Biomedical subjects

M L Chu

Publications and source records attributed to M L Chu.

At least 55 records · Page 3Linked to original sources

PubMed2001

Observation of diffractive J/psi production at the Fermilab Tevatron.

We report the first observation of diffractive J/psi(--> mu+mu-) production in pp collisions at root square[s] = 1.8 TeV. Diffractive events are identified by their rapidity gap signature. In a sample of events with two muons of transverse momentum p(mu)T>2 GeV/c within the pseudorapidity region /eta/ < 1.0, the ratio of diffractive to total J/psi production rates is found to be R(J/psi) = [1.45 +/- 0.25]%. The ratio R(J/psi)(x) is presented as a function of x-Bjorken. By combining it with our previously measured corresponding ratio R(jj)(x) for diffractive dijet production, we extract a value of 0.59 +/- 0.15 for the gluon fraction of the diffractive structure function of the proton.

Journal Article↗

PubMed2001

Charged-particle multiplicity pp collisions at square root of (s) = 1.8 TeV.

We report on a measurement of the mean charged-particle multiplicity of jets in dijet events with dijet masses in the range 80-630 GeV/c(2), produced at the Tevatron in pp collisions with square root (s) = 1.8 TeV and recorded by the Collider Detector at Fermilab. The data are fit to perturbative-QCD calculations carried out in the framework of the modified leading log approximation and the hypothesis of local parton-hadron duality. The fit yields values for two parameters in that framework: the ratio of parton multiplicities in gluon and quark jets, r identical withN(g-jet)(partons)/N(q-jet)(partons) = 1.7+/-0.3, and the ratio of the number of charged hadrons to the number of partons in a jet, K(charged)(LPHD) identical with N(charged)(hadrons)/N(partons) = 0.57+/-0.11.

Journal Article↗

PubMed2001

Search for quark-lepton compositeness and a heavy W' Boson using the enu channel in p p macro collisions at square root of [s] = 1.8 TeV.

We present searches for quark-lepton compositeness and a heavy W' boson at high electron-neutrino transverse mass. We use approximately 110 pb(-1) of data collected in p p macro collisions at square root of [s] = 1.8 TeV by the CDF Collaboration during 1992-1995. The data are consistent with standard model expectations. Limits are set on the quark-lepton compositeness scale Lambda, the ratio of partial cross sections sigma(W'-->enu)/sigma(W-->enu), and the mass of a W' boson with standard model couplings. We exclude Lambda<2.81 TeV and a W' boson with mass below 754 GeV/c(2) at the 95% confidence level. Combining with our previously published limit obtained using the muon channel, we exclude a W' boson with mass below 786 GeV/c(2) at the 95% confidence level.

Journal Article↗

PubMed2001

Double diffraction dissociation at the Fermilab Tevatron collider.

We present results from a measurement of double diffraction dissociation in pp collisions at the Fermilab Tevatron collider. The production cross section for events with a central pseudorapidity gap of width Deltaeta(0)>3 (overlapping eta = 0) is found to be 4.43+/-0.02(stat)+/-1.18(syst) mb [ 3.42+/-0.01(stat)+/-1.09(syst) mb] at square root of (s) = 1800[630] GeV. Our results are compared with previous measurements and with predictions based on Regge theory and factorization.

Journal Article↗

PubMed2001

Measurement of d sigma/dM and forward-backward charge asymmetry for high-mass Drell-Yan e(+)e(-) pairs from pp macro collisions at square root of s = 1.8 TeV.

We report on a measurement of the mass dependence of the forward-backward charge asymmetry, A(FB), and production cross section d sigma/dM for e(+)e(-) pairs with mass M(ee)>40 GeV/c(2). The data sample consists of 108 pb(-1) of pp macro collisions at square root of s = 1.8 TeV taken by the Collider Detector at Fermilab during 1992-1995. The measured asymmetry and d sigma/dM are compared with the predictions of the standard model and a model with an extra Z' gauge boson.

Journal Article↗

PubMed2001

Measurement of the top quark p(T) distribution.

We have measured the p(T) distribution of top quarks that are pair produced in pp collisions at sqrt[s] = 1.8 TeV using a sample of tt decays in which we observe a single high- p(T) charged lepton, a neutrino, and four or more jets. We use a likelihood technique that corrects for the experimental bias introduced due to event reconstruction and detector resolution effects. The observed distribution is consistent with the standard model prediction. We use these data to place limits on the production of high- p(T) top quarks suggested in some models of anomalous top quark pair production.

Journal Article↗

PubMed2001

Ullrich scleroatonic muscular dystrophy is caused by recessive mutations in collagen type VI.

Ullrich syndrome is a recessive congenital muscular dystrophy affecting connective tissue and muscle. The molecular basis is unknown. Reverse transcription-PCR amplification performed on RNA extracted from fibroblasts or muscle of three Ullrich patients followed by heteroduplex analysis displayed heteroduplexes in one of the three genes coding for collagen type VI (COL6). In patient A, we detected a homozygous insertion of a C leading to a premature termination codon in the triple-helical domain of COL6A2 mRNA. Both healthy consanguineous parents were carriers. In patient B, we found a deletion of 28 nucleotides because of an A --> G substitution at nucleotide -2 of intron 17 causing the activation of a cryptic acceptor site inside exon 18. The second mutation was an exon skipping because of a G --> A substitution at nucleotide -1 of intron 23. Both mutations are present in an affected brother. The first mutation is also present in the healthy mother, whereas the second mutation is carried by their healthy father. In patient C, we found only one mutation so far-the same deletion of 28 nucleotides found in patient B. In this case, it was a de novo mutation, as it is absent in her parents. mRNA and protein analysis of patient B showed very low amounts of COL6A2 mRNA and of COL6. A near total absence of COL6 was demonstrated by immunofluorescence in fibroblasts and muscle. Our results demonstrate that Ullrich syndrome is caused by recessive mutations leading to a severe reduction of COL6.

Base Sequence↗

PubMed2001

Search for neutral supersymmetric Higgs bosons in pp collisions at sqrt[s] = 1.8TeV.

We present the results of a search for neutral Higgs bosons produced in association with b quarks in pp-->bb(phi)-->bbb final states with 91+/-7 pb(-1) of pp collisions at sqrt[s] = 1.8 TeV recorded by the Collider Detector at Fermilab. We find no evidence of such a signal and the data are interpreted in the context of the neutral Higgs sector of the minimal supersymmetric extension of the standard model. With basic parameter choices for the supersymmetric scale and the stop-quark mixing, we derive 95% C.L. lower mass limits for neutral Higgs bosons for tan(beta) values in excess of 35.

Journal Article↗

PubMed2001

Production of chi(c1) and chi(c2) in pp collisions at sqrt[S] = 1.8 TeV.

We have measured the ratio of prompt production rates of the charmonium states chi(c1) and chi(c2) in 110 pb(-1) of pp collisions at sqrt[s] = 1.8 TeV. The photon from their decay into J/psi(gamma) is reconstructed through conversion into e+e- pairs. The energy resolution this technique provides makes the resolution of the two states possible. We find the ratio of production cross sections sigma(chi(c2))/sigma(chi(c1)) = 0.96+/-0.27(stat)+/-0.11(syst) for events with pT(J/psi) > 4.0 GeV/c, /eta(J/psi)/ < 0.6, and pT(gamma) > 1.0 GeV/c.

Journal Article↗

PubMed2001

First measurement of the ratio B(t --> Wb)/B(t --> Wq) and associated limit on the Cabibbo-Kobayashi-Maskawa element /V(tb)/.

We present the first measurement of the ratio of branching fractions R identical withB(t-->Wb)/B(t-->Wq) from p_p collisions at sqrt[s] = 1.8 TeV. The data set corresponds to 109 pb(-1) of data recorded by the Collider Detector at Fermilab during the 1992-95 Tevatron run. We measure R = 0.94(+0.31)(-0.24)(stat+syst) or R>0.61 (0.56) at 90% (95)% C.L., in agreement with the standard model predictions. This measurement yields a limit on the Cabibbo-Kobayashi-Maskawa quark mixing matrix element /V(tb)/ under the assumption of three generations and unitarity.

Journal Article↗

PubMed2001

Identification of novel TGF-beta /Smad gene targets in dermal fibroblasts using a combined cDNA microarray/promoter transactivation approach.

Despite major advances in the understanding of the intimate mechanisms of transforming growth factor-beta (TGF-beta) signaling through the Smad pathway, little progress has been made in the identification of direct target genes. In this report, using cDNA microarrays, we have focussed our attention on the characterization of extracellular matrix-related genes rapidly induced by TGF-beta in human dermal fibroblasts and attempted to identify the ones whose up-regulation by TGF-beta is Smad-mediated. For a gene to qualify as a direct Smad target, we postulated that it had to meet the following criteria: (1) rapid (30 min) and significant (at least 2-fold) elevation of steady-state mRNA levels upon TGF-beta stimulation, (2) activation of the promoter by both exogenous TGF-beta and co-transfected Smad3 expression vector, (3) up-regulation of promoter activity by TGF-beta blocked by both dominant-negative Smad3 and inhibitory Smad7 expression vectors, and (4) promoter transactivation by TGF-beta not possible in Smad3(-/-) mouse embryo fibroblasts. Using this stringent approach, we have identified COL1A2, COL3A1, COL6A1, COL6A3, and tissue inhibitor of metalloproteases-1 as definite TGF-beta/Smad3 targets. Extrapolation of this approach to other extracellular matrix-related gene promoters also identified COL1A1 and COL5A2, but not COL6A2, as novel Smad targets. Together, these results represent a significant step toward the identification of novel, early-induced Smad-dependent TGF-beta target genes in fibroblasts.

Animals↗

PubMed2001

Fibulin-2 expression marks transformed mesenchymal cells in developing cardiac valves, aortic arch vessels, and coronary vessels.

Previous studies showed that extracellular matrix protein, fibulin-2, is expressed during epithelial-mesenchymal transformation in the endocardial cushion matrix during embryonic heart development. Our current study revealed that, in addition to the cardiac valvuloseptal formation, fibulin-2 is synthesized by the smooth muscle precursor cells of developing aortic arch vessels and the coronary endothelial cells that are originated from neural crest cells and epicardial cells, respectively. In the cardiac valves and the aortic arch vessels, fibulin-2 expression shows robust up-regulation when the transformed mesenchymal cells migrate into the existing extracellular matrix. In the epicardium, epicardial cells produce fibulin-2 upon their migration over the myocardial surface and its expression persists throughout coronary vasculogenesis and angiogenesis. Fibulin-2 is produced by the endothelial cells of coronary arteries and veins but not by the capillary endothelial cells in the myocardium. Thus, fibulin-2 not only uniquely marks the transformed mesenchymal cells during mouse embryonic cardiovascular development, but also indicates vascular endothelial cells of coronary arteries and veins in postnatal life.

Animals↗

PubMed2001

Physical mapping of mouse collagen genes on chromosome 10 by high-resolution FISH.

Fluorescence in situ hybridization (FISH) on mechanically stretched chromosomes (MSCs) and extended DNA fibers enables construction of high-resolution physical maps by accurate ordering and orienting genomic clones as well as by measuring physical lengths of gaps and overlaps between them. These high-resolution FISH targets have hitherto been used mainly in the study of the human genome. Here we have applied both MSCs and extended DNA fibers to the physical mapping of the mouse genome. At first, five mouse collagen genes were localized by metaphase-FISH: Col10a1 to chromosomal bands 10B1-B3; Col13a1 to 10B4; and Col6a1, Col6a2, and Col18a1 to 10B5-C1. The mutual order of the genes, centromere--Col10a1--Col13a1--Col6a2--Col6a1--Col18a1--telomere, was determined by FISH on metaphase chromosomes, MSCs, and extended DNA fibers. To our knowledge, this is the first time mouse metaphase chromosomes have been stretched and used as targets for FISH. We also used MSCs to determine the transcriptional orientations, telomere--5'-->3'--centromere, of both Col13a1 and Col18a1. With fiber-FISH, Col18a1, Col6a1, and Col6a2 were shown to be in a head-to-tail configuration with respective intergenic distances of about 350 kb and 90 kb. Comparison of our physical mapping results with the homologous human data reveals both similarities and differences concerning the chromosomal distribution, order, transcriptional orientations, and intergenic distances of the collagen genes studied.

Animals↗

PubMed2001

Retropharyngeal abscess caused by group B Streptococcus in a previously healthy child.

Retropharyngeal cellulitis/abscess has not been recognized as a manifestation of group B streptococcal disease in the pediatric group beyond neonates. The purpose of this paper is to present a previously healthy 3-year-old boy with a retropharyngeal abscess due to group B Streptococcus which was successfully treated by surgical incision and drainage in combination with amoxicillin/clavulanate therapy.

Amoxicillin-Potassium Clavulanate Combination↗

PubMed2001

Intrathecal baclofen in X-linked adrenoleukodystrophy.

X-linked adrenoleukodystrophy is a progressive neurodegenerative disorder involving the destruction of white matter in the brain and adrenocortical hormone deficiency. Clinical symptoms first appear between 4 and 8 years of age and include spasticity, visual loss, dysphagia, and seizures. In this report, continuous infusion of intrathecal baclofen was used to treat the severe spasticity of an 8-year-old patient with X-linked adrenoleukodystrophy. The improvement in this patient's quality of life, including the elimination of pain and the increased ease of care, suggests that intrathecal baclofen should be considered as part of the treatment strategy for spasticity associated with X-linked adrenoleukodystrophy and other neurodegenerative disorders in children and adults.

Adrenoleukodystrophy↗

PubMed2001

Perinatal lethality and endothelial cell abnormalities in several vessel compartments of fibulin-1-deficient mice.

The extracellular matrix protein fibulin-1 is a distinct component of vessel walls and can be associated with other ligands present in basement membranes, microfibrils, and elastic fibers. Its biological role was investigated by the targeted inactivation of the fibulin-1 gene in mice. This led to massive hemorrhages in several tissues starting at midgestation, ultimately resulting in the death of almost all homozygous embryos upon birth. Histological analysis demonstrated dilation and ruptures in the endothelial lining of various small vessels but not in that of larger vessels. Kidneys displayed a distinct malformation of glomeruli and disorganization of podocytes. A delayed development of lung alveoli suggested impairment in lung inflation. Immunohistology demonstrated the absence of fibulin-1 in its typical localizations but no aberrant patterns for several other extracellular matrix proteins. Electron microscopy revealed intact basement membranes but very irregular cytoplasmic processes of capillary endothelial cells in the organs that were most severely affected. Absence of fibulin-1 caused considerable blood loss but did not compromise blood clotting. The data indicate a strong but restricted abnormality in some endothelial compartments which, together with some kidney and lung defects, may be responsible for early death.

Animals↗

PubMed2001

Chronic granulomatous disease: a case report.

Chronic granulomatous disease is one form of the phagocyte function disorder. Unlike most patients with chronic granulomatous disease who develop signs and symptoms of chronic and recurrent pyogenic infections during the first 2 years of life, patients with mild forms of the disease may not present until the teenage years or even adulthood. Thus, the diagnosis in these mild-form patients is often delayed. This paper describes a patient with the mild form of chronic granulomatous disease. A 7-year-old boy was admitted to our ward with intermittent high fever and a left neck mass present for about 1 week. He had a history of persistent infection in the bilateral lower face lasting for about 1 year during his fourth year of life. Family history was unremarkable except that the patient's elder sister had a history of persistent oral mucosal wound infection for about 1 year during the fifth year of life. On physical examination, there were scars over the patient's bilateral lower face. Bacterial culture of pus drained from the neck mass revealed Burkholderia cepacia, a rare species in patients without immunodeficiency. A series of antibiotics, including oxacillin, clindamycin, and piperacillin, was given, and two incision operations for drainage and debridement were performed. The neck mass resolved completely about 1.5 months later. This history indicated that the patient might have chronic granulomatous disease. A definite absence of superoxide activity in the patient's granulocytes detected by chemiluminescence and nitroblue tetrazolium dye test confirmed this diagnosis.

Child↗

PubMed2001

Meningitis due to penicillin-resistant Neisseria meningitidis in a 20-year-old man.

The emergence of meningococcal strains with reduced susceptibility to penicillin has been reported in several countries during the past two decades, but not in Taiwan. We report a case of meningococcal meningitis with intermediate resistance to penicillin. A 20-year-old male soldier complained of chills, fever, and headache for 2 days, followed by drowsiness. Physical examination revealed erythema of the pharynx, stiff neck, erythematous maculopapules, and petechiae over the trunk and four limbs including palms and soles. Analysis of the cerebrospinal fluid (CSF) showed a white blood cell count of 9.06 x 10(6)/L, a glucose concentration of 0.165 mmol/L, and a protein concentration of 7.85 g/L. CSF culture yielded Neisseria meningitidis, serogroup B. The minimum inhibitory concentration of penicillin was determined using an E-test (0.125 microgram/mL); there was no beta-lactamase production. He recovered after high-dose penicillin G treatment with six doses of 24 million units per day for 11 days. The emergence of penicillin resistance in N. meningitidis in Taiwan requires surveillance. High-dose penicillin may be successful in treating penicillin-insensitive meningococcal meningitis. Alternative treatment with third-generation cephalosporins should be considered if poor response to penicillin is encountered.

Adult↗