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S Chuang

Publications and source records attributed to S Chuang.

At least 37 records · Page 2Linked to original sources
PubMed2004

Measurement of the tt production cross section in pp collisions at sqrt[s]=1.96 TeV using dilepton events.

We report a measurement of the tt production cross section using dilepton events with jets and missing transverse energy in pp collisions at a center-of-mass energy of 1.96 TeV. Using a 197+/-12 pb(-1) data sample recorded by the upgraded Collider Detector at Fermilab, we use two complementary techniques to select candidate events. We compare the number of observed events and selected kinematical distributions with the predictions of the standard model and find good agreement. The combined result of the two techniques yields a tt production cross section of 7.0(+2.4)(-2.1)(stat)+1.6-1.1(syst)+/-0.4(lum) pb.

Journal Article↗
PubMed2004

Search for B0s-->micro+micro- and B0d-->micro+micro- decays in pp collisions at square root s = 1.96 TeV.

We report on a search for B(0)(s)-->micro(+)micro(-) and B(0)(d)-->micro(+)micro(-) decays in pp collisions at square root of s=1.96 TeV using 171 pb(-1) of data collected by the CDF II experiment at the Fermilab Tevatron Collider. The decay rates of these rare processes are sensitive to contributions from physics beyond the standard model. One event survives all our selection requirements, consistent with the background expectation. We derive branching ratio limits of B(B(0)(s)-->micro(+)micro(-))<5.8x10(-7) and B(B(0)(d)-->micro(+)micro(-))<1.5x10(-7) at 90% confidence level.

Journal Article↗
PubMed2002

IL-13-dependent autocrine signaling mediates altered responsiveness of IgE-sensitized airway smooth muscle.

In testing the hypothesis that interleukin-4 receptor alpha-subunit (IL-4R alpha)-coupled signaling mediates altered airway smooth muscle (ASM) responsiveness in the atopic sensitized state, isolated rabbit tracheal ASM segments were passively sensitized with immunoglobulin E (IgE) immune complexes, both in the absence and presence of an IL-4R alpha blocking antibody (anti-IL-4R alpha Ab). Relative to control ASM, IgE-sensitized tissues exhibited enhanced isometric constrictor responses to administered ACh and attenuated relaxation responses to isoproterenol. These proasthmatic-like effects were prevented in IgE-sensitized ASM that were pretreated with anti-IL-4R alpha Ab. In complementary experiments, IgE-sensitized cultured human ASM cells exhibited upregulated expression of IL-13 mRNA and protein, whereas IL-4 expression was undetected. Moreover, extended studies demonstrated that 1) exogenous IL-13 administration to naïve ASM elicited augmented contractility to ACh and impaired relaxation to isoproterenol, 2) these effects of IL-13 were prevented by pretreating the tissues with an IL-5 receptor blocking antibody, and 3) IL-13 administration induced upregulated mRNA expression and release of IL-5 protein from cultured ASM cells. Collectively, these findings provide new evidence demonstrating that the altered responsiveness of IgE-sensitized ASM is largely attributed to activation of an intrinsic Th2-type autocrine mechanism involving IL-13/IL-4R alpha-coupled release and action of IL-5 in the sensitized ASM itself.

Acetylcholine↗
PubMed2001

Neuromagnetic spectral distribution of implicit processing of words.

Neuromagnetic spectral distributions when silently viewing words and non-words were investigated using a 151-channel whole head MEG system. The data were analyzed with synthetic aperture magnetometry (SAM). The dominant changes of spectral power were identified in the parietal and occipital cortices in 15-30 Hz, 30-60 Hz and 60-125 Hz bands following both word and non-word stimulations. The changes in Broca's and Wernicke's areas were consistently observed in 60-125 Hz bands, mainly following word stimulation. The results indicated that the occipital and parietal cortices were most probably involved in visuospatial processing of words and non-words. The language areas, particularly Broca's and Wernickes's areas, might be involved in implicit word processing such as verbal searching and/or internal speech.

Adult↗
PubMed2001

Rhinovirus elicits proasthmatic changes in airway responsiveness independently of viral infection.

BACKGROUND: Rhinovirus (RV), the principal pathogen responsible for the common cold, is importantly implicated in triggering attacks of asthma secondary to changes in airway responsiveness. OBJECTIVE: Because the airway histopathologic features of RV infection are relatively modest, we tested the hypothesis that RV can directly elicit proasthmatic-like changes in airway smooth muscle (ASM) responsiveness independently of actual viral infection and its associated cytopathic effects. METHODS: Isolated ASM tissues and cultured ASM cells were inoculated with either infectious or noninfectious (UV-irradiated) RV16 and RV2, the latter serotypes belonging to the "major" and "minor" groups of RV subtypes, respectively. ASM constrictor and relaxant responsiveness, G(i) protein expression, and proinflammatory cytokine release were subsequently compared under the different treatment conditions. RESULTS: In contrast to RV2, which had no effect, RV16 inoculation elicited enhanced ASM contractility and impaired relaxation to cholinergic and beta-adrenergic agonists, respectively, in association with increased ASM membrane G(i) protein expression and induced release of the proinflammatory cytokines IL-5 and IL-1beta. These proasthmatic-like effects were also observed in ASM exposed to UV-irradiated RV16, wherein viral replication was completely inhibited. In contrast, pretreatment of ASM with a neutralizing antibody directed against ICAM-1, the host receptor for the "major" group of RVs, completely abrogated the proasthmatic effects of RV16. CONCLUSIONS: The results demonstrate that (1) RV16 elicits proasthmatic changes in ASM responsiveness that can occur independently of actual viral infection of the ASM and (2) the effects of RV16 are attributed solely to binding of the virus to its host receptor (ICAM-1) on the ASM cell surface. Collectively, these findings support the notion that RV-induced exacerbation of wheezing in asthmatic individuals can occur even in the absence of any cytopathology associated with viral infection.

Animals↗
PubMed2001

Mechanism of cooperative effects of rhinovirus and atopic sensitization on airway responsiveness.

To elucidate the mechanistic interplay between rhinovirus (RV) exposure and atopic sensitization in regulating airway smooth muscle (ASM) responsiveness, isolated rabbit ASM tissue and cultured human ASM cells were passively sensitized with sera from atopic asthmatic or nonatopic nonasthmatic (control) subjects in the absence and presence of inoculation with RV serotype 16. Relative to control subjects, atopic asthmatic serum-sensitized and RV-inoculated ASM exhibited significantly increased contractility to acetylcholine, impaired relaxation to isoproterenol, and enhanced release of the proinflammatory cytokine interleukin-1beta. These effects were potentiated in atopic asthmatic serum-sensitized ASM concomitantly inoculated with RV and inhibited by pretreating the tissues with monoclonal blocking antibodies against intercellular adhesion molecule (ICAM)-1 (CD54), the host receptor for RV serotype 16, or lymphocyte function-associated antigen (LFA)-1 (CD11a/CD18), the endogenous counterreceptor for ICAM-1. Moreover, RV inoculation was found to potentiate the induction of mRNA and surface protein expression of FcepsilonRII (CD23), the low-affinity receptor for IgE, in atopic asthmatic serum-sensitized ASM. Collectively, these observations provide new evidence demonstrating that 1) RV exposure and atopic sensitization act cooperatively to potentiate induction of proasthmatic changes in ASM responsiveness in association with upregulated proinflammatory cytokine release and FcepsilonRII expression and 2) the effects of RV exposure and atopic sensitization are mediated by cooperative ICAM-1-coupled LFA-1 signaling in the ASM itself.

Acetylcholine↗
PubMed2001

Autocrine signaling by IL-10 mediates altered responsiveness of atopic sensitized airway smooth muscle.

To elucidate the role and mechanism of action of interleukin (IL)-10 in regulating airway smooth muscle (ASM) responsiveness in the atopic asthmatic state, isolated rabbit tracheal ASM segments were passively sensitized with serum from atopic asthmatic patients or nonatopic nonasthmatic (control) subjects in both the absence and presence of an anti-IL-10 receptor blocking antibody (Ab). Relative to control ASM, atopic asthmatic serum-sensitized tissues exhibited enhanced isometric constrictor responses to administered acetylcholine and attenuated the relaxation responses to isoproterenol. These proasthmatic effects were prevented in atopic asthmatic serum-sensitized ASM that was pretreated with anti-IL-10 receptor Ab. In complementary experiments, exposure of cultured human ASM cells to atopic asthmatic serum induced upregulated expression of IL-10 mRNA. Moreover, extended studies demonstrated that 1) exogenous IL-10 administration to naive ASM elicited augmented contractility to acetylcholine and impaired relaxation to isoproterenol, 2) these effects of IL-10 were prevented by pretreating the tissues with an IL-5 receptor Ab, and 3) IL-10 administration induced upregulated mRNA expression and release of IL-5 protein from cultured ASM cells. Collectively, these findings provide new evidence demonstrating that the altered responsiveness of atopic asthmatic serum-sensitized ASM is largely attributed to activation of an intrinsic T helper type 2-type autocrine mechanism involving IL-10-mediated release and the action of IL-5 in the sensitized ASM itself.

Acetylcholine↗
PubMed2000

Comparative study of inter- and intrahemispheric somatosensory functions in children with partial and complete agenesis of the corpus callosum.

Inter- and intrahemispheric somatosensory functions were evaluated in blinded tests of 11 children with partial and complete agenesis of the corpus callosum (age range 2 years 8 months to 11 years 9 months) and compared with those of age- and sex-matched control individuals both normally developing and with neurological impairment. Tests included uni- and bimanual measures of stereognosis, haptic visual discrimination, kinaesthesis, and texture matching. Children with callosal absence displayed significant difficulties with many somatosensory functions, but most deficits were no greater than those of the children who had neurological dysfunction and an intact corpus callosum. Children with callosal absence, however, had significantly greater difficulty with bimanual texture matching, seemingly because this task required refined spatial interpretation of somatosensory input. Response times for the individuals with callosal absence were significantly greater than those for control participants with neurological impairment on several tasks in which overall accuracy of performance among groups did not significantly differ. These findings suggest that children with agenesis of the corpus callosum may have less efficient and slower processing capacity for certain types of somatosensory information. Possible compensatory mechanisms are discussed.

Agenesis of Corpus Callosum↗
PubMed2000

Autocrine cytokine signaling mediates effects of rhinovirus on airway responsiveness.

The airway responses to allergen exposure in allergic asthma are qualitatively similar to those elicited by specific viral respiratory pathogens, most notably rhinovirus (RV), suggesting that the altered airway responsiveness seen in allergic asthma and that elicited by viral respiratory tract infection may share a common underlying mechanism. To the extent that T helper cell type 2 (Th2) cytokines have been implicated in the pathogenesis of allergic asthma, this study examined the potential role(s) of Th2-type cytokines in mediating pro-asthmatic-like changes in airway smooth muscle (ASM) responsiveness after inoculation of naive ASM with human RV. Isolated rabbit ASM tissues and cultured human ASM cells were exposed to RV (serotype 16) for 24 h in the absence and presence of monoclonal blocking antibodies (MAbs) or antagonists directed against either the Th2-type cytokines interleukin (IL)-4 and IL-5, intercellular adhesion molecule (ICAM)-1 (the endogenous host receptor for most RVs), or the pleiotropic proinflammatory cytokine IL-1beta. Relative to control (vehicle-treated) tissues, RV-exposed ASM exhibited significantly enhanced isometric contractility to acetylcholine and impaired relaxation to isoproterenol. These pro-asthmatic-like changes in ASM responsiveness were ablated by pretreating the RV-exposed tissues with either IL-5-receptor-alpha blocking antibody or human recombinant IL-1-receptor antagonist, whereas IL-4 neutralizing antibody had no effect. Extended studies further demonstrated that inoculation of ASM cells with RV elicited 1) an increased mRNA expression and release of IL-5 protein, which was inhibited in the presence of anti-ICAM-1 MAb, and 2) an enhanced release of IL-1beta protein, which was inhibited in the presence of IL-5 receptor-alpha antibody. Collectively, these observations provide new evidence demonstrating that RV-induced changes in ASM responsiveness are largely attributed to ICAM-1-dependent activation of a cooperative autocrine signaling mechanism involving upregulated IL-5-mediated release of IL-1beta by the RV-exposed ASM itself.

Animals↗
PubMed2000

Intrinsic ICAM-1/LFA-1 activation mediates altered responsiveness of atopic asthmatic airway smooth muscle.

Cell adhesion molecules (CAMs) have been importantly implicated in the pathobiology of the airway responses in allergic asthma, including inflammatory cell recruitment into the lungs and altered bronchial responsiveness. To elucidate the mechanism of CAM-related mediation of altered airway responsiveness in the atopic asthmatic state, the expressions and actions of intercellular adhesion molecule-1 (ICAM-1) and its counterreceptor ligand lymphocyte function-associated antigen-1 (LFA-1; i.e., CD11a/CD18) were examined in isolated rabbit airway smooth muscle (ASM) tissues and cultured human ASM cells passively sensitized with sera from atopic asthmatic patients or nonatopic nonasthmatic (control) subjects. Relative to control tissues, the atopic asthmatic sensitized ASM exhibited significantly enhanced maximal contractility to acetylcholine and attenuated relaxation responses to isoproterenol. These proasthmatic changes in agonist responsiveness were ablated by pretreating the atopic sensitized tissues with a monoclonal blocking antibody (MAb) to either ICAM-1 or CD11a, whereas a MAb directed against the related beta(2)-integrin Mac-1 had no effect. Moreover, relative to control tissues, atopic asthmatic sensitized ASM cells displayed an autologously upregulated mRNA and cell surface expression of ICAM-1, whereas constitutive expression of CD11a was unaltered. Extended studies further demonstrated that 1) the enhanced expression and release of soluble ICAM-1 by atopic sensitized ASM cells was prevented when cells were pretreated with an interleukin (IL)-5-receptor-alpha blocking antibody and 2) administration of exogenous IL-5 to naive (nonsensitized) ASM cells induced a pronounced soluble ICAM-1 release from the cells. Collectively, these observations provide new evidence demonstrating that activation of the CAM counterreceptor ligands ICAM-1 and LFA-1, both of which are endogenously expressed in ASM cells, elicits autologously upregulated IL-5 release and associated changes in ICAM-1 expression and agonist responsiveness in atopic asthmatic sensitized ASM.

Animals↗
PubMed2000

Primary malignant rhabdoid tumor of the brain: CT and MR findings.

PURPOSE: To describe the CT and MR findings of primary malignant rhabdoid tumor (MRT) of the brain, which is a rare but very aggressive neoplasm in childhood. MATERIALS AND METHODS: Retrospectively, we evaluated the CT and MR findings of 5 patients of primary MRT of the brain with a review of clinical records. RESULTS: The primary MRTs of the brain were large (n = 4) with a tendency to be associated with necrosis, hemorrhage (n = 2) and calcification (n = 2). Solid components of the tumor showed increased attenuation on precontrast CT scan and iso- or slightly hyper-signal intensity on T2-weighted images probably due to hypercellularity. Solid components of the tumor were also well enhanced on contrast-enhanced CT scan (n = 5) and MRI (n = 2). In 1 case with intratumoral bleeding, MR findings were variable on T1-weighted and T2-weighted images. Intracranial and intraspinal metastasis were found in 2 cases on preoperative MR studies. Follow-up CT and MR studies showed recurrence of the tumor and/or leptomeningeal metastasis in 3 cases. CONCLUSIONS: Although CT and MR findings of primary MRT of the brain are nonspecific, a tendency toward large size, calcification and intratumoral bleeding may be attributed to CT and MR findings. The solid components of tumors could present hyperdense on precontrast CT scan and iso- or slightly hyper-signal intensity on T2-weighted MR image. Preoperative and follow-up MR studies are important to detect metastatic foci.

Adolescent↗
PubMed1999

Distribution of salicylic acid in human stratum corneum following topical application in vivo: a comparison of six different formulations.

Distribution of salicylic acid in human stratum corneum from treatment of six different formulations was assessed by quantitation of drug content in sequentially tape-stripped stratum corneum after a single 2-h dose was applied unoccluded to skin on the ventral forearm of four female subjects. The profile and total amounts of stratum corneum removed in 20 tape-strips varied among different types of formulations. With or without normalization by the total stratum corneum weights removed, the extent of drug delivery to the stratum corneum decreased in the following order: SA (5%) > > SAC (10%), Duofilm (16.7%) > TSSS (2%) > SAO (10%), Salic (2.5%), the percentage in parentheses indicating the salicylic acid concentration in each formulation. The greatest topical bioavailability was observed for the alcoholic solution containing glycerol (SA). The 10% collodion formulation (SAC) was found to deliver an amount of salicylic acid into the stratum corneum 2-fold greater than 10% ointment formulation (SAO). Use of absorption ointment (TSSS) also increased the uptake of salicylic acid into the stratum corneum in comparison with formulations based on simple ointment (SAO) and oil in water (o/w) cream (Salic). The partitioning of salicylic acid from collodion formulations (SAC and Duofilm) appeared to be concentration-independent. The results of this study indicate that topical bioavailability of salicylic acid in the stratum corneum varies substantially among different formulations.

Adhesives↗
PubMed1999

Autocrine interaction between IL-5 and IL-1beta mediates altered responsiveness of atopic asthmatic sensitized airway smooth muscle.

T-helper type 2 (Th2) cytokines have been implicated in the pathogenesis of the pulmonary inflammatory response and altered bronchial responsiveness in allergic asthma. To elucidate the mechanism of Th2-dependent mediation of altered airway responsiveness in the atopic asthmatic state, the expression and actions of specific cytokines were examined in isolated rabbit and human airway smooth muscle (ASM) tissues and cultured cells passively sensitized with sera from atopic asthmatic patients or nonatopic/nonasthmatic (control) subjects. Relative to control tissues, the atopic asthmatic sensitized ASM exhibited significantly enhanced maximal isometric contractility to acetylcholine and attenuated relaxation responses to isoproterenol. These proasthmatic changes in agonist responsiveness were ablated by pretreating the atopic sensitized tissues with either an IL-5 receptor blocking antibody (IL-5ra) or the human recombinant IL-1 receptor antagonist (IL-1ra), whereas an IL-4 neutralizing antibody had no effect. Moreover, relative to controls, atopic asthmatic sensitized ASM cells demonstrated an initial, early (after 3 hours of incubation) increased mRNA expression and protein release of IL-5. This was followed (after 6 hours of incubation) by an enhanced mRNA expression and release of IL-1beta protein, an effect that was inhibited in sensitized cells pretreated with IL-5ra. Extended studies demonstrated that naive ASM exposed to exogenously administered IL-5 exhibited an induced upregulated mRNA expression and protein release of IL-1beta associated with proasthmatic-like changes in ASM constrictor and relaxant responsiveness, and that these effects were ablated in tissues pretreated with IL-1ra. Taken together, these observations provide new evidence that (a) the Th2 cytokine IL-5 and the pleiotropic proinflammatory cytokine IL-1beta are endogenously released by atopic asthmatic sensitized ASM and mechanistically interact to mediate the proasthmatic perturbations in ASM responsiveness; and (b) the nature of this interaction is given by an initial endogenous release of IL-5, which then acts to induce the autologous release of IL-1beta by the sensitized ASM itself, resulting in its autocrine manifestation of the proasthmatic phenotype.

Adolescent↗
PubMed1998

Cerebellar arteriovenous malformations in children.

We review the presentation, imaging findings and outcome in 18 children with cerebellar arteriovenous malformations (AVM). This group is of particular interest because of the reported poor outcome despite modern imaging and neurosurgical techniques. All children had CT and 15 underwent catheter angiography at presentation. Several of the children in the latter part of the study had MRI. Of the 18 children, 17 presented with a ruptured AVM producing intracranial haemorrhage. The remaining child presented with temporal lobe epilepsy and was shown to have temporal, vermian and cerebellar hemisphere AVM. This child had other stigmata of Osler-Weber-Rendu syndrome. Three other children had pre-existing abnormalities of possible relevance. One had a vascular malformation of the cheek and mandible, one a documented chromosomal abnormality and another a midline cleft upper lip and palate. Six of the 17 children with a ruptured cerebellar AVM died within 7 days of the ictus. Vascular pathology other than an AVM was found in 10 of the 14 children with a ruptured cerebellar AVM who had angiography: 4 intranidal aneurysms, 5 venous aneurysms and 2 cases of venous outflow obstruction (one child having both an aneurysm and obstruction). The severity of clinical presentation was directly related to the size of the acute haematoma, which was a reasonable predictor of outcome.

Adolescent↗
PubMed1994

Localized scleroderma: imaging features.

Localized scleroderma is distinct from the diffuse form of scleroderma and does not show Raynaud's phenomenon and visceral involvement. The imaging features in 23 patients ranging from 2 to 17 years of age (mean 11.1 years) were reviewed. Leg length discrepancy and muscle atrophy were the most common findings (five patients), with two patients also showing modelling deformity of the fibula. One patient with lower extremity involvement showed abnormal bone marrow signals on MR. Disabling joint contracture requiring orthopedic intervention was noted in one patient. In two patients with "en coup de sabre" facial deformity, CT and MR scans revealed intracranial calcifications and white matter abnormality in the ipsilateral frontal lobes, with one also showing migrational abnormality. In a third patient, CT revealed white matter abnormality in the ipsilateral parietal lobe. In one patient with progressive facial hemiatrophy, CT and MR scans showed the underlying hypoplastic left maxillary antrum and cheek. Imaging studies of areas of clinical concern revealed positive findings in half our patients.

Adolescent↗
PubMed1993

Mitochondrial encephalomyopathy, lactic acidosis, stroke-like episodes (MELAS): clinical, radiological, pathological, and genetic observations.

We reviewed 10 patients (5 males, 5 females) with mitochondrial encephalomyopathy, lactic acidosis, and stroke-like episodes. The age of symptom onset ranged from 3 months to 12 years. All had lactic acidosis, multiple stroke-like events with secondary neurological deficits, radiological changes of progressive brain infarction, and muscle biopsy showing ragged-red fibers. In patients with earlier onset of symptoms (< 2 yr), involvement tended to be more diffuse, with failure to thrive and early onset of delayed development. Patients whose symptoms appeared later tended to have focal neurological deficits with migraine-like headache, and a rate of cognitive regression reflecting the rapidity of disease progression. Radiological changes included multiple areas of infarction with initial predilection for parietal occipital areas, progressing to generalized atrophy. Pathological findings in muscle biopsies included type 1 fiber predominance, ragged-red fibers, increased intermyofibrillar lipid deposition, and abnormal mitochondria. Four patients showed mitochondrial DNA tRNA mutation at position 3,243. No difference was noted in clinical, radiological, or pathological findings in patients with and without this mutation, suggesting that multiple sites of point mutation may give rise to mitochondrial encephalomyopathy, lactic acidosis, and stroke-like episodes.

Base Sequence↗