Publications by authors named "G T Bolger"

Introduction: Chronic disease management programs (CDMP) that include education and exercise enhance outcomes and reduce healthcare costs. Remote CDMP have the potential to provide convenient, cost-effective, and accessible options for individuals, but it is unclear how to best implement programs that include education and exercise. This review identified and synthesized resources for implementing remote CDMP programs that incorporate education and exercise.

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Article Synopsis
  • The development of new treatments for chronic obstructive pulmonary disease (COPD) focuses on expanding therapeutic options and targeting various biological pathways.
  • Recent success in clinical trials with the biologic agent dupilumab emphasizes the significance of targeting inflammation, but other mechanisms like airway remodeling and mucociliary function are also important therapeutic targets.
  • Identifying and classifying COPD based on these new targets can improve precision medicine approaches, helping to tailor treatments to patient subsets and speeding up drug discovery processes.
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The cAMP-signaling cancers, which are defined by functionally-significant somatic mutations in one or more elements of the cAMP signaling pathway, have an unexpectedly wide range of cell origins, clinical manifestations, and potential therapeutic options. Mutations in at least 9 cAMP signaling pathway genes (, and ) have been identified as driver mutations in human cancer. Although all cAMP-signaling pathway cancers are driven by mutation(s) that impinge on a single signaling pathway, the ultimate tumor phenotype reflects interactions between five critical variables: (1) the precise gene(s) that undergo mutation in each specific tumor type; (2) the effects of specific allele(s) in any given gene; (3) mutations in modifier genes (mutational "context"); (4) the tissue-specific expression of various cAMP signaling pathway elements in the tumor stem cell; and (5) and the precise biochemical regulation of the pathway components in tumor cells.

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Considerable interest continues to be focused on the development of curcumin either as an effective stand-alone therapeutic or as an adjunct therapy to established therapies. Curcumin (1, 7-bis (4-hydroxy-3-methoxyphenyl)-1, 6-heptadiene-3, 5- dione; also called diferuloylmethane) is a polyphenolic phytochemical extracted from the root of curcuma longa, commonly called turmeric. Despite evidence from in vitro (cell culture) and preclinical studies in animals, clinical studies have not provided strong evidence for a therapeutic effect of curcumin.

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Evaluation of the in vitro human liver microsome and hepatocyte metabolism of ketotifen demonstrated that norketotifen (NK) is the major demethylated hepatic metabolite of ketotifen. It is here reported that NK is completely devoid of the severe and dose-limiting sedative effects of ketotifen. Thus, while ketotifen is clinically dose-limited to 1 mg, bid, there are no dose-limiting sedative effects elicited by NK, even after the highest single-dose (16 mg) or after repeat-doses (8 mg × 7 days) in humans or after the highest doses given to dogs in repeat-dose toxicological studies (40 mg/kg × 14 days).

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