line, Tumor ; Cyclin D1/*antagonists & inhibitors/metabolism ; *Down-Regulation ; Humans ; Microtubule-Associated Proteins/*genetics/metabolism ; TNF-Related Apoptosis-Inducing Ligand/*metabolism ; Tunicamycin/*pharmacology