Objective To analyze current situation of incentive mechanism and investigate the countermeasures.Provide the evidence for improving the incentive mechanism of scientific research at the hospital.Methods Questionnaire survey was conducted to investigate current situation and countermeasures of incentive mechanism of scientific research.Database was building using EpiData3.1,and was performed by descriptive analysis.Results 194 questionnaires were available.For the current incentive mechanism,86.5％ respondents thought the content is comprehensive,The over 50 years old,bachelor or below,and clinical examination group thought the content were less comprehensive.Respectively,81％,82.5％,76.2％ of respondents thought stimulation on achievements has positive effect to research,team work,and individual accounted for.The over 41 years old college or bellow,clinical treatment group felt less effect.For improving measures of incentive mechanism,the top three positions of contents were technological reward,high level project and SCI paper;and incentive methods were promotion,material rewards and training.Conclusions Incentive mechanism can promote scientific research to some extent.To further promote scientific research development,individual incentive measures need to be taken,the contents need to be expanded,variety incentive methods need to be used.

Science is the power of improving the academic discipline in hospitals.Evaluation of research has always be the key issue for research management.Using stratification method to establish the evaluation system was constructed directly by high level research output and based on the process of scientific,which can conduct quantitative assessment for individual level.The contents included three parts:process indicators,basic achievement indicators and high level achievements indicators.The implementation effect was satisfied during last year.The evaluation system stimulates high level research output.

Objective:To observe the protective effect of deproteinized extract of calf blood (DECB) on the kidney injury of the diabetic rats, and to discuss its mechanism preliminarily.Methods:The male Wistar rats were intraperitoneally injected with STZ (65 mg·kg-1) to establish the diabetes models, then the model rats were randomly divided into model (M)group, and metformin (MMet, 105 mg·kg-1) group , low dose of combined administration (ML,105 mg·k-1 metformin+94.5 mg·kg-1 ,DECB) group, medium dose of combined administration(MM, 105 mg·kg-1 metformin+ 189 mg·kg-1 DECB) group, high dose of combined administration(MH, 105 mg·kg-1 metformin +378 mg·kg-1,DECB) group, another ten Wistar rats were selected as normal control(NC)group.The rats were intragastrically administed with metformin and intraperitoneally injected with DECB, once a day, total of 8 weeks.The rats in NC group and M group were given normal saline solution.The weights and blood glucose levels of the rats in various groups were determined;the levels of serum high density lipoprotein-cholesterol (HDL-C), low density lipoprotein-cholesterol (LDL-C), blood urea nitrogen (BUN), urinary albumin (UAlb), urine creatinine (UCR), serum creatinine (SCr), total cholesterol (TC), triglyceride (TG), uric acid (UA), glutathione (GSH), and malondialdehyde (MDA) were detected;the activities of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) were determined.The pathological changes of kidney tissue of the rats in various groups were detected by HE staining.Results:Compared with NC group, the weight of the rats in M group was reduced(P<0.05),and the levels of blood glucose,UAlb,UCr,SCr,UA,BUN,LDL-C,TC,TG,and MDA were increased(P<0.05);the levels of HDL-C and GSH were obviously reduced(P<0.05),and the activities of SOD adn GSH-Px were obviously reduced(P<0.05).Compared with M group,the weights of the rats in MM and MH groups were increased (P<0.05), and the levels of blood glucose,UAlb,UCr,SCr,UA,BUN,LDL-C,TC,TG, and MDA were decreased (P< 0.05);the levels of HDL-C and GSH were increased (P<0.05),and the activities of SOD and GSH-Px were increased (P<0.05).The pathological observation of kidney tissue showed that the rats in M group had obvios kidney tissue lesions with glomerular congestion and renal tubular edema compared with NC group;compared with M group,the pathological changes of the kidney tissue of the rats in drug administration groups were significantly improved, the renal tubular vacuoles were reduced, and the interstitial hyperplasia was not obvious.Conclusion:DECB combined with metformin can reduce the blood glucose level, regulate blood lipid, improve the pathological changes of kidney tissue in the diabetic rats, reduce the renal damage, and enhance the antioxidant capacity of the body.

Objective:To observe the protective effect of deproteinized extract of calf blood (DECB)on the ethanol-induced liver injury of the mice,and to preliminaryly discuss its mechanism. Methods:Sixty healthy ICR mice were divided into control group,model group,positive drug group,low,medium and high doses of DECB groups (n=10).By intragastric administration,the mice in control group were given 20 mL·kg-1 saline solution, the mice in low,medium and high doses of DECB groups were administrated with 0.125,0.250,0.500 g·kg -1 DECB,and the mice in positive drug group were administrated with 0.63 g·kg -1 Hugan Tablets;once a day for 30 d. 1 h after the last administration,except control group,the mice in other groups were administrated with one-time grant of 50% ethanol 14 mL·kg -1 ,and fasted for 16 h to establish the models of acute alcohol liver injury.The endurance alcohol time and drunk time of the mice were determined,the activities of aspartate aminotransferase (ALT)and alanine transaminase (AST)activity in serum of the mice were detected,the levels of triglyceride (TG),glutathione (GSH)and malonic dialdehyde (MDA)in liver tissue were determined,and the pathological changes of liver tissue were detected.Results:Compared with model group,the drunk symptoms of the mice in different doses of DECB groups were obviously reduced,the endurance time of the mice in high dose of DECB group and positive drug group was prolonged (P <0.05),and the drinking time was shortened (P <0.05);the ALT and AST activities in serum in mediun and high doses of DECB groups were significantly lower than those in model group (P <0.05).Compared with model group,the MDA and TG levels in liver tissue of the mice in medium and high doses of DECB groups and positive drug group were obviously reduced,and the GSH levels were increased (P <0.05);compared with model group,the pathological damages of liver tissue of the mice in high dose of DECB group caused by ethanol were significantly reduced.Conclusion:DECB can improve ethanol-induced liver injury which may be related to the inhibition of hepatic oxidative stress response.

Objective To investigate clinical and myopathological features and genetic mutations of GNE myopathy.Methods The clinical manifestations and pathological findings of 4 patients were reviewed who had been treated for GNE myopathy at Department of Neurology,The People's Hospital of Zhengzhou University from January 2016 to July 2017.The exons of GNE gene were sequenced to detect gene mutations in all of them.Results Onset of the disease started at late adolescence or early adulthood in the 4 patients (2 siblings).Gait disturbance appeared as an initial symptom.The disease progressed slowly and the distal muscles were more affected than the proximal ones.Muscle magnetic resonance imaging revealed that the soleus and the anterolateral muscles of the lower leg were the most severely involved and the internal and posterior compartments of the thigh muscles were more involved than the anterior one.The characteristic pathological finding was presence of rimmed vacuoles.Two siblings (Patients 1 and 2) both had the same compound heterozygous mutations of p.G395R and p.D207V,patient 3 had the compound heterozygous mutations of p.D207V and p.G166D,and patient 4 had the homozygous mutation ofp.G237D.Conclusions Sparing of the quadriceps relatively is a very unique feature of GNE myopathy.Missense mutations (G395R and G237D) may be 2 new ones in the GNE gene.