Anatomical morphometry for Cricothyrotomy puncture and incision.

PURPOSE: Emergency surgical airway securing techniques include cricothyrotomy, puncture, and incision. While the instruments used for these methods vary in size, no index of laryngeal morphology exists to guide instrument selection. Therefore, we measured the morphology of the cricothyroid ligament in Japanese individuals and assessed its correlations with height. METHODS: This retrospective study used 61 anatomical practice specimens. The cricothyroid ligament of the laryngeal area was dissected, and a frontal image was recorded. Next, images of the midsagittal sections of the larynx and trachea were recorded. The width and height of the cricothyroid ligament were measured from the frontal images, and the depth of the larynx and the angle to the lower edge of the cricothyroid plate were measured from the mid-sagittal cross-sectional images. The height was estimated from the tibial lengths of the specimens and statistically analyzed for correlations. 　 RESULTS: The width and depth were significantly greater in males. Overall, there was a slight correlation between the results of each laryngeal measurement and estimated height for all items. CONCLUSION: The morphology of cricothyrotomy revealed that the width and depth of the laryngeal area varied according to sex. Moreover, the results also showed a correlation with the estimated height. Thus, it is important to predict the morphology of the laryngeal area and cricothyroid ligament by considering factors such as patient sex, weight, and height.

Etidronate down-regulates Toll-like receptor 2 ligand-induced chemokine production by inhibiting MyD88 expression and NF-κB activation.

OBJECTIVE: Pretreatment of J774.1 cells with etidronate, a non-nitrogen-containing bisphosphonate (non-NBP) used as an antibone resorptive drug, was previously reported to inhibit Toll-like receptor (TLR) 2 agonist-induced proinflammatory cytokine production. The present study aimed to examine the effects of etidronate on chemokine production by human monocytic U937 cells incubated with Pam3Cys-Ser-(Lys)4 (Pam3CSK4, a TLR2 ligand) and lipid A (a TLR4 ligand). METHODS: U937 cells were pretreated with or without etidronate, and then incubated with or without Pam3CSK4 or lipid A. Levels of secreted human interleukin (IL)-8 and monocyte chemoattractant protein-1 (MCP-1) in culture supernatants and activation of nuclear factor-κB (NF-κB) p65 were measured by enzyme-linked immunosorbent assay (ELISA). Cytotoxicity was determined by measuring lactate dehydrogenase (LDH) activity in supernatants. Expression of intracellular adhesion molecule (ICAM)-1 and MyD88 was analyzed by flow cytometry and Western blot analysis, respectively. RESULTS: Etidronate down-regulated IL-8 and MCP-1 production and NF-κB p65 activation induced by Pam3CSK4, but not lipid A, in U937 cells. Etidronate also inhibited MyD88 expression in U937 cells incubated with Pam3CSK4. CONCLUSION: Etidronate down-regulates IL-8 and MCP-1 production in U937 cells by inhibiting both the expression of MyD88 and activation of NF-κB p65 in the TLR2, but not TLR4, pathway.