49 research outputs found

    Constraints on Nucleon Decay via "Invisible" Modes from the Sudbury Neutrino Observatory

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    Data from the Sudbury Neutrino Observatory have been used to constrain the lifetime for nucleon decay to ``invisible'' modes, such as n -> 3 nu. The analysis was based on a search for gamma-rays from the de-excitation of the residual nucleus that would result from the disappearance of either a proton or neutron from O16. A limit of tau_inv > 2 x 10^{29} years is obtained at 90% confidence for either neutron or proton decay modes. This is about an order of magnitude more stringent than previous constraints on invisible proton decay modes and 400 times more stringent than similar neutron modes.Comment: Update includes missing efficiency factor (limits change by factor of 2) Submitted to Physical Review Letter

    Toward allele-specific targeting therapy and pharmacodynamic marker for spinocerebellar ataxia type 3

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    Spinocerebellar ataxia type 3 (SCA3), caused by a CAG repeat expansion in the ataxin-3 gene (ATXN3), is characterized by neuronal polyglutamine (polyQ) ATXN3 protein aggregates. Although there is no cure for SCA3, gene-silencing approaches to reduce toxic polyQ ATXN3 showed promise in preclinical models. However, a major limitation in translating putative treatments for this rare disease to the clinic is the lack of pharmacodynamic markers for use in clinical trials. Here, we developed an immunoassay that readily detects polyQ ATXN3 proteins in human biological fluids and discriminates patients with SCA3 from healthy controls and individuals with other ataxias. We show that polyQ ATXN3 serves as a marker of target engagement in human fibroblasts, which may bode well for its use in clinical trials. Last, we identified a single-nucleotide polymorphism that strongly associates with the expanded allele, thus providing an exciting drug target to abrogate detrimental events initiated by mutant ATXN3. Gene-silencing strategies for several repeat diseases are well under way, and our results are expected to improve clinical trial preparedness for SCA3 therapies

    Molecular MRI of Inflammation in Atherosclerosis

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    Inflammatory activity in atherosclerotic plaque is a risk factor for plaque rupture and atherothrombosis and may direct interventional therapy. Inflammatory activity can be evaluated at the (sub)cellular level using in vivo molecular MRI. This paper reviews recent progress in contrast-enhanced molecular MRI to visualize atherosclerotic plaque inflammation. Various MRI contrast agents, among others ultra-small particles of iron oxide, low-molecular-weight Gd-chelates, micelles, liposomes, and perfluorocarbon emulsions, have been used for in vivo visualization of various inflammation-related targets, such as macrophages, oxidized LDL, endothelial cell expression, plaque neovasculature, MMPs, apoptosis, and activated platelets/thrombus. An enzyme-activatable magnetic resonance contrast agent has been developed to study myeloperoxidase activity in inflamed plaques. Agents creating contrast based on the chemical exchange saturation transfer mechanism were used for thrombus imaging. Transfer of these molecular MRI techniques to the clinic will critically depend on the safety profiles of these newly developed magnetic resonance contrast agents

    Чернiгiвськi бестселери

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    Огляд книжкових новинок: Дзюба С. Зима така маленька, мов японка: Пародiї та вiршики. -Чернiгiв: Чернiгiвськi обереги, 2004 - 80 с.; Бондаревич (Черненко) Л. На берегах любовi: Есеї, нариси та монологи / переклад з бiлоруської С. Дзюби/. - Чернiгiв: Чернiгiвськi обереги, 2004 - 298 с.; Кава для янголiв. Випуск другий: Збiрник поезiї та прози молодих лiтераторiв Чернiгiвщини /упорядники С. i Т. Дзюби/. -Чернiгiв: Чернiгiвськi обереги, 2004 - 128 с.; Ткач М. Багрянi громи: Проза. - Нiжин: Аспект-Полiграф, 2004. -496 с.; Брик О. I возлюби: Проза - Нiжин: Аспект-Полiграф, 2004. - 320 с.; Брик О. Шоколадка:Проза. - Нiжин: Аспект-Полiграф, 2004. - 240 с
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