Biomedical subjects

S Chen

Publications and source records attributed to S Chen.

At least 145 records · Page 8Linked to original sources

PubMed2002

Measurement of B(D+-->K(*0)l(+)nu(l)).

Using 13.53 fb(-1) of CLEO data, we have measured the ratios of the branching fractions R(+)(e),R(+)(mu) and the combined branching fraction ratio R(+)(l), defined by R(+)(l)=[B(D+-->K(*0)l(+)nu(l))]/[B(D+-->K-pi(+)pi(+))]. We find R(+)(e)=0.74+/-0.04+/-0.05, R(+)(mu)=0.72+/-0.10+/-0.05, and R(+)(l)=0.74+/-0.04+/-0.05, where the first and second errors are statistical and systematic, respectively. The known branching fraction B(D+-->K-pi(+)pi(+)) leads to B(D+-->K(*0)e(+)nu(e))=(6.7+/-0.4+/-0.5+/-0.4)%, B(D+-->K(*0)mu(+)nu(mu))=(6.5+/-0.9+/-0.5+/-0.4)%, and B(D+-->K(*0)l(+)nu(l))=(6.7+/-0.4+/-0.5+/-0.4)%, where the third error is due to the uncertainty in B(D+-->K-pi(+)pi(+)).

Journal Article↗

PubMed2002

Landauer-type transport theory for interacting quantum wires: application to carbon nanotube y junctions.

We propose a Landauerlike theory for nonlinear transport in networks of one-dimensional interacting quantum wires (Luttinger liquids). A concrete example of current experimental focus is given by carbon nanotube Y junctions. Our theory has three basic ingredients that allow one to explicitly solve this transport problem: (i) radiative boundary conditions to describe the coupling to external leads, (ii) the Kirchhoff node rule describing charge conservation, and (iii) density matching conditions at every node.

Journal Article↗

PubMed2002

Observation of the decay Omega(0)(c)-->Omega(-)e(+)nu(e).

Using the CLEO detector at the Cornell Electron Storage Ring we have observed the Omega(0)(c) (css ground state) in the decay Omega(0)(c)-->Omega(-)e(+)nu(e). We find a signal of 11.4+/-3.8(stat) events. The probability that we have observed a background fluctuation is 7.6x10(-5). We measure B(Omega(0)(c)-->Omega(-)e(+)nu(e)).sigma(e(+)e(-)-->Omega(0)(c)X)=(42.2+/-14.1(stat)+/-5.7(syst)) fb and R=[Gamma(Omega(0)(c)-->Omega(-)pi(+))]/[Gamma(Omega(0)(c)-->Omega(-)enu(e))]=00.41+/-0.19(stat)+/-0.04(syst). This is the first statistically significant observation of an individual decay mode of the Omega(0)(c) in e(+)e(-) annihilation and the first example of a baryon decaying via beta emission, where no quarks from the first generation participate in the reaction.

Journal Article↗

PubMed2002

Further evidence for the decay K+ -->pi+nu(nu).

Additional evidence for the rare kaon decay K+-->pi+nu(nu) has been found in a new data set with comparable sensitivity to the previously reported result. One new event was observed in the pion momentum region examined, 211 pi+nu(nu)) = 1.57(+1.75)(-0.82)x10(-10).

Journal Article↗

PubMed2002

Determination of toxicokinetic parameters for bioconcentration of water-soluble fraction of petroleum hydrocarbon associated with no. 0 diesel in Changjiang estuary and Jiaozhou bay: model versus mesocosm experiments.

A method is proposed for determination of toxicokinetic parameters for bioconcentration by phytoplankton of the water-soluble fraction (WSF) of petroleum hydrocarbon (PH) associated with No. 0 diesel, in which WSF-PH concentration in phytoplankton cells, C(A(d)), is estimated by subtracting concentration in water (S-bottle) containing a phytoplankton sample from that in a C-bottle without phytoplankton. It was demonstrated that C(A(d)) agrees well with the concentration found by direct ultrasonication extraction of collected cells, C(A(ind)) ( r = 0.88, p < 0.0001), and its uncertainty was about 17.6%. Mesocosms in 25-m3 ethylene vinyl acetate or 4-m3 polyethylene bags were performed at two sites in China: Changjiang Estuary in spring/summer 1998 and Jiaozhou Bay in autumn 1999 and spring/summer 2000. The experiments were designed to determine toxicokinetic parameters, including specific rates of uptake and elimination, and bioconcentration factor (BCF), for bioconcentration of WSF-PH by phytoplankton. A modified kinetic two-compartment model for bioconcentration of WSF-PH by phytoplankton was developed to estimate the toxicokinetic parameters. In the model, the influence of phytoplankton growth on bioconcentration and WSF-PH decline due to biotic and abiotic processes other than bioconcentration, such as volatilization, microbial degradation, phytolysis, and sorption expressed as an exponential-decay equation, are taken into account. Size-dependent BCF was observed in the laboratory experiment. BCFs were 1.0 x 10(4) in summer in Changjiang Estuary, 1.6 x 10(4) in summer, and 1.1 x 10(4) in autumn in Jiaozhou Bay. The difference in BCF may be interpreted by its size dependence.

Biological Availability↗

PubMed2002

Peritoneal mesothelioma: CT and MRI findings.

Two patients with histologically proven diagnosis of peritoneal mesothelioma are presented. Both patients had CT scans of the abdomen. The second patient was also examined with MRI.

Adult↗

PubMed2002

TGF beta-1 downregulates DMP-1 and DSPP in odontoblasts.

Transforming growth factor beta-1 (TGF beta-1) is a multifunctional growth factor that is expressed in numerous cell types. It has been shown to induce secretion of dentin extracellular matrix components associated with primary dentinogenesis and to play a role in tertiary or reparative dentinogenesis. In this study, we investigated the potential transcriptional regulation by TGF beta-1 of two dentin matrix proteins: dentin matrix protein 1 (DMP-1), and dentin sialophosphoprotein (DSPP). In vitro promoter studies were performed using plasmid constructs containing mouse DMP-1 and DSPP promoter sequences fused to the luciferase reporter gene. Constructs were transiently transfected in the mouse odontoblast cell line M06-G3 and cultured in the presence or absence of TGF beta-1. The integrity of the TGF beta-1 signaling pathway was investigated in the M06-G3 cells by identifying known key effectors of TGF beta-1 signal transduction. Transient transfection studies demonstrate for the first time that TGF beta-1 downregulates both DMP-1 and DSPP genes. Our findings indicate that the TGF beta-1 type I receptor ALK5 is expressed by odontoblasts as well as the signal transduction proteins Smad2, Smad3, and Smad4. These results suggest that TGF beta-1 regulates two key dentin proteins involved in matrix mineralization most likely mediated through the type I ALK5 receptor and transduced by Smads 2, 3, and 4.

Activin Receptors, Type I↗

PubMed2002

Isolation and characterization of human monoclonal autoantibodies to glutamic acid decarboxylase.

Production of human monoclonal autoantibodies to glutamic acid decarboxylase M(r) 65,000 (GAD65), characterization of their isotype, binding affinity, V region sequences and competition with autoantibodies in patients' sera is described. Lymphocytes from a patient with Addison's disease who had GAD65 autoantibodies without diabetes were immortalised and fused to a mouse/human hybridoma. In addition, mouse monoclonal antibodies to GAD65 were produced using standard techniques. F(ab')2S from our monoclonals and the GAD6 mouse monoclonal were used in competition with intact monoclonals and sera from diabetic patients for binding to 125I-labelled GAD65 (amino acids 46-586). Reactivities of the human monoclonals with GAD 65,000/67,000 M(r) chimeras were also studied. Variable region genes of human monoclonals were sequenced and analysed. The human monoclonals (n = 3) had affinity constants for GAD65 of 2.2 x 10(9), 5.8 x 10(9), 1.3 x 10(10) mol/l(-1); affinities of the mouse monoclonals (n = 5) ranged from 1.1 x 10(8) to 5.4 x 10(10) mol/l(-1). The binding of each of the human monoclonals was inhibited by GAD6 F(ab')2 and the binding of GAD6 antibody was inhibited by the human monoclonal F(ab')2S suggesting that the epitopes for these antibodies were overlapping. Studies with GAD65/GAD67 chimeras indicated that the human monoclonals reacted with C-terminal epitopes. The human monoclonals, GAD6 and 3/5 mouse monoclonals inhibited serum autoantibody binding to 125I-labelled GAD65. Overall, the human monoclonals were of high affinity, reacted with C-terminal epitopes and showed evidence of antigen driven maturation; they represented only a proportion of the repertoire of autoantibodies to GAD65 in the donor's serum and in the sera of patients with type-1 diabetes.

Addison Disease↗

PubMed2002

Linear free energy relationships on rate constants for dechlorination by zero-valent iron.

By correlation analysis, molecular structural factors governing surface area-normalized rate constants (k) for dechlorination by zero-valent iron, were identified. Twenty-nine quantum chemical descriptors computed by MNDO, AM1 and PM3 Hamiltonians for gas-phase and the conductor-like screening model (COSMO) for incorporating solvent (H2O) effects were studied. Besides the energy of the lowest unoccupied molecular orbital (E(LUMO)), the character of carbon-chlorine bonds (C-Cl bonds) and especially the strength of C-Cl bonds was found significant in governing the magnitude of log k. By PLS analysis, six two-parameter linear free energy relationships (LFER) were obtained. The best two-parameter LFER model was the one using E(LUMO) and C (the Coulombic interaction energy of the two-center term for the C-Cl bonds) computed by PM3/H2O method as molecular structural descriptors. Chlorinated compounds with high E(LUMO) and C values tend to have low dechlorination rate constants.

Carbon↗

PubMed2002

Anti-aromatase chemicals in red wine.

Estrogen synthesized in situ plays a more important role in breast cancer cell proliferation than does circulating estrogen. Aromatase is the enzyme that converts androgen to estrogen and is expressed at a higher level in breast cancer tissue than in surrounding noncancer tissue. A promising route of chemoprevention against breast cancer may be through the suppression of in situ estrogen formation using aromatase inhibitors. A diet high in fruits and vegetables may reduce the incidence of breast cancer, because they contain phytochemicals that can act as aromatase inhibitors. In our previous studies, we found that grapes and wine contain potent phytochemicals that can inhibit aromatase. We show that red wine was more effective than white wine in suppressing aromatase activity. Interestingly, our results from white wine studies suggest a weak inductive effect of alcohol on aromatase activity. On the other hand, the potent effect of anti-aromatase chemicals in red wine overcomes the weak inductive effect of alcohol in wine. Several purification procedures were performed on whole red wine to separate active aromatase inhibitors from non-active compounds. These techniques included liquid-liquid extraction, silica gel chromatography, various solid phase extraction (SPE) columns, and high performance liquid chromatography. An active Pinot Noir red wine SPE C18 column fraction (20% acetonitrile:water) was more effective than complete Pinot Noir wine in suppressing aromatase assay. This red wine extract was further analyzed in a transgenic mouse model in which aromatase was over-expressed in mammary tissue. Our gavaged red wine extract completely abrogated aromatase-induced hyperplasia and other neoplastic changes in mammary tissue. These results suggest that red wine or red wine extract may be a chemopreventive diet supplement for postmenopausal women who have a high risk of breast cancer. Further research is underway to purify and characterize the active compounds in red wine that are responsible for the inhibition of aromatase.

Aromatase Inhibitors↗

PubMed2002

SNP S1103Y in the cardiac sodium channel gene SCN5A is associated with cardiac arrhythmias and sudden death in a white family.

Cardiac arrhythmias cause 400 000 sudden deaths annually in the United States alone. Mutations in the cardiac sodium channel gene SCN5A on chromosome 3p21 cause cardiac arrhythmias and sudden death. In this study, we define an SCN5A mutation, S1103Y, in a white family associated with syncope, ventricular fibrillation, and sudden death. A very recent study reported the same mutation in 13.2% of African Americans, but not in the white population. Our study shows that mutation S1103Y does exist in the white population, and it is associated with a considerable risk of syncope, ventricular arrhythmia, ventricular fibrillation, and sudden death in this population.

Adult↗

PubMed2002

Hyperhexosemia induced functional and structural changes in the kidneys: role of endothelins.

BACKGROUND/AIMS: Glomerular basement membrane (GBM) thickening and mesangial matrix expansion are characteristic features of diabetic nephropathy. The present study investigates the role of endothelins (ETs) in the pathogenesis of such changes in diabetic nephropathy. METHODS: Diabetic (streptozotocin-induced, 65 mg/kg), galactose-fed (30%) and control animals were followed up for 1 and 6 months. Animal groups also included diabetic and galactose fed animals on dual ET(A)/ET(B) receptor antagonist bosentan (100 mg/kg). A semi-quantitative reverse transcription polymerase chain reaction method was used to quantify mRNA expression of ET-1, ET-3, ET(A), ET(B), fibronectin and collagen alpha2(IV). Histological analyses of the kidneys and ET-1, ET-3 and fibronectin immunohistochemistry were performed. Morphometric assessment of the GBM after 6 months was performed. RESULTS: Diabetes increased mRNA expression of ET-1, ET-3, ET(A), ET(B), fibronectin and collagen alpha2(IV) after one and six months. In contrast, although increased ET(A) and ET(B) mRNAs were present following galactose feeding both at 1 and 6 months, ET-1, ET-3, fibronectin and collagen alpha2(IV)mRNAs were increased after 6 months. Both diabetes and galactose feeding caused increased GBM thickening. Furthermore, diabetes caused an increase in mesangial matrix production. Bosentan prevented increased fibronectin and collagen alpha2(IV) mRNA expression, increased mesangial matrix deposition and GBM thickening. CONCLUSION: This study has demonstrated that diabetes and galactose feeding induced functional and structural changes in the kidney are mediated via ETs.

Animals↗

PubMed2002

Nanoindentation behavior of clay/poly(ethylene oxide) nanocomposites.

Depth-sensing nanoindentation of clay/poly(ethylene oxide) nanocomposites has shown significant differences in the mechanical behavior of the composites, depending on method of synthesis and clay content. In general, the clay/polymer nanocomposite approach can dramatically improve the hardness, stiffness, and creep resistance of the polymer. However, these improvements are dependent on the clay content. At lower concentrations, the improvements are not significant, because of an adverse effect on creep behavior.

Aluminum Silicates↗

PubMed2002

Effect of pasteurization on survival of Mycobacterium paratuberculosis in milk.

Mycobacterium paratuberculosis (Mptb) is the causative agent of Johne's disease of ruminant animals including cattle, goats, and sheep. It has been suggested that this organism is associated with Crohn's disease in humans, and milk is a potential source of human exposure to this organism. A total of 18, including 7 regular batch and 11 high temperature short time (HTST) pasteurization experiments, were conducted in this study. Raw milk or ultra-high temperature pasteurized milk samples were spiked at levels of 10(3), 10(5), and 10(7) cfu of Mptb/ml. Escherichia coli and Mycobacterium bovis BCG strains at 10(7) cfu/ml were used as controls. Pasteurization experiments were conducted using time and temperature standards specified in the Canadian National Dairy Code: regular batch pasteurization method: 63 degrees C for 30 min, and HTST method: 72 degrees C for 15 s. The death curve of this organism was assessed at 63 degrees C. No survivors were detected after 15 min. Each spiked sample was cultured in Middlebrook 7H9 culture broth and Middlebrook 7H11 agar slants. Samples selected from 15 experiments were also subjected to BACTEC culture procedure. Survival of Mptb was confirmed by IS900-based PCR of colonies recovered on slants. No survivors were detected from any of the slants or broths corresponding to the seven regular batch pasteurization trials. Mptb survivors were detected in two of the 11 HTST experiments. One was by both slant and broth culture for the sample spiked to 10(7) cfu/ml of Mptb, while the other was detected by BACTEC for the sample spiked to 10(5) cfu/ml. These results indicate that Mptb may survive HTST pasteurization when present at > or = 10(5) cfu/ml in milk. A total of 710 retail milk samples collected from retail store and dairy plants in southwest Ontario were tested by nested IS900 PCR for the presence of Mptb. Fifteen percent of these samples (n = 110) were positive. However, no survivors were isolated from the broth and agar cultures of 44 PCR positive and 200 PCR negative retail milk samples. The lack of recovery of live Mptb from the retail milk samples tested may be due to either the absence of live Mptb in the retail milk samples tested or the presence of low number of viable Mptb which were undetected by the culture method used in this study.

Animals↗

PubMed2002

Potentiation of tumor necrosis factor-mediated apoptosis of oral squamous cell carcinoma cells by adenovirus-mediated gene transfer of NF-kappaB inhibitor.

Oral squamous cell carcinoma (SCC) is a malignant tumor which is often resistant to cancer-therapy-mediated apoptosis. The stress-responsive transcription factor nuclear factor kappa B (NF-kappaB), which has been found to be associated with SCC development, plays an essential role in the suppression of tumor necrosis factor (TNF)-mediated apoptosis. Here, we report that an adenovirus-mediated gene transfer of NF-kappaB inhibitor, super-repressor I kappa B alpha (Adv-SR-IkappaBalpha), blocked TNF-induced NF-kappaB activation and sensitized oral SCC cells to TNF killing. Additionally, we found that the inhibition of NFkappaB by Adv-SR-IkappaBalpha enhanced TNF-mediated caspase-8 and -3 activation. These results suggest that NF-kappaB activation is a general mechanism by which oral squamous carcinoma cells are resistant to TNF killing and provide a molecular basis for gene therapy of oral cancer by IkappaBalpha gene transfer in vivo.

Adenoviridae↗

PubMed2001

Caspase-9 activation results in downstream caspase-8 activation and bid cleavage in 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-induced Parkinson's disease.

Parkinson's disease (PD) and 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) toxicity are both associated with dopaminergic neuron death in the substantia nigra (SN). Apoptosis has been implicated in this cell loss; however, whether or not it is a major component of disease pathology remains controversial. Caspases are a major class of proteases involved in the apoptotic process. To evaluate the role of caspases in PD, we analyzed caspase activation in MPTP-treated mice, in cultured dopaminergic cells, and in postmortem PD brain tissue. MPTP was found to elicit not only the activation of the effector caspase-3 but also the initiators caspase-8 and caspase-9, mitochondrial cytochrome c release, and Bid cleavage in the SN of wild-type mice. These changes were attenuated in transgenic mice neuronally expressing the general caspase inhibitor protein baculoviral p35. These mice also displayed increased resistance to the cytotoxic effects of the drug. MPTP-associated toxicity in culture was found temporally to involve cytochrome c release, activation of caspase-9, caspase-3, and caspase-8, and Bid cleavage. Caspase-9 inhibition prevented the activation of both caspase-3 and caspase-8 and also inhibited Bid cleavage, but not cytochrome c release. Activated caspase-8 and caspase-9 were immunologically detectable within MPP(+)-treated mesencephalic dopaminergic neurons, dopaminergic nigral neurons from MPTP-treated mice, and autopsied Parkinsonian tissue from late-onset sporadic cases of the disease. These data demonstrate that MPTP-mediated activation of caspase-9 via cytochrome c release results in the activation of caspase-8 and Bid cleavage, which we speculate may be involved in the amplification of caspase-mediated dopaminergic cell death. These data suggest that caspase inhibitors constitute a plausible therapeutic for PD.

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine↗

PubMed2001

Modulation of Lrp action in Escherichia coli by leucine: effects on non-specific binding of Lrp to DNA.

Lrp is a global regulator of metabolism in Escherichia coli that helps cells respond to changes in environmental conditions. The action of Lrp as a transcriptional activator or repressor is sometimes affected by whether the medium contains exogenous leucine. The abundance of Lrp in cells is relatively high (about 15 microM in monomer), and given the relatively high Lrp binding affinity in vitro for specific binding sites (nanomolar apparent dissociation constants), the expectation is that all binding sites will be saturated with Lrp in vivo. Here we consider the fraction of the total Lrp in cells that is free and the fraction that is bound to DNA. Using minicell-producing strains, we measured the distribution of Lrp between cytoplasm and nucleoid in cells grown under different nutritional conditions and in cells in different phases of growth. In E. coli cells grown in minimal medium to mid-log phase, the ratio of free to DNA-bound Lrp was about 0.67. This ratio decreased about threefold when the cells were grown in minimal medium supplemented with leucine. Our results also confirmed the previous finding that growth rate regulates lrp expression by as much as three to fourfold. Growth rate-regulated lrp expression, along with changes in the extent of non-specific binding, influences the level of free Lrp in vivo over a 16-fold range. We propose that the net effect of these processes is to regulate the relative concentrations of free Lrp hexadecamer and leucine-bound octamer, leading to promoter selection in response to environmental conditions.

Cytoplasm↗

PubMed2001

Search for the familon via B(+/-) --> pi+/-X(0), B(+/-) --> K(+/-)X(0), and B(0) --> K(0)(S)X(0) decays.

We have searched for the two-body decay of the B meson to a light pseudoscalar meson h = pi(+/-),K+/-,K(0)(S) and a massless neutral feebly interacting particle X(0) such as the familon, the Nambu-Goldstone boson associated with a spontaneously broken global family symmetry. We find no significant signal by analyzing a data sample containing 9.7x10(6) BBbar mesons collected with the CLEO detector at the Cornell Electron Storage Ring, and set 90% C.L. upper limits italicB(B(+/-) --> h(+/-)X(0)) = 4.9x10(-5) and italicB(B(0) --> K(0)(S)X(0)) = 5.3x10(-5). These limits correspond to a lower bound of approximately 10(8) GeV on the family symmetry breaking scale with vector coupling involving the third generation of quarks.

Journal Article↗