%0 Journal Article
%~ PubMed
%A Matthews, Slade
%A Succar, Petter
%A Jelinek, Herbert
%A McParland, Brent
%A Buckland, Michael
%A McLachlan, Craig S
%T Diagnosis of oligodendroglioma: Molecular and classical histological assessment in the twenty-first century.
%B Asia-Pacific Journal of Clinical Oncology
%D 2012
%C United Kingdom
%I Wiley-Blackwell Publishing Ltd.
%V 8
%N 3
%P 213-216
%@ 1743-7563
%X Advances in molecular genetics are currently challenging the traditional morphological categorization of gliomas. Recurrent molecular and cytogenetic aberrations add prognostic and predictive information over and above that provided by standard histomorphological techniques and may influence decisions to re-operate or observe, to deliver radiation or not, or to administer chemotherapy to glioma patients. The importance of routine hematoxylin and eosin (H-E pathological stains cannot be underestimated, especially in resource-poor areas and developing countries where there is likely to be a significant economic opportunity cost for molecular diagnosis services. New research tools for image analyses of histological H-E slides, such as the precise measures of cell area, curvature and nuclear roundness, may provide an increased ability to provide an accurate classification for an inherently subjective process of histological assessment. We discuss the current trends, limitations and impact of molecular classification in this mini review.
%Z FOR Codes: 10401 111202


%0 Journal Article
%~ PubMed
%A Trian, Thomas
%A Ge, Qi
%A Moir, Lyn M
%A Burgess, Janette K
%A Kuo, Curtis
%A King, Nicholas J C
%A Reddel, Helen K
%A Black, Judith L
%A Oliver, Brian G
%A McParland, Brent E
%T Rhinovirus-induced Exacerbations of Asthma - How is the {beta}2-adrenoceptor Implicated?
%B American journal of respiratory cell and molecular biology
%D 2010
%C United States
%I American Thoracic Society
%V 43
%N 2
%P 227-33
%@ 1535-4989
%X Rhinovirus (RV) infections are the major cause of asthma exacerbations in children and adults. Under normal circumstances, asthmatic airway obstruction improves spontaneously or characteristically briskly in response to inhaled beta(2)-adrenergic receptor (beta(2)AR) agonists. During virus-associated exacerbations, an impaired response to beta(2)AR agonists is observed; the reason for this is not known. The objective of this study was to determine the effect of RV infection on airway smooth muscle beta(2)AR function. The human cell line Beas-2B and primary human bronchial epithelial cells (HBECs) were infected with RV (multiplicity of infection = 1). After 1 or 5 days for primary and Beas-2B cells, respectively, cell culture supernatants were harvested, UV-irradiated to inactivate RV, and applied to human airway smooth muscle cells for 3 days to assess modifications of beta(2)AR function. RV conditioned medium from Beas-2B and HBECs decreased beta(2)AR agonist-induced cAMP by 50 and 65%, respectively (n = 5; P < 0.05). When cAMP was induced independently of the beta(2)AR using forskolin, no impairment was found. Using flow cytometry, we demonstrated that this decrease was likely the result of beta(2)AR desensitization because membrane but not total cell receptor beta(2)AR was decreased. Pretreatment of HBECs and Beas-2B cells but not human airway smooth muscle cells with the corticosteroids dexamethasone or fluticasone abolished virus-mediated beta(2)AR loss of function. This study shows that epithelial infection with RV induces a decrease of beta(2)AR function on airway smooth muscle cells, potentially explaining the clinical observation of loss of beta(2)AR agonist function during RV-induced asthma exacerbations.
%Z FOR Codes: 111501 110804 111601 110106


%0 Journal Article
%~ Isi
%A Cooper, P. R.
%A McParland, B. E.
%A Mitchell, H. W.
%A Noble, P. B.
%A Politi, A. Z.
%A Ressmeyer, A. R.
%A West, A. R.
%T Airway mechanics and methods used to visualize smooth muscle dynamics in vitro
%B Pulmonary Pharmacology & Therapeutics
%D 2009
%C United Kingdom
%I Academic Press
%V 22
%N 
%P 398-406
%@ 1094-5539
%X 
%Z FOR Codes: 111501 110203


%0 Journal Article
%~ PubMed
%A Chapman, David Geoffrey
%A Berend, Norbert
%A King, Gregory G
%A McParland, Brent E
%A Salome, Cheryl M
%T Deep Inspirations Protect Against Airway Closure in Non-asthmatic Subjects.
%B Journal of applied physiology (Bethesda, Md. : 1985)
%D 2009
%C United States
%I American Physiological Society
%V 107
%N 2
%P 564-9
%@ 8750-7587
%X The mechanism by which deep inspirations protect against increased airway responsiveness in nonasthmatic subjects is not known. The aim was to investigate the role of airway closure and airway narrowing in deep inspiration bronchoprotection. Twelve nonasthmatic and nine asthmatic subjects avoided deep inspirations (DI) for 20 min, then took five DI expired to functional residual capaciy (DI-FRC) or, on a separate day, no DI (no DI) before inhaling a single dose of methacholine. On another day, eight nonasthmatic subjects took five DI expired to residual volume (DI-RV). Peripheral airway function was measured by respiratory system reactance (Xrs), using the forced oscillation technique, and by forced vital capacity (FVC) as an index of airway closure. Respiratory system resistance (Rrs) and forced expiratory volume in 1 s (FEV1)/FVC were measured as indexes of airway narrowing. In nonasthmatic subjects, DI-FRC reduced the response measured by FEV1 (P=0.019), Xrs (P=0.02), and FVC (P=0.0005) but not by Rrs (P=0.15) or FEV1/FVC (P=0.52) compared with no DI. DI-RV had a less protective effect than DI-FRC on response measured by FEV1 (P=0.04) and FVC (P=0.016). There was no difference between all protocols when the response was measured by Xrs (P=0.20), Rrs (P=0.88), or FEV1/FVC (P=0.88). DI had no effect on methacholine response in asthmatic subjects. DI protect against airway responsiveness through an effect on peripheral airways involving reduced airway closure. The protective effect of DI on FEV1 and FVC was abolished by expiration to residual volume. We speculate that the reduced airway closure is due to reduced baseline ventilation heterogeneity and/or reduced airway surface tension.
%Z FOR Codes: 110203


%0 Journal Article
%~ PubMed
%A An, S S
%A Bai, T R
%A Bates, J H T
%A Black, J L
%A Brown, R H
%A Brusasco, V
%A Chitano, P
%A Deng, L
%A Dowell, M
%A Eidelman, D H
%A Fabry, B
%A Fairbank, N J
%A Ford, L E
%A Fredberg, J J
%A Gerthoffer, W T
%A Gilbert, S H
%A Gosens, R
%A Gunst, S J
%A Halayko, A J
%A Ingram, R H
%A Irvin, C G
%A James, A L
%A Janssen, L J
%A King, G G
%A Knight, D A
%A Lauzon, A M
%A Lakser, O J
%A Ludwig, M S
%A Lutchen, K R
%A Maksym, G N
%A Martin, J G
%A Mauad, T
%A McParland, B E
%A Mijailovich, S M
%A Mitchell, H W
%A Mitchell, R W
%A Mitzner, W
%A Murphy, T M
%A Paré, P D
%A Pellegrino, R
%A Sanderson, M J
%A Schellenberg, R R
%A Seow, C Y
%A Silveira, P S P
%A Smith, P G
%A Solway, J
%A Stephens, N L
%A Sterk, P J
%A Stewart, A G
%A Tang, D D
%A Tepper, R S
%A Tran, T
%A Wang, L
%T Airway smooth muscle dynamics: a common pathway of airway obstruction in asthma.
%B The European respiratory journal : official journal of the European Society for Clinical Respiratory Physiology
%D 2007
%C Switzerland
%I European Respiratory Society
%V 29
%N 5
%P 834-860
%@ 0903-1936
%X Excessive airway obstruction is the cause of symptoms and abnormal lung function in asthma. As airway smooth muscle (ASM) is the effecter controlling airway calibre, it is suspected that dysfunction of ASM contributes to the pathophysiology of asthma. However, the precise role of ASM in the series of events leading to asthmatic symptoms is not clear. It is not certain whether, in asthma, there is a change in the intrinsic properties of ASM, a change in the structure and mechanical properties of the noncontractile components of the airway wall, or a change in the interdependence of the airway wall with the surrounding lung parenchyma. All these potential changes could result from acute or chronic airway inflammation and associated tissue repair and remodelling. Anti-inflammatory therapy, however, does not "cure" asthma, and airway hyperresponsiveness can persist in asthmatics, even in the absence of airway inflammation. This is perhaps because the therapy does not directly address a fundamental abnormality of asthma, that of exaggerated airway narrowing due to excessive shortening of ASM. In the present study, a central role for airway smooth muscle in the pathogenesis of airway hyperresponsiveness in asthma is explored.
%Z FOR Codes: 110203


%0 Journal Article
%~ PubMed
%A Matsumoto, Hisako
%A Moir, Lyn M
%A Oliver, Brian Gg
%A Burgess, Janette K
%A Roth, Michael
%A Black, Judith L
%A McParland, Brent E
%T Comparison of gel contraction mediated by asthmatic and non-asthmatic airway smooth muscle cells.
%B Thorax
%D 2007
%C London
%I British Medical Journal Publishing Group
%V 62
%N 10
%P 848-54
%@ 1468-3296
%X Exaggerated bronchial constriction is the most significant and life threatening response of patients with asthma to inhaled stimuli. However, few studies have investigated the contractility of airway smooth muscle (ASM) from these patients. The purpose of this study was to establish a method to measure contraction of ASM cells by embedding them into a collagen gel, and to compare the contraction between subjects with and without asthma.
%Z FOR Codes: 110502 111601


%0 Journal Article
%~ PubMed
%A Paré, Peter D
%A McParland, Brent E
%A Seow, Chun Y
%T Structural basis for exaggerated airway narrowing.
%B Canadian Journal of Physiology and Pharmacology
%D 2007
%C Canada
%I N R C Research Press
%V 85
%N 7
%P 653-658
%@ 0008-4212
%X Airway hyperresponsiveness, particularly the ability of airways to narrow excessively in response to stimuli that normally cause little airway narrowing in nonasthmatic subjects, is a characteristic feature of asthma and the basis of its symptoms. Although airway hyperresponsiveness may be partly the result of alterations in the contractile phenotype of the airway smooth muscle, there is evidence that it may also be caused by structural changes in the airway wall, collectively termed airway remodeling. Airway remodeling is defined as changes in composition, quantity, and (or) organization of cellular and molecular constituents of the airway wall. Airway wall remodeling that occurs in asthma can result in functional alterations because of quantitative changes in airway wall compartments, and (or) because of changes in the biochemical composition or material properties of the various constituents of the airway wall. This brief review summarizes the quantitative changes in the dimensions and organization of the airway wall compartments that have been described and explains how structural alterations may lead to the exaggerated airway narrowing.
%Z FOR Codes: 1117 110203