Objective: To examine the protective effect and its mechanism of hawthorn on human vascular endothelial cells. [WT5HZ]Methods: [WT5BZ]Original human umbilical vein endothelial cells (ECs) were cultured, and the changes of cell morphology, cell growth condition, lactate dehydrogenase (LDH) released from cells, monocyte (MC) adhesion to EC, and thiobarbituric acid reaction substance (TBARS) were measured when ECs were incubated with oxidized low density lipoprotein (OxLDL,100 mg/L) in the presence or not of hawthorn, as well as with hawthorn alone at three different doses (25,50,100 mg/L). [WT5HZ]Results: [WT5BZ]ECs survival rate of oxLDL group was lower (P

Objective: To examine the effects of four organic acids (OA), namely chlorogenic acid (CHA), ascorbic acid (AA), citric acid (CA) and malic acid (MA), on monocyte chemotactic protein-1 (MCP-1) and monocyte colony stimulating factor (M-CSF), as well as on antioxidant function in human vascular endothelial cells (EC). Methods: Original human umbilical vein EC were cultured and incubated for 12 h respectively with ox-LDL, in the presence of CHA, AA, CA and MA at different concentrations(10, 20, 40 mg/L), to study the protective effect on human vascular EC and its mechanism . Results: (1) TBARS value of oxLDL group was 14.85 times higher than that of normal LDL group which was not different with blank group. TBARS values of the OA+oxLDL group were lower at different extents when compared with ox-LDL group, showing dose-effect response. The inhibitory effects of CHA and AA were better than those of CA and MA. (2) MCP-1 and M-CSF of ox-LDL group were higher than those of blank group. Both MCP-1 and M-CSF of OA+ox-LDL groups statistically decreased when compared with ox-LDL group; MCP-1 and M-CSF of single CHA or AA (40 mg/L)group were lower than those of blank group respectively. Conclusion: The protective effects of OA on human vascular EC were contributed to their antioxidant activities, probably through MCP-1 and M-CSF .

Objective To explore the modulation of chlorogenic acid (CGA) on glucose metabolism in HepG2 cells pretreated with high insulin and high oleic acid (OA). Methods Cultured HepG2 cells induced by high insulin and oleic acid for insulin resistance and steatosis respectively, were co-cultured with different concentrations of CGA (10,20,40,80 mg/L) for 24h. The morphological changes were observed and glucose consumptions of cells were measured by glucose oxidase method. Results Compared to control group, CGA could significantly increase glucose consumption of normal HepG2 cells and the dosedependent effect was noted between 10-40 mg/L(P

Objective: To study the nutritional status and problems of Chinese elite athletes for instructing training scientifically. Method: 599 elite athletes were investigated by means of dietary survey, physical measure and biochemical detection. Results: (1) The daily average energy intake reached the adequate intake (AI) recommended for athletes, but the energy ratio both of protein and fat higher, carbohydrate lower, being 18.9%, 38.6% and 42.5% respectively. Except vitamin A and B1, B2 the intakes of other vitamins and minerals were sufficient. (2) The average BMI and body fat percentage were 23.0?3.0 and (12.1?3.2)% in men and 21.9?3.0 and (20.5?3.9)% in women respectively. (3) The average hemoglobin levels were (145.7?13.3)g/L in men and (130.6?11.8)g/L in women. The rates of anemia and iron deficiency anemia were 12.6% and 5.2% respectively, female higher than male. (4)The hyperlipidemia rate was 22.3%, including 12.6% high TG, 9.7% high TC and 1.2% high LDL, female higher than male. (5) The rates of VB1 and VB2 insuficiency were 46.2% and 32.7% respectively, both including 9.6% deficiency. Conclusion: The nutritional status of Chinese elite athletes was good, but still with anemia, vitamin insufficiency and hyperlipidemia.

Purpose To study the effect of overexpressing either wild type or a familial Alzheimer disease mutant presenilin 1 (mPS1) on tau phosphorylation in neuroblastoma NG-108 cells. Methods Three different plasmids transfected NG-108 cells respectively. Immunostaining and confocal microscopic technique were used to study the distribution of presenilin 1 and phosphorylated tau. Immunoblot test was applied to investigate the change of tau phosphorylation. Results Immunostaining showed that in brain of sporadic Alzheimer disease, PS1 mainly distributed in neuron and partially colocalized with the phosphorylated tau. Immunoblot tests showed that the cells transected either wild type PS1 or mPS1 contained more phorphorylated tau than the control cells. However, MTT test showed no significant difference between mock transfected cells and the wPS1 or mPS1 transfected cells. In addition, after transfection of the constructed PS1-EGFP vector, overexpressed EGFP-PS1 was located at cell surface membrane and subcellular organelles at earlier time at 12 hr, then EGFP-PS1 diffused in cytosol. Immunocytochemical observations demonstrated that some of the PS1-EGFP transfected cells contained more phosphorylated tau protein, which formed aggresome with PS-1-EGFP. When treated with phosphotase inhibitor okadaic acid, in the PS1-EGFP transfected cells accumulated more phosphorylated tau than the un-transfected cells. Conclusions Wild type PS1 is possibly involved in tauopathy in sporadic Alzheimer's disease.

Purpose To explore the practical significance of TERC gene amplification by fluorescence in situ hybridization ( FISH) on the differential diagnosis of cervical intraepithelial neoplasias 1 and 2 by tissue microarray. Methods A total of 42 cases of cervical tissue samples were selected, including 20 cases of normal cervix, 22 cases of cervical intraepithelial neoplasia (CIN) 1/2 (8 cases of CIN1 and 14 CIN2). Homemade tissue microarray was prepared. TERC gene amplification was detected with FISH method. Results TERC gene showed no amplification in the normal cervical squamous epithelium. TERC gene amplification was detected in 22. 7%(5/22)CIN1 and 77. 3%(17/22) in CIN2. 1/8 cases of TERC gene amplification in CIN1, 4/14 cases of TERC gene amplification in CIN2. There were significant differences in TERC gene amplification between those groups (P<0. 05). Conclusion The method is feasible and reliable in the detection of TERC gene amplification in CIN1/2 on paraffin sections. It has practical values in differential diagnosis between CIN1 and CIN2.

Objective To find out the present situation and influence factor in core capabilities of nurses of blood purification, and offer reference frame for evaluation, selection, authentication and engagement of nursing post. Methods Core capability training module for nurses of blood purification was selected as theoretical basis for rough draft of evaluation index system establishment. The selected index underwent expert consultation with Delphi method. Results Four hierarchy were confirmed after 3 rounds of consultation (N1-1,N 1-2, N2, N3). Each hierarchy had three evaluation indexes, knowledge, technology and clinical practice. Number of grade one evaluation indexes of each hierarchy was 5,5,4; 5,5, 4;5,5,5; 5,5,1. Number of grade two evaluation indexes was 20,20,24;20,20,20;25,25,48;23,24,14.Only N1- 1,N1-2 and N2 had grade three evaluation indexes, 16, 5, 13 respectively. Conclusions Preliminary establishment of core capability evaluation index system can basically evaluate capability of nurses of blood purification.

Objective To find out the present situation and influence factor in core capabilities of nurses that with blood purification skills in 18 hospitals, and offer reference frame for training. Methods The questionnaires were used to investigate, theresults underwent analysis. Results Among three parts of core capabilities, total score of N1-2 made the highest,the mean score was 236.75,N3 score made the lowest,the mean score was 168.00. The percent of pass in every hierarchy didn't passed 50%. Using the multiple regression to analyze the factor,N1-1 was the work experience in department of nephrology;N3 was the training time of blood purification. Conclusions Percent of pass in core capabilities of nurses of blood purification is in a low level,every hospital should follow the principle of recruitment,and regulate the training of nurses in blood purification.

OBJECTIVE To investigate the effect of neferine （NEF） on mitophagy in Parkinson’s disease （PD） cells by regulating the adenosine monophosphate-activated protein kinase （AMPK）/mammalian target of rapamycin （mTOR）/UNC-51-like kinase 1 （ULK1） signaling pathway， and explore the mechanism of this drug to improve PD. METHODS SH-SY5Y cells were treated with 100 μmol/L 1-methyl-4-phenylpyridinium ion （MPP+） for 24 h to construct a PD cell model. PD model cells were divided into model group （PD group）， NEF low-， medium- and high-concentration groups （NEF-L， NEF-M， NEF-H group， 2.5， 5.0， 10.0 μmol/L）， and high concentration of NEF+AMPK inhibitor group （NEF-H+Compound C group， 10.0 μmol/L NEF+50 μmol/L Compound C）. The cells treated without MPP+ and NEF were used as the control group. The ultrastructure of the cells in each group was observed； the amount of autophagosomes， survival rate， apoptosis rate， mitochondrial membrane potential， and the protein expressions of Caspase-3， microtubule-associated protein 1 light chain 3 （LC3） and Beclin-1， as well as the phosphorylation levels of mTOR， AMPK and ULK1 were detected. RESULTS Compared with PD group， the amount of autophagosomes in NEF-L， NEF-M and NEF-H groups was increased， and membrane potential was increased； survival rate， LC3- Ⅱ/LC3-Ⅰ， protein expression of Beclin-1， and protein phosphorylation levels of AMPK and ULK1 were significantly increased or up-regulated； the apoptotic rate， protein expressions of Caspase-3 and p62， and protein phosphorylation level of mTOR were significantly decreased or down-regulated， and the above improvements were in a dose-dependent manner （P＜0.05）. Compound C could significantly reverse the above improvement effect of high concentration of NEF （P＜0.05）. CONCLUSIONS NEF can promote mitophagy and inhibit apoptosis of PD model cells by up-regulating protein phosphorylation levels of AMPK and ULK1， and down-regulating protein phosphorylation level of mTOR， thus playing a protective role in nerve cells.

OBJECTIVE To investigate the effect of neferine （NEF） on mitophagy in Parkinson’s disease （PD） cells by regulating the adenosine monophosphate-activated protein kinase （AMPK）/mammalian target of rapamycin （mTOR）/UNC-51-like kinase 1 （ULK1） signaling pathway， and explore the mechanism of this drug to improve PD. METHODS SH-SY5Y cells were treated with 100 μmol/L 1-methyl-4-phenylpyridinium ion （MPP+） for 24 h to construct a PD cell model. PD model cells were divided into model group （PD group）， NEF low-， medium- and high-concentration groups （NEF-L， NEF-M， NEF-H group， 2.5， 5.0， 10.0 μmol/L）， and high concentration of NEF+AMPK inhibitor group （NEF-H+Compound C group， 10.0 μmol/L NEF+50 μmol/L Compound C）. The cells treated without MPP+ and NEF were used as the control group. The ultrastructure of the cells in each group was observed； the amount of autophagosomes， survival rate， apoptosis rate， mitochondrial membrane potential， and the protein expressions of Caspase-3， microtubule-associated protein 1 light chain 3 （LC3） and Beclin-1， as well as the phosphorylation levels of mTOR， AMPK and ULK1 were detected. RESULTS Compared with PD group， the amount of autophagosomes in NEF-L， NEF-M and NEF-H groups was increased， and membrane potential was increased； survival rate， LC3- Ⅱ/LC3-Ⅰ， protein expression of Beclin-1， and protein phosphorylation levels of AMPK and ULK1 were significantly increased or up-regulated； the apoptotic rate， protein expressions of Caspase-3 and p62， and protein phosphorylation level of mTOR were significantly decreased or down-regulated， and the above improvements were in a dose-dependent manner （P＜0.05）. Compound C could significantly reverse the above improvement effect of high concentration of NEF （P＜0.05）. CONCLUSIONS NEF can promote mitophagy and inhibit apoptosis of PD model cells by up-regulating protein phosphorylation levels of AMPK and ULK1， and down-regulating protein phosphorylation level of mTOR， thus playing a protective role in nerve cells.