Entity

Time filter

Source Type

Iowa City, IA, United States

Goto M.,University of Iowa | Goto M.,Iowa City Veterans Affairs Medical Center | Al-Hasan M.N.,University of South Carolina | Al-Hasan M.N.,Rochester College
Clinical Microbiology and Infection | Year: 2013

In this systematic review, we estimated the total number of episodes of bloodstream infection (BSI) and deaths from BSI per year in North America and Europe, using data from population-based settings. Then, we estimated the number of episodes and deaths from nosocomial BSI from population-based studies and nosocomial infection surveillance systems. We estimated 575 000-677 000 episodes of BSI per year in North America (536 000-628 000 in the USA and 40 000-49 000 in Canada) and 79 000-94 000 deaths (72 000-85 000 in the USA and 7000-9000 in Canada), using estimates from three population-based studies. We estimated over 1 200 000 episodes of BSI and 157 000 deaths per year in Europe, using estimates from one population-based study in each of the following countries: Denmark (9100 episodes and 1900 deaths), Finland (8700 episodes and 1100 deaths) and England (96 000 episodes and 12 000-19 000 deaths). There were substantial differences in estimates of nosocomial BSI between population-based and nosocomial infection surveillance data. BSI has a major impact on the morbidity and mortality of the general population, as it ranks among the top seven causes of death in all included countries in North America and Europe. However, it is difficult to obtain precise estimates of nosocomial BSI, owing to the limited number of studies. This review highlights the need for a greater focus on BSI research in order to reduce the overall burden of disease by improving the outcome of patients with BSI. It also emphasizes the role of infection control and prevention methods in reducing the burden of nosocomial BSI. © 2013 The Authors. Clinical Microbiology and Infection © 2013 European Society of Clinical Microbiology and Infectious Diseases. Source


Vouri S.M.,Texas Tech University Health Sciences Center | Shaw R.F.,University of Iowa | Waterbury N.V.,Ambulatory Care | Egge J.A.,Ambulatory Care | Alexander B.,Iowa City Veterans Affairs Medical Center
Journal of Managed Care Pharmacy | Year: 2011

BACKGROUND: The "ABCs of Diabetes" are defined as hemoglobin A1c < 7.0%, blood pressure < 130/80 millimeters mercury (mm Hg), and lowdensity lipoprotein cholesterol (LDL-C) < 100 milligrams per deciliter (mg per dL). Assessments of 3-part goal attainment of A1c, blood pressure, and cholesterol have been reported using data from the National Health and Nutrition Examination Survey (NHANES) for several time periods (e.g., 1988-1994, 1999-2000, 1999-2002, and 2003-2004), Look Action for Health in Diabetes (Look AHEAD, 2001-2004), and community-based endocrinology practice (CBEP, 2000-2004). In 2002, an unpublished analysis of data from 2001-2002 at the Iowa City Veterans Affairs (ICVA) Medical Center found less than 50% of patients met each of the 3 individual goals. In the 5 years following the 2001-2002 assessment, the care for veterans with diabetes at the ICVA was enhanced to include (a) an increased number of diabetes classes and clinics, (b) implementation of the diabetes Care Coordination/Home Telehealth (CCHT) program, and (c) clinical reminders for diabetes performance measures that were added to the electronic medical record (EMR). OBJECTIVES: To (a) describe the prevalence of veterans meeting the ABC goals of diabetes in 1 VA medical center; (b) differentiate the proportion of diabetes patients who met the individual targets for A1c, blood pressure, and LDL-C and compare the results for 2008 through September 2009 with the earlier data from this facility (2001-2002); and (c) examine results reported previously in the literature for NHANES, Look AHEAD, and CBEP data sources. METHODS: Single-center, retrospective analysis of veterans at the ICVA for dates of service from January 1, 2008, through September 30, 2009, who (a) filled at least 1 prescription for an antidiabetic medication and (b) had each of the 3 biomarker values recorded in the EMR for A1c, blood pressure, and LDL-C after the antidiabetic prescription fill date. RESULTS: Of the 5,426 (97.6% male) patients meeting inclusion criteria in 2008-2009, 17.3% (n = 936) achieved the 3-part ABC goal. In this managed care setting, achievement of the 3-part ABC goal surpassed the proportions reported in previous studies in NHANES data (5.2% in 1988-1994, 7.3% in 1999-2000, 7.0% in 1999-2002, 13.2% in 2003-2004), and 10.1% in Look AHEAD 2001-2004, but fell short of the 22.0% reported in CBEP 2000-2004. When compared with the 2001-2002 results at ICVA, the proportion of patients achieving the individual A1c goal in 2008-2009 increased by 10.8 percentage points (from 43.2% to 54.0%), 12.6 percentage points for blood pressure (from 29.2% to 41.8%), and 17.1 percentage points for LDL-C (from 49.5% to 66.6%, P < 0.001) for the 3 individual comparisons. CONCLUSIONS: The proportion of patients achieving each of the 3 goals for A1c, blood pressure, and LDL-C improved significantly in 2008-2009 compared with the 2001-2002 assessment in this medical center, following RESEARCH implementation of yearly clinical reminders for diabetes care, enhanced patient education, and other program changes that included home-based telephone monitoring with diabetes case management for some patients. Achievement of the 3-part ABC goal in 2008-2009 (17.3%) surpassed 5 assessments reported in the literature but was lower than the CBEP (2000-2004) performance (22.0%). © 2011, Academy of Managed Care Pharmacy. All rights reserved. Source


Buchta C.M.,University of Iowa | Bishop G.A.,University of Iowa | Bishop G.A.,Iowa City Veterans Affairs Medical Center
Immunologic Research | Year: 2014

Numerous reports have described Toll-like receptor (TLR) functions in myeloid cells such as dendritic cells (DCs) and macrophages, but relatively fewer studies have examined TLR responses in B lymphocytes. B cells express a wide variety of TLRs and are highly activated after TLR ligation, leading to enhancements in B cell survival, surface molecule expression, cytokine and antibody production, and antigen presentation. During an immune response, B cells can receive signals through TLRs as well as the B cell antigen receptor (BCR) and/or CD40. TLR ligation synergizes with signals through these receptors and augments both innate and adaptive immune functions of B lymphocytes. Additionally, targeting B cell TLRs may provide new therapies against certain types of cancer as well as autoimmune diseases. Here, we summarize TLR expression and contributions to both normal and pathogenic functions in mouse and human B cells. © 2014 Springer Science+Business Media. Source


Swick B.L.,University of Iowa | Swick B.L.,Iowa City Veterans Affairs Medical Center | Srikantha R.,University of Iowa | Messingham K.N.,University of Iowa
Journal of Cutaneous Pathology | Year: 2013

Background The purpose of this study was to explore the immunohistochemical and mutational status of the tyrosine kinases KIT and platelet derived growth receptor-alpha (PDGFRA) in Merkel cell carcinoma (MCC). Specifically, we examined the mutated exons in gastrointestinal stromal cell tumors that may confer a treatment response to imatinib mesylate. Methods We evaluated KIT and PDGFRA immunostaining in 23 examples of MCC utilizing laser capture microdissection to obtain pure samples of tumor genomic DNA from 18 of 23 examples of MCC. PCR amplification and sequencing of KIT exons 9, 11, 13 and 17, and PDGFRA exons 10, 12, 14 and 18 for mutations was performed. Results Fifteen of 23 tumors (65%) demonstrated CD117 expression and 22 of 23 tumors (95%) demonstrated PDGFRA expression. A single heterozygous KIT exon 11 base change resulting in an E583K mutation was discovered in 12 of 18 (66%) examples of MCC. In addition, a single nucleotide polymorphism was detected in eight of 18 tumors (44%) in exon 18 of PDGFRA (codon 824; GTC > GTT). Conclusions We discovered a novel somatic KIT exon 11 E583K mutation in 66% of tumors. This mutation has been previously described in a human with piebaldism and appears to represent an inactivating mutation. Therefore, despite expression of CD117 and PDGFRA, the absence of activating mutations in these tyrosine kinases makes KIT and PDGFRA unlikely candidates of MCC oncogenesis. © 2013 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd. Source


Murthy S.,University of Iowa | Ryan A.J.,University of Iowa | Carter A.B.,University of Iowa | Carter A.B.,Iowa City Veterans Affairs Medical Center
Biochemical Journal | Year: 2012

Rac1, a small GTPase, regulates macrophage MMP (matrix metalloproteinase)-9 in an ERK (extracellular-signal-regulated kinase)- and SP (specificity protein)-1-dependent manner. SP-1 contains a PEST (Pro-Glu-Ser-Thr) domain that may modulate protein stability. We hypothesize that Thr578, Ser 586 and/or Ser587in the PEST domain are required for SP-1 stability and MMP-9 expression secondary to activation of ERK, a serine/threonine kinase. We determined the effects of Rac1 and ERK on MMP-9 expression driven by SP-1WT (wild-type) and the SP-1 mutants T578A, S586A and S587A. Expression of WT and mutant SP-1 increased MMP9 promoter activity in alveolar macrophages. However, constitutively active Rac1 suppressed MMP9 promoter activity in cells expressing SP-1WT, SP-1 T578A and SP-1S587A, but not SP-1S586A. Furthermore, constitutive ERK activation, which was inhibited by Rac1, significantly increased MMP9 transcription in cells expressing SP-1 WT, but not SP-1S586A. As Rac1 activation and ERK inactivation increased degradation of SP-1WT and not SP- 1S586A, the results of the present study suggest that SP-1 stability mediated at Ser586 regulates MMP9 transcription. Ex vivo, alveolar macrophages obtained from patients with asbestosis had less MMP-9 expression that was associated with decreased SP-1 expression and ERK activation. These observations demonstrate that Ser586 in the PEST domain of SP-1 is important for MMP9 gene expression in alveolar macrophages and highlight the importance of these proteins in pulmonary fibrosis. © The Authors Journal compilation © 2012 Biochemical Society. Source

Discover hidden collaborations