Imperial College London

DrMatthewHind

Faculty of MedicineNational Heart & Lung Institute

Honorary Research Officer
 
 
 
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Contact

 

m.hind

 
 
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Location

 

Royal BromptonRoyal Brompton Campus

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Summary

 

Publications

Publication Type
Year
to

82 results found

Hind M, Stinchcombe SV, 2010, Lung Regenerating Molecules, Cell Therapy for Lung Disease, Editors: Polak, Polak, ISBN: 9781848164390

Book chapter

Bazari F, Hind M, Ong YE, 2010, Horner's syndrome--not to be sneezed at., Lancet, Vol: 375

Journal article

Hind M, 2010, Signs and symptoms - Chest pain, ERS Handbook Respiratory Medicine, Editors: Palange, Simonds, Sheffield UK, Publisher: European Respiratory Society, Pages: 49-51, ISBN: 978-1-904097-99-0

Book chapter

Murphy P, Brignall K, Williams A, Davidson C, Hind M, Simonds A, Moxham J, Polkey M, Hart Net al., 2009, HEALTH-RELATED QUALITY OF LIFE IN OBESITY HYPOVENTILATION SYNDROME (OHS) PRIOR TO INITIATION OF HOME MECHANICAL VENTILATION (HMV), Winter Meeting of the British-Thoracic-Society, Publisher: BMJ PUBLISHING GROUP, Pages: A137-A137, ISSN: 0040-6376

Conference paper

Murphy P, Brignall K, Hind M, Simonds A, Davidson C, Williams A, Moxham J, Polkey M, Hart Net al., 2009, ACTIVITY LEVELS AT INITIATION OF HOME MECHANICAL VENTILATION IN PATIENTS WITH OBESITY HYPOVENTILATION SYNDROME, Winter Meeting of the British-Thoracic-Society, Publisher: BMJ PUBLISHING GROUP, Pages: A29-A29, ISSN: 0040-6376

Conference paper

Hind M, Stinchcombe S, 2009, Palovarotene, a novel retinoic acid receptor γ agonist for the treatment of emphysema, CURRENT OPINION IN INVESTIGATIONAL DRUGS, Vol: 10, Pages: 1243-1250, ISSN: 1472-4472

Journal article

Quinlan R, Hind M, Beales P, 2009, The role of BBS proteins in lung development, 16th Annual Conference of the International-Society-of-Development-Biologists, Publisher: ELSEVIER SCIENCE BV, Pages: S266-S266, ISSN: 0925-4773

Conference paper

Man W, Hind M, 2009, Unexplained Respiratory Failure, Oxford Desk Reference: Respiratory Medicine, Editors: Maskell, Millar, Publisher: Oxford University Press, Pages: 56-58, ISBN: 9780199239122

In the era of evidence-based medicine, clinicians draw upon a vast resource of research-based evidence to guide their practice.

Book chapter

Hind M, Gilthorpe A, Stinchcombe S, Maden Met al., 2009, Retinoid induction of alveolar regeneration: from mice to man?, THORAX, Vol: 64, Pages: 451-457, ISSN: 0040-6376

Journal article

Maden M, Hind M, 2004, Alveolization: does "A" stand for appropriate morphometry? Reply, EUROPEAN RESPIRATORY JOURNAL, Vol: 24, Pages: 332-332, ISSN: 0903-1936

Journal article

Maden M, Hind M, 2004, Retinoic acid in alveolar development, maintenance and regeneration., Philos Trans R Soc Lond B Biol Sci, Vol: 359, Pages: 799-808, ISSN: 0962-8436

Recent data suggest that exogenous retinoic acid (RA), the biologically active derivative of vitamin A, can induce alveolar regeneration in a rat model of experimental emphysema. Here, we describe a mouse model of disrupted alveolar development using dexamethasone administered postnatally. We show that the effects of dexamethasone are concentration dependent, dose dependent, long lasting and result in a severe loss of alveolar surface area. When RA is administered to these animals as adults, lung architecture and the surface area per unit of body weight are completely restored to normal. This remarkable effect may be because RA is required during normal alveolar development and administering RA re-awakens gene cascades used during development. We provide evidence that RA is required during alveologenesis in the mouse by showing that the levels of the retinoid binding proteins, the RA receptors and two RA synthesizing enzymes peak postnatally. Furthermore, an inhibitor of RA synthesis, disulphiram, disrupts alveologenesis. We also show that RA is required throughout life for the maintenance of lung alveoli because when rats are deprived of dietary retinol they lose alveoli and show the features of emphysema. Alveolar regeneration with RA may therefore be an important novel therapeutic approach to the treatment of respiratory diseases characterized by a reduced gas-exchanging surface area such as bronchopulmonary dysplasia and emphysema for which there are currently no treatments.

Journal article

Maden M, Hind M, 2004, Retinoic acid in alveolar development, maintenance and regeneration, PHILOSOPHICAL TRANSACTIONS OF THE ROYAL SOCIETY B-BIOLOGICAL SCIENCES, Vol: 359, Pages: 799-808, ISSN: 0962-8436

Journal article

Hind M, Maden M, 2004, Retinoic acid induces alveolar regeneration in the adult mouse lung., Eur Respir J, Vol: 23, Pages: 20-27, ISSN: 0903-1936

Recent data suggests that exogenous retinoic acid (RA) can induce alveolar regeneration in a mouse and a rat model of experimental emphysema and disrupted alveolar development. This may be because RA is required during normal alveolar development and the subsequent provision of RA reawakens the gene cascades used during development. Here, additional evidence that RA is required during alveologenesis in the mouse is provided by showing that disulphiram disrupts this process. A further model of disrupted alveolar development using dexamethasone administered postnatally is then described, and it is further shown that RA administered to these adult mice restores the lung architecture to normal. Alveolar regeneration with retinoic acid may therefore be an important novel therapeutic approach to the treatment of respiratory diseases characterised by a reduced gas-exchanging surface area, such as bronchopulmonary dysplasia and emphysema.

Journal article

Hind M, Maden M, 2004, Retinoic acid induces alveolar regeneration in the adult mouse lung, EUROPEAN RESPIRATORY JOURNAL, Vol: 23, Pages: 20-27, ISSN: 0903-1936

Journal article

Hind M, Maden M, 2003, Prolonged retinoid deficiency in the adult rat results in emphysematous change, Winter Meeting of the British Thoracic-Society, Publisher: B M J PUBLISHING GROUP, Pages: 10-10, ISSN: 0040-6376

Conference paper

Maden M, Hind M, 2003, Retinoic acid, a regeneration-inducing molecule., Dev Dyn, Vol: 226, Pages: 237-244, ISSN: 1058-8388

Retinoic acid (RA) is the biologically active metabolite of vitamin A. It is a low molecular weight, lipophilic molecule that acts on the nucleus to induce gene transcription. In amphibians and mammals, it induces the regeneration of several tissues and organs and these examples are reviewed here. RA induces the "super-regeneration" of organs that can already regenerate such as the urodele amphibian limb by respecifying positional information in the limb. In organs that cannot normally regenerate such as the adult mammalian lung, RA induces the complete regeneration of alveoli that have been destroyed by various noxious treatments. In the mammalian central nervous system (CNS), which is another tissue that cannot regenerate, RA does not induce neurite outgrowth as it does in the embryonic CNS, because one of the retinoic acid receptors, RAR beta 2, is not up-regulated. When RAR beta 2 is transfected into the adult spinal cord in vitro, then neurite outgrowth is stimulated. In all these cases, RA is required for the development of the organ, in the first place suggesting that the same gene pathways are likely to be used for both development and regeneration. This suggestion, therefore, might serve as a strategy for identifying potential tissue or organ targets that have the capacity to be stimulated to regenerate.

Journal article

Maden M, Hind M, 2003, Retinoic acid, a regeneration-inducing molecule, DEVELOPMENTAL DYNAMICS, Vol: 226, Pages: 237-244, ISSN: 1058-8388

Journal article

Hind M, Corcoran J, Maden M, 2002, Pre- and postnatal lung development, maturation, and plasticity - Temporal/spatial expression of retinoid binding proteins and RAR isoforms in the postnatal lung, AMERICAN JOURNAL OF PHYSIOLOGY-LUNG CELLULAR AND MOLECULAR PHYSIOLOGY, Vol: 282, Pages: L468-L476, ISSN: 1040-0605

Journal article

Hind M, Corcoran J, Maden M, 2002, Temporal/spatial expression of retinoid binding proteins and RAR isoforms in the postnatal lung., Am J Physiol Lung Cell Mol Physiol, Vol: 282, Pages: L468-L476, ISSN: 1040-0605

Endogenous retinoids have been implicated in alveologenesis in both the rat and the mouse, and exogenous retinoic acid (RA) can reverse or partially reverse experimental emphysema in adult rat and mouse models by an unknown mechanism. In this study, we examine the cellular and molecular biology of retinoid signaling during alveologenesis in the mouse. We describe the temporal and spatial expression of the retinoid binding proteins CRBP-I, CRBP-II, and CRABP-I using RT-PCR and immunohistochemistry. We identify the retinoic acid receptor isoforms RAR-alpha 1, RAR-beta 2, RAR-beta 4, and RAR-gamma 2 and describe their temporal and spatial expression using RT-PCR and in situ hybridization. We demonstrate that both retinoid binding proteins and RAR isoforms are temporally regulated and found within the alveolar septal regions during alveologenesis. These data support a role of dynamic endogenous RA signaling during alveolar formation.

Journal article

Hind M, Corcoran J, Maden M, 2002, Alveolar proliferation, retinoid synthesizing enzymes, and endogenous retinoids in the postnatal mouse lung. Different roles for Aldh-1 and Raldh-2., Am J Respir Cell Mol Biol, Vol: 26, Pages: 67-73, ISSN: 1044-1549

Alveoli are formed postnatally in the rat, mouse, and human. The molecular signals controlling the patterning of this developmental process are not well understood. Here we describe immunohistochemical studies that label proliferating alveolar wall cells which suggest two distinct patterns of alveologenesis: (1) a low grade, peripheral subpleural parenchymal process which occurs from P1 through to P15; and (2) a dramatic increase in central cell proliferation from P4 which is complete by P15, corresponding to the well described period of alveolar septation. We describe the temporal and spatial expression of the retinoid-synthesizing enzymes Aldh-1 and Raldh-2 in the postnatal mouse lung. Both enzymes are upregulated during the period of maximal alveolar wall cell proliferation. Aldh-1 is located in the bronchial epithelium and alveolar parenchyma, and Raldh-2 is restricted to the bronchial epithelium and pleural mesothelial cells. High-pressure liquid chromatography (HPLC) reveals that rapidly septating lungs have relatively simple chromatographic profiles; in contrast, the adult lungs have a complex profile that includes many novel retinoids. These data suggest two patterns of alveolar proliferation with temporal and spatial association of the enzymes Aldh-1 and Raldh-2 and a dynamic role for different retinoids in both the septating and adult mouse lung.

Journal article

Hind M, Corcoran J, Maden M, 2002, Alveolar proliferation, retinoid synthesizing enzymes, and endogenous retinoids in the postnatal mouse lung - Different roles for Aldh-1 and Raldh-2, AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY, Vol: 26, Pages: 67-73, ISSN: 1044-1549

Journal article

Tovar-Corona B, Hind MD, Torry JN, Vincent Ret al., 2001, Effects of respiration on heart sounds using time-frequency analysis, 28th Annual Meeting on Computers in Cardiology, Publisher: IEEE, Pages: 457-460, ISSN: 0276-6574

Conference paper

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