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Aim: This study aims to elucidate the foreign patient-specific factors associated with emergency department length of stay (EDLOS) in a regional core hospital emergency department (ED) in Japan. Methods: This retrospective observational study included non-Japanese patients who visited the ED in a Japanese regional core hospital between April 1, 2018, and March 31, 2020. The effects on EDLOS were assessed using multivariate linear regression analysis, which included factors such as age, sex, consultation language, interpreter usage, arrival time, day of visit, mode of arrival, underlying disease, triage level, diagnosis of injury/noninjury, diagnostic investigations, consultation with specialists, and treatments or procedures. Results: Of 65,297 ED patients, there were 777 study patients, with a median age of 37 years (interquartile range [IQR], 24.0-50.0). The median EDLOS was 101 min (IQR, 63.0-153.0). Multivariate linear regression analysis indicated that an extended EDLOS was associated with: language apart from Japanese, Chinese, or English (51.7 min; 95% confidence interval [CI], 17.8-85.6), helicopter arrival (115.6 min; 95% CI, 48.8-182.5), blood testing (60.5 min; 95% CI, 34.6-86.4), computed tomography (23.8 min; 95% CI, 3.7-43.9), consultation with specialists (36.2 min; 95% CI, 11.8-60.6), intravenous fluid/medication (29.7 min; 95% CI, 3.3-56.1), and surgical procedure/reduction/fixation in the ED (38.8 min; 95% CI, 14.2-63.4). Conclusions: Consultation in a language other than Japanese, English, or Chinese was associated with a longer EDLOS in a regional core hospital in Japan. Devising ways to accommodate patients who speak various languages could be important.
RESUMO
Neuroligin (NLG), a postsynaptic adhesion molecule, is involved in the formation of synapses by binding to a cognate presynaptic ligand, neurexin. Here we report that neuroligin-1 (NLG1) undergoes ectodomain shedding at the juxtamembrane stalk region to generate a secreted form of NLG1 and a membrane-tethered C-terminal fragment (CTF) in adult rat brains in vivo as well as in neuronal cultures. Pharmacological and genetic studies identified ADAM10 as the major protease responsible for NLG1 shedding, the latter being augmented by synaptic NMDA receptor activation or interaction with soluble neurexin ligands. NLG1-CTF was subsequently cleaved by presenilin/γ-secretase. Secretion of soluble NLG1 was significantly upregulated under a prolonged epileptic seizure condition, and inhibition of NLG1 shedding led to an increase in numbers of dendritic spines in neuronal cultures. Collectively, neuronal activity-dependent proteolytic processing of NLG1 may negatively regulate the remodeling of spines at excitatory synapses.