275 research outputs found

    An ecological approach to problems of Dark Energy, Dark Matter, MOND and Neutrinos

    Full text link
    Modern astronomical data on galaxy and cosmological scales have revealed powerfully the existence of certain dark sectors of fundamental physics, i.e., existence of particles and fields outside the standard models and inaccessible by current experiments. Various approaches are taken to modify/extend the standard models. Generic theories introduce multiple de-coupled fields A, B, C, each responsible for the effects of DM (cold supersymmetric particles), DE (Dark Energy) effect, and MG (Modified Gravity) effect respectively. Some theories use adopt vanilla combinations like AB, BC, or CA, and assume A, B, C belong to decoupled sectors of physics. MOND-like MG and Cold DM are often taken as opposite frameworks, e.g. in the debate around the Bullet Cluster. Here we argue that these ad hoc divisions of sectors miss important clues from the data. The data actually suggest that the physics of all dark sectors is likely linked together by a self-interacting oscillating field, which governs a chameleon-like dark fluid, appearing as DM, DE and MG in different settings. It is timely to consider an interdisciplinary approach across all semantic boundaries of dark sectors, treating the dark stress as one identity, hence accounts for several "coincidences" naturally.Comment: 12p, Proceedings to the 6-th Int. Conf. of Gravitation and Cosmology. Neutrino section expande

    Ischaemic strokes in patients with pulmonary arteriovenous malformations and hereditary hemorrhagic telangiectasia: associations with iron deficiency and platelets.

    Get PDF
    <div><p>Background</p><p>Pulmonary first pass filtration of particles marginally exceeding ∼7 µm (the size of a red blood cell) is used routinely in diagnostics, and allows cellular aggregates forming or entering the circulation in the preceding cardiac cycle to lodge safely in pulmonary capillaries/arterioles. Pulmonary arteriovenous malformations compromise capillary bed filtration, and are commonly associated with ischaemic stroke. Cohorts with CT-scan evident malformations associated with the highest contrast echocardiographic shunt grades are known to be at higher stroke risk. Our goal was to identify within this broad grouping, which patients were at higher risk of stroke.</p><p>Methodology</p><p>497 consecutive patients with CT-proven pulmonary arteriovenous malformations due to hereditary haemorrhagic telangiectasia were studied. Relationships with radiologically-confirmed clinical ischaemic stroke were examined using logistic regression, receiver operating characteristic analyses, and platelet studies.</p><p>Principal Findings</p><p>Sixty-one individuals (12.3%) had acute, non-iatrogenic ischaemic clinical strokes at a median age of 52 (IQR 41–63) years. In crude and age-adjusted logistic regression, stroke risk was associated not with venous thromboemboli or conventional neurovascular risk factors, but with low serum iron (adjusted odds ratio 0.96 [95% confidence intervals 0.92, 1.00]), and more weakly with low oxygen saturations reflecting a larger right-to-left shunt (adjusted OR 0.96 [0.92, 1.01]). For the same pulmonary arteriovenous malformations, the stroke risk would approximately double with serum iron 6 µmol/L compared to mid-normal range (7–27 µmol/L). Platelet studies confirmed overlooked data that iron deficiency is associated with exuberant platelet aggregation to serotonin (5HT), correcting following iron treatment. By MANOVA, adjusting for participant and 5HT, iron or ferritin explained 14% of the variance in log-transformed aggregation-rate (p = 0.039/p = 0.021).</p><p>Significance</p><p>These data suggest that patients with compromised pulmonary capillary filtration due to pulmonary arteriovenous malformations are at increased risk of ischaemic stroke if they are iron deficient, and that mechanisms are likely to include enhanced aggregation of circulating platelets.</p></div

    Spinal trigeminal neurons demonstrate an increase in responses to dural electrical stimulation in the orofacial formalin test

    Get PDF
    Primary headaches are often associated with pain in the maxillofacial region commonly classified under the term “orofacial pain” (OFP). In turn, long-lasting OFP can trigger and perpetuate headache as an independent entity, which is able to persist after the resolution of the main disorder. A close association between OFP and headache complicates their cause and effect definition and leads to misdiagnosis. The precise mechanisms underlying this phenomenon are poorly understood, partly because of the deficiency of research-related findings. We combined the animal models of OFP and headache—the orofacial formalin test and the model of trigeminovascular nociception—to investigate the neurophysiological mechanisms underlying their comorbidity. In anesthetized rats, the ongoing activity of single convergent neurons in the spinal trigeminal nucleus was recorded in parallel to their responses to the electrical stimulation of the dura mater before and after the injection of formalin into their cutaneous receptive fields. Subcutaneous formalin resulted not only in the biphasic increase in the ongoing activity, but also in an enhancement of neuronal responses to dural electrical stimulation, which had similar time profile. These results demonstrated that under tonic pain in the orofacial region a nociceptive signaling from the dura mater to convergent trigeminal neurons is significantly enhanced apparently because of the development of central sensitization; this may contribute to the comorbidity of OFP and headache

    A Markov computer simulation model of the economics of neuromuscular blockade in patients with acute respiratory distress syndrome

    Get PDF
    BACKGROUND: Management of acute respiratory distress syndrome (ARDS) in the intensive care unit (ICU) is clinically challenging and costly. Neuromuscular blocking agents may facilitate mechanical ventilation and improve oxygenation, but may result in prolonged recovery of neuromuscular function and acute quadriplegic myopathy syndrome (AQMS). The goal of this study was to address a hypothetical question via computer modeling: Would a reduction in intubation time of 6 hours and/or a reduction in the incidence of AQMS from 25% to 21%, provide enough benefit to justify a drug with an additional expenditure of 267(thedifferenceinacquisitioncostbetweenagenericandbrandnameneuromuscularblocker)?METHODS:Thebasecasewasa55yearoldmanintheICUwithARDSwhoreceivesneuromuscularblockadefor3.5days.AMarkovmodelwasdesignedwithhypotheticalpatientsin1of6mutuallyexclusivehealthstates:ICUintubated,ICUextubated,hospitalward,longtermcare,home,ordeath,overaperiodof6months.Thenetmonetarybenefitwascomputed.RESULTS:OurcomputersimulationmodelingpredictedthemeancostforARDSpatientsreceivingstandardcarefor6monthstobe267 (the difference in acquisition cost between a generic and brand name neuromuscular blocker)? METHODS: The base case was a 55 year-old man in the ICU with ARDS who receives neuromuscular blockade for 3.5 days. A Markov model was designed with hypothetical patients in 1 of 6 mutually exclusive health states: ICU-intubated, ICU-extubated, hospital ward, long-term care, home, or death, over a period of 6 months. The net monetary benefit was computed. RESULTS: Our computer simulation modeling predicted the mean cost for ARDS patients receiving standard care for 6 months to be 62,238 (5% – 95% percentiles 42,25942,259 – 83,766), with an overall 6-month mortality of 39%. Assuming a ceiling ratio of 35,000,evenifadrug(thatcost35,000, even if a drug (that cost 267 more) hypothetically reduced AQMS from 25% to 21% and decreased intubation time by 6 hours, the net monetary benefit would only equal $137. CONCLUSION: ARDS patients receiving a neuromuscular blocker have a high mortality, and unpredictable outcome, which results in large variability in costs per case. If a patient dies, there is no benefit to any drug that reduces ventilation time or AQMS incidence. A prospective, randomized pharmacoeconomic study of neuromuscular blockers in the ICU to asses AQMS or intubation times is impractical because of the highly variable clinical course of patients with ARDS
    corecore