77 research outputs found
Production and Decay of D_1(2420)^0 and D_2^*(2460)^0
We have investigated and final states and
observed the two established charmed mesons, the with mass
MeV/c and width MeV/c and
the with mass MeV/c and width
MeV/c. Properties of these final states, including
their decay angular distributions and spin-parity assignments, have been
studied. We identify these two mesons as the doublet predicted
by HQET. We also obtain constraints on {\footnotesize } as a function of the cosine of the relative phase of the two
amplitudes in the decay.Comment: 15 pages in REVTEX format. hardcopies with figures can be obtained by
sending mail to: [email protected]
Measurement of the branching fraction for
We have studied the leptonic decay of the resonance into tau
pairs using the CLEO II detector. A clean sample of tau pair events is
identified via events containing two charged particles where exactly one of the
particles is an identified electron. We find . The result is consistent with
expectations from lepton universality.Comment: 9 pages, RevTeX, two Postscript figures available upon request, CLNS
94/1297, CLEO 94-20 (submitted to Physics Letters B
Measurement of the Decay Asymmetry Parameters in and
We have measured the weak decay asymmetry parameters (\aLC ) for two \LC\
decay modes. Our measurements are \aLC = -0.94^{+0.21+0.12}_{-0.06-0.06} for
the decay mode and \aLC = -0.45\pm 0.31 \pm
0.06 for the decay mode . By combining these
measurements with the previously measured decay rates, we have extracted the
parity-violating and parity-conserving amplitudes. These amplitudes are used to
test models of nonleptonic charmed baryon decay.Comment: 11 pages including the figures. Uses REVTEX and psfig macros. Figures
as uuencoded postscript. Also available as
http://w4.lns.cornell.edu/public/CLNS/1995/CLNS95-1319.p
Observation of the Charmed Baryon Decays to , , and
We have observed two new decay modes of the charmed baryon into
and using data collected with the
CLEO II detector. We also present the first measurement of the branching
fraction for the previously observed decay mode . The branching fractions for these three modes relative to
are measured to be , , and , respectively.Comment: 12 page uuencoded postscript file, postscript file also available
through http://w4.lns.cornell.edu/public/CLN
Early- Onset Stroke and Vasculopathy Associated with Mutations in ADA2
Adenosine deaminase 2 (ADA2) is an enzyme involved in purine metabolism and a growth factor that influences the development of endothelial cells and leukocytes. This study shows that defects in ADA2 cause recurrent fevers, vascular pathologic features, and mild immunodeficiency. Patients with autoinflammatory disease sometimes present with clinical findings that encompass multiple organ systems.(1) Three unrelated children presented to the National Institutes of Health (NIH) Clinical Center with intermittent fevers, recurrent lacunar strokes, elevated levels of acute-phase reactants, livedoid rash, hepatosplenomegaly, and hypogammaglobulinemia. Collectively, these findings do not easily fit with any of the known inherited autoinflammatory diseases. Hereditary or acquired vascular disorders can have protean manifestations yet be caused by mutations in a single gene. Diseases such as the Aicardi-Goutieres syndrome,(2),(3) polypoidal choroidal vasculopathy,(4) sickle cell anemia,(5) livedoid vasculopathy,(6) and the small-vessel vasculitides(7),(8) are examples of systemic ...</p
CSF1R inhibitor JNJ-40346527 attenuates microglial proliferation and neurodegeneration in P301S mice
Neuroinflammation and microglial activation are significant processes in Alzheimer's disease pathology. Recent genome-wide association studies have highlighted multiple immune-related genes in association with Alzheimer's disease, and experimental data have demonstrated microglial proliferation as a significant component of the neuropathology. In this study, we tested the efficacy of the selective CSF1R inhibitor JNJ-40346527 (JNJ-527) in the P301S mouse tauopathy model. We first demonstrated the anti-proliferative effects of JNJ-527 on microglia in the ME7 prion model, and its impact on the inflammatory profile, and provided potential CNS biomarkers for clinical investigation with the compound, including pharmacokinetic/pharmacodynamics and efficacy assessment by TSPO autoradiography and CSF proteomics. Then, we showed for the first time that blockade of microglial proliferation and modification of microglial phenotype leads to an attenuation of tau-induced neurodegeneration and results in functional improvement in P301S mice. Overall, this work strongly supports the potential for inhibition of CSF1R as a target for the treatment of Alzheimer's disease and other tau-mediated neurodegenerative diseases
Inflammatory biomarkers in Alzheimer's disease plasma
Introduction: Plasma biomarkers for Alzheimer's disease (AD) diagnosis/stratification are a \u201cHoly Grail\u201d of AD research and intensively sought; however, there are no well-established plasma markers. Methods: A hypothesis-led plasma biomarker search was conducted in the context of international multicenter studies. The discovery phase measured 53 inflammatory proteins in elderly control (CTL; 259), mild cognitive impairment (MCI; 199), and AD (262) subjects from AddNeuroMed. Results: Ten analytes showed significant intergroup differences. Logistic regression identified five (FB, FH, sCR1, MCP-1, eotaxin-1) that, age/APO\u3b54 adjusted, optimally differentiated AD and CTL (AUC: 0.79), and three (sCR1, MCP-1, eotaxin-1) that optimally differentiated AD and MCI (AUC: 0.74). These models replicated in an independent cohort (EMIF; AUC 0.81 and 0.67). Two analytes (FB, FH) plus age predicted MCI progression to AD (AUC: 0.71). Discussion: Plasma markers of inflammation and complement dysregulation support diagnosis and outcome prediction in AD and MCI. Further replication is needed before clinical translation
A measurement of B(D+S → φl+ν) B(D+S → φπ+)
Using the CLEO II detector at CESR, we have measured the ratio of branching fractions B (D + S → φl + ν) B (D + S → φπ + ) = 0.54 ± 0.05 ± 0.04 . We use this measurement to obtain a model dependent estimate of B (D + S → φπ + )
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