ED syndromic surveillance for novel H1N1 spring 2009.

Purpose: The aim of this study is to demonstrate the use of emergency department (ED) syndromic surveillance in the setting of a novel and unexpected H1N1 influenza outbreak.

Basic Procedures: Data collection from ED electronic medical records was used to track initial chief complaint and discharge International Classification of Diseases, Ninth Revision, codes related to influenza-like illness (ILI). An alert threshold was generated using cumulative sum sequential analysis technique.

Insulin receptor substrate-2-dependent interleukin-4 signaling in macrophages is impaired in two models of type 2 diabetes mellitus.

We have shown previously that hyperinsulinemia inhibits interferon-alpha-dependent activation of phosphatidylinositol 3-kinase (PI3-kinase) through mammalian target of rapamycin (mTOR)-induced serine phosphorylation of insulin receptor substrate (IRS)-1. Here we report that chronic insulin and high glucose synergistically inhibit interleukin (IL)-4-dependent activation of PI3-kinase in macrophages via the mTOR pathway. Resident peritoneal macrophages (PerMPhis) from diabetic (db/db) mice showed a 44% reduction in IRS-2-associated PI3-kinase activity stimulated by IL-4 compared with PerMPhis from heterozygote (db/+) control mice.