Objective To explore the expression of pentraxin-3 (PTX3) in placentas from patients with severe preeclampsia and the relationship between PTX3 and the pathogenesis of severe preeclampsia.Methods Fifty-three pregnant women who delivered from October 2010 to March 2011 in the First Affiliated Hospital of Chongqing Medical University were included in the study.Twenty-three women with severe preeclampsia were chosen as the preeclampsia group,and thirty healthy pregnant women were identified as the control group.All the women received cesarean section.The location of PTX3 protein in placentas was studied by immunohistochemical SP method.Quantitative real-time PCR technique and western blot analysis were employed to assay the levels of PTX3 mRNA and protein in placentas,respectively.Results ( 1 ) The location of PTX3 protein in placentas:PTX3 protein was expressed in placentas from both groups,and there was no difference of PTX3 distribution between normal and preeclamptic placentas.PTX3 was mainly located in perivascular stroma,decidual cells and terminal villi.Neutrophilic infiltration was observed in the preeclamptic placentas.(2)The expression of PTX3 mRNA and protein in placentas:the level of PTX3 mRNA in placentas from the preeclampsia group was higher than that in the control group( 1.98 ± 0.54 vs.0.87 ± 0.27,P ＜ 0.05 ).Compared with the control group,the level of PTX3 protein was significantly elevated in the preeclampsia group ( 1.42 ± 0.29 vs.0.56 ± 0.25,P ＜ 0.01 ).Conclusion The high expression of PTX3 in placentas from the preeclamptic patients suggests that PTX3 may be involved in the pathologic process of preeclampsia.

Objective To analyze the clinical characteristics and perinatal outcome of early-onset intrahepatic cholestasis of pregnancy (ICP).Methods A total of 305 ICP cases were collected in the First Affiliated Hospital of Chongqing Medical University between June 2006 and May 2012.According to the onset time of ICP,patients were divided into early-onset ICP group (onset time ＜ 28 gestational weeks) and lateonset ICP group (onset time ≥28 gestational weeks).The late-onset ICP group was further divided into 28-31 +6 gestational weeks and ≥32 gestational weeks according to the onset time.The biochemical indices and perinatal outcome of each group were assessed.Results (1) When the diagnosis was made for the first time,the maternal serum concentrations of total bile acid (TBA) and total bilirubin (TBIL) in early-onset ICP group were (41 ±9) and (32 ±9) μmol/L,respectively; while TBA and TBIL in late-onset ICP group were (32 ± 6) and (22 ± 9) μmol/L,and the difference between the two groups was statistically significant (P ＜ 0.05).(2) There was no significant difference in alanine aminotran-sferase (ALT) and aspartate aminotransferase (AST) between early-onset ICP group and late-onset ICP group (P ＞ 0.05).The ALT of early-onset ICP group and late-onset ICP group were (159 ± 50) and (145 ± 52) U/L,respectively; and AST were (151 ±49) and (138 ± 44) U/L,respectively.(3) The early-onset ICP group had significant higher (P ＜ 0.05) incidence of meconium staining (18.8％ vs.7.4％),fetal distress (22.9％ vs.8.9％),newborn asphyxia (14.6％ vs.5.4％),premature delivery (33.3％ vs.15.6％),developing into severe ICP (41.7％ vs.25.3％) and cesarean section (91.7％ vs.78.6％) when compared to the late-onset ICP group.No significant difference in the incidence of premature delivery,developing into severe ICP and cesarean section was found between the two types of late-onset ICE (4) There was significant differences in average birth weight and gestational weeks at delivery between the two groups [early-onset ICP group:(3113 ± 443) g and (36.3 ± 2.6) weeks] ; late-onset ICP group:[(3513 ± 450) g and (37.7 ±1.6) weeks].Conclusion The early-onset ICP patients presented worse clinical manifestations than lateonset ICP patients,and early-onset ICP is more likely to lead to premature delivery and fetal distress.

Objective To discuss the value of video-assisted thoracoscopic repair in the treatment of pectus excavatum in children.Methods Thoracoscopic sternum elevation with an internal steel bar(Nuss procedure) was performed in 45 children with pectus excavatum.Preoperatively,a curved steel bar was prepared and the site of incision and the lowest part of the depression were labeled with methylene blue.Under right-sided thoracoscopic vision,the bar was inserted into the retrosternal tunnel thereby correcting deformity. Results The steel bar was placed safely in all the 45 patients.The operation time was 35~80 min(mean,60 min).The intraoperative blood loss was less than 5 ml.The length of postoperative hospital stay was 4~10 days(mean,7 days).Forty children were followed for 3~30 months(mean,16.5 months).Short-term complications included pneumothorax in 1 patient and pneumonia in 1 patient.Long-term complications included bar shift after 1 year in 1 patient and persistent sternal pain in 2 patients(which had been cured by oral and local analgetic administration).The bar had been removed in 10 children,all of whom had good cosmetic results.Conclusions Video-assisted thoracoscopic Nuss procedure is safe and effective in the management of pectus excavatum in children,with advantages of short operation time,simple performance,satisfactory cosmetic results,and fewer complications.

Furthering of the health reform calls for better health care system,greater public financing,and deepened reform of public hospitals.Introduced in this paper are the actions taken and outcomes of the health reform in Changchun city,including the essential medicines system to minimize drug prices,improvement of the primary healthcare system to minimize people's financial burden,greater public spending to enhance public welfare nature of medical institutions,enhanced competencies of primary medical institutions to introduce rational classification of patient flow,and enhanced equity of public services to promote people's health.On such basis,further reform proposals were made for Changchun's health reform.

The axon guidance molecule Slit is a secreted glucoprotein which is conserved during evolution. Slit has been implicated in regulating a variety of life activities, such as axon guidance, neuronal migration, neuronal morphological differentiation, tumor metastasis, angiogenesis and heart morphogenesis. Slit function mainly depends on the binding of its LRR-2 domain to the Ig1 domain of Roundabout (Robo) receptor, meanwhile Slit function is also mediated by a range of signaling molecules, including the heparan sulfate proteoglycans (HSPGs), GTPase-activating proteins (GAPs), tyrosine kinase Abelson, calcium ions, MicroRNA-218 and other axon guidance molecules. Several transcription factors, including Single-minded, Irx and Midline, were shown to regulate slit expression. In addition, multiple Slit isoforms exist as a consequence of alternative spliced transcripts. The research on guidance mechanism of Slit will facilitate the understanding of molecular mechanism underlying neural networks formation in the process of neural development and regeneration. Meanwhile, the studying of Slit guidance mechanism could promote the prevention and treatment of human neurological diseases and cancer metastasis.
Animals ; Axons ; metabolism ; physiology ; Cell Movement ; physiology ; Drosophila Proteins ; physiology ; Gene Expression Regulation ; Humans ; Intercellular Signaling Peptides and Proteins ; genetics ; physiology ; Nerve Tissue Proteins ; genetics ; metabolism ; physiology ; Neurons ; cytology ; Receptors, Immunologic ; metabolism

AIM:To investigate the influence of matrine (MA) on the phenotype switching of mouse mono-cytes and alveolar macrophages induced by bleomycin ( BLM) .METHODS:All mice were randomly divided into normal saline (NS) group, BLM group, BLM+NS group and BLM +MA group.The mice were administered with BLM at 2.5 mg/kg via oropharyngeal instillation .The mice in BLM+MA group were treated with MA (15 mg· kg-1 · d-1 ) by oral gavage following BLM administration .The mice were sacrificed on days 3, 7, 14, and 21.The lungs were removed for pathological analysis .The circulating monocyte subsets and polarization state of bronchoalveolar lavage fluid ( BALF)-de-rived alveolar macrophages were analyzed by flow cytometry .RESULTS:The results of HE and Masson trichrome staining in BLM and BLM+NS groups exhibited classical pathological stages of lung fibrosis , including acute inflammation phase and later fibrosis phase .Compared with BLM +NS group, MA treatment alleviated the inflammatory response and the de-gree of fibrosis induced by BLM (P<0.05).There was a rapid change of circulating Ly6Chi monocytes and its magnitude was positively associated with the pulmonary inflammatory response .An expansion of M2-like alveolar macrophages was positively correlated with the magnitude of lung fibrosis .Moreover , MA treatment partially normalized the phenotype switc-hing of monocytes and alveolar macrophages .CONCLUSION:Matrine treatment attenuates BLM-induced pulmonary injury partially via modulating the phenotype switching of monocytes and alveolar mocrophages .

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 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

AIMTo study the effects of sodium magnesium fructose diphosphate (SMFD) on free calcium concentration and nitric oxide synthase activity of ischemic synaptosome, so as to explore the protective mechanisms of SMFD on cerebral ischemia.

METHODSThe synaptosomes from normal rat brain were prepared by phase partition and cultured with oxygen-glucose deprivation to establish ischemic synaptosome model. The intrasynaptosomal free calcium concentration and nitric oxide synthase activity were detected separately after the synaptosomes were co-incubated with SMFD (1.3 mmol.L-1) or fructose-1, 6-diphosphate (FDP, 4.0 mmol.L-1) for 60 min.

RESULTSSMFD decreased the free calcium concentration and reduced the activity of nitric oxide synthase (NOS) of ischemic synaptosomes. Its effects were more powerful than those of FDP.

CONCLUSIONSMFD may protect neurons from ischemic injury by preventing intracellular Ca2+ overload and inhibiting the activity of nitric oxide synthase.

Animals ; Brain Ischemia ; enzymology ; metabolism ; Calcium ; metabolism ; Chelating Agents ; pharmacology ; Fructosediphosphates ; pharmacology ; Magnesium ; chemistry ; Male ; Nitric Oxide Synthase ; drug effects ; metabolism ; Rats ; Rats, Wistar ; Sodium ; chemistry ; Synaptosomes ; metabolism

Interleukin-1 receptor antagonist (IL-1ra), a member of IL-1 family, is a naturally occurring IL-1 inhibitor as "receptor antagonist", which blocks biological responses mediated by IL-1. Recombinant human IL-1ra (rhIL-1ra, Kineret) was introduced in clinical trials involving patients with RA. Between 2001 to approximately 2002, rhIL-1 ra was approved by the US Food and Drug Administration and the European Agency for the Evaluation of Medicine Procedure. Unfortunately, 10,000 to 100,000-fold excess amounts of IL-1ra are needed to relieve disease because minimal IL-1 can induce complete biological responses, and the dosage of 100 to approximately 150mg/day in a RA patient is so big that it greatly influence patients' physical, psychological and economical situation. In this study, IL-1ra mutants were established by site-specific mutagenesis to improve its stability. The sites of mutagenesis included R6 K7-AA,R93 K94-AA and K97 R98-AA. IL-1ra and its mutants were expressed in E. coli BL21 (DE3) using pTIG-Trx expressing system with the induction of IPTG. The recombinant proteins were purified by Ni2+ chelate chromatography and Sephadex G75 gel filtration chromatography. The activity of mutants is as high as IL-1ra. We characterized the pharmacokinetic profile of IL-1ra and its mutants. The third mutant's half life is 2.26 times than wt IL-1ra. The study has provided some approaches and experience for further research to improve the metabolism stability of IL-1ra.
Animals ; Escherichia coli ; genetics ; metabolism ; Female ; Humans ; Interleukin 1 Receptor Antagonist Protein ; biosynthesis ; genetics ; pharmacokinetics ; Mutagenesis, Site-Directed ; methods ; Mutant Proteins ; biosynthesis ; pharmacokinetics ; Recombinant Proteins ; biosynthesis ; genetics ; pharmacokinetics