450 research outputs found
On single and double soft behaviors in NLSM
In this paper, we study the single and double soft behaviors of tree level
off-shell currents and on-shell amplitudes in nonlinear sigma model(NLSM). We
first propose and prove the leading soft behavior of the tree level currents
with a single soft particle. In the on-shell limit, this single soft emission
becomes the Adler's zero. Then we establish the leading and sub-leading soft
behaviors of tree level currents with two adjacent soft particles. With a
careful analysis of the on-shell limit, we obtain the double soft behaviors of
on-shell amplitudes where the two soft particles are adjacent to each other. By
applying Kleiss-Kuijf (KK) relation, we further obtain the leading and
sub-leading behaviors of amplitudes with two nonadjacent soft particles.Comment: 41 pages, 6 tables, 9 figures, minor revised, more content about
nonadjacent double soft limit, update the reference
CHY representations for gauge theory and gravity amplitudes with up to three massive particles
We show that a wide class of tree-level scattering amplitudes involving
scalars, gauge bosons, and gravitons, up to three of which may be massive, can
be expressed in terms of a Cachazo-He-Yuan representation as a sum over
solutions of the scattering equations. These amplitudes, when expressed in
terms of the appropriate kinematic invariants, are independent of the masses
and therefore identical to the corresponding massless amplitudes.Comment: 20 pages, 1 figure; v2: minor typos corrected, published versio
The epistemological model of disability, and its role in understanding passive exclusion in eighteenth and nineteenth century protestant educational asylums
This article examines how the process of constructing knowledge on impairment has affected the institutional construction of an ethic of disability. Its primary finding is that the process of creating knowledge in a number of historical contexts was influenced more by traditions and the biases of philosophers and educators in order to signify moral and intellectual superiority, than by a desire to improve the lives of disabled people through education. The article illustrates this epistemological process in a case study of the development of Protestant asylums in the latter years of the nineteenth century
Collegial nests can Foster Critical Thinking, Innovative Ideas, and Scientific Progress.
How can management and strategy scholars organize to generate more productive, more innovative, and more impactful research? With appropriate cultures and leaders, small and egalitarian discussion groups that we call “collegial nests” can become powerful generators of innovative ideas and creators of extraordinary scholars. Collegial nests need cultures that free participants to think critically, to cherish new viewpoints, and to speak freely without fear of ridicule. They also need leaders who model such cultures and facilitate frequent discussions. Two case examples illustrate how productive collegial nests can create better science and better scientists. To generate scientific innovation and progress on a large scale, many autonomous groups tackling related issues are desirable. Modern communication technology is making it feasible for groups to operate over large distances and to coordinate with each other at very low cost. Collegial nests offer greater potential for enhancing scholarly productivity and innovation than do attempts to regulate scholarship via hierarchical structures. Multiplicity can lower the probability of wasting resources on low-yield paths, egalitarian control can reduce the influence of vested interests, and a combination of shared goals and partial autonomy can integrate enthusiasm with sensible risk taking
Borrelia valaisiana resist complement-mediated killing independently of the recruitment of immune regulators and inactivation of complement components
Spirochetes belonging to the Borrelia (B.) burgdorferi sensu lato complex differ in their resistance to complement-mediated killing, particularly in regard to human serum. In the present study, we elucidate the serum and complement susceptibility of B. valaisiana, a genospecies with the potential to cause Lyme disease in Europe as well as in Asia. Among the investigated isolates, growth of ZWU3 Ny3 was not affected while growth of VS116 and Bv9 was strongly inhibited in the presence of 50% human serum. Analyzing complement activation, complement components C3, C4 and C6 were deposited on the surface of isolates VS116 and Bv9, and similarly the membrane attack complex was formed on their surface. In contrast, no surface-deposited components and no aberrations in cell morphology were detected for serum-resistant ZWU3 Ny3. While further investigating the protective role of bound complement regulators in mediating complement resistance, we discovered that none of the B. valaisiana isolates analyzed bound complement regulators Factor H, Factor H-like protein 1, C4b binding protein or C1 esterase inhibitor. In addition, B. valaisiana also lacked intrinsic proteolytic activity to degrade complement components C3, C3b, C4, C4b, and C5. Taken together, these findings suggest that certain B. valaisiana isolates differ in their capability to resist complement-mediating killing by human serum. The molecular mechanism utilized by B. valaisiana to inhibit bacteriolysis appears not to involve binding of the key host complement regulators of the alternative, classical, and lectin pathways as already known for serum-resistant Lyme disease or relapsing fever borreliae
EARLYDRAIN- outcome after early lumbar CSF-drainage in aneurysmal subarachnoid hemorrhage: study protocol for a randomized controlled trial
<p>Abstract</p> <p>Background</p> <p>Aneurysmal subarachnoid hemorrhage (SAH) may be complicated by delayed cerebral ischemia, which is a major cause of unfavorable clinical outcome and death in SAH-patients. Delayed cerebral ischemia is presumably related to the development of vasospasm triggered by the presence of blood in the basal cisterns. To date, oral application of the calcium antagonist nimodipine is the only prophylactic treatment for vasospasm recognized under international guidelines.</p> <p>In retrospective trials lumbar drainage of cerebrospinal fluid has been shown to be a safe and feasible measure to remove the blood from the basal cisterns and decrease the incidence of delayed cerebral ischemia and vasospasm in the respective study populations. However, the efficacy of lumbar drainage has not been evaluated prospectively in a randomized controlled trial yet.</p> <p>Methods/Design</p> <p>This is a protocol for a 2-arm randomized controlled trial to compare an intervention group receiving early continuous lumbar CSF-drainage and standard neurointensive care to a control group receiving standard neurointensive care only. Adults suffering from a first aneurysmal subarachnoid hemorrhage whose aneurysm has been secured by means of coiling or clipping are eligible for trial participation. The effect of early CSF drainage (starting < 72 h after securing the aneurysm) will be measured in the following ways: the primary endpoint will be disability after 6 months, assessed by a blinded investigator during a personal visit or standardized telephone interview using the modified Rankin Scale. Secondary endpoints include mortality after 6 months, angiographic vasospasm, transcranial Doppler sonography (TCD) mean flow velocity in both middle cerebral arteries and rate of shunt insertion at 6 months after hospital discharge.</p> <p>Discussion</p> <p>Here, we present the study design of a multicenter prospective randomized controlled trial to investigate whether early application of a lumbar drainage improves clinical outcome after aneurysmal subarachnoid hemorrhage.</p> <p>Trial registration</p> <p>www.clinicaltrials.gov Identifier: <a href="http://www.clinicaltrials.gov/ct2/show/NCT01258257">NCT01258257</a></p
The glial growth factors deficiency and synaptic destabilization hypothesis of schizophrenia
BACKGROUND: A systems approach to understanding the etiology of schizophrenia requires a theory which is able to integrate genetic as well as neurodevelopmental factors. PRESENTATION OF THE HYPOTHESIS: Based on a co-localization of loci approach and a large amount of circumstantial evidence, we here propose that a functional deficiency of glial growth factors and of growth factors produced by glial cells are among the distal causes in the genotype-to-phenotype chain leading to the development of schizophrenia. These factors include neuregulin, insulin-like growth factor I, insulin, epidermal growth factor, neurotrophic growth factors, erbB receptors, phosphatidylinositol-3 kinase, growth arrest specific genes, neuritin, tumor necrosis factor alpha, glutamate, NMDA and cholinergic receptors. A genetically and epigenetically determined low baseline of glial growth factor signaling and synaptic strength is expected to increase the vulnerability for additional reductions (e.g., by viruses such as HHV-6 and JC virus infecting glial cells). This should lead to a weakening of the positive feedback loop between the presynaptic neuron and its targets, and below a certain threshold to synaptic destabilization and schizophrenia. TESTING THE HYPOTHESIS: Supported by informed conjectures and empirical facts, the hypothesis makes an attractive case for a large number of further investigations. IMPLICATIONS OF THE HYPOTHESIS: The hypothesis suggests glial cells as the locus of the genes-environment interactions in schizophrenia, with glial asthenia as an important factor for the genetic liability to the disorder, and an increase of prolactin and/or insulin as possible working mechanisms of traditional and atypical neuroleptic treatments
Optomechanical Crystals
Structured, periodic optical materials can be used to form photonic crystals
capable of dispersing, routing, and trapping light. A similar phenomena in
periodic elastic structures can be used to manipulate mechanical vibrations.
Here we present the design and experimental realization of strongly coupled
optical and mechanical modes in a planar, periodic nanostructure on a silicon
chip. 200-Terahertz photons are co-localized with mechanical modes of Gigahertz
frequency and 100-femtogram mass. The effective coupling length, which
describes the strength of the photon-phonon interaction, is as small as 2.9
microns, which, together with minute oscillator mass, allows all-optical
actuation and transduction of nanomechanical motion with near quantum-limited
sensitivity. Optomechanical crystals have many potential applications, from
RF-over-optical communication to the study of quantum effects in mesoscopic
mechanical systems.Comment: 16 pages, 7 figure
Effect of educational intervention on medication timing in Parkinson's disease: a randomized controlled trial
<p>Abstract</p> <p>Background</p> <p>Medicine usage in Parkinson's disease patients is often imperfect, in particular irregular timing of medication. The effect of informing Parkinson's disease patients about the continuous dopaminergic hypothesis (to encourage regular medicine intake) on medication adherence and motor control was tested.</p> <p>Methods</p> <p>Patients were randomised either to the active group (receiving the intervention) or control group (no extra information). Antiparkinson medicine usage was monitored for 3 months before and after the intervention using electronic pill bottles which record the date and time of opening (MEMS<sup>®</sup>, Aardex, Switzerland) and data used to calculate the percentage of doses taken at correct time intervals.</p> <p>Results</p> <p>43 patients (52%) were randomised to active counselling, and 40 (48%) were controls (standard management). The intervention effect (difference in timing adherence pre- to post-intervention between the 2 groups) was 13.4% (CI 5.1 to 21.7), p = 0.002. Parkinson motor scores did not change significantly (active group 0.1, CI -3.4 to 3.7) versus controls (4.5, CI 1.6 to 7.1), p = 0.06.</p> <p>Conclusion</p> <p>Timing adherence, but not motor scores, improves by providing patients with extra information. Therapy timing is of potential importance in Parkinson's disease management.</p> <p>Trial registration number</p> <p>NCT00361205</p
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