The Harley School

Only half of US schoolchildren receive influenza vaccine. School-located influenza vaccination (SLIV) might raise vaccination rates but conducting flu vaccine clinics at schools is challenging to implement. We compared 2 school-based programs designed to raise influenza vaccination rates: parent reminder/educational messages sent to parents from schools which is a low-intensity intervention vs the combination of reminder/educational messages plus SLIV clinics which is a high-intensity intervention. We assigned 36 schools (6 school districts, 2 per group) to 3 groups: (1) control, ie, no SLIV and no parent reminder/education, (2) parent reminder/education emailed by schools, and (3) parent reminder/education plus SLIV clinics. Some schools had SLIV clinics in prior years. Health department nurses conducted SLIV clinics. Among 24,832 children at 36 schools, vaccination rates were control (51.3%), parent reminder/education-only (41.2%), and reminder/education + SLIV (58.7%). On multivariate analyses which controlled for vaccination in prior seasons, children in reminder/education + SLIV schools had higher vaccination rates (OR 1.27, 95% CI 1.10-1.47), but children in reminder/education-only schools had lower rates (OR 0.87, 95% CI 0.75-1.00) than children in control schools. Parent reminder/education combined with SLIV clinics raise vaccination rates, but parent reminder/education alone does not.

Treatment planning to reduce challenging behavior (e.g., aggression and property destruction) can be complex and requires a prescriptive interprofessional team-based approach. As with other problems that interfere with an individual’s quality of life, such as health issues, the best course of treatment is one that accurately assesses the problem, leads to effective treatment for the issue of concern, and is empirically supported. This is especially important when treating individuals who display problem behavior which frequently interfere with their opportunities to learn and to live and be educated in less-restrictive settings (Matson, Mayville, & Laud, 2003). The utility of functional behavior assessments (FBAs) and functional analyses (FAs) in the identification of the specific function or purpose of challenging behavior has been embraced commonly by persons charged with supporting individuals who display challenging behavior (e.g., behavior analysts and educators). This is demonstrated by the laws requiring FBAs be conducted when individuals are struggling in educational environments (Individuals with Disabilities Education Improvement Act, 2004) and the belief that the assessments conducted should result in the development of interventions that help preserve the child’s placement in the least restrictive appropriate educational setting. The utility of these assessments has been repeatedly demonstrated in the published literature (e.g., Derby et al., 1992; Iwata, Dorsey, Slifer, Bauman, & Richman, 1994; Kennedy & Souza, 1995; Kern, Childs, Dunlap, Clarke & Falk, 1994; McCord, Thompson, & Iwata, 2001; Ellingson, Miltenberger, Stricker, Galensky, & Garlinghouse, 2000). Several excellent reviews of this extensive literature have been conducted and have independently identified functional analysis and assessment as best practice (e.g., Carr, 1994; Hanley, Iwata, & McCord, 2003).

Cyclosporin A (CsA), a widely used immunosuppressant, causes distal renal tubular acidosis (dRTA). It exerts its immunosuppressive effect by a calcineurin-inhibitory complex with its cytosolic receptor, cyclophilin A. However, CsA also inhibits the peptidyl prolyl cis-trans isomerase (PPIase) activity of cyclophilin A. We studied HCO(3)(-) transport and changes in beta-intercalated cell pH on luminal Cl(-) removal in isolated, perfused rabbit cortical collecting tubules (CCDs) before and after exposure to media pH 6.8 for 3 h. Acid incubation causes adaptive changes in beta-intercalated cells by extracellular deposition of hensin (J Clin Invest 109: 89, 2002). Here, CsA prevented this adaptation. The unidirectional HCO(3)(-) secretory flux, estimated as the difference between net flux and that after Cl(-) removal from the lumen, was -6.7 +/- 0.2 pmol.min(-1).mm(-1) and decreased to -1.3 +/- 0.2 after acid incubation. CsA in the bath prevented the adaptive decreases in HCO(3)(-) secretion and apical Cl(-):HCO(3)(-) exchange. To determine the mechanism, we incubated CCDs with FK-506, which inhibits calcineurin activity independently of the host cell cyclophilin. FK-506 did not prevent the acid-induced adaptive decrease in unidirectional HCO(3)(-) secretion. However, [AD-Ser](8) CsA, a CsA derivative, which does not inhibit calcineurin but inhibits PPIase activity of cyclophilin A, completely blocked the effect of acid incubation on apical Cl(-):HCO(3)(-) exchange. Acid incubation resulted in prominent "clumpy" staining of extracellular hensin and diminished apical surface of beta-intercalated cells [smaller peanut agglutinin (PNA) caps]. CsA and [AD-Ser](8) CsA prevented most hensin staining and the reduction of apical surface; PNA caps were more prominent. We suggest that hensin polymerization around adapting beta-intercalated cells requires the PPIase activity of cyclophilins. Thus CsA is able to prevent this adaptation by inhibition of a peptidyl prolyl cis-trans isomerase activity. Such inhibition may cause dRTA during acid loading.

Temperature and density histories of direct-drive laser fusion implosions are important to an understanding of the reaction`s progress. Such measurements also document phenomena such as preheating of the core and improper compression that can interfere with the thermonuclear reaction. Model x-ray spectra from the non-LTE (local thermodynamic equilibrium) radiation transport post-processor for LILAC have recently been fitted to OMEGA data. The spectrum fitting code reads in a grid of model spectra and uses an iterative weighted least-squares algorithm to perform a fit to experimental data, based on user-input parameter estimates. The purpose of this research was to upgrade the fitting code to compute formal uncertainties on fitted quantities, and to provide temperature and density estimates with error bars. A standard error-analysis process was modified to compute these formal uncertainties from information about the random measurement error in the data. Preliminary tests of the code indicate that the variances it returns are both reasonable and useful.

Embryonic cardiovascular function has been extensively studied in vivo in the chick embryo. However, the geometry of mammalian and avian hearts differs; the mammalian cardiovascular system is coupled to both yolk sac and placental circulations, and unique murine genetic models associated with structural and functional cardiovascular defects are now available. We therefore adapted techniques validated for the chick embryo to define cardiovascular dimensions and function in the mouse embryo. We bred C3HeB female and C57B1/J6 male mice and ICR pairs for experiments on embryonic days (EDs) 10.5 to 14.5 (n = 130 dams). After maternal anesthesia (pentobarbital, 60 mg/kg IP), laparotomy, and sequential regional hysterotomy, we exposed and then imaged individual embryos at 60 Hz (video) in the ventral and/or left anterior oblique views while maintaining uteroplacental continuity. We measured epicardial chamber dimensions and then calculated right and left ventricular elliptical volumes from ares. In addition, we measured pulsed-Doppler blood velocity across the atrioventricular cushions and ventricular outflow tract. We maintained embryonic temperature with a heated surgical platform, topical oxygenated and warmed buffer, and warming lamps. Embryonic heart rate increased from 124.7 +/- 5.2 to 194.3 +/- 13.2 bpm from EDs 10.5 to 14.5 (P < .01). Right and left ventricular end-diastolic and end-systolic dimensions increased (P < .05 by ANOVA for each). Maximal ventricular mean inflow and outflow velocities increased from 62.33 +/- 4.06 to 106.23 +/- 11.59 and from 55.79 +/- 6.11 to 91.61 +/- 6.93 mm/s, respectively (P < .05 by ANOVA for each). Thus, as has been done for chick and rat embryos, the maturation of murine embryonic cardiovascular function can be quantified in vivo, setting the stage for the investigation of structure-function relations in mouse models of cardiovascular development and disease.