Inpatient urine cultures are frequently performed without urinalysis or microscopy: Findings from a large academic medical center

OBJECTIVETo describe the frequency of urine cultures performed in inpatients without additional testing for pyuriaDESIGNRetrospective cohort studySETTINGA 1,250-bed academic tertiary referral centerPATIENTSHospitalized adultsMETHODSThis study included urine cultures drawn on 4 medical and 2 surgical wards from 2009 to 2013 and in the medical and surgical intensive care units (ICUs) from 2012 to 2013. Patient and laboratory data were abstracted from the hospital’s medical informatics database. We identified catheter-associated urinary tract infections (CAUTIs) in the ICUs by routine infection prevention surveillance. Cultures without urinalysis or urine microscopy were defined as “isolated.” The primary outcome was the proportion of isolated urine cultures obtained. We used multivariable logistic regression to assess predictors of isolated cultures.RESULTSDuring the study period, 14,743 urine cultures were obtained (63.5 cultures per 1,000 patient days) during 11,820 patient admissions. Of these, 2,973 cultures (20.2%) were isolated cultures. Of the 61 CAUTIs identified, 31 (50.8%) were identified by an isolated culture. Predictors for having an isolated culture included male gender (adjusted odds ratio [aOR], 1.22; 95%; confidence interval [CI], 1.11–1.35], urinary catheterization (aOR, 2.15; 95% CI, 1.89–2.46), ICU admission (medical ICU aOR, 1.72; 95% CI, 1.47–2.00; surgical ICU aOR, 1.82; 95% CI, 1.51–2.19), and obtaining the urine culture ≥1 calendar day after admission (1–7 days aOR, 1.91; 95% CI. 1.71–2.12; &gt;7 days after admission aOR, 2.81; 95% CI, 2.37–3.34).CONCLUSIONSIsolated urine cultures are common in hospitalized patients, particularly in patients with urinary catheters and those in ICUs. Interventions targeting inpatient culturing practices may improve the diagnosis of urinary tract infections.Infect Control Hosp Epidemiol2017;38:455–460</jats:sec

CDH11 inhibits proliferation and invasion in head and neck cancer

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/135974/1/jop12471_am.pdfhttp://deepblue.lib.umich.edu/bitstream/2027.42/135974/2/jop12471.pd

The course of etoposide-induced apoptosis from damage to DNA and p53 activation to mitochondrial release of cytochrome c.

Treatment of L929 fibroblasts by the topoisomerase II inhibitor etoposide killed 50% of the cells within 72 h. The cell killing was preceded by the release of cytochrome c from the mitochondria. Simultaneous treatment of the cells with wortmannin, cycloheximide, furosemide, cyclosporin A, or decylubiquinone prevented the release of cytochrome c and significantly reduced the loss of viability. Etoposide caused the phosphorylation of p53 within 6 h, an effect prevented by wortmannin, an inhibitor of DNA-dependent protein kinase (DNA-PK). The activation of p53 by etoposide resulted in the up-regulation of the pro-apoptotic protein Bax, a result that was prevented by the protein synthesis inhibitor cycloheximide. The increase in the content of Bax was followed by the translocation of this protein from the cytosol to the mitochondria, an event that was inhibited by furosemide, a chloride channel inhibitor. Stably transfected L929 fibroblasts that overexpress Akt were resistant to etoposide and did not translocate Bax to the mitochondria or release cytochrome c. Bax levels in these transfected cells were comparable with the wild-type cells. The release of cytochrome c upon translocation of Bax has been attributed to induction of the mitochondrial permeability transition (MPT). Cyclosporin A and decylubiquinone, inhibitors of MPT, prevented the release of cytochrome c without affecting Bax translocation. These data define a sequence of biochemical events that mediates the apoptosis induced by etoposide. This cascade proceeds by coupling DNA damage to p53 phosphorylation through the action of DNA-PK. The activation of p53 increases Bax synthesis. The translocation of Bax to the mitochondria induces the MPT, the event that releases cytochrome c and culminates in the death of the cells

Regulation of Intracellular pH Mediates Bax Activation in HeLa Cells Treated with Staurosporine or Tumor Necrosis Factor-α

Induction of apoptosis in HeLa cells with staurosporine produced a rise in the intracellular pH (pH(i)). Intracellular alkalinization was accompanied by translocation of Bax to the mitochondria, cytochrome c release, and cell death. The chloride channel inhibitor furosemide prevented intracellular alkalinization, Bax translocation, cytochrome c release, and cell death. Translocation of full-length Bid to the mitochondria was also prevented by furosemide. The cleavage product of Bid degradation (truncated Bid, tBid) was not detectable in the mitochondria. Its accumulation in the cytosol was prevented by furosemide. Apoptosis induced by tumor necrosis factor-alpha (TNF) lowered pH(i), an effect also accompanied by Bax translocation, cytochrome c release, and cell killing. Furosemide prevented all of these events. TNF induced a depletion of full-length Bid from the mitochondria and the cytosol but induced an accumulation of mitochondrial tBid. Furosemide only delayed full-length Bid depletion and tBid accumulation. The caspase 8 inhibitor IETD did not prevent the translocation of Bax. Although IETD did inhibit the cleavage of Bid and the accumulation of tBid, cell killing was reduced only slightly. It is concluded that with either staurosporine or TNF a furosemide-sensitive change in pH(i) is linked to Bax translocation, cytochrome c release, and cell killing. With TNF Bax translocation occurs as Bid is depleted and can be dissociated from the accumulation of tBid. With staurosporine a role for full-length Bid in Bax translocation cannot be excluded but is not necessary as evidenced by the data with TNF

Renewable Energy Opportunities at Fort Sill, Oklahoma

This document provides an overview of renewable resource potential at Fort Sill, based primarily upon analysis of secondary data sources supplemented with limited on-site evaluations. This effort focuses on grid-connected generation of electricity from renewable energy sources and on ground source heat pumps for heating and cooling buildings. The effort was funded by the U.S. Army Installation Management Command (IMCOM) as follow-on to the 2005 Department of Defense (DoD) Renewables Assessment. The site visit to Fort Sill took place on June 10, 2010