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Biomedical subjects

J Tao

Publications and source records attributed to J Tao.

At least 19 recordsLinked to original sources
PubMed2006

Arterial elasticity identified by pulse wave analysis and its relation to endothelial function in patients with coronary artery disease.

Patients with coronary artery disease (CAD) have impaired endothelial function. Arterial elasticity is modulated by endothelial function. The association between arterial elasticity and endothelial function has not been reported in patients with CAD. The present study was designed to investigate whether endothelial dysfunction contributes to impaired arterial elasticity. Thirty patients with CAD and 30 control subjects were recruited. Large and small artery elasticity indices were non-invasively assessed using pulse wave analysis. Brachial artery endothelium-dependent and -independent function were assessed by vascular response to flow-mediated vasodilation (FMD) and sublingual nitroglyceride (NTG), respectively. C1 large artery elasticity index was not different in the CAD group compared with the control group. However, C2 small artery elasticity index was significantly reduced in the CAD group compared with the control group. Flow-mediated vasodilation (FMD) was also impaired in the CAD group compared with the control group. Flow-mediated vasodilation (FMD) in the brachial artery correlated with C2 small arterial elasticity index. But NTG-mediated brachial artery vasodilation was similar between the two groups. The present findings suggest that the patients with CAD have reduced C2 small arterial elasticity index and impaired FMD. Endothelial dysfunction is involved in diminished arterial elasticity, suggesting that C2 small arterial elasticity index is a novel surrogate measure for the clinical evaluation of endothelial function.

Aged↗
PubMed2006

Circulating endothelial progenitor cell deficiency contributes to impaired arterial elasticity in persons of advancing age.

Reduced arterial elasticity is a hallmark of ageing in healthy humans and appears to occur independently of coexisting disease processes. Endothelial-cell injury and dysfunction may be responsible for this fall in arterial elasticity. We hypothesized that circulating endothelial progenitor cells (EPCs) are involved in endothelial repair and that lack of EPCs contributes to impaired arterial elasticity. A total of 56 healthy male volunteers were divided into young (n=26) and elderly (n=30) groups. Large and small artery elasticity indices were noninvasively assessed using pulse wave analysis. The number of circulating EPCs was measured by using flow cytometry. Cells demonstrating DiI-acLDL and FITC-ulex lectin double-positive fluorescence were identified as EPCs. C1 large artery elasticity and C2 small artery elasticity indices were significantly reduced in the elderly group compared with the young group (11.73+/-1.45 vs 16.88+/-1.69 ml/mm Hg x 10, P<0.001; 8.40+/-1.45 vs 10.58+/-1.18 ml/mm Hg x 100, P<0.001, respectively). In parallel, the number of circulating EPCs was significantly reduced in the elderly group compared with the young group (0.13+/-0.02 vs 0.17+/-0.04%, P<0.05). The number of circulating EPCs correlated with C1 large and C2 small artery elasticity indices (r=0.47, P<0.01; r=0.4, P<0.01). The present findings suggest that the fall in circulating EPCs with subsequently impaired endothelial-cell repair and function contributes to reduced arterial elasticity in humans with ageing. The decrease in circulating EPCs may serve as a surrogate biologic measure of vascular function and human age.

Adult↗
PubMed2006

Endogenous production of nitric oxide contributes to proliferation effect of vascular endothelial growth factor-induced malignant melanoma cell.

The objectives of this study were to observe the effect of overexpression of vascular endothelial growth factor (VEGF) on the proliferation of the malignant melanoma (MM) cell line A375, and to study the role of nitric oxide (NO) in this process and the mechanism of VEGF induced-A375 cell proliferation. The VEGF(165) cDNA was transfected into A375 cells by electroporation. VEGF mRNA and protein in A375 cells were detected by RT-PCR and ELISA. The proliferation of A375 cells was assessed by cell counting and MTT assay. Protein expression of iNOS, eNOS and nNOS was detected by Western blotting. NO production in A375 cell supernatant was measured by the nitrate reductase method. VEGF mRNA in A375 cells was significantly increased 72 h and 96 h after transfection of VEGF(165) cDNA, as were VEGF protein, NO and iNOS levels. However, protein expression of eNOS and nNOS was not detected in either transfected or untransfected cells. Proliferation of A375 cells transfected with VEGF(165) cDNA was enhanced. The nitric oxide synthase inhibitor l-NAME could dose-dependently inhibit the proliferation of A375 cells evoked by VEGF. These results indicate that VEGF enhances the expression of iNOS in A375 cells and results in an increase in NO formation, which may be important in the process of VEGF-induced proliferation of A375 cells.

Cell Division↗
PubMed2006

Expression of endothelial nitric oxide synthase and vascular endothelial growth factor in human malignant melanoma and their relation to angiogenesis.

BACKGROUND: Angiogenesis is the major and key factor for growth and invasion of tumours, including malignant melanoma (MM), but the factors that contribute to tumour angiogenesis are still unclear. OBJECTIVE: To study expression of endothelial nitric oxide synthase (eNOS) and vascular endothelial growth factor (VEGF) in human MM and their relation to angiogenesis. To investigate the correlation between eNOS and VEGF and the role of nitric oxide (NO) generated by eNOS in the process of mediating angiogenesis by VEGF. METHODS: Tissue sections from 31 patients with MM were examined using immunohistochemistry and morphological quantitative analysis for protein expression of eNOS and VEGF. Microvessel density (MVD) was counted in endothelial cells in immunostained by anti-FVIII:RAg antibody. RESULTS: Positive eNOS and VEGF immunostaining were observed in 77.4% and 83.9% of MM lesions, respectively, whereas pigmented naevi never expressed eNOS and VEGF. A positive correlation between eNOS and VEGF in MM was observed. Expression of eNOS and VEGF was positively correlated with MVD expression in MM, and MVD expression in MM was stronger than in pigmented naevi. Expression of eNOS and VEGF was not correlated with lymph node metastasis. CONCLUSIONS. On the basis of the current data showing that malignant melanocytic tumours displayed strong VEGF and eNOS expression, whereas benign melanocytic proliferations showed no immunoreactivity for VEGF and eNOS, such expression may be used as a discriminating factor to distinguish malignant melanoma from pigmented naevi. Expression of eNOS and VEGF may contribute to angiogenesis of MM, eNOS probably plays an important role in mediating VEGF-induced angiogenesis.

Adult↗
PubMed2006

Current asthma and respiratory symptoms among pupils in Shanghai, China: influence of building ventilation, nitrogen dioxide, ozone, and formaldehyde in classrooms.

We investigated 10 naturally ventilated schools in Shanghai, in winter. Pupils (13-14 years) in 30 classes received a questionnaire, 1414 participated (99%). Classroom temperatures were 13-21 degrees C (mean 17 degrees C), relative air humidity was 36-82% (mean 56%). The air exchange rate was 2.9-29.4 ac/h (mean 9.1), because of window opening. Mean CO2 exceeded 1000 ppm in 45% of the classrooms. NO2 levels were 33-85 microg/m3 indoors, and 45-80 microg/m3 outdoors. Ozone were 1-9 microg/m3 indoors and 17-28 microg/m3 outdoors. In total, 8.9% had doctors' diagnosed asthma, 3.1% wheeze, 23.0% daytime breathlessness, 2.4% current asthma, and 2.3% asthma medication. Multiple logistic regression was applied. Observed indoor molds was associated with asthma attacks [odds ratio (OR) = 2.40: P < 0.05]. Indoor temperature was associated with daytime breathlessness (OR = 1.26 for 1 C; P < 0.001), and indoor CO2 with current asthma (OR = 1.18 for 100 ppm; P < 0.01) and asthma medication (OR = 1.15 for 100 ppm; P < 0.05). Indoor NO2 was associated with current asthma (OR = 1.51 for 10 microg/m3; P < 0.01) and asthma medication (OR = 1.45 for 10 microg/m3; P < 0.01). Outdoor NO2 was associated with current asthma (OR = 1.44 for 10 microg/m3; P < 0.05). Indoor and outdoor ozone was negatively associated with daytime breathlessness. In conclusion, asthma symptoms among pupils in Shanghai can be influenced by lack of ventilation and outdoor air pollution from traffic. Practical Implications Most urban schools in Asia are naturally ventilated buildings, often situated in areas with heavy ambient air pollution from industry or traffic. The classes are large, and window opening is the only way to remove indoor pollutants, but this results in increased exposure to outdoor air pollution. There is a clear need to improve the indoor environment in these schools. Building dampness and indoor mold growth should be avoided, and the concept of mechanical ventilation should be introduced. City planning aiming to situate new schools away from roads with heavy traffic should be considered.

Adolescent↗
PubMed2005

A bio-inspired approach to the synthesis of CaCO3 spherical assemblies in a soluble ternary-additive system.

Two different soluble polymers, poly(ethylene glycol) (PEG) and poly(methacrylic acid) (PMAA), with individual functions were successfully employed in combination with a third additive, sodium dodecyl sulfate (SDS), in one system, and spherical assemblies (e.g., hollow spheres) with multiscale constructs of CaCO3 were obtained. The variation of polymer concentration drastically changed both the morphology and polymorph of the produced CaCO3 crystals due to the corresponding transformation of the micelle structure. This study suggests that noncovalent interaction and cooperation between soluble macromolecules play key roles in controlling the growth of biominerals. The results also suggest a novel and facile route toward biomimetic inorganic synthesis.

Calcium Carbonate↗
PubMed2005

Lamellar phase separation and dynamic competition in La0.23Ca0.77MnO3.

We report the coexistence of lamellar charge-ordered (CO) and charge-disordered (CD) domains, and their dynamical behavior, in La0.23Ca0.77MnO3. Using high-resolution transmission electron microscopy (TEM), we show that below T(CD) approximately 170 K a CD-monoclinic phase forms within the established CO-orthorhombic matrix. The CD phase has a sheetlike morphology, perpendicular to the q vector of the CO superlattice (a axis of the Pnma structure). For temperatures between 64 and 130 K, both the TEM and resistivity experiments show a dynamic competition between the two phases: at constant T, the CD phase slowly advances over the CO one. This slow dynamics appears to be linked to the magnetic transitions occurring in this compound, suggesting important magnetoelastic effects.

Journal Article↗
PubMed2005

Investigation of serum protein systems in Chinese pigs.

Polymorphisms of transferrin (Tf), pre-albumin (Pa), haemopexin (Hpx), ceruloplasmin (Cp) and amylase (Am) of Duroc pigs and Hunan indigenous pigs were investigated using horizontal starch gel electrophoresis. Allele frequencies of Durocs determined in 2004 were compared with frequencies presented in the paper by Baker L.N. (1968) Serum protein variation in Duroc and Hampshire pigs. Vox Sanguinis15, 154-8. The number of serum protein alleles decreased over time and allele frequencies aggregated across certain alleles, including TfB, PaA, Hpx3, CpB and AmB. Differences in allele frequencies, average heterozygosities and standard genetic distances between the Duroc pigs and Hunan indigenous pig populations were examined. The relationship between Durocs and Hunan indigenous pigs was found to be more distant than those among the three Hunan indigenous pig populations.

Amylases↗
PubMed2005

Inhibiting the growth of malignant melanoma by blocking the expression of vascular endothelial growth factor using an RNA interference approach.

BACKGROUND: Vascular endothelial growth factor (VEGF) is overexpressed in malignant melanoma (MM). OBJECTIVES: To develop an RNA interference approach that specifically targets VEGF by constructing a eukaryotic expression plasmid containing short interfering RNA (siRNA), and to evaluate the effects of this vector on the proliferation and apoptosis of MM in vitro and in vivo. METHODS: pU-VEGF-siRNA plasmid was transfected into MM cell line A375 and colorectal carcinoma cell line Lovo by electroporation. Expression of VEGF mRNA and protein in A375 and Lovo cells after gene transfer was detected by reverse transcription-polymerase chain reaction and enzyme-linked immunosorbent assay, respectively. Proliferation of pU-VEGF-siRNA-transfected A375 and Lovo cells and control cells was observed by cell counting through the microscope. The proliferation of human umbilical vein endothelial cells (ECV-304) cultured in medium containing supernatants of transfected and control A375 cells was measured by the cell counting method. Flow cytometry (FCM) was used to analyse the apoptosis of transfected and control groups. In a mouse model, tumorigenicity and tumour growth of transfected cells were studied in vivo. VEGF expression and microvessel density (MVD) in tumour tissue were measured by immunohistochemistry. Apoptosis in tumours was detected by terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick end labelling. RESULTS: Expression of VEGF mRNA and protein in pU-VEGF-siRNA-transfected A375 and Lovo cells was significantly decreased on days 3, 10, 17 and 24 post-transfection, compared with controls. The greatest suppression occurred on days 3 and 10 post-transfection. The proliferation of transfected A375 cells and ECV-304 cocultured with supernatants of transfected A375 cells was inhibited. FCM analysis showed that a hypodiploidy peak was found only in A375 cells transfected by pU-VEGF-siRNA. After subcutaneous inoculation with pU-VEGF-siRNA-transfected A375 cells, tumour growth in mice was inhibited, VEGF expression and MVD were decreased, and tumour apoptosis was increased significantly, in comparison with mice inoculated with untransfected A375 cells. CONCLUSIONS: The delivery of siRNA directed against VEGF was shown not only to give efficient and specific downregulation of the expression of VEGF, inhibit proliferation of A375 and ECV-304 cells and induce apoptosis of A375 cells in vitro, but also to suppress growth of MM in vivo. These results suggest that a strategy based on siRNA targeting of VEGF may build the foundation to the clinical management of MM.

Animals↗
PubMed2004

Absolute and convective instabilities of natural convection flow in boundary-layer regime.

The spatiotemporal instability of the buoyancy-driven flow adjacent to a vertically heated wall, which is immersed in thermally stratified medium, is studied theoretically and numerically. The temperature gradients ratio between the wall and the ambient fluid is shown to lead to rich scenario of absolute-convective instability transitions. The direct numerical simulations consistent with the theoretical prediction are presented. The supercritical steady state, found in previous simulations of the natural convection in vertically heated square cavity, is explained in terms of the convective instability, and the nonlinear effect on the convectively unstable waves is discussed as well.

Journal Article↗
PubMed2004

Coherent nano-area electron diffraction.

We describe the new coherent nano-area electron diffraction (NED) and its application for structure determination of individual nanostructures. The study is motivated by the challenge and the general lack of analytical techniques for characterizing nanometer-sized, heterogeneous phases. We show that by focusing electrons on the focal plane of the pre-objective lens using a 3rd condenser lens and a small condense aperture, it is possible to achieve a nanometer-sized highly parallel illumination or probe. The high angular resolution of diffraction pattern from the parallel illumination allows over-sampling and consequently the solution of phase problem based on the recently developed ab initio phase retrieval technique. From this, a high-contrast and high-resolution image can be reconstructed at resolution beyond the performance limit of the image-forming objective lens. The significance of NED for nanostructure characterization will be exemplified by single-wall carbon nanotubes and small metallic clusters. Imaging from diffraction patterns, or diffractive imaging, will be demonstrated using double-wall carbon nanotubes.

Computer Simulation↗
PubMed2004

Rapid induction of cAMP/PKA pathway during retinoic acid-induced acute promyelocytic leukemia cell differentiation.

The second messenger cyclic adenosine monophosphate (cAMP) plays an important role in cell proliferation, differentiation and apoptosis. In the present work, we evaluated the cAMP signaling in acute promyelocytic leukemia (APL) cells in the context of differentiation induced by all-trans retinoic acid (ATRA). There was a marked increase in the intracellular cAMP level within a few minutes after treatment with ATRA in APL cell line NB4 and fresh APL cells, whereas no such phenomenon was observed in NB4-R1 cells that are resistant to ATRA-induced maturation. In addition, the basal level of intracellular cAMP was lower in NB4-R1 than in NB4 cells. Mechanistic study showed that this induction of cAMP was mediated through the activation of adenylate cyclase. Moreover, we found that cAMP-dependent protein kinase (PKA) activity was quickly upregulated in parallel in ATRA-treated NB4 cells, and the phosphorylation of RARalpha by PKA could increase its transactivation effect. Use of H-89, an inhibitor of PKA, could partially suppress the transcriptional expression of ATRA target genes and ATRA-induced differentiation of APL cells. Taken together, we suggested a crosstalk between ATRA-induced cytosolic pathway and nuclear pathway in APL cell differentiation.

Adenylyl Cyclases↗
PubMed2004

AKAP (A-kinase anchoring protein) domains: beads of structure-function on the necklace of G-protein signalling.

AKAPs (A-kinase anchoring proteins) are members of a diverse family of scaffold proteins that minimally possess a characteristic binding domain for the RI/RII regulatory subunit of protein kinase A and play critical roles in establishing spatial constraints for multivalent signalling assemblies. Especially for G-protein-coupled receptors, the AKAPs provide an organizing centre about which various protein kinases and phosphatases can be assembled to create solid-state signalling devices that can signal, be modulated and trafficked within the cell. The structure of AKAP250 (also known as gravin or AKAP12), based on analyses of milligram quantities of recombinant protein expressed in Escherichia coli, suggests that the AKAP is probably an unordered scaffold, acting as a necklace on which 'jewels' of structure-function (e.g. the RII-binding domain) that provide docking sites on which signalling components can be assembled. Recent results suggest that AKAP250 provides not only a 'tool box' for assembling signalling elements, but may indeed provide a basis for spatial constraint observed for many signalling paradigms. The spatial dimension of the integration of cell signalling will probably reflect many functions performed by members of the AKAP family.

A Kinase Anchor Proteins↗
PubMed2004

Identification of Escherichia coli O172 O-antigen gene cluster and development of a serogroup-specific PCR assay.

AIM: To characterize the locus for O-antigen biosynthesis from Escherichia coli O172 type strain and to develop a rapid, specific and sensitive PCR-based method for identification and detection of E. coli O172. METHODS AND RESULTS: DNA of O-antigen gene cluster of E. coli O172 was amplified by long-range PCR method using primers based on housekeeping genes galF and gnd Shot gun bank was constructed and high quality sequencing was performed. The putative genes for synthesis of UDP-FucNAc, O-unit flippase, O-antigen polymerase and glycosyltransferases were assigned by the homology search. The evolutionary relationship between O-antigen gene clusters of E. coli O172 and E. coli O26 is shown by sequence comparison. Genes specific to E. coli O172 strains were identified by PCR assays using primers based on genes for O-unit flippase, O-antigen polymerase and glycosyltransferases. The specificity of PCR assays was tested using all E. coli and Shigella O-antigen type strains, as well as 24 clinical E. coli isolates. The sensitivity of PCR assays was determined, and the detection limits were 1 pg microl(-1) chromosomal DNA, 0.2 CFU g(-1) pork and 0.2 CFU ml(-1) water. The total time required from beginning to end of the procedure was within 16 h. CONCLUSION: The O-antigen gene cluster of E. coli O172 was identified and PCR assays based on O-antigen specific genes showed high specificity and sensitivity. SIGNIFICANCE AND IMPACT OF THE STUDY: An O-antigen gene cluster was identified by sequencing. The specific genes were determined for E. coli O172. The sensitivity of O-antigen specific PCR assay was tested. Although Shiga toxin-producing O172 strains were not yet isolated from clinical specimens, they may emerge as pathogens.

Base Sequence↗
PubMed2001

Galpha(i2) enhances insulin signaling via suppression of protein-tyrosine phosphatase 1B.

Suppression of the expression of the heterotrimeric G-protein Galpha(i2) in vivo has been shown to provoke insulin resistance, whereas enhanced insulin signaling is observed when Galpha(i2) is overexpressed in vivo. The basis for Galpha(i2) regulation of insulin signaling was explored in transgenic mice with targeted expression of the GTPase-deficient, constitutively active Q205L Galpha(i2) in fat and skeletal muscle. Phosphorylation of insulin receptor and IRS-1 in response to insulin challenge in vivo was markedly amplified in fat and skeletal muscle expressing Q205L Galpha(i2). The expression and activity of the protein-tyrosine phosphatase 1B (PTP1B), but not protein-tyrosine phosphatases SHP-1, SHP-2, and LAR, were constitutively decreased in tissues expressing the Q205L Galpha(i2), providing a direct linkage between insulin signaling and Galpha(i2). The loss of PTP1B expression may explain, in part, the loss of PTP1B activity in the iQ205L transgenic mice. Activation of Galpha(i2) in mouse adipocytes with lysophosphatidic acid was shown to decrease PTP1B activity, whereas pertussis toxin inactivates Galpha(i2), blocks lysophosphatidic acid-stimulated inhibition of PTP1B activity, and blocks tonic suppression of PTP1B activity by Galpha(i2). Elevation of intracellular cAMP in fat cells is shown to increase PTP1B activity, whereas either depression of cAMP levels or direct activation of Galpha(i2) suppresses PTP1B. These data provide the first molecular basis for the interplay between Galpha(i2) and insulin signaling, i.e. activation of Galpha(i2) can suppress both the expression and activity of PTP1B in insulin-sensitive tissues.

Adipose Tissue↗
PubMed2001

15-deoxy-Delta 12,14-prostaglandin J2 induces apoptosis of human hepatic myofibroblasts. A pathway involving oxidative stress independently of peroxisome-proliferator-activated receptors.

Hepatic myofibroblasts (hMFs) play a key role in the development of liver fibrosis associated with chronic liver diseases. Apoptosis of these cells is emerging as a key process in the resolution of liver fibrosis. Here, we examined the effects of cyclopentenone prostaglandins on apoptosis of human hMFs. Cyclopentenone prostaglandins of the J series markedly reduced hMF viability, with 15-deoxy-Delta(12,14)-prostaglandin J2 (15-d-PGJ2) being the most potent. This effect was independent of peroxisome-proliferator-activated receptors (PPARs), because PPARgamma and PPARalpha agonists did not affect hMF cell viability, and PPARgamma, the nuclear receptor for 15-d-PGJ2, was not expressed in hMFs. Moreover, 15-d-PGJ2 did not act via a cell surface G protein-coupled receptor, as shown in guanosine-5'-O-(3-thiotriphosphate) binding assays. Cell death resulted from an apoptotic process, because 15-d-PGJ2-treated hMFs exhibited condensed nuclei, fragmented DNA, and elevated caspase-3 activity. Moreover, the caspase inhibitor Z-Val-Ala-Asp(OCH3)-fluoromethyl ketone blocked the cytotoxic effect of 15-d-PGJ2. The apoptotic effects of 15-d-PGJ2 were reproduced by H2O2 and blocked by the antioxidants N-acetylcysteine (NAC), N-(2-mercapto-propionyl)-glycine (NMPG) and pyrrolidine dithiocarbamate (PDTC). Accordingly, 15-d-PGJ2 generated rapid production of reactive oxygen species in hMFs, via a NAC/NMPG/PDTC-sensitive pathway. In conclusion, 15-d-PGJ2 induces apoptosis of human hMFs via a novel mechanism involving oxidative stress and unrelated to activation of its nuclear receptor PPARgamma. These data underline the antifibrogenic potential of 15-d-PGJ2.

Apoptosis↗
PubMed2001

Akt activation preserves cardiac function and prevents injury after transient cardiac ischemia in vivo.

BACKGROUND: The serine-threonine kinase Akt is activated by several ligand-receptor systems previously shown to be cardioprotective. Akt activation reduces cardiomyocyte apoptosis in models of transient ischemia. Its role in cardiac dysfunction or infarction, however, remains unclear. METHODS AND RESULTS: We examined the effects of a constitutively active Akt mutant (myr-Akt) in a rat model of cardiac ischemia-reperfusion injury. In vivo gene transfer of myr-Akt reduced infarct size by 64% and the number of apoptotic cells by 84% (P<0.005 for each). Ischemia-reperfusion injury decreased regional cardiac wall thickening as well as the maximal rate of left ventricular pressure rise and fall (+dP/dt and -dP/dt). Akt activation restored regional wall thickening and +dP/dt and -dP/dt to levels seen in sham-operated rats. To better understand this benefit, we examined the effects of myr-Akt on hypoxic cardiomyocyte dysfunction in vitro. myr-Akt prevented hypoxia-induced abnormalities in cardiomyocyte calcium transients and shortening. Akt activation also enhanced sarcolemmal expression of Glut-4 in vivo and increased glucose uptake in vitro to the level seen with insulin treatment. CONCLUSIONS: Akt activation exerts a powerful cardioprotective effect after transient ischemia that probably reflects its ability to both inhibit cardiomyocyte death and improve function of surviving cardiomyocytes. Akt may represent an important nodal target for therapy in ischemic and other heart disease.

Adenoviridae↗