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Biomedical subjects

Q Wang

Publications and source records attributed to Q Wang.

At least 127 records · Page 7Linked to original sources
PubMed2001

Kinetic model and optimization of 2,4-D degradation by anodic Fenton treatment.

Anodic Fenton treatment (AFT) is a new technology derived from chemical Fenton treatment. It has several advantages as compared with classic Fenton treatment and electrochemical Fenton treatment. On the basis of assumptions about a second-order reaction between pesticides and hydroxyl radicals and about AFT technology, a new kinetic model was developed to accurately describe the degradation kinetics of 2,4-D and to quantitatively investigate the effect of operating conditions. 2,4-D (2,4-dichlorophenoxyacetic acid) was employed as a probe in this study to investigate the AFT system. It was found that an increased delivery rate of Fenton reagent increased the degradation rate of 2,4-D, but the efficiency was decreased. The effects of the H2O2:Fe2+ ratio, the temperature, the initial concentration of 2,4-D, and the presence of other organic compounds have also been investigated. Quantitative correlations have been established that allow the use of this technology as a controlled Fenton reaction to determine the reaction rate constants of other compounds with hydroxyl radicals easily and accurately.

2,4-Dichlorophenoxyacetic Acid↗
PubMed2001

Identification of a trafficking determinant localized to the Kv1 potassium channel pore.

The repertoire of Kv1 potassium channels expressed in presynaptic terminals of mammalian central neurons is shaped by intrinsic trafficking signals that determine surface-expression efficiencies of homomeric and heteromeric Kv1 channel complexes. Here, we show that a determinant controlling surface expression of Kv1 channels is localized to the highly conserved pore region. Point-mutation analysis revealed two residues as critical for channel trafficking, one in the extracellular "turret" domain and one in the region distal to the selectivity filter. Interestingly, these same residues also form the binding sites for polypeptide neurotoxins. Our findings demonstrate a previously uncharacterized function for the channel-pore domain as a regulator of channel trafficking.

Amino Acid Sequence↗
PubMed2001

Light and electron microscopic study of cholinergic and noradrenergic elements in the basolateral nucleus of the rat amygdala: evidence for interactions between the two systems.

Pharmacological studies have suggested that the cholinergic (ACh) and noradrenergic (NA) systems in the amygdala (AM) play an important role in learning and memory storage and that the two systems interact to modulate memory storage. To obtain anatomical evidence for the interaction, the organization of the ACh and NA fibers in rat AM was investigated by immunocytochemistry for choline acetyltransferase (ChAT) and dopamine-beta-hydroxylase (DBH) in conjunction with light, confocal laser scanning, and electron microscopy (LM, CLSM, and TEM, respectively). LM showed that the ChAT immunoreactivity was densest in the basolateral nucleus (BL), whereas the DBH immunoreactivity was densest in the posterior BL. CLSM demonstrated that the ChAT-immunoreactive profiles in the BL were frequently located in juxtaposition to the DBH-immunoreactive axons. The TEM observations were as follows: The majority of the synapses formed by ChAT-immunoreactive terminals were symmetric, but DBH-immunoreactive axons formed both asymmetric and symmetric synapses. The ChAT-immunoreactive terminals usually established the symmetric synaptic contacts with the DBH-immunoreactive terminals and varicosities. The DBH-immunoreactive terminals formed the asymmetric synapses with the ChAT-immunoreactive dendrites of the intrinsic neurons within the AM. The results provide anatomical substrates for mnemonic functions of the ACh and NA systems and for the interactions between the two systems in the AM.

Amygdala↗
PubMed2001

[Electrophsiological study of rabbits with axonal form Guillain-Barre syndrome].

OBJECTIVE: To investigate the electrophysiological changes of common pheroneal nerve in rabbit model of axonal form of Guillain-Barre syndrome (GBS). METHODS: Lipopolysaccaride (LPS) was inoculated into six rabbits. Three of them got GBS and three remained healthy. The motor nerve conduction velocity of common peroneal nerve, compound muscle action potential, and latency of F wave were determined, and electromyography of anterior tibial muscle was made in the 3 rabbits modal of axonal form GBS, the 3 rabbits without symptom after inoculation of LPS, and 8 control rabbits. RESULTS: The three rabbits with axonal form GBS showed normal motor nerve conduction velocity and normal latency of F waves, and remarkably reduced compound muscle action potential amplitudes. Needle electromyography of anterior tibial muscle showed fibrillations and positive sharp waves. CONCLUSION: The electrophysiological characters of rabbits with axonal form GBS are consistent with those of patients with axonal form GBS. Electrophysiology plays an important role in diagnosing axonal form GBS.

Action Potentials↗
PubMed2001

Present-day crustal deformation in China constrained by global positioning system measurements.

Global Positioning System (GPS) measurements in China indicate that crustal shortening accommodates most of India's penetration into Eurasia. Deformation within the Tibetan Plateau and its margins, the Himalaya, the Altyn Tagh, and the Qilian Shan, absorbs more than 90% of the relative motion between the Indian and Eurasian plates. Internal shortening of the Tibetan plateau itself accounts for more than one-third of the total convergence. However, the Tibetan plateau south of the Kunlun and Ganzi-Mani faults is moving eastward relative to both India and Eurasia. This movement is accommodated through rotation of material around the eastern Syntaxis. The North China and South China blocks, east of the Tibetan Plateau, move coherently east-southeastward at rates of 2 to 8 millimeters per year and 6 to 11 millimeters per year, respectively, with respect to the stable Eurasia.

Journal Article↗
PubMed2001

Plasma nitric oxide level in heart failure secondary to left ventricular diastolic dysfunction.

Nitric oxide (NO) is a free radical that is elevated in the plasma of patients with systolic heart failure. However, its relation to diastolic function is unknown. This study investigated the relation between the level of stable end-products of plasma NO (NOx level) and diastolic function in patients with heart failure. We performed echocardiographic Doppler studies in 76 patients (mean age of 66 +/- 10 years, 75% men) with congestive heart failure. Left ventricular (LV) diastolic dysfunction was classified as either a restrictive (RFP) or nonrestrictive filling pattern (non-RFP). Same day venous total nitrite plus nitrate levels were measured by chemiluminscence. Both patients with isolated diastolic heart failure (ejection fraction >50%) (77 +/- 9 micromol/L, n = 33) and systolic failure (ejection fraction < or = 50%) (115 +/- 17 micromol/L, n = 43) had significantly higher plasma NOx levels than controls (37 +/- 2 micromol/L, both p <0.001). RFP coexists mostly in patients with systolic heart failure (15 of 18), and these patients had a higher NOx level than patients with systolic failure and a non-RFP (n = 28) (163 +/- 35 vs 88 +/- 16 micromol/L, p <0.05). Patients who were not on oral nitrate drugs had insignificant lower plasma NOx levels than those on regular nitrate therapy, although it was still higher than controls. Plasma NOx level did not correlate with LV ejection fraction. Stepwise multiple regression analysis confirmed that the presence of RFP was the only independent predictor of NOx, and hence NO production. Plasma NOx level is elevated in patients with isolated diastolic heart failure. In addition, in patients with LV systolic failure, the severity of LV diastolic dysfunction determines the amount of NO production.

Aged↗
PubMed2001

CD4 promotes breadth in the TCR repertoire.

A diverse population of MHC class II-restricted CD4 lineage T cells develops in mice that lack expression of the CD4 molecule. In this study, we show that the TCR repertoire selected in the absence of CD4 is distinct, but still overlapping in its properties with that selected in the presence of CD4. Immunization of mice lacking CD4 caused the clonal expansion of T cells that showed less breadth in the range of Ag-binding properties exhibited by their TCRs. Specifically, the CD4-deficient Ag-specific TCR repertoire was depleted of TCRs that demonstrated low-affinity binding to their ligands. The data thus suggest a key role for CD4 in broadening the TCR repertoire by potentiating productive TCR signaling and clonal expansion in response to the engagement of low-affinity antigenic ligands.

Animals↗
PubMed2001

The role of cytochrome 2B1 substrate recognition site residues 115, 294, 297, 298, and 362 in the oxidation of steroids and 7-alkoxycoumarins.

At least two substitutions were made at each of five amino acid residues in rat cytochrome P450 2B1 that align to residues of known importance in other P450s. The mutants were histidine tagged for purification from Escherichia coli, and the proteins were assessed for testosterone and 7-alkoxycoumarin oxidation. Alteration of each of the sites studied, Phe-115, Ser-294, Phe-297, Ala-298, and Leu-362, was found to affect overall enzyme activity or the metabolite profile. In particular, most of the mutants, excluding F297A, A298G, and L362F, exhibited significantly altered ratios of 16alpha-hydroxytestosterone:16beta-hydroxytestosterone, with the most dramatic alteration being displayed by A298V. Four 7-butoxycoumarin metabolites were produced by CYP2B1, of which two, 7-hydroxycoumarin and 7-(3-hydroxybutoxy)coumarin, were formed at nearly equal rates. Several mutants, F115A, F297A, F297I, and A298V, exhibited an increased predominance of one of the metabolites. The results from this study illustrate the conservation of functionally important residues across P450 subfamilies and families.

Amino Acid Substitution↗
PubMed2001

The tyrosine phosphatase SHP-2 is required for mediating phosphatidylinositol 3-kinase/Akt activation by growth factors.

SHP-2 is a ubiquitously expressed non-transmembrane tyrosine phosphatase with two SH2 domains. Multiple reverse-genetic studies have indicated that SHP-2 is a required component for organ and animal development. SHP-2 wild-type and homozygous mutant mouse fibroblast cells in which the N-terminal SH2 domain was target-deleted were used to examine the function of SHP-2 in regulating Phosphatidylinositol 3-Kinase (PI3K) activation by growth factors. In addition, SHP-2 and various mutants were introduced into human glioblastoma cells as well as SHP-2(-/-) mouse fibroblasts. We found that EGF stimulation and EGFR oncoprotein (DeltaEGFR) expression independently induced the co-immunoprecipitation of the p85 subunit of PI3K with SHP-2. Targeted deletion of the N-terminal SH2 domain of SHP-2 severely impaired PDGF- and IGF-induced Akt phosphorylation. Ectopic expression of SHP-2 in U87MG gliobastoma cells elevated EGF-induced Akt phosphorylation, and the effect was abolished by mutation of its N-terminal SH2 domain. Likewise, the reconstitution of SHP-2 expression in the SHP-2(-/-) cells enhanced Akt phosphorylation induced by EGF while rescuing that induced by PDGF and IGF. Further lipid kinase activity assays confirmed that SHP-2 modulation of Akt phosphorylation correlated with its regulation of PI3K activation. Based on these results, we conclude that SHP-2 is required for mediating PI3K/Akt activation, and the N-terminal SH2 domain is critically important for a "positive" role of SHP-2 in regulating PI3K pathway activation.

Animals↗
PubMed2001

Dendritic cells support hematopoiesis of bone marrow cells.

BACKGROUND: We previously observed that vaccination of normal mice with bone marrow (BM) -derived dendritic cells (DCs) could increase the number of peripheral white blood cells (WBCs) and platelets. In the present study, we investigated the potential of DCs to support the hematopoiesis of BM cells in vitro and in vivo. METHODS: In the absence of exogenous cytokines, the expansion of CD34+ stem cells was observed when cultured with DC-derived supernatant or contact cocultured with DC. After culture in supernatant of DCs or contact coculture with DCs for 3 days, CD34+ progenitor cells were cultured in the semisolid media to test their ability to generate the clonogeneic cells. Then, BM cells combined with DCs or not were transferred into lethally irradiated syngeneic recipients to determine the effects of DCs on hematopoietic recovery. RESULTS: After culture in the supernatant of DCs, especially in the supernatant of OVA-DCs (OVA-stimulated DC), the proliferation of CD34+ stem cells and generation of clonogeneic cells were augmented in correspondence with the concentration of DCs. After contact coculture with DCs, the proliferation of CD34+ stem cells and generation of clonogeneic cells were more significant than that in noncontact cultures. Moreover, when cultured with DCs or supernatant of DCs, CD34+ progenitor cells were preferentially differentiated to megakaryocytes. After coculture with OVA-DCs, markedly greater generation of colony forming units-granulocyte/macrophages (CFU-GM): colony forming units-megakaryocytes (CFU-MK) was found than that in coculture with unstimulated DCs. Pretreatment of DC with antibodies to thrombopoietin (TPO), interleukin (IL) -6, IL-12, or anti-mouse intercellular adhesion molecule-1 (ICAM-1) could inhibit the ability of DCs to support the generation of CFU-GM, CFU-MK. After transplant with BM cells and DCs, the number of peripheral platelets of the recipients increased significantly and, to a lesser extent, peripheral WBC counts increased. The survival periods were significantly prolonged when the lethally irradiated mice were transplanted with BM cells combined with DCs or OVA-DCs. High levels of TPO, IL-6, and IL-12 could be detectable in the supernatant of DCs, and TPO expression by DCs was further confirmed by reverse transcription-polymerase chain reaction analysis and intracellular staining with anti-TPO antibody. CONCLUSIONS: We first demonstrated that DCs, especially antigen-stimulated DCs, can promote the expansion of hematopoietic progenitors and support hematopoiesis, preferentially support megakaryopoiesis of BM cells, by expressing soluble factors, including TPO, IL-6, IL-12, and by direct cell-to-cell interaction with stem cells in vitro and in vivo.

Animals↗
PubMed2001

Plk3 functionally links DNA damage to cell cycle arrest and apoptosis at least in part via the p53 pathway.

Polo-like kinase 3 (Plk3, previously termed Prk) contributes to regulation of M phase of the cell cycle (Ouyang, B., Pan, H., Lu, L., Li, J., Stambrook, P., Li, B., and Dai, W. (1997) J. Biol. Chem. 272, 28646-28651). Plk3 physically interacts with Cdc25C and phosphorylates this protein phosphatase predominantly on serine 216 (Ouyang, B., Li, W., Pan, H., Meadows, J., Hoffmann, I., and Dai, W. (1999) Oncogene 18, 6029-6036), suggesting that the role of Plk3 in mitosis is mediated, at least in part, through direct regulation of Cdc25C. Here we show that ectopic expression of a kinase-active Plk3 (Plk3-A) induced apoptosis. In response to DNA damage, the kinase activity of Plk3 was rapidly increased in an ATM-dependent manner, whereas that of Plk1 was markedly inhibited. Recombinant Plk3 phosphorylated in vitro a glutathione S-transferase fusion protein containing p53, but not glutathione S-transferase alone. Recombinant Plk1 also phosphorylated p53 but on residues that differed from those targeted by Plk3. Co-immunoprecipitation and pull-down assays demonstrated that Plk3 physically interacted with p53 and that this interaction was enhanced upon DNA damage. In vitro kinase assays followed by immunoblotting showed that serine 20 of p53 was a target of Plk3. Furthermore, expression of a kinase-defective Plk3 mutant (Plk3(K52R)) resulted in significant reduction of p53 phosphorylation on serine 20, which was correlated with a decrease in the expression of p21 and with a concomitant increase in cell proliferation. These results strongly suggest that Plk3 functionally links DNA damage to cell cycle arrest and apoptosis via the p53 pathway.

Apoptosis↗
PubMed2001

Control of laser high-harmonic generation with counterpropagating light.

Relatively weak counterpropagating light is shown to disrupt the emission of laser high-harmonic generation. Harmonic orders ranging from the teens to the low thirties produced by a 30-femtosecond pulse in a narrow argon jet are "shut down" with a contrast as high as 2 orders of magnitude by a chirped 1-picosecond counterpropagating laser pulse (60 times less intense). Alternatively, under poor phase-matching conditions, the counterpropagating light boosts harmonic production by similar contrast through quasiphase matching where out-of-phase emission is suppressed.

Journal Article↗
PubMed2001

Phenylalanine and tryptophan scanning mutagenesis of CYP3A4 substrate recognition site residues and effect on substrate oxidation and cooperativity.

Phenylalanine and/or tryptophan scanning mutagenesis was performed at 15 sites within CYP3A4 proposed to be involved in substrate specificity or cooperativity. The sites were chosen on the basis of previous studies or from a comparison with the structure of P450(eryF) containing two molecules of androstenedione. The function of the 25 mutants was assessed in a reconstituted system using progesterone, testosterone, 7-benzyloxy-4-(trifluoromethyl)coumarin (7-BFC), and alpha-naphthoflavone (ANF) as substrates. CYP3A4 wild type displayed sigmoidal kinetics of ANF 5,6-oxide formation and 7-BFC debenzylation. Analysis of 12 mutants with significant steroid hydroxylase activity showed a lack of positive correlation between ANF oxidation and stimulation of progesterone 6beta-hydroxylation by ANF, indicating that ANF binds at two sites within CYP3A4. 7-BFC debenzylation was stimulated by progesterone and ANF, and 7-BFC did not inhibit testosterone or progesterone 6beta-hydroxylation. Correlational analysis showed no relationship between 7-BFC debenzylation and either progesterone or testosterone 6beta-hydroxylation. These data are difficult to explain with a two-site model of CYP3A4 but suggest that three subpockets exist within the active site. Interestingly, classification of the mutants according to their ability to oxidize the four substrates utilized in this study suggested that substrates do bind at preferred locations in the CYP3A4 binding pocket.

Amino Acid Sequence↗
PubMed2001

Sites of nucleic acid binding in type I-IV intermediate filament subunit proteins.

A combination of enzymatic and chemical ladder sequencing of photo-cross-linked protein-single-stranded oligodeoxyribonucleotide complexes and analysis by MALDI-TOF mass spectrometry was employed to identify the amino acid residues responsible for the stable binding of nucleic acids in several intermediate filament (IF) subunit proteins. The IF proteins studied included the type I and type II cytokeratins K8, K18, and K19; the type III proteins desmin, glial fibrillary acidic protein (GFAP), peripherin, and vimentin; and the type IV neurofilament triplet protein L (NF-L). The site of nucleic acid binding was localized to the non-alpha-helical, amino-terminal head domain of all of the IF proteins tested. GFAP, which has the shortest head domain of the proteins tested, cross-linked via only two amino acid residues. One of these residues was located within a conserved nonapeptide domain that has been shown to be required for filament formation. One or more cross-linked residues were found in a similar location in the other proteins studied. The major binding site for nucleic acids for most of the proteins appears to be localized within the middle of the head domain. The two exceptions to this generalization are GFAP, which lacks these residues, and NF-L, in which a large number of cross-linked residues were found scattered throughout the first half of the head domain. Control experiments were also done with two bacteriophage ssDNA-binding proteins, as well as actin and tubulin. The single sites of cross-linkage observed with the bacteriophage proteins, Phe(183) for the T4 gene 32 protein and Phe(73) for the M13 gene 5 protein, were in good agreement with literature data. Actin and tubulin could not be cross-linked to the oligonucleotide. Aside from the insight into the biological activity of IF proteins that these data provide, they also demonstrate that this analytical method can be employed to study a variety of protein-nucleic acid interactions.

Amino Acid Sequence↗
PubMed2001

Comparative pharmacokinetics and pharmacodynamics of lansoprazole oral capsules and suspension in healthy subjects.

The pharmacokinetics and pharmacodynamics of lansoprazole suspension and lansoprazole capsules were studied. Thirty-six healthy males and females were randomized in a single-dose, open-label, two-period crossover study. Lansoprazole 30 mg was administered via a nasogastric tube as simplified lansoprazole suspension (in 8.4% sodium bicarbonate) or orally as the intact capsule after a minimum 12-hour fast and 5 hours before lunch. Ambulatory 24-hour intragastric pH was monitored at baseline and on day 1 of each treatment period to assess lansoprazole's pharmacodynamics. Blood samples were collected before drug administration and at predetermined intervals up to 24 hours after each dose to assess lansoprazole's pharmacokinetics. Both formulations effectively raised the mean 24-hour intragastric pH (mean 24-hour pH of 3.75 with suspension and 3.52 with intact capsule) and maintained it above threshold values of 3 and 4 for more than 40% of the 24-hour postdose period. The suspension was associated with a significantly shorter mean time to the maximum observed concentration (tmax) compared with the intact capsule. The mean maximum observed plasma concentration (Cmax) of the suspension was significantly higher and the mean area under the concentration-time curve from time zero to infinity (AUC infinity) was significantly lower than those of the intact capsule (879 versus 810 ng/mL and 1825 versus 2229 ng.hr/mL). The 90% confidence intervals obtained by two one-sided tests for both Cmax and AUC infinity were contained within the 0.80 to 1.25 range, confirming the bioequivalence of the two regimens. Simplified lansoprazole suspension effectively controls intragastric pH, is bioequivalent to the intact capsule, and represents an effective therapeutic option for patients who have difficulty swallowing or are unable to swallow lansoprazole capsules.

2-Pyridinylmethylsulfinylbenzimidazoles↗
PubMed2001

Differential dependence of the D1 and D5 dopamine receptors on the G protein gamma 7 subunit for activation of adenylylcyclase.

The D(1) dopamine receptor, G protein gamma(7) subunit, and adenylylcyclase are selectively expressed in the striatum, suggesting their potential interaction in a common signaling pathway. To evaluate this possibility, a ribozyme strategy was used to suppress the expression of the G protein gamma(7) subunit in HEK 293 cells stably expressing the human D(1) dopamine receptor. Prior in vitro analysis revealed that the gamma(7) ribozyme possessed cleavage activity directed exclusively toward the gamma(7) RNA transcript (Wang, Q., Mullah, B., Hansen, C., Asundi, J., and Robishaw, J. D. (1997) J. Biol. Chem. 272, 26040-26048). In vivo analysis of cells transfected with the gamma(7) ribozyme showed a specific reduction in the expression of the gamma(7) protein. Coincident with the loss of the gamma(7) protein, there was a noticeable reduction in the expression of the beta(1) protein, confirming their interaction in these cells. Finally, functional analysis of ribozyme-mediated suppression of the beta(1) and gamma(7) proteins revealed a significant attenuation of SKF81297-stimulated adenylylcyclase activity in D(1) dopamine receptor-expressing cells. By contrast, ribozyme-mediated suppression of the beta(1) and gamma(7) proteins showed no reduction of SKF81297-stimulated adenylylcyclase activity in D(5) dopamine receptor-expressing cells. Taken together, these data indicate that the structurally related D(1) and D(5) dopamine receptor subtypes utilize G proteins composed of distinct betagamma subunits to stimulate adenylylcyclase in HEK 293 cells. Underscoring the physiological relevance of these findings, single cell reverse transcriptase-polymerase chain reaction analysis revealed that the D(1) dopamine receptor and the G protein gamma(7) subunit are coordinately expressed in substance P containing neurons in rat striatum, suggesting that the G protein gamma(7) subunit may be a new target for drugs to selectively alter dopaminergic signaling within the brain.

Adenylyl Cyclases↗