211 research outputs found
Heat Transfer Mechanisms in Porous Materials and Contemporary Problems in Thermophysical Properties Investigations: Analyses and Solutions
This article is an overview of the topical problems in the investigation of thermophysical properties and the development of a database for porous materials. Determination of both apparent/measured and true thermophysical properties is discussed taking into account combined heat and mass transfer, latent heat effects during chemical and physical transformations, as well as structural changes. The approaches to the solution of these problems are demonstrated for a number of different classes of materials: Industrial refractories, ceramics, highly porous insulation; Moist materials and materials undergoing phase, chemical and structural transformations; Materials semitransparent for heat radiation.
The approaches being used in the development of a thermophysical properties database consist in a combination of theoretical and experimental methods.
The analysis, generalization, and extrapolation of available reference data can be conducted based on the models for classical (conduction, heat radiation, gas convection) and additional (novel) mechanisms and processes affecting the apparent thermophysical properties. The novel heat transfer mechanisms include: Heterogeneous heat and mass transfer processes occurring in pores existing at grain boundaries and in cracks, in particular, surface segregation and diffusion of impurities on pore surfaces and transport of gases produced from chemical reactions, evaporation, and sublimation. Microstructure changes due to non-uniform thermal expansion of particles and grains. These changes are caused by the mismatch of thermal expansion coefficients of different phases in the material and anisotropic thermal expansion of crystals
Conducting clinical trials in persons with Down syndrome : summary from the NIH INCLUDE Down syndrome clinical trials readiness working group
The recent National Institute of Health (NIH) INCLUDE (INvestigation of Co-occurring conditions across the Lifespan to Understand Down syndromE) initiative has bolstered capacity for the current increase in clinical trials involving individuals with Down syndrome (DS). This new NIH funding mechanism offers new opportunities to expand and develop novel approaches in engaging and effectively enrolling a broader representation of clinical trials participants addressing current medical issues faced by individuals with DS. To address this opportunity, the NIH assembled leading clinicians, scientists, and representatives of advocacy groups to review existing methods and to identify those areas where new approaches are needed to engage and prepare DS populations for participation in clinical trial research. This paper summarizes the results of the Clinical Trial Readiness Working Group that was part of the INCLUDE Project Workshop: Planning a Virtual Down Syndrome Cohort Across the Lifespan Workshop held virtually September 23 and 24, 2019
Reductive Stress Causes Pathological Cardiac Remodeling and Diastolic Dysfunction.
Aims: Redox homeostasis is tightly controlled and regulates key cellular signaling pathways. The cells antioxidant response provides a natural defense against oxidative stress, but excessive antioxidant generation leads to reductive stress (RS). This study elucidated how chronic RS, caused by constitutive activation of nuclear erythroid related factor-2 (caNrf2)-dependent antioxidant system, drives pathological myocardial remodeling. Results: Upregulation of antioxidant transcripts and proteins in caNrf2-TG hearts (TGL and TGH; transgenic-low and -high) dose dependently increased glutathione (GSH) redox potential and resulted in RS, which over time caused pathological cardiac remodeling identified as hypertrophic cardiomyopathy (HCM) with abnormally increased ejection fraction and diastolic dysfunction in TGH mice at 6 months of age. While the TGH mice exhibited 60% mortality at 18 months of age, the rate of survival in TGL was comparable with nontransgenic (NTG) littermates. Moreover, TGH mice had severe cardiac remodeling at ∼6 months of age, while TGL mice did not develop comparable phenotypes until 15 months, suggesting that even moderate RS may lead to irreversible damages of the heart over time. Pharmacologically blocking GSH biosynthesis using BSO (l-buthionine-SR-sulfoximine) at an early age (∼1.5 months) prevented RS and rescued the TGH mice from pathological cardiac remodeling. Here we demonstrate that chronic RS causes pathological cardiomyopathy with diastolic dysfunction in mice due to sustained activation of antioxidant signaling. Innovation and Conclusion: Our findings demonstrate that chronic RS is intolerable and adequate to induce heart failure (HF). Antioxidant-based therapeutic approaches for human HF should consider a thorough evaluation of redox state before the treatment
Consensus statement on surgical pathology of the aorta from the Society for Cardiovascular Pathology and the Association for European Cardiovascular Pathology: I. Inflammatory diseases
Abstract Inflammatory diseases of the aorta include routine atherosclerosis, aortitis, periaortitis, and atherosclerosis with excessive inflammatory responses, such as inflammatory atherosclerotic aneurysms. The nomenclature and histologic features of these disorders are reviewed and discussed. In addition, diagnostic criteria are provided to distinguish between these disorders in surgical pathology specimens. An initial classification scheme is provided for aortitis and periaortitis based on the pattern of the inflammatory infiltrate: granulomatous/giant cell pattern, lymphoplasmacytic pattern, mixed inflammatory pattern, and the suppurative pattern. These inflammatory patterns are discussed in relation to specific systemic diseases including giant cell arteritis, Takayasu arteritis, granulomatosis with polyangiitis (Wegener's), rheumatoid arthritis, sarcoidosis, ankylosing spondylitis, Cogan syndrome, Behcet's disease, relapsing polychondritis, syphilitic aortitis, and bacterial and fungal infections
Thermal conductivity of refractory glass fibres
In the present study, the current international
standards and corresponding apparatus for measuring the
thermal conductivity of refractory glass fibre products have
been reviewed. Refractory glass fibres are normally produced
in the form of low-density needled mats. A major
issue with thermal conductivity measurements of these
materials is lack of reproducibility in the test results due to
transformation of the test material during the test. Also
needled mats are inherently inhomogeneous, and this poses
additional problems. To be able to compare the various
methods of thermal conductivity measurement, a refractory
reference material was designed which is capable of
withstanding maximum test temperatures (1673 K) with
minimum transformation. The thermal conductivity of this
reference material was then measured using various
methods according to the different standards surveyed. In
order to compare different materials, samples have been
acquired from major refractory glass fibre manufacturers
and the results have been compared against the newly
introduced reference material. Materials manufactured by
melt spinning, melt blowing and sol–gel have been studied,
and results compared with literature values
Signal Transmission in the Auditory System
Contains table of contents for Section 3, an introduction and reports on six research projects.National Institutes of Health Grant RO1-DC-00194-11National Institutes of Health Grant PO1-DC00119 Sub-Project 1National Institutes of Health Grant F32-DC00073-3National Institutes of Health Contract P01-DC00119National Institutes of Health Grant R01 DC00238National Institutes of Health Grant P01-DC00119National Institutes of Health Grant T32-DC00038National Institutes of Health Contract P01-DC00361National Institutes of Health Grant R01-DC00235National Institutes of Health Contract NO1-DC2240
Signal Transmission in the Auditory System
Contains table of contents for Section 3, an introduction and reports on seven research projects.National Institutes of Health Grant P01-DC-00119National Institutes of Health Grant R01-DC-00194National Institutes of Health Grant R01 DC00238National Institutes of Health Grant R01-DC02258National Institutes of Health Grant T32-DC00038National Institutes of Health Grant P01-DC00361National Institutes of Health Grant 2RO1 DC00235National Institutes of Health Contract N01-DC2240
From Vulnerable Plaque to Vulnerable Patient
Atherosclerotic cardiovascular disease results in >19 million deaths annually, and coronary heart disease accounts for the majority of this toll. Despite major advances in treatment of coronary heart disease patients, a large number of victims of the disease who are apparently healthy die suddenly without prior symptoms. Available screening and diagnostic methods are insufficient to identify the victims before the event occurs. The recognition of the role of the vulnerable plaque has opened new avenues of opportunity in the field of cardiovascular medicine. This consensus document concludes the following. (1) Rupture-prone plaques are not the only vulnerable plaques. All types of atherosclerotic plaques with high likelihood of thrombotic complications and rapid progression should be considered as vulnerable plaques. We propose a classification for clinical as well as pathological evaluation of vulnerable plaques. (2) Vulnerable plaques are not the only culprit factors for the development of acute coronary syndromes, myocardial infarction, and sudden cardiac death. Vulnerable blood (prone to thrombosis) and vulnerable myocardium (prone to fatal arrhythmia) play an important role in the outcome. Therefore, the term "vulnerable patient" may be more appropriate and is proposed now for the identification of subjects with high likelihood of developing cardiac events in the near future. (3) A quantitative method for cumulative risk assessment of vulnerable patients needs to be developed that may include variables based on plaque, blood, and myocardial vulnerability. In Part I of this consensus document, we cover the new definition of vulnerable plaque and its relationship with vulnerable patients. Part II of this consensus document will focus on vulnerable blood and vulnerable myocardium and provide an outline of overall risk assessment of vulnerable patients. Parts I and II are meant to provide a general consensus and overviews the new field of vulnerable patient. Recently developed assays (eg, C-reactive protein), imaging techniques (eg, CT and MRI), noninvasive electrophysiological tests (for vulnerable myocardium), and emerging catheters (to localize and characterize vulnerable plaque) in combination with future genomic and proteomic techniques will guide us in the search for vulnerable patients. It will also lead to the development and deployment of new therapies and ultimately to reduce the incidence of acute coronary syndromes and sudden cardiac death. We encourage healthcare policy makers to promote translational research for screening and treatment of vulnerable patients
Molecular imaging of inflammation and intraplaque vasa vasorum: A step forward to identification of vulnerable plaques?
Current developments in cardiovascular biology and imaging enable the noninvasive molecular evaluation of atherosclerotic vascular disease. Intraplaque neovascularization sprouting from the adventitial vasa vasorum has been identified as an independent predictor of intraplaque hemorrhage and plaque rupture. These intraplaque vasa vasorum result from angiogenesis, most likely under influence of hypoxic and inflammatory stimuli. Several molecular imaging techniques are currently available. Most experience has been obtained with molecular imaging using positron emission tomography and single photon emission computed tomography. Recently, the development of targeted contrast agents has allowed molecular imaging with magnetic resonance imaging, ultrasound and computed tomography. The present review discusses the use of these molecular imaging techniques to identify inflammation and intraplaque vasa vasorum to identify vulnerable atherosclerotic plaques at risk of rupture and thrombosis. The available literature on molecular imaging techniques and molecular targets associated with inflammation and angiogenesis is discussed, and the clinical applications of molecular cardiovascular imaging and the use of molecular techniques for local drug delivery are addressed
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