Radiative Decay of Vector Quarkonium: Constraints on Glueballs and Light Gluinos

Given a resonance of known mass, width, and J^{PC}, we can determine its gluonic branching fraction, b(R->gg), from data on its production in radiative vector quarkonium decay, V -> gamma+R. For most resonances b(R->gg) is found to be O(10%), consistent with being q-qbar states, but we find that both pseudoscalars observed in the 1440 MeV region have b(R->gg) ~ 1/2 - 1, and b(f_0^{++}->gg) ~ 1/2. As data improves, b(R->gg) should be a useful discriminator between q-qbar and gluonic states and may permit quantitative determination of the extent to which a particular resonance is a mixture of glueball and q-qbar. We also examine the regime of validity of pQCD for predicting the rate of V -> gamma+eta_gluino, the ``extra'' pseudoscalar bound state which would exist if there were light gluinos. From the CUSB limit on peaks in Upsilon -> gamma X, the mass range 3 GeV < m(eta_gluino) < 7 GeV can be excluded. An experiment must be significantly more sensitive to exclude an eta_gluino lighter than this.Comment: 36pp (inc figs),RU-94-04. (Replaces original which didn't latex correctly and didn't have figures.

Meson Decay Constants from Isospin Mass Splittings in the Quark Model

Decay constants of $D$ and $B$ mesons are estimated within the framework of a heavy-quark approach using measured isospin mass splittings in the $D$, $D^*$, and $B$ states to isolate the electromagnetic hyperfine interaction between quarks. The values $f_D = (262 \pm 29)$ MeV and $f_B = (160 \pm 17)$ MeV are obtained. Only experimental errors are given; possible theoretical ambiguities, and suggestions for reducing them, are noted.Comment: 7 pages, LaTeX, EFI-92-3

Anti-PrP antibodies block PrPSc replication in prion-infected cell cultures by accelerating PrPC degradation.

manuscript received October 15, 2003; revised manuscript received December 15, 2003; accepted December 16, 2003. We thanks P. Rondard, O Bischof, J.-L. Laplanche and J.-P. Pin for their fruitful discussions. we are grateful to S. barrère for her assistance in the statistical analysis of the data and H. McMahon for her assistance in reading the manuscript

Wissenschaftliche Monitoringkonzepte für die Deutsche Bucht (WIMO) - Abschlussbericht

The state and development of coastal marine systems and an understanding of the interaction of organisms, sea floor, water column, and biochemical and physical processes can only be obtained by a combination of long-term monitoring and modelling approaches of different complexity. A need for the development and evaluation of monitoring strategies is driven by a framework of different European and German regulations. The research project WIMO (Scientific Monitoring Concepts for the German Bight) has developed concepts and methods that aim at a fundamental scientific understanding of marine systems and also meet monitoring requirements of European legislation and regulations like the EU Marine Strategy Framework Directive. In this final report examples of common descriptors of ecosystem state like seabed integrity, eutrophication, and biodiversity are discussed. It has been assessed to what extent established measuring procedures used to survey the characteristics of the sea floor, and newly developed technologies are eligible for governmental monitoring. The significance of integrative modelling for linking and visualising results of measurements and models is illustrated. It is shown how new concepts have been implemented into governmental monitoring in the form of web based data sheets. These insights enable continuous analyses and developments in the future

Leptonic and Semileptonic Decays of Charm and Bottom Hadrons

We review the experimental measurements and theoretical descriptions of leptonic and semileptonic decays of particles containing a single heavy quark, either charm or bottom. Measurements of bottom semileptonic decays are used to determine the magnitudes of two fundamental parameters of the standard model, the Cabibbo-Kobayashi-Maskawa matrix elements $V_{cb}$ and $V_{ub}$. These parameters are connected with the physics of quark flavor and mass, and they have important implications for the breakdown of CP symmetry. To extract precise values of $|V_{cb}|$ and $|V_{ub}|$ from measurements, however, requires a good understanding of the decay dynamics. Measurements of both charm and bottom decay distributions provide information on the interactions governing these processes. The underlying weak transition in each case is relatively simple, but the strong interactions that bind the quarks into hadrons introduce complications. We also discuss new theoretical approaches, especially heavy-quark effective theory and lattice QCD, which are providing insights and predictions now being tested by experiment. An international effort at many laboratories will rapidly advance knowledge of this physics during the next decade.Comment: This review article will be published in Reviews of Modern Physics in the fall, 1995. This file contains only the abstract and the table of contents. The full 168-page document including 47 figures is available at http://charm.physics.ucsb.edu/papers/slrevtex.p

Inoculation route-dependent Lassa virus dissemination and shedding dynamics in the natural reservoir – Mastomys natalensis

Lassa virus (LASV), a Risk Group-4 zoonotic haemorrhagic fever virus, affects sub-Saharan African countries. Lassa fever, caused by LASV, results in thousands of annual deaths. Although decades have elapsed since the identification of the Natal multimammate mouse (Mastomys natalensis) as a natural reservoir of LASV, little effort has been made to characterize LASV infection in its reservoir. The natural route of infection and transmission of LASV within M. natalensis remains unknown, and the clinical impact of LASV in M. natalensis is mostly undescribed. Herein, using an outbred colony of M. natalensis, we investigate the replication and dissemination dynamics of LASV in this reservoir following various inoculation routes. Inoculation with LASV, regardless of route, resulted in a systemic infection and accumulation of abundant LASV-RNA in many tissues. LASV infection in the Natal multimammate mice was subclinical, however, clinical chemistry values were transiently altered and immune infiltrates were observed histologically in lungs, spleens and livers, indicating a minor disease with coordinated immune responses are elicited, controlling infection. Intranasal infection resulted in unique virus tissue dissemination dynamics and heightened LASV shedding, compared to subcutaneous inoculation. Our study provides important insights into LASV infection in its natural reservoir using a contemporary infection system, demonstrating that specific inoculation routes result in disparate dissemination outcomes, suggesting intranasal inoculation is important in the maintenance of LASV in the natural reservoir, and emphasizes that selection of the appropriate inoculation route is necessary to examine aspects of viral replication, transmission and responses to zoonotic viruses in their natural reservoirs.Peer Reviewe

Evidence of beta amyloid independent small vessel disease in familial Alzheimer\u27s disease

\ua9 2022 The Authors. Brain Pathology published by John Wiley &amp; Sons Ltd on behalf of International Society of Neuropathology. We studied small vessel disease (SVD) pathology in Familial Alzheimer\u27s disease (FAD) subjects carrying the presenilin 1 (PSEN1) p.Glu280Ala mutation in comparison to those with sporadic Alzheimer\u27s disease (SAD) as a positive control for Alzheimer\u27s pathology and Cerebral Autosomal Dominant Arteriopathy with Subcortical Infarcts and Leukoencephalopathy (CADASIL) bearing different NOTCH3 mutations, as positive controls for SVD pathology. Upon magnetic resonance imaging (MRI) in life, some FAD showed mild white matter hyperintensities and no further radiologic evidence of SVD. In post-mortem studies, total SVD pathology in cortical areas and basal ganglia was similar in PSEN1 FAD and CADASIL subjects, except for the feature of arteriosclerosis which was higher in CADASIL subjects than in PSEN1 FAD subjects. Further only a few SAD subjects showed a similar degree of SVD pathology as observed in CADASIL. Furthermore, we found significantly enlarged perivascular spaces in vessels devoid of cerebral amyloid angiopathy in FAD compared with SAD and CADASIL subjects. As expected, there was greater fibrinogen-positive perivascular reactivity in CADASIL but similar reactivity in PSEN1 FAD and SAD groups. Fibrinogen immunoreactivity correlated with onset age in the PSEN1 FAD cases, suggesting increased vascular permeability may contribute to cognitive decline. Additionally, we found reduced perivascular expression of PDGFRβ AQP4 in microvessels with enlarged PVS in PSEN1 FAD cases. We demonstrate that there is Aβ-independent SVD pathology in PSEN1 FAD, that was marginally lower than that in CADASIL subjects although not evident by MRI. These observations suggest presence of covert SVD even in PSEN1, contributing to disease progression. As is the case in SAD, these consequences may be preventable by early recognition and actively controlling vascular disease risk, even in familial forms of dementia

Possible Explanation Why \tau_{B^{\pm}}\sim\tau_{B^0} But \tau_{D^{\pm}}\sim \tau_{D^0}

Data show that \tau_{B^{\pm}}\sim\tau_{B^0}, but \tau_{D^{\pm}}\sim 2\tau_{D^0}. The naive interpretation which attributes \tau_{D^{\pm}}\sim 2\tau_{D^0} to a destructive interference between two quark diagrams for D^{\pm} decays, definitely fails in the B-case. We investigate Close and Lipkin's suggestion that the phases for producing radially excited states \psi_{2s} in the decay products of B-mesons can possess an opposite sign to the integrals for \psi_{1s} decay products. Their contributions can partially compensate each other to result in \tau_{B^{\pm}}\sim\tau_{B^0}. Since D-mesons are much lighter than B-mesons, such possibilities do not exist in D-decays.Comment: 14 pages, latex, 4 ps figures. to appear in Phys. Rev.

The POM Monoclonals: A Comprehensive Set of Antibodies to Non-Overlapping Prion Protein Epitopes

PrPSc, a misfolded and aggregated form of the cellular prion protein PrPC, is the only defined constituent of the transmissible agent causing prion diseases. Expression of PrPC in the host organism is necessary for prion replication and for prion neurotoxicity. Understanding prion diseases necessitates detailed structural insights into PrPC and PrPSc. Towards this goal, we have developed a comprehensive collection of monoclonal antibodies denoted POM1 to POM19 and directed against many different epitopes of mouse PrPC. Three epitopes are located within the N-terminal octarepeat region, one is situated within the central unstructured region, and four epitopes are discontinuous within the globular C-proximal domain of PrPC. Some of these antibodies recognize epitopes that are resilient to protease digestion in PrPSc. Other antibodies immunoprecipitate PrPC, but not PrPSc. A third group was found to immunoprecipitate both PrP isoforms. Some of the latter antibodies could be blocked with epitope-mimicking peptides, and incubation with an excess of these peptides allowed for immunochromatography of PrPC and PrPSc. Amino-proximal antibodies were found to react with repetitive PrPC epitopes, thereby vastly increasing their avidity. We have also created functional single-chain miniantibodies from selected POMs, which retained the binding characteristics despite their low molecular mass. The POM collection, thus, represents a unique set of reagents allowing for studies with a variety of techniques, including western blotting, ELISA, immunoprecipitation, conformation-dependent immunoassays, and plasmon surface plasmon resonance-based assays

APOE3 Christchurch Heterozygosity and Autosomal Dominant Alzheimer’s Disease

BackgroundVariants in APOE and PSEN1 (encoding apolipoprotein E and presenilin 1, respectively) alter the risk of Alzheimer's disease. We previously reported a delay of cognitive impairment in a person with autosomal dominant Alzheimer's disease caused by the PSEN1 E280A variant who also had two copies of the apolipoprotein E3 Christchurch variant (APOE3 Ch). Heterozygosity for the APOE3 Ch variant may influence the age at which the onset of cognitive impairment occurs. We assessed this hypothesis in a population in which the PSEN1 E280A variant is prevalent.MethodsWe analyzed data from 27 participants with one copy of the APOE3 Ch variant among 1077 carriers of the PSEN1 E280A variant in a kindred from Antioquia, Colombia, to estimate the age at the onset of cognitive impairment and dementia in this group as compared with persons without the APOE3 Ch variant. Two participants underwent brain imaging, and autopsy was performed in four participants.ResultsAmong carriers of PSEN1 E280A who were heterozygous for the APOE3 Ch variant, the median age at the onset of cognitive impairment was 52 years (95% confidence interval [CI], 51 to 58), in contrast to a matched group of PSEN1 E280A carriers without the APOE3 Ch variant, among whom the median age at the onset was 47 years (95% CI, 47 to 49). In two participants with the APOE3 Ch and PSEN1 E280A variants who underwent brain imaging, 18F-fluorodeoxyglucose positron-emission tomographic (PET) imaging showed relatively preserved metabolic activity in areas typically involved in Alzheimer's disease. In one of these participants, who underwent 18F-flortaucipir PET imaging, tau findings were limited as compared with persons with PSEN1 E280A in whom cognitive impairment occurred at the typical age in this kindred. Four studies of autopsy material obtained from persons with the APOE3 Ch and PSEN1 E280A variants showed fewer vascular amyloid pathologic features than were seen in material obtained from persons who had the PSEN1 E280A variant but not the APOE3 Ch variant.ConclusionsClinical data supported a delayed onset of cognitive impairment in persons who were heterozygous for the APOE3 Ch variant in a kindred with a high prevalence of autosomal dominant Alzheimer's disease. (Funded by Good Ventures and others.)