Today's Hours: 12:00pm - 8:00pm
Lane Medical Library

Search

Filter Results

Did You Mean:

Search Results

Sort by
relevance
  • Book
    Allan R. Brasier, editor.
    Summary: Asthma is a chronic relapsing airways disease that represents a major public health problem worldwide. Intermittent exacerbations are provoked by airway mucosal exposure to pro-inflammatory stimuli, with RNA viral infections or inhaled allergens representing the two most common precipitants. In this setting, inducible signaling pathways the airway mucosa play a central role in the initiation of airway inflammation through production of antimicrobial peptides (defensins), cytokines, chemokines and arachidonic acid metabolites that coordinate the complex processes of vascular permeability, cellular recruitment, mucous hyper-secretion, bronchial constriction and tissue remodeling. These signals also are responsible for leukocytic infiltration into the submucosa, T helper-lymphocyte skewing, and allergic sensitization. Currently, it is well appreciated that asthma is a heterogeneous in terms of onset, exacerbants, severity, and treatment response. Current asthma classification methods are largely descriptive and focus on a single aspect or dimension of the disease. An active area of investigation on how to collect, use and visualize multidimensional profiling in asthma. This book will overview multidimensional profiling strategies and visualization approaches for phenotyping asthma. As an outcome, this work will facilitate the understanding of disease etiology, prognosis and/or therapeutic intervention.

    Contents:
    Spectrum of Asthma: an introduction
    Genetics and Genomics in Asthma
    Proteomics, Metabolomics, and Systems Biology of Asthma
    Modeling Complex Data in Asthma
    Conclusions and Future Directions.
    Digital Access Springer 2014
    Access via Advances in experimental medicine and biology ; 2014 ; 795
    Location
    Version
    Call Number
    Items
    Advances in experimental medicine and biology ; 2014 ; 795
    2014
  • Article
    Madden KS, Van der Kloot W.
    J Physiol. 1978 Mar;276:227-32.
    1. When motor nerve terminals are slightly depolarized with increased [K+]o, progressive increases in [Ca2+]o raise min.e.p.p. frequencies until a maximum is reached; further increases then produce a depression (Cook & Quastel, 1973; Matthews & Wickelgren, 1977). 2. Increases in [Mg2+]o also produce the depression. 3. It has been suggested that the depression results from this sequence of events: (a) the divalent cations screen the fixed negative surface charges on the outer face of the nerve terminal, which (b) decreases the negativity of the surface potential, which (c) increases the voltage gradient within the membrane itself, which (d) tends to shut depolarization-gated channels for Ca2+ entry, which (e) decreases min.e.p.p. frequency. 4. In agreement with the interpretation, in frog neuromuscular junctions slightly depolarized with 11 mM-[K+]o, min.e.p.p. frequency is a monotonically increasing function of [Ca2+]o, as long as the sum of [Ca2+]o plus [Mg2+]o is kept constant. 5. The decrease in min.e.p.p. frequency caused by raising [Mg2+]o by 5 mM can be counterbalanced by raising [K+]o by about 9 mM. Using the Grahame equation (1947), assuming that the elevated divalent cations act solely by screening and have no effect on conductance, the negative surface charge is estimated to be roughly 1 electronic charge/75 A2.
    Digital Access Access Options