The clinical practice in Pediatrics of Chinese medicine is the first step of the students to combine the theory with the clinical practice. The optimization teaching methods for clinical practice in Pediatrics of Chinese medicine was formed by using Delphi method of the extensive consultation from experts in colleges and universities of Pediatrics of Chinese medicine. We used this teaching method in students of Beijing University of Chinese medicine in 2011. Comprehensive evaluation to the implementation of effect was from assessment from students and analysis of exam results. The results showed that based on the survey of the students in the practice, the students in the experimental group give more positive evaluation than the control group on the necessity, satisfaction and harvest in the clinical practice in pediatrics of Chinese medicine.

Objective To observe the effects of blood nourishing and wind expel formulae on learning and memory capabilities of rats with tic disorders. Methods Intradialytic Parenteral Nutrition peritoneal injection was used to establish the rat model of tic disorders. The successful test subjects were categorized into 5 different groups, namely the model group, the Chinese medicine groups (low dosage, medium dosage and high dosage) and the western medicine group. The test groups were each given gastric perfusion of the related medicine, whereas the control and model groups were each given equal amounts of saline solution continuously for 8 weeks. Open field test and water maze test were carried out in the 1st, 4th and 8th weeks to evalute the learning and memory capabilities. Results In comparison with the control group, the model group showed obvious increase in movement across grid and decrease in vertical locomotion. Statistical significance was obtained showing an increase in vertical locomotion in the treatment groups compared with the model group. In the Chinese medicine groups, the medium and high dosage groups exhibited shorter escape latency and increased exploratory behavior (P<0.05) in the 4th and 8th weeks. Conclusion Among the blood nourishing and wind expel formula, the medium and high dosage showed ameliorating effects on the memory and learning capabilities of rats with tic disorders.

Obesity is an established risk factor for endometrial cancer. Leptin, a secreted protein of the ob gene by white adipose tissue, plays an important role in the regulation of food intake and energy consumption in the brain and acts as a potential growth stimulator in normal and neoplastic cancer cells. However, a direct role for leptin in endometrial cancer has not been demonstrated. In the present study, the effect of leptin on the proliferation of Ishikawa endometrial cancer cells was investigated as well as the possible mechanism(s) underlying this action in endometrial cancers which express both short and long isoforms of leptin receptors. The expression of leptin receptor (ObRb) in Ishikawa cells was detected by RT-PCR and Western blotting. The cells after serum starvation, were treated by leptin with various concentrations (0, 10, 50, 100, 150 ng/mL) for different durations (6, 12, 24 h). The effect of leptin treatment on cell proliferation was examined by MTT assay. Meanwhile, inhibitory effect of Janus tyrosine kinase 2 (JAK2)/signal transducer and activator of transcription 3 (STAT3) inhibitor AG490 or extracellular signal-regulated kinase 1/2 (ERK1/2) inhibitor PD98059 on the proliferation of Ishikawa cells induced by leptin was also studied. Ishikawa cells were treated with 100 ng/mL leptin for various periods (0, 20, 40, 60 min), and the levels of STAT3 phosphorylation and ERK1/2 phosphorylation were examined by Western blotting. The results showed that leptin induced the phosphorylation of STAT3 and the activation of ERK1/2 in a time- and dose-dependent manner in the Ishikawa endometrial cancer cells. Blocking STAT3 phosphorylation with the inhibitor AG490, or blocking ERK1/2 activation by the specific ERK1/2 kinase inhibitor, PD98059, abolished leptin-induced proliferation of Ishikawa cells. In addition, leptin was found to potently induce the invasion of endometrial cancer cells in a Matrigel invasion assay. Leptin-stimulated invasion was effectively blocked by pharmacological inhibitors of STAT3 (AG490) and ERK1/2 kinase (PD98059). These results suggested that leptin promotes endometrial cancer growth and invasiveness by activating STAT3 and ERK1/2 signaling pathways and therefore blocking its action at the receptor level can be a rational therapeutic strategy.

Objective To investigate the changes of gene expression profile in Beagle dogs' peripheral blood lymphocytes after acute irradiation.Methods Totally 20 male adult Beagle dogs were randomly divided into four groups including non-treatment blank control group and three radiation groups exposed to 0.5,2.0,and 5.0 Gy of γ-rays,respectively.Six hours after radiation,the peripheral blood were collected for lymphocytes isolation.Total RNA was extracted from the lymphocytes and analyzed by microarray hybridization.The differential gene profiles of radiation groups were analyzed by gene ontology (GO) analysis and kyoto encyclopedia of genes and genomes (KEGG) pathways analysis,and the alerted genes were further confirmed by the real time quantitative PCR (qRT-PCR) assay.Results Compared to the blank control group,the expressions of 308 genes in the radiation groups were perturbed over 2-fold of control,including 61 genes up-regulated and 247 genes down-regulated,which were mainly associated with immune response and cancer occurrence.The GO analysis indicated that the differential expressed genes were associated with cell connection,signal transduction,oxidation-reduction reaction and metabolism.The KEGG pathway analysis showed that some physiological and biochemical processes were involved,such as phagocytosis,tumor pathway,p53 signaling pathway,JAK-STAT signal pathway,cell differentiation,and proliferation,oxidative phosphorylation,glycogen dysplasia and other pathways.The microarray data of the alterations of apoptosis enhancing nuclease (AEN) and mitogenactivated protein kinase 13 (MAP3K13) gene expressions were further confirmed by qRT-PCR.Conclusions Exposure to different doses of acute γ-ray irradiation had significant impact on the gene expressions in Beagle dogs' peripheral blood lymphocytes and those differential expressed genes were related to a series of biological processes and pathways including immune response,metabolism and carcinogenesis.

AIM: To investigate the mechanism of the AP-1 signal transduction pathway inhibited by JIP in nasopharyngeal carcinoma cells. METHODS: AP-1 activity was triggered by Dox-induced LMP1 expression in Tet-on-LMP1-HNE 2 cells (L7). The retention of phospho-JNK in the cytoplasm caused by JIP was examined with immunofluroscence assay. RESULTS: 24 h after transfection of L7 cells with the JIP expression plasmid, the translocation of activated JNK was inhibited, which resulted in the retention of phospho-JNK in the cytoplasm and down-regulation of the AP-1 activity. CONCLUSION: JIP down-regulates the activity of AP-1 through the inhibition of the translocation of JNK.

Abstract:Objective To elucidate the mechanisms by which Epstein-Barr virus-encoded latent membrane protein 1 activates NF-κB in nasopharyngeal carcinoma cells.Methods A tetracycline-regulated LMP1-expressing nasopharyngeal carcinoma cell line, Tet-on-LMP1-HNE2, was used as the cell model. The kinetics of the expression of proteins, including LMP1, IκBα and IκBβ, was analyzed by Western blotting. The subcellular localization of NF-κB (p65) was detected by indirect immunofluorescence assay. The NF-κB transactivity was studied by transient transfection and reporter gene assay. Results IκBα was phosphorylated and degraded after the inducible expression of LMP1, although the total protein levels remained stable. The steady-state level of total IκBβ protein may have resulted from the initiation of an autoregulation loop after the activation of NF-κB. No change in the IκBβ level was detected. NF-κB (p65) was translocated from the cytoplasm to the nucleus following degradation of IκBα. After the introduction of the dominant-negative mutant of IκBα (Del 71) into Tet-on-LMP1-HNE2 cells, both nuclear translocation and transactivation of NF-κB induced by LMP1 was significantly inhibited. Conclusions The results indicated that in nasopharyngeal carcinoma cells, LMP1 activated NF-κB via phosphorylation and degradation of IκBα, but not IκBβ. The dominant-negative mutant of IκBα (Del 71) could completely inhibit both the nuclear translocation and transactivation of NF-κB induced by LMP1.

Objective To elucidate the clinical characteristics and coronary angiographic findings of patients underwent PCI before and after drug-eluting stents(DES).Methods DESIRE(Drug-Eluting Stent Impact on revascularization) was a retrospective registry of patients who received revascularization therapy during July,2001 through June,2002(non-DES era) and July,2003 through February,2004(DES era).In this analysis,we used the DISIRE data to examine the clinical and angiographic features of patients who received PCI in the different era.Results Among 3763 patients in the registry,2180 patients were analyzed(763 were in the non-DES era and 1417 were in the DES era).In the DES era,more diseased vessels(1.31?0.54 vs 1.39?0.61,P

Objective To determine the median effective plasma concentration (Cp50) of remifentanil inhibiting cardiovascular response to CO2 pneumoperitoneum stimulus when combined with propofol in patients undergoing laparoscopic gynaecological surgery.Methods Twenty-two female patients scheduled for elective laparoscopic gynaecological surgery under general anesthesia, aged20-60 years, with a BMI 18-30 kg/m2, falling into ASA physical statusⅠ orⅡ, were enrolled in this study.Anesthesia was induced with propofol and remifentanil target-controlled infusion and iv injection of rocuronium 0.6 mg/kg.The target plasma concentration (Cp) of remifentanil and propofol were set at 5 ng/ml and 4μg/ml respectively.3 minutes after endotracheal intubation, the Cp of remifentanil was adjusted.The target Cp was set at 6 ng/ml in the first patient.CO2 pneumoperitoneum was performed after the target effect-site concentration and Cp were balanced.Each time Cp increased/decreased by 20％in the next patient depending on whether or not the cardiovascular response to CO2 pneumoperitoneum occurred.The positive cardiovascular response was defined as HR and/or MAP increasing by 20％ within 3 minutes after CO2 pneumoperitoneum.The Cp50 and 95％ confidence interval (CI) of remifentanil required to inhibit cardiovascular response to CO2 pneumoperitoneum stimulus when combined with propofol in patients undergoing laparoscopic gynaecological surgery were calculated.Results The Cp50 (95％ CI) of remifentanil required to inhibit cardiovascular response to CO2 pneumoperitoneum stimulus was 4.58 (4.14-5.08) ng/ml when combined with propofol in patients undergoing laparoscopic gynaecological surgery.Conclusion The Cp50 of remifentanil required to inhibit cardiovascular response to CO2 pneumoperitoneum stimulus was 4.58 ng/ml when combined with propofol in patients undergoing laparoscopic gynaecological surgery.

Objective:To explore the effect of small private online course (SPOC) in basic nursing course teaching.Methods:In September 2019, convenience sampling was used to select 150 second-year nursing undergraduates of the 2018 grade from the School of Nursing, Qiqihar Medical College, as the research subject. This study relied on the Chaoxing learning platform to build a SOPC-based pre-class + in-class + after-class blended teaching model, and evaluated the implementation effect.Results:Among 150 students, the online learning score was (93.13±7.76) , and the final offline examination score was (85.61±10.09) . The number of visits to the online platform was 9 428 person-times, a total of 55 topics were discussed by teachers and students, and 172 task points were completed. In the evaluation of each item of the teaching effect of basic nursing based on SPOC by 150 students, more than 80% of students strongly agreed and agreed, and there was no evaluation that strongly disagreed.Conclusions:The SPOC-based teaching model is applied to the teaching of basic nursing courses, which can meet the learning needs of students and improve the quality of education and teaching.

Obesity is an established risk factor for endometrial cancer.Leptin,a secreted protein of the ob gene by white adipose tissue,plays an important role in the regulation of food intake and energy consumption in the brain and acts as a potential growth stimulator in normal and neoplastic cancer cells.However,a direct role for leptin in endometrial cancer has not been demonstrated.In the present study,the effect of leptin on the proliferation of Ishikawa endometrial cancer cells was investigated as well as the possible mechanism(s) underlying this action in endometrial cancers which express both short and long isoforms of leptin receptors.The expression of leptin receptor (ObRb) in Ishikawa cells was detected by RT-PCR and Western blotting.The cells after serum starvation,were treated by leptin with various concentrations (0,10,50,100,150 ng/mL) for different durations (6,12,24 h).The effect of leptin treatment on cell proliferation was examined by MTT assay.Meanwhile,inhibitory effect of Janus tyrosine kinase 2 (JAK2)/signal transducer and activator of transcription 3 (STAT3) inhibitor AG490 or extracellular signal-regulatedkinase 1/2 (ERK1/2) inhibitor PD98059 on the proliferation of Ishikawa cells induced by leptin was also studied.Ishikawa cells were treated with 100 ng/mL leptin for various periods (0,20,40,60 min),and the levels of STAT3 phosphorylation and ERK1/2 phosphorylation were examined by Western blotting.The results showed that leptin induced the phosphorylation of STAT3and the activation of ERK 1/2 in a time-and dose-dependent manner in the Ishikawa endometrial cancer cells.Blocking STAT3 phosphorylation with the inhibitor AG490,or blocking ERK1/2 activation by the specific ERK1/2 kinase inhibitor,PD98059,abolished leptin-induced proliferation of Ishikawa cells.In addition,leptin was found to potently induce the invasion of endometrial cancer cells in a Matrigel invasion assay.Leptin-stimulated invasion was effectively blocked by pharmacological inhibitors of STAT3 (AG490) and ERK1/2 kinase (PD98059).These results suggested that leptin promotes endometrial cancer growth and invasiveness by activating STAT3 and ERK1/2 signaling pathways and therefore blocking its action at the receptor level can be a rational therapeutic strategy.