Strategic Facilities Planning: A Focus On Health Care

Turbulent market conditions have forced the health care sector to re-examine its business and operational practices.  Health care has become increasingly complex as decisions and planning are reframed in light of the current lagging economy, an increased demand for services, new global competition, and impending legislation reform.  The stress is felt most keenly within the nation’s hospitals and consortia of health care facilities.  Facility planning decisions are no exception.  Hospital administrators are abandoning the once commonplace rules governing aging infrastructure renovations.  Instead, administrators are basing decisions within their respective strategic context and are attempting to align buildings, services, personnel, and technology to an overall plan that looks at markets, operations, and finances as resources for competitive advantage.  This paper reviews the strategic facilities planning literature and applies those best practices which support this organizational alignment for health care.  An application in the mid-Atlantic demonstrates that hospital facilities, by design, need to support the current and future needs of health care delivery systems, while dated structures impede industry advances.  Health care infrastructure improvements must proactively address technological, regulatory, and financial changes facing the sector

ATM activation accompanies histone H2AX phosphorylation in A549 cells upon exposure to tobacco smoke

<p>Abstract</p> <p>Background</p> <p>In response to DNA damage or structural alterations of chromatin, histone H2AX may be phosphorylated on <it>Ser</it>139 by phosphoinositide 3-kinase related protein kinases (PIKKs) such as <it>ataxia telangiectasia </it>mutated (ATM), ATM-and Rad-3 related (ATR) kinase, or by DNA dependent protein kinase (DNA-PKcs). When DNA damage primarily involves formation of DNA double-strand breaks (DSBs), H2AX is preferentially phosphorylated by ATM rather than by the other PIKKs. We have recently reported that brief exposure of human pulmonary adenocarcinoma A549 cells or normal human bronchial epithelial cells (NHBE) to cigarette smoke (CS) induced phosphorylation of H2AX.</p> <p>Results</p> <p>We report here that H2AX phosphorylation in A549 cells induced by CS was accompanied by activation of ATM, as revealed by ATM phosphorylation on <it>Ser</it>1981 (ATM-S1981^P) detected immunocytochemically and by Western blotting. No cell cycle-phase specific differences in kinetics of ATM activation and H2AX phosphorylation were observed. When cells were exposed to CS from cigarettes with different tobacco and filter combinations, the expression levels of ATM-S1981^Pcorrelated well with the increase in expression of phosphorylated H2AX (γH2AX) (R = 0.89). In addition, we note that while CS-induced γH2AX expression was localized within discrete foci, the activated ATM was distributed throughout the nucleoplasm.</p> <p>Conclusion</p> <p>These data implicate ATM as the PIKK that phosphorylates H2AX in response to DNA damage caused by CS. Based on current understanding of ATM activation, expression and localization, these data would suggest that, in addition to inducing potentially carcinogenic DSB lesions, CS may also trigger other types of DNA lesions and cause chromatin alterations. As checkpoint kinase (Chk) 1, Chk2 and the p53 tumor suppressor gene are known to be phosphorylated by ATM, the present data indicate that exposure to CS may lead to their phosphorylation, with the downstream consequences related to the halt in cell cycle progression and increased propensity to undergo apoptosis. Defining the nature and temporal sequence of molecular events that are disrupted by CS through activation and eventual dysregulation of normal defense mechanisms such as ATM and its downstream effectors may allow a more precise understanding of how CS promotes cancer development.</p

Tissue registration and exploration user interfaces in support of a human reference atlas

Seventeen international consortia are collaborating on a human reference atlas (HRA), a comprehensive, high-resolution, three-dimensional atlas of all the cells in the healthy human body. Laboratories around the world are collecting tissue specimens from donors varying in sex, age, ethnicity, and body mass index. However, harmonizing tissue data across 25 organs and more than 15 bulk and spatial single-cell assay types poses challenges. Here, we present software tools and user interfaces developed to spatially and semantically annotate ( register ) and explore the tissue data and the evolving HRA. A key part of these tools is a common coordinate framework, providing standard terminologies and data structures for describing specimen, biological structure, and spatial data linked to existing ontologies. As of April 22, 2022, the registration user interface has been used to harmonize and publish data on 5,909 tissue blocks collected by the Human Biomolecular Atlas Program (HuBMAP), the Stimulating Peripheral Activity to Relieve Conditions program (SPARC), the Human Cell Atlas (HCA), the Kidney Precision Medicine Project (KPMP), and the Genotype Tissue Expression project (GTEx). Further, 5,856 tissue sections were derived from 506 HuBMAP tissue blocks. The second exploration user interface enables consortia to evaluate data quality, explore tissue data spatially within the context of the HRA, and guide data acquisition. A companion website is at https://cns-iu.github.io/HRA-supporting-information/

A Computational Simulation Study of Benzamidine Derivatives Binding to Arginine-Specific Gingipain (HRgpA) from Periodontopathogen Porphyromonas gingivalis

We have shown that the binding free energy calculation from molecular dynamics can be adapted successfully to cysteine proteinases, such as arginine-specific gingipain (HRgpA) from Porphyromonas gingivalis. The binding free energy obtained is in good agreement with the available experimental data for eight benzamidine derivatives including urea and ether linker. The calculations showed that the electrostatic energies between HRgpA and inhibitors were important in determining the relative affinities of the inhibitors to the HRgpA, with an average binding free energy of about −5 kcal/mol. The average structures of the eight complexes suggest that benzamidine inhibitors interact with Asp387, His435, and Cys468 by hydrogen bonding and with Trp508 by hydrophilic interactions that are essential for the activities of benzamidine inhibitors. It can therefore be expected that the method provides a reliable tool for the investigation of new HRgpA inhibitors. This finding could significantly benefit the future design of HRgpA inhibitors

Learning to Believe in Papua New Guinea

This chapter examines how witchcraft and sorcery beliefs are reproduced among the educated working and middle classes in Papua New Guinea. In a context where tertiary schooling is accessible only to a tiny segment of the population, many educated people in PNG feel anxious about their social position and worry that their upward mobility will provoke envy and resentment in the less fortunate. This anxiety is projected most strongly onto the “ples lain” or rural population, who are thought to maintain many traditional practices, including witchcraft and sorcery. Drawing on ethnographic research among nursing students in the Eastern Highlands, I examine the ways that class identity and Pentecostal social forms coalesce, giving students resources for narrating, understanding, and resisting the dangers they face as social outsiders and (future) employees of a neglectful state. Looking specifically at events during a nursing practicum in rural Eastern Highlands Province, I describe how students and their teachers collapsed different forms of invisible violence—both traditional and contemporary—into a generic evil to be discerned and resisted. Following Robbins (2009) I argue that witchcraft talk is exceptionally socially productive—in this case, productive of a distinctly Christian, professional class identity in which the problems created by “the villagers” and “pasin tumbuna” (ancestral practices) are objects of profound concern.falseAccepte

Geospatial Resolution of Human and Bacterial Diversity with City-Scale Metagenomics

The panoply of microorganisms and other species present in our environment influence human health and disease, especially in cities, but have not been profiled with metagenomics at a city-wide scale. We sequenced DNA from surfaces across the entire New York City (NYC) subway system, the Gowanus Canal, and public parks. Nearly half of the DNA (48%) does not match any known organism; identified organisms spanned 1,688 bacterial, viral, archaeal, and eukaryotic taxa, which were enriched for harmless genera associated with skin (e.g., Acinetobacter). Predicted ancestry of human DNA left on subway surfaces can recapitulate U.S. Census demographic data, and bacterial signatures can reveal a station’s history, such as marine-associated bacteria in a hurricane-flooded station. Some evidence of pathogens was found (Bacillus anthracis), but a lack of reported cases in NYC suggests that the pathogens represent a normal, urban microbiome. This baseline metagenomic map of NYC could help long-term disease surveillance, bioterrorism threat mitigation, and health management in the built environment of citie