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Hines, IL, United States

Gerding D.N.,Hines Veterans Administration Hospital | Johnson S.,Loyola University Chicago
Clinical Infectious Diseases | Year: 2010

Treatment of Clostridium difficile infection (CDI) has relied on 2 antimicrobial agents, metronidazole and vancomycin, since the recognition of this disease entity. While effective, these "inside the box" approaches to CDI management have the disadvantage of further microbial disruption of the host indigenous microflora. "Outside the box" therapies use non-antimicrobial approaches to management and are theoretically less prone to causing recurrent CDI episodes. Recent advances in understanding of "inside the box" approaches include appreciation of the decreased efficacy of metronidazole overall and the superior efficacy of vancomycin for treatment of severe CDI, as well as a new agent under development, fidaxomicin, which appears to be equal in efficacy to vancomycin but with less risk of subsequent CDI recurrences. Several "outside the box" approaches have also entered clinical development, including use of monoclonal antibodies, active vaccination, luminal toxin binders, and nontoxigenic C. difficile. These reports provide optimism that more-effective management of CDI is forthcoming. © 2010 by the Infectious Diseases Society of America. All rights reserved.

Venkatachalam M.A.,University of Texas Health Science Center at San Antonio | Weinberg J.M.,University of Michigan | Kriz W.,University of Heidelberg | Bidani A.K.,Hines Veterans Administration Hospital
Journal of the American Society of Nephrology | Year: 2015

The transition of AKI to CKDhasmajor clinical significance. As reviewed here, recent studies show that a subpopulation of dedifferentiated, proliferating tubules recovering from AKI undergo pathologic growth arrest, fail to redifferentiate, and become atrophic. These abnormal tubules exhibit persistent, unregulated, and progressively increasing profibrotic signaling along multiple pathways. Paracrine products derived therefrom perturb normal interactions between peritubular capillary endothelium and pericyte-like fibroblasts, leading to myofibroblast transformation, proliferation, and fibrosis as well as capillary disintegration and rarefaction. Although signals from injured endothelium and inflammatory/immune cells also contribute, tubule injury alone is sufficient to produce the interstitial pathology required for fibrosis. Localized hypoxia produced by microvascular pathology may also prevent tubule recovery. However, fibrosis is not intrinsically progressive, and microvascular pathology develops strictly around damaged tubules; thus, additional deterioration of kidney structure after the transition of AKI to CKD requires new acute injury or other mechanisms of progression. Indeed, experiments using an acute-on-chronic injury model suggest that additional loss of parenchyma caused by failed repair of AKI in kidneys with prior renal mass reduction triggers hemodynamically mediated processes that damage glomeruli to cause progression. Continued investigation of these pathologic mechanisms should reveal options for preventing renal disease progression after AKI. © 2015 by the American Society of Nephrology.

Fortenbaugh F.C.,Hines Veterans Administration Hospital
Journal of vision | Year: 2012

Previous studies of localization of stationary targets in the peripheral visual field have found either underestimations (foveal biases) or overestimations (peripheral biases) of target eccentricity. In the present study, we help resolve this inconsistency by demonstrating the influence of visual boundaries on the type of localization bias. Using a Goldmann perimeter (an illuminated half-dome), we presented targets at different eccentricities across the visual field and asked participants to judge the target locations. In Experiments 1 and 2, participants reported target locations relative to their perceived visual field extent using either a manual or verbal response, with both response types producing a peripheral bias. This peripheral localization bias was a non-linear scaling of perceived location when the visual field was not bounded by external borders induced by facial features (i.e., the nose and brow), but location scaling was linear when visual boundaries were present. Experiment 3 added an external border (an aperture edge placed in the Goldmann perimeter) that resulted in a foveal bias and linear scaling. Our results show that boundaries that define a spatial region within the visual field determine both the direction of bias in localization errors for stationary objects and the scaling function of perceived location across visual space.

Jubran A.,Hines Veterans Administration Hospital | Jubran A.,Loyola University Chicago
Critical Care | Year: 2015

Pulse oximetry is universally used for monitoring patients in the critical care setting. This article updates the review on pulse oximetry that was published in 1999 in Critical Care. A summary of the recently developed multiwavelength pulse oximeters and their ability in detecting dyshemoglobins is provided. The impact of the latest signal processing techniques and reflectance technology on improving the performance of pulse oximeters during motion artifact and low perfusion conditions is critically examined. Finally, data regarding the effect of pulse oximetry on patient outcome are discussed. © 2015 Jubran.

Recruitment and trafficking of autoreactive leucocytes across the BNB (blood-nerve barrier) is an early pathological insult in GBS (Guillain-Barré syndrome), an aggressive autoimmune disorder of the PNS (peripheral nervous system). Whereas the aetiology and pathogenesis of GBS remain unclear, pro-inflammatory cytokines, including TNFα (tumour necrosis factor α), are reported to be elevated early in the course of GBS and may initiate nerve injury by activating the BNB. Previously, we reported that disrupting leucocyte trafficking in vivo therapeutically attenuates the course of an established animal model of GBS. Here, PNMECs (peripheral nerve microvascular endothelial cells) that form the BNB were harvested from rat sciatic nerves, immortalized by SV40 (simian virus 40) large T antigen transduction and subsequently challenged with TNFα. Relative changes in CCL2 (chemokine ligand 2) and ICAM-1 (intercellular adhesion molecule 1) expression were determined. We report that TNFα elicits marked dose- and time-dependent increases in CCL2 and ICAM-1 mRNA and protein content and promotes secretion of functional CCL2 from immortalized and primary PNMEC cultures. TNFα-mediated secretion of CCL2 promotes, in vitro, the transendothelial migration of CCR2-expressing THP-1 monocytes. Increased CCL2 and ICAM-1 expression in response to TNFα may facilitate recruitment and trafficking of autoreactive leucocytes across the BNB in autoimmune disorders, including GBS.

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