Publications
82 results found
Hind M, Polkey MI, Simonds AK, 2017, Homeward bound: a centenary of home mechanical ventilation, American Journal of Respiratory and Critical Care Medicine, Vol: 195, Pages: 1140-1149, ISSN: 1073-449X
The evolution of home mechanical ventilation is an intertwined chronicle of negative and positive pressure modes and their role in managing ventilatory failure in neuromuscular diseases and other chronic disorders. The uptake of noninvasive positive pressure ventilation has resulted in widespread growth in home ventilation internationally and fewer patients being ventilated invasively. As with many applications of domiciliary medical technology, home ventilatory support has either led or run in parallel with acute hospital applications and has been influenced by medical and societal shifts in the approach to chronic care, the creation of community support teams, a preference of recipients to be treated at home, and economic imperatives. This review summarizes the trends and growing evidence base for ventilatory support outside the hospital.
Hind M, Jordan S, Hansell DM, et al., 2017, A man with progressive type II respiratory failure, Lancet Respiratory Medicine, Vol: 5, Pages: 456-456, ISSN: 2213-2600
Pavitt MJ, Swanton LL, Hind M, et al., 2017, Choking on a foreign body: a physiological study of the effectiveness of abdominal thrust manoeuvres to increase thoracic pressure, THORAX, Vol: 72, Pages: 576-578, ISSN: 0040-6376
The Heimlich manoeuvre is a well-known intervention for the management of choking due to foreign body airway occlusion, but the evidence base for guidance on this topic is limited and guidelines differ. We measured pressures during abdominal thrusts in healthy volunteers. The angle at which thrusts were performed (upthrust vs circumferential) did not affect intrathoracic pressure. Self-administered abdominal thrusts produced similar pressures to those performed by another person. Chair thrusts, where the subject pushed their upper abdomen against a chair back, produced higher pressures than other manoeuvres. Both approaches should be included in basic life support teaching.
Poobalasingam T, Yates LL, Walker SA, et al., 2017, Heterozygous Vangl2 looptail mice reveal novel roles for the planar cell polarity pathway in adult lung homeostasis and repair, Disease Models & Mechanisms, Vol: 10, Pages: 409-423, ISSN: 1754-8403
Lung diseases impose a huge economic and health burden worldwide. A key aspect of several adult lung diseases, such as Idiopathic pulmonary fibrosis (IPF) and Chronic Obstructive pulmonary Disease (COPD), including emphysema, is aberrant tissue repair, which leads to an accumulation of damage and impaired respiratory function. Currently, there are few effective treatments available for these diseases and their incidence is rising.The Planar Cell Polarity (PCP) pathway is critical for the embryonic development of many organs, including kidney and lung. We have previously shown that perturbation of the PCP pathway impairs tissue morphogenesis, which disrupts the number and shape of epithelial tubes formed within these organs during embryogenesis. However, very little is known about the role of the PCP pathway beyond birth, partly due to the perinatal lethality of many PCP mouse mutant lines.Here we have investigated heterozygous Looptail (Lp) mice, in which a single copy of the core PCP gene, Vangl2, is disrupted. We show that these mice are viable but display severe airspace enlargement and impaired adult lung function. Underlying these defects, we find that Vangl2Lp/+ lungs exhibit altered distribution of actin microfilaments and abnormal regulation of the actin modifying protein cofilin. In addition, we show that Vangl2Lp/+ lungs exhibit many of the hallmarks of tissue damage including an altered macrophage population, abnormal elastin deposition and elevated levels of the elastin-modifying enzyme, Mmp12, all of which are observed in the lung disease, emphysema.In vitro, VANGL2 disruption impairs directed cell migration and reduces the rate of repair following scratch wounding of human alveolar epithelial cells. Moreover, using population data from a birth cohort of young adults, all aged 31, we found evidence of an interactive effect between VANGL2 and smoking (a tissue damaging insult) on lung function. Finally, we show that that PCP genes VANGL2 and SCRIBBLE (SC
Ng-Blichfeldt JP, Alçada J, Montero MA, et al., 2017, Deficient retinoid-driven angiogenesis may contribute to failure of adult human lung regeneration in emphysema, Thorax, Vol: 72, Pages: 510-521, ISSN: 0040-6376
BACKGROUND: Molecular pathways that regulate alveolar development and adult repair represent potential therapeutic targets for emphysema. Signalling via retinoic acid (RA), derived from vitamin A, is required for mammalian alveologenesis, and exogenous RA can induce alveolar regeneration in rodents. Little is known about RA signalling in the human lung and its potential role in lung disease. OBJECTIVES: To examine regulation of human alveolar epithelial and endothelial repair by RA, and characterise RA signalling in human emphysema. METHODS: The role of RA signalling in alveolar epithelial repair was investigated with a scratch assay using an alveolar cell line (A549) and primary human alveolar type 2 (AT2) cells from resected lung, and the role in angiogenesis using a tube formation assay with human lung microvascular endothelial cells (HLMVEC). Localisation of RA synthetic (RALDH-1) and degrading (cytochrome P450 subfamily 26 A1 (CYP26A1)) enzymes in human lung was determined by immunofluorescence. Regulation of RA pathway components was investigated in emphysematous and control human lung tissue by quantitative real-time PCR and Western analysis. RESULTS: RA stimulated HLMVEC angiogenesis in vitro; this was partially reproduced with a RAR-α agonist. RA induced mRNA expression of vascular endothelial growth factor A (VEGFA) and VEGFR2. RA did not modulate AT2 repair. CYP26A1 protein was identified in human lung microvasculature, whereas RALDH-1 partially co-localised with vimentin-positive fibroblasts. CYP26A1 mRNA and protein were increased in emphysema. CONCLUSIONS: RA regulates lung microvascular angiogenesis; the endothelium produces CYP26A1 which is increased in emphysema, possibly leading to reduced RA availability. These data highlight a role for RA in maintenance of the human pulmonary microvascular endothelium.
Hopkinson NS, Polkey, Shah P, et al., 2016, Endobronchial valves for patients with heterogeneous emphysema and without interlobar collateral ventilation – open label treatment following the BeLieVeR-HIFi study, Thorax, Vol: 72, Pages: 277-279, ISSN: 1468-3296
Outcomes in early trials of bronchoscopic lung volume reduction using endobronchial valves for the treatment of patients with advanced emphysema were inconsistent. However improvements in patient selection with focus on excluding those with interlobar collateral ventilation and homogeneous emphysema resulted in significant benefits in the BeLieVeR-HIFi study compared to sham treated controls. In this manuscript we present data from the control patients in the BeLieVeR-HIFi study who went on to have open label endobronchial valve treatment after completion of the clinical trial (n=12), combined with data from those in the treatment arm who did not have collateral ventilation (n=19). Three months after treatment the forced expiratory volume in the 1st second increased by 27.3(36.4)%, residual volume reduced by 0.49(0.76)L, the 6 minute walk distance increased by 32.6(68.7) m, and the St George Respiratory Questionnaire for COPD score improved by 8.2(20.2) points. These data extend the evidence for endobronchial valve placement in appropriately selected patients with COPD.
Hadjiphilippou S, Shah PL, Rice A, et al., 2016, Bronchial Dieulafoy lesion. A 20-year history of unexplained hemoptysis, American Journal of Respiratory and Critical Care Medicine, Vol: 195, Pages: 397-397, ISSN: 1073-449X
Minelli C, Dean CH, Hind M, et al., 2016, Association of Forced Vital Capacity with the Developmental Gene NCOR2, PLOS One, Vol: 11, ISSN: 1932-6203
BackgroundForced Vital Capacity (FVC) is an important predictor of all-cause mortality in the absenceof chronic respiratory conditions. Epidemiological evidence highlights the role of early lifefactors on adult FVC, pointing to environmental exposures and genes affecting lung developmentas risk factors for low FVC later in life. Although highly heritable, a small number ofgenes have been found associated with FVC, and we aimed at identifying further geneticvariants by focusing on lung development genes.PLOS ONE | DOI:10.1371/journal.pone.0147388 February 2, 2016 1 / 17OPEN ACCESSCitation: Minelli C, Dean CH, Hind M, Alves AC,Amaral AFS, Siroux V, et al. (2016) Association ofForced Vital Capacity with the Developmental GeneNCOR2. PLoS ONE 11(2): e0147388. doi:10.1371/journal.pone.0147388Editor: Philipp Latzin, University Children's HospitalBasel, SWITZERLANDReceived: August 28, 2015Accepted: January 4, 2016Published: February 2, 2016Copyright: © 2016 Minelli et al. This is an openaccess article distributed under the terms of theCreative Commons Attribution License, which permitsunrestricted use, distribution, and reproduction in anymedium, provided the original author and source arecredited.Data Availability Statement: All relevant data arewithin the paper and its Supporting Information files.Funding: The authors have no support or funding toreport.Competing Interests: The authors have declaredthat no competing interests exist.MethodsPer-allele effects of 24,728 SNPs in 403 genes involved in lung development were tested in7,749 adults from three studies (NFBC1966, ECRHS, EGEA). The most significant SNP forthe top 25 genes was followed-up in 46,103 adults (CHARGE and SpiroMeta consortia) and5,062 children (ALSPAC). Associations were considered replicated if the replication p-valuesurvived Bonferroni correction (p<0.002; 0.05/25), with a nominal p-value considered assuggestive evidence. For SNPs with evidence of replication, effects on the expression levelsof n
Davey C, Zoumot Z, Jordan S, et al., 2015, Bronchoscopic lung volume reduction with endobronchial valves for patients with heterogeneous emphysema and intact interlobar fissures (the BeLieVeR-HIFi study): a randomised controlled trial, Lancet, Vol: 386, Pages: 1066-1073, ISSN: 1474-547X
BackgroundLung volume reduction surgery improves survival in selected patients with emphysema, and has generated interest in bronchoscopic approaches that might achieve the same effect with less morbidity and mortality. Previous trials with endobronchial valves have yielded modest group benefits because when collateral ventilation is present it prevents lobar atelectasis.MethodsWe did a single-centre, double-blind sham-controlled trial in patients with both heterogeneous emphysema and a target lobe with intact interlobar fissures on CT of the thorax. We enrolled stable outpatients with chronic obstructive pulmonary disease who had a forced expiratory volume in 1 s (FEV1) of less than 50% predicted, significant hyperinflation (total lung capacity >100% and residual volume >150%), a restricted exercise capacity (6 min walking distance <450 m), and substantial breathlessness (MRC dyspnoea score ≥3). Participants were randomised (1:1) by computer-generated sequence to receive either valves placed to achieve unilateral lobar occlusion (bronchoscopic lung volume reduction) or a bronchoscopy with sham valve placement (control). Patients and researchers were masked to treatment allocation. The study was powered to detect a 15% improvement in the primary endpoint, the FEV1 3 months after the procedure. Analysis was on an intention-to-treat basis. The trial is registered at controlled-trials.com, ISRCTN04761234.Findings50 patients (62% male, FEV1 [% predicted] mean 31·7% [SD 10·2]) were enrolled to receive valves (n=25) or sham valve placement (control, n=25) between March 1, 2012, and Sept 30, 2013. In the bronchoscopic lung volume reduction group, FEV1 increased by a median 8·77% (IQR 2·27–35·85) versus 2·88% (0–8·51) in the control group (Mann-Whitney p=0·0326). There were two deaths in the bronchoscopic lung volume reduction group and one control patient was unable to attend for follow-up asse
Nanzer AM, Jordan S, Padley S, et al., 2015, A deadly web, THORAX, Vol: 70, Pages: 101-101, ISSN: 0040-6376
Proudfoot AG, Juss J, Appleby S, et al., 2014, EFFECTS OF DIFFERENTIAL TNF RECEPTOR SIGNALLING IN MODULATING NEUTROPHIL-ENDOTHELIAL INTERACTIONS IN THE PULMONARY MICROVASCULATURE, Meeting of the British-Thoracic-Society, Publisher: BMJ PUBLISHING GROUP, Pages: A53-A53, ISSN: 0040-6376
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Alcada J, Ng-Blichfeldt JP, Proudfoot AG, et al., 2014, A NOVEL HUMAN MODEL TO STUDY ALVEOLAR INJURY AND REPAIR, Meeting of the British-Thoracic-Society, Publisher: BMJ PUBLISHING GROUP, Pages: A53-A53, ISSN: 0040-6376
Nanzer AM, Janssen J, Hind M, 2014, Sniffing out a hidden cause of breathlessness., BMJ Case Rep, Vol: 2014
A 78-year-old man presented with severe exertional dyspnoea. He suffered from mild chronic obstructive pulmonary disease, congestive cardiac failure and seropositive myasthaenia gravis. Clinical examination of his chest and heart were unremarkable but he had speech dyspnoea and was unable to count to 20 in a single breath. Consecutive sniff nasal inspiratory measurements (SNIP) fell from 55 to 33 cm H2O and forced vital capacity (FVC) fell from 3.4 to 2.4 L. A diagnosis of myasthenic crisis was carried out and treatment with non-invasive ventilation, intravenous immunoglobulis and high-dose oral prednisolone was initiated. The patient responded well and was discharged following a short period of rehabilitation. A high index of suspicion and a careful clinical examination with the help of two simple bedside tests, FVC and SNIP, allowed correct and timely treatment of his condition.
Proudfoot AG, O'Kane CM, Bayliffe A, et al., 2014, A Novel Tnfr1-Targeting Domain Antibody Attenuates Pulmonary Inflammation In A Human Model Of Lung Injury, Via Actions On The Lung Micro-Vascular Endothelium, AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE, Vol: 189, ISSN: 1073-449X
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- Citations: 4
Dean C, Bingle C, Hind M, 2013, Delivering and phenotyping mouse models for the respiratory community: a report on the Biochemical Society Workshop, CLINICAL SCIENCE, Vol: 125, Pages: 495-500, ISSN: 0143-5221
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- Citations: 1
Hare A, Chatwin M, Hind M, et al., 2013, Percutaneous gastrostomy (PEG) insertion under general anaesthesia (GA) in ventilator-dependent patients with neuromuscular disease (NMD), EUROPEAN RESPIRATORY JOURNAL, Vol: 42, ISSN: 0903-1936
Hopkinson NS, Moxham J, Montgomery H, et al., 2013, Tobacco industry lobbyists and their health-care clients, LANCET, Vol: 381, Pages: 445-445, ISSN: 0140-6736
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- Citations: 3
Proudfoot AG, Cordy J, Fiddler C, et al., 2013, Differential Tnfr Signalling In Human Models Of Acute Lung Injury, AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE, Vol: 187, ISSN: 1073-449X
Hasan NA, Hind M, Dean CH, 2012, MECHANISMS OF LUNG REPAIR POST INJURY: THE ROLE FOR NON-CANONICAL WNT SIGNALLING AND PLANAR CELL POLARITY, Winter Meeting of the British-Thoracic-Society 2012, Publisher: BMJ PUBLISHING GROUP, Pages: A36-A36, ISSN: 0040-6376
Proudfoot A, Summers C, Jackson T, et al., 2012, LSC 2012 abstract - Neutrophil trafficking in acute lung injury: A novel human ex vivo model, Publisher: EUROPEAN RESPIRATORY SOC JOURNALS LTD, ISSN: 0903-1936
Murphy PB, Davidson C, Hind MD, et al., 2012, Volume targeted versus pressure support non-invasive ventilation in patients with super obesity and chronic respiratory failure: a randomised controlled trial, THORAX, Vol: 67, Pages: 727-734, ISSN: 0040-6376
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- Citations: 150
Proudfoot AG, Hind M, Griffiths MJD, 2011, Biomarkers of acute lung injury: worth their salt?, BMC MEDICINE, Vol: 9, ISSN: 1741-7015
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- Citations: 17
Ng-Blichfeldt JP, Griffiths M, Griesenbach U, et al., 2011, THE ROLE OF THE RETINOIC ACID PATHWAY IN HUMAN LUNG REGENERATION, Winter Meeting of the British-Thoracic-Society, Publisher: B M J PUBLISHING GROUP, Pages: A115-A115, ISSN: 0040-6376
Cho M, Beales P, Hind M, et al., 2011, THE RESPIRATORY PHENOTYPE OF THE BBS4 NULL MOUSE LUNG, Winter Meeting of the British-Thoracic-Society, Publisher: B M J PUBLISHING GROUP, Pages: A168-A168, ISSN: 0040-6376
Proudfoot AG, McAuley DF, Hind M, et al., 2011, Translational research: what does it mean, what has it delivered and what might it deliver?, CURRENT OPINION IN CRITICAL CARE, Vol: 17, Pages: 495-503, ISSN: 1070-5295
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- Citations: 10
Hind M, 2011, Stem Cells in the Respiratory System, British Journal Clinical Pharmacology, Vol: 72
Shah PL, Slebos DJ, Cardoso PF, et al., 2011, Bronchoscopic lung-volume reduction with Exhale airway stents for emphysema (EASE trial): randomised, sham-controlled, multicentre trial., Lancet, Vol: 378, Pages: 997-1005
Hind M, Maden M, 2011, Is a regenerative approach viable for the treatment of COPD?, BRITISH JOURNAL OF PHARMACOLOGY, Vol: 163, Pages: 106-115, ISSN: 0007-1188
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- Citations: 26
Proudfoot AG, McAuley DF, Griffiths MJD, et al., 2011, Human models of acute lung injury, DISEASE MODELS & MECHANISMS, Vol: 4, Pages: 145-153, ISSN: 1754-8403
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- Citations: 86
Murphy P, Davidson C, Williams A, et al., 2011, Interim Data From A Randomised Controlled Trial Of Average Volume-Assured Pressure Support (AVAPS) Versus Spontaneous-Timed (ST) Pressure Support In Obesity Hypoventilation Syndrome (OHS), Publisher: AMER THORACIC SOC, ISSN: 1073-449X
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