The mammalian target of rapamycin (mTOR) plays key roles in cellular metabolism and hypertrophic-hyperplasic growth, and it acts as a central regulator of protein synthesis and ribosome biogenesis at the transcriptional and translational levels by sensing and integrating signals from mitogens and nutrients. Hormonal and stress factors can affect the mTOR-signaling pathway via their receptors and signal transduction pathways. Nutritional regulation of the mTOR-signaling pathway is mediated by their corresponding plasma membrane transporters, other unknown mechanisms, or both. Adenine monophosphate-activated protein kinase, an important cellular energy sensor, can interact with the mTOR-signaling pathway to maintain cellular energy homeostasis. Interactions of mTOR with regulatory-associated protein of TOR or rapamycin-insensitive companion of mTOR result in 2 mTOR complexes, with the former (mTOR complex-1) being the primary controller of cell growth and the latter (mTOR complex-2) mediating effects that are insensitive to rapamycin, such as cytoskeletal organization. Upstream elements of the mTOR-signaling pathway include Ras-homolog enriched in brain, and tuberous sclerosis complex 1 and 2, with tuberous sclerosis complex 2 as the linker between phosphatidylinositol 3-kinase/protein kinase B or Ras-Raf-mitogen-activated protein kinase-extracellular signal-regulated protein kinase pathways and the mTOR pathway. Ribosomal protein S6 protein kinase 1 and eukaryotic initiation factor 4E binding protein 1 are currently the 2 best-known downstream effectors of mTOR signaling. Hormonal factors, stressors, and nutrients can differentially mediate cellular metabolism and growth via the mTOR pathway with effectors specific to the organ or tissue types involved.

This is the first report documenting a difference in laryngohyoid morphology following the application of a tongue tie, providing evidence that the use of a tongue tie has a measurable effect on upper airway structure. The functional implications of this finding are yet to be elucidated.

This study was conducted to examine colonic abundances of anti‐inflammatory cytokine interleukin 10 (IL‐10) and pro‐inflammatory cytokines tumor necrosis factor‐alpha (TNF‐α) and interleukin‐6 (IL‐6) in pigs fed a high‐fat basal diet supplemented with 15% guar gum and resistant starch. A total of 24 Yorkshire grower barrows were assigned into a high‐fat basal diet as the control and two basal diets supplemented with 15% guar gum and retrograded high amylose cornstarch, i.e., resistant starch, according to a randomized block design for 4 weeks. Compared with the control group, guar gum and resistant starch consumption at 15% increased (P<0.05) colonic IL‐10 abundance. However, there was no difference (P>0.05) in colonic IL‐10 abundance between the 15%‐guar gum and the 15%‐resistant starch groups. Furthermore, the consumption of guar gum and resistant starch did not affect (P>0.05) colonic abundances of TNF‐α and IL‐6. We conclude that consumption of guar gum and resistant starch supplemented in a high‐fat basal diet may protect the colon from developing inflammation by enhancing IL‐10 abundance. Supported by OMAFRA of Canada.