Purpose: To assess OSA prevalence, comorbidities, and the influence of sleep stages and body positions on respiratory events distribution in toddlers aged 12-24 months.
Methods: A single center retrospective study that included toddlers aged 12-24 months old who underwent overnight PSG. OSA severity was categorized by obstructive apnea-hypopnea index (OAHI) as mild (1-4.
Recent evidence indicates that the presence of a primary cilium (PC), and of selective cAMP signaling within this smallest of organelles, promotes adipogenic differentiation of 3T3-L1 preadipocytes incubated in media supplemented with either a natural (docosahexaenoic acid, DHA), or a synthetic (TUG-891), free fatty acid receptor 4 (FFAR4) agonist. Indeed, in this earlier work, activation of ciliary FFAR4 in 3T3-L1 cells was correlated with selective increases in PC cAMP and adipogenesis in these cells. However, this study was silent on the role of local PC cAMP phosphodiesterases (PDEs)-mediated events in regulating these adipogenic responses and on the identity of cAMP PDEs that could regulate the "pool" of ciliary cAMP accessed by FFAR4 agonists.
View Article and Find Full Text PDFAm J Orthod Dentofacial Orthop
November 2021
Introduction: The objectives of this study were to assess the changes in right vs left nasal cavity volumes and minimum cross-sectional width, nasopharyngeal, and oropharyngeal volumes of the upper airway in response to rapid maxillary expansion (RME).
Methods: Pretreatment and posttreatment cone-beam computed tomography scans of 28 patients with a mean age of 9.86 ± 2.
There are five Ubiquilin proteins (UBQLN1-4, UBQLN-L), which are evolutionarily conserved and structurally similar. UBQLN proteins have three functional domains: N-terminal ubiquitin-like domain (UBL), C-terminal ubiquitin-associated domain (UBA), and STI chaperone-like regions in the middle. Alterations in UBQLN1 gene have been detected in a variety of disorders ranging from Alzheimer's disease to cancer.
View Article and Find Full Text PDFAdv Exp Med Biol
December 2011
Although obesity is a complex metabolic disorder often associated with insulin resistance, hyperinsulinemia and Type 2 diabetes, as well as with accelerated atherosclerosis, the molecular changes in obesity that promote these disorders are not completely understood. Several mechanisms have been proposed to explain how increased adipose tissue mass affects whole body insulin resistance and cardiovascular risk. One theory is that increased adipose derived inflammatory cytokines induces a chronic inflammatory state that not only increases cardiovascular risk, but also antagonizes insulin signaling and mitochondrial function and thereby impair glucose hemostasis.
View Article and Find Full Text PDFObesity increases the risk for metabolic and cardiovascular disease, and adipose tissue plays a central role in this process. Ceramide, the key intermediate of sphingolipid metabolism, also contributes to obesity-related disorders. We show that a high fat diet increased ceramide levels in the adipose tissues and plasma in C57BL/6J mice via a mechanism that involves an increase in gene expression of enzymes mediating ceramide generation through the de novo pathway (e.
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