Climate change. Recent reductions in China's greenhouse gas emissions.
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Bioelectric Energy Sources↗
Biomedical subjects
X Q Zhang
Publications and source records attributed to X Q Zhang.
Stromal cells expressing ephrin-B2 promote the growth and sprouting of ephrin-B2(+) endothelial cells.
Ephrin-B2 is a transmembrane ligand that is specifically expressed on arterial endothelial cells (ECs) and surrounding cells and interacts with multiple EphB class receptors. Conversely, EphB4, a specific receptor for ephrin-B2, is expressed on venous ECs, and both ephrin-B2 and EphB4 play essential roles in vascular development. The bidirectional signals between EphB4 and ephrin-B2 are thought to be specific for the interaction between arteries and veins and to regulate cell mixing and the making of particular boundaries. However, the molecular mechanism during vasculogenesis and angiogenesis remains unclear. Manipulative functional studies were performed on these proteins in an endothelial cell system. Using in vitro stromal cells (OP9 cells) and a paraaortic splanchnopleura (P-Sp) coculture system, these studies found that the stromal cells expressing ephrin-B2 promoted vascular network formation and ephrin-B2(+) EC proliferation and that they also induced the recruitment and proliferation of alpha-smooth muscle actin (alpha-SMA)-positive cells. Stromal cells expressing EphB4 inhibited vascular network formation, ephrin-B2(+) EC proliferation, and alpha-SMA(+) cell recruitment and proliferation. Thus, these data suggest that ephrin-B2 and EphB4 mediate reciprocal interactions between arterial and venous ECs and surrounding cells to form each characteristic vessel. (Blood. 2001;98:1028-1037)
Animals↗
Protein kinase C pathway is involved in regulating the secretion of prostatic acid phosphatase in human prostate cancer cells.
The stimulated secretion of prostatic acid phosphatase (PAcP) has been known to be a hallmark of androgen action on human prostate epithelial cells for the last five decades. The molecular mechanism of androgen action on PAcP secretion, however, has remained mostly unknown. We investigated the molecular mechanism that promotes PAcP secretion in LNCaP human prostate carcinoma cells which express PAcP and are androgen-responsive. Treatment with 12-o-tetradecanoyl phorbol-13-acetate (TPA), a protein kinase C (PKC) activator, resulted in an increased secretion of PAcP in a dose- and time-dependent fashion. 4Alpha-phorbol, a biologically inactive isomer of TPA, had no effect. This TPA stimulation of PAcP secretion was observed 2 h after exposure, while TPA did not have a significant effect on the mRNA level even with a 6 h treatment. A23187 calcium ionophore, known to mobilize cellular calcium which is a co-factor of PKC, also activated PAcP secretion. This TPA stimulation of PAcP secretion was more potent than the conventional stimulating agent 5alpha-dihydrotestosterone (DHT) at the same concentration of 50 nM. Furthermore, the action of TPA and DHT on PAcP secretion was blocked by five different PKC inhibitors. Results also showed that DHT, as well as TPA, could rapidly modulate PKC activity. Therefore, PKC can regulate PAcP secretion, and may also be involved in DHT action on PAcP secretion.
Acid Phosphatase↗
A stable glucose biosensor prepared by co-immobilizing glucose oxidase into poly(p-chlorophenol) at a platinum electrode.
An amperometric glucose biosensor was successfully developed by electrochemical polymerization of p-chlorophenol (4-CP) at a Pt electrode in the presence of glucose oxidase. The amperometric response of this biosensor to hydrogen peroxide, formed as the product of enzymatic reaction, was measured at a potential of 0.6 V (vs. SCE) in phosphate buffer solution. The performances of sensors, prepared at different monomer concentrations and polymerization potentials, were investigated in detail. The biosensor prepared under optimal conditions had a linear response to glucose ranging from 2.5 x 10(-4) to 1.5 x 10(-2) mol L(-1) with a correlation coefficient of 0.997 and a response time of less than 2 s. Substrate selectivity of the polymer-based enzyme electrode was tested for coexisting interferents such as uric acid and ascorbic acid, and no discernible response was observed. After 90 days, the response of the biosensor remained almost unchanged, indicating very good stability.
Biosensing Techniques↗
Nested genetic algorithm for resolving overlapping spectra.
A nested genetic algorithm, including a genetic parameter level and a genetic implemented level, has been proposed and applied for resolving simulated overlapping spectra. Parameters of genetic algorithms (GA) were optimized by use of the genetic parameter level. The number of overlapping peaks was, moreover, detected simultaneously. Parameters of individual peaks in multiplets were computed by use of the genetic implemented level. It is obvious that the parameters of GA can be optimized and the number of overlapping peaks can be detected by itself. The optimization results are less affected than in traditional curve-fitting by the initial values of the parameters of the overlapping bands. Consequently, the nested genetic algorithm is superior to the curve-fitting technique for resolution of overlapping peaks.
Algorithms↗
Effects of nitrovasodilators on the human fetal-placental circulation in vitro.
This study examines the vasorelaxation of isolated human placental chorionic plate arteries and the perfused fetal-placental vasculature, in vitro, to a variety of nitrovasodilator compounds including glyceryl trinitrate (GTN) sodium nitroprusside (SNP), S-nitroso-N-acetylpenicillamine (SNAP), S-nitroso-N-glutathione (SNG) and NaNO(2). The effects of these compounds were also examined under conditions of high (>450 mmHg) and low oxygen (<50 mmHg) tension. In a separate series of experiments the effects of GTN and NaNO(2)were further investigated with addition of the antioxidants cysteine (100 microm), glutathione (100 microm) or superoxide dismutase (SOD) (30 I.U./ml). The order of nitrovasodilator potency, when added directly to isolated fetal vessels was GTN=SNP>SNAP=SNG>NaNO(2). The order under low oxygen tension was similar, GTN=SNP>SNG= SNAP>or=NaNO(2). SNG ( approximately fourfold) and NaNO(2)( approximately 50-fold) were significantly more potent under low oxygen conditions. Cysteine, glutathione and SOD were without effect on GTN induced vasodilatation. However, all three agents significantly enhanced (six- to ninefold) the effects of NaNO(2)under similar conditions. When infused directly into the fetal-placental circulation during in vitro perfusion experiments the order of potency was GTN>SNP>or=SNG>or=SNAP>or=NaNO(2). When the nitrovasodilators were infused indirectly via the maternal intervillous space the order of potency was GTN>or=SNP>or=NaNO(2)>or=SNAP=SNG. Our observations suggest that there are important differences in the action of different classes of nitrovasodilator compounds on the fetal-placental circulation. The changes observed with SNG and NaNO(2)may be influenced by levels of tissue oxygenation.
Adolescent↗
Overexpression of Na+/Ca2+ exchanger alters contractility and SR Ca2+ content in adult rat myocytes.
The functional consequences of overexpression of rat heart Na+/Ca2+ exchanger (NCX1) were investigated in adult rat myocytes in primary culture. When maintained under continued electrical field stimulation conditions, cultured adult rat myocytes retained normal contractile function compared with freshly isolated myocytes for at least 48 h. Infection of myocytes by adenovirus expressing green fluorescent protein (GFP) resulted in >95% infection as ascertained by GFP fluorescence, but contraction amplitude at 6-, 24-, and 48-h postinfection was not affected. When they were examined 48 h after infection, myocytes infected by adenovirus expressing both GFP and NCX1 had similar cell sizes but exhibited significantly altered contraction amplitudes and intracellular Ca2+ concentration ([Ca2+]i) transients, and lower resting and diastolic [Ca2+]i when compared with myocytes infected by the adenovirus expressing GFP alone. The effects of NCX1 overexpression on sarcoplasmic reticulum (SR) Ca2+ content depended on extracellular Ca2+ concentration ([Ca2+]o), with a decrease at low [Ca2+]o and an increase at high [Ca2+]o. The half-times for [Ca2+]i transient decline were similar, suggesting little to no changes in SR Ca2+-ATPase activity. Western blots demonstrated a significant (P < or = 0.02) threefold increase in NCX1 but no changes in SR Ca2+-ATPase and calsequestrin abundance in myocytes 48 h after infection by adenovirus expressing both GFP and NCX1 compared with those infected by adenovirus expressing GFP alone. We conclude that overexpression of NCX1 in adult rat myocytes incubated at high [Ca2+]o resulted in enhanced Ca2+ influx via reverse NCX1 function, as evidenced by greater SR Ca2+ content, larger twitch, and [Ca2+]i transient amplitudes. Forward NCX1 function was also increased, as indicated by lower resting and diastolic [Ca2+]i.
Adenoviridae↗
Sprint training shortens prolonged action potential duration in postinfarction rat myocyte: mechanisms.
Two electrophysiological manifestations of myocardial infarction (MI)-induced myocyte hypertrophy are prolongation of action potential duration (APD) and reduction of transient outward current (I(to)) density. Because high-intensity sprint training (HIST) ameliorated myocyte hypertrophy and improved myocyte Ca(2+) homeostasis and contractility after MI, the present study evaluated whether 6-8 wk of HIST would shorten the prolonged APD and improve the depressed I(to) in post-MI myocytes. There were no differences in resting membrane potential and action potential amplitude (APA) measured in myocytes isolated from sham-sedentary (Sed), MI-Sed, and MI-HIST groups. Times required for repolarization to 50 and 90% APA were significantly (P < 0.001) prolonged in MI-Sed myocytes. HIST reduced times required for repolarization to 50 and 90% APA to values observed in Sham-Sed myocytes. The fast and slow components of I(to) were significantly (P < 0.0001) reduced in MI-Sed myocytes. HIST significantly (P < 0.001) enhanced the fast and slow components of I(to) in MI myocytes, although not to levels observed in Sham-Sed myocytes. There were no significant differences in steady-state I(to) inactivation and activation parameters among Sham-Sed, MI-Sed, and MI-HIST myocytes. Likewise, recovery from time-dependent inactivation was also similar among the three groups. We suggest that normalization of APD after MI by HIST may be mediated by restoration of I(to) toward normal levels.
Action Potentials↗
[Analysis of association between gene polymorphisms of microsomal epoxide hydrolase (EPHX1) and infant birthweight].
We investigated association between genetic polymorphisms of EPHX1 in mother and infant birthweight. Data of 342 female workers were collected in textile mill. A total of 342 mothers were genotyped for the His139Arg polymorphism of EPHX1 by a polymerase chain reaction-restriction fragment length polymorphism assay. Using multiple linear regression models, we estimated the adjusted association between polymorphisms of EPHX1 and birthweight, with adjusted for potential confounders. We found that polymorphisms of EPHX1 were closely associated with reduced birthweight (beta +/- SE = -149 g +/- 56, P = 0.0083) after adjustment for major cofounders. In subgroup of passive smoking analysis, the polymorphisms of EPHX1 were highly associted with birthweight for those with passive smoking (beta +/- SE = -234 g +/- 88, P = 0.0088); The significant association of EPHX1 polymorphisms with reduced birthweight were showed for those with working stress (beta +/- SE = -157 g +/- 59, P = 0.0079). Our data provide polymorphisms of EPHX1 in mothers were significant association with birthweight of their infant, and showed gene-environmental interaction in relation to birthweight.
Birth Weight↗
[Cloning and sequencing of prolactin gene cDNA in three chicken breeds].
The total RNA was extracted from the pituitary of two Chinese native chicken breeds, Yuehuang and Taihe Silkies, and one layer Isa, using RNeasy Kit (QIAGEN, Germany). The total RNA was used to synthesize a specific fragment with RT-PCR, in which the primers were designed based on the sequence of broiler prolactin gene cDNA. The specific fragment was ligated to a linear plasmid pBSSK and cloned with XL1-Blue. The sequencing of prolactin cDNA was carried out with ABI PRISH 377XL DNA Sequencer after cloning. The cDNA sequences and deduced amino acid sequences of prolactin gene of two Chinese native chicken breeds and one layer were compared with that of broiler, dwarf chicken and turkey. There was 93.97%-99.89% cDNA sequence homology among Chinese native, layer, broiler and dwarf chickens, in which there was the highest (99.87%) between those of Taihe and dwarf chickens. There was 98.25%-100% deduced amino acid sequence homology among Chinese native, layer, broiler and dwarf chickens, in which there was the highest (100%) between those of Taihe Silkies and dwarf chickens. It was found that Yuehuang and Taihe Silkies had the same signal peptide cleavage site Leu-Pro-Ile-Cys among amino acids sequence deduced from pre-prolactin cDNA as broiler, dwarf and turkey, while layer Isa had a different cleavage site Pro-Pro-Ile-Cys. Such difference might cause a different translation processing of pre-prolactin, which could make layer Isa non-broody. There were different amino acids in the positions 71, 141, 150 and 175 of deduced prolactin amino acid sequences among Yuehuang, Taihe Silkies, layer, broiler and dwarf chickens. There was a heparin-binding site in positions 175-181 (L-R-R-D-S-H-K) among prolactin amino acid sequences of broiler and Taihe Silkies.
Amino Acid Sequence↗
[Chromosomal location and molecular marker of resistance gene to Puccinia striiformis west. in Leymus mollis Trin. Hara].
The hybrid wheat line, 93784 is a stable line selected from progenies of Leymus molli Trin. Hara x common wheat, which shows a very high level of resistance to yellow rust. The results of GISH using genomic DNA of Leymus mollis as probe indicated that the 93784 was a wheat-Leymus mollis small segment translocation line, and the translocated alien chromosome fragment were located on a pair of short arm terminals of what chromosomes. Using this translocation line, we established F2 segregation population and identified its yellow rust resistance in adult stage. Genetic analysis suggested that the yellow rust resistance of 93784 was controlled by a single gene. The gene was located on the translocated chromosome segments of Leymus mollis. We called it YrLm. By AFLP analysis with Taq I (T1-T4)/Pst I (P1-P6) primes in individuals of F2 segregation population and their susceptive and resistant parents, we screened a molecular marker that linked to yellow rust resistance gene YrLm. We also cloned and sequenced the molecular marker. The length of the marker is 205 bp, named P1T(3)205.
Chromosome Mapping↗
Characterization of a prostate-specific tyrosine phosphatase by mutagenesis and expression in human prostate cancer cells.
The cellular form of human prostatic acid phosphatase (PAcP) is a neutral protein-tyrosine phosphatase (PTP) and may play a key role in regulating the growth and androgen responsiveness of prostate cancer cells. The functional role of the enzyme is at least due in part to its dephosphorylation of c-ErbB-2, an in vivo substrate of the enzyme. In this study, we investigated the molecular mechanism of phosphotyrosine dephosphorylation by cellular PAcP. We mutated several amino acid residues including one cysteine residue that was proposed to be involved in the PTP activity of the enzyme by serving as the phosphate acceptor. The cDNA constructs of mutant enzymes were transiently transfected into C-81 LNCaP and PC-3 human prostate cancer cells that lack the endogenous PAcP expression. The phosphotyrosine level of ErbB-2 in these transfected cells was subsequently analyzed. Our results demonstrated that the phosphotyrosine level of ErbB-2 in cells expressing H12A or D258A mutant PAcP is similar to that in control cells without PAcP expression, suggesting that these mutants are incapable of dephosphorylating ErbB-2. In contrast, cells expressing C183A, C281A, or wild-type PAcP had a decreased phosphotyrosine level of ErbB-2, compared with the control cells. Similar results were obtained from in vitro dephosphorylation of immunoprecipitated ErbB-2 by these mutant enzymes. Furthermore, transient expression of C183A, C281A, or the wild-type enzyme, but not H12A or D258A, decreased the growth rate of C-81 LNCaP cells. The data collectively indicate that His-12 and Asp-258, but not Cys-183 or Cys-281, are required for the PTP activity of PAcP.
Acid Phosphatase↗
A transactivation-deficient mouse model provides insights into Trp53 regulation and function.
The gene Trp53 is among the most frequently mutated and studied genes in human cancer, but the mechanisms by which it suppresses tumour formation remain unclear. We generated mice with an allele encoding changes at Leu25 and Trp26, known to be essential for transcriptional transactivation and Mdm2 binding, to enable analyses of Trp53 structure and function in vivo. The mutant Trp53 was abundant, its level was not affected by DNA damage and it bound DNA constitutively; however, it showed defects in cell-cycle regulation and apoptosis. Both mutant and Trp53-null mouse embryonic fibroblasts (MEFs) were readily transformed by oncogenes, and the corresponding mice were prone to tumours. We conclude that the determining pathway for Trp53 tumour-suppressor function in mice requires the transactivation domain.
Alleles↗
Patterns and levels of genetic differentiation in North American populations of the Alaskan wheatgrass complex.
Levels and distribution of genetic variation were assessed using six allozymes in 27 populations of Alaskan wheatgrass (Elymus alaskanus) from different locations in Canada, USA, Greenland and Russia to obtain information on the genetic structure of these populations. The enzyme systems were ACO, DIA, GPI, MDH, PGM and SKD. Allozyme variation at the species level was high, with 64.3% (Ps) of the loci being polymorphic, an average number of alleles per locus of 1.9 (As), and an average genetic diversity of 0.17 (Hes). Differentiation was found in the populations studied, with the following findings: (1) statistically significant differences were found in allele frequencies among populations for every polymorphic locus (P < 0.001); (2) 63% of the total allozyme variation at polymorphic loci was partitioned among populations (GST = 0.63); (3) relatively low mean genetic distances between the populations were obtained (mean D = 0.029); (4) the genetic structure of Russian populations are clearly distinct from the other populations, the cluster and principal component analyses revealed the same genetic patterns of relationships among populations. This study also indicates that E. alaskanus contains different levels of allozyme variation in its populations. Furthermore, some banding patterns at the loci Aco-1, Aco-2, Gpi-2, Mdh-1, Skd-1, Skd-2 can be used as markers to identify individual populations.
Canada↗
Sprint training normalizes Ca(2+) transients and SR function in postinfarction rat myocytes.
Previous studies have shown that myocytes isolated from sedentary (Sed) rat hearts 3 wk after myocardial infarction (MI) undergo hypertrophy, exhibit altered intracellular Ca(2+) concentration ([Ca(2+)](i)) dynamics and abnormal contraction, and impaired sarcoplasmic reticulum (SR) function manifested as prolonged half-time of [Ca(2+)](i) decline. Because exercise training elicits positive adaptations in cardiac contractile function and myocardial Ca(2+) regulation, the present study examined whether 6-8 wk of high-intensity sprint training (HIST) would restore [Ca(2+)](i) dynamics and SR function in MI myocytes toward normal. In MI rats, HIST ameliorated myocyte hypertrophy as indicated by significant (P </= 0.05) decreases in whole cell capacitances [Sham-Sed 179 +/-12 (n = 20); MI-Sed 226 +/- 7 (n = 20); MI-HIST 183 +/- 11 pF (n = 19)]. HIST significantly (P < 0.0001) restored both systolic [Ca(2+)](i) [Sham-Sed 421 +/- 9 (n = 79); MI-Sed 350 +/- 6 (n = 70); MI-HIST 399 +/- 9 nM (n = 70)] and half-time of [Ca(2+)](i) decline (Sham-Sed 0. 197 +/- 0.005; MI-Sed 0.247 +/- 0.006; MI-HIST 0.195 +/- 0.006 s) toward normal. Compared with Sham-Sed myocytes, SR Ca(2+)-ATPase expression significantly (P < 0.001) decreased by 44% in MI-Sed myocytes. Surprisingly, expression of SR Ca(2+)-ATPase was further reduced in MI-HIST myocytes to 26% of that measured in Sham-Sed myocytes. There were no differences in calsequestrin expression among the three groups. Expression of phospholamban was not different between Sham-Sed and MI-Sed myocytes but was significantly (P < 0.01) reduced in MI-HIST myocytes by 25%. Our results indicate that HIST instituted shortly after MI improves [Ca(2+)](i) dynamics in surviving myocytes. Improvement in SR function by HIST is mediated not by increased SR Ca(2+)-ATPase expression, but by modulating phospholamban regulation of SR Ca(2+)-ATPase activity.
Animals↗
Sprint training restores normal contractility in postinfarction rat myocytes.
The significance of 6-8 wk of high-intensity sprint training (HIST) on contractile abnormalities of myocytes isolated from rat hearts with prior myocardial infarction (MI) was investigated. Compared with the sedentary (Sed) condition, HIST attenuated myocyte hypertrophy observed post-MI primarily by reducing cell lengths but not cell widths. At high extracellular Ca(2+) concentration (5 mM) and low pacing frequency (0.1 Hz), conditions that preferentially favored Ca(2+) influx over efflux, MI-Sed myocytes shortened less than Sham-Sed myocytes did. HIST significantly improved contraction amplitudes in MI myocytes. Under conditions that favored Ca(2+) efflux, i.e., low extracellular Ca(2+) concentration (0.6 mM) and high pacing frequency (2 Hz), MI-Sed myocytes contracted more than Sham-Sed myocytes. HIST did not appreciably affect contraction amplitudes of MI myocytes under these conditions. Compared with MI-Sed myocytes, HIST myocytes showed significant improvement in time required to reach one-half maximal contraction amplitude shortening, maximal myocyte shortening and relengthening velocities, and half time of relaxation. Our results indicate that HIST instituted shortly after MI improved cellular contraction in surviving myocytes. Because our previous studies demonstrated that, in post-MI myocytes, HIST improved intracellular Ca(2+) dynamics, enhanced sarcoplasmic reticulum Ca(2+) uptake and Ca(2+) content, and restored Na(+)/Ca(2+) exchange current toward normal, we hypothesized that improvement in MI myocyte contractile function by HIST was likely mediated by normalization of cellular Ca(2+) homeostatic mechanisms.
Animals↗
[Characterization of a wheat-Agropyron intermedium translocation line by sequential GISH and FISH].
The chromosome constitution on H96276-2, which is a stable line derived from a sterile wheat-Agropyron intermedium partial amphiploid Zhong 3 cross to common wheat Hui 75, was analyzed by sequential GISH and FISH. The results of GISH using genomic DNA of Agropyron intermedium as probe showed that H96276-2 possessed 20 pairs of wheat chromosomes and one pair of translocation chromosomes of wheat and Ag. intermedium. The translocated alien chromosome fragments located on the terminals of one pair of wheat chromosomes. Furthermore, reprobing of repeat sequence pSc119 was used to identify the wheat chromosomes involved in the translocation. It was determined that the alien fragments located in the terminals of the short arms of 2B chromosomes of wheat.
In Situ Hybridization, Fluorescence↗
Soybean nodule sucrose synthase (nodulin-100): further analysis of its phosphorylation using recombinant and authentic root-nodule enzymes.
Sucrose synthase (SS) is a known phosphoserine-containing enzyme in legume root nodules and various other plant "sink" tissues. In order to begin to investigate the possible physiological significance of this posttranslational modification, we have cloned a full-length soybean nodule SS (nodulin-100) cDNA and overexpressed it in Escherichia coli. Authentic nodule SS and recombinant wild-type and mutant forms of the enzyme were purified and characterized. We document that a conserved serine near the N-terminus (Ser(11)) is the primary phosphorylation site for a nodule Ca(2+)-dependent protein kinase (CDPK) in vitro. Related tryptic digestion and mass spectral analyses indicated that this target residue was also phosphorylated in planta in authentic nodulin-100. In addition, a secondary phosphorylation site(s) in recombinant nodule SS was implicated given that all active mutant enzyme forms (S11A, S11D, S11C, and N-terminal truncation between Ala(2) and Arg(13)) were phosphorylated, albeit weakly, by the CDPK. This secondary site(s) likely resides between Glu(14) and Met(193) as evidenced by CNBr cleavage and phosphopeptide mapping. Phosphorylation of the recombinant and authentic nodule Ser(11) enzymes in vitro by the nodule CDPK had no major effect on the sucrose-cleavage activity and/or kinetic properties. However, phosphorylation decreased the apparent surface hydrophobicity of the recombinant wild-type enzyme, suggesting that this covalent modification could potentially play some role in the documented partitioning of nodulin-100 between the nodule symbiosome/plasma membranes and cytosol in planta.
Amino Acid Sequence↗