According to the requirement of promoting the reform of personnel system reform in the public hos -pital reform, based on characteristics of labor dispatch and the meaning of job insecurity , analysis the impact on em-ployee job performance of job insecurity factors .We put forward the improvement proposal in four aspects that are hospital culture , perceived organizational support , organizational justice and employee number , which is combined with the requirements of the medical and health system reform .

As a new biotechnology, protein transduction connects the target fragment with biology active and protein transduction domain, and transducer it in to cells, exert its biological effects. Protein transduc-tion domain is a small molecule peptide, not only the protein transduction domain can penetrate through cell membrane, but could maintain the activity of its fusion protein. Protein transduction is an emerging biology technology, it has been applied into all aspects of cell gene regulation since its invention. In this article, we take Tat, Pdx-1 and Beta/NeuroD for instance and review the application of transduction protein in the dif-ferentiation of pancreatic stem cell.

Objective To observe the effect of wheel running exercise on subventricular zone neurogenesis and the neural function in rats post cerebral ischemia. Methods 48 adult male Sprague-Dawley rats were induced cortical infarcts with left middle artery occlusion and were housed in either standard (control group, n=24) or wheel running (exercise group, n=24). They were assessed with neurological severi-ty scores (NSS), and the expression of Ki67 was determined with immunofluorescence, 3, 7, 14 and 21 days after training. Results Com-pared with the control group, the number of Ki67-labeled cells in subventricular significantly increased in the exercise group 14 and 21 days after ischemia (P<0.05), and the NSS decreased since 7 days after ischemia (P<0.05). Conclusion Wheel running may promote the neuro-genesis in subventricular of adult rats after cerebral infarction, which may associate with the recovery of neural function.

Objective To observe the clinical effect of recombinant human growth hormone(rhGH) in the treatment of Turner syndrome(TS).Methods The clinical data of 40 children with TS who were treated with rhGH were retrospectively analyzed.Results After treatment for 6 months,the GV,IGF-1 levels [(9.4 ± 2.7) cm/a,(433.9 ± 164.9)μg/L] were significantly higher than those before treatment [(2.5 ± 0.4)cm/a,(186.7 ± 7.33) μg/L],the differences were statistically significant(t =45.562 5,5.061 0,all P ＜ 0.05).The treatment dose of rhGH,initial treatment age had no significant relationship with GV,the GH peak before treatment had no significant correlation with GV.There was no obvious adverse reactions in the treatment process.Conclusion For children with TS,rhGH can improve the height,improve the therapeutic effect,reduce the burden of family and society.Low dose of rhGH in the treatment of TS can achieve better curative effect,the initial treatment age and growth rate in children had no obvious relationship,the insulin growth factor is an important index during the treatment,and the changes of insulin growth should be closely monitored,and adjusting the dosage of the drug in order to achieve the best therapeutic effect.

Objective To study the effect of growth hormone on serum levels of Ghrelin, leptin(LP), insulin like growth factor-1(IGF-1) and insulin-like growth factor binding protein 3(IGFBP3) in children with idiopathic short stature(ISS).Methods 86 patients of ISS who received therapy from September 2013 to September 2015 were selected.According to random number table,those patients were divided into observation group ( n=43) and the control group (n=43).Control group was treated with routine nutrition therapy, while the observation group was added with recombinant human growth hormone.The Ghrelin, LP, IGF-1, IGFBP3 levels and height pre-and post-treatment were compared.Results After treatment, the level of Ghrelin in observation group [ ( 4.85 ±0.41 ) ng/mL ] was lower than that of control group [ ( 5.63 ±0.62 ) ng/mL ] , the level of LP [ ( 6.53 ± 0.78)mg/L] was higher than that of control group[(5.49 ±0.62)mg/L](all P<0.05); the levels of IGF-1[(387.94 ±47.38)ng/mL] and IGFBP3 [(6.74 ±0.73)μg/mL]in the observation group were higher than that of the control group[(243.54 ±36.82)ng/mL,(4.85 ±0.61)μg/mL](all P<0.05); the height in the observation group[(110.17 ±8.12)cm] was higher than that of control group[(114.58 ±9.40)cm](P<0.05).Conclusion Recombinant human growth hormone is well for ISS, which can effectively improve Ghrelin, LP, promote physical growth IGF-1, IGFBP3 levels, promote growth.

Objective_To explore the effect and the mechanism of isoflurane on human cardiac myocytes ( HCM) injury induced by anoxia/reoxygenation ( AR) .Methods_HCM cells were divided into control group ( con) , an-oxia/reoxygenation group (AR) and isoflurane (0.5%, 1%, 1.5%and 2%) treatment group (n=6).Cell via-bility, LDH activity, apoptosis and the expression level of Anoxia inducible factor-1α( HIF-1α) were detected using CCK-8 assay, LDH activity assay kit, Annexin V-FITC/PI staining, PCR and western blot, respectively. Results_Compared with the con group, cell viability decreased, LDH activity and apoptosis cells increased in AR group.Isoflurane can significantly relieve the decrease of cell viability, the increase of LDH activity and apoptosis cells, and the down-regulation of the mRNA and protein expression level of HIF-1αinduced by AR ( P<0.05 ) . Compared with AR group, the mRNA and protein expression level of HIF-1αin siRNA transfected group signifi-cantly decreased (P<0.05).2%isoflurane significantly relieve the increase of cell viability, the decrease of LDH activity and apoptotic cells induced by HIF-siRNA in AR injuried HCM cells(P<0.05).Conclusions_Isoflurane can protect HCM cells from AR injury partly through up-regulate the expression of HIF-1α.

Immune thrombocytopenia (ITP) is the most common hemorrhagic disease in childhood,and immunological abnormality is the most common cause of this disease.Humoral immune abnormalities are the major cause of ITP,involving platelet,platelet membrane surface glycoproteins associated antibodies,impaired Breg cells and upregulation of platelet Toll like receptors.Cellular immune abnormalities include the imbalance of Th1/Th2 cells results in increased inhibitory cytokines [interleukin (IL)-2,interferon-α,tumor necrosis factor-β],IL-17 and Th17 cells in patients with chronic ITP are higher than those in control group,and Treg decline is also common seen in ITP.Increased expression of apoptosis related genes Bak and Bax are also the cause of chronic ITP.Helicobacter pylori is an important cause of chronic ITP,which can be eased in some cases but not effective in new diagnosed cases.Vaccination can lead to ITP,repeated vaccines are applied usually in 3-6 months after the onset.

Adolescent ; Child ; Electroencephalography ; Female ; Fructose ; analogs & derivatives ; therapeutic use ; Humans ; Male ; Migraine Disorders ; diagnostic imaging ; drug therapy ; physiopathology ; Ultrasonography, Doppler, Transcranial

Adolescent ; Adult ; Female ; Herbicides ; poisoning ; Humans ; Male ; Middle Aged ; Paraquat ; poisoning ; Rural Population ; Young Adult