Developmental deglutition and intrinsic tongue muscle maturation phenotypes in the Ts65Dn mouse model of Down syndrome.

Introduction: Down syndrome (DS) is associated with difficulties with feeding during infancy and childhood. Weaning, or transitioning from nursing to independent deglutition, requires developmental progression in tongue function. However, little is known about whether postnatal tongue muscle maturation is impacted in DS.

Effectiveness of pharmacological therapies for fibromyalgia syndrome in adults: an overview of Cochrane Reviews.

Objectives: To summarise and evaluate Cochrane reviews of pharmacological therapies for adults with fibromyalgia syndrome (FMS) pain.

Methods: Systematic search of Cochrane Database of Systematic Reviews to May 2024. Generic quality assessment used AMSTAR-2 criteria, validity checks of potentially critical factors in evaluation of analgesic efficacy, and assessment of susceptibility of results to publication bias.

Effectiveness of pharmacological therapies for fibromyalgia syndrome in adults: an overview of Cochrane Reviews.

Objectives: To summarise and evaluate Cochrane reviews of pharmacological therapies for adults with fibromyalgia syndrome (FMS) pain.

Methods: Systematic search of Cochrane Database of Systematic Reviews to May 2024. Generic quality assessment used AMSTAR-2 criteria, validity checks of potentially critical factors in evaluation of analgesic efficacy, and assessment of susceptibility of results to publication bias.

Type I IFN induces long-chain acyl-CoA synthetase 1 to generate a phosphatidic acid reservoir for lipotoxic saturated fatty acids.

Long-chain acyl-CoA synthetase 1 (ACSL1) catalyzes the conversion of long-chain fatty acids to acyl-CoAs. ACSL1 is required for β-oxidation in tissues that rely on fatty acids as fuel, but no consensus exists on why ACSL1 is induced by inflammatory mediators in immune cells. We used a comprehensive and unbiased approach to investigate the role of ACSL1 induction by interferon type I (IFN-I) in myeloid cells in vitro and in a mouse model of IFN-I overproduction.