Zobrazeno 1 - 10
of 17
pro vyhledávání: '"HM Haitchi"'
Autor:
H Rupani, D Edwards, J Richards, R Chaudhuri, S Smith, DJ Jackson, A Hearn, M Edwards, S Johnston, H Moyses, RJ Kurukulaaratchy, HM Haitchi, R Djukanovic
Publikováno v:
‘Infinity War’ – Ongoing clinical challenges in COVID-19.
Publikováno v:
‘Finding Neverland’ – T2 inflammation and its absence.
Publikováno v:
Deciphering ‘The Da Vinci Code’ – Biomarkers in airways disease.
Autor:
Joanne Kelly, Donna E. Davies, Marieke Wandel, Elizabeth R. Davies, Stephen T. Holgate, HM Haitchi
Publikováno v:
Airway cell biology and immunopathology.
Background: Maternal asthma is a risk factor for asthma and airway hyperresponsiveness (AHR) in children. The asthma susceptibility gene, ADAM33, has been associated with AHR and impaired lung function in early life. Aims and Objectives: Our aim was
Autor:
HM Haitchi, Jfc Kelly, Elizabeth R. Davies, Stephen T. Holgate, Donna E. Davies, JA Whitsett, Marieke Wandel
Publikováno v:
Mucosal and microbial drivers of asthma.
Background Maternal allergy is a strong risk factor for developing asthma and airway hyperresponsiveness (AHR). ADAM33 has been identified as an asthma susceptibility gene and is associated with AHR and impaired lung function in early life. Our aim w
Autor:
HM Haitchi, Marieke Wandel, Jfc Kelly, Elizabeth R. Davies, S. T. Holgate, JA Whitsett, Donna E. Davies
Publikováno v:
Mucosal and microbial drivers of asthma.
Introduction Most asthma has its origin in early life and probably involves gene-environment interactions. The asthma susceptibility gene ADAM33 is associated with bronchial hyperresponsiveness (BHR) and reduced lung function in young children. It en
Publikováno v:
Mechanisms of asthma.
Rationale Severe corticosteroid refractory asthma is a significant unmet medical need. It accounts for 10% of the asthma population and 50% of the health economic burden. Recent understanding of asthma heterogeneity has evolved beyond clinical charac
Publikováno v:
Thorax. 61:313-319
Background: Transforming growth factor beta (TGFβ) upregulates a number of smooth muscle specific genes in (myo)fibroblasts. As asthma is characterised by an increase in airway smooth muscle, we postulated that TGFβ 2 favours differentiation of ast