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Feng Gao

Publications and source records attributed to Feng Gao.

At least 91 records · Page 5Linked to original sources
PubMed2006

Isochore structures in the chicken genome.

The availability of the complete chicken genome sequence provides an unprecedented opportunity to study the global genome organization at the sequence level. Delineating compositionally homogeneous G + C domains in DNA sequences can provide much insight into the understanding of the organization and biological functions of the chicken genome. A new segmentation algorithm, which is simple and fast, has been proposed to partition a given genome or DNA sequence into compositionally distinct domains. By applying the new segmentation algorithm to the draft chicken genome sequence, the mosaic organization of the chicken genome can be confirmed at the sequence level. It is shown herein that the chicken genome is also characterized by a mosaic structure of isochores, long DNA segments that are fairly homogeneous in the G + C content. Consequently, 25 isochores longer than 2 Mb (megabases) have been identified in the chicken genome. These isochores have a fairly homogeneous G + C content and often correspond to meaningful biological units. With the aid of the technique of cumulative GC profile, we proposed an intuitive picture to display the distribution of segmentation points. The relationships between G + C content and the distributions of genes (CpG islands, and other genomic elements) were analyzed in a perceivable manner. The cumulative GC profile, equipped with the new segmentation algorithm, would be an appropriate starting point for analyzing the isochore structures of higher eukaryotic genomes.

Algorithms↗
PubMed2006

Insulin improves cardiomyocyte contractile function through enhancement of SERCA2a activity in simulated ischemia/reperfusion.

AIM: Insulin exerts anti-apoptotic effects in both cardiomyocytes and coronary endothelial cells following ischemia/reperfusion (I/R) via the Akt-endothelial nitric oxide synthase survival signal pathway. This important insulin signaling might further contribute to the improvement of cardiac function after reperfusion. In this study, we tested the hypothesis that sarcoplasmic reticulum calcium-ATPase (SERCA2a) is involved in the insulin-induced improvement of cardiac contractile function following I/R. METHODS: Ventricular myocytes were enzymatically isolated from adult SD rats. Simulated I/R was induced by perfusing cells with chemical anoxic solution for 15 min followed by reperfusion with Tyrode's solution with or without insulin for 30 min. Myocyte shortening and intracellular calcium transients were assessed and underlying mechanisms were investigated. RESULTS: Reperfusion with insulin (10(-7) mol/L) significantly improved the recovery of contractile function (n=15-20 myocytes from 6-8 hearts, P<0.05), and increased calcium transients, as evidenced by the increased calcium [Ca2+] fluorescence ratio, shortened time to peak Ca2+ and time to 50% diastolic Ca2+, compared with those in cells reperfused with vehicle (P<0.05). In addition, Akt phosphorylation and SERCA2a activity were both increased in insulin-treated I/R cardiomyocytes, which were markedly inhibited by pretreatment of cells with a specific Akt inhibitor. Moreover, inhibition of Akt activity abolished insulin-induced positive contractile and calcium transients responses in I/R cardiomyocytes. CONCLUSION: These data demonstrated for the first time that insulin improves the recovery of contractile function in simulated I/R cardiomyocytes in an Akt-dependent and SERCA2a-mediated fashion.

Animals↗
PubMed2006

Cross-subtype T-cell immune responses induced by a human immunodeficiency virus type 1 group m consensus env immunogen.

The genetic diversity among globally circulating human immunodeficiency virus type 1 (HIV-1) strains is a serious challenge for HIV-1 vaccine design. We have generated a synthetic group M consensus env gene (CON6) for induction of cross-subtype immune responses and report here a comparative study of T-cell responses to this and natural strain env immunogens in a murine model. Three different strains of mice were immunized with CON6 as well as subtype A, B, or C env immunogens, using a DNA prime-recombinant vaccinia virus boost strategy. T-cell epitopes were mapped by gamma interferon enzyme-linked immunospot analysis using five overlapping Env peptide sets from heterologous subtype A, B, and C viruses. The CON6-derived vaccine was immunogenic and induced a greater number of T-cell epitope responses than any single wild-type subtype A, B, and C env immunogen and similar T-cell responses to a polyvalent vaccine. The responses were comparable to within-clade responses but significantly more than between-clade responses. The magnitude of the T-cell responses induced by CON6 (measured by individual epitope peptides) was also greater than the magnitude of responses induced by individual wild-type env immunogens. Though the limited major histocompatibility complex repertoire in inbred mice does not necessarily predict responses in nonhuman primates and humans, these results suggest that synthetic centralized env immunogens represent a promising approach for HIV-1 vaccine design that merits further characterization.

AIDS Vaccines↗
PubMed2006

Trans-cyclopropanation of mycolic acids on trehalose dimycolate suppresses Mycobacterium tuberculosis -induced inflammation and virulence.

Recent studies have shown that fine structural modifications of Mycobacterium tuberculosis cell envelope lipids mediate host cell immune activation during infection. One such alteration in lipid structure is cis-cyclopropane modification of the mycolic acids on trehalose dimycolate (TDM) mediated by proximal cyclopropane synthase of alpha mycolates (pcaA), a proinflammatory lipid modification during early infection. Here we examine the pathogenetic role and immunomodulatory function of mycolic acid cyclopropane stereochemistry by characterizing an M. tuberculosis cyclopropane-mycolic acid synthase 2 (cmaA2) null mutant (Delta cmaA2) that lacks trans-cyclopropanation of mycolic acids. Although titers of WT and Delta cmaA2 organisms were identical during mouse infection, Delta cmaA2 bacteria were hypervirulent while inducing larger granulomas than WT M. tuberculosis. The hypervirulence of the Delta cmaA2 strain depended on host TNF-alpha and IFN-gamma. Loss of trans-cyclopropanation enhanced M. tuberculosis-induced macrophage inflammatory responses, a phenotype that was transferable with petroleum ether extractable lipids. Finally, purified TDM lacking trans-cyclopropane rings was 5-fold more potent in stimulating macrophages. These results establish cmaA2-dependent trans-cyclopropanation of TDM as a suppressor of M. tuberculosis-induced inflammation and virulence. In addition, cyclopropane stereochemistries on mycolic acids interact directly with host cells to both positively and negatively influence host innate immune activation.

Animals↗
PubMed2006

Histidine 89 is an essential residue for Hsp70 in the phosphate transfer reaction.

Autophosphorylation of Hsp70 is detected in the process of substrate refolding in the presence of adenosine triphosphate (ATP) in the reaction mixture. But to date, the role and mechanism of Hsp70 autophosphorylation have not been elucidated. In this study we determined the site of histidine phosphorylation of Hsp70 as an intermediate in the process of phosphate transfer reaction by site-directed mutagenesis. We selected two possible sites (ie, His89 and His227) of intermediate histidine phosphorylation based on our hypothesis of the transfer of gamma-phosphoryl groups and replacement by glycine and serine. Although an acid labile autophosphorylation intermediate of Hsp70 and its cytidine diphosphate-dependent dephosphorylation were detected in wild-type Hsp70, they were markedly suppressed in the H89S mutation of Hsp70, but not on the H227S mutation. The ATPase activity and ATP synthesis activity of Hsp70 were almost completely suppressed in the H89S and H89G mutations. The role of His89 in the phosphate transfer reaction of Hsp70 is discussed.

Adenosine Diphosphate↗
PubMed2006

Maternal antenatal administration of vitamin K1 results in increasing the activities of vitamin K-dependent coagulation factors in umbilical blood and in decreasing the incidence rate of periventricular-intraventricular hemorrhage in premature infants.

AIMS: Infants less than 35 weeks' gestation age are susceptible to periventricular-intraventricular hemorrhage (PIVH). This may be partially attributable to low concentrations of vitamin K-dependent coagulation factors. The purposes of this study were: (1) to determine the umbilical blood activity levels of vitamin K-dependent coagulation factors II, VII, IX and X; (2) to investigate the change in activities of these factors in premature infants' umbilical blood after prenatal administration of vitamin K1 to the mothers; and (3) to study the prophylactic effects on PIVH after maternal antenatal supplemental vitamin K1. METHODS: Pregnant women in preterm labor at less than 35 weeks of gestation were randomly selected to receive antenatal vitamin K1 10 mg per day injection intramuscularly or intravenously for 2-7 days (vitamin K1 group, n = 40), or no such treatment (control group, n = 50). At the same period, cord blood samples were collected from thirty full-term neonates to compare the factor levels with those of premature infants. Intracranial ultrasound was performed by the same sonographer to determine the presence and severity of PIVH. RESULTS: The activities of vitamin K-dependent coagulation factors in umbilical blood in the control group were: factor II 25.64+/-9.49%, factor VII 59.00+/-17.66%, factor IX 24.67+/-8.88%, and factor X 30.16+/-5.02%. In full-term infants, the respective values were: factor II 36.70+/-4.88%, factor VII 64.54+/-10.62%, factor IX 30.18+/-5.69%, and factor X 34.32+/-12.63%. In vitamin K1 group these factors were: factor II 36.35+/-6.88%, factor VII 69.59+/-16.55%, factor IX 25.71+/-10.88%, and factor X 39.26+/-8.02%. The data suggest the absence of vitamin K-dependent coagulation factors in preterm infants, and antenatal supplement of vitamin K1 may increase the cord blood activity of factor II, VII and factor X (P < 0.001). In addition, the overall rates of PIVH in the vitamin K1 group and in controls were 32.4 and 52.0%, respectively (P = 0.036), and the frequency of severe PIVH was 5.0 and 20.0%, respectively (P = 0.038). CONCLUSIONS: Administration of vitamin K1 to pregnant women at less than 35 weeks' gestation age may result in improved coagulation and may reduce the incidence as well as the severity degree of PIVH.

Blood Coagulation Factors↗
PubMed2006

Application of chemical arrays in screening elastase inhibitors.

Protein chip technology provides a new and useful tool for high-throughput screening of drugs because of its high performance and low sample consumption. In order to screen elastase inhibitors on a large scale, we designed a composite microarray integrating enzyme chip containing chemical arrays on glass slides to screen for enzymatic inhibitors. The composite microarray includes an active proteinase film, screened chemical arrays distributed on the film, and substrate microarrays to demonstrate change of color. The detection principle is that elastase hydrolyzes synthetic colorless substrates and turns them into yellow products. Because yellow is difficult to detect, bromochlorophenol blue (BPB) was added into substrate solutions to facilitate the detection process. After the enzyme had catalyzed reactions for 2 h, effects of samples on enzymatic activity could be determined by detecting color change of the spots. When chemical samples inhibited enzymatic activity, substrates were blue instead of yellow products. If the enzyme retained its activity, the yellow color of the products combined with blue of BPB to make the spots green. Chromogenic differences demonstrated whether chemicals inhibited enzymatic activity or not. In this assay, 11,680 compounds were screened, and two valuable chemical hits were identified, which demonstrates that this assay is effective, sensitive and applicable for high-throughput screening (HTS).

Bromphenol Blue↗
PubMed2006

[Receptor mechanisms underlying the modulation of lipopolysaccharide-induced nuclear factor-kappaB expression in vascular endothelial cells by cholecystokinin octapeptide].

OBJECTIVE: To elucidate the receptor mechanisms underlying the modulation of lipopolysaccharide (LPS)-induced nuclear factor-kappaB (NF-kappaB) expression in human umbilical vein endothelial cell line ECV-304 cells by cholecystokinin octapeptide (CCK-8). METHODS: Human umbilical vein endothelial cell line ECV-304 cells were stimulated with vehicle, LPS, CCK-8 (10(-9)-10(-7) mol/L), CCK receptor non-specific antagonist proglumide, CCK-A receptor (CCK-AR) specific antagonist CR-1409 or CCK-B receptor (CCK-BR) specific antagonist CR-2945 singularly or in combination. The NF-kappaB p65 protein level was determined by Western blot and immunocytochemistry technique. RESULTS: LPS resulted in an increase in the up-regulatory expression and nuclear translocation of NF-kappaB p65 protein in ECV-304 compared with vehicle stimulation. CCK-8 obviously inhibited LPS-induced the changes in NF-kappaB p65 protein in a dose-dependent manner. The inhibitory effects of CCK-8 on NF-kappaB p65 protein expression were attenuated by proglumide>CR-2945>CR-1409. CONCLUSION: CCK-AR and CCK-BR are involved in the mediation of CCK-8 inhibitive regulation for LPS-induced NF-kappaB protein expression in ECV-04 cells, whereas the effect of CCK-BR are more than that of CCK-R.

Benzodiazepines↗
PubMed2006

[Proliferation of natural killer T cells in umbilical cord blood and peripheral blood and their different phenotypes].

Purpose of this study was to establish an effective method in vitro to proliferate natural killer T (NKT) cells from umbilical cord blood (UCB) and peripheral blood (PB), and to study their different phenotype. Mononuclear cells (MNC) from UCB and PB were cultured in the presence of IL-2 (100 U/ml), with or without alpha-Galcer. TCR Valpha24 Vbeta11 double positive natural killer T-cells (NKT cells) and their other phenotypes were determined by flow cytometry. The results showed that after expansion for 7 days, TCRValphabeta(+) NKT cells from UCB-MNCs increased by (8.74 +/- 4.37) x 10(2) times as much, but most of them did not express NK1.1 and its TCR Vbeta11(+) was higher than TCR Valpha24(+). After expansion for 14 days, TCR Valphabeta(+) NKT cells from PB-MNCs increased by (3.72 +/- 2.01) x 10(2) times, the expression of NK1.1 was high and its TCR Vbeta11(+) was almost equal to TCR Valpha24(+). It is concluded that human TCR Valpha24 Vbeta11 double positive NKT cells can expand by addition of alpha-Galcer. The proliferation efficiency in UCB-MNCs is greater than that in PB-MNCs. Most of the UCB-NKT is NK1.1(-), while the PB-NKT is NK1.1(+), a new subset of NKT cells.

Cell Proliferation↗
PubMed2006

Expression of thioredoxin-binding protein-2/vitamin D3 upregulated protein-1 in peripheral blood eosinophils of asthma patients.

OBJECTIVE: To investigate the expression of vitamin D3 upregulated protein-1 (VDUP1) in peripheral eosinophils at different stages of asthma and its correlation with clinical manifestations of asthma. METHODS: Fourteen normal volunteers and 51 mild to moderate asthma patients, including 16 untreated patients with asthma attack and 35 with asthma remission by continuously corticosterone inhalation. The symptom severity and pulmonary function indices were evaluated and induced sputum eosinophil counts and blood eosinophil count measured. VDUP1 and beta-actin gene fragments were amplified simultaneously by RT-PCR from the total RNA of peripheral eosinophils, and 10 microl of the RT-PCR product underwent agarose gel electrophoresis and the VDUP1/beta-actin ratio was obtained by Gel-Pro software. RESULTS: VDUP1/beta-actin ratio significantly decreased in untreated patients with asthma attacks in comparison with normal volunteers (0.314+/-0.242 vs 0.532 +/-0.279) but not in patients with asthma remission (0.612+/-0.381). In the former patients, a positive correlation of VDUP1/beta-actin ratio was found with FEV1.0% (r=0.587, P=0.046) and %PEF (r=0.563, P=0.033), whereas an inverse one observed with sputum eosinophil count (r=-0.436, P=0.049). CONCLUSION: VDUP1 expression in the eosinophils correlates to eosinophil activation and may influence the disease severity of asthma patients.

Actins↗
PubMed2006

[Insulin prevents injury and enhances survival of rat hepatocytes via its anti-inflammatory effects].

AIM: To investigate whether insulin exerts protective effects against hepatocytes injury indirectly induced by LPS and if so, the mechanism involved. METHODS: Kupffer cells and hepatocytes were isolated from male Sprague-Dawley rats by pronasecollagenase perfusion and cultured. Kupffer cells were stimulated by lipopolysaccharide (LPS) or LPS+insulin for 4 h, the supernatant of different groups were collected to detect TNF-alpha and IL-10 by ELISA and to stimulate the primary cultured rat hepatocytes with or without anti-TNF-alpha antibody. After the hepatocytes were stimulated for 12 h, cell survival rate and injury indexes were detected. RESULTS: (1) The supernatant of LPS-activated Kupffer cells caused significant hepatocytes injury. Treatment with insulin produced a potent protective effect as evidenced by decreased ALT and AST levels (P<0.01, n=8) and improved hepatocytes survival rate (P<0.01, n=8). (2) Compared with the LPS group, insulin significantly decreased TNF-alpha secretion (P<0.01, n=8) and increased IL-10 secretion (P<0.05, n=8) from Kupffer cell stimulated by LPS. (3) Incubating hepatocytes with anti-TNF-alpha antibody attenuated hepatocytes injury induced by the supernatant of LPS-activated Kupffer cells. But treatment with anti-TNF-alpha antibody and insulin did not exert additive effect compared with treatment with insulin alone. CONCLUSION: Insulin has protective effects on rat hepatocytes injury indirectly induced by LPS, which is associated with suppression of the pro-inflammatory cytokine TNF-alpha and increment of the anti-inflammatory cytokine IL-10 both from Kupffer cells.

Animals↗
PubMed2006

[Behaviors of Propylaea japonica (Coleoptera: Coccinellidae) in searching and preying cotton aphid Aphis gossypii (Coleoptera: Coccinellidae) in the cotton plant].

The study showed that the searching activity of P. japonica on cotton aphid Aphis gossypii decreased gradually with decreasing aphid density. When enough A. gossypii existed, P. japonica had a preferential searching and preying activity on the top of cotton plant. There was no significant difference in the preying activity of P. japonica at different positions of cotton plant, while the searching activity of the ladybird beetle was significantly lower on cotton M9101 than on cotton Zhongmian 13. The preying behavior of P. japonica was significantly correlated with the density and distribution of A. gossypii.

Animals↗
PubMed2006

[Studies on gene expression and the 5' CpG islands methylation status of E-cadherin in acute myeloid leukemia].

OBJECTIVE: To study the relationship between E-cadherin gene expression and the methylation status of E-cadherin 5' CpG islands in acute myeloid leukemia (AML). METHODS: Reverse transcription-PCR (RT-PCR), flow cytometry and methylation specific PCR were used to analyze the E-cadherin gene and protein expression and its 5' CpG island methylation status respectively in bone marrow cells from 55 AML patients and 7 normal controls. RESULTS: AML cells displayed a significant reduction or lack of E-cadherin gene and protein expression, the positive rates were 23.6% and 18.2% (P < 0.01), respectively. All normal bone marrow cells were E-cadherin positive. Thirty-eight of the 55 patients (69.1%) were E-cadherin 5' CpG island methylated whereas the normal controls were completely unmethylated. Twenty-nine of thirty-one (93.5%) E-cadherin-negative samples showed abnormal hypermethylation of the E-cadherin CpG islands. CONCLUSION: Expression downregulation and methylation of E-cadherin gene in AML suggest that it might be an important event in AML. E-cadherin methylation was associated with the inhibition of E-cadherin gene and protein expression in AML.

Cadherins↗
PubMed2006

[Platelet-derived microparticles stimulate proliferation of granulocyte-macrophage progenitor cells from umbilical cord blood].

This study was aimed to investigate the effect of platelet-derived microparticles (PMP) on stimulating the proliferation of granulocyte-macrophage progenitors (CFU-GM) from umbilical cord blood. Different concentrations of thrombin were adopted to activate the platelets for releasing PMP. Flow cytometry was adopted to evaluate the efficiencies of different concentrations of thrombin to produce PMP. Umbilical cord blood mononuclear cells (MNC) were obtained from healthy donors and the MNC were isolated by Ficoll density gradient centrifugation. MNC were cultured in 2.7% methylcellulose containing different concentration of PMP and colonies were counted under an inverted microscope after 7 days. The result showed that the release rate of PMP activated by 2.0, 1.5, 1.0 and 0.5 U/ml thrombin were 28.7%, 47.7%, 50.1% and 43.9% respectively. The PMP enhanced colony formation in dose-dependent manner. The number of colonies per 2 x 10(5) MNCs in groups of PMP at different concentrations (10, 50 and 100 microg/ml) were 119.8 +/- 32.2,142.8 +/- 45.2 and 180.8 +/- 85.1 respectively. The number of colonies in the groups of PMP at 100 microg/ml and 50 microg/ml were statistically significant when compared with control group (103.0 +/- 24.8) (P < 0.05). The number of colonies per 2 x 10(5) MNC in the group of PMP (10 microg/ml) was 119.8 +/- 32.2 which was higher than that in control group, but there was no statistical significance between two groups. It is concluded that platelet activated with 1.0 U/ml thrombin can get the best release efficiency of PMP and PMP can enhance the proliferation of granulocyte-macrophage progenitor cells of umbilical cord blood.

Blood Platelets↗
PubMed2006

[Expression of P33ING1, P53 and their relationship with apoptosis in anal canal carcinoma].

OBJECTIVE: To explore the expressions of P33ING1, P53 and their relationships with apoptosis in anal canal carcinoma (ACC). METHODS: The expressions of P33ING1, P53 proteins were measured by immunohistochemistry method (SP method), and apoptosis was detected in 42 cases with ACC, 36 cases with anal canal adenoma (ACA) or anal canal papilloma (ACP), and 40 cases with paraanal inflammatory mass(PAIM). RESULTS: The positive expression rates of P33ING1 and P53 proteins were 40.5% (17/42), 97.2% (35/36) and 97.5% (39/40), 50.0% (21/42), 22.2% (8/36) and 27.5% (11/40) respectively, and the average apoptosis indexes(AI) were (10.27+/- 1.23) per thousand, (42.75+/- 0.98) per thousand and (42.67+/- 1.04) per thousand respectively in ACC, ACA or ACP and PAIM. There were significant differences in the positive expression rates of P33ING1, P53 and apoptosis index between ACC and the other two groups respectively (P< 0.05). Among 21 cases of ACC with positive expression of P53 protein,there were 18 cases with P33ING1 negative expression. CONCLUSIONS: P33ING1 expression decrease in ACC, which may play an important role in the carcinogenesis and progression of ACC. P33ING1 and P53 may have an synergistic effect of suppressing cell growth and accelerating cell apoptosis.

Adult↗
PubMed2006

[Nitroglycerin tolerance aggravates arterial ischemia/reperfusion injury by increasing nitrotyrosine and ONOO- production].

OBJECTIVE: To investigate the influence of nitroglycerin tolerance (NT) on arterial ischemia (90 min) and reperfusion (120 min). METHODS: Male Sprague-Dawley rats were infused with nitroglycerin (GTN) or saline for 12 h and ascending aorta was rapidly isolated. The isolated aorta was subjected to one of the following treatments: stimulative ischemia/reperfusion, stimulative ischemia/reperfusion (I/R) plus glutathione (GSH, 0.1 mmol/L) during reperfusion, or control solution (Kreb's solution for 3.5 h). RESULTS: Compared with I/R group, contractile function, vasorelaxation responses to Ach, NO production were significantly decreased and CK, LDH activity as well as nitrotyrosine formation in reperfusion solution were significantly increased in I/R + NT group and these effects could be prevented with addition of GSH in I/R + NT aortas. CONCLUSIONS: Our results demonstrated that NT could aggravate arterial I/R injury by increasing the production of ONOO- and GSH may play a cardioprotective role against NT-induced myocardial injury by attenuating the formation of ONOO-.

Animals↗