Objectives:To understand the patients' cognition and satisfaction with public welfare in public hospitals.Methods:A questionnaire survey was conducted among 600 patients in Beijing municipal public hospitals and the data was statistically analyzed by SPSS 22.0.Results:Patients' understanding of public welfare was not ideal,the satisfaction was quite well,and the satisfaction of the patients in the experimental hospitals was more satisfactory than those in non-experimental hospitals.The patients have urgent needs on rational drug use,mutual recognition of medical results,smooth channels of patient rights,reduced medical expense and shortened waiting time.Conclusions:It should strengthen the publicity and governance of the public welfare of public hospitals to enhance the patients' understanding,breakthrough the urgent needs of public welfare to improve patients' satisfaction,and intensify the policy linkage and explore diversified implement forms of public welfare to improve service level.

Aged ; Female ; Humans ; Leukocyte Common Antigens ; metabolism ; Peroxidase ; metabolism ; Sarcoma, Myeloid ; metabolism ; pathology ; Vulva ; metabolism ; pathology ; Vulvar Neoplasms ; metabolism ; pathology

Action Potentials ; Animals ; Female ; Heart ; physiology ; Male ; Membrane Transport Proteins ; genetics ; Mice ; Mice, Knockout ; Myocardium ; metabolism ; Patch-Clamp Techniques ; Sodium Channels ; physiology

Adult ; Aged ; Asteraceae ; Drugs, Chinese Herbal ; adverse effects ; Female ; Hepatic Veno-Occlusive Disease ; chemically induced ; Humans ; Male ; Middle Aged ; Retrospective Studies

Objective To evaluate the cost-effectiveness of early enteral nutrition (EEN) in elder patients undergoing gastrectomy for gastric carcinoma. Methods An outcome-based retrospective review of 52 patients who had undergone gastrectomy for gastric carcinoma between July 1999 and June 2002 was performed .There were 27 patients in the EEN group, and 25 in the TPN group. Results The mean postoperative hospital days of the EEN group was significantly less than that of the TPN group (16.3 d vs. 21.3 d, t =4.6814, P

Objective To investigate if the 23 strains of highly-resistant P.aeruginosa isolated from different patients in the in- tensive care unit (ICU) have the same origin;and explore the related mechanisms of carbapenem resistance in these multidrug- resistant P.aeruginosa.MethOds Antimicrobial susceptibility testing was performed using disk-diffusion technique.The strains were genotyped by rep-PCR with the primer ERIC2 followed by electrophoresis in agarose gel.We used a previously described imipenem-EDTA double-disk test for screening MBL-producing P.aeruginosa.Polymerase chain reaction for amplification of blaOprD, blaIMP, and bla VIM were performed to detect corresponding mutants.Results The result of antimicrobial suscepti- bility testing showed that 20 of the 23 P.aeruginosa isolates were muhidrug-resistant and highly resistant to imipenem and meropenem, and at least 5 antimicrobial agents tested in this study.The analysis of the rep-PCR products indicated that all the 19 carbapenem-resistant strains had an identical band pattern, which was different from that seen in the sensitive strains.Al- though imipenem-EDTA double-disk test identified 5 MBL-producing strains, PCR found that all the 23 strains were negative for bla VIM and blaIMP.Only one OprD-deficient mutant was identified.Conclusions The 19 highly-resistant strains of P. aeruginosa derive from a common origin.More researches are needed to clarify their mechanism of carbapenem resistance.

Objective To identify whether cisplatin can induce autophagy of bladder cancer T24 cells and the possible mechanism, and to observe the relationship between outophagy and apoptosis.Methods MTT assay was applied to investigate the effects of various concentration of cisplatin( 0 , 10 , 20 and 40 μg/mL) on T24 survival.TEM was performed to detect the autophagosome formation .Western blot assay was used to analyze the expression changes of LC3-Ⅱ, P62 and extracellular signal-regulated kinase ( ERK1/2 ) and p-ERK at the protein level.The effects of autophagy on the survival and apoptosis of bladder cancer cells were investiga-ted.Results DDP observably inhibited proliferation of bladder cancer cells in a dose-dependent manner ( P<0.05), the 50% inhibiting concentration(IC50) was (30.3 ±2.4)μg/mL;DDP induced autophagy of bladder cancer cells, observably increased autophagosome induced by DDP; up-regulated expression levels of LC3-Ⅱproteins ( P<0.05 ) , down-regulated expression of P62 proteins ( P<0.05 );DDP increased the protein level of p-ERK (P<0.05); The inhibitor of ERK pathway U0126 inhibited DDP-induced autophagy, as evidenced by decrease in the expression of LC3-Ⅱproteins ( P<0.05 ) .After inhibition of autophagy by WTM in DDP-treated cells, cell viability was obviously decreased and apoptosis was increased (P<0.05);DDP combined with WTM observably enhanced cleavage of poly ADP-ribose polymerase 1 ( PARP-1 ) and cleaved-caspase-3 which is apop-tosis related proteins ( P<0.05 ) .Conclusions Autophagy can protect T24 cells against ciplatin-induced apop-tosis, the possible mechanism of autophagy is the ERK signaling pathway is activated .

2cm~2.Conclusions The auto-cranial pedicle flap via endonasal repairing blow-out fractures of or- bital inferior wails is an effective technique.The results are good for improving eye movement especially for fracture ranged≤2cm~2. (Ophthalmol CHN,2007,16:388-390)

OBJECTIVETo investigate the effects and underlying mechanism of notoginsenoside R1 on amyloid-β (1-42) (Aβ(1-42)) induced mitochondrial apoptotic death in SH-SY5Y cells.

METHODCell viability was assayed by MTT, apoptotic rates were analyzed with PI/Annexin V flow cytometry, Bax and Bcl-2 expression were detected with Western blotting, enzymatic activity of caspase-3, caspase-8 and caspase-9 were measured by ELISA assay.

RESULTThe 6.25-100 nmol x L(-1) of notoginsenoside R1 attenuate Aβ(1-42) induced apoptotic death of SH-SY5Y in dose dependent manner. The ratio of Bcl-2/Bax was elevated in SH-SY5Y with notoginsenoside R1 treatment. Caspase-3 and caspase-9 were activated with notoginsenoside R1 treatment while caspase-8 was not affected.

CONCLUSIONNotoginsenoside R1 could protect SH-SY5Y cells from Aβ(1-42) induced apoptosis via mitochondria related apoptotic pathway.

Amyloid beta-Peptides ; antagonists & inhibitors ; Apoptosis ; drug effects ; Caspases ; metabolism ; Cell Line, Tumor ; Cell Survival ; drug effects ; Cytoprotection ; Ginsenosides ; pharmacology ; Humans ; Mitochondria ; drug effects ; Peptide Fragments ; antagonists & inhibitors

OBJECTIVETo study the effect of Jinlida on changes in expression of skeletal muscle lipid transport enzymes in fat-induced insulin resistance ApoE -/- mice.

METHODEight male C57BL/6J mice were selected in the normal group (NF), 40 male ApoE -/- mice were fed for 16 weeks, divided into the model group (HF), the rosiglitazone group ( LGLT), the Jinlida low-dose group (JLDL), the Jinlida medium-dose group (JLDM), the Jinlida high-dose group (JLDH) and then orally given drugs for 8 weeks. The organization free fatty acids, BCA protein concentration determination methods were used to determine the skeletal muscle FFA content. The Real-time fluorescent quantitative reverse transcription PCR ( RT-PCR) and Western blot method were adopted to determine mRNA and protein expressions of mice fatty acids transposition enzyme (FAT/CD36), carnitine palm acyltransferase 1 (CPT1), peroxide proliferators-activated receptor α( PPAR α).

RESULTJinlida could decrease fasting blood glucose (FBG), cholesterol (TC), triglyceride (TG), free fatty acid (FFA) and fasting insulin (FIns) and raise insulin sensitive index (ISI) in mice to varying degrees. It could also up-regulate mRNA and protein expressions of CPT1 and PPARα, and down-regulate mRNA and protein levels of FAT/CD36.

CONCLUSIONJinlida can improve fat-induced insulin resistance ApoE -/- in mice by adjusting the changes in expression of skeletal muscle lipid transport enzymes.

Animals ; Apolipoproteins E ; deficiency ; genetics ; Blood Glucose ; metabolism ; CD36 Antigens ; genetics ; metabolism ; Carnitine O-Palmitoyltransferase ; genetics ; metabolism ; Dietary Fats ; adverse effects ; metabolism ; Drugs, Chinese Herbal ; administration & dosage ; Humans ; Hypoglycemic Agents ; administration & dosage ; Insulin ; metabolism ; Insulin Resistance ; Lipid Metabolism ; drug effects ; Male ; Metabolic Diseases ; drug therapy ; enzymology ; genetics ; metabolism ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Muscle, Skeletal ; drug effects ; metabolism