Prevalence of Nasal Colonization by Methicillin-Resistant in Persons Using a Homeless Shelter in Kansas City.

Nasal colonization of methicillin-resistant (MRSA) plays an important role in the epidemiology and pathogenesis of disease. Situations of close-quarter contact in groups are generally regarded as a risk factor for community-acquired MRSA strains due to transmission fomites and person-to-person contact. With these criteria for risk, homeless individuals using shelter facilities, including showers and toilets, should be considered high risk for colonization and infection.

A Versatile Method for Immunofluorescent Staining of Cells Cultured on Permeable Membrane Inserts.

BACKGROUND Obtaining high-quality images of cellular structures via immunofluorescence staining is critical for cellular localization studies. Often, these studies cannot be performed in parallel with certain oncology, virology, pharmacokinetic, and drug absorption studies due to model system technicalities requiring the cells to be cultured on porous membranes rather than glass or plastic. MATERIAL AND METHODS Here, we report a method of immunofluorescent staining of cells cultured on permeable membranes.

The TGF-β pathway mediates doxorubicin effects on cardiac endothelial cells.

Elevated ALK4/5 ligands including TGF-β and activins have been linked to cardiovascular remodeling and heart failure. Doxorubicin (Dox) is commonly used as a model of cardiomyopathy, a condition that often precedes cardiovascular remodeling and heart failure. In 7-8-week-old C57Bl/6 male mice treated with Dox we found decreased capillary density, increased levels of ALK4/5 ligand and Smad2/3 transcripts, and increased expression of Smad2/3 transcriptional targets.

The effects of human immunodeficiency virus infection on the expression of the drug efflux proteins P-glycoprotein and breast cancer resistance protein in a human intestine model.

Objectives: In human immunodeficiency virus (HIV) infection, decreased penetration of antiretroviral drugs is postulated to contribute to HIV persistence within lymphoid-rich regions of the gastrointestinal (GI) tract. However, mechanistic explanations for this phenomenon remain unclear. Specifically, investigations of HIV effects on drug efflux proteins within intestinal models are minimal.

Functional PAK-2 knockout and replacement with a caspase cleavage-deficient mutant in mice reveals differential requirements of full-length PAK-2 and caspase-activated PAK-2p34.

p21-Activated protein kinase 2 (PAK-2) has both anti- and pro-apoptotic functions depending on its mechanism of activation. Activation of full-length PAK-2 by the monomeric GTPases Cdc42 or Rac stimulates cell survival, whereas caspase activation of PAK-2 to the PAK-2p34 fragment is involved in the apoptotic response. In this study we use functional knockout of PAK-2 and gene replacement with the caspase cleavage-deficient PAK-2D212N mutant to differentiate the biological functions of full-length PAK-2 and caspase-activated PAK-2p34.

Prevalence of multi-gastrointestinal infections with helminth, protozoan and Campylobacter spp. in Guatemalan children.

Background: The prevalence of multi-infections with helminthes, protozoans and Campylobacter spp. in Guatemalan children is a reflection of differences in the risk factors related to pathogen transmission.

Methodology: Two hundred and eighty-nine fecal samples were collected from children of the Guatemalan highlands and patterns of pathogen occurrences were evaluated using an immunoassay for Campylobacter spp.

Elevated p21-activated kinase 2 activity results in anchorage-independent growth and resistance to anticancer drug-induced cell death.

p21-activated kinase 2 (PAK-2) seems to be a regulatory switch between cell survival and cell death signaling. We have shown previously that activation of full-length PAK-2 by Rac or Cdc42 stimulates cell survival, whereas caspase activation of PAK-2 to the proapoptotic PAK-2p34 fragment is involved in the cell death response. In this study, we present a role of elevated activity of full-length PAK-2 in anchorage-independent growth and resistance to anticancer drug-induced apoptosis of cancer cells.

RhoA mediates cyclooxygenase-2 signaling to disrupt the formation of adherens junctions and increase cell motility.

Cyclooxygenase-2 (COX-2) represents an important target for treatment and prevention of colorectal cancer. Although COX-2 signaling is implicated in promoting tumor cell growth and invasion, the molecular mechanisms that mediate these processes are largely unknown. In this study, we show that the RhoA pathway mediates COX-2 signaling to disrupt the formation of adherens junctions and increase cell motility.