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Q Tang

Publications and source records attributed to Q Tang.

At least 19 recordsLinked to original sources

TL and OSL of SrSO4 phosphors doped with Eu.

The thermoluminescence (TL) and optically stimulated luminescence (OSL) of SrSO4:Eu (0.1 mol%) powder sample were studied. The TL and OSL emission spectrum are measured after irradiation (absorbed dose 100 Gy) of 90Sr source; both of them showed that the emission wavelength is at approximately 375 nm, which indicates that TL and OSL have the same luminescence centres, and the luminescence comes from transitions between the energy levels of Eu2+. The TL glow curves and OSL decay curves illustrate that there is only one main TL peak but two main components in OSL curves. By a comparative study of TL and OSL it is concluded that OSL traps are different from TL traps. The TL and OSL dose responses of SrSO4:Eu phosphor were measured, and it showed that phosphor has similar dose responses for OSL and TL.

Computer Simulation↗

Thermoluminescence glow curves and optical stimulated luminescence of undoped alpha-Al2O3 crystals.

The characteristics of thermoluminescence (TL) and optical stimulated luminescence (OSL) in undoped alpha-Al2O3 single crystals were studied. The TL glow curves of the crystal samples irradiated at various dose levels were measured by RisØ TL/OSL-DA-15B/C reader with U-340 or 7-59 filters at different heating rates. The glow peaks measured with U-340 at approximately 210 degrees C of the undoped alpha-Al2O3 can be well fitted by first-order kinetic equation whereas the glow peaks measured with 7-59 filters are a composite of two first-order glow peaks. It indicates that the TL glow curves are dependent upon the filter used in the reader that is related to the emission spectra of luminescence materials. The OSL were also measured and fitted by two exponential functions to get the luminescence intensities. The TL and OSL dose responses of the undoped alpha-Al2O3 crystal were obtained in the dose range of 0.12-248 Gy and fitted by the composite action dose-response function to get nonlinear characteristic parameters. The TL and OSL dose responses are linear-sublinear.

Aluminum Oxide↗

Defect complexes in Re3+-doped magnesium sulphate phosphors.

A series of magnesium sulphate phosphors MgSO4:RE3+,X ( RE = Dy, Tm, Eu and X = P, Mn) have been prepared and studied. Based on the experimental results of thermoluminescence (TL) emission spectra and dose responses studies, it is proposed that in these phosphors large defect complexes are formed, which include intrinsic imperfections and dopants. These defect complexes were formed in the course of preparation of phosphors and could be regarded as basic elements in the TL multi-stage processes. This defect model might be applicable to the most of TL materials.

Artifacts↗

Elimination of metformin-croscarmellose sodium interaction by competition.

During analytical method development and validation, a strong charge interaction between metformin and croscarmellose sodium was observed when the aqueous solution containing metformin was spiked with croscarmellose sodium. The charge interaction resulted in the retention of metformin in croscarmellose sodium and caused a serious drug recovery problem. The percent recovery of metformin in the solution was much lower than its theoretical values, especially in the low metformin concentration range. To overcome the metformin-croscarmellose interaction, arginine was selected as a competitor for the binding sites on croscarmellose sodium. Because of the competition and stronger interaction between arginine and croscarmellose sodium than metformin and croscarmellose sodium, a complete recovery of metformin in presence of arginine in both low and high concentration ranges was achieved. The effect of arginine on the recovery of metformin and the competition mechanism are discussed in this paper.

Arginine↗

The effect of renal ischemia-reperfusion injury on expression of RAE-1 and H60 in mice kidney.

INTRODUCTION: NKG2D, an activating receptor, may trigger NK and CD8+ T cells. Ligands for NKG2D and major histocompability complex class I chain-related antigen (MIC) have been reported to be expressed in rejected human renal allografts. MIC-NKG2D engagement may induce natural killer (NK) cell activation providing T-cell costimulation. We hypothesized that this interaction between innate and adaptive immunity may occur during kidney ischemia-reperfusion injury (IRI). METHODS: Male C57BL/6 mice after right renal resection were subjected to 35 minutes of left renal ischemia: the ischemic group. Sham-operated mice underwent the same protocol without vascular occlusion. The sham and ischemic kidneys were removed at 2 to 7, 10, 14, or 28 days postoperatively. The normal, sham, and ischemic kidney tissues were collected for reverse-transcriptase polymerase chain reaction, and immunohistochemistry analysis of MIC homologues in mice (Rae-1 and H60). RESULTS: Compared with no expression in sham control and normal kidneys, IRI caused mRNA expression of Rae-1 from 2 to 10 days postoperatively and protein expression of Rae-1 from 2 to 14 days postoperatively in ischemic kidneys. We observed no expression of H60 mRNA or protein in any kidney. CONCLUSION: H60 transcripts have been reported to be present in the BALB/c background but not in C57BL/6. We found IRI did not cause H60 mRNA on protein expression in C57BL/6 kidneys. Rae-1 was absent in normal C57BL/6 kidneys. The IRI-induced expression of the NKG2D ligand, Rae-1, might activate NK and CD8+ T cells. Our results suggested that MIC may be an important link between innate and adaptive immunity in kidney IRI.

Animals↗

Study on energy metabolism in perioperative infants.

OBJECTIVES: To evaluate resting energy expenditure (REE) in surgical infants and define the effects of the degree of stress on its level. SUBJECTS AND METHODS: Between June 1999 and June 2003 forty-five infants awaiting surgery (boys/girls: 32/13) from the Department of Pediatric Surgery were entered in the study. Indirect calorimetry was used to measure the REE of all the patients before operation and 1 - 7 days after operation. Clinical data were collected, including age, weight, height, diagnosis, operative method, site and duration, and first day postoperative C-reactive protein (CRP) levels. RESULTS: The REE before operation did not differ significantly from the postoperative values (paired t-test, p > 0.05). The predicted REE was significantly higher than the measured REE even before and after the operation (p < 0.01). REE values in the first three postoperative days were lower in the mild stress group than in the severe surgical stress group. CONCLUSIONS: REE variation among the patients is relatively large. Changes in REE may be related to the degree of stress. Predicted REE values may be not a good reflection of measured REE.

Calorimetry↗

[Preparation and characterization of the monoclonal antibodies against Japanese encephalitis virus.].

BACKGROUND: To prepare mouse monoclonal antibodies (McAbs) against Japanese encephalitis virus (JEV)and evaluate their biological characteristics. METHODS: McAbs against JEV were prepared by immunizing, fusing, cloning and screening. Their sensitivity, specificity, universality and neutralizing function were analyzed with ELISA, IFA, NT and Western blot. RESULTS: Titers of three McAbs against JEV were higher than 106. Three McAbs only reacted with JEV and not with other nine arboviruses. F12.37 could react with ten strains of JEV and sensitively detected ten replicating strains of viruses in BHK cell. The strains P3 and SH03-103 of JEV were neutralized by F12.37, its titers of protecting 50% cell were 3.2x105 and 105. Western blot showed that F12.37 reacted with envelop(E)protein of JEV. CONCLUSION: Three McAbs against JEV had high titer and good specificity. And F12.37 was very sensitive and universal in reacting with JEV, and neutralized JEV of Genotype I and Genotype .The binding site of F12.37 lays in E protein of JEV.

Animals↗

In vitro expanded human CD4+CD25+ regulatory T cells suppress effector T cell proliferation.

Regulatory T cells (Tregs) have been shown to be critical in the balance between autoimmunity and tolerance and have been implicated in several human autoimmune diseases. However, the small number of Tregs in peripheral blood limits their therapeutic potential. Therefore, we developed a protocol that would allow for the expansion of Tregs while retaining their suppressive activity. We isolated CD4+CD25 hi cells from human peripheral blood and expanded them in vitro in the presence of anti-CD3 and anti-CD28 magnetic Xcyte Dynabeads and high concentrations of exogenous Interleukin (IL)-2. Tregs were effectively expanded up to 200-fold while maintaining surface expression of CD25 and other markers of Tregs: CD62L, HLA-DR, CCR6, and FOXP3. The expanded Tregs suppressed proliferation and cytokine secretion of responder PBMCs in co-cultures stimulated with anti-CD3 or alloantigen. Treg expansion is a critical first step before consideration of Tregs as a therapeutic intervention in patients with autoimmune or graft-versus-host disease.

Autoimmune Diseases↗

Recombinant adeno-associated virus-mediated alpha-1 antitrypsin gene therapy prevents type I diabetes in NOD mice.

Type I diabetes results from an autoimmune destruction of the insulin-producing pancreatic beta cells. Although the exact immunologic processes underlying this disease are unclear, increasing evidence suggests that immunosuppressive, immunoregulatory and anti-inflammatory agents can interrupt the progression of the disease. Alpha 1 antitrypsin (AAT) is a multifunctional serine proteinase inhibitor (serpin) that also displays a wide range of anti-inflammatory properties. To test the ability of AAT to modulate the development of type I diabetes, we performed a series of investigations involving recombinant adeno-associated virus vector (rAAV)-mediated gene delivery of human alpha-1 antitrypsin (hAAT) to nonobese diabetic (NOD) mice. Recombinant AAV-expressing hAAT (rAAV2-CB-AT) was administered intramuscularly to 4-week-old female NOD mice (1 x 10(10) i.u./mouse). A single injection of this vector reduced the intensity of insulitis, the levels of insulin autoantibodies, and the frequency of overt type I diabetes (30% (3/10) at 32 weeks of age versus 70% (7/10) in controls). Transgene expression at the injection sites was confirmed by immunostaining. Interestingly, antibodies against hAAT were present in a majority of the vector-injected mice and circulating hAAT was undetectable when assessed 10 weeks postinjection. This study suggests a potential therapeutic role for AAT in preventing type I diabetes as well as the ability of AAV gene therapy-based approaches to ameliorate disease effectively.

Animals↗

Mathematical analysis of a model describing evolution of an asexual population in a changing environment.

We investigate a mathematical model for an asexual population with non-overlapping (discrete) generations, that exists in a changing environment. Sexual populations are also briefly discussed at the end of the paper. It is assumed that selection occurs on the value of a single polygenic trait, which is controlled by a finite number of loci with discrete-effect alleles. The environmental change results in a moving fitness optimum, causing the trait to be subject to a combination of stabilising and directional selection. This model is different from that investigated by Waxman and Peck [Genetics 153 (1999) 1041] where overlapping generations and continuous effect alleles were considered. In this paper, we consider non-overlapping generations and discrete effect alleles. However in [Genetics 153 (1999) 1041] and the present work, there is the same pattern of environmental change, namely a constant rate of change of the optimum. From [Genetics 153 (1999) 1041], no rigorous theoretical conclusion can be drawn about the form of the solutions as t grows large. Numerical work carried out in [Genetics 153 (1999) 1041] suggests that the solution is a lagged travelling wave solution, but no mathematical proof exists for the continuous model. Only partial results, regarding existence of travelling wave solutions and perturbed solutions, have been established (see [Nonlin. Anal. 53 (2003) 683; An integral equation describing an asexual population in a changing environment, Preprint]). For the discrete case of this paper, under the assumption that the ratio between the unit of genotypic value and the speed of environment change is a rational number, we are able to give rigorous proof of the following conclusion: the population follows the environmental change with a small lag behind, moreover, the lag is represented using a calculable quantity.

Biological Evolution↗

Targeting recombinant adeno-associated virus vectors to enhance gene transfer to pancreatic islets and liver.

Human pancreatic islet cells and hepatocytes represent the two most likely target cells for genetic therapy of type I diabetes. However, limits to the efficiency of rAAV serotype 2 (rAAV2)-mediated gene transfer have been reported for both of these cell targets. Here we report that nonserotype 2 AAV capsids can mediate more efficient transduction of islet cells, with AAV1 being the most efficient serotype in murine islets, suggesting that receptor abundance could be limiting. In order to test this, we generated rAAV particles that display a ligand (ApoE) that targets the low-density lipoprotein receptor, which is present on both of these cell types. The rAAV/ApoE viruses greatly enhanced the efficiency of transduction of both islet cells ex vivo and murine hepatocytes in vivo when compared to native rAAV2 serotype (220- and four-fold, respectively). The use of receptor-targeted rAAV particles may circumvent the lower abundance of receptors on certain nonpermissive cell types.

Animals↗

Swimming and ammonia toxicity in salmonids: the effect of sub lethal ammonia exposure on the swimming performance of coho salmon and the acute toxicity of ammonia in swimming and resting rainbow trout.

This study tested the hypothesis that swimming exacerbates ammonia toxicity in fish. Both sub-lethal and acute toxicity testing was conducted in a swim tunnel on swimming and resting coho salmon and rainbow trout, respectively. The sub lethal tests on coho salmon also considered the compartmentalization of ammonia within the fish. Coho salmon showed a significant linear decrease in U(crit) both with increasing water ammonia (0, 0.02, 0.04 and 0.08 mg per l NH3) and increasing plasma ammonia. Data collected included plasma pH and ammonia, muscle pH and ammonia and muscle membrane potential. Based on results found in these experiments it was concluded that the reduction in swimming performance was due to both metabolic challenges as well as depolarization of white muscle. Acute toxicity testing on swimming and resting rainbow trout revealed that swimming at (60% U(crit) or approximately 2.2 body lengths/s) decreased the LC50 level from 207+/-21.99 mg N per l in resting fish to 32.38+/-10.81. The LC50 for resting fish was significantly higher than that for swimming fish. The acute value set forth by the US EPA at the same pH is 36.1 mg N per l and may not protect swimming fish. In addition the effect of water hardness on ammonia toxicity was considered. It was found that increased water calcium ameliorates ammonia toxicity in fish living in high pH water.

Ammonia↗

Thermoluminescence of MgSO4 doped with Eu and P impurities.

CaSO4:Eu, MgSO4:Eu and MgSO4:Eu,P phosphors have been prepared and their thermoluminescence (TL) characteristics were studied. A main glow peak due to Eu2+ ions is seen at approximately 146 degrees C and 440 nm and glow peaks at approximately 145 degrees C, approximately 190 degrees C, approximately 260 degrees C and approximately 360 degrees C for 590 nm and 625 nm wavelengths are identified as Eu3+ ion emissions in MgSO4:Eu. Emission spectra in MgSO4:Eu and the MgSO4:Eu,P show that the MgSO4:Eu3+ glow peak at 260 degrees C for 590 nm and 625 nm shifts to 280 degrees C with enhanced intensity while the Eu2+ ion glow peak at 146 degrees C remains but with reduced intensity. The main glow peak at approximately 146 degrees C and 440 nm from Eu2+ ions shows significant difference from the characteristic glow peaks of Eu3+ ions. It is observed that the wavelength of the Eu2+ ion glow peak is inversely proportional to the radius of the cation of the host sulphate in alkaline-earth sulphate phosphors. By contrast the wavelengths of the Eu3+ ion glow peaks remain unchanged in different sulphates. Besides, the glow curve at approximately 146 degrees C obtained using a conventional blue sensitive reader shows simply the first order kinetics. It is concluded that the luminescence centres and distribution of traps related to Eu2+ ions are different from that of Eu3+ ions in MgSO4:Eu and MgSO4:Eu,P phosphors.

Europium↗

Antigen-specific blockade of T cells in vivo using dimeric MHC peptide.

Ag-specific immune tolerance in clinical organ transplantation is currently an unrealized but critical goal of transplant biology. The specificity and avidity of multimerized MHC-peptide complexes suggests their potential ability to modulate T cell sensitization and effector functions. In this study, we examined the ability of MHC-peptide dimers to modulate T cell function both in vitro and in vivo. Soluble MHC dimers induced modulation of surface TCR expression and inhibited T cell cytolytic activity at nanomolar concentrations in vitro. Furthermore, engagement of TCR by soluble dimers resulted in phosphorylation of the TCR zeta-chain and recruitment and phosphorylation of zeta-associated protein-70 to the signaling complex, the latter of which increased upon dimer cross-linking. Significantly, Ag-specific inhibition of an alloreactive TCR-transgenic T cell population in vivo resulted in consequent outgrowth of an allogeneic tumor. The prolonged Ag-specific suppression of expansion and/or effector function of cognate T cells in vivo suggests that soluble MHC dimers may be a means of inducing sustained Ag-specific T cell unresponsiveness in vivo.

Animals↗

Role of cyclic AMP responsive element in the UVB induction of cyclooxygenase-2 transcription in human keratinocytes.

It has been shown that UVB irradiation induces expression of COX-2 and up-regulation of COX-2 plays a functional role in UVB tumor promotion. In this study, we examined the cis-elements in the human COX-2 promoter that may be responsible for the UVB induction of COX-2. Analyses with the COX-2 promoter region revealed that the cyclic AMP responsive element near the TATA box was essential for both basal and UVB induced COX-2 expression. This was further supported by studies using a dominant negative mutant of CREB, which strongly inhibited the activity of COX-2 promoter. Electrophoretic mobility shift assays indicated that CREB and ATF-1 were the major proteins binding to the COX-2 CRE. CREB and ATF-1 were phosphorylated upon UVB treatment, and SB202190, a p38 MAPK inhibitor, decreased the phosphorylation of CREB/ATF-1 and suppressed COX-2 promoter activity. In contrast, treatment with forskolin, an activator of adenylyl cyclase, led to phosphorylation of CREB and ATF-1 and activation of COX-2 promoter. Finally, enhanced binding of phospho-CREB/ATF-1 to the COX-2 CRE was observed after UVB induction. Thus, one signaling pathway for UVB induction of human COX-2 involves activation of p38, subsequent phosphorylation of CREB/ATF-1, and activation of the COX-2 CRE through enhanced binding of phosphorylated CREB/ATF-1.

Activating Transcription Factor 1↗

Role of p38 MAP kinases and ERK in mediating ultraviolet-B induced cyclooxygenase-2 gene expression in human keratinocytes.

The roles of p38 MAP kinases and ERK in UVB induced cox-2 gene expression were studied in a human keratinocyte cell line, HaCaT. UVB significantly increased cox-2 gene expression at both protein and mRNA levels. As we reported previously, p38 and ERK were significantly activated after UVB irradiation in HaCaT cells. In addition, treating the cells with p38 inhibitor SB202190 or MEK inhibitor PD98059 specifically inhibited UVB induced p38 or ERK activation, respectively. In this study, we further examined the roles of p38 and ERK in UVB induced cox-2 gene expression in HaCaT cells. We found that SB202190 strongly inhibited UVB induced COX-2 protein expression at different time points and various UVB doses. Furthermore, SB202190 markedly inhibited UVB induced cox-2 mRNA. Our data indicated that ERK did not play a role in UVB induced cox-2 gene expression in human keratinocytes since suppression of ERK did not significantly alter UVB induced increase of COX-2 protein and mRNA. These results suggested, for the first time, that activation of p38 is required for UVB induced cox-2 gene expression in human keratinocytes. Since cox-2 expression plays an important role in UV carcinogenesis, p38 could be a potential molecular target for chemoprevention of skin cancer.

Cell Line↗

Roles of Akt and glycogen synthase kinase 3beta in the ultraviolet B induction of cyclooxygenase-2 transcription in human keratinocytes.

Ultraviolet B (UVB)-induced cyclooxygenase-2 (COX-2) expression plays an important role in UVB tumor promotion. We examined whether Akt and glycogen synthase kinase 3beta (GSK-3beta), components of the phosphatidylinositol 3'-kinase pathway, are involved in UVB induction of COX-2 transcription. UVB caused Akt phosphorylation at both Thr-308 and Ser-473 that was inhibited by LY294002, a phosphatidylinositol 3'-kinase inhibitor. LY294002 also decreased the expression of endogenous COX-2 protein and a luciferase construct driven by COX-2 promoter. Similarly, UVB caused phosphorylation of GSK-3beta (Ser-9) and presumably inactivation of GSK-3beta. Inhibition of GSK-3beta by lithium induced endogenous COX-2 protein expression and COX-2 promoter activity. Finally, overexpression of a dominant-negative Akt mutant or wild-type GSK-3beta suppressed UVB-mediated induction of COX-2 promoter. These studies suggest that inactivation of GSK-3beta through activation of Akt plays an important role in the UVB induction of COX-2 transcription.

Calcium-Calmodulin-Dependent Protein Kinases↗

Development and applications of surface-linked single chain antibodies against T-cell antigens.

In this report the use of surface-linkage to expand the potential experimental and therapeutic applications of single chain antibody (scFv) constructs is reviewed. A strategy for the generation and functional characterization of surface-linked scFvs that bind selectively to the T-cell proteins CD3epsilon, CD28, and CD152 (CTLA-4) is described in detail. Experimental examples are provided of the use of these constructs to study the positive and negative regulation of T-cell activation and to manipulate the in vivo immunogenicity of tumor cells. In addition, a novel system for Simultaneous T-cell Activation and Retroviral Transduction (START) is described in which retroviral packaging cells are rendered mitogenic for T lymphocytes by combined expression of surface-linked scFvs. Finally, the use of random mutagenesis and yeast surface display to increase the affinity and functional efficacy of scFv constructs is demonstrated.

Abatacept↗