Learning induces unique transcriptional landscapes in the auditory cortex.

Learning can induce neurophysiological plasticity in the auditory cortex at multiple timescales. Lasting changes to auditory cortical function that persist over days, weeks, or even a lifetime, require learning to induce gene expression. Indeed, transcription is the molecular determinant for long-term memories to form with a lasting impact on sound-related behavior.

NEUROPSYCHOLOGICAL PREDICTORS OF SAFETY IN URBAN LEFT-TURN SCENARIOS.

Left turns at urban intersections can be dangerous, especially when views are obstructed or pedestrians are present. Impairments in driver vision, motor, and cognition functions may further increase left-turn risk. We examined this problem in a simulated environment that included left-turn scenarios to study the driving behaviors of 28 drivers, ages 37 to 88 years, six of whom had "Useful Field of View" (UFOV) impairments.

EFFECTS OF ENVIRONMENTAL FACTORS ON NATURALISTIC DRIVING IN OBSTRUCTIVE SLEEP APNEA.

Reduced visibility and other environmental factors can impair driver ability to respond to roadway hazards. We examined the effects of reduced visibility on naturalistic driving in 66 drivers, including 45 at-risk drivers with obstructive sleep apnea (OSA) and 21 controls. We analyzed three months of electronic data using "black box" recorder technology and assessed the extent to which driver speed, longitudinal acceleration, and lateral acceleration metrics depend on ambient visibility from web-based environmental data archives.

Vascular nitric oxide and superoxide anion contribute to sex-specific programmed cardiovascular physiology in mice.

Intrauterine environmental pertubations have been linked to the development of adult hypertension. We sought to evaluate the interrelated roles of sex, nitric oxide, and reactive oxygen species (ROS) in programmed cardiovascular disease. Programming was induced in mice by maternal dietary intervention (DI; partial substitution of protein with carbohydrates and fat) or carbenoxolone administration (CX, to increase fetal glucocorticoid exposure).

Cerebral vascular dysfunction in TallyHo mice: a new model of Type II diabetes.

The purpose of this study was to characterize vascular responses and to examine mechanisms of vascular dysfunction in TallyHo mice, a new polygenic model of Type II diabetes. Responses of cerebral arterioles and carotid arteries were examined in vivo by using a cranial window and in vitro by using tissue baths, respectively. Dilatation of cerebral arterioles (baseline diameter = 33 +/- 1 micro m) in response to acetylcholine, but not to nitroprusside, was markedly reduced (P < 0.

Myocardial vascular and metabolic adaptations in chronically anemic fetal sheep.

Little is known about the vascular and metabolic adaptations that take place in the fetal heart to maintain cardiac function in response to increased load. Chronic fetal anemia has previously been shown to result in increased ventricular mass, increased myocardial vascularization, and increased myocardial expression of hypoxia-inducible factor-1 (HIF-1) and vascular endothelial growth factor (VEGF). We therefore sought to determine whether chronic fetal anemia induces expression of HIF-1-regulated angiogenic factors and glycolytic enzymes in the fetal myocardium.

14,15-Dihydroxyeicosatrienoic acid activates peroxisome proliferator-activated receptor-alpha.

Epoxyeicosatrienoic acids (EETs), lipid mediators synthesized from arachidonic acid by cytochrome P-450 epoxygenases, are converted by soluble epoxide hydrolase (SEH) to the corresponding dihydroxyeicosatrienoic acids (DHETs). Originally considered as inactive degradation products of EETs, DHETs have biological activity in some systems. Here we examined the capacity of EETs and DHETs to activate peroxisome proliferator-activated receptor-alpha (PPARalpha).

Vascular interleukin-10 protects against LPS-induced vasomotor dysfunction.

We tested the hypotheses that 1) systemic IL-10, after adenoviral gene transfer, protects arteries from impaired relaxation produced by LPS; 2) local expression of IL-10 within the arterial wall protects against vasomotor dysfunction after LPS; and 3) IL-10 protects against vascular dysfunction mediated by inducible NO synthase (iNOS) after LPS. In IL-10-deficient (IL-10-/-) and wild-type (WT, IL-10+/+) mice, LPS in vivo impaired relaxation of arteries to acetylcholine and gene transfer of IL-10 improved responses to acetylcholine. Superoxide levels were elevated in arteries after LPS, and increased levels of superoxide were prevented by gene transfer of IL-10.

Responses of cerebral arterioles to ADP: eNOS-dependent and eNOS-independent mechanisms.

ADP mediates platelet-induced relaxation of blood vessels and may function as an important intercellular signaling molecule in the brain. We used pharmacological and genetic approaches to examine mechanisms that mediate responses of cerebral arterioles to ADP, including the role of endothelial nitric oxide synthase (eNOS). We examined responses of cerebral arterioles (control diameter approximately 30 microm) in anesthetized wild-type (WT, eNOS+/+) and eNOS-deficient (eNOS-/-) mice using a cranial window.

Modulation of airway inflammation and bacterial clearance by epithelial cell ICAM-1.

Many cell types in the airway express the adhesive glycoprotein for leukocytes intercellular adhesion molecule-1 (ICAM-1) constitutively and/or in response to inflammatory stimuli. In this study, we identified functions of ICAM-1 on airway epithelial cells in defense against infection with Haemophilus influenzae. Initial experiments using a mouse model of airway infection in which the bacterial inoculum was mixed with agar beads that localize inflammation in airways demonstrated that ICAM-1 expression was required for efficient clearance of H.