Biomedical subjects

J Chapman

Publications and source records attributed to J Chapman.

At least 91 records · Page 5Linked to original sources

PubMed2003

Search for a W' boson decaying to a top and bottom quark pair in 1.8 TeV pp collisions.

We report the results of a search for a W' boson produced in pp; collisions at a center-of-mass energy of 1.8 TeV using a 106 pb(-1) data sample recorded by the Collider Detector at Fermilab. We observe no significant excess of events above background for a W' boson decaying to a top and bottom quark pair. In a model where this boson would mediate interactions involving a massive right-handed neutrino (nu(R)) and have standard model strength couplings, we use these data to exclude a W' boson with mass between 225 and 536 GeV/c(2) at 95% confidence level for M(W')>>M(nu(R)) and between 225 and 566 GeV/c(2) at 95% confidence level for M(W')<M(nu(R)).

Journal Article↗

PubMed2003

Biochemical characterization of atherosclerotic plaque constituents using FTIR spectroscopy and histology.

The behavior of vulnerable atherosclerotic plaques is believed to be closely related to plaque composition. There is a need for an effective in vivo technique for examining plaque constituent properties. In this study, Fourier transform infrared spectroscopy using attenuated total reflectance (FTIR-ATR) was used to assess and analyze the biochemical properties of human atherosclerotic plaques. FTIR spectra clearly revealed prominent spectral features corresponding to plaque constituents of interest: the 2930 cm(-1) and 2850 cm(-1) peaks (indicating the presence of lipids), the 1730 cm(-1) peak (lipid esters), the 1550 cm(-1) and 1650 cm(-1) peaks (fibrous tissues), and the 1100-1000 cm(-1) broad phosphate peak (calcification). Spectral data examined on a qualitative basis correlated well with both gross tissue anatomy and histologic features. Gross spatial mappings of tissue sections of both lipidic and calcified plaques were performed. Spectra from various regions of the plaques demonstrated the evolution of lipid peaks, fibrous tissue peaks, and the phosphate calcification band within the plaques. Histologic analysis corroborated the spectral findings in this study.

Arteriosclerosis↗

PubMed2003

One-year posttransplant renal function is a strong predictor of long-term kidney function: results from the Neoral-MOST Observational Study.

BACKGROUND: Peritransplant risk factors influence short-term and long-term graft survival, and 1-year serum creatinine is known to predict long-term graft survival. To examine interrelationships between risk factors, renal function at 1 year, and long-term graft function in patients maintained on cyclosporine, we analyzed data collected from 10,692 de novo or maintenance renal transplant recipients in an ongoing international, prospective, observational study--Neoral-MOST (Multinational Observational Study in renal Transplantation). The effect of donor age, delayed graft function, acute rejection, donor type, panel-reactive antibodies, and previous graft on 1- and 5-year renal function and their relationship to 1-year serum creatinine was assessed. RESULTS: Donor age, delayed graft function, acute rejection, and donor type significantly increased the risk for serum creatinine > 130 micromol/L at 1 year posttransplant, and 1-year serum creatinine was the strongest predictor of 5-year renal function. After adjustment for 1-year serum creatinine, an ongoing influence was observed for donor age, donor type, and previous graft. Delayed graft function and acute rejection had a significant effect on serum creatinine at year 1 but no additional impact on long-term graft function. CONCLUSIONS: Serum creatinine at 1 year is influenced by risk factors known to affect overall graft survival and is predictive of 5-year renal graft function. The effects of delayed graft function and acute rejection appear to be limited to their influence on serum creatinine at 1 year, whereas donor type and previous graft predominantly affect later stages of graft life.

Creatinine↗

PubMed2003

10th International Congress on Antiphospholipid Antibodies--summary.

The 10th International Congress on Antiphospholipid Antibodies (Sicily, Italy, September 29-October 3, 2002) (Fig. 1) provided enlightening aspects on the recent developments in antiphospholipid syndrome (APS) and antiphospholipid antibodies in more than 150 lectures and posters. Researchers from all aspects of medicine attended the meeting, implicating the systemic characteristics of APS. The important breakthroughs are summarized.

Animals↗

PubMed2003

Stroke and the antiphospholipid syndrome: consensus meeting Taormina 2002.

Ischaemic stroke is the only neurological manifestation accepted as a clinical diagnostic criterion for the antiphospholipid syndrome (APS). This association is reasonably well established in patients first diagnosed with APS but is less clear in randomly selected stroke patients who test positive on one occasion for antiphospholipid antibodies and who have no other evidence of systemic autoimmune disease. We propose a grading system that posits stroke to be definitely, likely or possibly associated with antiphospholipid antibodies (aPL). Further, there are limited prospective data to determine appropriate treatment. There is controversy as to whether the presence of aPL even increases risk of a recurrent stroke or other thromboembolic event, although data point to persistent medium-high titre aCL and/or LA as risk factors for recurrence. In the absence of data to guide clinicians on the best treatment, we cannot make strong recommnendations as to optimal therapy, nor can we propose clear consensus treatment guidelines.

Administration, Oral↗

PubMed2003

Non-stroke neurological syndromes associated with antiphospholipid antibodies: evaluation of clinical and experimental studies.

Although many types of neurological disorders and events have been described in association with antiphospholipid antibodies (aPL) and the antiphospholipid syndrome (APS), only ischaemic stroke is reasonably well established and accepted as a diagnostic criterion for the syndrome. We propose to evaluate, classify and rank the association of other neurological manifestations as possible, probable, or definite according to the data available from clinical studies and animal models. By these criteria, none of the neurological disorders or events such as epilepsy, psychiatric disease, dementia, transverse myelitis, multiple sclerosis-like disease, chorea, migraine, Guillian-Barrè syndrome, and sensory-neural hearing loss, can be definitely associated with aPL or APS.

Antibodies, Antiphospholipid↗

PubMed2003

Neuronal-binding antibodies from patients with antiphospholipid syndrome induce cognitive deficits following intrathecal passive transfer.

Antiphospholipid antibodies (aPL) have been suggested to play a role in causing cognitive and behavioral impairments. In the present study we investigated the pathogenic potential of aPL by intracerebro-ventricular (ICV) administration of immunoglobulins (IgG) from patients with antiphospholipid syndrome (APS). IgG, purified from the sera of four APS patients, was tested for binding to normal mouse brain by immunohistological staining. These IgG (7.5 microg) were injected ICV unilaterally to male C3H mice. Mice injected with IgG purified from pooled sera derived from healthy subjects served as controls. The mice were examined neurologically for motor function and coordination, and cognitively in a Morris water maze. The cognitive tests were performed with the experimenter blinded to the treatment. The performance of the mice in four separate experiments was compared by analysis of variance with repeated measures. IgG from one APS patient was found to bind best to neuronal structures in the hippocampus and cerebral cortex. Mice (n = 43) injected with this IgG performed worse in the water maze compared to the controls (n = 45) with significant effects of the aPL IgG on the overall performance of the mice (treatment, P < 0.03), on learning throughout the experiment (treatment x day, P < 0.02) and on short term memory (treatment x day xtrial, P < 0.002). IgG injected from two of the three other patients also bound specifically to mouse brain neurons and produced an impairment in performance of the water maze. These results support the hypothesis that aPL that gain access to the central nervous system may play a direct role in the pathogenesis of neurological manifestations of APS.

Adult↗

PubMed2003

CNS dysfunction in the antiphospholipid syndrome.

Though many neurological deficits have been described in the antiphospholipid syndrome (APS), only stroke is well established and accepted as a diagnostic criterion in this disease. We review clinical data obtained from a large series of cases regarding stroke, dementia, epilepsy, chorea, migraine, white matter disease and behavioral changes in APS or linked to laboratory criteria such as antiphospholipid antibodies (aPL). The contribution of animal models to our understanding of these manifestations of APS is stressed, especially regarding the cognitive and behavioral aspects for which we have established model systems in the mouse. These models utilize immunization of mice with beta2-glycoprotein I, a central autoantigen in APS, which induces persistent high levels of aPL. These mice develop hyperactive behavior after a period of four to five months as well as deficits in learning and memory and are potentially valuable as a system in which to study the pathogenesis and treatment of cognitive and behavioral aspects of APS. Another model we have developed, in which IgG from APS patients induce depolarization of brain synaptoneurosomes, may serve as a model for the pathogenesis of epilepsy in APS.

Animals↗

PubMed2003

Lack of apolipoprotein-E exacerbates experimental allergic encephalomyelitis.

Experimental autoimmune encephalomyelitis (EAE) was found to have a chronic and significantly worse course in apolipoprotein-E (apoE) deficient female mice when compared with matched controls. Disease measures compared included incidence of EAE (64% versus 31%, P < 0.05, chi2 test), maximal clinical score (average +/- SD 2.81 +/- 2.5 versus 0.75 +/- 1.1, P < 0.01, Mann-Whitney test) and mortality (27.3% versus 0%, P = 0.02, Mann-Whitney test and chi2 test). ApoE deficient mice had significantly increased lymphocyte proliferation responses to both myelin antigens and mitogens and significantly more infiltrating lesions in the central nervous system (CNS) in histopathology. Defective neuronal repair mechanisms and enhanced immune reactivity in apoE deficient mice may explain our findings. Clinical implications for MS are discussed.

Alzheimer Disease↗

PubMed2002

Limits on extra dimensions and new particle production in the exclusive photon and missing energy signature in pp collisions at square root [s]=1.8 TeV.

The exclusive gammaE(T) signal has a small standard model cross section and is thus a channel sensitive to new physics. This signature is predicted by models with a superlight gravitino or with large extra spatial dimensions. We search for such signals at the Collider Detector at Fermilab, using 87 pb(-1) of data at square root [s]=1.8 TeV, and extract 95% C.L. limits on these processes. A limit of 221 GeV is set on the scale |F|(1/2) in supersymmetric models. For 4, 6, and 8 extra dimensions, model-dependent limits on the fundamental mass scale M(D) of 0.55, 0.58, and 0.60 TeV, respectively, are found. We also specify a "pseudo-model-independent" method of comparing the results to theoretical predictions.

Journal Article↗

PubMed2002

Search for new physics in photon-lepton events in pp collisions at sqrt[s] = 1.8 TeV.

We present the results of a search in pp collisions at sqrt[s] = 1.8 TeV for anomalous production of events containing a photon and a lepton (e or mu), both with large transverse energy, using 86 pb(-1) of data collected with the Collider Detector at Fermilab during the 1994-1995 collider run at the Fermilab Tevatron. The presence of large missing transverse energy (E(T)), additional photons, or additional leptons in these events is also analyzed. The results are consistent with standard model expectations, with the possible exception of photon-lepton events with large E(T), for which the observed total is 16 events and the expected mean total is 7.6+/-0.7 events.

Journal Article↗

PubMed2002

Upsilon production and polarization in p p macro collisions at square root of s = 1.8 TeV.

We report on measurements of the Upsilon(1S), Upsilon(2S), and Upsilon(3S) differential cross sections (d(2)sigma/dp(T)dy)(/y/<0.4), as well as on the Upsilon(1S) polarization in p p macro collisions at square root of s = 1.8 TeV using a sample of 77+/-3 pb(-1) collected by the collider detector at Fermilab. The three resonances were reconstructed through the decay Upsilon-->mu(+)mu(-). The measured angular distribution of the muons in the Upsilon(1S) rest frame is consistent with unpolarized meson production.

Journal Article↗

PubMed2002

Diffractive dijet production at sqrt[s] = 630 and 1800 GeV at the Fermilab Tevatron.

We report a measurement of the diffractive structure function F(D)(jj) of the antiproton obtained from a study of dijet events produced in association with a leading antiproton in pp collisions at sqrt[s] = 630 GeV at the Fermilab Tevatron. The ratio of F(D)(jj) at sqrt[s] = 630 GeV to F(D)(jj) obtained from a similar measurement at sqrt[s] = 1800 GeV is compared with expectations from QCD factorization and other theoretical predictions. We also report a measurement of the xi ( x-Pomeron) and beta ( x of parton in Pomeron) dependence of F(D)(jj) at sqrt[s] = 1800 GeV. In the region 0.035<xi<0.095, /t/<1 GeV2, and beta<0.5, F(D)(jj)(beta,xi) is found to be of the form beta(-1.0+/-0.1)xi(-0.9+/-0.1), which obeys beta-xi factorization.

Journal Article↗

PubMed2002

Peroxisome proliferator-activated receptor (PPAR) agonists decrease lipoprotein lipase secretion and glycated LDL uptake by human macrophages.

Lipoprotein lipase (LPL) acts independently of its function as triglyceride hydrolase by stimulating macrophage binding and uptake of native, oxidized and glycated LDL. Peroxisome proliferator-activated receptors (PPARs) are nuclear receptors expressed in monocyte/macrophages, where they control cholesterol homeostasis. Here we study the role of PPARs in the regulation of LPL expression and activity in human monocytes and macrophages. Incubation of human monocytes or macrophages with PPARalpha or PPARgamma ligands increases LPL mRNA and intracellular protein levels. By contrast, PPAR activators decrease secreted LPL mass and enzyme activity in differentiated macrophages. These actions of PPAR activators are associated with a reduced uptake of glycated LDL and could influence atherosclerosis development associated with diabetes.

Biological Transport↗

PubMed2002

Search for new heavy particles in the WZ0 final state in pp collisions at square root[s] = 1.8 TeV.

We present the first general search for new heavy particles, X, which decay via X --> WZ0 --> e(nu)+jj as a function of M(X) and Gamma(X) in pp collisions at square root[s] = 1.8 TeV. No evidence is found for production of X in 110 pb(-1) of data collected by the Collider Detector at Fermilab. General cross section limits are set at the 95% C.L. as a function of mass and width of the new particle. The results are further interpreted as mass limits on the production of new heavy charged vector bosons which decay via W' --> WZ0 in an extended gauge model as a function of the width, Gamma(W'), and mixing factor between the W' and the standard model W bosons.

Journal Article↗

PubMed2002

Study of B0 --> J/psiK(*)0pi(+)pi(-) decays with the collider detector at Fermilab.

We report a study of the decays B0 --> J/psiK(*)0pi(+)pi(-), which involve the creation of a uu or dd quark pair in addition to a b -->c(cs) decay. The data sample consists of 110 pb(-1) of pp collisions at square root[s] = 1.8 TeV collected by the CDF detector at the Fermilab Tevatron collider during 1992-1995. We measure the branching fractions to be B(B0 --> J/psiK(*0)pi(+)pi(-)) = (6.6 +/- 1.9 +/- 1.1)x10(-4) and B(B0 --> J/psiK0pi(+)pi(-)) = (10.3 +/- 3.3 +/- 1.5)x10(-4). Evidence is seen for contributions from psi(2S)K(*)0, J/psiK0rho(0), J/psiK(*+)pi(-), and J/psiK1(1270).

Journal Article↗

PubMed2002

Measurement of the strong coupling constant from inclusive jet production at the Tevatron pp collider.

We report a measurement of the strong coupling constant, alpha(s)(MZ), extracted from inclusive jet production in pp collisions at square root[s] = 1800 GeV. The QCD prediction for the evolution of alpha(s) with jet transverse energy ET is tested over the range 40<ET<450 GeV using ET for the renormalization scale. The data show good agreement with QCD in the region below 250 GeV. The value of alpha(s) at the mass of the Z0 boson averaged over the range 40<ET<250 GeV is found to be alpha(s)(MZ) = 0.1178+/-0.0001(stat)+0.0081(-0.0095)(expt. syst). The associated theoretical uncertainties are mainly due to the choice of renormalization scale ((+6%)(-4%)) and input parton distribution functions (5%).

Journal Article↗

PubMed2002

Search for gluinos and scalar quarks in pp collisions at square root[s] = 1.8 TeV using the missing energy plus multijets signature.

We have performed a search for gluinos (g) and scalar quarks (q) in a data sample of 84 pb(-1) of pp collisions at square root[s] = 1.8 TeV, recorded by the Collider Detector at Fermilab. We investigate the final state of large missing transverse energy and three or more jets, a characteristic signature in R-parity-conserving supersymmetric models. The analysis has been performed "blind," in that the inspection of the signal region is made only after the predictions from standard model backgrounds have been calculated. Comparing the data with predictions of constrained supersymmetric models, we exclude gluino masses below 195 GeV/c2 (95% C.L.), independent of the squark mass. For the case m(q) approximately m(g), gluino masses below 300 GeV/c2 are excluded.

Journal Article↗