11β-hydroxysteroid dehydrogenase type 1 gene knockout attenuates atherosclerosis and in vivo foam cell formation in hyperlipidemic apoE⁻/⁻ mice.

Background: Chronic glucocorticoid excess has been linked to increased atherosclerosis and general cardiovascular risk in humans. The enzyme 11β-hydroxysteroid dehydrogenase type 1 (11βHSD1) increases active glucocorticoid levels within tissues by catalyzing the conversion of cortisone to cortisol. Pharmacological inhibition of 11βHSD1 has been shown to reduce atherosclerosis in murine models.

Rating the overall secondary safety of vehicles from real world crash data: the Australian and New Zealand Total Secondary Safety Index.

Various systems for rating secondary safety of particular makes and models of vehicles have been developed internationally. These measures generally evaluate crashworthiness (the ability of the vehicle to protect its own occupants in the event of a crash) separately from aggressivity (the harm a vehicle is liable to impose on other road users into which it crashes). This paper describes an approach using Australian and New Zealand data that combines these two facets of secondary safety into one 'Total Secondary Safety Index' estimated from real world crash outcomes.

Children with cochlear implants: the communication journey.

Cochlear implantation is now a well-established procedure for profoundly deaf children providing access to speech through hearing for many of them. Much attention has focused on which communication mode to adopt with this group of children but very little work has looked at the choices that parents make before and after cochlear implantation. This study, following on from two earlier studies, looked in depth at the experiences of 12 families.

Children's communication mode five years after cochlear implantation: changes over time according to age at implant.

One hundred and seventy six children who had received cochlear implants at one centre in the UK were followed up for five years post-implant. The cohort was divided into three groups by age at implant. 1: Under three years of age; 2: Between three and five; 3: Over five.

Urine acidification has no effect on peroxisome proliferator-activated receptor (PPAR) signaling or epidermal growth factor (EGF) expression in rat urinary bladder urothelium.

We previously reported prevention of urolithiasis and associated rat urinary bladder tumors by urine acidification (via diet acidification) in male rats treated with the dual peroxisome proliferator-activated receptor (PPAR)alpha/gamma agonist muraglitazar. Because urine acidification could potentially alter PPAR signaling and/or cellular proliferation in urothelium, we evaluated urothelial cell PPARalpha, PPARdelta, PPARgamma, and epidermal growth factor receptor (EGFR) expression, PPAR signaling, and urothelial cell proliferation in rats fed either a normal or an acidified diet for 5, 18, or 33 days. A subset of rats in the 18-day study also received 63 mg/kg of the PPARgamma agonist pioglitazone daily for the final 3 days to directly assess the effects of diet acidification on responsiveness to PPARgamma agonism.

Parents' views on changing communication after cochlear implantation.

We sent questionnaires to families of all 288 children who had received cochlear implants at one center in the United Kingdom at least 5 years previously. Thus, it was a large, unselected group. We received 142 replies and 119 indicated that the child and family had changed their communication approach following cochlear implantation.

Role of CCR2 in macrophage migration into the liver during acetaminophen-induced hepatotoxicity in the mouse.

The biological effects of monocyte chemoattractant protein (MCP) 1 are mediated by binding to C-C chemokine receptor (CCR) 2. In the present studies, we used CCR2 knockout (CCR2-/-) mice to examine the role of MCP-1 in acetaminophen-induced macrophage accumulation in the liver, expression of inflammatory cytokines, and hepatotoxicity. We found that hepatic expression of CCR2 and MCP-1 was increased 10-fold and 20-fold, respectively, 12 to 72 hours after administration of acetaminophen to wild-type mice.