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Clarke G. Tankersley

Researcher at Johns Hopkins University

Publications -  97
Citations -  4100

Clarke G. Tankersley is an academic researcher from Johns Hopkins University. The author has contributed to research in topics: Leptin & Lung. The author has an hindex of 37, co-authored 97 publications receiving 3912 citations. Previous affiliations of Clarke G. Tankersley include Uniformed Services University of the Health Sciences & Cincinnati Children's Hospital Medical Center.

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Leptin prevents respiratory depression in obesity.

TL;DR: The results suggest that leptin can prevent respiratory depression in obesity, but a deficiency in central nervous system leptin levels or activity may induce hypoventilation and the Pickwickian syndrome in some obese subjects.
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Leptin, obesity, and respiratory function.

TL;DR: The possibility exists that a relative deficiency in leptin, or a leptin resistance, may play a role in obesity-related breathing disorders such as obesity hypoventilation syndrome (OHS) or obstructive sleep apnea (OSA).
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Differential control of ventilation among inbred strains of mice

TL;DR: The role genetic factors play in ventilatory control was examined by challenging eight inbred strains of mice to acute hypercapnia under normoxic and hypoxic conditions, and it is suggested that genetic determinants interstrain variation in the magnitude and pattern of breathing during hypoxia andhypercapnia are influenced by different genetic mechanisms.
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Leptin attenuates respiratory complications associated with the obese phenotype

TL;DR: The results suggested that respiratory complications associated with the obese phenotype, including rapid breathing pattern at baseline, diminished lung compliance, and abnormal respiratory muscle adaptations, are attenuated with prolonged leptin treatment.
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Quantitative trait loci controlling allergen-induced airway hyperresponsiveness in inbred mice.

TL;DR: The strain distribution patterns for the asthma-related phenotypes airway hyperresponsiveness, lung eosinophils, and ovalbumin (OVA)-specific serum immunoglobulin (Ig) E induced by allergen exposure protocols are characterized and two distinct quantitative trait loci for susceptibility toallergen-induced AHR are identified.