نتایج جستجو برای: adam33
تعداد نتایج: 149 فیلتر نتایج به سال:
My research career has focused on the causes of asthma and its treatment. After establishing the key role that mast cells play in the inflammatory response in asthma, attention was turned towards understanding disease chronicity and variability across the lifecourse. Through a combination of studies on airway biopsies and primary cell cultures we have established that asthma is primarily an epi...
Acute and chronic lung inflammation is driven and controlled by several endogenous mediators that undergo proteolytic conversion from surface-expressed proteins to soluble variants by a disintegrin and metalloproteinase (ADAM)-family members. TNF and epidermal growth factor receptor ligands are just some of the many substrates by which these proteases regulate inflammatory or regenerative proce...
OBJECTIVES Asthma is a childhood disease that is strongly influenced by genetic factors. We sought to replicate an association between single nucleotide polymorphisms (SNPs) of the top-ranked candidate genes and childhood atopic asthma in Perinatal Risk of Asthma in Infants of Asthmatic Mothers (PRAM) study subjects. METHODS Using data from a systematic literature search and an exploratory ge...
BACKGROUND A substantial proportion of the general population has low lung function, and lung function is known to decrease as we age. Low lung function is a feature of several pulmonary disorders, such as uncontrolled asthma and chronic obstructive pulmonary disease. The objective of this study is to investigate the association of polymorphisms in asthma and chronic obstructive pulmonary disea...
PURPOSE OF REVIEW Irreversible airflow limitation develops in some patients with asthma and is related to poorer prognosis. This paper reviews recent literature on natural course, risk factors, and potential mechanisms of persistent airflow limitation in asthma. RECENT FINDINGS The natural course of persistent airflow limitation in asthma is poorly known, but reduced lung function at disease ...
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