0.05) in age, sex, disease course and disease activities (SLEDAI). Fever, oral ulcer, Raynaud′s phenomenon and cardiac involvement in infection group were more common than in disease flare group (P

Because the influence of fibrin on the reaction of plasm inogen activation by various plasminogen activators is different, the kinetic co nstant of the reaction of plasminogen activation catalyzed by InB with and witho ut fibrin were detected. The result is: Kfibrinm＝4.2 μmol*L -1，greater than the normal Km=0.379 μmol*L-1; kfib rincat＝0.107 s-1，greater than the normal kcat=0.0165 s-1. The results suggest that existence of fibrin in the reaction system of plasminogen activation depress the affinity between InB and plasminog en, but accelerates the hydrolysis of plasminogen by InB. The count up effect is inhibition.

Humans ; Muscular Dystrophy, Duchenne ; Research ; trends

Cervical Ripening ; Female ; Humans ; Integrative Medicine ; Pregnancy

Objective To explore the roles of reactive oxygen species(ROS) and TGF-?1 in aldosterone-induced PAI-1 production.Methods Quiescent rat mesangial cells (MCs) were treated by aldosterone.The level of ROS in MCs induced by aldosterone was measured by confecal laser scanning microscopy and the TGF-?1 activity in the supematant of culture was measured by mink lung epithelial cell (Mvllu) proliferation inhibition MTT assay.Then,before the addition of aldosterone,MCs were pretreated with NAC or TGF-?1 neutralizing antibody to decrease cellular ROS or inhibit activity of TGF-?1 induced by aldosterone respectively.PAI-1 mRNA was examined by semi-quantification RT-PCR and PAI-1 protein by Western blotting.Results The intracellular ROS induced by aldosterone increased by 5-fold compared to that of control group,and the activity of TGF-?1 stimulated by aldosterone increased markedly.TGF-?1 neutralizing antibody and NAC effectively decreased aldosterone-induced PAI-1 mRNA expression by 30% and 32%,and PAI-1 protein expression by 21% and 11%,respectively.However,neither TGF-?1 neutralizing antibody nor NAC alone could regulate aldosterone-induced PAI-1 mRNA and protein expression to normal level in 24 hours.Conclusions ROS and TGF-?1 play important roles in up-regulation of aldosterone- induced PAI-1 in MCs.ROS and TGF-?1 are not the exclusive pathway of PAI-1 expression induced by aldosterone in MCs.

Purpose:To investigate the prevention and treatment protocol for Af after resection of esophageal and car- dia carcinoma.Methods:Analyses for clinical materials of 1527 patients underwent resection for esophageal and cardiac carcinoma.Results:There were Af 23 cases.Age older than 60 years,abnormal ECG or/and pulmonary function before operation,gastro-esophageal anastomosis above the aortic arch and histological staging Ⅲ～Ⅳ were risk factors for AF.Fa- tal AF was rarely seen.In our 23 cases after treatment in time AF disappeared.Conclusions:Further recognition for post- operative AF and management of perioperative period complication,may reduce the danger of postoperative AF.

Objective To investigate the effects of adenosine 5'-monophosphate-activated protein kinase (AMPK) and phosphated AMPK (pAMPK) signals in ischemic preconditioning (IPC), and the effect of pharmacological intervention of AMPK on infarct size of the brain. Methods A brief (3min) middle cerebral artery occlusion (MCAO) was employed to induce IPC in male rat, and another 90-min MCAO was performed 4 or 72h later. The levels of AMPK and pAMPK were assessed after IPC. A pharmacological activator metformin, or inhibitor compound C of AMPK, was used to analyze the correlation of IPC to AMPK signaling in MCAO rats. Results The infarct size of total cerebral hemisphere and cortex was significantly decreased in MCAO animals by IPC for 72h (P<0.05, n=8), and the neurological deficit scores (NDS) of MCAO rats were also improved (P<0.05, n=8). There was a significant increase in pAMPK expression after a 90min MCAO (P<0.05, n=6), and a significant decrease in induced pAMPK expression (P<0.05, n=6) achieved only by a 72h IPC treatment. Intraperitoneal injection of an AMPK inhibitor, compound C, could decrease the infarct size in MCAO rats (P<0.05, n=6), but combined IPC (72h) and injection of compound C did not result in further decrease of the infarct size (P>0.05, n=6). The AMPK activator metformin can significantly reverse the protective effect of IPC (P<0.05, n=6). Conclusions The signals of AMPK and pAMPK play an important role in neuroprotective effect of IPC on cerebral ischemic injury. The neuroprotective effect of IPC may be associated with the down-regulation of pAMPK.

OBJECTIVE: To assess the patterns of linkage disequilibrium (LD) of 16 STR loci on X chromo- some and investigate the genetic stability. METHODS: Genomic DNA samples extracted from blood stains from 500 unrelated individuals and 885 lineage members from Eastern Chinese Han population were genotyped through multiplex amplification using IDtyperX-16 kit by our independent research followed by capillary electrophoresis. LD was assessed by PowerMarker v3.25 software and mutation rate of every locus was analyzed. RESULTS: LD were not found at the 16 X-STR loci. Allele mutations were observed at 10 loci. Among them, mutation rates of DXS6809 and DXS7132 were both up to 0.0048. CONCLUSION When the 16 X-STR loci included in IDtyperX-16 kit were used for parentage testing, product princi- ples can be applied to calculate the likelihood, but mutation should be taken into consideration in the case that the genotypes do not meet the genetic law (especially at DXS6809 and DXS7132).
Alleles ; Asian People/genetics* ; Blood Stains ; China ; Chromosomes, Human, X/genetics* ; Electrophoresis, Capillary ; Female ; Forensic Genetics/methods* ; Gene Frequency ; Genetic Loci/genetics* ; Genotype ; Humans ; Linkage Disequilibrium/genetics* ; Microsatellite Repeats/genetics* ; Multiplex Polymerase Chain Reaction ; Mutation ; Mutation Rate

We isolated 61 endophyte isolates from the bark of 4 plants, Ginkgo biloba L, Albizzia julibrissin Durazz, Ailanthus sltissima (Mill) Swingle and Melia azedarach L. At the test concentration of 200 ?g/mL, higher than 50% of antitumor activities were demonstrated with crude extracts from 45.9% of fungal culture in MTT assay. Six isolates, YX5, YX17, YX36, KL1, CC1 and CC5, still showed higher cytotoxicity at 50 ?g/mL. No isolates from A. julibrissin had inhibitory effect towards EC109 at the test concentration of 50 ?g/mL; while about 15.8% of isolates from G. biloba were active. IC50 of the extract from the most active isolate YX5 against EC109, HONE1 and HeLa were 18.3 ?g/mL, 3.6 ?g/mL and 6.5 ?g/mL, respectively. Our results indicate that endophytes from G. biloba could be regarded as a potent source of antitumor drugs.

Melatonin has been reported to inhibit hepatic fibrosis and the mechanism may be correlated to its anti-oxidant effect.Nevertheless,the mechanism is not completely identified.This study was conducted to investigate the effects of melatonin on TGF-β1/Smad signaling pathway in liver fibrosis in rats.The liver fibrosis model was made by the subcutaneous injection of CCl4.The liver pathology changes were detected using hematoxylin and eosin (H&E) staining and Van Gieson (VG) staining.Serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) activities were measured with an autoanalyzer.Glutathione peroxidase (GPx) activities and levels of malondialdehyde (MDA) and hydroxyproline (Hyp) in liver were evaluated by spectrophotometry.Expression levels of TGF-β1,Smad2/3,phosphorylated Smad2/3 (p-Smad2/3) and Smad7 in liver were detected by immunohistochemistry and Western blot analysis.Results showed that melatonin suppressed CC14-induced liver fibrosis,along with an improvement in histological changes,significant decreases in pathologic grading sores and obvious decreases in Hyp levels in liver.Melatonin improved liver function indicated by decreased serum ALT and AST activities.In addition,melatonin exerted its anti-oxidant effects,as supported by decreased MDA levels and increased GPx activities in liver.Furthermore,melatonin inhibited TGF-β1/Smad pathway,as evidenced by decreased TGF-β1,Smad2/3 and p-Smad2/3 expression and increased Smad7 expression in liver.In conclusion,melatonin may suppress CCl4-induced hepatic fibrosis in rats via inhibiting TGF-β1/Smad pathway.It is possible for melatonin to be a potential reagent to treat and cure liver fibrosis.