BackgroundA wide variety of specialty textiles are used in health care settings for bedding, clothing, and privacy. The ability of textiles to host or otherwise sequester microbes has been well documented; however, their reciprocal potential for liberating airborne bacteria remains poorly characterized. In response, a multi-season survey of bacterial bioaerosols was conducted in the origin and terminus of residual paths which are specifically designed to isolate soiled hospital textiles as they are moved to laundering. This survey used conventional optical particle counting which incorporated multi-channel fluorescence in conjunction with molecular phylogenetic analyses to characterize the bioaerosols liberated during soiled textile storage—immediately before and after the occupation of a modern hospital. Although outfitted with a HEPA filtration system, the number of airborne particles presenting fluorescing optical signatures consistent with airborne bacteria and fungi significantly increased in textile holding rooms soon after the hospital’s commissioning, even though these isolated residual areas rarely host personnel. The bioaerosol liberated during textile storage was characterized using Illumina MiSeq sequencing of bacterial 16S ribosomal ribonucleic acid (rRNA) genes. Gene copies recovered by quantitative PCR from aerosol collected in co-located impingers were consistent with fluorescence gated optical particle counting.ResultsThe relative abundance patterns of proximal bacterial bioaerosol were such that the air in the origin and terminus of textile storage rooms could not be differentiated once the hospital began processing soiled linens. Genes from microbes typically associating with human skin, feces, and hair—Staphylococcus, Propionibacteria, Corynebacteria, Lactobacillus, and Streptococcus spp.—dominated the aerosol abundance profiles in textile holding rooms, which were generally far less diverse than communities recovered from surfaces in patient rooms.ConclusionsThese results suggest that aerosol partitioning from the routine handling of soiled textiles can contribute to airborne exposures in the health care environment.

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Epidemiological studies have shown that exposure to airborne particulate matter can be an important risk factor for some common respiratory diseases. While many studies have shown that particulate matter exposures are associated with inflammatory reactions, the role of specific cellular responses in the manifestation of primary hypersensitivities, and the progression of respiratory diseases remains unclear. In order to better understand mechanisms by which particulate matter can exert adverse health effects, more robust approaches to support in vitro studies are warranted. In response to this need, a group of accepted toxicology assays were adapted to create an analytical suite for screening and evaluating the effects of important, ubiquitous atmospheric pollutants on two model human lung cell lines (epithelial and immature macrophage). To demonstrate the utility of this suite, responses to intact diesel exhaust particles, and mass-based equivalent doses of their organic extracts were examined. Results suggest that extracts have the potential to induce greater biological responses than those associated with their colloidal counterpart. Additionally, macrophage cells appear to be more susceptible to the cytotoxic effects of both intact diesel exhaust particles and their organic extract, than epithelial cells tested in parallel. As designed, the suite provided a more robust basis for characterizing toxicity mechanisms than the analysis of any individual assay. Findings suggest that cellular responses to particulate matter are cell line dependent, and show that the collection and preparation of PM and/or their extracts have the potential to impact cellular responses relevant to screening fundamental elements of respiratory toxicity.

Public reporting burden for this collection of information is estimated to average 1 hour per response, including the time for reviewing instructions, searching existing data sources, gathering and maintaining the data needed, and completing and reviewing this collection of information. Send comments regarding this burden estimate or any other aspect of this collection of information, including suggestions for reducing this burden to Department of Defense, Washington Headquarters Services, Directorate for Information Operations and Reports (0704-0188), 1215 Jefferson Davis Highway, Suite 1204, Arlington, VA 22202-4302. Respondents should be aware that notwithstanding any other provision of law, no person shall be subject to any penalty for failing to comply with a collection of information if it does not display a currently valid OMB control number. PLEASE DO NOT RETURN YOUR FORM TO THE ABOVE ADDRESS. REPORT DATE 30-04-2008 REPORT TYPE PERFORMING ORGANIZATION NAME(S) AND ADDRESS(ES) 8. PERFORMING ORGANIZATION REPORT NUMBERUniversity of Colorado Health Science Center Aurora, CO 80045-0508 SPONSORING / MONITORING AGENCY NAME(S) AND ADDRESS(ES) 10. SPONSOR/MONITOR'S ACRONYM(S) U.S. Army Medical Research and Materiel Command Fort Detrick, Maryland 21702-5012 SPONSOR/MONITOR'S REPORT NUMBER(S) DISTRIBUTION / AVAILABILITY STATEMENTApproved for Public Release; Distribution Unlimited SUPPLEMENTARY NOTES ABSTRACTAim 1: Loss of CD44 standard and increased splice variant form CD44v7-10 facilitate prostate cancer (PC) invasion. Mitogen-activated protein kinase (MAPK) pathways and paracrine calcitonin may dysregulate CD44. CD44 total and CD44v7-10 RNA or protein were assessed in androgen-independent PC with known high CD44v7-10 expression and in BPH-1 cells in response to exogenous calcitonin and to inhibitors of protein kinase A, MEK, JNK, or p38 kinase. Inhibition of MEK or p38 but not JNK reduced CD44 RNA in cancer and benign cells. Calcitonin, in calcitonin receptor-positive cells only, caused suppression of CD44 total but increase in variant, the latter apparently dependent on the p38 pathway. See the attached, submitted manuscript. Aim 2: In vivo trials of altering CD44 in mouse xenografts. We spent several months cloning our DNA sequences for CD44 standard overexpression and CD44 variant RNAi out of pTracer and into pAAV-IRES-GFP to use the latter plasmid to establish therapeutic adenoassociated virus (AAV). However, when C4-2 prostate cancer cells were infected, only 30% were GFP+ infected cells, and the low percent of viable cells, due to viral cytopathic effect, prohibited in vitro or in vivo use of AAV. We decided to revert to the pTracer approach with blasticidin cell selection. Matrigel invasion assay demonstrates that non-invaded cells have much higher GFP+ than invaded ones and by western blot analysis, non-invasion correlates with altered CD44 standard and variant. Aim 1: Mitogenic Pathway Effects on Splicing: Mr. Robbins' duties from July 1-December 1 were primarily concerned with Aim 1's first sub-Aim inv...

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