The implementation of CPOE resulted in almost a complete elimination of MPEs and RVs and a significant but less dramatic effect on potential ADEs.

No abstract

SUMMARYCBA mice, inoculated intravenously with large doses of adenovirus type 5, showed raised levels of serum aspartate aminotransferase (SAAT; EC 2.6.1.1) and died within a few days from histologically demonstrable hepatic necrosis. After inoculation of I LDs0, virus was rapidly taken up by the tissues where infectivity then declined greatly. Organ titres then increased about Ioo-fold by 48 h p.i. but, in the liver, which showed intranuclear inclusion bodies, and by electron microscopy, scattered intranuclear and intracytoplasmic adenovirions, the increase was IOOOO-to iooooo-fold. P antigen was detected by single radial diffusion in liver extracts, and by immunofluorescence in 80 % of liver cells at 36 h p.i. Hexon, penton base and fibre antigens appeared later and in fewer cells. The maximum amount of hexon, of demonstrable type 5 specificity, was shown by radioimmunoassay to be equivalent to up to 5 x io 11 whole adenovirions/g liver. It is concluded that human adenovirus type 5 undergoes an abortive but lytic infection in most liver cells but that replication may proceed to completion in a few.

Hyphal development in the dimorphic pathogenic fungus Candida albicans is thought to facilitate the primary invasion of surface epithelia during superficial infections. When mycelia were grown on Nuclepore membrane filters that were placed over serum-containing agar, the hyphae grew over the membrane surface and through the pores thereby crossing to the other side of the membrane. Hyphae that did not contact the lip of a pore did not enter it. The response was likely to be due to contact guidance (thigmotropism) and not chemotropism towards the nutrients since hyphae growing on the underside of the membrane also entered the pores then grew away from the underlying nutrient agar. The response therefore seems to be due to sensation of the substrate topography, and tropic movement in relation to changes in contour. This behaviour may enable the hyphae to penetrate epithelia at microscopic wound sites, membrane invaginations and other foci where the integrity of the epithelium is weak.

Background— Medication errors and adverse drug events are common after hospital discharge due to changes in medication regimens, suboptimal discharge instructions, and prolonged time to follow-up. Pharmacist-based interventions may be effective in promoting the safe and effective use of medications, especially among high-risk patients such as those with low health literacy. Methods and Results— The Pharmacist Intervention for Low Literacy in Cardiovascular Disease (PILL-CVD) study is a randomized controlled trial conducted at 2 academic centers—Vanderbilt University Hospital and Brigham and Women’s Hospital. Patients admitted with acute coronary syndrome or acute decompensated heart failure were randomly assigned to usual care or intervention. The intervention consisted of pharmacist-assisted medication reconciliation, inpatient pharmacist counseling, low-literacy adherence aids, and tailored telephone follow-up after discharge. The primary outcome is the occurrence of serious medication errors in the first 30 days after hospital discharge. Secondary outcomes are health care utilization, disease-specific quality of life, and cost-effectiveness. Enrollment was completed September 2009. A total of 862 patients were enrolled, and 430 patients were randomly assigned to receive the intervention. Analyses will determine whether the intervention was effective in reducing serious medication errors, particularly in patients with low health literacy. Conclusions— The PILL-CVD study was designed to reduce serious medication errors after hospitalization through a pharmacist-based intervention. The intervention, if effective, will inform health care facilities on the use of pharmacist-assisted medication reconciliation, inpatient counseling, low-literacy adherence aids, and patient follow-up after discharge. Clinical Trial Registration— clinicaltrials.gov. Identifier: NCT00632021.