Linac primary barrier transmission: Flattening filter free and field size dependence.

There is widespread consensus in the literature that flattening filter free (FFF) beams have a lower primary barrier transmission than flattened beams. Measurements presented here, however, show that for energy compensated FFF beams, the barrier transmission can be as much as 70% higher than for flattened beams. The ratio of the FFF barrier transmission to the flattened beam barrier transmission increases with increasing barrier thickness.

Evaluation of machine log files/MC-based treatment planning and delivery QA as compared to ArcCHECK QA.

Purpose: A treatment planning/delivery QA tool using linac log files (LF) and Monte Carlo (MC) dose calculation is investigated as a standalone alternative to phantom-based patient-specific QA (ArcCHECK (AC)).

Methods: Delivering a variety of fields onto MapCHECK2 and ArcCHECK, diode sensitivity dependence on dose rate (in-field) and energy (primarily out-of-field) was quantified. AC and LF QAs were analyzed with respect to delivery complexity by delivering 12 × 12 cm static fields/arcs comprised of varying numbers of abutting sub-fields onto ArcCHECK.

Smooth muscle specific overexpression of p22phox potentiates carotid artery wall thickening in response to injury.

We hypothesized that transgenic mice overexpressing the p22(phox) subunit of the NADPH oxidase selectively in smooth muscle (Tg(p22smc)) would exhibit an exacerbated response to transluminal carotid injury compared to wild-type mice. To examine the role of reactive oxygen species (ROS) as a mediator of vascular injury, the injury response was quantified by measuring wall thickness (WT) and cross-sectional wall area (CSWA) of the injured and noninjured arteries in both Tg(p22smc) and wild-type animals at days 3, 7, and 14 after injury. Akt, p38 MAPK, and Src activation were evaluated at the same time points using Western blotting.

Slingshot isoform-specific regulation of cofilin-mediated vascular smooth muscle cell migration and neointima formation.

Objective: We hypothesized that cofilin activation by members of the slingshot (SSH) phosphatase family is a key mechanism regulating vascular smooth muscle cell (VSMC) migration and neoinitima formation following vascular injury.

Methods And Results: Scratch wound and modified Boyden chamber assays were used to assess VSMC migration following downregulation of the expression of cofilin and each SSH phosphatase isoform (SSH1, SSH2, and SSH3) by small interfering RNA (siRNA), respectively. Cofilin siRNA greatly attenuated the ability of VSMC migration into the "wound," and platelet-derived growth factor (PDGF)-induced migration was virtually eliminated versus a 3.

National hospital antibiotic timing measures for pneumonia and antibiotic overuse.

The development of drug-resistant bacteria from the overuse of antibiotics is a serious problem, with overutilization threatening to disarm caregivers and their patients even as together they face increasingly virulent strains of microbes. On the other hand, the speedy treatment of pneumonia with antibiotics is a firmly established, evidence-based practice, enshrined in Joint Commission on Accreditation for Healthcare Organizations Core Measures used in hospital accrediting and public reporting, and in Centers for Medicare and Medicaid Services (CMS) public-reporting and pay-for-performance hospital measures. This sets the stage for a potential conflict between (a) not doing the wrong thing by overprescribing antibiotics and (b) prescribing antibiotics on time for pneumonia.

Phosphoinositide 3-kinase, Src, and Akt modulate acute ventilation-induced vascular permeability increases in mouse lungs.

To determine the role of phosphoinositide 3-OH kinase (PI3K) pathways in the acute vascular permeability increase associated with ventilator-induced lung injury, we ventilated isolated perfused lungs and intact C57BL/6 mice with low and high peak inflation pressures (PIP). In isolated lungs, filtration coefficients (K(f)) increased significantly after ventilation at 30 cmH(2)O (high PIP) for successive periods of 15, 30 (4.1-fold), and 50 (5.