Objective To describe self-care agency and its influence factors of the patients with temporary ileum stoma. Methods The descriptive statistics of non-experimental study was performed in the study. The convenience sample consisted of 144 patients from 3 hospitals in Shanghai. The self-care agency was measured by the Colostomy Self-care Agency Scale. Results 144 cases of colorectal cancer temporary ileum stoma patients′ self-care ability scored an average of 57.02 ± 7.00, including self- care willingness (37.19 ± 4.04) points, self-care knowledge 17 points, self-care skills 3 points. The multiple stepwise regression analysis showed that seven factors were statistically significant including age, gender, culture level, living area, postoperative months, presence of complications, whether to accept professional nursing training or education. Conclusions Temporary ileum stoma in patients of rectal cancer with medium self-care ability, but self-care skill level is relatively not high and should be strengthen attention in patients with rectal cancer undergoing ileum stoma. Targeted nursing intervention should be carried out to improve the self-care ability and improve the quality of life of patients with stoma.

This study examined the effects of arsenic trioxide on apoptosis and interleukin4 release in T cells of asthmatic patients in vitro and investigated the role of Bcl2 in the active mechanism. Tcells were isolated from asthmatic patients (n=21) and healthy controls (n=20), and then treated with arsenic trioxide and dexamethasone. Cell apoptosis was measured using fluorescence microscopy, flow cytometry and a cytochrome c ELISA kit. Interleukin4 levels in the serum and in supernatants from T cells were quantified by ELISA. Flow cytometric analysis and immunofluorescence studies were performed to determine Bcl 2 expression. Tcells of the asthmatic patients (I.e. without treatment) exhibited decelerated spontaneous apoptosis after 24 h incubation in vitro when compared to T cells of the healthy controls. With dexamethasone treatment, an increase in apoptosis of Tcells was not significantly different between both groups, irrespective of the method used. Arsenic trioxide treatment, however, significantly increased the apoptosis of T cells of the asthmatic group and showed a slight effect on the control group. In asthmatic patients, elevated levels of interleukin 4 and upregulated Bcl 2 expression were detected. Moreover, in vitro, T cells of asthmatic patients spontaneously released more interleukin4 and exhibited more Bcl 2 expression than T cells from the control group. Arsenic trioxide treatment significantly decreased interleukin4 release and downregulated Bcl 2 expression in asthmatic patients, while it only slightly affected healthy controls. Dexamethasone treatment decreased interleukin4 release in both groups examined. It did not significantly influence Bcl2 expression. These results suggest that arsenic trioxide induces T cell apoptosis and decreases interleukin4 release in T cells of asthmatic patients in vitro and that downregulation of Bcl2 expression may be an important mechanism.

AIM To study the possible mechanism of the treatment of arsenic trioxide on asthma. METHODS T cells isolated from 21 asthmatic patients and 20 healthy controls were treated with arsenic trioxide (0.1 mg·L-1) or dexamethasone (5 mg·L-1),in vitro, for 24 h. Interleukin-4 (IL-4) levels in supernatants from T cells were quantified with ELISA. Cell apoptosis was measured by using fluorescence microscopy, flow cytometry and cytochrome c ELISA kit. RESULTS T cells of asthmatic patients spontaneously released more IL-4 than that of healthy controls. Arsenic trioxide significantly decreased IL-4 release of T cells from asthmatic patients, which was more obvious compared with healthy controls. Dexamethasone decreased IL-4 release in both groups. Apoptosis percentage and cytochrome c content in cytoplasm of T cells from asthmatic patients were lower than those from healthy controls. Arsenic trioxide significantly increased the apoptosis percentage and cytochrome c content in cytoplasm of T cells in the asthmatic group, and had slighter effects on that in healthy controls. Dexamathasone increased the apoptosis percentage and cytochrome c content of T cells in both groups. CONCLUSION The mechanism of the treatment of arsenic trioxide on asthma involves the induction of T cell apoptosis and decrease of IL-4 release in asthmatic patients.

OBJECTIVE: To observe the effects of glycyrrhizin on hydroxyproline(HYP),hyaluronic acid(HA) and laminin(LN) in pulmonary fibrosis model rats.METHODS: A total of 80 SD rats were randomly divided into normal control group,model group,hormone group(prednisone 0.6 mg?kg?d-1),and glycyrrhizin group(10 g?kg?d-1).The latter 3 groups were established into pulmonary fibrosis model with bleomycin,and on the second day after modelling,each group was given corresponding test drugs(the normal group and model group were treated with same amount of normal saline) then the changes of the levels of HYP in lung tissues,and serum levels of HA and LN in every group were observed at 7 and 28 days respectively.RESULTS: In glycyrrhizin group compared with model group,the contents of HYP in lung tissue,HA and LN in serum decreased significantly(P

OBJECTIVE: To explore the effect of glycyrrhizin on eotaxin expression in lung tissue from asthmatic model mice and the mechanism for glycyrrhizin to treat bronchial asthma.METHODS: The mice were randomized to asthma model group,prednisone-treated group and glycyrrhizin-treated group and normal control group.Egg protein asthma mouse model was established before being giving the corresponding drugs.Then the mice were sacrificed after 4 weeks for the counting of eosinophils in bronchoalveolar lavage fluid(BALF) and detection of Eotaxin expression in lung tissues by immunohistochemistry,with the results compared with normal control group.RESULTS: In glycyrrhizin-treated group compared with model group,the counting of eosinophils in BALF were decreased(P

ObjectiveTo investigate the effects of controlled subcutaneous analgesia(PCSA) with sufentanil in patients underwent abdominal surgery and the occurrence of adverse reactions. Methods90 patients underwent abdominal surgery were randomly divided intothree groups with 30 cases each. Group Ⅰ :sufentanil 0. 04μg · kg-1 ·h-1 for postoperative analgesia; Group Ⅱ : sufentanil 0. 06μg · kg-1 · h-1 for postoperative analgesia; Group Ⅲ :sufentanil 0.08μg/kg · h for postoperative analgesia;PCSA started at the end of operation with catheter buried in deltoid muscle. Visual analgesia scale(VAS) ,Rasmay scale and side effects were recorded at 4,8,16,24 and 48h after operation. ResultsVAS scores decreased significantly in group Ⅱ and group Ⅲ compared with that in group Ⅰ ( all P ＜ 0.05) ;There were no differences of Ramsay scores between groups ( all P ＞ 0. 05) ;There were three cases of respiratory depression in group Ⅲ. ConclusionPCSA with sufentanil (0.06μg/kg) had exact analgesic effects for postoperative abdominal surgery patients with less adverse reactions.

Objective To explore the effect of nicotine on rats callus content and maturity in the process of fracture healing.Methods Sixty male Sprague-Dawley rats were randomly divided into model group,mild nicotine group and severe nicotine group (n =20/each group).The 3-mm bone defects fracture models were made in the junction of the lower 1/3 of the rat left radial.Five rats of each group were sacrificed randomly in the 3,7,14,21 days after surgery,respectively.The left radial were collected as the observed object.The callus thickness and maturity of the specimens were detected by HE staining.Results At the 3rd days after modeling,the difference in specimens callus thickness between each treatment group and the model group was not statistically significant (P ＞ 0.05),no difference in the maturity of the callus under the microscope; callus thickness in mild and severe nicotine groups and model group was (1.59 ± 0.09) mm,(1.43 ± 0.12) mm,(1.39 ± 0.09) mm at the 7th day after modeling,(1.98 ± 0.12) mm,(1.78 ± 0.08)mm and (1.68 ± 0.09) mm at the 14th day after modeling,and (2.39 ± 0.09) mm,(1.93 ± 0.11) mm,(1.89 ± 0.09) mm at the 21 st day after modeling; The difference of callus thickness in specimens between each treatment group and the model group had statistical significance (P ＜ 0.05,P ＜0.01),callus thickness and maturity of the treatment group were lower than that in the model group.Conclusions Nicotine affects the proliferation and differentiation of callus,reduces callus formation,inhibits maturity transformation of bone,and delays the healing process of fracture.

AIM To investigate the effects of D galactose on bone contents of hydroxyproline(HOP), calcium, microelements and activities of antioxidation in mice. METHODS Twenty female kunming mice at three months of age were used in this study. D galactose at dose of 1 g?kg -1 ?d -1 was given subcutaneous injection daily to the mice for 42 days. The right femurs were collected to determine the bone dry weight, bone hydroxyproline content, bone calcium, and bone microelements. The activities of catalase (CAT), glutathione peroxidase (GSH Px) and superozide dismutases (SOD) in blood, and contents of methylenedioxyamphetamine (MDA) in serum, lipofuscin in liver were determined. RESULTS The bone dry weight, hydroxyproline, calcium of bone decreased significantly in D galactose treaded group(compared with control group, P

Aim To investigate the effects of glycyrrhizin on the proliferation of ASMC stimulated by fetal calf or histamine in rats. Methods Cell culture of rat ASMC, MTT assay, flow cytometry and cell growth counts were used in this study. Results ①In the culture medium containing 100g?L -1 fetal calf serum, Glycyrrhizin at low concentration(6?10 -5 mol?L -1 ) stimulated the increase of A 570 in ASMC. This effect descended with increasing glycyrrhizin concentration and changed to be inhibitory at high concentration (from 384?10 -5 mol?L -1 to 1 536 ?10 -5 mol?L -1 ). In the culture medium containing 10 -2 mol?L -1 histamine, Glycyrrhizin at both low and high concentration inhibited the increase of A 570 in ASMC. ②In the culture medium containing 100 g?L -1 fetal calf, Glycyrrhizin at low concentration(6?10 -5 mol?L -1 ) stimulated the proliferation of ASMC. This effect descended with increasing glycyrrhizin concentration and changed to be inhibitory at high concentration (from 384?10 -5 mol?L -1 to 1 536 ?10 -5 mol?L -1 ). In the culture medium containing 1 g?L -1 histamine, Glycyrrhizin at both low and high concentration inhibited the proliferation of ASMC. ③In the culture medium containing 100 g?L -1 fetal calf or 10 -2 mol?L -1 histamine, with increasing glycyrrhizin concentration, the cell count in G 1 phase increase, the cell count in G 2 and M phase decrease. Conclusion ①Glycyrrhizin accelerated the proliferation of ASMC stimulated by fetal calf at low concentration, inhibited the proliferation at high concentration. ②Glycyrrhizin inhibited the proliferation of ASMC stimulated by histamine at both low concentration and high concentration.

Objective To evaluate effects of simultaneous inhibition of mammalian target of rapamycin complex 1(mTORC1)kinase and glycogen synthase kinase-3β(GSK-3β)on phosphorylation of 4E-binding protein-1(4EBP1), cap-dependent translation, as well as survival and apoptosis of melanoma cells. Methods Cultured A375 cells were classified into several groups to be treated with dimethyl sulfoxide (DMSO group), the mTORC1 kinase inhibitor everolimus at a concentration of 5 nmol/L (everolimus group), the GSK-3β kinase inhibitor AR-A014418 at a concentration of 10 μmol/L (AR-A014418 group), or 5 nmol/L everolimus and 10 μmol/L AR-A014418(combined treatment group). After additional culture, Western-blot analysis was performed to measure protein expressions of phosphorylated 4EBP1 (p4EBP1)and survivin in A375 cells, m7GTP pull down assay to estimate interaction between eukaryotic initiation factor-4E (eIF4E)and eIF4G, cell counting kit 8 (CCK8)assay to evaluate cell proliferation, and flow cytometry to detect cell apoptosis. Results Both everolimus and AR-A014418 had inhibitory effects on 4EBP1 phosphorylation and survivin expression. The expressions of p4EBP1-65 and survivin were both significantly decreased in the everolimus group (0.74 ± 0.05 and 0.71 ± 0.06 respectively), AR-A014418 group (0.62 ± 0.06 and 0.58 ± 0.07 respectively)and combined treatment group (0.14 ± 0.04 and 0.09 ± 0.05 respectively)compared with the DMSO group (1.00 ± 0.07 and 1.00 ± 0.06, respectively, all P < 0.001), with the most significant decrease observed in the combined treatment group. As m7GTP pull-down assay showed, the everolimus group, AR-A014418 group and combined treatment group all showed significantly lower relative expression levels of eIF4G(0.72 ± 0.04, 0.67 ± 0.05 and 0.12 ± 0.05 vs. 1.00 ± 0.06, all P < 0.001), but significantly higher relative expression levels of 4EBP1 (1.98 ± 0.16, 2.32 ± 0.17 and 7.58 ± 0.25 vs. 1.00 ± 0.08, all P < 0.001)than the DMSO group, and the combined treatment group showed the lowest eIF4G expression but highest 4EBP1 expression. After 24-hour culture, the proliferation of A375 cells was inhibited by 18.5% ± 1.3% in the everolimus group, 19.8% ± 1.8% in the AR-A014418 group, and 61.2% ± 2.1% in the combined treatment group compared with the DMSO group, with the strongest inhibition noted in the combined treatment group. The inhibitory effects of everolimus and AR-A014418 on cell proliferation increased over time, and showed the same trend at 48 hours. Flow cytometry showed that the apoptosis of A375 cells was accelerated by the 24-hour treatments with everolimus and AR-A014418 alone or in combination, with the apoptosis rate being 14.28% ± 2.18%, 14.57% ± 2.35% and 55.18% ± 6.27% in the everolimus group, AR-A014418 group and combined treatment group respectively, and the combined treatment showed the strongest accelerating effect. Conclusion The combined treatment with everolimus and AR-A014418 can evidently inhibit 4EBP1 phosphorylation and eIF4F complex formation in A375 cells, which then suppress cap-dependent translation and promote apoptosis of melanoma cells.