4,870 research outputs found

    Dirac type operators for spin manifolds associated to congruence subgroups of generalized modular groups

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    Fundamental solutions of Dirac type operators are introduced for a class of conformally. at spin manifolds. This class consists of manifolds obtained by factoring out the upper half-space of R-n by congruence subgroups of generalized modular groups. Basic properties of these fundamental solutions are presented together with associated Eisenstein and Poincare type series

    Multi-Prover Commitments Against Non-Signaling Attacks

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    We reconsider the concept of multi-prover commitments, as introduced in the late eighties in the seminal work by Ben-Or et al. As was recently shown by Cr\'{e}peau et al., the security of known two-prover commitment schemes not only relies on the explicit assumption that the provers cannot communicate, but also depends on their information processing capabilities. For instance, there exist schemes that are secure against classical provers but insecure if the provers have quantum information processing capabilities, and there are schemes that resist such quantum attacks but become insecure when considering general so-called non-signaling provers, which are restricted solely by the requirement that no communication takes place. This poses the natural question whether there exists a two-prover commitment scheme that is secure under the sole assumption that no communication takes place; no such scheme is known. In this work, we give strong evidence for a negative answer: we show that any single-round two-prover commitment scheme can be broken by a non-signaling attack. Our negative result is as bad as it can get: for any candidate scheme that is (almost) perfectly hiding, there exists a strategy that allows the dishonest provers to open a commitment to an arbitrary bit (almost) as successfully as the honest provers can open an honestly prepared commitment, i.e., with probability (almost) 1 in case of a perfectly sound scheme. In the case of multi-round schemes, our impossibility result is restricted to perfectly hiding schemes. On the positive side, we show that the impossibility result can be circumvented by considering three provers instead: there exists a three-prover commitment scheme that is secure against arbitrary non-signaling attacks

    Carotid shunt provides cerebral protection during emergency coronary artery bypass grafting in a patient with bilateral high grade carotid stenosis: a case report

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    <p>Abstract</p> <p>Background</p> <p>Management of patients with co-existent coronary and carotid disease is a controversial and challenging issue. The risk for stroke after coronary artery bypass grafting (CABG) in patients with hemodynamically significant carotid stenosis is up to 30%. In these patients a common practice is to proceed first with the restoration of cerebral perfusion and then perform the coronary revascularization. The rationale is that this strategy will reduce perioperative neurological morbidity and mortality. However, what happens when the carotid procedure is acutely complicated by cardiac instability which necessitates the interruption of the carotid procedure?</p> <p>Case report</p> <p>We describe a case of a patient with unstable angina and high grade asymptomatic bilateral carotid stenosis who underwent emergency combined CABG and carotid endarterectomy (CEA). Due to hemodynamic instability, ST-T changes, hypotension and bradycardia, upon completion of endarterectomy we placed a carotid shunt and the patient was put on cardiopulmonary bypass through median sternotomy. After triple CABG (duration of 90 minutes) we concluded the interrupted CEA procedure with primary closure of the carotid arteriotomy with the shunt in place. The postoperative course was uneventful and the patient was discharged after a week. In extreme cases with bilateral severe carotid stenosis and coronary artery disease where the carotid procedure should be interrupted, we suggest the use of carotid shunt which can provide adequate cerebral perfusion giving time to cardiac surgeon to perform the life saving cardiac procedure first.</p

    Effects of asenapine on depressive symptoms in patients with bipolar I disorder experiencing acute manic or mixed episodes: a post hoc analysis of two 3-week clinical trials

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    <p>Abstract</p> <p>Background</p> <p>Asenapine demonstrated superiority over placebo for mania in bipolar I disorder patients experiencing acute current manic or mixed episodes in 2 randomized, placebo-and olanzapine-controlled trials. We report the results of exploratory pooled post hoc analyses from these trials evaluating asenapine's effects on depressive symptoms in patients from these trials with significant baseline depressive symptoms.</p> <p>Methods</p> <p>In the original trials (A7501004 [NCT00159744], A7501005 [NCT00159796]), 977 patients were randomized to flexible-dose sublingual asenapine (10 mg twice daily on day 1; 5 or 10 mg twice daily thereafter), placebo, or oral olanzapine 5-20 mg once daily for 3 weeks. Three populations were defined using baseline depressive symptoms: (1) Montgomery-Asberg Depression Rating Scale (MADRS) total score ≥20 (n = 132); (2) Clinical Global Impression for Bipolar Disorder-Depression (CGI-BP-D) scale severity score ≥4 (n = 170); (3) diagnosis of mixed episodes (n = 302) by investigative site screening. For each population, asenapine and olanzapine were independently compared with placebo using least squares mean change from baseline on depressive symptom measures.</p> <p>Results</p> <p>Decreases in MADRS total score were statistically greater with asenapine versus placebo at days 7 and 21 in all populations; differences between olanzapine and placebo were not significant. Decreases in CGI-BP-D score were significantly greater with asenapine versus placebo at day 7 in all categories and day 21 in population 1; CGI-BP-D score reductions were significantly greater with olanzapine versus placebo at day 21 in population 1 and day 7 in populations 2 and 3.</p> <p>Conclusions</p> <p>These post hoc analyses show that asenapine reduced depressive symptoms in bipolar I disorder patients experiencing acute manic or mixed episodes with clinically relevant depressive symptoms at baseline; olanzapine results appeared to be less consistent. Controlled studies of asenapine in patients with acute bipolar depression are necessary to confirm the generalizability of these findings.</p

    Turing instabilities in a mathematical model for signaling networks

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    GTPase molecules are important regulators in cells that continuously run through an activation/deactivation and membrane-attachment/membrane-detachment cycle. Activated GTPase is able to localize in parts of the membranes and to induce cell polarity. As feedback loops contribute to the GTPase cycle and as the coupling between membrane-bound and cytoplasmic processes introduces different diffusion coefficients a Turing mechanism is a natural candidate for this symmetry breaking. We formulate a mathematical model that couples a reaction-diffusion system in the inner volume to a reaction-diffusion system on the membrane via a flux condition and an attachment/detachment law at the membrane. We present a reduction to a simpler non-local reaction-diffusion model and perform a stability analysis and numerical simulations for this reduction. Our model in principle does support Turing instabilities but only if the lateral diffusion of inactivated GTPase is much faster than the diffusion of activated GTPase.Comment: 23 pages, 5 figures; The final publication is available at http://www.springerlink.com http://dx.doi.org/10.1007/s00285-011-0495-

    Discussion on a possible neutrino detector located in India

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    We have identified some important and worthwhile physics opportunitites with a possible neutrino detector located in India. Particular emphasis is placed on the geographical advantage with a stress on the complimentary aspects with respect to other neutrino detectors already in operation.Comment: 9 pages; arXiv copy of published proceedings contributio

    Phenothiazine-mediated rescue of cognition in tau transgenic mice requires neuroprotection and reduced soluble tau burden

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    Abstract Background It has traditionally been thought that the pathological accumulation of tau in Alzheimer's disease and other tauopathies facilitates neurodegeneration, which in turn leads to cognitive impairment. However, recent evidence suggests that tau tangles are not the entity responsible for memory loss, rather it is an intermediate tau species that disrupts neuronal function. Thus, efforts to discover therapeutics for tauopathies emphasize soluble tau reductions as well as neuroprotection. Results Here, we found that neuroprotection alone caused by methylene blue (MB), the parent compound of the anti-tau phenothiaziazine drug, Rember&#8482;, was insufficient to rescue cognition in a mouse model of the human tauopathy, progressive supranuclear palsy (PSP) and fronto-temporal dementia with parkinsonism linked to chromosome 17 (FTDP17): Only when levels of soluble tau protein were concomitantly reduced by a very high concentration of MB, was cognitive improvement observed. Thus, neurodegeneration can be decoupled from tau accumulation, but phenotypic improvement is only possible when soluble tau levels are also reduced. Conclusions Neuroprotection alone is not sufficient to rescue tau-induced memory loss in a transgenic mouse model. Development of neuroprotective agents is an area of intense investigation in the tauopathy drug discovery field. This may ultimately be an unsuccessful approach if soluble toxic tau intermediates are not also reduced. Thus, MB and related compounds, despite their pleiotropic nature, may be the proverbial "magic bullet" because they not only are neuroprotective, but are also able to facilitate soluble tau clearance. Moreover, this shows that neuroprotection is possible without reducing tau levels. This indicates that there is a definitive molecular link between tau and cell death cascades that can be disrupted.http://deepblue.lib.umich.edu/bitstream/2027.42/78314/1/1750-1326-5-45.xmlhttp://deepblue.lib.umich.edu/bitstream/2027.42/78314/2/1750-1326-5-45.pdfhttp://deepblue.lib.umich.edu/bitstream/2027.42/78314/3/1750-1326-5-45-S1.PDFPeer Reviewe

    Study protocol: a randomised controlled trial investigating the effect of exercise training on peripheral blood gene expression in patients with stable angina

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    Background: Exercise training has been shown to reduce angina and promote collateral vessel development in patients with coronary artery disease. However, the mechanism whereby exercise exerts these beneficial effects is unclear. There has been increasing interest in the use of whole genome peripheral blood gene expression in a wide range of conditions to attempt to identify both novel mechanisms of disease and transcriptional biomarkers. This protocol describes a study in which we will assess the effect of a structured exercise programme on peripheral blood gene expression in patients with stable angina, and correlate this with changes in angina level, anxiety, depression, and exercise capacity. Methods/Design: Sixty patients with stable angina will be recruited and randomised 1: 1 to exercise training or conventional care. Patients randomised to exercise training will attend an exercise physiology laboratory up to three times weekly for supervised aerobic interval training sessions of one hour in total duration. Patients will undergo assessments of angina, anxiety, depression, and peripheral blood gene expression at baseline, after six and twelve weeks of training, and twelve weeks after formal exercise training ceases. Discussion: This study will provide comprehensive data on the effect of exercise training on peripheral blood gene expression in patients with angina. By correlating this with improvement in angina status we will identify candidate peripheral blood transcriptional markers predictive of improvements in angina level in response to exercise training

    Chronic bilateral heel pain in a child with Sever disease: case report and review of literature

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    We are presenting a case report of a 10-year-old male with a 1 year history of bilateral heel pain. Sever disease is self limiting condition of calcaneal apophysis. It is the most common cause of heel pain in the growing child. There is no documented case of this condition in this region. This case highlights the clinical features of this self limiting disorder as seen in this patient and reviews the current literature
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