Infrared tympanic thermometry in comparison with other temperature measurement techniques in febrile children.

OBJECTIVE: : To determine whether infrared tympanic thermometry (ITT) measurements more accurately reflect core body temperatures than axillary, forehead, or rectal measurements during fever cycles in children. DESIGN: : Prospective cohort study. SETTING: : Pediatric and cardiac intensive care units at a tertiary care children's hospital. PATIENTS: : Critically ill children <7 yrs of age with indwelling bladder catheters. INTERVENTIONS: : Simultaneous temperatures were recorded during both febrile and nonfebrile periods using ITT, indwelling bladder (core), axillary, forehead, and indwelling rectal measurements in 36 children. MEASUREMENTS AND MAIN RESULTS: : Overall ITT measurements were 0.03 +/- 1.43 degrees F less than core temperature measurements. In comparison, rectal, forehead, and axillary measurements averaged 0.62 +/- 1.44, 0.56 +/- 1.81, and 1.25 +/- 1.73 degrees F less than core temperature measurements. ITT measurements had better agreement with core measurements during increasing and decreasing temperature cycles. Receiver operating characteristic analysis performed on increasing and decreasing temperature cycle data revealed that ITT measurements performed well, with an area under the curve of 0.855 (95% confidence interval, 0.797-0.913) in comparison with rectal measurement area under the curve of 0.777 (95% confidence interval, 0.701-0.853), forehead measurement area under the curve of 0.710 (95% confidence interval, 0.715-0.888), and axillary measurement area under the curve of 0.664 (95% confidence interval, 0.579-0.750). CONCLUSIONS: : ITT measurements more accurately reflect core temperatures than any other measurement site during febrile and nonfebrile periods in children. ITT measurements are a reproducible and relatively noninvasive substitute for bladder or rectal measurements in febrile children.

The A2A receptor mediates an endogenous regulatory pathway of cytokine expression in THP-1 cells.

Adenosine is an endogenous nucleoside that regulates numerous cellular functions including inflammation. Adenosine acts via cell-surface receptors subtyped as A1, A2A, A2B, and A3. The A2A receptor (A2AR) has been linked to anti-inflammatory effects of adenosine. Furthermore, microarray analysis revealed increased A2AR mRNA in lipopolysaccharide (LPS)-stimulated monocytes. We hypothesized that endogenous adenosine inhibited LPS-mediated tumor necrosis factor (TNF) production via A2AR stimulation. Using THP-1 cells, our results demonstrated that LPS increased expression of cellular A2AR and adenosine. A2AR agonism with 2-p-(2-carboxyethyl)phenethylamino-5'-N-ethylcarboxamido adenosine (CGS 21680) after LPS decreased TNF production in a dose- and time-dependent manner, whereas A2AR antagonism significantly increased TNF and blocked the inhibitory effect of CGS 21680. This inhibitory pathway involved A2AR stimulation of cyclic adenosine monophosphate (cAMP) to activate protein kinase A, resulting in phosphorylation of cAMP response element-binding protein (CREB). Phospho-CREB had been shown to inhibit nuclear factor-kappaB transcriptional activity, as was observed with CGS 21680 treatment. Thus, following immune activation with LPS, endogenous adenosine mediates a negative feedback pathway to modulate cytokine expression in THP-1 cells.

Heat shock inhibits tnf-induced ICAM-1 expression in human endothelial cells via I kappa kinase inhibition.

The pulmonary vascular endothelium plays a critical role in lung inflammation. As a result of proinflammatory cytokine expression, adhesion molecules are upregulated on the surface of the endothelial cells. Adhesion molecules facilitate recruitment of leukocytes and thus, have been targeted for potential anti-inflammatory strategies. Prior induction of the stress response through thermal stimulation, or heat shock, alters proinflammatory gene expression by attenuating NF-kappaB signaling. As intercellular adhesion molecule-(ICAM) 1 expression is, in part, NF-kappaB-dependent, we hypothesized that heat shock would inhibit ICAM-1 expression. Heat shocking endothelial cells resulted in heat shock protein (HSP) expression as measured by HSP-70 induction, and decreased TNF-alpha-induced ICAM-1 expression in a manner that appeared to be transcriptionally mediated. Following heat shock, decreased TNF-alpha-induced NF-kappaB activation was observed and was associated with preservation of IkappaB-alpha and a decrease in phosphorylated IkappaB-alpha that correlated to inhibition of I kappa kinase (IKK) activity. Interestingly, exposing respiratory epithelial cells to heat shock, which results in NF-kappaB inhibition, did not affect TNF-induced ICAM-1 expression. We conclude that heat shock decreases endothelial cell ICAM-1 expression via inhibition of IKK activity.