Biomedical subjects
Publications and source records attributed to L Yang.
A Arachnia sp. P163 producing alcohol dehydrogenase which is able to reduce aminoacetophenone to R-1-phenyl-2-aminoethanol was obtained from soil and cultures. The maximum activity of enzyme was produced by the LB medium containing 1% sodium citrate and peptone, 0.1% phenylaminoethanol as inducer at 30 degrees C for 48 hs.
The effect of zinc deficiency and zinc replenishment on HOX3.5 gene expression in mouse embryos was investigated. Sixty Kunming female mice (25-30 g) were divided into three groups: zinc-deficient groups (ZD), zinc-replenished group (ZR) and zinc normal controlled group (ZN). ZD mice fed with ZD diet (Zn 3.0 +/- 0.5 mg/kg), ZN mice fed with ZN diet (Zn 30 mg/kg), and ZR mice fed with ZD diet at first and then with ZN diet from the 7th day of pregnancy. After feeding different diet for 25 days, the mice were made to copulate (female: male = 2:1). At the 12th day of pregnancy, the mice were killed and the embryos were stored at -70 degrees C. The content of mRNA of HOX3.5 in the embryos were determined by in situ hybridization with digxigenin-labeled cDNA probes. The result showed that the expression on area density and L-density (average optical density) of Hox3.5 in ZD and ZR groups were decreased in comparing with those in ZN group (P < 0.05). It was suggested that the decreased HOX3.5 gene expression by zinc deficiency might influence the normal growth of mouse embryos, and this effect might occurr in the early stage of embryo development, which can not be prevented by replenishing zinc at the 7th day of pregnancy.
OBJECTIVE: To investigate the role of calcitonin gene related peptide(CGRP) and endothelin-1 (ET-1) in cirrhotic cardiomyopathy (CCM). METHODS: We measured the level of CGRP and ET-1 in the samples of rat heart collected from 15 liver cirrhosis rats and 15 controls by using radio immunoassay. RESULTS: The data showed that the levels of CGRP (74.2130 +/- 10.3776 pg/mg protein) and ET-1 level (1.4780 +/- 0.9235 pg/mg protein) were significantly higher in the cirrhotic rat hearts than those in controls (P < 0.05). The increase of ET-1 in the cirrhotic rat hearts was closely associated with the severity of liver cirrhosis (P = 0.004); whereas no significant association was seen between the CGRP concentration and the severity of liver cirrhosis (P = 0.307). CONCLUSION: We infer that the increasing of CGRP level in the cirrhotic rat heart may be a protective or antagonistic reaction to ET-1 or other pathogenic factors for cardiac dysfunction. The disturbance of the balance between CGRP and ET-1 in the liver cirrhosis rat hearts may contribute to the pathologic process of CCM.
OBJECTIVE: The aims of this study were to determine 1. the variation of blood TGF beta 1 and ET-1 in patients with liver cirrhosis; 2. the relationship of the blood TGF beta 1 and ET-1 with Child degree of liver function and the severity of esophageal varices. METHODS: Peripheral blood samples were obtained from 72 patients and 24 normal controls. The blood levels of TGF beta 1 and ET-1 were measured by using a standard bioassay and the radioimmunoassay. RESULTS: TGF beta 1 level (11.77 +/- 1.32 ng/ml) and ET-1 level (78.37 +/- 17.54 pg/ml) were significantly higher in the patients than those in controls(P < 0.05). The increase of the ET-1 in the patients is closely associated with Child degree of liver function (r = 0.94) and the severity of esophageal varices(r = 0.87). TGF beta 1 concentration is not associated with Child degree of liver function (r = 0.11) and the severity of esophageal varices (r = 0.03). CONCLUSION: TGF beta 1 and ET-1 may play an important role in the pathophysiologic process of cirrhosis. ET-1 concentration may reflect portal hypertension development.
OBJECTIVE: To observe the activity of c-Jun N-terminal kinase/stress-activated protein kinase (JNK/SAPK) and assess the correlation between JNK/SAPK activity and ICAM-1 expression on mesangial cells in mesangial proliferative glomerulonephritis(MSPGN). METHODS: Seven patients with MSPGN and 6 controls were selected for this study. JNK/SAPK activity was detected by immunoprecipitation and western blotting; RT-PCR was used to detect ICAM-1 mRNA expression, and flow cytometry was used to analyze cell surface ICAM-1 expression. RESULTS: Either in spontaneous condition or under the stimulus of TNF alpha, the activity of JNK/SAPK on mesangial cells in vitro in MSPGN was higher than that of the controls(P < 0.05); the activity of JNK/SAPK in MSPGN was found to have a positive correlation with the levels of ICAM-1 mRNA and protein. The levels of ICAM-1 mRNA and protein were increased by TNF alpha stimulation while the levels ICAM-1 mRNA and protein were decreased by DMAP inhibition (P < 0.01). CONCLUSION: JNK/SAPK may have been aberrantly activated in MSPGN, which may involve in the overexpression of ICAM-1 in MSPGN.
OBJECTIVE: To observe the effects of transforming growth factors beta 1 (TGF beta 1) on the expression of integrin beta 3 and the activity of focal adhesion kinase (FAK). METHODS: This study was performed on cultured human endothelial cells (EC) by using cell-ELISA and immunoprecipitation-tyrosine kinase assay respectively. RESULTS: Under the stimulus of TGF beta 1, there a dose-dependent increase in the expression of integrin beta 3 chain in the surface of EC. And after the cultured EC were treated with 5 ng/ml or 10 ng/ml TGF beta 1 for 6 or 24 hours, the FAK activity in EC increased significantly as compared with the control group (P < 0.05). CONCLUSION: The expression of integrin beta 3 and the activity of FAK on EC were regulated by TGF beta 1, and this regulation may be important in cell adherence, angiogenesis, and in the pathophysiology of atherosclerosis.
OBJECTIVE: To analyze and predict the trends of incidence and mortality rates of esophageal cancer in areas of Taihang Mountains, and explore the strategies for facilitating the reduction of the incidence and mortality of esophageal cancer. METHODS: The data were collected from Linxian and Cixian Counties registries between 1988-1997. The trends of the incidence and mortality rates for esophageal cancer had been fitted and predicted by the model of BP (Back Propagation) Neural Networks. Then Linqi Xiang in Linxian County was taken as an example, to determine the power for reducing incidence and mortality of esophageal cancer using endoscopic technology as an early detection and treatment method. RESULTS: There were slowly declining trends for both incidence and mortality rates during past 10 years in Taihang Mountains. The predicting rates of the esophageal cancer incidence in 2,002 are 115. 70/100,000 for male and 79.88/100,000 for female; mortality rates are 94.00/100,000 and 56.29/100,000 respectively. Both incidence and mortality rates a still in high level. But when using endoscopic technology as an early detection and treatment method, the incidence rate is nearly 1/3 of a control group and the power is 88.30% at the end of eight years. The mortality rate is 1/4 of the control group and power is 89.44% after five years intervention (both powers based on 0.05 significant levels). CONCLUSIONS: The incidence and mortality rates for esophageal cancer are still on high levels in Taihang Mountains. We should continue to enhance our preventive effort there. After using endoscopic technology as an early detection and treatment method, the incidence and mortality rates will be decreased markedly during 5 to 8 years. It is recommended to implement a large-scale secondary prevention strategy in these areas.
OBJECTIVE: The effect of platelet factor four (PF4) on human neutrophil function was studied. METHODS: Crystal violet dye staining, immunofluorescence labeling, PKC kit assay, NBT and HVA fluoro-spectrophotometry were applied to study the effect of PF4 on total adherence, integrin CD11b level, PKC level and respiratory burst level of resting human neutrophils and FMLP/or PMA-stimulated human neutrophils. RESULTS: It was found that PF4 slightly increased the total adherence of resting human neutrophils. There was no change on integrin CD11b level and respiratory burst level of resting human neutrophils after interaction with PF4. However, PF4 significantly down-regulated the total adherence, integrin CD11b level and respiratory burst level of human neutrophils stimulated by FMLP/or PMA. In addition, PF4 did not influence PKC level on resting and activated human neutrophil. CONCLUSION: These results indicate that PF4 plays a down regulation of the function of human neutrophils. Differing from other members of classical CXC-chemokine family, the signaling of PF4 is not through PLC-PKC signal pathway.
OBJECTIVE: To investigate hnRNPA2/B1's role in rheumatoid synovitis by obtaining its cDNA sequence and analyzing its expression in synovium. METHODS: Total RNA was isolated from peripheral blood mononuclear cells (PBMC) and the RT-PCR was performed. The fragment was cloned into PUC-T1 plasmids and further sequenced. We detected it's expression in synovium with monoclonal antibodies and specific cDNA probes by immunohistochemistry and in situ hybridization. RESULTS: The fragment was identified by DNA sequencing. The expression in rheumatoid synovium was higher than that from osteoarthritis and the normal controls (P < 0.05). CONCLUSION: hnRNP A2/B1 cDNA has been cloned successfully and hnRNP A2/B1 might play an important role in rheumatoid synovitis.
OBJECTIVE: To evaluate the efficacy and safety of single-dose oral antibiotic prophylaxis in the METHODS: Between prevention of post-procedure infections in patients undergoing transrectal prostate biopsy. September 1998 and March 2001, a total of 192 patients who had an abnormal digital rectal examination and/or prostate specific antigen 4 ng/ml or greater underwent transrectal ultrasound guided systematic 13 cores prostate biopsy. The patients were randomly divided into three groups. Group A (62) received a placebo (Vit C) tablet twice a day for 3 days, group B (64) a single dose of ciprofloxacin (0.5 g) and metronidazole (0.4 g), and group C (66) the same combination twice a day for 3 days. Urine cultures were obtained 48 h after the biopsy and blood cultures when patients who developed fever. RESULTS: Noninfective complications included were rectal bleeding, haematuria and pain. Infective complications included urinary tract infection and fever. There was no significant difference among the three groups in noninfective complications but the incidence of infective complications in group A was significantly higher than in groups B and C (P < 0.01). There was no significant difference among group B and C in infective complications (P > 0.05). CONCLUSIONS: Our study shows single-dose oral antibiotic prophylaxis is effective and safe to prevent infectious complications follow transrectal prostate biopsy.
OBJECTIVE: To study the effect of arsenic trioxide (As2O3) or all-trans retinoic acid (ATRA) on coagulopathy in patients with acute promyelocytic leukemia (APL), and the mechanism of hemorrhage in these patients. METHODS: Thrombomodulin (TM) or tissue factor (TF) transcription of mRNA of freshly isolated bone marrow blast from APL patients was detected by semi-quantitative RT-PCR. The parameters of coagulation and cell procoagulation activity (PCA) were assessed in plasmic levels. Bleeding symptom was observed during As2O3 or ATRA treatment. RESULTS: TM expression in the APL cell surface was significantly upregulated from (14.31 +/- 1.60) ng/10(7) to (21.61 +/- 6.82) ng/10(7) cells. The levels of P-selectin, soluble fibrin monomer complex (SFMC) and D-dimer (D-D) decreased after ATRA or As2O3 treatment. Abnormal high expression of TF in APL cell was downregulated in patients treated with ATRA or As2O3. The expression level was (14.81 +/- 6.23) ng/L before treatment, but undetected after 20 days of treatment. In addition, the membrane PCA of fresh APL cells was predominantly FVII-dependent after ATRA or As2O3 treatment. Bleeding symptom was ameliorated during As2O3 or ATRA treatment. CONCLUSION: Bleeding symptom was controlled in patients with APL after As2O3 or ATRA treatment.
The non-essential amino acids L-serine (Ser) and glycine (Gly) have recently been shown to exhibit specific actions in the nervous system. In the present study, L-Ser and Gly promoted the survival of cultured rat cerebrocortical neurons in a concentration-dependent manner as revealed by Alamar blue assay and microtubule-associated protein-2 (MAP2) immunoblotting. The maximum effects of the amino acids were detected at the concentrations of 30-100 microM. L-Ser was more effective than Gly. D-Ser failed to promote neuronal survival. L-Ser and Gly upregulated expression of the anti-apoptotic gene product Bcl-w, while they did not affect the expression of Bcl-xL. The promotion of neuronal survival by L-Ser and Gly may be, at least in part, attributable to the upregulated Bcl-w.
The title compound, PrCl3.C6H12O6.9 H2O crystallized in the monoclinic space group P2(1)/n with cell dimensions a = 15.8293(3), b = 8.67750(10), c = 16.2292(3) A, beta = 107.0788(8) degrees, V = 2130.92(6) A3 and Z = 4. Each Pr ion is coordinated to nine oxygen atoms, two from the inositol and seven from water molecules, with Pr-O distances from 2.4729 to 2.6899 A; the other two water molecules are hydrogen-bonded. No direct contacts exist between Pr and Cl. There is an extensive network of hydrogen bonds formed by hydroxyl groups, water molecules, and chloride ions. The IR spectra of Pr-, Nd-, and Sm-inositol complexes are similar, which shows that the three metal ions have the same coordination mode. The IR results are consistent with the crystal structure.
Ewing's sarcoma displays a characteristic chromosomal translocation that results in fusion of the N-terminal domain of the Ewing's sarcoma protein (EWS) to the C-terminal DNA-binding domain of the ETS family transcription factor Fli-1 (Friend leukemia integration-1). EWS possesses structural motifs suggesting a role in transactivation as well as RNA binding. We demonstrate that wild-type EWS protein functions as an adapter molecule coupling transcription to RNA splicing by binding to hyperphosphorylated RNA polymerase II through the N-terminal domain of EWS and recruiting serine-arginine (SR) splicing factors through the C-terminal domain of EWS. The oncogenic EWS.Fli-1 fusion protein retains the ability to bind to hyperphosphorylated RNA polymerase II but lacks the ability to recruit SR proteins because of replacement of the C-terminal domain of EWS by Fli-1. In an in vivo splicing assay, the EWS.Fli-1 fusion protein inhibits SR protein-mediated E1A pre-mRNA splicing in a dominant-negative manner. These results indicate that EWS.Fli-1 interferes with the normal function of EWS and implicate uncoupling of gene transcription from RNA splicing in the pathogenesis of Ewing's sarcoma.
We have previously shown that 25-hydroxycholesterol (25-OHC) treated CHO-K1 cells could be used as a model to investigate the signaling pathway of apoptosis induced by oxidized LDL in vascular cells. In the present study, we examine the execution phase of the apoptotic pathway in CHO-K1 cell death induced by 25-OHC. Oxysterol-induced apoptosis in CHO-K1 was accompanied by caspase activation and was preceded by mitochondrial cytochrome c release. The addition of a competitive caspase-3 inhibitor, Ac-DEVD-CHO, prevented 25-OHC-induced apoptotic cell death. Furthermore, immunoblot analysis showed that 25-OHC treatment induced the degradation of poly(ADP-ribose) polymerase (PARP)-a substrate for caspase 3 and a key enzyme involved in genome surveillance and DNA repair. Thus, we could demonstrate in CHO-K1 cells that 25-OHC activates the apoptotic machinery through induction of the release of cytochrome c from mitochodria into the cytosol and activation of a typical caspase cascade.
TRAF6 is a signal transducer in the NF-kappaB pathway that activates IkappaB kinase (IKK) in response to proinflammatory cytokines. We have purified a heterodimeric protein complex that links TRAF6 to IKK activation. Peptide mass fingerprinting analysis reveals that this complex is composed of the ubiquitin conjugating enzyme Ubc13 and the Ubc-like protein Uev1A. We find that TRAF6, a RING domain protein, functions together with Ubc13/Uev1A to catalyze the synthesis of unique polyubiquitin chains linked through lysine-63 (K63) of ubiquitin. Blockade of this polyubiquitin chain synthesis, but not inhibition of the proteasome, prevents the activation of IKK by TRAF6. These results unveil a new regulatory function for ubiquitin, in which IKK is activated through the assembly of K63-linked polyubiquitin chains.
The p38 family of mitogen-activated protein kinases (MAPKs) mediates signaling in response to environmental stresses and inflammatory cytokines, but the requirements for the p38 MAPK pathway in normal mammalian development have not been elucidated. Here, we show that targeted disruption of the p38alpha MAPK gene results in homozygous embryonic lethality because of severe defects in placental development. Although chorioallantoic placentation is initiated appropriately in p38alpha null homozygotes, placental defects are manifest at 10.5 days postcoitum as nearly complete loss of the labyrinth layer and significant reduction of the spongiotrophoblast. In particular, p38alpha mutant placentas display lack of vascularization of the labyrinth layer as well as increased rates of apoptosis, consistent with a defect in placental angiogenesis. Furthermore, p38alpha mutants display abnormal angiogenesis in the embryo proper as well as in the visceral yolk sac. Thus, our results indicate a requirement for p38alpha MAPK in diploid trophoblast development and placental vascularization and suggest a more general role for p38 MAPK signaling in embryonic angiogenesis.
Mitotic root micronucleus (MCN) frequency in Vicia faba as a bioassay, is primarily based on the extent of the sentinel Vicia response in terms of cytogenetic damage quantitatively or qualitatively to indicate the presence of mutagenic contaminants. This paper describes an investigation designed to assess changes in MCN frequencies of Vicia faba from three generation plants obtained, respectively from a reference site (RS) and a metal-contaminated experimental field (EF) in the bioassay of mutagenic Cd(2+) and NaN(3). The background value, dose-response to Cd(2+) and to NaN(3) in three generation (F(1), F(2) and F(3)) plants of the EF and the initial (F(0)) plants were determined in terms of MCN frequencies. With more generations of growing Vicia plants in the EF, a higher background value of MCN frequency, a lower slope value in the regression equation, a smaller ratio of MCN frequency between the control and treatment in the same generation and larger perturbation values were observed. This denotes that the decreased reliability and efficiency are represented in Vicia plants from the EF if the plants are used as sentinels in the bioassay of mutagenic Cd(2+) and NaN(3). It was concluded that the Vicia MCN bioassay should be used as an endpoint biomarker acceptable in biomonitoring environmental mutagens when the sentinel plants were collected from clean areas. Because no place is absolutely without pollutants, it is suggested that several seed stock centers should be established for providing sentinel Vicia if Vicia MCN bioassay is used as a biomarker to identify the global environmental status.