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 (TLR) 2 ligand-induced proinflammatory cytokine production by inhibiting NF-κB activation.

BACKGROUND: Etidronate is a non-nitrogen-containing bisphosphonate (non-NBP) used for anti-bone resorptive therapy as well as having inhibitory effects on atherosclerotic plaques. The present study examined the effects of etidronate on the production of proinflammatory cytokines and chemokines by the macrophage-like cell line, J774.1, incubated with Pam3Cys-Ser-(Lys)4 (Pam3CSK4, a Toll-like receptor (TLR) 2 agonist) and lipid A (a TLR4 agonist). METHODS: J774.1 cells and human monocytic THP-1 cells were pretreated with or without etidronate for 5min, and then incubated with or without Pam3CSK4 or lipid A for 24h. Levels of secreted interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), monocyte chemoattractant protein-1 (MCP-1), and macrophage inflammatory protein-1α (MIP-1α) in culture supernatants were measured by enzyme-linked immunosorbent assay (ELISA). Cytotoxicity was determined by LDH activity in the supernatants. We also examined the effects of etidronate on the activation of nuclear factor-κB (NF-κB) and p38 mitogen-activated protein kinase (MAPK) in J774.1 cells by ELISA and Western blotting. RESULTS: Treatment of J774.1 cells with etidronate down-regulated TLR2 ligand-induced production of IL-6, TNF-α, MCP-1, and MIP-1α. Etidronate also inhibited Pam3CSK4-induced MCP-1 and TNF-α production by THP-1 cells. However, etidronate did not induce cytotoxicity and reduced lipid A-induced cytotoxicity in J774.1 cells. In addition, this agent did not down-regulate TLR4 ligand-induced proinflammatory cytokine production. Furthermore, etidronate inhibited the translocation of NF-κB but not p38 MAPK in J774.1 cells stimulated with Pam3CSK4 or lipid A. CONCLUSION: Etidronate likely inhibits proinflammatory cytokine production in J774.1 cells by suppressing NF-κB activation in the TLR2 and not the TLR4 pathway.