Objective To study the views of clinical nursing staff about current nursing quality evaluation so as to find the problems in nursing quality evaluation.Method 25 head nurses and nurses were interviewed using semi-structured open interview about nursing quality evaluation.Result The current nursing quality evaluation system was lower in sensitivity,focusing more on nursing skills but less on nursing evaluation of nursing specialties.Conclusions The system of current nursing quality evaluation lacks of nursing evaluation of nursing specialties and therefore cannot meet the requirements for the development of nursing specialty. Therefore,it is urgent to regulate an evaluation system for nursing specialties.

0.05),respectively.The fractured adheisive dentin surface was mainly a mixed failue mode.Conclusions:There is no significant difference in the bond strengths of each of the three bonding agents to ND and CAD.

Adenoma, Acidophil ; metabolism ; Adult ; Angiomyolipoma ; genetics ; metabolism ; pathology ; Carcinoma, Renal Cell ; metabolism ; Codon ; Diagnosis, Differential ; Exons ; Female ; Follow-Up Studies ; Gene Deletion ; Genes, p53 ; Humans ; Kidney Neoplasms ; genetics ; metabolism ; pathology ; Male ; Melanoma-Specific Antigens ; metabolism ; Middle Aged ; Retrospective Studies ; Tumor Suppressor Protein p53 ; genetics ; metabolism

To investigate the effect of C/EBP βon the neuroinflammation.Recently,neuroinflamma-tion research mainly focused on C/EBP β,more and more researches indicated that C/EBP βmay play an important role in neurodegenerative diseases.We searched the published papers in PubMed,CNKI,and Wan Fang date bases in June 2015.The key words were used asCCAAT enhancer binding protein beta,Neu-ron,Neuroinflammationand so on.According to the inclusion and exclusion criteria, we summaried and analyzed the literatures.Eventually,42 articles were adapted,most of which were foused on the functions and mechanisms of C/EBP βin neuroinflammation.C/EBP βparticipate in multiple signaling pathways of neu-roinflammation,and the regulation mechanism is complicated.Abrogation of C/EBPβexpression or its down-regulation by gene regulation may may serve as a therapeutic target to attenuate deleterious effects in neural tissue and ultimately prevent the development of neurodegenerative disorders.

Objective: To study the effects of vitamin E and selenium on apoptosis and c-Myc expression in human leukemia cells. Methods: DNA gel electrophoresis and Northern blotting hybridization were used to detect the apoptosis and the expression of c-Myc gene, respectively. Human leukemia cell line HL-60 and K562 were cultured in vitro. Results: The apoptosis of HL-60 and K562 cells were induced after being exposed to vitamin E (100 ?mol/L) and selenium (8 ?mol/L) for 24 hours, respectively. In HL-60 cell line, c-Myc mRNA was down-regulated significantly by vitamin E(100 ?mol/L),but not selenium(8 ?mol/L).In contrast, the expression of c-Myc gene was repressed by selenium(8 ?mol/L) and not by vitamin E(100 ?mol/L) in K562 cell. Conclusion: Our observations suggest that c-Myc down-regulation and induction of apoptosis by selenium and vitamin E are important pathways in repressing leukemia cell proliferation.The results suggest there are different mechanisms of repressing leukemia cell proliferation for selenium and vitamin E.

Objective To investigate the correhtion between cognitive impairment and cerebral atherosclerosis in patients with acute ischemic stroke.Methods Acute ischemic stroke patients without cognitive impairment were recruited before symptom onset.The Montreal cognitive assessment (MoCA) was used to evaluate the cognitive function.Magnetic resonance imaging (MRI) was used to identify the infarct locations and sides.Magnetic resonance angiography,CT angiography and digital subtraction angiography were used to identify atherosclerotic arteries.Resul~ A total of 101 patients with acute ischemic stroke were enrolled,including 75 (74.3％) with cognitive impairment.The proportions of age (54.54 ± 12.59 years vs.64.43 ± 10.37 years;t =-3.960,P ＜0.001),years of education ≤6 years (50.7％ vs.11.5％;x2 =12.257,P ＜ 0.001),and cerebral atherosclerosis (89.3％ vs.50.0％;x2 =18.137,P ＜0.001) of the cognitive impairment group were significantly higher than those of the normal cognitive function group.Multivariate logistic regression analysis showed that cerebral atherosclerosis was an independent risk factor for cognitive impairment in patients with acute ischemic stroke (odds ratio 1.720,95％ confidence interval 1.005-2.942;P=0.048).MoCA score was negatively correlated with the offending vessels (r=-0.365,P＜ 0.001) and the most severe vessels of atherosclerotic degree (r=-0.243,P =0.014).Conclusions Most patients with acute ischemic stroke had cognitive impairment in the early stage after onset,and the MoCA scores was negatively correlated with the degree of cerebral atherosclerosis.Cerebral atherosclerosis was an independent risk factor for cognitive impairment in patientswith acute ischemic stroke.

Objective To survey the knowledge requested by patients with coronary artery disease (CAD) after stent implantation.Methods A survey on CAD and stent-related knowledge requested by CAD patients with stent implantation was conducted with a self-designed questionnaire from September 2013 to November 2013.Total 362 patients (235 males and 127 females) aged (67 ± 12) years participated in the survey in Yuetan Community Health Service Center and Fuxing Hospital in Beijing.Open questions and heuristic questions were used together during the survey.Results The knowledge requested by patients were:diet management(255,70.4％),side effects of medication(241,66.6％),management of physical activity (221,61.0％),prevention of CAD(181,50.0％),withdrawal of medication(176,48.6％),the life of stents (168,46.4％),post-operation check-up items (162,44.8％),the causes of CAD (156,43.1％)and drug mechanisms(134,37.0％).Patients with stent implantation less than one year requested more knowledge about the cause of CAD (x2 =37.4,P ＜ 0.001),life-time of stent (x2 =39.9,P ＜0.001),prevention of CAD (x2 =13.4,P =0.001),post-operation check-up items (x2 =21.2,P =0.001) and requested less knowledge about withdrawal of medication (x2 =9.56,P =0.008),diet management (x2 =6.49,P =0.04) than those with more than one year.Patients aged ＜ 70 years requested more knowledge about the cause of CAD (x2 =31.6,P ＜ 0.001),prevention of CAD (x2 =9.99,P =0.007),life-time of stent (x2 =79.1,P ＜ 0.001),side effects of medication (x2 =7.84,P =0.02) than patients aged ＞ 70 years.Patients with education higher than junior high school requested more knowledge about the cause of CAD (x2 =26.6,P ＜ 0.001),prevention of CAD (x2 =14.4,P =0.001) and life-time of stents (x2 =7.82,P =0.02) than those with education lower than junior high school.Patients with education higher than junior college requested more knowledge about the cause of CAD (x2 =26.6,P ＜ 0.001) and post-operation check-up items (x2 =10.7,P =0.005) than those with education lower than junior college.Conclusion Some factors affect the knowledge requested by patients with coronary artery disease (CAD) after stent implantation,which should be considered in health education for CAD patients.

Objective To study the effect of lentinan on cisplatin’s inhibition on cervical cancer Hela cell line. Method Cervical cancer Hela cell line were divided into LEN group (only lentinan treatment), CIS group (only Cisplatin treatment), LEC group (Both Lentinan and Cisplatin treatment) and CON group (no Lentinan and Cisplatin treatment) according to their treatment methods. The differences of cell proliferation, cell cycle, PI and apoptosis were compared. Results The differences of absorbance between LEN group and CON group were not significant d1-d8 after treatment, but significant between CIS and LEC group (P<0.05). The absorbance in LEC group was significantly lower than in CIS group (P<0.05). The differences of PI and apoptosis rate in LEC and CIS group were significant (P<0.05), but not between LEN and group. The PI in LEC group was lower than in CIS group (P<0.05), while apoptosis rate was higher (P<0.05). Conclusion Lentinan could significantly promote Cisplatin’s inhibition effects on cervical cancer Hela cell line.

HSP90, which is the biomarker of cell stress and endogenous protective protein, functions as a molecular chaperone. Many client proteins of HSP90, including EGFR, Met, Raf-1, IKK and p53, play important roles in the occurrence and development of tumor. Binding of HSP90 inhibitors triggers the deactivation of HSP90, resulting in client protein degradation, and hence inhibits the tumor growth by blocking multiple targets involved in signaling of tumor proliferation. This review summarizes recent development of small molecule inhibitors bound to N-terminal of HSP90.

To investigate whether glutamate and voltage-gated calcium channels-independent calcium influx exists during acute anoxic neuronal damage and its possible relationship to neuronal protective function of NGF. In in vitro model of acute anoxia, hippocampal cultures from newborn rats were exposed to 3 mmol/L KCN. Changes of intracellular Ca(2+) concentration ([Ca(2+)](i)) were monitored by con-focal imaging and cell viability was assayed by PI and cFDA staining. The results showed that after treatment with primary hippocampal cultures with 3 mmol/L KCN for 15 min, [Ca(2+)](i) was significantly increased 6.27-fold compared to pre-anoxia level and 73.3% of the cells died. When combination of 20 mumol/L MK-801 (glutamate receptor antagonist), 40 mumol/L CNQX (AMPA receptor antagonist) and 5 mumol/L nimodipine (voltage-gated calcium channel antagonist) (hereafter denoted as MCN) were administrated to hippocampal cultures, levels of [Ca(2+)](i) and cell death rate induced by KCN were partially reduced by 35.9% and 47.5% respectively. However, Gd(3+) (10 mumol/L) almost completely blocked KCN-mediated [Ca(2+)](i) elevation by 81.9% and reduced neuronal death by 88.8% in the presence of MCN. It is noteworthy that NGF, used in combination with MCN, inhibited KCN-induced [Ca(2+)](i) increase by 77.4% and reduced cell death by 87.1%. Only PLC inhibitor U73122 (10 mumol/L) abolished NGF effects. It is concluded that Gd(3+)-sensitive calcium influx, which is NMDA (glutamate receptor) and voltage-gated calcium channels-independent, is responsible for acute anoxic neuronal death. NGF can inhibit Gd(3+)-sensitive calcium influx and reduce anoxic neuronal death through activating PLC pathway.