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Biomedical subjects

Qin Wang

Publications and source records attributed to Qin Wang.

At least 55 records · Page 3Linked to original sources
PubMed2006

[Construction and identification of recombinant adenovirus containing the polyproteins coding regions of O type foot-and-mouth disease virus by homologous recombination in Escherichia coli].

The gene coding for the polyprotein (PP) of foot-and-mouth disease virus (FMDV)was obtained by PCR from recombinant plasmid rpMD18-T/PP. The PCR product was digested with Xba I and Not I and inserted into the cloning site of the adenovirus shuttle vector pAdTrack-CMV, previously digested with the same enzymes. This recombinant shuttle plasmid was designated rpAd-CMV/PP. The recombinant adenovirus vector rpAd/PP was obtained by homologous recombination of plasmid rpAd-CMV/PP and adenovirus skeletal vector pAdeasy-1 in E. coli. Plasmid rpAd/PP was linearized by Pme I and transformed into 293 competent cells to pack the adenovirus using liposome mediated gene transfer method and, as a result, the recombinant adenovirus rAd/PP that contained the polyprotein coding gene was obtained. Obvious CPE could be observed under an inverted microscope, the green fluorescence protein expression can be detected under fluorescence microscope and the empty capsid of FMDV was observed under electron microscope. These results indicated that the recombinant adenovirus rAd/PP expressed the PP protein and that this protein could be assembled into the empty capsid of FMDV. The recombinant adenovirus obtained in this study can be used for further research for making FMDV recombinant adenovirus vaccine.

Adenoviridae↗
PubMed2006

[Full length nucleotide sequence analysis of L and M segments of Hantavirus Q32 strain gene].

BACKGROUND: To study the full length L and M sequence of Hantavirus Q32 strain gene and explore its molecular characters. METHODS: The L and M segment cDNA of Hantavirus Q32 strain was amplified by RT-PCR. The purified PCR products were sequenced directly or cloned into pGEM-T Vector and then sequenced. RESULTS: The L genome segment of Q32 virus was found to be 6533 nucleotides in length. One large open reading frame was found located at bases 38 to 6493. This was predicted to encode an L protein 2151 amino acids in length with a molecular mass of 2.46 x 10(5). The M genome segment was 3616 nucleotides in length. One open reading frame was located at bases 41 to 3488. This was predicted to encode an M protein 1135 amino acids with a molecular mass of 1.26 x 10(5). CONCLUSION: The nucleotides sequence of M and L segments of strain Q32 was similar to that of other Hantavirus M and L segments. Deduced amino acid sequences of glycoprotein and RNA polymerase revealed high homologue to other Hantavirus.

Amino Acid Sequence↗
PubMed2006

[Eco-hydrological characteristics of a subtropical evergreen broadleaved forest in Japan].

A three years (1998-2000) observation on the eco-hydrological characteristics of Castanopsis sieboldii and Schima wallichii dominated subtropical evergreen broadleaved forest on the Okinawa Island of Japan showed that during the observation period, the mean annual precipitation was 3325 mm, and 42.3% of it was directly or indirectly contributed by typhoon rainfall, implying that typhoon played a very important role in the hydrology of the forest. Through-fall and stem-flow contributed to 53.9% and 30.9% of the annual rainfall, respectively. The higher stem-flow could be due to the high wind velocity, intense rainfall, and the crown morphology of dominant species C. sieboldii with inclined branches and concave-shaped leaves. Interception loss occupied 15.2% of the total rainfall, being the lowest in the range of 15%-30% widely reported for many broadleaved evergreen forests. The annual surface runoff and lateral flow were 1092 mm and 613 mm, respectively, and the high proportion of surface runoff (32.8%) was probably due to the poor physical properties of soil, particularly the low noncapillary porosity (8%-12%), high clay content (51.9%-60.5%), and low infiltration rate (12 ml x min(-1)) in deeper soil layers. The effective and maximum water storage capacity of 0-70 cm soil layer were 85 mm and 324 mm, respectively, and the maximum water-holding capacity of forest floor was 2. 8 mm, which were close to or lower than those of the subtropical and tropical rain forests in China.

Conservation of Natural Resources↗
PubMed2005

Increased divalent metal transporter 1 expression might be associated with the neurotoxicity of L-DOPA.

Based on the available data, we speculated that changes in brain iron metabolism induced by L-DOPA might be associated with the neurotoxicity of L-DOPA. To investigate this possibility, the effects of L-DOPA on the expression of iron influx proteins [transferrin receptor (TfR) and divalent metal transporter 1 (DMT1)], iron efflux protein (ferroportin 1), and iron uptake in C6 glioma cells were determined in this study using Northern blot and Western blot analysis and the calcein method. The findings showed that treatment of C6 cells with different concentrations of L-DOPA (0-100 microM) did not affect the expression of mRNA and protein of TfR and DMT1 with iron-responsive element (+IRE) and protein of ferroportin 1. However, a significant increase in the expression of DMT1(-IRE) mRNA and protein was found in cells treated, respectively, with 10 and 30 microM L-DOPA (mRNA) and 1, 5, 10 and 30 microM L-DOPA (protein). The increase in DMT(-IRE) protein induced by L-DOPA treatment was in parallel with the increase in DMT(-IRE) mRNA. The levels of DMT1(-IRE) mRNA and protein peaked in the cells treated with 10 microM L-DOPA and then decreased progressively with increasing concentrations of L-DOPA. Further study demonstrated that treatment of the cells with 10 microM L-DOPA induced a significant increase in ferrous uptake by C6 glioma cells. The findings suggested that the increased DMT1(-IRE) expression might be partly associated with the neurotoxicity of L-DOPA. Clinical relevance of the findings needs to be investigated further.

Animals↗
PubMed2005

Synthesis, characterization, cytotoxic activities, and DNA-binding properties of the La(III) complex with Naringenin Schiff-base.

A new Naringenin Schiff-base ligand (H3L) and its complex, [La(H2L)2(NO3).3H2O], have been synthesized and characterized on the basis of elemental analyses, molar conductivities, mass spectra, 1H NMR, thermogravimetry/differential thermal analysis (TG-DTA), UV spectra, and IR spectra. Spectrometric titrations, ethidium bromide displacement experiments, and viscosity measurements indicate that the two compounds, especially the La(III) complex, strongly bind with calf-thymus DNA, presumably via an intercalation mechanism. The intrinsic binding constants of the La(III) complex and ligand with DNA were 1.83 x 10(7) and 9.46 x 10(5) M(-1), respectively. Comparative cytotoxic activities of the La(III) complex and ligand were also determined by MTT [3-(4,5-dimethyl-2-thiazoyl)-2,5-diphenyl-2H-tetrazolium bromide] and SRB (sulforhodamine B) methods. The results showed that the La(III) complex had significant cytotoxic activity against the tested cells.

Antineoplastic Agents↗
PubMed2005

Gonadotropin-releasing hormone agonists and fracture risk: a claims-based cohort study of men with nonmetastatic prostate cancer.

PURPOSE: Gonadotropin-releasing hormone (GnRH) agonists decrease bone mineral density, a surrogate for fracture risk, in men with prostate cancer. We conducted a claims-based cohort study to characterize the relationship between GnRH agonists and risk for clinical fractures in men with nonmetastatic prostate cancer. PATIENTS AND METHODS: Using medical claims data from a 5% national random sample of Medicare beneficiaries, we identified a study group of men with nonmetastatic prostate cancer who initiated GnRH agonist treatment from 1992 to 1994 (n = 3,887). A comparison group of men with nonmetastatic prostate cancer who did not receive GnRH agonist treatment during the study period (n = 7,774) was matched for age, race, geographic location, and comorbidity. Clinical fractures were identified using inpatient, outpatient, and physician claims during 7 years of follow-up. RESULTS: In men with nonmetastatic prostate cancer, GnRH agonists significantly increased fracture risk. The rate of any clinical fracture was 7.88 per 100 person-years at risk in men receiving a GnRH agonist compared with 6.51 per 100 person-years in matched controls (relative risk, 1.21; 95% CI, 1.14 to 1.29; P < .001). Rates of vertebral fractures (relative risk, 1.45; 95% CI, 1.19 to 1.75; P < .001) and hip/femur fractures (relative risk, 1.30; 95% CI, 1.10 to 1.53; P = .002) were also significantly higher in men who received a GnRH agonist. GnRH agonist treatment independently predicted fracture risk in multivariate analyses. Longer duration of treatment conferred greater fracture risk. CONCLUSION: GnRH agonists significantly increase risk for any clinical fracture, hip fractures, and vertebral fractures in men with prostate cancer.

Aged↗
PubMed2005

Effects of mercuric ion on the conformation and activity of Penaeus Vannamei beta-N-acetyl-d-glucosaminidase.

beta-N-acetyl-d-glucosaminidase (NAGase, EC.3.2.1.52), a composition of the chitinases, catalyzes the cleavage of N-acetylglucosamine polymers into N-acetylglucosamine. In this paper, the effects of mercuric ion on the activity of NAGase from Penaeus vannamei for the hydrolysis of pNP-NAG have been studied. The results show that HgCl2 can lead to irreversible inactivation to this enzyme. The inactivation process follows a first-order reaction and the inactivation rate constants have been determined. The relationship between the inactivation rate constants and HgCl2 concentration has been studied and the result shows that only one molecule of HgCl2 binds to the enzyme molecule to lead the enzyme lose its activity. Moreover, the conformational changes of the enzyme inactivated by HgCl2 were studied by following changes in the intrinsic fluorescence emission and ultraviolet absorption spectra.

Acetylglucosaminidase↗
PubMed2005

Nonsynaptic GABA signaling in postnatal subventricular zone controls proliferation of GFAP-expressing progenitors.

In the postnatal subventricular zone (SVZ), local cues or signaling molecules released from neuroblasts limit the proliferation of glial fibrillary acidic protein (GFAP)-expressing progenitors thought to be stem cells. However, signals between SVZ cells have not been identified. We show that depolarization of neuroblasts induces nonsynaptic SNARE-independent GABA(A) receptor currents in GFAP-expressing cells, the time course of which depends on GABA uptake in acute mouse slices. We found that GABA(A) receptors are tonically activated in GFAP-expressing cells, consistent with the presence of spontaneous depolarizations in neuroblasts that are sufficient to induce GABA release. These data demonstrate the existence of nonsynaptic GABAergic signaling between neuroblasts and GFAP-expressing cells. Furthermore, we show that GABA(A) receptor activation in GFAP-expressing cells limits their progression through the cell cycle. Thus, as GFAP-expressing cells generate neuroblasts, GABA released from neuroblasts provides a feedback mechanism to control the proliferation of GFAP-expressing progenitors by activating GABA(A) receptors.

Animals↗
PubMed2005

Irreversibly inhibitory kinetics of 3,5-dihydroxyphenyl decanoate on mushroom (Agaricus bisporus) tyrosinase.

3,5-Dihydroxyphenyl decanoate (DPD) is found to inhibit the diphenolase activity of tyrosinase from mushroom (Agaricus bisporus). The effects of DPD on the diphenolase activity of mushroom tyrosinase have been studied. The results show that the enzyme activity decreases very slowly with an increase in DPD concentrations at lower concentrations of DPD (between 5 and 60 microM). But at higher concentrations of DPD, DPD can strongly inhibit the diphenolase activity of the enzyme and the inhibition is irreversible. The IC50 value was estimated to be 96.5 microM. The inhibition mechanism of DPD has been investigated and the results show that DPD can bind to the free enzyme molecule and enzyme-substrate complex and lose the enzyme activity completely. The inhibition kinetics has been studied in detail by using the kinetic method of the substrate reaction described by Tsou. The microscopic rate constants of the enzyme inhibited by DPD at higher concentrations have been determined.

Agaricus↗
PubMed2005

Properties of zein films coated with drying oils.

Zein films prepared by resin were coated with either flax oil or tung oil and cured by UV- or gamma-radiation. Coated zein films were then evaluated for tensile and water barrier properties. Film microstructure was examined by transmitted light microscope. Tensile strength, elongation, and toughness of oil-coated samples increased substantially with respect to uncoated films. Flax oil coated samples showed an increase in elongation of 300%. It was suggested that oil coatings fill in pinholes and cracks existing in zein films, affecting their mechanical properties. Water vapor permeability also decreased statistically for coated film (except for tung oil coated-UV treated films), suggesting water vapor transfer was controlled by film hydrophobicity and microstructure. Moreover, the liquid water transmission rate of coated films was at least 10 times slower than for control films. Examination of film microstructure revealed that flax oil coatings had uniform coverage and smooth finish, which explained their high elongation, low water vapor permeability. Tung oil coatings cured under UV light showed patterns of intertwined dark and light regions, which may be caused by cross-linking and drying at different times. The oriented structures were found when tung oil coatings were cured by gamma-radiation.

Chemical Phenomena↗
PubMed2005

GaAs-based multiple-quantum-well spatial light modulators fabricated by a wafer-scale process.

The design, fabrication, and characterization of large, two-dimensional multiple-quantum-well modulator arrays are presented. Such arrays present a speed advantage compared with competing technologies such as liquid crystals and micromirrors, which are intrinsically limited to the kilohertz range. We discuss the design compromises to reach high-contrast, low-voltage swing optical structures compatible with complementary metal-oxide semiconductor-based integrated circuits and present experimental results. Contrast ratio of 5:1 (limited by the fill factor), variations in uniformity below 1nm, and frame rates in excess of 10kHz are demonstrated. Technology maturity for volume production is also discussed.

Journal Article↗
PubMed2005

Proteomic analysis of neurofibrillary tangles in Alzheimer disease identifies GAPDH as a detergent-insoluble paired helical filament tau binding protein.

We performed proteomic analysis of neurofibrillary tangles (NFTs) obtained by laser capture microdissection from pyramidal neurons in hippocampal sector CA1 in patients with Alzheimer disease (AD) using liquid chromatography (LC)-mass spectrometry (MS)/MS. We discovered a total of 155 proteins in laser captured NFT's, 72 of which were identified by multiple unique peptides. Of these 72 proteins, 63 had previously unknown association with NFTs; one of these was glyceraldehyde-3-phosphate dehydrogenase (GAPDH). We validated by immunohistochemistry that GAPDH co-localized with the majority of NFTs as well as plaque-like structures in AD brain and was co-immunoprecipitated by antibodies to abnormal forms of tau in AD, but not tau from AD temporal cortex. Characterization of GAPDH showed that it, along with phosphorylated tau and Abeta peptides, was present in detergent-insoluble fractions from AD temporal cortex but not from age-matched controls. These data are the first proteomic investigation of NFTs. Moreover, our results validate this approach by demonstrating that GAPDH, a glycolytic and microtubule binding protein, not only co-localized to NFTs and immunoprecipitated with PHF-tau, but also is one of the few proteins known to undergo conversion to a detergent-insoluble form in AD.

Alzheimer Disease↗
PubMed2005

Mitochondrial function is a critical determinant of IL-1-induced ERK activation.

Interleukin-1 (IL-1) is a potent, proinflammatory cytokine, but local environmental factors in inflamed sites or in sepsis may affect cell metabolism and energetics, including the amplitude and duration of IL-1-induced signals, thereby leading to loss of tissue homeostasis. Currently, the mechanisms by which disruption of cell energetics affects inflammatory signaling are incompletely understood. Here, we examined the impact of cell energetics and mitochondrial function on the regulation of IL-1-induced Ca2+ signals and ERK activation in human gingival fibroblasts, cells that are important targets for IL-1-induced destruction of extracellular matrix in inflamed connective tissues. In untreated cells, IL-1 induced a prolonged increase of free intracellular calcium, which was required for ERK activation. Inhibition of cellular energetics by selective depolarization of mitochondria blocked Ca2+ uptake and almost completely abolished IL-1-induced cytosolic Ca2+ signals and ERK activation. IL-1 caused rapid Ca2+ release from the endoplasmic reticulum (ER), concomitant with mitochondrial Ca2+ uptake from ER and non-ER stores. Disruption of mitochondrial energetics abrogated IL-1 induced Ca2+ release from the ER but left other vital cellular functions intact. The negative effect of mitochondrial depolarization on ER release was bypassed by BAPTA/AM, indicating that mitochondrial Ca2+ buffering is the key mechanism in regulating ER release. Thus, in gingival fibroblasts, mitochondrial Ca2+ uptake is essential not only for shaping the kinetics and duration, but also the generation of, IL-1-induced Ca2+ signals. Consequently, mitochondria regulate key downstream effectors of IL-1, including MAP kinases.

Adenosine Triphosphate↗
PubMed2005

Alpha 2-adrenergic agonist enrichment of spinophilin at the cell surface involves beta gamma subunits of Gi proteins and is preferentially induced by the alpha 2A-subtype.

Agonist activation regulates reciprocal interactions of spinophilin and arrestin with the alpha2A- and alpha2B -adrenergic receptor (AR) subtypes via their 3i loop. Because arrestin association with G protein-coupled receptor is preceded by redistribution of arrestin to the cell surface, the present studies explored whether agonist activation of the alpha2A- and alpha2B -AR subtypes also led to spinophilin enrichment at the cell surface. Live cell imaging studies using a green fluorescent protein-tagged spinophilin examined spinophilin localization and its regulation by alpha2 -AR agonist. Agonist activation of alpha2A-AR preferentially, compared with the alpha2B-AR, led to spinophilin enrichment at the cell surface in human embryonic kidney 293 cells and in mouse embryo fibroblasts derived from spinophilin null mice. Activation of the delta LEESSSS alpha2A-AR, which has enriched association with spinophilin compared with the wild-type (WT) alpha2A-AR, does not show an enhanced redistribution of spinophilin to the surface compared with WT alpha2A-AR, demonstrating that the ability or affinity of the receptor in binding spinophilin may be independent of the ability of the receptor to effect spinophilin redistribution to the surface. Agonist-evoked enrichment of spinophilin at the cell surface seems to involve downstream signaling events, manifested both by the pertussis toxin sensitivity of the process and by the marked attenuation of spinophilin redistribution in cells expressing the beta-adrenergic receptor kinase-C tail, which sequesters beta gamma subunits of G proteins. Together, the data suggest that agonist-evoked spinophilin enrichment at the cell surface is caused by receptor-evoked signaling pathways and is independent of the affinity of the receptor for the spinophilin molecule.

Adrenergic alpha-2 Receptor Agonists↗
PubMed2005

Hyperinsulinemia provokes synchronous increases in central inflammation and beta-amyloid in normal adults.

BACKGROUND: Inflammation has been implicated as a pathogenetic factor in Alzheimer disease, possibly via effects on beta-amyloid (Abeta). Hyperinsulinemia induces inflammation and is a risk factor for Alzheimer disease. Thus, insulin abnormalities may contribute to Alzheimer disease pathophysiology through effects on the inflammatory network. OBJECTIVES: To determine the effects of induced hyperinsulinemia with euglycemia on Abeta, transthyretin, and inflammatory markers and modulators in plasma and cerebrospinal fluid (CSF). DESIGN: Randomized crossover trial. SETTING: Veterans Affairs hospital clinical research unit. PARTICIPANTS: Sixteen healthy adults ranging from 55 to 81 years of age (mean age, 68.2 years). INTERVENTIONS: On separate mornings, fasting participants received randomized infusions of saline or insulin (1.0 mU.kg(-1).min(-1)) with variable dextrose levels to maintain euglycemia, achieving plasma insulin levels typical of insulin resistance. Plasma and CSF were collected after an approximately 105-minute infusion. MAIN OUTCOME MEASURES: Plasma and CSF levels of interleukin 1alpha, interleukin 1beta, interleukin 6, tumor necrosis factor alpha, F2-isoprostane (CSF only), Abeta, norepinephrine, transthyretin, and apolipoprotein E. RESULTS: Insulin increased CSF levels of F2-isoprostane and cytokines (both P<.01), as well as plasma and CSF levels of Abeta42 (both P<.05). The changes in CSF levels of Abeta42 were predicted by increased F2-isoprostane and cytokine levels (both P<.01) and reduced transthyretin levels (P = .02). Increased inflammation was modulated by insulin-induced changes in CSF levels of norepinephrine and apolipoprotein E (both P<.05). CONCLUSION: Moderate hyperinsulinemia can elevate inflammatory markers and Abeta42 in the periphery and the brain, thereby potentially increasing the risk of Alzheimer disease.

Age Factors↗
PubMed2005

Effects of development and iron status on ceruloplasmin expression in rat brain.

The increased iron content in the brain of subjects with aceruloplasminemia has implicated ceruloplasmin (CP) as a major factor in the regulation of regional brain iron content. In this study, we investigated the effects of age and iron on CP expression in rat brain. In all four regions, the iron concentrations increased with developmental age. There is a similar trend in age-induced changes in CP mRNA and protein. The CP mRNA and protein levels were both lowest at postnatal day (PND) 7. The expression increased gradually with age, reaching the highest at PND196 in the striatum and substantia nigra, and at PND21 and PND63 in the cortex and hippocampus, respectively. This suggests the existence of an age-dependent pre-transcriptional regulation and a regionally specific effect of age on CP expression in the brain. Although total iron in all four regions was significantly lower in the rats fed with a low-iron diet for 6 weeks and higher in the rats with a high-iron diet than those in the control animals, no significant between-group differences in CP mRNA and protein were found in these animals, except in the substantia nigra where a significant increase in CP protein in high-iron rats was observed, and the reverse in low-iron rats. These findings suggested that the effects of iron on CP expression in the brain may be region-specific, and that regulation of CP expression by iron in the substantia nigra was at the post-transcriptional level.

Aging↗