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J Ye

Publications and source records attributed to J Ye.

At least 37 records · Page 2Linked to original sources
PubMed2003

The role of intramuscular lipid in insulin resistance.

There is interest in how altered lipid metabolism could contribute to muscle insulin resistance. Many animal and human states of insulin resistance have increased muscle triglyceride content, and there are now plausible mechanistic links between muscle lipid accumulation and insulin resistance, which go beyond the classic glucose-fatty acid cycle. We postulate that muscle cytosolic accumulation of the metabolically active long-chain fatty acyl CoAs (LCACoA) is involved, leading to insulin resistance and impaired insulin signalling or impaired enzyme activity (e.g. glycogen synthase or hexokinase) either directly or via chronic translocation/activation of mediators such as a protein kinase C (particularly PKC theta and epsilon ). Ceramides and diacylglycerols (DAGs) have also been implicated in forms of lipid-induced muscle insulin resistance. Dietary lipid-induced muscle insulin resistance in rodents is relatively easily reversed by manipulations that lessen cytosolic lipid accumulation (e.g. diet change, exercise or fasting). PPAR agonists (both gamma and alpha) also lower muscle LCACoA and enhance insulin sensitivity. Activation of AMP-activated protein kinase (AMPK) by AICAR leads to muscle enhancement (especially glycolytic muscle) of insulin sensitivity, but involvement of altered lipid metabolism is less clear cut. In rodents there are similarities in the pattern of muscle lipid accumulation/PKC translocation/altered insulin signalling/insulin resistance inducible by 3-5-h acute free fatty acid elevation, 1-4 days intravenous glucose infusion or several weeks of high-fat feeding. Recent studies extend findings and show relevance to humans. Muscle cytosolic lipids may accumulate either by increased fatty acid flux into muscle, or by reduced fatty acid oxidation. In some circumstances muscle insulin resistance may be an adaptation to optimize use of fatty acids when they are the predominant available energy fuel. The interactions described here are fundamental to optimizing therapy of insulin resistance based on alterations in muscle lipid metabolism.

Acyl Coenzyme A↗
PubMed2003

Independent activation of MAP kinase and MPF during the initiation of meiotic maturation in pig oocytes.

Mitogen-activated protein (MAP) kinase is universally activated during oocyte maturation in all vertebrates studied to date. Its role in the resumption of meiosis and in the activation of maturation-promoting factor (MPF) remains unclear, especially in domestic species such as the pig. This study aimed to clarify the temporal and causal relationships between MAP kinase and MPF during meiotic maturation, particularly during the resumption of meiosis. Pig oocytes were matured synchronously in culture by treatment with cycloheximide. Kinase activities were analysed using a sensitive in vitro double-kinase assay and the specific MAP kinase pathway inhibitor U0126. MAP kinase and MPF were activated simultaneously at the time of germinal vesicle breakdown (GVBD; 6 h after removal of cycloheximide); they reached significant activity at 7 h (P < 0.05). The activities increased in parallel during GVBD (6-10 h) and peaked when the oocytes entered metaphase I (MI; 10 h). Whereas MAP kinase remained stable at peak activity thereafter, MPF activity significantly declined during the MI-MII transition (16-20 h) but increased to a second peak at MII (22 h). MAP kinase activity in denuded and cumulus-cell enclosed oocytes was completely inhibited by 20 and 80 mmicro mol U0126 l(-1), respectively. Oocytes without detectable MAP kinase activity underwent normal GVBD in terms of nuclear morphology and timing, although later meiotic stages were abnormal. The kinetics of MPF activity during GVBD were unaffected by U0126. This study has demonstrated that MAP kinase is activated simultaneously with MPF at GVBD, but that its activation is not essential for the activation of MPF nor for the resumption of the first meiosis in pig oocytes.

Animals↗
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

Observation of B(0) --> D0pi(0) and B(0) -->D(*0)pi(0).

We have studied the color-suppressed hadronic decays of neutral B mesons into the final states D*0pi(0). Using 9.67 x 10(6) BB pairs collected with the CLEO detector, we observe the decays B( 0) --> D0pi(0) and B( 0) -->D(*0)pi(0) with the branching fractions BB( 0) -->D0pi(0)) = (2.74(+0.36)(-0.32) +/- 0.55)x10(-4) and BB( 0) -->D(*0)pi(0)) = (2.20(+0.59)(-0.52) +/- 0.79)x10(-4). The first error is statistical and the second systematic. The statistical significance of the D0pi(0) signal is 12.1sigma ( 5.9sigma for D(*0)pi(0)). Utilizing the B( 0) -->D*0)pi(0) branching fractions we determine the strong phases delta(I,D(*)) between isospin 1/2 and 3/2 amplitudes in the Dpi and D*pi final states to be cosdelta(I,D) = 0.89 +/-0.08 and cosdelta(I,D*) = 0.89 +/- 0.08, respectively.

Journal Article↗
PubMed2002

Alterations in cytokine regulation in aged epidermis: implications for permeability barrier homeostasis and inflammation. I. IL-1 gene family.

Acute disruption of the cutaneous permeability barrier with either solvents or tape-stripping stimulates a homeostatic metabolic response in the subjacent nucleated layers of the epidermis that results in a rapid restoration of normal permeability barrier function. When the aged epidermal permeability barrier is stressed, it reveals a diminished capacity for recovery, in comparison to young epidermis, analogous to other organs in the aged when stressed. Although the signals that regulate this homeostatic response by the epidermis have not yet been resolved, acute permeability barrier disruption stimulates release of prestored IL-1alpha, and increased production of potentially regulatory cytokines, including IL-1alpha and TNFalpha in the epidermis. In these studies, we addressed the hypothesis that cytokine dysregulation explains the permeability barrier abnormality in aged epidermis, assessing the regulation of IL-1 and TNF signaling in aged vs young mice. To determine whether the IL-1 family of cytokines plays a key role in the permeability barrier abnormality of the aged, permeability barrier recovery rates were compared in transgenic mice lacking the functional IL-1 type 1 receptor vs wild-type mice at various ages. Knockout of the IL-1 type 1 receptor exacerbates the defect in permeability barrier homeostasis that is seen in age-matched, wild-type counterparts. Furthermore, the sluggish permeability barrier recovery in aged epidermis is associated with, and at least in part attributable to, altered expression of the IL-1 family of cytokines and receptors both under basal conditions and after acute barrier perturbations. Whereas modulations in cytokine expression with epidermal permeability barrier perturbation are qualitatively similar in aged epidermis, they greatly differ quantitatively. In contrast, examination of TNFalpha mRNA and protein basally, and following barrier perturbation revealed no alterations in aged epidermis. Together, these results show that selective alterations in the IL-1 family of cytokines occur with aging and that defects in IL-1 signaling may contribute to the epidermal permeability barrier abnormality of aged skin.

Animals↗
PubMed2002

Synchronization of porcine oocyte meiosis using cycloheximide and its application to the study of regulation by cumulus cells.

This paper describes the use of the protein synthesis inhibitor cycloheximide (CHX) to synchronize nuclear progression during meiotic maturation in porcine oocytes, and also the time-dependence of nuclear maturation on exposure of the oocyte to cumulus cells. Prior to culture, the majority of oocytes were at the germinal vesicle (GV) stage (95-100%), but distributed from GVI to GVIV (GVI 56.1 +/- 9.1%, GVII 15.3 +/- 1.4%, GVIII 21.5 +/- 7.1%, GVIV 7.1 +/- 3.5%). During culture of cumulus-enclosed oocytes (COCs) from 12 h to 48 h in a conventional culture system, all meiotic stages were represented at any time point examined, with 63.6 +/- 4.2% of oocytes maturing to metaphase II (MII). Cycloheximide blocked the progression of nuclear development in a dose-dependent manner. Treatment for 12 h with CHX at 1-25 microg mL(-1) resulted in 95-100% oocytes being arrested and synchronized at GVII. With >5 microg mL(-1) CHX, all oocytes were arrested before germinal vesicle breakdown (GVBD) (mostly at GVIII) by 24 h. A 12 h preincubation with 5 microg mL(-1) CHX followed by 24 h of further culture without CHX resulted in >80% of oocytes maturing to MII. The profile of nuclear progression during maturation revealed discrete peaks of occurrence of different meiotic stages, with GVBD at 6-12 h, metaphase I (MI) at 10-18 h and anaphase I/telophase I at 16-20 h. After 12 h preincubation with 5 microg mL(-1) CHX, denuded oocytes (DOs) matured to MI as COCs. However, DOs matured to MII as normal when denuded at MI. In conclusion, CHX not only efficiently blocks and synchronizes the meiotic progression of porcine oocytes at a specific GV stage, but it also effectively synchronizes subsequent meiotic progression to MII, resulting in discrete peaks of occurrence of different meiotic stages. Using this technique, the study showed that cumulus cells are essential for oocytes to mature from MI to MII but exposure to cumulus cells must occur before MI.

Animals↗
PubMed2002

Muscle long-chain acyl CoA esters and insulin resistance.

A common observation in animal models and in humans is that accumulation of muscle triglyceride is associated with the development of insulin resistance. In animals, this is true of genetic models of obesity and nutritional models of insulin resistance generated by high-fat feeding, infusion of lipid, or infusion of glucose. Although there is a strong link between the accumulation of triglycerides (TG) in muscle and insulin resistance, it is unlikely that TG are directly involved in the generation of muscle insulin resistance. There are now other plausible mechanistic links between muscle lipid metabolites and insulin resistance, in addition to the classic substrate competition proposed by Randle's glucose-fatty acid cycle. The first step in fatty acid metabolism (oxidation or storage) is activation to the long-chain fatty acyl CoA (LCACoA). This review covers the evidence suggesting that cytosolic accumulation of this active form of lipid in muscle can lead to impaired insulin signaling, impaired enzyme activity, and insulin resistance, either directly or by conversion to other lipid intermediates that alter the activity of key kinases and phosphatases. Actions of fatty acids to bind specific nuclear transcription factors provide another mechanism whereby different lipids could influence metabolism.

Acyl Coenzyme A↗
PubMed2002

Nonaqueous capillary electrophoretic analysis of hexetidine in a commercial liquid formulation.

A non-aqueous capillary electrophoresis method has been proposed to analyse hexetidine and its degradation products in a commercial liquid pharmaceutical formulation. The separation was achieved using a 37 cm fused silica capillary with a 75 microns internal diameter, an electrolyte of 120 mM sodium acetate buffer in methanol, at 16 kV and 25 degrees C. The results show that the proposed method is able to resolve hexetidine from its degradation products and/or impurities.

Antifungal Agents↗
PubMed2001

Molecular iodine clock.

We demonstrate a simple optical clock based on an optical transition of iodine molecules, providing a frequency stability superior to most rf sources. Combined with a femtosecond-laser-based optical comb to provide the phase coherent clock mechanism linking the optical and microwave spectra, we derive an rf clock signal of comparable stability over an extended period. Measurements suggest the stability ( 5x10(-14) at 1 s) of the cw laser locked on the iodine transition is transferred to every comb component throughout the optical octave bandwidth (from 532 to 1064 nm) with a precision of 3.5x10(-15). Characterization of the performance of the optical clock shows (in-)stability below 3x10(-13) at 1 s (currently limited by the microwave sources), and 4.6x10(-13) over one year.

Journal Article↗
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↗
PubMed2001

Direct splitting of water under visible light irradiation with an oxide semiconductor photocatalyst.

The photocatalytic splitting of water into hydrogen and oxygen using solar energy is a potentially clean and renewable source for hydrogen fuel. The first photocatalysts suitable for water splitting, or for activating hydrogen production from carbohydrate compounds made by plants from water and carbon dioxide, were developed several decades ago. But these catalysts operate with ultraviolet light, which accounts for only 4% of the incoming solar energy and thus renders the overall process impractical. For this reason, considerable efforts have been invested in developing photocatalysts capable of using the less energetic but more abundant visible light, which accounts for about 43% of the incoming solar energy. However, systems that are sufficiently stable and efficient for practical use have not yet been realized. Here we show that doping of indium-tantalum-oxide with nickel yields a series of photocatalysts, In(1-x)Ni(x)TaO(4) (x = 0-0.2), which induces direct splitting of water into stoichiometric amounts of oxygen and hydrogen under visible light irradiation with a quantum yield of about 0.66%. Our findings suggest that the use of solar energy for photocatalytic water splitting might provide a viable source for 'clean' hydrogen fuel, once the catalytic efficiency of the semiconductor system has been improved by increasing its surface area and suitable modifications of the surface sites.

Journal Article↗
PubMed2001

Branching fraction and photon energy spectrum for b --> s gamma.

We have measured the branching fraction and photon energy spectrum for the radiative penguin process b-->s gamma. We find Beta(b-->s gamma) = (3.21+/-0.43+/-0.27(+0.18)(-0.10))x10(-4), where the errors are statistical, systematic, and from theory corrections. We obtain first and second moments of the photon energy spectrum above 2.0 GeV, = 2.346+/-0.032+/-0.011 GeV, and - (2) = 0.0226+/-0.0066+/-0.0020 GeV(2), where the errors are statistical and systematic. From the first moment, we obtain (in the modified minimal subtraction renormalization scheme, to order 1/M(3)(B) and beta(0)alpha(2)(s)) the heavy quark effective theory parameter Lambda = 0.35+/-0.08+/-0.10 GeV.

Journal Article↗
PubMed2001

Hadronic mass moments in inclusive semileptonic B meson decays.

We have measured the first and second moments of the hadronic mass-squared distribution in B-->X(c)l nu, for P(lepton)>1.5 GeV/c. We find = 0.251+/-0.066 GeV(2), <(M(2)(X)- )(2)> = 0.576+/-0.170 GeV(4), where M macro(D) is the spin-averaged D meson mass. From that first moment and the first moment of the photon energy spectrum in b-->s gamma, we find the heavy quark effective theory parameter lambda(1) (in the modified minimal subtraction renormalization scheme, to order 1/M(3)(B) and beta(0)alpha(2)(s)) to be -0.24+/-0.11 GeV(2). Using these first moments and the B semileptonic width, and assuming parton-hadron duality, we obtain absolute value of V(cb) = 0.0404+/-0.0013.

Journal Article↗
PubMed2001

First measurement of gamma(D*(+)).

We present the first measurement of the D*(+) width using 9/fb of e(+)e(-) data collected near the Upsilon(4S) resonance by the CLEO II.V detector. Our method uses advanced tracking techniques and a reconstruction method that takes advantage of the small vertical size of the Cornell Electron-positron Storage Ring beam spot to measure the energy release distribution from the D*(+)-->D(0)pi(+) decay. We find gamma(D*(+)) = 96+/-4 (stat)+/-22 (syst) keV. We also measure the energy release in the decay and compute Delta m identical with m(D*(+))-m(D(0)) = 145.412+/-0.002 (stat)+/-0.012 (syst) MeV/c(2).

Journal Article↗
PubMed2001

Thermally generated vortices, gauge invariance, and electron spectral function in the pseudogap regime.

Starting from the classical vortex fluctuation picture, we study the single electron properties in the pseudogap regime. We show that it is the gauge invariant Green function of spinon which is directly related to ARPES data in the pseudogap regime instead of the nongauge invariant one. We find that the random gauge field from the thermally generated vortices destroys the coherent spinon motion. The energy distribution curves show broad peaks, while the momentum distribution curves show sharp peaks with Lorenz form. The local density of state at zero energy scales as the inverse of Kosterlitz-Thouless length. These results are qualitatively consistent with the ARPES data in the pseudogap regime.

Journal Article↗
PubMed2001

Effects of phospholipid surfactant on apoptosis induction by respirable quartz and kaolin in NR8383 rat pulmonary macrophages.

Apoptosis was measured in rat alveolar macrophage NR8383 cells challenged in vitro with respirable quartz or kaolin dust and with the dusts pretreated with dipalmitoyl phosphatidylcholine (DPPC) to model conditioning of respired dusts by interaction with a primary phospholipid component of pulmonary surfactant. Quartz dust is known to induce apoptosis in vitro and in vivo. For this study, quartz and kaolin were compared as dusts of similar cytotoxicity in some in vitro assays but of differing pathogenic potential: quartz can cause significant pulmonary fibrosis while kaolin generally does not. NR8383 cells exposed to native quartz at concentrations from 50 to 400 microg/ml for 6 h showed a dose-dependent increase in apoptosis measured by the TdT-mediated dUTP-fluorescein nick end labeling (TUNEL), cell death ELISA, and DNA ladder formation assays, while native kaolin induced significant response only at the higher concentrations and only in the TUNEL and ELISA assays. For cell challenge from 6 h to 5 days at 100 microg/ml of dust, quartz was active at all times while kaolin was active only at 5 days. DPPC pre-treatment suppressed quartz activity until 3 days and kaolin activity through 5 days. Cellular release of lactate dehydrogenase, measured in parallel experiments to compare dust apoptotic and necrotic activities, indicated that components of serum as well as surfactant may affect kaolin in vitro expression of those activities.

1,2-Dipalmitoylphosphatidylcholine↗
PubMed2001

Search for the decay upsilon(1S) --> gammaeta(').

We report on a search for the radiative decay Upsilon(1S)-->gammaeta(') in 61.3 pb(-1) of data taken with the CLEO II detector at the Cornell Electron Storage Ring. Three decay chains were investigated, all involving eta(')-->pi(+)pi(-)eta, followed by eta-->gammagamma, eta-->pi(0)pi(0)pi(0), or eta-->pi(+)pi(-)pi(0). We find no candidate events in any of the three cases and set a combined upper limit of 1.6x10(-5) at 90% C.L., significantly smaller than the previous limit. We compare our result to other radiative Upsilon decays, to radiative J/psi decays, and to theoretical predictions.

Journal Article↗