395 research outputs found
Dynamics from elastic neutron-scattering via direct measurement of the running time-integral of the van Hove distribution function
We present a new neutron-scattering approach to access the van Hove
distribution function directly in the time domain, I(t), which reflects the
system dynamics. Currently, I(t) is essentially determined from neutron
energy-exchange. Our method consists of the straightforward measurement of the
running time-integral of I(t), by computing the portion of scattered neutrons
corresponding to species at rest within a time t, (conceptually elastic
scattering). Previous attempts failed to recognise this connection. Starting
from a theoretical standpoint, a practical realisation is assessed via
numerical methods and an instrument simulation.Comment: 11 pages, 5 figures, new results, supplementary material (14 pages, 5
figures, 21 main equations, new results
Spin-gap opening accompanied by a strong magnetoelastic response in the S=1 magnetic dimer system Ba3BiRu2O9
Neutron diffraction, magnetization, resistivity, and heat capacity
measurements on the 6H-perovskite Ba3BiRu2O9 reveal simultaneous magnetic and
structural dimerization driven by strong magnetoelastic coupling. An
isostructural but strongly displacive first-order transition on cooling through
T*=176 K is associated with a change in the nature of direct Ru-Ru bonds within
Ru2O9 face-sharing octahedra. Above T*, Ba3BiRu2O9 is an S=1 magnetic dimer
system with intradimer exchange interactions J0/kB=320 K and interdimer
exchange interactions J'/kB=-160 K. Below T*, a spin-gapped state emerges with
\Delta\approx220 K. Ab initio calculations confirm antiferromagnetic exchange
within dimers, but the transition is not accompanied by long range-magnetic
order.Comment: 5 pages, 5 figures, accepted by Physical Review
B-type natriuretic peptide-guided treatment for heart failure
Background
Heart failure is a condition in which the heart does not pump enough blood to meet all the needs of the body. Symptoms of heart failure include breathlessness, fatigue and fluid retention. Outcomes for patients with heart failure are highly variable; however on average, these patients have a poor prognosis. Prognosis can be improved with early diagnosis and appropriate use of medical treatment, use of devices and transplantation. Patients with heart failure are high users of healthcare resources, not only due to drug and device treatments, but due to high costs of hospitalisation care. Bâtype natriuretic peptide levels are already used as biomarkers for diagnosis and prognosis of heart failure, but could offer to clinicians a possible tool to guide drug treatment. This could optimise drug management in heart failure patients whilst allaying concerns over potential side effects due to drug intolerance.
Objectives
To assess whether treatment guided by serial BNP or NTâproBNP (collectively referred to as NP) monitoring improves outcomes compared with treatment guided by clinical assessment alone.
Search methods
Searches were conducted up to 15 March 2016 in the Cochrane Central Register of Controlled Trials (CENTRAL) in the Cochrane Library; MEDLINE (OVID), Embase (OVID), the Database of Abstracts of Reviews of Effects (DARE) and the NHS Economic Evaluation Database in the Cochrane Library. Searches were also conducted in the Science Citation Index Expanded, the Conference Proceedings Citation Index on Web of Science (Thomson Reuters), World Health Organization International Clinical Trials Registry and ClinicalTrials.gov. We applied no date or language restrictions.
Selection criteria
We included randomised controlled trials of NPâguided treatment of heart failure versus treatment guided by clinical assessment alone with no restriction on followâup. Adults treated for heart failure, in both inâhospital and outâofâhospital settings, and trials reporting a clinical outcome were included.
Data collection and analysis
Two review authors independently selected studies for inclusion, extracted data and evaluated risk of bias. Risk ratios (RR) were calculated for dichotomous data, and pooled mean differences (MD) (with 95% confidence intervals (CI)) were calculated for continuous data. We contacted trial authors to obtain missing data. Using the Grading of Recommendations Assessment, Development and Evaluation (GRADE) approach, we assessed the quality of the evidence and GRADE profiler (GRADEPRO) was used to import data from Review Manager to create a 'Summary of findings' table.
Main results
We included 18 randomised controlled trials with 3660 participants (range of mean age: 57 to 80 years) comparing NPâguided treatment with clinical assessment alone. The evidence for allâcause mortality using NPâguided treatment showed uncertainty (RR 0.87, 95% CI 0.76 to 1.01; patients = 3169; studies = 15; low quality of the evidence), and for heart failure mortality (RR 0.84, 95% CI 0.54 to 1.30; patients = 853; studies = 6; low quality of evidence).
The evidence suggested heart failure admission was reduced by NPâguided treatment (38% versus 26%, RR 0.70, 95% CI 0.61 to 0.80; patients = 1928; studies = 10; low quality of evidence), but the evidence showed uncertainty for allâcause admission (57% versus 53%, RR 0.93, 95% CI 0.84 to 1.03; patients = 1142; studies = 6; low quality of evidence).
Six studies reported on adverse events, however the results could not be pooled (patients = 1144; low quality of evidence). Only four studies provided cost of treatment results, three of these studies reported a lower cost for NPâguided treatment, whilst one reported a higher cost (results were not pooled; patients = 931, low quality of evidence). The evidence showed uncertainty for quality of life data (MD â0.03, 95% CI â1.18 to 1.13; patients = 1812; studies = 8; very low quality of evidence).
We completed a 'Risk of bias' assessment for all studies. The impact of risk of bias from lack of blinding of outcome assessment and high attrition levels was examined by restricting analyses to only low 'Risk of bias' studies.
Authors' conclusions
In patients with heart failure lowâquality evidence showed a reduction in heart failure admission with NPâguided treatment while lowâquality evidence showed uncertainty in the effect of NPâguided treatment for allâcause mortality, heart failure mortality, and allâcause admission. Uncertainty in the effect was further shown by very lowâquality evidence for patient's quality of life. The evidence for adverse events and cost of treatment was low quality and we were unable to pool results.</p
Th2-driven, allergen-induced airway inflammation is reduced after treatment with anti-Tim-3 antibody in vivo
T cell immunoglobulin and mucin domainâcontaining molecule-3 (Tim-3) is a surface molecule that is preferentially expressed on activated Th1 cells in comparison to Th2 cells. Blockade of Tim-3 has been shown to enhance Th1-driven pathology in vivo, suggesting that blockade of Tim-3 may improve the development of Th2-associated responses such as allergy. To examine the effects of Tim-3 blockade on the Th2 response in vivo, we administered antiâTim-3 antibody during pulmonary inflammation induced by transfer of ovalbumin (OVA)-reactive Th2 cells, and subsequent aerosol challenge with OVA. In this model, antiâTim-3 antibody treatment before each airway challenge significantly reduced airway hyperreactivity, with a concomitant decrease in eosinophils and Th2 cells in the lung. We examined Th1 and Th2 cytokine levels in the lung after allergen challenge and found that pulmonary expression of the Th2 cytokine IL-5 was significantly reduced, whereas IFN-Îł levels were significantly increased by antiâTim-3 antibody treatment. Thus, blocking Tim-3 function has a beneficial effect during pulmonary inflammation by skewing the Th2 response toward that of a Th1 type, suggesting an important role for Tim-3 in the regulation of allergic disease
Resolution of airway inflammation and hyperreactivity after in vivo transfer of CD4(+) CD25(+) regulatory T cells is interleukin 10 dependent
Th2-driven, allergen-induced airway inflammation is reduced after treatment with antiâTim-3 antibody in vivo
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