Bridge stents in the management of obstructive vascular lesions in children.
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Adolescent↗
Biomedical subjects
S Chen
Publications and source records attributed to S Chen.
FTY720: altered lymphocyte traffic results in allograft protection.
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Animals↗
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↗
[Tumor targeted expression of adenovirus mediated CDglyTK gene regulated by irradiation via Egr-1 promoter].
OBJECTIVE: To construct adenoviral vecter of AdEgr-CD/TK in which CDglyTK gene was driven by Egr-1 promoter, and control the tumor targeted expression of CDglyTK gene by gamma irradiation so as to observe the effects of gene-radiotherapy of liver cancer. METHODS: Adenoviral vector of AdEgr-CD/TK was generated through homologous recombination in bacteria. The expression of CDglyTK gene in MM45T. Li cells infected with AdEgr-CD/TK and exposed to different doses of gamma irradiation were analyzed, and the relative survival rate of the cells in presence of prodrugs 5-FC and GCV was tested. In addition, the tumor suppression effects of different treatments were investigated in 64 mice bearing liver cancer by observing the size of tumor at interval of four days. RESULTS: In vitro experiment showed that gamma irradiation markedly and dose-dependently induced CDglyTK expression in MM45T. Li tumor cells, and significantly enhanced the sensitivity of MM45T. Li cells infected with AdEgr-CD/TK to prodrugs 5-FC or GCV resulting in cell being killed (P < 0.01). A synergetic cytotoxic effect was found when both 5-FC and GCV were added. In vivo experiment revealed that, compared with other control treatments, intratumoral injection of AdEgr-CD/TK combined with intraperitoneal injection of GCV + 5-FC and TLI obviously suppressed tumor growth (P < 0.01), with 30% of the tumor eradicated completely while without causing the increase of whole body cytotoxic effect. CONCLUSION: Tumor targeted expression of CDglyTK gene under the control of irradiation represents a novel strategy for safe and effective gene therapy of cancer and might have wide application in the future.
Adenoviridae↗
Targeted alpha(1A)-adrenergic receptor overexpression induces enhanced cardiac contractility but not hypertrophy.
Activation of the alpha(1A)-adrenergic receptor (alpha(1A)-AR)/Gq pathway has been implicated as a critical trigger for the development of cardiac hypertrophy. However, direct evidence from in vivo studies is still lacking. To address this issue, transgenic mice with cardiac-targeted overexpression of the alpha(1A)-AR (4- to 170-fold) were generated, using the rodent alpha-myosin heavy chain promoter. Heterozygous animals displayed marked enhancement of cardiac contractility, evident from increases in dP/dt(max) (80%, P<0.0001), dP/dt(max)/LVP(inst) (76%, P<0.001), dP/dt(max):dP/dt(min) (104%, P<0.0001), and fractional shortening (33%, P<0.05). Moreover, changes in the dP/dt(max)-end-diastolic volume relationship provided load-independent evidence of a primary increase in contractility. Blood pressure and heart rate were largely unchanged, and there was a small increase in (-)norepinephrine-stimulated, but not basal, phospholipase C activity. Increased contractility was directly related to the level of receptor overexpression and could be completely reversed by acute alpha(1A)- but not beta-AR blockade. Despite the robust changes in contractility, transgenic animals displayed no morphological, histological, or echocardiographic evidence of left ventricular hypertrophy. In addition, apart from an increase in atrial natriuretic factor mRNA, expression of other hypertrophy-associated genes was unchanged. To our knowledge, these data provide the first in vivo evidence for an inotropic action of the alpha(1A)-AR.
Adenylyl Cyclases↗
A microtiter plate assay for polyglutamine aggregate extension.
Polyglutamine (polyGln) aggregates are neuropathological markers of expanded CAG repeat disorders, and may also play a critical role in the development of these diseases. We have established a highly sensitive, fast, reproducible, and specific assay capable of monitoring aggregate-dependent deposition of polyglutamine peptides. This assay allows detailed studies on various aspects of aggregation kinetics, and also makes possible the detection and quantitation of low levels of "extension-competent" aggregates. In the simplest form of this assay, polyGln aggregates are made from chemically synthesized peptides and immobilized onto microplate wells. These wells are incubated for different times with low concentrations of a soluble biotinylated polyGln peptide. Europium-streptavidin complexation of the immobilized biotin, followed by time-resolved fluorescence detection of the deposited europium, allows us to calculate the rate (fmol/h) of incorporation of polyGln peptides into polyGln aggregates. This assay will make possible basic studies on the assembly mechanism of polyGln aggregates and on critical features of the reaction, such as polyGln length dependence. The assay also will be a valuable tool for screening and characterizing anti-aggregation inhibitors. It will also be useful for detection and quantitation of aggregation-competent polyGln aggregates in biological materials, which may prove to be of critical importance in understanding the disease mechanism.
Humans↗
Suppression of tumor necrosis factor-mediated apoptosis by nuclear factor kappaB-independent bone morphogenetic protein/Smad signaling.
The activation of nuclear factor kappaB (NF-kappa B) plays a pivotal role in the regulation of tumor necrosis factor (TNF)-mediated apoptosis. However, little is known about the regulation of TNF-mediated apoptosis by other signaling pathways or growth factors. Here, unexpectedly, we found that bone morphogenetic protein (BMP)-2 and BMP-4 inhibited TNF-mediated apoptosis by inhibition of caspase-8 activation in C2C12 cells, a pluripotent mesenchymal cell line that has the potential to differentiate into osteoblasts depending on BMP stimulation. Utilizing both a trans-dominant IkappaBalpha inhibitor of NF-kappaB expressed in C2C12 cells and IkappaB kinase beta-deficient embryonic mouse fibroblast, we show that BMP-mediated survival was independent of NF-kappaB activation. Rather, the antiapoptotic activity of BMPs functioned through the Smad signaling pathway. Thus, these findings provide the first report of a BMP/Smad signaling pathway that can inhibit TNF-mediated apoptosis, independent of the prosurvival activity of NF-kappaB. Our results suggest that BMPs not only stimulate osteoblast differentiation but can also promote cell survival during the induction of bone formation, offering new insight into the biological functions of BMPs.
Animals↗
A novel method for the preparation of amino-substituted hypocrellin B.
A series of amino-substituted hypocrellins derived from hypocrellin B (HB) were synthesized by a novel mild method, in which the peri-hydroxylated perylenequinone structure of hypocrellin was preserved by the reaction of HB with an amine. The red absorption of the resulting products was significantly enhanced relative to the parent hypocrellins, which will significantly improve its photodynamic therapy effectiveness.
Anti-HIV Agents↗
Novel differences between two human prion strains revealed by two-dimensional gel electrophoresis.
The phenotype of human sporadic prion diseases is affected by patient genotype at codon 129 of the prion protein (PrP) gene, the site of a common methionine/valine polymorphism, and by the type of the scrapie PrP (PrP(Sc)), which likely reflects the prion strain. However, two distinct disease phenotypes, identified as sporadic Creutzfeldt-Jakob disease (M/M2 sCJD) and sporadic fatal insomnia (sFI), share methionine homozygosity at codon 129 and PrP(Sc) type 2. One-dimensional gel electrophoresis and immunoblotting reveal no difference between the M/M2 sCJD and sFI species of PrP(Sc) in gel mobility and glycoform ratio. In contrast, the two-dimensional immunoblot demonstrates that in M/M2 sCJD the full-length PrP(Sc) form is overrepresented and carries glycans that are different from those present in the PrP(Sc) of sFI. Because the altered glycans are detectable only in the PrP(Sc) and not in the normal or cellular PrP (PrP(C)), they are likely to result from preferential conversion to PrP(Sc) of rare PrP(C) glycoforms. This is the first evidence that a qualitative difference in glycans contributes to prion diversity.
Electrophoresis, Gel, Two-Dimensional↗
Phase diagram of an asymmetric spin ladder.
We investigate an asymmetric zigzag spin ladder with different exchange integrals on both legs using bosonization and renormalization group approaches. When the leg exchange integrals and frustration both are sufficiently small, renormalization group analysis shows that the Heisenberg critical point flows to an intermediate-coupling fixed point with gapless excitations and a vanishing spin velocity. When they are large, a spin gap opens and a dimer liquid is realized. Here, we find a continuous manifold of Hamiltonians with dimer product ground states, interpolating between the Majumdar-Ghosh and sawtooth spin-chain model.
Journal Article↗
Polyglutamine aggregation behavior in vitro supports a recruitment mechanism of cytotoxicity.
In expanded CAG repeat diseases such as Huntington's disease, proteins containing polyglutamine (poly(Gln)) sequences with repeat lengths of about 37 residues or more are associated with development of both disease symptoms and neuronal intranuclear inclusions (NIIs). Disease physiology in animal and cellular models does not always correlate with NII formation, however, and the mechanism by which aggregate formation might lead to cytotoxicity is unknown. To help evaluate various possible mechanisms, we determined the biophysical properties of a series of simple poly(Gln) peptides. The circular dichroism spectra of poly(Gln) peptides with repeat lengths of five, 15, 28 and 44 residues are all nearly identical and are consistent with a high degree of random coil structure, suggesting that the length-dependence of disease is not related to a conformational change in the monomeric states of expanded poly(Gln) sequences. In contrast, there is a dramatic increase in both the kinetics and the thermodynamic favorability of the spontaneous formation of ordered, amyloid-like aggregates for poly(Gln) peptides with repeat lengths of greater than 37 residues. At the same time, poly(Gln) peptides with repeat lengths in the 15-20 residue range, despite their poor abilities to support spontaneous, self-nucleated aggregation, are capable of efficiently adding to an already-formed aggregate. We also find that morphologically small, finely divided aggregates are much more efficient at recruiting poly(Gln) peptides than are large aggregates, suggesting a possible explanation for why disease pathology does not always correlate with the observable NII burden. Together, these data are consistent with a model for disease pathology in which critical cellular proteins possessing poly(Gln) sequences of modest length become inactivated when they are recruited into aggregates of an expanded poly(Gln) protein.
Aluminum Silicates↗
Rate measurement of D(0)-->K+pi(-)pi(0) and constraints on D(0) -- D(0) mixing.
We present an observation and time-integrated rate measurement of the decay D(0)-->K(+)pi(-)pi(0) produced in 9 fb(-1) of e(+)e(-) collisions near the Upsilon(4S) resonance. The signal is inconsistent with an upward fluctuation of the background by 4.9 standard deviations. We measured the time-integrated rate of D(0)-->K(+)pi(-)pi(0) normalized to the rate of D(0)-->K(+)pi(-)pi(0) to be 0.0043(+0.0011)(-0.0010) (stat)+/-0.0007 (syst). This decay can be produced by doubly Cabibbo-suppressed decays or by the D(0) evolving into a D(0) through mixing, followed by a Cabibbo-favored decay to K(+)pi(-)pi(0). We also found the CP asymmetry A = (9(+25)(-22))% be consistent with zero.
Journal Article↗
Experimental investigation of the two-photon widths of the chi(c0) and the chi(c2) mesons.
Using 12.7 fb(-1) of data collected with the CLEO detector at CESR, we observed two-photon production of the cc states chi(c0) and chi(c2) in their decay to pi(+)pi(-)pi(+)pi(-). We measured gamma(gammagamma)(chi(c))xB(chi(c)-->pi(+)pi(-)pi(+)pi(-)) to be 75+/-13(stat)+/-8(syst) eV for the chi(c0) and 6.4+/-1.8(stat)+/-0.8(syst) eV for the chi(c2), implying gamma(gammagamma)(chi(c0)) = 3.76+/-0.65(stat)+/-0.41(syst)+/-1.69(br) keV and gamma(gammagamma)(chi(c2)) = 0.53+/-0.15(stat)+/-0.06(syst)+/-0.22(br) keV. Also, cancellation of dominant experimental and theoretical uncertainties permits a precise comparison of gamma(gammagamma)(chi(c0))/gamma(gammagamma)(chi(c2)), evaluated to be 7.4+/-2.4(stat)+/-0.5(syst)+/-0.9(br), with QCD-based predictions.
Journal Article↗
Effects of sulfur impregnation temperature on the properties and mercury adsorption capacities of activated carbon fibers (ACFs).
Laboratory studies were conducted to determine the role of sulfur functional groups and micropore surface area of carbon-based adsorbents on the adsorption of Hg0 from simulated coal combustion flue gases. In this study, raw activated carbon fibers that are microporous (ACF-20) were impregnated with elemental sulfur between 250 and 650 degrees C. The resulting samples were saturated with respect to sulfur content. Total sulfur content of the sulfur impregnated ACF samples decreased with increasing impregnation temperatures from 250 and 500 degrees C and then remained constant to 650 degrees C. Results from sulfur K-edge X-ray absorption near-edge structure (S-XANES) spectroscopy showed that sulfur impregnated on the ACF samples was in both elemental and organic forms. As sulfur impregnation temperature increased, however, the relative amounts of elemental sulfur decreased with a concomitant increase in the amount of organic sulfur. Thermal analyses and mass spectrometry revealed that sulfur functional groups formed at higher impregnation temperatures were more thermally stable. In general, sulfur impregnation decreased surface area and increased equilibrium Hg0 adsorption capacity when compared to the raw ACF sample. The ACF sample treated with sulfur at 400 degrees C had a surface area of only 94 m2/g compared to the raw ACF sample's surface area of 1971 m2/g, but at least 86% of this sample's surface area existed as micropores and it had the largest equilibrium Hg0 adsorption capacities (2211-11,343 micrograms/g). Such a result indicates that 400 degrees C is potentially an optimal sulfur impregnation temperature for this ACF. Sulfur impregnated on the ACF that was treated at 400 degrees C was in both elemental and organic forms. Thermal analyses and CS2 extraction tests suggested that elemental sulfur was the main form of sulfur affecting the Hg0 adsorption capacity. These findings indicate that both the presence of elemental sulfur on the adsorbent and a microporous structure are important properties for improving the performance of carbon-based adsorbents for the removal of Hg0 from coal combustion flue gases.
Adsorption↗
Differential gene regulation in human versus rodent hepatocytes by peroxisome proliferator-activated receptor (PPAR) alpha. PPAR alpha fails to induce peroxisome proliferation-associated genes in human cells independently of the level of receptor expresson.
We compared the ability of rat and human hepatocytes to respond to fenofibric acid and a novel potent phenylacetic acid peroxisome proliferator-activated receptor (PPAR) alpha agonist (compound 1). Fatty acyl-CoA oxidase (FACO) activity and mRNA were increased after treatment with either fenofibric acid or compound 1 in rat hepatocytes. In addition, apolipoprotein CIII mRNA was decreased by both fenofibric acid and compound 1 in rat hepatocytes. Both agonists decreased apolipoprotein CIII mRNA in human hepatocytes; however, very little change in FACO activity or mRNA was observed. Furthermore, other peroxisome proliferation (PP)-associated genes including peroxisomal 3-oxoacyl-CoA thiolase (THIO), peroxisomal enoyl-CoA hydratase/3-hydroxyacyl-CoA dehydrogenase (HD), peroxisomal membrane protein-70 (PMP-70) were not regulated by PPAR alpha agonists in human hepatocytes. Moreover, other genes that are regulated by PPAR alpha ligands in human hepatocytes such as mitochondrial HMG-CoA synthase and carnitine palmitoyl transferase-1 (CPT-1) were also regulated in HepG2 cells by PPAR alpha agonists. Several stably transfected HepG2 cell lines were established that overexpressed human PPAR alpha to levels between 6- and 26-fold over normal human hepatocytes. These PPAR alpha-overexpressing cells had higher basal mRNA levels of mitochondrial HMG-CoA synthase and CPT-1; however, basal FACO mRNA levels and other PP-associated genes including THIO, HD, or PMP-70 mRNA were not substantially affected. In addition, FACO, THIO, HD, and PMP-70 mRNA levels did not increase in response to PPAR alpha agonist treatment in the PPAR alpha-overexpressing cells, although mitochondrial HMG-CoA synthase and CPT-1 mRNAs were both induced. These results suggest that other factors besides PPAR alpha levels determine the species-specific response of human and rat hepatocytes to the induction of PP.
3-Hydroxyacyl CoA Dehydrogenases↗
Controlling dissipative and Hamiltonian chaos by a constant periodic pulse method.
A constant periodic pulse method is proposed to control dissipative and Hamiltonian chaos. Using the convergence of the chaotic orbit in finite time, the stable segment of the chaotic orbit that satisfies the desired dynamical features can be made to form a closed orbit by the action of a proper perturbation on the system variables. A way to determine the intensity of the perturbation and the corresponding fixed points is presented. The method is robust against the presence of external noise.
Journal Article↗
Transcription factor RF2a alters expression of the rice tungro bacilliform virus promoter in transgenic tobacco plants.
The promoter from rice tungro bacilliform badnavirus (RTBV) is expressed only in phloem tissues in transgenic rice plants. RF2a, a b-Zip protein from rice, is known to bind to the Box II cis element near the TATA box of the promoter. Here, we report that the full-length RTBV promoter and a truncated fragment E of the promoter, comprising nucleotides -164 to +45, result in phloem-specific expression of beta-glucuronidase (GUS) reporter genes in transgenic tobacco plants. When a fusion gene comprising the cauliflower mosaic virus 35S promoter and RF2a cDNA was coexpressed with the GUS reporter genes, GUS activity was increased by 2-20-fold. The increase in GUS activity was positively correlated with the amount of RF2a, and the expression pattern of the RTBV promoter was altered from phloem-specific to constitutive. Constitutive expression of RF2a did not induce morphological changes in the transgenic plants. In contrast, constitutive overexpression of the b-ZIP domain of RF2a had a strong effect on the development of transgenic plants. These studies suggest that expression of the b-Zip domain can interfere with the function of homologues of RF2a that regulate development of tobacco plants.
Agrobacterium tumefaciens↗
Bimp1, a MAGUK family member linking protein kinase C activation to Bcl10-mediated NF-kappaB induction.
Bcl10 and MALT1, products of distinct chromosomal translocations in mucosa-associated lymphoid tissue lymphoma, cooperate in activating NF-kappaB. Mice lacking Bcl10 demonstrate severe immunodeficiency associated with failure of lymphocytes to activate nuclear factor kappaB (NF-kappaB) in response to antigen receptor stimulation and protein kinase C activation. We characterize Bimp1, a new signaling protein that binds Bcl10 and activates NF-kappaB. Bimp1-mediated NF-kappaB activation requires Bcl10 and IkappaB kinases, indicating that Bimp1 acts upstream of these mediators. Bimp1, Bcl10, and MALT1 form a ternary complex, with Bcl10 bridging the Bimp1/MALT1 interaction. A dominant negative Bimp1 mutant inhibits NF-kappaB activation by anti-CD3 ligation, phorbol ester, and protein kinase C expression. These results suggest that Bimp1 links surface receptor stimulation and protein kinase C activation to Bcl10/MALT1, thus leading to NF-kappaB induction.
Adaptor Proteins, Signal Transducing↗