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G Wu

Publications and source records attributed to G Wu.

At least 73 records · Page 4Linked to original sources
PubMed2001

Oxidative damage induced by the injection of HIV-1 Tat protein in the rat striatum.

Oxidative stress has been hypothesized to play a role in the pathogenesis of different neurodegenerative disorders, including HIV-related dementia. Tat, a nonstructural protein of HIV, is implicated in potentiation of neuronal apoptosis by mechanisms involving the disruption of calcium homeostasis and oxidative stress. The injection of Tat caused an increase of protein carbonyl formation in the rat striatum. Increased oxidative modification of proteins occurred early after Tat injection and preceded Tat-mediated astrogliosis. Immunostaining of brain sections demonstrated that an area of prominent protein carbonyl immunoreactivity surrounded an injection site in the striatum of Tat-injected rats. Intense protein carbonyl immunoreactivity was localized in cell bodies. Our study suggests that increased protein oxidation may be an important part of the mechanism of Tat neurotoxicity.

Animals↗
PubMed2001

Atomic carbon as a terminal ligand: studies of a carbidomolybdenum anion featuring solid-state (13)C NMR data and proton-transfer self-exchange kinetics.

Anion [CMo(N[R]Ar)(3)](-) (R = C(CD(3))(2)CH(3) or (t)Bu, Ar = 3,5-C(6)H(3)Me(2)) containing one-coordinate carbon as a terminal substituent and related molecules have been studied by single-crystal X-ray crystallography, solution and solid-state (13)C NMR spectroscopy, and density functional theory (DFT) calculations. Chemical reactivity patterns for [CMo(N[R]Ar)(3)](-) have been investigated, including the kinetics of proton-transfer self-exchange involving HCMo(N[R]Ar)(3), the carbidomolybdenum anion's conjugate acid. While the Mo triple bond C bond lengths in [K(benzo-15-crown-5)(2)][CMo(N[R]Ar)(3)] and the parent methylidyne, HCMo(N[R]Ar)(3), are statistically identical, the carbide chemical shift of delta 501 ppm is much larger than the delta 282 ppm shift for the methylidyne. Solid-state (13)C NMR studies show the carbide to have a much larger chemical shift anisotropy (CSA, 806 ppm) and smaller (95)Mo--(13)C coupling constant (60 Hz) than the methylidyne (CSA = 447 ppm, (1)J(MoC) = 130 Hz). DFT calculations on model compounds indicate also that there is an increasing MoC overlap population on going from the methylidyne to the terminal carbide. The pK(a) of methylidyne HCMo(N[R]Ar)(3) is approximately 30 in THF solution. Methylidyne HCMo(N[R]Ar)(3) and carbide [CMo(N[R]Ar)(3)](-) undergo extremely rapid proton-transfer self-exchange reactions in THF, with k = 7 x 10(6) M(-1) s(-1). Besides being a strong reducing agent, carbide [CMo(N[R]Ar)(3)](-) reacts as a nucleophile with elemental chalcogens to form carbon-chalcogen bonds and likewise reacts with PCl(3) to furnish a carbon-phosphorus bond.

Journal Article↗
PubMed2001

Effects of dopaminergic agents on carrageenan hyperalgesia after intrathecal administration to rats.

The present study explored the role of dopaminergic transmission in spinal cord in a model of carrageenan-induced inflammatory pain by examining the effects of selective agonists and antagonists of dopamine receptors. The results were as follows: (1) trans-(-)-4aR-4,4a,5,6,7,8,8a,9-octahydro-5-propyl-1H-pyrazolo[3,4-g] quinoline hydrochloride (LY171555), a dopamine D(2) receptor agonist, produced anti-hyperalgesia (150 and 300 nmol) or hypoalgesia (300 nmol) in the inflamed hindpaws and non-inflamed hindpaws, respectively; spiperone hydrochloride (8-[4-(4-fluorophenyl)-4-oxobutyl]-1-phenyl-1,3,8-triazaspiro[4,5]decan-4-one hydrochloride), a dopamine D(2) receptor antagonist, decreased the pain threshold of non-inflamed hindpaws (300 nmol). (2) (+/-)-SKF38393 hydrochloride ((+/-)-1-phenyl-2,3,4,5-tetrahydro-(1H)-3-benzazepine-7,8-diol hydrochloride), a dopamine D(1) receptor agonist, had no effect on either hindpaw, even at a higher dose (300 nmol); R(+)-7-Chloro-8-hydroxy-3-methyl-1-phenyl-2,3,4,5-tetrahydro-1H-3-benzazepine hydrochloride (R(+)-SCH23390 hydrochloride), a dopamine D(1) receptor antagonist, induced anti-hyperalgesia in the inflamed hindpaws (300 nmol). The present results suggest that the dopaminergic system in the spinal cord is involved in the central modulation of inflammatory hyperalgesia, and that the different effects are probably induced by different receptors.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗
PubMed2001

Early onset of spontaneous activity in uninjured C-fiber nociceptors after injury to neighboring nerve fibers.

Ligation and transection of the L5 spinal nerve in the rat lead to behavioral signs of pain and hyperalgesia. Discharge of injured nociceptors has been presumed to play a role in generating the pain. However, A fibers, but not C fibers, in the injured L5 spinal nerve have been shown to develop spontaneous activity. Moreover, an L5 dorsal root rhizotomy does not reverse this pain behavior, suggesting that signals from other uninjured spinal nerves are involved. We asked if abnormal activity develops in an adjacent, uninjured root. Single nerve fiber recordings were made from the L4 spinal nerve after ligation and transection of the L5 spinal nerve. Within 1 d of the lesion, spontaneous activity developed in approximately half of the C fiber afferents. This spontaneous activity was at a low level (median rate, seven action potentials/5 min), originated distal to the dorsal root ganglion, and was present in nociceptive fibers with cutaneous receptive fields. The incidence and level of spontaneous activity were similar 1 week after injury. The early onset of spontaneous activity in uninjured nociceptive afferents could be the signal that produces the central sensitization responsible for the development of mechanical hyperalgesia. Because L4 afferents comingle with degenerating L5 axons in the peripheral nerve, we hypothesize that products associated with Wallerian degeneration lead to an alteration in the properties of the adjacent, uninjured afferents.

Action Potentials↗
PubMed2001

Cantilever-based optical deflection assay for discrimination of DNA single-nucleotide mismatches.

Characterization of single-nucleotide polymorphisms is a major focus of current genomics research. We demonstrate the discrimination of DNA mismatches using an elegantly simple microcantilever-based optical deflection assay, without the need for external labeling. Gold-coated silicon AFM cantilevers were functionalized with thiolated 20- or 25-mer probe DNA oligonucleotides and exposed to target oligonucleotides of varying sequence in static and flow conditions. Hybridization of 10-mer complementary target oligonucleotides resulted in net positive deflection, while hybridization with targets containing one or two internal mismatches resulted in net negative deflection. Mismatched targets produced a stable and measurable signal when only a four-base pair stretch was complementary to the probe sequence. This technique is readily adaptable to a high-throughput array format and provides a distinct positive/negative signal for easy interpretation of oligonucleotide hybridization.

Base Pair Mismatch↗
PubMed2001

Role of the arginine-nitric oxide pathway in the regulation of vascular smooth muscle cell proliferation.

The objective of this study was to elucidate the mechanisms by which nitric oxide (NO) inhibits rat aortic smooth muscle cell (RASMC) proliferation. Two products of the arginine-NO pathway interfere with cell growth by distinct mechanisms. N(G)-hydroxyarginine and NO appear to interfere with cell proliferation by inhibiting arginase and ornithine decarboxylase (ODC), respectively. S-nitroso-N-acetylpenicillamine, (Z)-1-[N-(2-aminoethyl)-N-(2-aminoethyl)-amino]-diazen-1-ium-1,2-diolate, and a nitroaspirin derivative (NCX 4016), each of which is a NO donor agent, inhibited RASMC growth at concentrations of 1-3 microM by cGMP-independent mechanisms. The cytostatic action of the NO donor agents as well as alpha-difluoromethylornithine (DFMO), a known ODC inhibitor, was prevented by addition of putrescine but not ornithine. These observations suggested that NO, like DFMO, may directly inhibit ODC. Experiments with purified, recombinant mammalian ODC revealed that NO inhibits ODC possibly by S-nitrosylation of the active site cysteine in ODC. DFMO, as well as the NO donor agents, interfered with cellular polyamine (putrescine, spermidine, spermine) production. Conversely, increasing the expression and catalytic activity of arginase I in RASMC either by transfection of cells with the arginase I gene or by induction of arginase I mRNA with IL-4 resulted in increased urea and polyamine production as well as cell proliferation. Finally, coculture of rat aortic endothelial cells, which had been pretreated with lipopolysaccharide plus a cytokine mixture to induce NO synthase and promote NO production, caused NO-dependent inhibition of target RASMC proliferation. This study confirms the inhibitory role of the arginine-NO pathway in vascular smooth muscle proliferation and indicates that one mechanism of action of NO is cGMP-independent and attributed to its capacity to inhibit ODC.

Animals↗
PubMed2001

Peroxidase self-inactivation in prostaglandin H synthase-1 pretreated with cyclooxygenase inhibitors or substituted with mangano protoporphyrin IX.

Self-inactivation imposes an upper limit on bioactive prostanoid synthesis by prostaglandin H synthase (PGHS). Inactivation of PGHS peroxidase activity has been found to begin with Intermediate II, which contains a tyrosyl radical. The structure of this radical is altered by cyclooxygenase inhibitors, such as indomethacin and flurbiprofen, and by replacement of heme by manganese protoporphyrin IX (forming MnPGHS-1). Peroxidase self-inactivation in inhibitor-treated PGHS-1 and MnPGHS-1 was characterized by stopped-flow spectroscopic techniques and by chromatographic and mass spectrometric analysis of the metalloporphyrin. The rate of peroxidase inactivation was about 0.3 s(-)1 in inhibitor-treated PGHS-1 and much slower in MnPGHS-1 (0.05 s(-)1); as with PGHS-1 itself, the peroxidase inactivation rates were independent of peroxide concentration and structure, consistent with an inactivation process beginning with Intermediate II. The changes in metalloporphyrin absorbance spectra during inactivation of inhibitor-treated PGHS-1 were similar to those observed with PGHS-1 but were rather distinct in MnPGHS-1; the kinetics of the spectral transition from Intermediate II to the next species were comparable to the inactivation kinetics in each case. In contrast to the situation with PGHS-1 itself, significant amounts of heme degradation occurred during inactivation of inhibitor-treated PGHS-1, producing iron chlorin and heme-protein adduct species. Structural perturbations at the peroxidase site (MnPGHS-1) or at the cyclooxygenase site (inhibitor-treated PGHS-1) thus can influence markedly the kinetics and the chemistry of PGHS-1 peroxidase inactivation.

Chromatography, High Pressure Liquid↗
PubMed2001

[Effect of thyroxine upon prevention of recurrence of Graves' disease treated with antithyroid drugs].

OBJECTIVE: To investigate the effect of thyroxine upon the prevention of recurrence of Graves disease after treatment by antithyroid drugs. METHODS: Sixty patients newly diagnosed as Graves disease were treated with methimazole for 6 months and then randomly distributed into three groups. Patient in group A and group C received small dose of methimazole plus L-T(4) 50 microgram/d, and patients in group B were treated with methimazole in small dose only. Twenty four months later, only L-T(4) 50 microgram/d, without methimazole, was administered to the patients of group A; methimazole in maintenance dose was administered continuously to the patients of group B, and patients in group C were treated with methimazole in maintenance dose plus L-T(4) 50 microgram/d. Such treatments lasted 6 months. Post-treatment follow-up survey was conducted to the three groups. RESULTS: The titers of thyroid-stimulating Ab (TSAb) in groups A and C were lower than that in group B. However, the recurrence rates among the three groups (4/20, 20%; 4/20, 25%; and 4/20, 20% respectively) were not significantly different. CONCLUSION: Both treatment of Graves' disease with methimazole plus L-T4 and treatment with prolonged use of methimazole cannot reduce the recurrence rate more effectively than treatment with only methimazole. The level of TSAb is not the only factor that influences the recurrence of Graves disease.

Adolescent↗
PubMed2001

Isolation and characterization of mouse MUC18 cDNA gene, and correlation of MUC18 expression in mouse melanoma cell lines with metastatic ability.

The cell surface adhesion molecule human MUC18 (huMUC18 or Mel-CAM) has been postulated to play a key pathogenic role in metastatic melanoma progression. To establish an immunocompetent syngeneic mouse model that would greatly facilitate our understanding of the role of MUC18 in the metastatic behavior of melanoma, we cloned and characterized the mouse MUC18 (muMUC18) cDNA gene. The gene was amplified by RT-PCR and RACE of the poly(A)+RNA isolated from the mouse melanoma cell line B16F10/Queens. The cloned muMUC18 cDNA gene contained 28 nucleotides of 5'-UTR, 908 nucleotides of 3'-UTR, and an open reading frame (ORF) of 1947 nucleotides encoding a protein of 648 amino acids, which is two amino acids longer than huMUC18. The size of the muMUC18 mRNA is about 3 kb with a shorter 3'-UTR than the huMUC18 mRNA (about 3.3 kb). Besides, the sequence in the 3' UTR of the two mRNAs is diverse with only 31% identity. The 5'-UTR and coding sequences of the muMUC18 cDNA are 72.4 and 80.6% identical to those of huMUC18, respectively. The deduced amino acid sequence of the muMUC18 cDNA is 76.2% identical to that of huMUC18. The amino acid sequences deduced from MUC18 cDNA sequences from six other mouse melanoma cell lines are identical except one to three residues, suggesting that the muMUC18 cDNA sequence determined in this report is correct. The muMUC18 protein is predicted to be slightly more acidic than the human protein. The levels of muMUC18 mRNA and protein in nine mouse melanoma cell lines were directly proportional to their ability to establish metastatic colonies in lungs of syngeneic mice. Most biological functions of the muMUC18 may be similar to the huMUC18.

Amino Acid Sequence↗
PubMed2001

Rop GTPase-dependent dynamics of tip-localized F-actin controls tip growth in pollen tubes.

Tip-growing pollen tubes provide a useful model system to study polar growth. Although roles for tip-focused calcium gradient and tip-localized Rho-family GTPase in pollen tube growth is established, the existence and function of tip-localized F-actin have been controversial. Using the green fluorescent protein-tagged actin-binding domain of mouse talin, we found a dynamic form of tip-localized F-actin in tobacco pollen tubes, termed short actin bundles (SABs). The dynamics of SABs during polar growth in pollen tubes is regulated by Rop1At, a Rop GTPase belonging to the Rho family. When overexpressed, Rop1At transformed SAB into a network of fine filaments and induced a transverse actin band behind the tip, leading to depolarized growth. These changes were due to ectopic Rop1At localization to the apical region of the plasma membrane and were suppressed by guanine dissociation inhibitor overexpression, which removed ectopically localized Rop1At. Rop GTPase-activating protein (RopGAP1) overexpression, or Latrunculin B treatments, also recovered normal actin organization and tip growth in Rop1At-overexpressing tubes. Moreover, overexpression of RopGAP1 alone disrupted SABs and inhibited growth. Finally, SAB oscillates and appears at the tip before growth. Together, these results indicate that the dynamics of tip actin are essential for tip growth and provide the first direct evidence to link Rho GTPase to actin organization in controlling cell polarity and polar growth in plants.

Actins↗
PubMed2001

Photon-stimulated ion desorption from molybdenum oxides following Mo 2p3/2 excitation.

Photon-stimulated ion desorption from solid MoO3 following the Mo 2p3/2 resonant transition has been investigated. In the XANES spectrum, Mo 2p3/2 peak is split into two components corresponding to the excitations from Mo 2p3/2 into the t2g and e(g) orbitals. It was observed that the desorption yield of O+ ions at the Mo 2p3/2-->e(g) resonance is higher than that at the Mo 2p3/2-->t2g resonance. The Auger decay spectra reveal that there exist two kinds of spectator Auger decays. The high desorption yield at the 2p3/2-->e(g) resonance is interpreted by the fast breaking of the Mo-O bond due to the localization of the electrons in the highly antibonding e(g).

Journal Article↗
PubMed2001

Comparison of ganglioside profiles in nuclei and whole cells of NG108-15 and NG-CR72 lines: changes in response to different neuritogenic stimuli.

The plasma and nuclear membranes of neural cells have been shown to express gangliosides to a limited extent before, and at increasing levels during, differentiation. Recent studies employing qualitative cytochemistry have shown that GM1 expression in particular is significantly elevated in both membranes by specific neuritogenic agents. The present study provides a more complete description of ganglioside patterns of the 2 membranes of NG108-15 cells and a mutated form of the latter lacking gangliotetraose gangliosides. Nuclei of wild type NG108-15 cells were found to contain predominantly GM1 and GD1a, whereas whole cells had those in addition to substantial amounts of GM2 and GM3. GM1 and GD1a levels increased 2--3.5-fold in both whole cells and nuclei following axonogenic stimulation, but changed little in response to dendritogenic agents. GM2 expression, limited to the plasma membrane, showed little if any change with axonogenic stimuli but a 1.5--2-fold increase following treatment with dendritogenic agents. GM3 resembled GM2 in being virtually absent from the nuclear membrane, while its presence in the plasma membrane showed only modest change at most with any of the stimuli. The gangliotetraose ganglioside-deficient mutant cell line, NG-CR72, had significantly higher basal levels of GM2 in the plasma membrane compared to wild type NG108-15 cells, and this level increased significantly on treatment with dendritogenic agents. Basal GM3 levels were greatly reduced in the mutant cells and changed little with any of the stimuli. As expected, nuclei of NG-CR72 cells were virtually devoid of gangliosides. These mutant cells were previously shown to extend well defined dendritic neurites but were incapable of forming stable axonal processes. This study thus demonstrates major differences in the ganglioside content of wild type and mutated NG108-15 cells and their nuclei, and in their response to different neuritogenic stimuli.

Animals↗
PubMed2001

Evolutionary relationships of the glucokinase from the amitochondriate protist, Trichomonas vaginalis.

Two genes coding for Trichomonas vaginalis glucokinase were isolated and sequenced. The putative translation products have molecular masses of 41,584 and 41,772 Da, corresponding to 375 and 377 amino acids, respectively. These values agree with data determined by sodium dodecylsulfate-polyacrylamide gel electrophoresis (SDS-PAGE) for the enzyme purified from the organism. The two sequences showed 78% amino acid identity. The sequences and their phylogenetic reconstruction show that they are members of a glucokinase/fructokinase protein family found in eubacteria and also in the eukaryote Giardia lamblia and are only distantly related to typical eukaryotic hexokinases. The results indicate that the evolutionary past of this enzyme, catalyzing the first step of glycolysis in T. vaginalis, is different from that of the enzyme performing this key role in almost all other eukaryotes.

Amino Acid Sequence↗
PubMed2001

Origin of nanomechanical cantilever motion generated from biomolecular interactions.

Generation of nanomechanical cantilever motion from biomolecular interactions can have wide applications, ranging from high-throughput biomolecular detection to bioactuation. Although it has been suggested that such motion is caused by changes in surface stress of a cantilever beam, the origin of the surface-stress change has so far not been elucidated. By using DNA hybridization experiments, we show that the origin of motion lies in the interplay between changes in configurational entropy and intermolecular energetics induced by specific biomolecular interactions. By controlling entropy change during DNA hybridization, the direction of cantilever motion can be manipulated. These thermodynamic principles were also used to explain the origin of motion generated from protein-ligand binding.

DNA, Single-Stranded↗
PubMed2001

Ciliary neurotrophic factor induces preprotachykinin A gene expression in the rat carotid body.

Substance P (SP), a translational product of preprotachykinin-A (PPT-A) mRNA plays an important role in hypoxic chemotransmission in the rat carotid body. Although hypoxic exposure has been associated with an increase in SP content in the carotid body, factors that cause induction, regulation and release of PPT-A and SP in the carotid body remain to be elucidated. The purpose of this study was to investigate whether ciliary neurotrophic factor (CNTF), a factor that has been shown to regulate neurotransmitter phenotype in tissue from neural crest origin, could induce PPT-A gene expression in the rat carotid body. We used in situ hybridization histochemistry with radioactive ribonucleotide probes to investigate the effect of CNTF on PPT-A gene induction in the carotid body. Exposure of the rat superior cervical ganglia and carotid body to increasing concentrations of CNTF in culture resulted in up-regulation and induction of PPT-A mRNA, respectively.

Animals↗
PubMed2001

Effects of baseline skin temperature on pain ratings to suprathreshold temperature-controlled stimuli.

Variations in baseline skin temperature can be encountered in experimental and clinical pain states. Such variations have been shown to greatly alter the response to radiant heat stimuli when the temperature of the stimulus is not controlled. We carried out a psychophysical investigation to examine the influence of baseline skin temperature on pain ratings to temperature-controlled heat stimuli. A CO(2) laser thermal stimulator was used to deliver heat stimuli under radiometer feedback temperature control to the volar forearm. Each stimulus consisted of a 30 s controlled baseline interval (at 34 or 38 degrees C) followed by a stepped increase in temperature (to 46 or 47 degrees C for 1, 2 or 4 s). A run comprised one presentation of each of these12 different stimuli to different locations. Each experiment contained three runs. In runs 2 and 3, the stimulus intensity and duration at a given location were not changed, but the baseline temperature was alternated between 34 degrees C and 38 degrees C. The intensity of pain was rated using the technique of magnitude estimation. Mean normalized pain ratings for suprathreshold stimuli applied from the higher base temperature (1.03+/-0.03) were slightly greater than from the lower base temperature (0.96+/-0.03). In contrast, pain ratings to the 47 degrees C stimuli (1.11+/-0.03) were substantially greater than to the 46 degrees C stimuli (0.88+/-0.03). Thus a 4 degrees C change in baseline temperature has a smaller affect (about 8%) on pain ratings than a 1 degrees C change in stimulus temperature (about 27%). This suggests that variations in baseline skin temperature encountered in experimental and clinical pain states have only a minor impact on pain sensitivity to suprathreshold temperature-controlled stimuli.

Adult↗
PubMed2001

Sino-MONICA project: a collaborative study on trends and determinants in cardiovascular diseases in China, Part i: morbidity and mortality monitoring.

BACKGROUND: The Sino-MONICA project is a 7-year study monitoring trends and determinants of cardiovascular disease (CVD) in geographically defined populations in different parts of China. METHODS AND RESULTS: The study is a community-based prospective disease surveillance that uses the methodology and criteria of the World Health Organization's Monitoring Trends and Determinants in Cardiovascular Disease (WHO MONICA) project, with slight modifications for local use. After a pilot study of 2 years (1985 through 1986), data collection started formally on January 1, 1987, and ended on December 31, 1993. The main results were as follows. By international standards, both the incidence and mortality rate of coronary heart disease in Chinese populations were low. The highest incidence was 108.7 of 100,000 (1987 to 1989), and the lowest was 3.3 of 100,000 for men 35 to 64 years of age, a 33-fold difference. Both the incidence and mortality rate of cerebrovascular disease were high. The highest incidence was 553.3 of 100,000 (1987 to 1989), and the lowest was 33.0 of 100,000 for men 35 to 64 years of age, a 17-fold difference. There were significant geographic variations in both CVD incidence and mortality rate, with higher rates in the north and lower rates in the south. During 1987 to 1993, increasing trends were found in CVD rates in some populations, whereas decreasing trends were found in others. The trends were not significant statistically in most cases. CONCLUSIONS: Monitoring CVD with international standardized methods in China is feasible and urgently needed in view of the rapid socioeconomic development and transition of disease patterns taking place in China. The results are of significance in combating CVD both at home and abroad.

Adult↗