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.

Endoplasmic reticulum stress(ERS) is a kind of subcellular pathological state,and associated with many diseases.Recently,the research of ERS on chondrocyte is at the beginning stage,and may be involved in pathogenisis of rheumatoid arthritis(RA) and osteoarthritis(OA).It has been proved that ERS can interfere the differentiation of chondrocyte,decrease the synthesis of abnormal protein,attenuate the injury of cell.But overreaction of ERS can cause chondrocyte apoptosis through an independent pathway without of Fas and NO.There are three signal transmission passages in ERS:ATF-6(activating transcription factor 6)、Ire 1(inositol-requiring 1)and PERK(PKR-like ER kinase).The three protein molecules activate apoptotic genes by TRAF-2(TNF receptor-associated factor 2)and GADD153(growth arrest and DNA-damage-inducible gene 153),initiate the chondrocyte apoptosis.Therefore,ERS may effect the pathogensis of RA and OA by modulating chondrocyte function and inducing apoptosis,but more research are needed to reveal the mechanism.

Adolescent ; Child ; Child, Preschool ; CpG Islands ; Cyclin-Dependent Kinase Inhibitor p15 ; genetics ; DNA Methylation ; Female ; Humans ; Leukemia, Myeloid, Acute ; genetics ; Male ; Promoter Regions, Genetic

Objective To prospectively assess the nutritional status in the patients with alimentary tract malignancy,and to elucidate the factors related to malnutrition.Methods The nutritional status of 328 patients with newly diagnosed alimentary tract malignancy was assessed using subjective global assessment(SGA)and serum levels of prealbumin and albumin.And the factors influencing the nutritional status of the patients with alimentary tract malignancy in different locations were analyzed.Results The prevalence of malnutrition was 64.43% in all,75.81% in colon cancer,63.24% in esophageal cancer,62.40% in gastric cancer and 60.27% in rectal cancer.The changes of nutritional status mainly manifested weight loss with the incidence of 67.39%,serum prealbumin level under 200 g/L with the incidence of 24.1% and serum albumin level less than 35 g/L with the incidence of 31.70%.And there was significant difference in weight loss and serum levels of prealbumin and albumin among the patients with different nutritional status(P=0.000).The factors that influence the nutritional status of the patients with alimentary tract malignancy include the location and TNM staging of tumors,and the age,appetite and digestive symptoms of the patients.Conclusion The patients with alimentary tract malignancy are susceptible to malnutrition due to the multiple factors such as the tumor location and metabolic impacts of tumor on host.Nutritional screening,assessment and early intervention should be emphasized in the inpatients with alimentary tract malignancy.

AIM To establish a high performance liquid chromatographic method (HPLC) to determine the concentration of valsartan in human plasma. METHODS Separation was achieved on the lichrospher C 18 column. The mobile phaseconsisted of pH 3 1 phosphate buffer acetonitrile (53∶47, V/V) was used at a flow rate of 1 0 ml?min -1 . The fluorimetric excitation and emission wavelengths were set at 265 nm and 378 nm, respectively. The plasma samples were acidified with HCl, extracted with ethyl acetate. Separate the organic phase, remove the solvent and then residue was dissolved in mobile phase. RESULTS The retention time of valsartan was 12 5 min. The calibration curves were linear in the range of 5 9～ 2 360 ?g?L -1 . The precision values (RSD) of intra day and inter day were determined to be 2 83%～7 07% and 1 57%～8 41% respectively. The absolute recovery rate were 80 30%?5 13%. The method was applied to determine the peak and valley concentrations in plasma of the hypertensive treated with 80mg valsartan per day. CONCLUSION The assay was sensitive and simple. It is suitable for the study of the pharmacokinetics of valsartan.

Objective To reveal the role of inhibitor of nuclear factor kappa B kinase alpha (IKKα) in renal inflammation after renal ischemia-reperfusion (IR) injury and its potential associated mechanism.Methods Ischemia-reperfusion injury models were induced in a total of 24 healthy C57BL/6 male mice.Renal function and histological changes were estimated.The expression and site of IKKα,p52,RelB,IL-10 and IL-18 were determined by immunohistochemistry and Western blotting.After the short hairpin RNA(shRNA)targeting IKKα was injected into renal parenchyma,renal function and protein expressions of IKKα,p52,RelB,IL-10,IL-18 were detected.Results Compared with sham-operated group[Scr(7.30±0.13) μmol/L,BUN (8.39± 0.30) mmol/L],levels of Scr [(29.80± 2.10)μmol/L,(27.00±3.40) μmol/L,(23.00±3.70) μmol/L] and BUN [(9.47±3.50) mmol/L,(11.68 ±4.30)mmol/L,(13.12±2.10) mmol/L] were higher on day 1,3,7 and the injury of kidney was serious in IR injury group.Immunohistochemical expression of both IL-18 and IL-10 were increased.Markedly increased IKKα,p52 and RelB protein expression were noted in experiments from day 1 to day 7 during kidney recovery period,with a peak on day 3 and then decreasing toward baseline after day 7.Compared with IR injury group,low-expression of IKKα by injection of shRNA up-regulated the expression of IL-18 and down-regulated the expression of IKKα,p52,RelB and IL-10.Conclusions The NF-κB pathway is activated and IKKα expression is up-regulated during the kidney ischemiareperfusion injury,low-expression of IKKα may block inflammation resolution via down-regulation of alternative NF-κB pathway family members of both p52 and RelB.

Objective To evaluate the relationship between neoadjuvant chemotherapy (combination of taxanes and anthracyclines ) induced-neutropenia and the efficacy of neoadjuvant chemotherapy and long-term survival in operable breast cancer patients. Methods Two hundred and eleven patients received 4 cycles of neoadjuvant chemotherapy (combination of taxanes and anthracyclines).Clinicopathological characteristics were compared between patients with neoadjuvant chemotherapy-induced neutropenia and patients without neutropenia. The efficacy of neoadjuvant chemotheray and long-term survival rate were analyzed. Results Among 211 patients there were 51 (24. 2% ) cases suffering from neutropenia and 160 (75.8%) cases were of no-neutropenia. The response to chemotherapy in patients with neutropenia were more effective than in no- neutropenia ones ( P ＜ 0. 05 ). The 5-year disease-free survival (DFS) in patients with neutropenia was 82. 4%, while the 5-year disease-free survival ( DFS) with nonneutropenia was 60% ( P ＜ 0. 01 ). Additionally, the 5-year overall survival ( OS ) in patients with neutropenia was 90. 2% and in patients with non-neutropenia patients was 67. 5% ( P ＜ 0. 01 ).Conclusions Chemotherapy-induced neutropenia during neoadjuvant chemotherapy combination of taxanes and anthracyclines in patients with operable breast cancer has a better prognosis. The sensitivity of tumors given to chemotherapeutic drugs could be evaluated by chemotherapy-induced neutropenia.

Objective To investigate the effects of Epigallocatechin gallate(EGCG)on IL-1βinduced MIN6 cells apoptosis. M.Methods The experiment group was divided into control group,IL-1β group,IL-1β+ EGCG low concentration group and IL-1β+EGCG high concentration group.Cell activity was detected by CCK8.Insulin secretion was detected by ELISA.cell apoptosis was detected by flow cytometry.The mitochondrial membrane potential was detected by flow cytometry.ATP content and cell ac-tivity of ROS were detected by colorimetry and chemiluminescence method.Results Compared with normal group,IL-1β group showed much lower cell activity,insulin secretion,cell mitochondrial membrane potential and ATP content,and at the same time IL-1βgroup had significantly higher cell apoptosis and ROS activities.After given EGCG,both low concentration group and high con-centration group had higher cell activity,insulin secretion,cell mitochondrial membrane potential and ATP content,at the same time lower cell apoptosis and ROS activities was showed.And the IL-1β+EGCG high concentration group worked more powerful.Con-clusion EGCG has protective effects on IL-1βinduced MIN6 cells apoptosis.Its mechanism may be related to increasing the content of the ATP and mitochondrial membrane potential and protecting mitochondrial function as well reducing the activity of ROS.

Objective To observe the expression of stromal cell-derived factor 1 (SDF-1) in the kidney after ischemic reperfusion injury (IRI),and explore its relationship with macrophage during the IRI kidney.Methods A total of 28 healthy C57BL/6 male mice were used to establish renal IRI model by clamping both pedicles for 35 min followed by reperfusion.Kidney tissue samples were collected at indicated time points.Renal histological changes were estimated.The expression of SDF-1 was determined by immunohistochemistry,ELISA and real-time PCR.After the liposomal clodronate was injected intraperitoneally,the location of CD68 was observed by immunofluorescence.Renal histology and protein expression of SDF-1 were also detected.Results Compared with sham-operated group,classical tubular damage was found in IRI group,accompanied by a large number of inflammatory cells.The expression of total renal SDF-1 peaked on day 1 and decreased to control levels in the following days.SDF-1 in healthy kidney was localized at cortex,but spread to the corticomedullary area of the kidney during IRI.Compared with IRI groups,elimination of macrophage by injection of liposomal clodronate alleviated renal IRI and down-regulated the expressions of CD68 while up-regulating SDF-1.Conclusions SDF-1 expression is up-regulated in IRI kidney and is associated with macrophage.SDF-1 may play a role in the early phase of acute kidney injury and it may be a new marker in diagnosis of AKI.

Objective To study the effect of interleukin (IL)-10 knockout (IL-10-/-) on renal repair after renal ischemia-reperfusion injury in mice.Methods Eighteen IL-10-/-mice (KO) aged 8-10 weeks and 18 C57BL/6 wild type mice (WT) aged 8-10 weeks were divided into control group (Sham) and renal ischemia-reperfusion injury (IRI) group.The renal tissue morphology change was observed by Hematoxylin and eosin (HE) staining and Masson staining.The expressions of IL-18, Ki67 and TGF-β1 were detected by immunohistochemistry.The expression of TGF-beta1 and IL-18 were detected by Western blotting.Results Compared with that in WT-IRI group, in KO-IRI group renal pathological damage was more severe, renal interstitial fibrosis was visible, Ki67 expression of renal tubular epithelial cells decreased distinctly (P＜0.01), the expression of TGF-betal increased significantly (P＜0.01).Conclusion Repair slows down significantly after kidney ischemia-reperfusion injury and fibrosis occurs gradually in IL-10-/-mice, eventually progressing to chronic kidney disease.