Objective Analyze the relationship between high sensitivity C‐reactive protein (hs‐CRP) ,homocysteine (Hcy) ,D‐di‐mer (D‐D) levels and atherosclerosis (AS) .Methods A total of 92 patients with AS were analyzed retrospectively ,including acute coronary syndrome (ACS) group with 61 cases ,stable angina pectoris (SAP) group with 31 cases .According to the result of coro‐nary artery plaque CT detection was further divided into plaque group ,non plaque group ,stable plaque subgroup ,and unstable plaque subgroup .Meanwhile 42 healthy subjects were selected as control group .The levels of the three indicators were compared . Results The serum hs‐CRP ,Hcy and plasma D‐D concentration in the ACS group and SAP group were significant higher than those of the control group (P< 0 .05) ,and those of the ACS group were significant higher than those of the SAP group(P< 0 .05) . The serum hs‐CRP ,Hcy and plasma D‐D concentration in the plaque group were significant higher than those of the non plaque group ,those in the unstable plaque subgroup were significant higher than those of the stable plaque subgroup(P< 0 .05) .The serum hs‐CRP ,Hcy and plasma D‐D concentration of the ACS patients were all correlated positively .Conclusion Serum hs‐CRP ,Hcy and plasma D‐D levels are closely related to the development of AS ,the combined detection of three indexes is value for the prevention , treatment and prognosis of AS .

Objectives To study the expression patterns of steroid receptor coactivators (SRC) and steroid-induced stromal cell-derived factor-1 (SDF-1) in endometriosis,and to explore the roles of SRC in the steroid-induced SDF-1 expression endometriosis.Methods From May 2010 to October 2012,16 endometriosis cases at stages Ⅲ or Ⅳ according to the revised American Society for Reproductive Medicine classification undergoing surgery in the First Affiliated Hospital to Nanjing Medical University were enrolled in this study.Their ectopic endometrium were from ovarian endometriomata which were identified pathologically with 9 cases at proliferative phase and 7 cases at secretory phase.The normal endometrium were acquired from the healthy women with normal menstrual cycle (n =10,proliferative phase =5,secretory phase =5).The mnRNA levels of SRC and SDF-1α during the menstrual cycle were detected by quantitative real-time polymerase chain reaction.Ectopic endometrium stromal cells were purified and cultured in medium containing 17β-estradiol (10-8mol/L) or 17β-estradiol (10-8 mol/L) + progesterone (10-6 mol/L).At 24,48,72 and 96 hours,the supernatants were collected to measure SDF-1α expression by ELISA.Ectopic endometrium stromal cells were transfected respectively with siRNA of SRC-1 and SRC-2 using lipofectamine.Two days after transfection,17β-estradiol (10-8 moL/L) or 17β-estradiol (10-8 mol/L) + progesterone (10-6 mol/L) were added into the media.On the third day after the steroid hormones treatment,the media were collected to quantify SDF-1α expression with ELISA.Results (1) Cyclical changes: the SRC-1,SRC-2 and SDF-1 α showed marked cyclic differences in normal endometrium (P ＜ 0.05).In proliferative phase and secretory phase,the SRC-1,SRC-2 and SDF-1 α were 5.6 ± 1.2,3.8 ± 1.1,2.7 ± 0.5 and 2.6 ± 1.0,2.1 ± 1.0,1.6-± 0.5,respectively.There was no periodic variation in the expression of SRC-1,SRC-2 and SDF-1α in ectopic endometrium throughout the menstrual cycle.(2) Steroid-induced SDF-1α expression in ectopic endometrium stromal cells: the 17β-estradiol-induced SDF-1α expression was (1 803 ± 196),(2 272 ± 261) and (2 162 ± 258) ng/L at 48,72 and 96 hours.At the same time points,the SDF-1α expression induced by 17β-estradiol and progesterone was (1 307 ± 150),(1 518 ± 301) and (1 550 ± 144) ng/L,respectively.There was significant difference between two groups (P ＜0.05).(3) The effects of SRC silencing on steroid hormones-induced SDF-1 α expression in ectopic endometrium stromal cells: the expression of 17β-estradiol-induced SDF-1α at 72 hours was significantly decreased from (2 313 ± 357) ng/L to (1 155 ± 244) ng/L after the silencing of SRC-1 (P ＜ 0.05).After the silencing of SRC-2,the 17β-estradiol-induced SDF-1 α at 72 hours was (1 958 ±324) ng/L.There was no significant difference compared with the before the silencing (P ＞ 0.05).The expression of SDF-1 α at 72 hours induced by 17β-estradiol + progesterone was (1 534 ± 449) ng/L and (2 051 ± 380) ng/L respectively before and after the silencing of SRC-2 and showed the significant difference (P ＜ 0.05).Conclusion During the expression of SDF-1 α regulated by steroids in ectopic endometrium cells,SRC-1 is the major coactivator of 17β-estradiol and SRC-2 is the major coactivator of progesterone.

Objective To investigate the effect of cobalt chloride on tumor cell proliferation and apoptosis in vitro, to explore the reasonable strategy of chemical hypoxia induced by CoCl2. Methods Two tumor cell lines (A549 and HeLa) were respectively exposed to CoCl2(0.05～2 mmol/L) for different time period (4～48 h), cells viability、proliferation and apoptosis were maesured by MTT and FCM methods. HIF-1? and related apoptosis proteins expression were detected by Western blot. Results Cells viability was weakly changed in low concentration(≤200 ?mol/L)of CoCl2 within 24 h. However, higher dose or prolonged challenge of CoCl2 significantly decreased cell survival rate (P

ObjectiveTo observe the influence of polyethylene glycol-conjugated hemoglobin (PEG-Hb) solution combined with cisplatin on the expression of erythropoietin/erythropoietin receptor (EPO/EPOR) and tumor angiogenesis in cancer treatment.MethodsHeLa cells were injected subcutaneously into the right oxter of 3-4 weeks old BALB/c nude mice to establish cervical tumor xenograft model.Then animals were randomly assigned to 4 groups (n=10) and treated respectively:group 1(control); group 2,cisplatin (5 mg/kg); group 3,PEG-Hb (0.6 g/kg); group 4 cisplatin (5 mg/kg) plus PEG-Hb (0.6 g/kg).The volume oftumors in each groups were measured in 4 weeks treatment period.Efficacy was measured as percent tumor growth inhibition (TGI) relative to salinetreated group.CD31 was detected by immunohistochemistry and its expression was identified as microvascular density (MVD).Expressions of hypoxia inducible factor-1α(HIF-1α) and EPO/EPOR in tumor tissues were analyzed by irnmunohistochemistry.EPOR protein level was tested by western blot.ELISA method was used in measuring EPO concentration in serum.ResultsTumor volume was significantly decreased in group 4 compared with other groups.Immunoreactivity data demonstrated lower expression of CD31,HIF-1α and EPO/EPOR in group 4.The expression of EPOR in the endothelial cells was also significantly decreased in group 4.Western-blot data indicated lower EPOR protein level in group 4.Serum level of EPO was also decreased in group 4.ConclusionPEG-Hb plus cisplatin is benefit to tumor tissue oxygenation,therefore it can inhibit the tumor angiogenesis and down regulate the erythropoietin/erythropoietin receptor system.The result can provide more evidence for the enhanced sensitivity effect of the artificial oxygen carrier in cancer therapy.

The quality and integrity of clinical trials and associated data are not only derived from accuracy of trial data analyses, but also closely embodied to the authenticity and integrity of those data and data documents as well as the compliant procedures obtaining those data and relevant files in the life cycle of clinical trials. The compliances of good clinical practices and standards suggest the reliability, complete and accuracy of data and data documents, which is constructing the convincible foundation of drug efficacy and safety validated via clinical trials. Therefore, the monitoring and auditing on clinical trials and associated data quality keep eyes on not only verifications of reliability and correctness on the data analytic outcomes, but also validation of science and compliance of the trial management procedure and documentations in the process of data collections.
Clinical Trials as Topic ; standards ; Data Accuracy ; Reproducibility of Results

Adult ; Asthma ; metabolism ; physiopathology ; Basic-Leucine Zipper Transcription Factors ; genetics ; physiology ; Fanconi Anemia Complementation Group Proteins ; genetics ; physiology ; Female ; Glutamate-Cysteine Ligase ; metabolism ; Humans ; Inflammation ; metabolism ; pathology ; Male ; NF-E2-Related Factor 2 ; genetics ; physiology ; RNA, Messenger ; genetics ; metabolism ; Sputum ; cytology

Type 2 diabetes is a hypermetabolic disease characterized with disorders of glucose/lipid metabolism, absolute or relative lack of insulin, and can induce skeletal muscle atrophy. Hyperglycemia, hyperlipidemia, insulin resistance, and abnormal release of inflammatory factors can lead to abnormal signal transduction in skeletal muscle, thus make protein synthesis and degradation imbalance and eventually causing muscle atrophy. Under normal conditions, insulin-like growth factor 1 (IGF-1)/insulin can activate phosphoinositide 3-kinase (PI3K)/protein kinase B (AKT). AKT not only increases protein synthesis through mammalian target protein of rapamycin (mTOR), but also phosphorylates forkhead box O (FoxO) transcription factor and then inhibits the transcription of several ubiquitin ligases (such as MAFbx/atrogin-1 and MuRF1), or autophagy related genes. The weakened IGF-1/PI3K/AKT pathway in type 2 diabetes is an important factor leading to skeletal muscle atrophy. Studies have shown that the commonly used anti-type 2 diabetic drugs have different effects in regulating the synthesis and degradation of skeletal muscle protein. Studies reported that drugs with effect of anti-diabetic muscle atrophy include thiazolidinediones, glucagon-like peptide analogs, glucose-sodium cotransporter 2 inhibitors, etc.; drugs that are still in controversial or even promote skeletal muscle atrophy include metformin, and some sulfonylurea or non-sulfonylurea insulin secretagogues. This article overviewed and analyzed the currently commonly used drugs for type 2 diabetes and summarized the related mechanisms, with the aim to provide references for the rational applications of drugs for type 2 diabetes.

ObjectiveTo explore the effect and safety of intravenous sodium valproate in treatment of pediatric patients with status epilepticus (SE).MethodsTwenty-five children suffering from convulsive SE were treated with intravenous sodium valproate after failure of the conventional treatment, in a dose of tolerability 15 mg/kg and 1～2 mg/kg daily.ResultsIn 25 cases, there were 23 cases (92%) with ≥50% seizure reduction and 11 cases (44%) with complete cessation. Except for winking in 7 cases (28%), no other adverse effects had been found.ConclusionIntravenous sodium valproate is effective and safe on pediatric patients with SE who are resistant to conventional drugs.

The kinetics of batch and fed-batch cultures of recombinant Escherichia coli to produce humanlike collagen were investigated. Through examining the density of substrate and the amount of mushrooms and the density of products during the process of fermenting, a set of kinetic models are set up. The influence of cell without plasmid was considered. The results show that the kinetic model may well simulate the fermenting process.

The volatile oils of endophyte isolates R1 (Acremonium sp.) and R2 (Acremonium sp.) from Aqui-laria sinensis were extracted by solvent method. Twenty and sixteen ingredients were identified from the volatile oils of R1 and R2 by GC-MS, respectively. Fatty acids, such as oleic acid, linoleic acid, hexa-decanoic acid etc., were the main components, whereas terpenoids like 1,8-cineole, zingiberene, ar-curcumene were also found in both oils. It’s the first report about the volatile oil constituents of endophyte isolates from A. sinensis.