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Li Yao

Publications and source records attributed to Li Yao.

At least 19 recordsLinked to original sources
PubMed2006

Evidence of the formation and conversion of unstable thionyl isocyanate: Gas-phase spectroscopic studies.

Thionyl diisocyanate which is unstable at ambient temperature is generated from a heterogeneous reaction of gaseous thionyl dichloride with silver cyanate and studied for the first time in the gas phase at 298 K. N-isocyanatoformyl sulfinylimide is also observed with photoelectron spectroscopy in the gas phase for the first time. The conversion of thionyl diisocyanate to N-isocyanatoformyl sulfinylimide via 1,3 shift at different temperatures is studied by using photoelectron spectroscopy and mass spectroscopy with the help of theoretical computations. On the basis of combined observations and quantum chemical calculations, possible 1,3-isocyanato shifts and dissociation processes for thionyl isocyanate and its cation have been discussed in detail.

Electrons↗
PubMed2006

The effect of cholecyst-derived extracellular matrix on the phenotypic behaviour of valvular endothelial and valvular interstitial cells.

Cholecyst-derived extracellular matrix (CEM) is a novel, proteinaceous biomaterial, derived from the porcine cholecyst, which may have potential applications as a scaffold in the area of heart valve tissue engineering. In this study the potential of CEM to support the proliferation of valvular endothelial cells (VECs) and valvular interstitial cells (VICs), while maintaining their phenotypic mRNA synthesis, protein expression and morphology was assessed by biochemical assays, electron microscopy, immunostaining and reverse-transcriptase polymerase chain reaction. VICs and VECs were isolated from the porcine aortic valve and techniques were developed for the isolation of CEM for cell culture. VECs and VICs cultured on CEM adhered and proliferated, maintaining their phenotypic morphology. VECs synthesised von Willebrand factor mRNA and endothelial nitric oxide synthase (eNOS) mRNA and expressed eNOS and VICs synthesised alpha-smooth muscle actin (alphaSMA) mRNA and expressed alphaSMA. Cellular area fraction of VICs expressing alphaSMA was 87.7+/-6.8% and cellular area fraction of VECs expressing eNOS was 93.8+/-9.3%. Findings of this study support the hypothesis that CEM is a potential biomaterial for tissue engineered heart valve scaffold design.

Animals↗
PubMed2006

Analysis of diversity and activity of sulfate-reducing bacterial communities in sulfidogenic bioreactors using 16S rRNA and dsrB genes as molecular markers.

Here we describe the diversity and activity of sulfate-reducing bacteria (SRB) in sulfidogenic bioreactors by using the simultaneous analysis of PCR products obtained from DNA and RNA of the 16S rRNA and dissimilatory sulfite reductase (dsrAB) genes. We subsequently analyzed the amplified gene fragments by using denaturing gradient gel electrophoresis (DGGE). We observed fewer bands in the RNA-based DGGE profiles than in the DNA-based profiles, indicating marked differences in the populations present and in those that were metabolically active at the time of sampling. Comparative sequence analyses of the bands obtained from rRNA and dsrB DGGE profiles were congruent, revealing the same SRB populations. Bioreactors that received either ethanol or isopropanol as an energy source showed the presence of SRB affiliated with Desulfobulbus rhabdoformis and/or Desulfovibrio sulfodismutans, as well as SRB related to the acetate-oxidizing Desulfobacca acetoxidans. The reactor that received wastewater containing a diverse mixture of organic compounds showed the presence of nutritionally versatile SRB affiliated with Desulfosarcina variabilis and another acetate-oxidizing SRB, affiliated with Desulfoarculus baarsii. In addition to DGGE analysis, we performed whole-cell hybridization with fluorescently labeled oligonucleotide probes to estimate the relative abundances of the dominant sulfate-reducing bacterial populations. Desulfobacca acetoxidans-like populations were most dominant (50 to 60%) relative to the total SRB communities, followed by Desulfovibrio-like populations (30 to 40%), and Desulfobulbus-like populations (15 to 20%). This study is the first to identify metabolically active SRB in sulfidogenic bioreactors by using the functional gene dsrAB as a molecular marker. The same approach can also be used to infer the ecological role of coexisting SRB in other habitats.

Bacterial Typing Techniques↗
PubMed2006

Gas-phase generation and electronic structure investigation of chlorosulfanyl thiocyanate, ClSSCN.

The chlorosulfanyl thiocyanate molecule, ClSSCN, was generated in the gas phase through heterogeneous reaction of SCl2 on the surface of finely powdered AgSCN for the first time. The reaction products were detected and characterized in situ by ultraviolet photoelectron and photoionization mass spectrometry. The molecular geometry and electronic structures of ClSSCN were investigated by a combination of PES experiment and theoretical calculations with the density functional theory and ab initio methods. It was found that the outermost electrons of ClSSCN reside in the Cl-S antibonding pi orbital, predominantly localized on the sulfur atom, and the experimental first vertical ionization potential of ClSSCN is 10.20 eV. The dominant fragment SSCN+ in the mass spectrum indicates that the ClSSCN cation prefers the dissociation of the Cl-S bond.

Journal Article↗
PubMed2006

Gas-phase spectroscopy of the unstable sulfur diisocyanate molecule S(NCO)2.

Sulfur diisocyanate is generated from a heterogeneous reaction of gaseous sulfur dichloride with silver cyanate and studied for the first time in the gas phase. Combined with quantum chemical calculations, the electronic structure is characterized by photoelectron spectroscopy (PES). Simultaneously, an investigation of the possible ionization and dissociation processes for the molecular cation is presented based on experimental soft ionization mass spectrometry. From the calculated bond-dissociation energies, the dissociation pathway is determined. S(NCO)2+ undergoes 1,3-sigmatropic rearrangement with a smaller barrier height (9.9 kcal mol(-1)) than the neutral counterpart. Thus, the 1,3-sigmatropic rearrangement is preferred for the molecular cation, and OCNCO+ and NS+ is produced by subsequent dissociation of the rearrangement product. The analysis agrees very well with the experimental mass spectrum.

Journal Article↗
PubMed2006

Electronic structures of acyl nitrites and nitrates.

The gas phase electronic structures of CM(3)C(O)ONO and CM(3)C(O)ONO(2) (M=H, Cl, F) are studied by photoelectron spectroscopy (PES) combined with the outer valence Green's function (OVGF) calculations at 6-311+G(d, p) basis sets. The highest occupied molecular orbital (HOMO) for each compound is the carbonyl oxygen lone pair (n(O)), the ionizations of these orbitals are associated with the vibrational frequency about 1750 and 1820 cm(-1) reflected on the first band, respectively, for acyl nitrites and nitrate. Comparing with the calculated energies, it can be concluded that the syn conformers with Cs overall symmetry, a planar CC(O)ONO skeleton in nitrites, and a planar CC(O)ON skeleton in nitrates, respectively, are the most stable in the gas phase.

Electrons↗
PubMed2006

Potent potentiating diuretic effects of prednisone in congestive heart failure.

UNLABELLED: Animal studies showed glucocorticoids could specifically dilate renal vasculature, regulate synthesis and release of atrial natriuretic peptide (ANP), upregulate ANP receptors on vascular endothelial cells, and thus have potent potentiating diuresis and natriuresis effects in animal studies; however, their diuretic efficacy in humans is yet to be known. Therefore, we designed this randomized, double- blind, placebo-controlled, clinical study to determine the diuretic efficacy of prednisone, a glucocorticoid, in patients with congestive heart failure (CHF). METHODS: Twenty clinically stable patients with CHF without overt fluid retention were randomized to a prednisone group or placebo group. Prednisone (1 mg/kg/day with a maximum dose of 60 mg/day) was added to standard care for 7 days, leaving other medications unchanged. Variables included urine volume and electrolytes, serum electrolytes, and change from baseline in serum creatinine. RESULTS: Adding prednisone resulted in striking diuresis and natriuresis with time. As compared with the placebo group, the maximum of mean daily urine volume was 810.5 mL larger than those in the placebo group (95% confidence intervals [CI] 276.25 to 1344.86, P < 0.05). The maximum mean daily sodium excretion was 123.8 mmol higher than those patients given placebo (95% CI 11.4 to 236.2, P < 0.05). The placebo-corrected effect on change from baseline in serum creatinine was -19.5 mumol/L (95% CI -7.4 to -31.6, P < 0.01), favoring prednisone. CONCLUSIONS: This pilot study showed that prednisone had potent potentiating diuretic effects in patients with heart failure and might improve renal function in the same time. Further prospective randomized clinical studies are warranted to determine the preferable dose and its efficacy in decompensated congestive heart failure.

Adult↗
PubMed2006

[Construction of the prokaryotic expression vector and expression of human CIDE-3 gene].

AIM: To construct a prokaryotic expression vector for human CIDE-3 gene, and to express the gene in E.coli BL21(DE3). METHODS: The total RNA was extracted from human hepatocellular carcinoma cell line HepG2. CIDE-3 gene fragment was amplified by RT-PCR and was cloned into the pET28a(+) vector. The recombinant vector was identified by restriction endonuclease digestion analysis and DNA sequencing, and then it was transformed into E.coli BL21(DE3) through IPTG induction to express the target protein bearing His tag. RESULTS: A 516 bp of CIDE-3 gene fragment was obtained. After E.coli BL21(DE3) was transformed with recombinant vector pET28a(+)-CIDE-3 and through IPTG induction, the recombinant protein with relative molecular masse about 23,000 was obtained. SDS-PAGE analysis showed that the expressed product was mainly inclusion bodies, accounting for 32% of the total bacterial proteins. CONCLUSION: Recombinant expression vector pET28a(+)-CIDE-3 is constructed successfully. The expressed CIDE-3 protein will be helpful to our further research.

Apoptosis Regulatory Proteins↗
PubMed2006

[The expression and clinical significance of hematopoietic cell phosphatase and cysteinyl aspartate-specific proteinase in leukemia].

OBJECTIVE: To evaluate the relationship between the expression of hematopoietic cell phosphatase (SHP-1) gene or cysteinyl aspartate-specific proteinases (Caspase-1, 3) gene and the effect of chemotherapy in leukemia patients. METHODS: The expression of SHP-1 and Caspase-1, 3 gene was measured in leukemia patients with reverse transcriptase-polymerase chain reaction. RESULTS: The positive rate of SHP-1 and Caspase-1, 3 gene in acute leukemia was 33.3%, 80.0% and 100.0%. The positive rate of SHP-1 in chronic myeloid leukemia (CML)-blastic phase and CML-chronic phase was 0.0%, 37.5%. The first complete remission (CR) rate of SHP-1 and Caspase-1, 3 positive group was 85.0%, 64.3% and 55.8%, which were higher than that of SHP-1 and Caspase-1, 3 negative group (P < 0.05). There was a positive correlation between SHP-1 and Caspase-1, 3. CONCLUSIONS: SHP-1 gene is potentially an anti-oncogene and may play a role through activation of Caspase-1, 3 gene. The expression of SHP-1 and Caspase-1, 3 is associated with remission rate and it is shown that they participate in the prognosis of leukemia. They could be used as indices for evaluating therapeutic efficacy and judging prognosis in leukemia patients.

Adolescent↗
PubMed2006

[Expression and clinical value of SHP-1 and c-kit in acute leukemia].

The aim of study is to investigate the expression of hematopoietic cell phosphatase (SHP-1) gene and c-kit pro-oncogene in acute leukemia (AL) and its impact on prognosis in AL. Semi-quantity reverse transcriptase-polymerase chain reaction (RT-PCR) was used to detect the expression of SHP-1 mRNA and c-kit mRNA in 60 AL patients and 33 normal controls (NC). The results showed that the positive rates of SHP-1 expression from high to low level were found orderly in complete remission group, newly diagnosed group and relapsed group, there was significance difference between each group and NC group (P < 0.05). The positive rates of c-kit expression were opposite order in each groups as compared with SHP-1. there was also significance difference between each group and NC group (P < 0.05). The positive rate of SHP-1 and c-kit expressions in AML was higher than that in ALL (P < 0.05), there was negative correlation between expressions of SHP-1 and c-kit (r = -0.502, P < 0.05); The difference between the complete remission rate in SHP-1 positive and in SHP-1 negative patients from 30 newly diagnosed AML patients was significant (P < 0.05), the same result was found between c-kit(+) complete remission and c-kit(-) complete remission. It is concluded that SHP-1 gene is a potentially anti-oncogene and inhibits the growing of tumor by negatively modulating c-kit gene. Simultaneous detection of SHP-1 and c-kit gene may act as a factor for predicting prognosis in AL.

Adolescent↗
PubMed2005

Trans-activation of EphA4 and FGF receptors mediated by direct interactions between their cytoplasmic domains.

A yeast two-hybrid analysis has shown that the juxtamembrane region of FGF receptor 3 (FGFR3) interacts with the cytoplasmic domain of EphA4, which is a member of the largest family of receptor tyrosine kinases. Complex formation between the two receptors was shown to be mediated by direct interactions between the juxtamembrane domain of FGFR1, FGFR2, FGFR3, or FGFR4 and the N-terminal portion of the tyrosine kinase domain of EphA4. Activation of FGFR1 in transfected cells resulted in tyrosine phosphorylation of a kinase-negative EphA4 mutant and activation of EphA4 led to tyrosine phosphorylation of a kinase-negative FGFR1 mutant. Moreover, both receptors stimulate tyrosine phosphorylation of the docking protein FRS2alpha and induce mitogen-activated protein kinase stimulation with a time course and intensity that depends on the ligand that is applied. We also demonstrate that FGF-receptor-mediated mitogen-activated protein kinase stimulation is potentiated in cells costimulated with ephrin-A1. The direct interaction between EphA4 and FGFRs and the potentiation of FGF response that is induced by ephrin-A1 stimulation may modulate the biological responses that are mediated by these receptor families in cells or tissues in which the two receptors are coexpressed.

Antibodies, Monoclonal↗
PubMed2005

Role of NAD(P)H oxidase- and mitochondria-derived reactive oxygen species in cardioprotection of ischemic reperfusion injury by angiotensin II.

Reactive oxygen species (ROS) participate in cardioprotection of ischemic reperfusion (I/R) injury via preconditioning mechanisms. Mitochondrial ROS have been shown to play a key role in this process. Angiotensin II (Ang II) exhibits pharmacological preconditioning; however, the involvement of NAD(P)H oxidase, known as an ROS-generating enzyme responsive to Ang II stimuli, in the preconditioning process remains unclear. We compared the effects of 5-hydroxydecanoate (5-HD; an inhibitor of mitochondrial ATP-sensitive potassium channels), apocynin (an NAD(P)H oxidase inhibitor), and 4-hydroxy-2,2,6,6-tetramethyl piperidinoxyl (tempol; a membrane permeable radical scavenger) on pharmacological preconditioning by Ang II in rat cardiac I/R injury in vivo. Treatment with a pressor dose of Ang II before a 30-minute coronary occlusion reduced infarct size as determined 24 hours after reperfusion. The protective effects of Ang II were eliminated by pretreatment with 5-HD or apocynin, similar to tempol. Both 5-HD and apocynin suppressed the enhanced cardiac lipid peroxidation and activation of the apoptosis signal-regulating kinase/p38, c-Jun NH2-terminal kinase (JNK) pathways, but not the Raf/MEK/extracellular signal-regulated kinase pathway, elicited by acutely administered Ang II. Apocynin but not 5-HD suppressed Ang II-induced augmentations of the NAD(P)H oxidase complex formation (p47phox, p22phox, and Rac-1) and its activity in the heart. Finally, 5-HD suppressed superoxide production by isolated cardiac mitochondria without any effect on their respiration. These results suggest that the preconditioning effects of Ang II for cardiac I/R injury may be mediated by cardiac mitochondria-derived ROS enhanced through NAD(P)H oxidase via JNK and p38 mitogen-activated protein kinase activation.

Acetophenones↗
PubMed2005

Involvement of aldosterone and mineralocorticoid receptors in rat mesangial cell proliferation and deformability.

We demonstrated recently that chronic administration of aldosterone to rats induces glomerular mesangial injury and activates mitogen-activated protein kinases including extracellular signal-regulated kinases 1/2 (ERK1/2). We also observed that the aldosterone-induced mesangial injury and ERK1/2 activation were prevented by treatment with a selective mineralocorticoid receptor (MR) antagonist, eplerenone, suggesting that the glomerular mesangium is a potential target for injuries induced by aldosterone via activation of MR. In the present study, we investigated whether MR is expressed in cultured rat mesangial cells (RMCs) and involved in aldosterone-induced RMC injury. MR expression and localization were evaluated by Western blotting analysis and fluorolabeling methods. Cell proliferation and micromechanical properties were determined by [3H]-thymidine uptake measurements and a nanoindentation technique using an atomic force microscope cantilever, respectively. ERK1/2 activity was measured by Western blotting analysis with an anti-phospho-ERK1/2 antibody. Protein expression and immunostaining revealed that MR was abundant in the cytoplasm of RMCs. Aldosterone (1 to 100 nmol/L) dose-dependently activated ERK1/2 in RMCs with a peak at 10 minutes. Pretreatment with eplerenone (10 micromol/L) significantly attenuated aldosterone-induced ERK1/2 phosphorylation. Aldosterone (100 nmol/L) treatment for 30 hours increased [3H]-thymidine incorporation and decreased the elastic modulus, indicating cellular proliferative and deforming effects of aldosterone, respectively. These aldosterone-induced changes in cellular characteristics were prevented by pretreatment with eplerenone or an ERK (MEK) inhibitor, PD988059 (100 micromol/L). The results indicate that aldosterone directly induces RMC proliferation and deformability through MR and ERK1/2 activation, which may contribute to the pathogenesis of glomerular mesangial injury.

Aldosterone↗
PubMed2005

Mitochondria-derived reactive oxygen species and vascular MAP kinases: comparison of angiotensin II and diazoxide.

Reactive oxygen species (ROS) are key mediators in signal transduction of angiotensin II (Ang II). However, roles of vascular mitochondria, a major intracellular ROS source, in response to Ang II stimuli have not been elucidated. This study aimed to examine the involvement of mitochondria-derived ROS in the signaling pathway and the vasoconstrictor mechanism of Ang II. Using 5-hydroxydecanoate (5-HD; a specific inhibitor of mitochondrial ATP-sensitive potassium [mitoK(ATP)] channels) and tempol (a superoxide dismutase mimetic), the effects of Ang II and diazoxide (a mitoK(ATP) channel opener) were compared on redox-sensitive mitogen-activated protein (MAP) kinase activation in rat vascular smooth muscle cells (RVSMCs) in vitro and in rat aorta in vivo. Stimulation of RVSMCs by Ang II or diazoxide increased phosphorylated MAP kinases (ERK1/2, p38, and JNK), as well as superoxide production, which were then suppressed by 5-HD pretreatment in a dose-dependent manner, except for ERK1/2 activation by Ang II. The same events were reproduced in rat aorta in vivo. Ang II-like diazoxide depolarized the mitochondrial membrane potential (DeltaPsi(M)) of RVSMCs determined by JC-1 fluorescence, which was inhibited by 5-HD. 5-HD did not modulate Ang II-induced calcium mobilization in RVSMCs and did not affect on the vasoconstrictor effect in either acute or chronic phases of Ang II-induced hypertension. These results reveal that Ang II stimulates mitochondrial ROS production through the opening of mitoK(ATP) channels in the vasculature-like diazoxide, leading to reduction of DeltaPsi(M) and redox-sensitive activation of MAP kinase; however, generated ROS from mitochondria do not contribute to Ang II-induced vasoconstriction.

Angiotensin II↗
PubMed2005

Temporary angiotensin II blockade at the prediabetic stage attenuates the development of renal injury in type 2 diabetic rats.

Whether temporary angiotensin II (AngII) blockade at the prediabetic stage attenuates renal injury in type 2 diabetic OLETF rats later in life was investigated. OLETF rats were treated with an AT(1) receptor antagonist (olmesartan, 0.01% in food), angiotensin-converting enzyme inhibitor (temocapril, 0.01% in food), a combination of the two, or hydralazine (25 mg/kg per d) at the prediabetic stage (4 to 11 wk of age) and then monitored without further treatment until 50 wk of age. At 11 wk of age, blood glucose levels and urinary protein excretion (U(protein)V) were similar between OLETF and control LETO rats. However, OLETF rats showed higher kidney AngII contents and type IV collagen mRNA expression than LETO rats at this age. These decreased with olmesartan, temocapril, and a combination of these but not with hydralazine. At 50 wk of age, diabetic OLETF rats showed higher BP, U(protein)V, and intrarenal AngII levels than LETO rats. Temporary AngII blockade did not affect glucose metabolism or the development of hypertension in OLETF rats but significantly suppressed proteinuria and ameliorated glomerular injury. However, no parameters were affected by temporary hydralazine treatment. The present study demonstrated that intrarenal AngII and type IV collagen expression are already augmented long before diabetes becomes apparent in OLETF rats. Furthermore, temporary AngII blockade at the prediabetic stage attenuates the progression of renal injury in these animals. These data suggest that early AngII blockade could be an effective strategy for preventing the development of type 2 diabetic renal injury later in life.

Angiotensin II↗
PubMed2005

Cardiac oxidative stress in acute and chronic isoproterenol-infused rats.

OBJECTIVE: Sympathetic nervous system activity in the myocardium is increased in patients with heart failure. However, the in vivo mechanisms responsible for beta-adrenoceptor-mediated cardiac hypertrophy or remodeling remain unclear. This study aimed to clarify the role of reactive oxygen species (ROS) in mitogen-activated protein (MAP) kinase activation and tissue remodeling of the heart of isoproterenol (ISO)-infused rats. METHODS AND RESULTS: Different doses of ISO (up to 1000 ng/kg/min) were given intravenously to conscious rats for 30 min. Phosphorylated MAP kinase levels (ERK1/2, JNK, p38) and lipid peroxidation were measured in the cardiac left ventricle, revealing the dose-dependent augmentation of MAP kinase phosphorylation and increased lipid peroxidation levels. Simultaneous treatment with 4-hydroxy-2,2,6,6-tetramethyl piperidinoxyl (Tempol), a membrane-permeable radical scavenger, completely eliminated the increases of phosphorylated MAP kinases and their upstream elements (Raf-1, Rac-1, ASK-1) as well as the increases of cardiac lipid peroxidation induced by the highest dose of ISO infusion. In chronically ISO-infused rats (3 mg/kg/day, s.c. for 10 days), cardiac hypertrophy developed with accompanying increases of collagen content, whereas cardiac phosphorylated MAP kinases returned to normal. Tempol treatment prevented increases of collagen accumulation and type I collagen mRNA without any significant reduction of cardiac mass enlargement induced by chronic ISO infusion. CONCLUSION: beta-Adrenoceptor stimulation provokes cardiac oxidative stress. In the acute phase of ISO infusion, ROS are important activators of cardiac MAP kinase cascades; while, in the chronic phase, ROS may participate in cardiac remodeling, especially in respect to wall stiffness, based on fibrogenesis.

Adrenergic beta-Agonists↗
PubMed2005

Fibroblast growth factor 23 reduces expression of type IIa Na+/Pi co-transporter by signaling through a receptor functionally distinct from the known FGFRs in opossum kidney cells.

Fibroblast growth factor (FGF) 23 is an important phosphaturic factor that inhibits inorganic phosphate (Pi) reabsorption from the renal proximal tubule. Its overproduction and proteolysis-resistant mutation such as R179Q cause tumor-induced osteomalacia and autosomal dominant hypophosphatemic rickets, respectively. To clarify the signaling mechanisms of FGF23 that mediate the reduction of Pi reabsorption, we inhibited the function of the known FGFRs in opossum kidney (OK-E) cells by expressing a dominant-negative (DN) form of FGFR. OK-E cells, which represent the renal proximal tubular cells, expressed all four known FGFRs. FGF23(R179Q) bound to and activated FGFR2, a prominent FGFR expressed in OK-E cells. The activated receptor transmitted a signal to increase the expression of type IIa Na(+)/Pi co-transporter and the Pi uptake. Expression of FGFR2(DN), which suppresses the major FGFR-mediated signal through the FRS2alpha-ERK pathway, reversed the function of FGF23(R179Q). When FGF23(R179Q) was applied to the basolateral side of polarized OK-E cells, regardless of the FGFR2(DN) expression, the apical Pi uptake decreased significantly. The apical application of FGF23(R179Q) in the polarized cells did not show such decrease but increase. The exogenously expressed FGFR2 was detectable only at the apical membrane. These results suggest that an FGF23 receptor, which is functionally distinct from the known FGFRs, is expressed at the basolateral membrane of OK-E cells.

Animals↗