OBJECTIVE:To analyze the relevant factors contributing to ARDs of Co-Salvia Miltiorrhiza injection (CSMI).METHODS:The ARDs of CSMI,reported in domestic literature in recent years,were collected and analyzed.RESULTS:About 7 kinds of clinical manifestation of ARDs were reported,of which,the allergic reaction was the commonest one.CONCLUSION:Clinical physicians should pay attention to the ARDs of CSMI and rationally use the preparation.

Objective To know the influence of psychological intervention on delivery results of par-turient women, and then reference to certain effective psychological nursing cares for clinical field. Methods Divided 226 partreient women of spontaneous labor into the experimental group and the control group randomly, there were 113 eases in each group. Traditional routine nursing cares was used in the control group, psychological intervention was used in the experimental group in addition. Compared the condi-tion of birth process and the incidence rate of labor-related complications between the two groups. Re-sults There were significant differences between the two groups about all the indexes which had indicated the delivery. Conclusions Correct psychoanalysis and proper nursing intervention and effective release the pains for parturient women, and then decrease the incidence rate of medical negligence.

Objective:To study the anti proliferation and inducing apoptosis effects of cytokine induced killer cells CIK cells on MGC 803 gastric cancer cell lines and to probe its underlying mechanism.Methods:To detect the anti proliferation and the cytotoxicity of CIK cells on MGC 803 gastric cancer line by MTT assay.The morphological changes of the apoptosis cell were observed by HE stain, scanning and transmission electron microscope. The positive expression of p53, p16,C myc were determined by immunocytochemistry (ICC).Results:MTT assay showed that the inhibitive rate inhanced obviously with the addition of Effect/Target rate and extension of time ( P

Objective To observe the survival,migration and differentiation of grafted neural stem cells(NSCs)transfected with cardiotrophin-1(CT1)in hippocampus in status epilepticus(SE)rats,and investigate its effect on neuron loss and mossy fiber sprouting(MFS)in hippocampus of SE rats.Methods (1)Lithium-pilocarpine induced SE model rats were divided into 3 groups randomly:CT1-NSCs transplantation group(n=18);NScs transplantation group(n=18)and SE model group(n=18).Another 18 rats served as normal control group.Each group was further divided into 3 time points testing groups(n=6 at each point)corresponding to 1,4 and 8 weeks after transplantation respectively.(2)Under the confocal microscopy,the survival,migration and differentiation of the grafted cells were observed by immunofluorescenee.(3)Morphological changes and neuron loss in the hippocampal CA1 region were examined by Nissl staining.(4)MFS in hippocampal dentate gyrus in rats was obserred by Timm histochemistry.Results(1)At 4 and 8 weeks post-tmusplantation,the numbers of double-labeled NF-200 and EGFP pesitive cells in the CT1-NSCs group were significantly hisher than those in NSCs group.In the former group most of the grafted NSCs migrated away from the needle tract,but in the latter group,grafted ceHs remained at the transplantation site.(2)The numbers of neuron in the hippocampal CA1 region reduced gradually after SE.The numbers of neuron in the CA1 region in CT1-NSCs transplantation rats (68.85±11.49,60.89±12.17 and 51.51±13.34 in 1,4,8 weeks after transplantation respectivelv)were greater than that in NSCs transplantation rats(67.92±10.78,42.56±11.47 and 30.49±10.12).tvalue were 4.650 and 5.334 in 4 and 8 weeks after transplantation(P<0.05).(3)Aberrant MFS in the inner molecular layer of dentate gyrus was observed,and the scores of MFS gradually increased with timelapse.The scores of MFS in CT1-NSCs transplantation rats(0.77±0.04,2.48±0.89 and 2.39±0.82 in 1,4,8 weeks after transplantation respectively)were significant lower than that in NSCs transplantation rats (1.12±0.62,3.17±0.64 and 3.88±0.51,t=6.059,9.511 and 9.728,P<0.05).Conclusions CT1 could promote the survival,migration and differentiation of engrafted NSCs in hippocampud in SE rats.Engrafted NSCs transfected with CT1 have effect on repair of the injured hippocampus,and could inhibit hippocampus MFS in SE rats.

AIM:To set up a glutamate-induced cell damage model in cultured hippocampal neurons, and to determine whether glutamate-induced neuronal apoptosis changes and whether this process is mediated by mitochondrial signal transduction pathways involving the release of cytochrome C. METHODS: Hippocampal neurons, isolated and cultured from new born Wistar rats, were exposed to various concentrations of glutamate. Extent of cell death was assessed by measuring the release of lactate dehydrogenase (LDH) in the culture media. Based on these data, an appropriate concentration of glutamate was selected, and all subsequent experiments were carried out under the concentration. Kinetics of glutamate-induced both apoptotic and necrotic cell death after exposure to glutamate for various times(3-24 h) were determined by flow cytometry and LDH release. The caspase-3 protein levels and cytochrome C release from mitochondria into cytosol in hippocampal neurons were determined by Western blotting. RESULTS: Glutamate treatment induced hippocampal neurons death in dose-dependent and time-dependent manners. A significant increase in LDH release (18.4%) was induced in the cells treated with 50 ?mol/L glutamate, compared to control untreated cells(P

Objective To investigate the effects of interleukin-17 (IL-17) on the cell proliferation, apoptosis and migration of human laryngeal carcinoma Hep-2 cells.Methods IL-17 was transiently transfected into Hep-2 cells, and at the same time empty vector group (pEGFP-N1) and normal control group were set up.The efficiency of transfection was evaluated by fluorescence microscope, and the mRNA and protein expressions of IL-17 were detected by reverse transcription-polymerase chain reaction (RT-PCR) and Western blotting.The proliferation of cells was detected by methyl thiazolyl tetrazolium (MTT) method, and the apoptosis was detected by flow cytometry.The migration ability was detected by wound-healing assay and Transwell assay.ResultsHep-2 cells transfected with empty vector pEGFP-N1 and IL-17 showed green fluorescence under the fluorescence microscope.Hep-2 cells expressed IL-17 at both mRNA and protein levels after transfection with IL-17.Compared with the normal control group, the proliferation of IL-17 transfected Hep-2 cells was significantly inhibited after 48 h transfection (0.34±0.03 vs.0.46±0.04, P=0.006).The apoptotic rate of IL-17 transfected cells was higher than that of normal control group (26.80%±0.80% vs.2.90%±0.31%, P=0.000).According to the wound-healing assay, compared with the normal control group, the scratch width of IL-17 transfected cells was significantly greater (1.59±0.01 vs.1.36±0.01, P=0.000).Transwell migration experiment showed that the migration of IL-17 transfected cells was significantly lower than that of the normal control group (26.33±2.08 vs.49.33±1.53, P=0.000).Conclusion IL-17 can inhibit the proliferation of human laryngeal carcinoma Hep-2 cells, reduce their migration ability and enhance their apoptosis ability.Therefore, IL-17 may inhibit the occurrence and development of laryngeal carcinoma through a variety of mechanisms.

Objective To investigate the inhibition effect of liraglutide (lira) on high glucose-induced adhesion of endothelial cells to monocyte.Methods Human umbilical vascular endothelial cells (HUVECs) induced by high glucose (20 mmol/L) were incubated with different concentrations of liraglutide (0,0.3,3,30 nmol/L) for different time.THP-1 cells were pre-labeled with Calcein-AM and then incubated with HUVECs for 1 h,M199 medium were used for washing the nonadherent cells for 3 times,and the adhesion of HUVECs to THP-1 cells were measured by Fluorence microplate reader;real-time polymerase chain reaction (qPCR) and enzyme-linked immunosorbent assay (ELISA) were employed to detect the mRNA and protein expression of vascular cell adhesion molecule-1 (VCAM-1) and intercellular adhesion molecule-1 (ICAM-1),respectively.Western blot was used to measure the content of IκBα,p-IκBα and the distribution of p65 in plasma and nuclear.GST-IκBα was introduced as substrate to test the activity of IκB-kinase (IKK).Results The adhesion of HUVECs to THP-1 (P ＜ 0.01),the mRNA and protein expression of VCAM-1 and ICAM-1 (P ＜ 0.05,P ＜ 0.01),the phosphorylation of κBα (P ＜ 0.05,P ＜ 0.01),the translocation of p65 subunit from plasma to nuclear and the activity of IKK (P ＜ 0.01) in HUVECs were all elevated by stimulation with 20 mmol/L glucose,and the content of IκBα was decreased accordingly (P ＜0.01).Pre-incubation with lira could reverse the above effect of high concentration of glucose.Conclusions Lira could reduce VCAM-1 and ICAM-1 expression through IKK/NF-κB pathways in 20 mmol/L glucose-induced HUVECs,which finally suppress THP-1-HUVECs adhesion.

OBJECTIVETo investigate the effect of 17-AAG combined with paclitaxel (PTX) on the proliferation and apoptosis of esophageal squamous cell carcinoma cell line Eca-109 in vitro.

METHODSEca-109 cells were treated with 17-AAG and PTX either alone or in combination. The proliferation of Eca-109 cells was detected by MTT assay, and the cell cycle changes and cell apoptosis were determined by flow cytometry.

RESULTSCompared with the control group, both 17-AAG and PTX significantly inhibited the proliferation of Eca-109 cells. A combined treatment of the cells with 0.5 µmol/L PTX and 0.625 µmol/L 17-AAG produced an obviously stronger inhibitory effect on the cell proliferation than either of the agents used alone (P<0.01). Flow cytometry showed that, 17-AAG and PTX used alone caused Eca-109 cell cycle arrest in G2/M phase and S phase, respectively, and their combined use caused cell cycle arrest in both G2/M and S phases. The cell apoptosis rates of Eca-109 cells treated with 17-AAG, PTX and their combination were 4.52%, 10.91%, and 29.88%, respectively, all significantly higher than that in the control group (1.32%); the combined treatment resulted in a distinct apoptotic peak that was significantly higher than that caused by either of the agents alone.

CONCLUSION17-AAG and PTX can inhibit cell proliferation and promote apoptosis of Eca-109 cells, and their combination produces stronger effects in inhibiting cell proliferation and increasing cell apoptosis.

Apoptosis ; Benzoquinones ; pharmacology ; Carcinoma, Squamous Cell ; pathology ; Cell Cycle Checkpoints ; Cell Line, Tumor ; drug effects ; Cell Proliferation ; Esophageal Neoplasms ; pathology ; Humans ; Lactams, Macrocyclic ; pharmacology ; Paclitaxel ; pharmacology

Objective To investigate the effect of 17-AAG combined with paclitaxel (PTX) on the proliferation and apoptosis of esophageal squamous cell carcinoma cell line Eca-109 in vitro. Methods Eca-109 cells were treated with 17-AAG and PTX either alone or in combination. The proliferation of Eca-109 cells was detected by MTT assay, and the cell cycle changes and cell apoptosis were determined by flow cytometry. Results Compared with the control group, both 17-AAG and PTX significantly inhibited the proliferation of Eca-109 cells. A combined treatment of the cells with 0.5μmol/L PTX and 0.625μmol/L 17-AAG produced an obviously stronger inhibitory effect on the cell proliferation than either of the agents used alone (P<0.01). Flow cytometry showed that, 17-AAG and PTX used alone caused Eca-109 cell cycle arrest in G2/M phase and S phase, respectively, and their combined use caused cell cycle arrest in both G2/M and S phases. The cell apoptosis rates of Eca-109 cells treated with 17-AAG, PTX and their combination were 4.52%, 10.91%, and 29.88%, respectively, all significantly higher than that in the control group (1.32%); the combined treatment resulted in a distinct apoptotic peak that was significantly higher than that caused by either of the agents alone. Conclusion 17-AAG and PTX can inhibit cell proliferation and promote apoptosis of Eca-109 cells, and their combination produces stronger effects in inhibiting cell proliferation and increasing cell apoptosis.

Objective To investigate the effect of 17-AAG combined with paclitaxel (PTX) on the proliferation and apoptosis of esophageal squamous cell carcinoma cell line Eca-109 in vitro. Methods Eca-109 cells were treated with 17-AAG and PTX either alone or in combination. The proliferation of Eca-109 cells was detected by MTT assay, and the cell cycle changes and cell apoptosis were determined by flow cytometry. Results Compared with the control group, both 17-AAG and PTX significantly inhibited the proliferation of Eca-109 cells. A combined treatment of the cells with 0.5μmol/L PTX and 0.625μmol/L 17-AAG produced an obviously stronger inhibitory effect on the cell proliferation than either of the agents used alone (P<0.01). Flow cytometry showed that, 17-AAG and PTX used alone caused Eca-109 cell cycle arrest in G2/M phase and S phase, respectively, and their combined use caused cell cycle arrest in both G2/M and S phases. The cell apoptosis rates of Eca-109 cells treated with 17-AAG, PTX and their combination were 4.52%, 10.91%, and 29.88%, respectively, all significantly higher than that in the control group (1.32%); the combined treatment resulted in a distinct apoptotic peak that was significantly higher than that caused by either of the agents alone. Conclusion 17-AAG and PTX can inhibit cell proliferation and promote apoptosis of Eca-109 cells, and their combination produces stronger effects in inhibiting cell proliferation and increasing cell apoptosis.