Objective To observe the short-term clinical effect of compound sophora injection combined with Java brucea fruit oil emulsion injection for palliative treatment of advanced malignant tumors. Methods Totally 120 cases of advanced malignant tumor patients were randomly divided into treatment group and control group, each contains 60 cases. The control group was treated with Java brucea fruit oil emulsion, and the treatment group took compound sophora injection additionally by intravenous infusion one time daily. The cycle was 24 d. After 3 cycles, the curative effect, pain relief, improvement situation of quality of life and adverse reactions of the two groups were observed. Results Feasible curative effect evaluation of 112 patients showed:The disease control rate in the treatment group was 89.5% (51/57), and the control group was 74.5% (41/55). The total effective rate of cancer pain relief of the treatment group was 91.2%(52/57), and the control group was 70.9% (39/55). The improvement rate of life quality of the treatment group was 70.2% (40/57), and the control group was 49.1% (27/55). The differences between the two groups was significant (P<0.05). There was no difference in hematology toxicity, liver and kidney function, gastrointestinal adverse reactions and itchy skin incidence between the two groups (P>0.05). And the treatment group had a lower incidence of phlebitis than the control group (P<0.05). Conclusion Compound sophora injection combined with Java brucea fruit oil emulsion for palliative treatment can improve curative effect, significantly improve patients’ quality of life, it was a safe and effective way in treating advanced malignant tumors.

Based on comprehensive vocational ability,this article analyzed lesson presentation of nursing pharmacology by introducing the nature and function of this course,design idea,curriculum goal,curriculum content,curriculum implementation and curriculum evaluation.Through this activity,higher vocational teachers may change the comprehension of curriculum and improve the quality of teaching.

Objective To investigate the effect of transforming growth factor β receptor-Ⅱ(TGF-βRⅡ) on AngⅡ inducing glomerular mesangial cell(GMC) proliferation and the expressions of TGF-β1 and psmad3 through transfecting TGF-βRⅡsmall interfering RNA(siRNA)into GMC. Methods Through transfecting fluo-rescence control siRNA into GMC ,we observed the transfection efficiency under fluorescence microscope after 6 hours. Transfecting TGF-βRⅡsiRNA and negative control siRNA into GMC respectively ,we detected the expres-sion of TGF-βRⅡ by western blot after 24 hours. The cells were divided into four groups:control group,AngⅡgroup,negative siRNA control group and TGF-βRⅡ siRNA group. Each group was stimulated by AngⅡ except the control group. After 24 hours,we detected the TGF-β1 and psmad3 protein levels by western blot and detected GMC proliferation by CCK8 kit. Results (1) Comparing with the scrambled control group,the expression of TGFβRⅡin the TGF-βRⅡsiRNA group was significantly decreased(P<0.05).(2)AngⅡcould accelerate the expression of TGF-β1. Transfecting TGF-βRⅡsiRNA into GMC decreased the expression of TGF-β1 protein(P<0.05).(3)AngⅡ could stimulate the phosphorylation of smad3. Transfecting TGF-βRⅡ siRNA into GMC de-creased the expression of psmad3 protein(P < 0.05).(4)Transfecting TGF-βRⅡ siRNA into GMC relieved the GMC proliferation AngⅡ-promoted(P < 0.05). Conclusions The AngⅡ stimulates the GMC proliferation,de-pending on the expression of TGF-βRⅡ. It is related to the expressions of TGF-β1 and psmad3.

Objective To investigate the current situation and the development of autism rehabilitation service institutions in China. Methods The finance, supervision and management, recipients and rehabilitation standards of 117 autism rehabilitation service institutions were investigated with questionnaire and interview. Results Private service played an important role in autism rehabilitation, as 67.5% of all. The supervision was poor, and the age of the recipients were limited, and varied in standards of rehabilitation. Conclusion It is needed to support the private autism rehabilitation services with more supervision to make their service for all-age and more standardized.

Objective To study the molecular regulation mechanism of VEGF in the model of ATRA induced differentiation in HL-60 cells,and to provide new targets for leukemia anti-angiogenic therapy.Methods The morphology was observed by Wright-Gimesa staining; HL-60 cells differentiation was detected by NBT reduction experiment.VEGF,STAT3,c-myc mRNAs were measured by reverse transcription-PCR;VEGF,STAT3 and c-myc proteins were determined by Western blot.Results The proliferation of HL-60 cells was inhibited obviously by ATRA(1 μmol/L) with the induction of differentiation,NBT positive rate was 82.59％ (t =-24.157,P ＜ 0.01) ; VEGF mRNA (t =7.339,P ＜ 0.05),STAT3 mRNA (t =3.667,P ＜0.05) and c-myc mRNA (t =6.858,P ＜ 0.05) were all down-regulated.VEGF protein (t =3.386,P ＜0.05),STAT3 protein(t =4.074,P ＜ 0.05) and c-myc protein (t =3.333,P ＜ 0.05) were all down-regulated.Conclusion VEGF expression level is reduced with the procession of differentiation of HL-60 cells,which may be largely correlated with the down regulation of STAT3 and c-myc.

Objective To investigate the effect of hosphocreatine therapy on the plasma cardiotrophin-1(CT-1) and N terminal probrain natriuretic (NT-proBNP) in elderly hypertensive patients with heart failure. Methods A total of 76 hy-pertensive patients with heart failure, aged 65 or over, were randomly divided into treatment group and control group (n=38 for each group). The control group received routine anti-heart failure treatment. The treatment group received conventional therapy plus creatine phosphate sodium for 2 weeks. The plasma levels of CT-1 and NT-proBNP were determined in two groups. The plasma CT-1 level was measured by a double antibody sandwich enzyme-linked immunosorbent assay (ELISA). The plasma level of NT-proBNP was tested by Rui Pu fluorescent dry quantitative analyzer. Results The plasma levels of CT-1 and NT-proBNP were significantly lower after treatment in two groups (P＜0.01). The plasma levels of CT-1 and NT-proBNP were significantly decreased in treatment group than those in control group (P＜0.05). The total effective rate was 89.47%in treatment group, which was significantly higher than that of control group (71.05%, P＜0.05). Symptoms of heart failure improved in one week (21 cases in treatment group/9 cases in control group) and in two weeks (13 cases in treatment group/18 cases in control group). Conclusion The conventional therapy plus creatine phosphate sodium can decrease the plasma CT-1 and NT-proBNP levels in elderly hypertensive patients with heart failure, which improves symptoms of heart failure in a shorter period of time.

Objective To screen the mutation of KATP channel mutations in Chinese pedigrees with infantile onset type 1 diabetes mellitus (T1DM) and neonatal diabetes mellitus.Methods A cohort of 12 children of infant onset T1DM and neonatal diabetes mellitus admitted into Beijing Children's Hospital between March 2004 and June 2013 were selected.PCR amplification and direct sequencing were used to analyze the 39 exons of ABCC8 gene and one exon of KCNJ11.And the mutational sites of the parents of the probands was sequenced in order to identify the inheritance.Results Analysis revealed ABCC8 mutation in 25％ (3/12 cases) of the patients,a case of transient neonatal diabetes (TNDM),a case of permanent neonatal diabetes mellitus (PNDM) and a case of infant onset T1DM.All positive patients showed a known heterozygosis mutation in the ABCC8 gene(R1182Q,c.3545G ＞ A,D209E,c.627C ＞ G,E208K c.622G ＞ A).The residue R1182Q,which was located at a position involved in joining transmembrane domain 2 to nucleotide binding domain 2,the mutations E208K and D209E were located in the intracellular region that links the transmembrane domain with the gatekeeper module.All the three mutations were located throughout the cytoplasm part of SUR1 protein.The TNDM successfully transferred from insulin to oral sulfonylureas therapy.Conclusions There is a complex genetic pathogenesis in neonatal and infant-onset diabetes.The KATP channel activating mutations is one of the main causes of neonatal diabetes mellitus and may cause T1DM in infants in China.Oral Glibenclamide therapy seems highly effective for some patients with the KATP channel activating mutations.

Objective For Genistein has been reported to inhibit many tumors ,we investigate the role of autophagy in the proliferation inhibition to Hela cells by Genistein and the machanism of autophagy plays in this process.Methods Human cervical cancer Hela cells were divided into control group,Genistein group and 3-MA+Genistein group,the control group were cultured in RPMI 1640 medium supplemented with 10% fetal bovine serum(FBS),Genistein group were cultured in various concentrations Genistein(25,50,100μmol/L),3-MA+Genistein group were treated with 5mmol/L 3-MA for 1h before cultured in 100μmol/L Genistein.The proliferation inhibitory rate of Hela cells was detected by MTT method.The ultrastructure changes of Hela cells was observed under transmission electronic microscope(TEM).The levels of autophagy-associated protein P62 and Beclin-1 were detected by Western blotting analysis.The expressions of autophagy-associated proteins LC3A/B in Hela cells were determined by fluorescent staining to analyse the autophagy induced by Genistein in Hela cells.Results Compared with control group ,the proliferation inhibitory rate of Hela cells was 20.9%±1.3%,33.5%±1.6% and 46.5%±3.2% when cultured in 25,50,100μmol/L Genistein(P<0.01).After treated with various concentrations Genistein for 48h, we observed a dose-dependent increase in the expression of Beclin-1 and decrease of P62.Confocal laser scanning microscopy confirmed the fluorescent density of LC3A/B expression in Hela cells treated with 100μmol/L Genistein increased significantly as compared with control group.TEM showed there are many vacuoles and double-membrane autophagosomes which involved cytoplasmic components in Hela cells treated with 100μmol/L Genistein.The proliferation inhibitory rate of Hela cells of Genistein group is decreased as compared with those in 3-MA+Genistein group[(46.5±3.2)% vs (58.2±2.2)%,P<0.01].Conclusion Genistein could inhibit Hela cells proliferation and induce autophagy.

Aim To observe the ameliorating effects of sophocarpine on mice with neuropathic pain induced by spared nerve injury(SNI), and to explore the analgesic mechanism.Methods Sixty male ICR mice were randomly divided into six groups: sham-operated, neuropathic-pain model(SNI), SNI+Pregabalin(Pre) 10 mg·kg-1, SNI+SC 40 mg·kg-1, 20 mg·kg-1 and 10 mg·kg-1 group.Neuropathic-pain mouse models were established by SNI of the sciatic nerve.The paw withdrawal mechanical threshold(PWMT), paw withdrawal thermal latency(PWTL), and cold withdrawal times(CWT) were detected to assess the analgesic effects of sophocarpine on mice with neuropathic pain induced by spared nerve injury.The expressions levels of TLR4, p38 MAPK, IL-1β and TNF-α mRNA and protein in spinal cord tissue were detected by reverse transcription-polymerase chain reaction(RT-PCR) and Western blot methods.Results Compared with sham group, the SNI group′s PWMT decreased, PWTL was shorten, CWT increased, and the expression levels of p38 MAPK, TLR4, TNF-α and IL-1β mRNA and protein in spinal cord tissue were up-regulated.Compared with SNI model group, the sophocarpine 40 mg·kg-1 group′s PWMT increased, PWTL was lengthened, CWT decreased, and the expression levels of p38 MAPK, TLR4, TNF-α and IL-1β mRNA and protein in spinal cord tissue were down-regulated.Conclusion Sophocarpine has the analgesic effects on neuropathic pain induced by SNI, and its mechanism may be related to the down-regulation of TLR4, p38 MAPK, IL-1β and TNF-α expression levels.

Objective:To explore the effects of human recombinant erythropoietin (rhEPO) on inflammation of hyperoxic lung injury in neonatal rats.Methods:Seventy-two neonatal rats were randomly divided into 4 groups: control group, BPD group, hyperoxia + low-dose recombinant erythropoietin [EPO(L)]group, and hyperoxia + high-dose recombinant erythropoietin [EPO(H)]group.The neonatal rats in BPD group, hyperoxia + EPO(L)group and hyperoxia + EPO(H)group were exposed to 850 mL/L oxygen.Then the neonatal rats in hyperoxia + EPO(L)group and hyperoxia + EPO(H)group were given 800 IU/kg and 2 000 IU/kg rhEPO by subcutaneous injection respectively at 1 d, 3 d and 7 d, while the control group and BPD group were given the same amount of 9 g/L saline water.Initially, the body weight of each group was recorded at 3 d, 7 d and 14 d. The morphological structure changes of lung tissues were observed by HE staining under light microscope, and the radial alveolar count(RAC) in lung tissues were detected.The expression of nuclear factor kappa B(NF-κB) was detected by immunofluorescence staining; Western blot was applied to determine the protein expression of phosphorylated NF-κB(pNF-κB), inhibitor protein(IκB) and Caspase-3 in lung tissues; and the expression of interleukin-1β(IL-1β) in bronchoalveolar lavage fluid was determined using enzyme linked immunosorbent assay (ELISA).Results:(1) On the 14 th day, the body weight of neonatal rats in the BPD group was lower than that in the control group [(18.97±3.21) g vs.(27.97±2.30) g], and the difference was statistically significant( P<0.01); however, the body weights of neonatal rats in the hyperoxia+ EPO(L)group and hyperoxia+ EPO(H)group[(24.16±2.15) g, (26.04±1.97) g] was much heavier than that in the BPD group, and the differences was statistically significant(all P<0.05). (2) The morphological structure of lung tissues which was observed by HE staining showed that in the BPD group, there were a few inflammatory cells infiltration in alveolar septum on the 3 rd day, the inflammatory response was more evident on the 7 th day, when exudation could be seen in the alveolar cavity; and on the 14 th day, the number of pulmonary alveoli decreased, pulmonary bulla formed, and septa were thickened.Besides, it was also observed that compared with control group, RAC was significantly decreased in BPD group on the 14 th day(5.50±1.29 vs.14.33±2.80), and the difference was statistically significant( P<0.01). Pathological changes were ameliorated and the infiltration of inflammatory reaction cells was reduced in the hyperoxia+ EPO(L)group and hyperoxia + EPO(H)group.RAC was remarkably higher in the hyperoxia+ EPO(L)group and hyperoxia+ EPO(H)group than that in the BPD group on the 14 th day, and the differences were statistically significant (all P<0.05). (3)Immunofluorescence results showed that: the number of NF-κB p65 positive cells increased significantly and fluorescence intensity increased in the BPD group, while EPO could greatly reduce the number of NF-κB p65 positive cells and lower the fluorescence intensity.(4)Western blot results indicated that compared with the control group, the expressions of pNF-κB p65 and Cleaved Caspase-3 was significantly increased, and the differences were statistically significant (all P<0.05); and IκB was significantly lower, and the difference was statistically significant ( P<0.05). The expression of NF-κB p65 and Cleaved Caspase-3 was significantly lower, but IκB was significantly higher in the hyperoxia+ EPO(L)group and the hyperoxia+ EPO(H)group than those in the BPD group, and the differences were statistically significant (all P<0.05). (5) ELISA results revealed that the expression of IL-1β in the BPD group was significantly higher than that in the control group, and the difference was statistically significant ( P<0.05); Compared with BPD group, the expression of IL-1β was significantly lower in the hyperoxia+ EPO(L)group and hyperoxia+ EPO(H)group, and the differences were statistically significant (all P<0.05). Conclusions:EPO can reduce hyperoxia-induced lung tissue apoptosis and protect newborn rats against hyperoxic lung injury by decreasing the inflammatory response of cells through the NF-κB pathway on BPD.