PubMed Health⌕ Search

Biomedical subjects

W Xiong

Publications and source records attributed to W Xiong.

At least 37 records · Page 2Linked to original sources
PubMed2001

Measurement of the branching ratios of D(+) and D(+)(s) hadronic decays to four-body final states containing a K(S).

We have studied hadronic four-body decays of D(+) and D(+)(s) mesons with a K(S) in the final state using data recorded during the 1996-1997 fixed-target run of the Fermilab high energy photoproduction experiment FOCUS. We report a new branching ratio measurement of gamma(D(+)-->K(S)K-pi(+)pi(+))/gamma(D(+)-->K(S)pi(+)pi(+)pi(-)) = 0.0768+/-0.0041+/-0.0032. We make the first observation of three new decay modes with branching ratios gamma(D(+)-->K(S)K+pi(+)pi(-))/gamma(D(+)-->K(S)pi(+)pi(+)pi(-)) = 0.0562+/-0.0039+/-0.0040, gamma(D(+)-->K(S)K+K-pi(+))/gamma(D(+)-->K(S)pi(+)pi(+)pi(-)) = 0.0077+/-0.0015+/-0.0009, and gamma(D(+)(s)-->K(S)K+pi(+)pi(-))/gamma(D(+)(s)-->K(S)K-pi(+)pi(+)) = 0.586+/-0.052+/-0.043, where in each case the first error is statistical and the second error is systematic.

Journal Article↗
PubMed2001

The effect of galanin on wide-dynamic range neuron activity in the spinal dorsal horn of rats.

The present study investigated the effect of galanin on wide-dynamic range (WDR) neuron activity in the dorsal horn of the spinal cord of rats. The evoked discharge of WDR neurons was elicited by transdermic electrical stimulation applied on the ipsilateral hindpaw of rats. Galanin was administered directly on the spinal dorsal surface of L3-L5. The evoked discharge frequency of the WDR neurons decreased significantly after the administration of galanin and the effect lasted for more than 30 min. Furthermore, the inhibitory effect of galanin on the evoked discharge frequency of WDR neurons was blocked by following administration of the galanin antagonist galantide, indicating that the inhibitory effect of galanin on the activity of WDR neurons was induced by activating galanin receptors in the dorsal horn of the spinal cord. The results suggest that galanin has an inhibitory role in the transmission of presumed nociceptive information in the dorsal horn of the spinal cord in rats.

Animals↗
PubMed2001

Regulation of CCAAT/enhancer-binding protein-beta isoform synthesis by alternative translational initiation at multiple AUG start sites.

The mRNA of the intronless, single-copy CCAAT/enhancer-binding protein-beta (C/EBPbeta) gene encodes several isoforms that have truncated transcription activation domains. This occurs by the alternative translational initiation (ATI) at multiple AUG start sites. The C/EBPbeta mRNA has four in-frame AUGs and an internal out-of-frame AUG associated with a small open reading frame (sORF). Initiation of translation at the in-frame AUGs forms 40-kDa (AUG-1), 35-kDa (AUG-2), 20-kDa (AUG-3) and 8.5-kDa (AUG-4) isoforms. We show that in COS-1 cells the 20-kDa isoform is not a product of proteolysis of the higher molecular weight isoforms. The sORF contains an AUG and termination signal that may produce the oligopeptide MPPAAARRL. Our studies suggest that ATI involves three mRNA structural features: (i) the cap structure, (ii) the context of the Kozak sequences that flank the AUG and (iii) the integrity of the sORF. We propose that formation of C/EBPbeta isoforms is accomplished by a leaky ribosomal scanning mechanism that facilitates ATI of multiple internal AUGs.

Alternative Splicing↗
PubMed2001

Study of the decay D0 --> K+pi-.

Using a large sample of photoproduced charm mesons from the FOCUS experiment at Fermilab (FNAL-E831), we observe the decay D0-->K+pi- with a signal yield of 149+/-31 events compared to a similarly cut sample consisting of 36 760+/-195 D0-->K-pi+ events. We use the observed ratio of D0-->K+pi- to D0-->K-pi+ (0.404+/-0.085+/-0.025)% to obtain a relationship between the D0 mixing and doubly Cabibbo suppressed decay parameters.

Journal Article↗
PubMed2001

Effects of mercuric chloride on the regulation of expression of the acute phase response components alpha(1)-acid glycoprotein and C/EBP transcription factors.

We have previously shown that in response to treatment with HgCl(2), the adult mouse liver exhibits both transcriptional and translational regulation of the acute phase response genes. In this study we asked whether the heavy metal treatment affects the regulation of the C/EBP transcription factors which play a key role in regulation of the acute phase response gene. Our studies have shown that the AGP gene is transcriptionally activated while transcription of the CCAAT/enhancer-binding trans-activating protein (C/EBP)alpha gene is slightly down-regulated and that of the C/EBPbeta gene does not respond. Both the C/EBPalpha and C/EBPbeta mRNAs produce multiple isoforms possibly by alternative translation initiation (ATI) of multiple internal AUG initiation sites. The C/EBPbeta mRNA appears to be stabilized. Although similar regulatory processes occur in response HgCl(2) vs. LPS, our data suggest that the translational processes (ATI) are differentially affected. In addition, a major difference lies in the fact that the C/EBPbeta gene is not transcriptionally activated by HgCl(2). Our data show decreased binding activity and pool levels of the C/EBPalpha isoform (p42(C/EBPalpha)) and increased binding activity and pool levels of C/EBPbeta isoform (p35(C/EBPbeta)) in response to HgCl(2). We propose that this isoform may be involved in the regulation of AGP gene expression in response to heavy metals and that there is a significant difference between the HgCl(2)-mediated and LPS-mediated inflammatory response.

Alternative Splicing↗
PubMed2001

c-Jun N-terminal kinase activation in Xenopus laevis eggs and embryos. A possible non-genomic role for the JNK signaling pathway.

The c-Jun N-terminal kinases (JNKs) are members of the mitogen-activated protein kinase family that play critical roles in stress responses and apoptosis. We have discovered that JNK is present in Xenopus oocytes, an experimental system that offers a variety of powerful experimental approaches to questions of protein function and regulation. Like ERK2/p42 MAPK, JNK is activated just prior to germinal vesicle breakdown during Xenopus oocyte maturation and remains active throughout meiosis I and II. However, unlike p42 MAPK, which is inactivated about 30 min after eggs are fertilized or parthenogenetically activated, JNK stays constitutively active until the early gastrula stage of embryogenesis. These findings suggest that the JNK pathway may play a role in oocyte maturation and embryogenesis. JNK was activated by microinjection of Mos, by activation of an estrogen-inducible form of Raf, and by a constitutively active MEK-1 (MEK R4F), indicating that the p42 MAPK cascade can trigger JNK activation. However, the MEK inhibitor U0126 blocked progesterone-induced p42 MAPK activation but not progesterone-induced JNK activation. Thus, progesterone can stimulate JNK activation both through the MEK/p42 MAPK pathway and through MEK/p42 MAPK-independent pathways. Many of the key substrates of JNKs identified to date are transcriptional regulators. However, since transcription is not required for germinal vesicle breakdown in progesterone-treated oocytes or for the early embryonic cell cycles, our findings suggest that in these contexts the JNK pathway exerts nongenomic effects.

Animals↗
PubMed2001

An experimental study on the regulation of expression of Th2 cytokines from T lymphocytes by protein kinase C in asthma.

To explore the regulatory role of protein kinase C (PKC) in the expression of Th2 cytokines, interleukin-4 (IL-4) and interleukin-5 (IL-5) by T lymphocytes in asthma. T lymphocytes were isolated and purified from blood and bronchial alveolus lavage fluid (BALF) of each guinea pig of normal control group and asthmatic group and from peripheral blood of the asthmatic patients and normal controls, and were stimulated with PKC accelerant phorbol 12-myristate 13-acetate (PMA) and inhibitor Ro31-8220. The expression of IL-4 and IL-5 mRNA and protein was detected by using in situ hybridization staining and ELISA respectively. The expression of IL-4 and IL-5 mRNA and protein of asthmatic T lymphocytes stimulated with PMA was significantly higher than that of asthmatic T lymphocytes stimulated without PMA respectively (P < 0.01) and that of normal T lymphocytes stimulated with PMA respectively (P < 0.01). The expression of IL-4 and IL-5 mRNA and protein of asthmatic T lymphocytes stimulated with PMA and Ro31-8220 was significantly lower than that of asthmatic T lymphocytes stimulated only with PMA respectively (P < 0.01). It was concluded that PKC might participate in regulating the expression of IL-4 and IL-5 in asthmatic T lymphocytes, and the activation of PKC in T lymphocytes might play an important role in the pathogenesis of asthma.

Adult↗
PubMed2001

Interactions between antiarrhythmic drugs and cardiac memory.

OBJECTIVE: Ventricular pacing or arrhythmias can induce cardiac memory (CM). We hypothesized that clinically administered antiarrhythmic drugs alter the expression of CM, and that the repolarization changes characteristic of CM can modulate the effects of antiarrhythmic drugs. METHODS: We studied conscious, chronically-instrumented dogs paced for two 1-h periods to study the effects of drugs on the evolution of memory (protocol 1) or for 21 days (protocol 2) to observe the effects of steady-state memory on drug actions. Dogs were treated in both settings with quinidine, lidocaine or E4031, in random order, and within therapeutic serum concentration ranges. RESULTS: Pacing, alone, for 2 h significantly prolonged ERP only near the left ventricular pacing site, whereas pacing alone for 21 days prolonged ERP at all sites (P<0.05). Quinidine and E4031, but not lidocaine, prolonged repolarization and ERP and suppressed evolution of CM in protocol 1. However, quinidine's effect in prolonging repolarization was diminished in both protocols, while its effect in prolonging ERP was diminished in the 21-day protocol only. In contrast, the effects of E4031 were additive to those of CM, prolonging repolarization and ERP in both protocols, while lidocaine showed no changes in effect at all. CONCLUSIONS: Pacing to induce CM significantly affects ventricular repolarization and refractoriness, and there are interactions between CM, quinidine and E4031. Depending on the specific drug, these interactions have the potential to be anti- or proarrhythmic, and may impact importantly on the clinical efficacy of drugs as well as on electrophysiologic testing of drug actions.

Animals↗
PubMed2001

Nucleoside transporter subtype expression: effects on potency of adenosine kinase inhibitors.

1. Adenosine kinase (AK) inhibitors can enhance adenosine levels and potentiate adenosine receptor activation. As the AK inhibitors 5' iodotubercidin (ITU) and 5-amino-5'-deoxyadenosine (NH(2)dAdo) are nucleoside analogues, we hypothesized that nucleoside transporter subtype expression can affect the potency of these inhibitors in intact cells. 3. Three nucleoside transporter subtypes that mediate adenosine permeation of rat cells have been characterized and cloned: equilibrative transporters rENT1 and rENT2 and concentrative transporter rCNT2. We stably transfected rat C6 glioma cells, which express rENT2 nucleoside transporters, with rENT1 (rENT1-C6 cells) or rCNT2 (rCNT2-C6 cells) nucleoside transporters. 3. We tested the effects of ITU and NH(2)dAdo on [(3)H]-adenosine uptake and conversion to [(3)H]-adenine nucleotides in the three cell types. NH(2)dAdo did not show any cell type selectivity. In contrast, ITU showed significant inhibition of [(3)H]-adenosine uptake and [(3)H]-adenine nucleotide formation at concentrations < or =100 nM in rENT1-C6 cells, while concentrations > or =3 microM were required for C6 or rCNT2-C6 cells. 4. Nitrobenzylthioinosine (NBMPR; 100 nM), a selective inhibitor of rENT1, abolished the effects of nanomolar concentrations of ITU in rENT1-C6 cells. 5. This study demonstrates that the effects of ITU, but not NH(2)dAdo, in whole cell assays are dependent upon nucleoside transporter subtype expression. Thus, cellular and tissue differences in expression of nucleoside transporter subtypes may affect the pharmacological actions of some AK inhibitors.

Adenine Nucleotides↗
PubMed2001

Altering ventricular activation remodels gap junction distribution in canine heart.

INTRODUCTION: Prolonged arrhythmic or paced ventricular activation causes persistent changes in myocardial conduction and repolarization that may result from altered electrotonic current flow, for which gap junctional coupling is the principal determinant. Remodeling of gap junctions and their constituent connexins modifies conduction and has been causally implicated in reentrant arrhythmogenesis. We hypothesized conversely that altering the pattern of ventricular activation causes gap junctional remodeling. METHODS AND RESULTS: Seven dogs were paced from the left ventricular (LV) epicardium (VVO, approximately 120 beats/min) for 21 days before excision of transmural LV samples that were divided into endomyocardial, mid-myocardial, and epimyocardial layers. Another five paced dogs had recording electrodes attached to multiple LV sites. All 12 dogs developed characteristic pacing-induced persistent T wave changes of cardiac memory. After 21 days of pacing, the ventricularly paced QRS duration prolonged by a mean of 4 msec over baseline (P < 0.05), a change that was associated with significant slowing of intraventricular conduction to local sites. These changes in QRS duration and repolarization were associated with a reduction in epimyocardial connexin43 expression on quantitative Western blotting of LV myocardium from close to, but not distant from, the pacing site (61.7+/-18.4 vs 100.9+/-34.0; P < 0.02) and a marked disruption in immunolabeled connexin43 distribution in epimyocardium only. CONCLUSION: Spatially distinct transmural and regional gap junctional remodeling is a consequence of abnormal ventricular activation and is associated with consistent changes in activation that may alter patterns of repolarization and facilitate reentrant arrhythmogenesis.

Activation Analysis↗
PubMed2001

In contrast to forskolin and 3-isobutyl-1-methylxanthine, amrinone stimulates the cardiac voltage-sensitive release mechanism without increasing calcium-induced calcium release.

The objective of this study was to determine whether the voltage-sensitive release mechanism (VSRM) can be stimulated independently from Ca(2+)-induced Ca(2+) release (CICR) by drugs that elevate intracellular cAMP. Contractions were measured in voltage-clamped guinea pig ventricular myocytes at 37 degrees C. Na(+) current was blocked. We compared effects of agents that elevate cAMP through activation of adenylyl cyclase (1 microM forskolin), nonspecific inhibition of phosphodiesterases (PDEs) [100 microM 3-isobutyl-1-methylxanthine (IBMX)], and selective inhibition of PDE III (100-500 microM amrinone) on contractions initiated by the VSRM and CICR. Forskolin and IBMX significantly increased peak Ca(2+) current and CICR. In addition, these agents also markedly increased contractions elicited by test steps from -65 to -40 mV, which activate the VSRM. However, because these steps also induced inward current in the presence of forskolin or IBMX, CICR could not be excluded. In contrast, amrinone caused a large, concentration-dependent increase in VSRM contractions but had no effect on CICR contractions or Ca(2+) current. Sarcoplasmic reticulum Ca(2+), assessed by rapid application of caffeine (10 mM), was increased only modestly by all three drugs. Normalization of contractions to caffeine contractures indicated that amrinone increased fractional release by the VSRM, but not CICR. Forskolin and IBMX increased fractional release elicited by steps to -40 mV. Increases in CICR induced by forskolin and IBMX were proportional to caffeine contractures. Thus, positive inotropic effects of cAMP on VSRM contractions may be compartmentalized separately from effects on Ca(2+) current and CICR.

1-Methyl-3-isobutylxanthine↗
PubMed2001

[An experimental study on the regulation of the expression of Th2 cytokines by nuclear factor-kappaB and protein kinase C in asthma].

OBJECTIVE: To explore the role of nuclear factor-kappaB (NF-kappaB) in the signal pathway of protein kinase C (PKC) regulating the expression of Th2 cytokines, interleukin 4 (IL-4) and IL-5, by T lymphocyte in asthma. METHODS: 16 guinea pigs were randomly divided into 2 groups, normal control and asthmatic group. 16 asthmatic patients and 16 normal control persons also participated in the study. T lymphocytes were isolated and purified from blood of each guinea pig and each person and divided into 3 groups: cells of 1st group were control group, cells of 2nd group were stimulated with phorbol 12-myristate 13-acetate (PMA), cells of 3rd group were stimulated with PMA and pyrrolidine dithiocarbamate (PDTC). The expression of NF-kappaB were observed by immunocytochemical staining, the expression of IL-4 and IL-5 mRNA were observed by in situ hybridization staining, IL-4 and IL-5 protein in supernatants were measured by ELISA. RESULTS: The percentage of cells of active NF-kappaB, the percentage of positive cells of IL-4 and IL-5 mRNA, IL-4 and IL-5 protein in supernatants of asthmatic T lymphocyte stimulated with PMA were significantly higher than those of asthmatic T lymphocyte stimulated without PMA (q = 8.44 approximately 38.66, P < 0.01) and those of normal control T lymphocyte stimulated with PMA (q = 8.11 approximately 40.12, P < 0.01), and were significant reduced by PDTC (q = 6.50 approximately 35.63, P < 0.01). There were good positive correlation between the percentage of cells of active NF-kappaB and the percentage of positive cells of IL-4 and IL-5 mRNA (r = 0.60 approximately 0.82, P < 0.001, respectively), and also good positive correlation between the percentage of active NF-kappaB and IL-4 and IL-5 protein in supernatants (r = 0.42 approximately 0.70, P < 0.005 or < 0.001, respectively). CONCLUSIONS: The active PKC of asthmatic T lymphocyte increasing the expression of IL-4 and IL-5 may be mediated by activating NF-kappaB, the activation of PKC-NF-kappaB signal pathway of T lymphocyte NF-kappab may play an important role in the pathogenesis of asthma.

Adult↗
PubMed2001

[Determination of trace mercury in soil by hydride generation atomic fluorescence spectrometry].

A method for the rapid determination of trace mercury in soil by hydride atomic fluorescence spectrometry is reported in this paper. The sample of soil is leached (at 80 degrees C-100 degrees C) with aqua regia (H2O + aqua regia, 1 + 1). The concentration of KBH4 used in this method is studied. Trace mercury in reference material (polluted farming soil) is determined by the described method too. The result obtained is in good agreement with standard value. The RSD is 1.4% and the recovery of mercury is 87%-105%. This method is proved to be rapid, simple and accurate.

Mercury↗
PubMed2000

Sequence analysis of the human glycoprotein hormone alpha-subunit gene 5'-flanking DNA and identification of a potential regulatory element as an alu repetitive sequence.

The nucleotide sequence of the human glycoprotein hormone alpha-subunit (GPHalpha) gene 5'-flanking DNA was determined from -1637 to +49 relative to the cap site (+1). Comparison of the upstream sequence of the human gene with those of rhesus and mouse demonstrates regions with variable identity. When the 1.7 kb fragment was used to drive the expression of chloramphenicol acetyltransferase (CAT) in transiently transfected HeLa cells, it was found that CAT activity was elevated about 3-fold when the fragment was truncated from -1637 to -846, suggesting the presence of a negative regulatory element in the distal 5'-flanking DNA. This overlaps an Alu repetitive sequence (ARS) located between nucleotides -1330 and -1007. Gel mobility shift and DNase protection analyses identified a protein binding site centered around -1100 in the ARS second monomer. The GPHalpha upstream ARS was cloned in both orientations in positions upstream and downstream from the bacterial CAT gene under control of the herpes simplex virus thymidine kinase (tk) promoter. DNA-mediated transient transfection of these plasmids revealed a marked inhibition (79-82%) of CAT production by the ARS when it was cloned upstream from the tk promoter and in the same orientation as that found in the GPHalpha 5'-flanking DNA. Smaller decreases (29-57%) were produced by the ARS cloned upstream from the tk promoter in the reverse orientation. In marked contrast, the Alu repetitive element had little or no effect when cloned in either orientation downstream from the tk-CAT gene. Introduction of a second ARS downstream from the CAT reporter gene in vectors already containing an ARS upstream from the tk promoter significantly reduced the strong negative effect elicited by the upstream repetitive element. When compared to the Blur 8 Alu element, the GPHalpha upstream ARS differs markedly with respect to its effect on tk-CAT expression in transient assays and as a substrate for DNA binding proteins present in HeLa nuclear extracts. Together, the transient expression results demonstrate that ARS elements can influence expression of nearby class II promoters. The extent of this effect depends on element position and orientation, cell type, the particular ARS (e.g., GPHalpha or Blur 8), and whether copies were present both upstream and downstream from the transcription unit.

Alu Elements↗
PubMed2000

Analysis of relations between NMDA receptors and GABA release at olfactory bulb reciprocal synapses.

In the mammalian olfactory bulb, signal processing is mediated by synaptic interactions between dendrites. Glutamate released from mitral cell dendrites excites dendritic spines of granule cells, which in turn release GABA back onto the mitral cell dendrites, forming a reciprocal synaptic pair. This feedback synaptic circuit was shown to be mediated predominantly by NMDA receptors. We further utilized caged Ca2+ compounds to obtain insight into the mechanism that couples NMDA receptor activation to GABA release. Feedback inhibition elicited by photo-release of caged Ca2+ in mitral cell secondary dendrites persisted when voltage-gated Ca2+ channels were blocked by cadmium (Cd2+) and nickel (Ni2+). These results indicate that Ca2+ influx through NMDA receptors can directly trigger presynaptic GABA release for local dendrodendritic feedback inhibition.

2-Amino-5-phosphonovalerate↗
PubMed2000

[Optimized models of logging-tending system in cutting areas].

The comprehensive advantages of different logging-tending systems in Pinus massoniana forest cutting area were evaluated by set-pair analysis, based on the comparison of their economic and ecological benefits. The results showed that the optimized model for P. massoniana forests in Northern Fujian comprised 40% selective cutting, manual skidding, clear-cutting in ribbon, and natural regeneration with artificial aids, which could also be used in the nearby forests with conditions similar to the experimental area.

China↗
PubMed2000

P16 overexpression in pituitary adenomas studied by immunohistochemistry and in situ hybridization.

OBJECTIVES: To examine the expression of p16 gene and the clinicopathological characteristics of 31 pituitary adenomas. To investigate the relationship between p16 expression and cell proliferative activity by analyzing the expression of proliferating cell nuclear antigens (PCNA). METHODS: Immunohistochemistry and in situ hybridization were performed on freshly-prepared paraffin-embedded specimens of 31 pituitary adenomas. RESULTS: Varying degrees of overexpression of the p16 gene was found in the tumors specimens. A higher proportion of p16 positive tumor cells was associated with bigger size, more frequent invasion and higher recurrence of the tumors. The expression of p16 was found to be significantly associated with the degree of PCNA expression. CONCLUSION: Though inactivation of the p16 gene is known in wide range of tumors, our study suggested that p16 overexpression might play a role in the development and progression of pituitary adenomas.

Adenoma↗