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Nowak M.A.,California Northstate University | Nelson R.E.,ViroPharma | Breidenbach J.L.,Sanford Medical Center | Thompson P.A.,University of South Dakota | Carson P.J.,Sanford Medical Center
American Journal of Health-System Pharmacy | Year: 2012

Purpose. A pre-post analysis of an antimicrobial stewardship program (ASP) involving the use of data-mining software to prospectively identify cases for ASP intervention was conducted. Methods. The investigators evaluated clinical outcomes and cost metrics before and after implementation of the ASP, which entailed daily physician review of summary reports on all adult inpatients receiving antimicrobial therapy. The primary outcome measures were annual antimicrobial expenditures and rates of infections due to common nosocomial pathogens; secondary outcome measures included patient survival and length of stay (LOS) in cases involving the indicator diagnoses of pneumonia and abdominal sepsis. Results. Antimicrobial expenditures, which had increased by an average of 14.4% annually in the years preceding ASP implementation, decreased by 9.75% in the first year of the program and remained relatively stable in subsequent years, with overall cumulative cost savings estimated at $1.7 million. Rates of nosocomial infections involving Clostridium difficile, methicillin-resistant Staphylococcus aureus, and vancomycin-resistant enterococci all decreased after ASP implementation. A pre-post comparison of survival and LOS in patients with pneumonia (n = 2186) or abdominal sepsis (n = 225) showed no significant differences in those outcomes in either patient group, possibly due to the hospital's initiation of other, concurrent infection-control programs during the study period. Conclusion. A prospective collaborative ASP employed automated reports to efficiently identify key data for ASP review. After ASP implementation, antimicrobial expenditures and rates of nosocomial infections caused by resistant pathogens dropped without significant changes in patient survival, LOS, and readmissions for the two studied illness categories. Copyright © 2012, American Society of Health-System Pharmacists, Inc. All rights reserved. Source

Arias H.R.,California Northstate University | Feuerbach D.,Novartis | Targowska-Duda K.M.,Medical University of Lublin | Aggarwal S.,Duquesne University | And 2 more authors.
Neurochemistry International | Year: 2012

The pharmacological properties of (±)-2-(N-tert-butylamino)- 3′-iodo-4′-azidopropiophenone [(±)-SADU-3-72], a photoreactive analog of bupropion (BP), were characterized at different muscle nicotinic acetylcholine receptors (AChRs) by functional and structural approaches. Ca2+ influx results indicate that (±)-SADU-3-72 is 17- and 6-fold more potent than BP in inhibiting human (h) embryonic (hα1β1γδ) and adult (hα1β1δ) muscle AChRs, respectively. (±)-SADU-3-72 binds with high affinity to the [ 3H]TCP site within the resting or desensitized Torpedo AChR ion channel, whereas BP has higher affinity for desensitized AChRs. Molecular docking results indicate that both SADU-3-72 enantiomers interact with the valine (position 13′) and serine (position 6′) rings. However, an additional domain, between the outer (position 20′) and valine rings, is observed in Torpedo AChR ion channels. Our results indicate that the azido group of (±)-SADU-3-72 may enhance its interaction with polar groups and the formation of hydrogen bonds at AChRs, thus supporting the observed higher potency and affinity of (±)-SADU-3-72 compared to BP. Collectively our results are consistent with a model where BP/SADU-3-72 and TCP bind to overlapping sites within the lumen of muscle AChR ion channels. Based on these results, we believe that (±)-SADU-3-72 is a promising photoprobe for mapping the BP binding site, especially within the resting AChR ion channel. © 2012 Elsevier Ltd. All rights reserved. Source

Mandal A.,Northeast Ohio Medical University | Bishayee A.,California Northstate University
International Journal of Molecular Sciences | Year: 2015

Trianthema portulacastrum, a medicinal and dietary plant, has gained substantial importance due to its various pharmacological properties, including anti-inflammatory and anticarcinogenic activities. We have recently reported that a characterized T. portulacastrum extract (TPE) affords a considerable chemoprevention of 7,12-dimethylbenz(a)anthracene (DMBA)-induced rat mammary tumorigenesis though the underlying mechanisms are not completely understood. The objective of this study was to investigate anti-inflammatory mechanisms of TPE during DMBA mammary carcinogenesis in rats by monitoring cyclooxygenase-2 (COX-2), heat shock protein 90 (HSP90), nuclear factor-kappaB (NF-κB) and nuclear factor erythroid 2-related factor 2 (Nrf2). Mammary tumors were harvested from our previous study in which TPE (50-200 mg/kg) was found to inhibit mammary tumorigenesis in a dose-response manner. The expressions of intratumor COX-2, HSP90, NF-κB, inhibitory kappaB-alpha (IκBα) and Nrf2 were determined by immunohistochemistry. TPE downregulated the expression of COX-2 and HSP90, blocked the degradation of IκBα, hampered the translocation of NF-κB from cytosol to nucleus and upregulated the expression and nuclear translocation of Nrf2 during DMBA mammary carcinogenesis. These results in conjunction with our previous findings suggest that TPE prevents DMBA-induced breast neoplasia by anti-inflammatory mechanisms mediated through simultaneous and differential modulation of two interconnected molecular circuits, namely NF-κB and Nrf2 signaling pathways. © 2015 by the authors; licensee MDPI, Basel, Switzerland. Source

Feng X.,California Northstate University | Tonnesen M.G.,State University of New York at Stony Brook | Tonnesen M.G.,Veterans Affairs Medical Center | Mousa S.A.,Albany College of Pharmacy and Health Sciences | Clark R.A.F.,State University of New York at Stony Brook
International Journal of Cell Biology | Year: 2013

Angiogenesis is a highly regulated event involving complex, dynamic interactions between microvascular endothelial cells and extracellular matrix (ECM) proteins. Alteration of ECM composition and architecture is a hallmark feature of wound clot and tumor stroma. We previously reported that during angiogenesis, endothelial cell responses to growth factors are modulated by the compositional and mechanical properties of a surrounding three-dimensional (3D) extracellular matrix (ECM) that is dominated by either cross-linked fibrin or type I collagen. However, the role of 3D ECM in the regulation of angiogenesis associated with wound healing and tumor growth is not well defined. This study investigates the correlation of sprout angiogenesis and ECM microenvironment using in vivo and in vitro 3D angiogenesis models. It demonstrates that fibrin and type I collagen 3D matrices differentially but synergistically regulate sprout angiogenesis. Thus blocking both integrin alpha v beta 3 and integrin alpha 2 beta 1 might be a novel strategy to synergistically block sprout angiogenesis in solid tumors. © 2013 Xiaodong Feng et al. Source

Khansari P.S.,California Northstate University | Sperlagh B.,Hungarian Academy of Sciences
Inflammopharmacology | Year: 2012

In recent years, compelling evidence suggests that inflammation plays a critical role in the pathology of a vast number of neurological diseases such as stroke, Parkinson's disease, Alzheimer's disease and amyotrophic lateral sclerosis as well as neuropsychiatric diseases such as major depression and schizophrenia. Despite emerging evidence in human and animal models alike, modulating inflammatory responses have yet to be proven as an effective treatment to prevent or delay the progression of these diseases. The primary focus of this special edition is to highlight some of our current findings on the complexities of targeting neuroinflammation as a novel therapy, and its role in neurological and psychiatric disorders. © 2011 CARS. Source

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