Showing papers by "University of Pittsburgh published in 2007"
TL;DR: The Acute Kidney Injury Network (AKI Network) as discussed by the authors is a multidisciplinary collaborative network focused on AKI, which was established to improve care for patients with or at risk for AKI.
Abstract: Acute kidney injury (AKI) is a complex disorder for which currently there is no accepted definition. Having a uniform standard for diagnosing and classifying AKI would enhance our ability to manage these patients. Future clinical and translational research in AKI will require collaborative networks of investigators drawn from various disciplines, dissemination of information via multidisciplinary joint conferences and publications, and improved translation of knowledge from pre-clinical research. We describe an initiative to develop uniform standards for defining and classifying AKI and to establish a forum for multidisciplinary interaction to improve care for patients with or at risk for AKI. Members representing key societies in critical care and nephrology along with additional experts in adult and pediatric AKI participated in a two day conference in Amsterdam, The Netherlands, in September 2005 and were assigned to one of three workgroups. Each group's discussions formed the basis for draft recommendations that were later refined and improved during discussion with the larger group. Dissenting opinions were also noted. The final draft recommendations were circulated to all participants and subsequently agreed upon as the consensus recommendations for this report. Participating societies endorsed the recommendations and agreed to help disseminate the results. The term AKI is proposed to represent the entire spectrum of acute renal failure. Diagnostic criteria for AKI are proposed based on acute alterations in serum creatinine or urine output. A staging system for AKI which reflects quantitative changes in serum creatinine and urine output has been developed. We describe the formation of a multidisciplinary collaborative network focused on AKI. We have proposed uniform standards for diagnosing and classifying AKI which will need to be validated in future studies. The Acute Kidney Injury Network offers a mechanism for proceeding with efforts to improve patient outcomes.
5,669 citations
01 Mar 2007
TL;DR: An initiative to develop uniform standards for defining and classifying AKI and to establish a forum for multidisciplinary interaction to improve care for patients with or at risk for AKI is described.
Abstract: Acute kidney injury (AKI) is a complex disorder for which currently there is no accepted definition. Having a uniform standard for diagnosing and classifying AKI would enhance our ability to manage these patients. Future clinical and translational research in AKI will require collaborative networks of investigators drawn from various disciplines, dissemination of information via multidisciplinary joint conferences and publications, and improved translation of knowledge from pre-clinical research. We describe an initiative to develop uniform standards for defining and classifying AKI and to establish a forum for multidisciplinary interaction to improve care for patients with or at risk for AKI. Members representing key societies in critical care and nephrology along with additional experts in adult and pediatric AKI participated in a two day conference in Amsterdam, The Netherlands, in September 2005 and were assigned to one of three workgroups. Each group's discussions formed the basis for draft recommendations that were later refined and improved during discussion with the larger group. Dissenting opinions were also noted. The final draft recommendations were circulated to all participants and subsequently agreed upon as the consensus recommendations for this report. Participating societies endorsed the recommendations and agreed to help disseminate the results. The term AKI is proposed to represent the entire spectrum of acute renal failure. Diagnostic criteria for AKI are proposed based on acute alterations in serum creatinine or urine output. A staging system for AKI which reflects quantitative changes in serum creatinine and urine output has been developed. We describe the formation of a multidisciplinary collaborative network focused on AKI. We have proposed uniform standards for diagnosing and classifying AKI which will need to be validated in future studies. The Acute Kidney Injury Network offers a mechanism for proceeding with efforts to improve patient outcomes.
5,467 citations
Pierre-and-Marie-Curie University1, University of British Columbia2, University of Pittsburgh3, French Institute of Health and Medical Research4, University of California, Los Angeles5, University of California, San Diego6, McGill University7, University of Kentucky8, Tohoku University9, Brown University10, NewYork–Presbyterian Hospital11, VU University Medical Center12
TL;DR: The NINCDS-ADRDA and DSM-IV-TR criteria for Alzheimer's disease (AD) are the prevailing diagnostic standards in research; however, they have now fallen behind the unprecedented growth of scientific knowledge as discussed by the authors.
Abstract: The NINCDS-ADRDA and the DSM-IV-TR criteria for Alzheimer's disease (AD) are the prevailing diagnostic standards in research; however, they have now fallen behind the unprecedented growth of scientific knowledge. Distinctive and reliable biomarkers of AD are now available through structural MRI, molecular neuroimaging with PET, and cerebrospinal fluid analyses. This progress provides the impetus for our proposal of revised diagnostic criteria for AD. Our framework was developed to capture both the earliest stages, before full-blown dementia, as well as the full spectrum of the illness. These new criteria are centred on a clinical core of early and significant episodic memory impairment. They stipulate that there must also be at least one or more abnormal biomarkers among structural neuroimaging with MRI, molecular neuroimaging with PET, and cerebrospinal fluid analysis of amyloid beta or tau proteins. The timeliness of these criteria is highlighted by the many drugs in development that are directed at changing pathogenesis, particularly at the production and clearance of amyloid beta as well as at the hyperphosphorylation state of tau. Validation studies in existing and prospective cohorts are needed to advance these criteria and optimise their sensitivity, specificity, and accuracy.
3,951 citations
Leiden University Medical Center1, University Hospital of Lausanne2, University of Oxford3, Cochrane Collaboration4, University of Texas Health Science Center at San Antonio5, University of London6, University of North Carolina at Chapel Hill7, University of Pittsburgh8, University of Bern9, University of Cape Town10
TL;DR: The STROBE Statement provides guidance to authors about how to improve the reporting of observational studies and facilitates critical appraisal and interpretation of studies by reviewers, journal editors and readers.
3,567 citations
TL;DR: This research presents a meta-analysis of 125 cases of central giant cell apoptosis, a type of cell death that is known as a “cell death” and which has been associated with Parkinson’s disease for more than 40 years.
Abstract: Timothy H. Dellit, Robert C. Owens, John E. McGowan, Jr., Dale N. Gerding, Robert A. Weinstein, John P. Burke, W. Charles Huskins, David L. Paterson, Neil O. Fishman, Christopher F. Carpenter, P. J. Brennan, Marianne Billeter, and Thomas M. Hooton Harborview Medical Center and the University of Washington, Seattle; Maine Medical Center, Portland; Emory University, Atlanta, Georgia; Hines Veterans Affairs Hospital and Loyola University Stritch School of Medicine, Hines, and Stroger (Cook County) Hospital and Rush University Medical Center, Chicago, Illinois; University of Utah, Salt Lake City; Mayo Clinic College of Medicine, Rochester, Minnesota; University of Pittsburgh Medical Center, Pittsburgh, and University of Pennsylvania, Philadelphia, Pennsylvania; William Beaumont Hospital, Royal Oak, Michigan; Ochsner Health System, New Orleans, Louisiana; and University of Miami, Miami, Florida
2,831 citations
TL;DR: A checklist of items that should be addressed in Reports of Observational Studies in Epidemiology (STROBE) Statement, a general reporting recommendations for descriptive observational studies and studies that investigate associations between exposures and health outcomes is developed.
Abstract: Much medical research is observational. The reporting of observational studies is often of insufficient quality. Poor reporting hampers the assessment of the strengths and weaknesses of a study and the generalizability of its results. Taking into account empirical evidence and theoretical considerations, a group of methodologists, researchers, and editors developed the Strengthening the Reporting of Observational Studies in Epidemiology (STROBE) recommendations to improve the quality of reporting of observational studies. The STROBE Statement consists of a checklist of 22 items, which relate to the title, abstract, introduction, methods, results, and discussion sections of articles. Eighteen items are common to cohort studies, case-control studies, and cross-sectional studies, and 4 are specific to each of the 3 study designs. The STROBE Statement provides guidance to authors about how to improve the reporting of observational studies and facilitates critical appraisal and interpretation of studies by reviewers, journal editors, and readers. This explanatory and elaboration document is intended to enhance the use, understanding, and dissemination of the STROBE Statement. The meaning and rationale for each checklist item are presented. For each item, 1 or several published examples and, where possible, references to relevant empirical studies and methodological literature are provided. Examples of useful flow diagrams are also included. The STROBE Statement, this document, and the associated Web site (www.strobe-statement.org) should be helpful resources to improve reporting of observational research.
2,813 citations
TL;DR: Treatment with zoledronic acid reduced the risk of morphometric vertebral fracture by 70% during a 3-year period, as compared with placebo.
Abstract: Background A single infusion of intravenous zoledronic acid decreases bone turnover and improves bone density at 12 months in postmenopausal women with osteoporosis. We assessed the effects of annual infusions of zoledronic acid on fracture risk during a 3-year period. Methods In this double-blind, placebo-controlled trial, 3889 patients (mean age, 73 years) were randomly assigned to receive a single 15-minute infusion of zoledronic acid (5 mg) and 3876 were assigned to receive placebo at baseline, at 12 months, and at 24 months; the patients were followed until 36 months. Primary end points were new vertebral fracture (in patients not taking concomitant osteoporosis medications) and hip fracture (in all patients). Secondary end points included bone mineral density, bone turnover markers, and safety outcomes. Results Treatment with zoledronic acid reduced the risk of morphometric vertebral fracture by 70% during a 3-year period, as compared with placebo (3.3% in the zoledronic-acid group vs. 10.9% in the ...
2,451 citations
University of Düsseldorf1, University of Pittsburgh2, University of New South Wales3, Icahn School of Medicine at Mount Sinai4, University of California, San Diego5, Washington University in St. Louis6, Children's Memorial Hospital7, University of Miami8, University of Gothenburg9, National Institutes of Health10, Columbia University11, University of Washington12, Johns Hopkins University13, University of California, San Francisco14, University of North Carolina at Chapel Hill15, University of Hawaii at Manoa16, University of Puerto Rico17
TL;DR: This report reviews the collective experience with HIV-associated neurocognitive disorders (HAND), particularly since the advent of highly active antiretroviral treatment, and their definitional criteria; discusses the impact of comorbidities; and suggests inclusion of the term asymptomatic neuroc cognitive impairment to categorize individuals with subclinical impairment.
Abstract: In 1991, the AIDS Task Force of the American Academy of Neurology published nomenclature and research case definitions to guide the diagnosis of neurologic manifestations of HIV-1 infection. Now, 16 years later, the National Institute of Mental Health and the National Institute of Neurological Diseases and Stroke have charged a working group to critically review the adequacy and utility of these definitional criteria and to identify aspects that require updating. This report represents a majority view, and unanimity was not reached on all points. It reviews our collective experience with HIV-associated neurocognitive disorders (HAND), particularly since the advent of highly active antiretroviral treatment, and their definitional criteria; discusses the impact of comorbidities; and suggests inclusion of the term asymptomatic neurocognitive impairment to categorize individuals with subclinical impairment. An algorithm is proposed to assist in standardized diagnostic classification of HAND.
2,292 citations
TL;DR: Current literature examining associations between components of the family context and children and adolescents' emotion regulation (ER) and a tripartite model of familial influence posited that children learn about ER through observational learning, modeling and social referencing.
Abstract: This article reviews current literature examining associations between components of the family context and children and adolescents' emotion regulation (ER). The review is organized around a tripartite model of familial influence. Firstly, it is posited that children learn about ER through observational learning, modeling and social referencing. Secondly, parenting practices specifically related to emotion and emotion management affect ER. Thirdly, ER is affected by the emotional climate of the family via parenting style, the attachment relationship, family expressiveness and the marital relationship. The review ends with discussions regarding the ways in which child characteristics such as negative emotionality and gender affect ER, how socialization practices change as children develop into adolescents, and how parent characteristics such as mental health affect the socialization of ER.
2,091 citations
TL;DR: The STROBE Statement provides guidance to authors about how to improve the reporting of observational studies and facilitates critical appraisal and interpretation of studies by reviewers, journal editors and readers.
Abstract: Much medical research is observational. The reporting of observational studies is often of insufficient quality. Poor reporting hampers the assessment of the strengths and weaknesses of a study and the generalizability of its results. Taking into account empirical evidence and theoretical considerations, a group of methodologists, researchers, and editors developed the Strengthening the Reporting of Observational Studies in Epidemiology (STROBE) recommendations to improve the quality of reporting of observational studies. The STROBE Statement consists of a checklist of 22 items, which relate to the title, abstract, introduction, methods, results and discussion sections of articles. Eighteen items are common to cohort studies, case-control studies and cross-sectional studies and four are specific to each of the three study designs. The STROBE Statement provides guidance to authors about how to improve the reporting of observational studies and facilitates critical appraisal and interpretation of studies by reviewers, journal editors and readers.This explanatory and elaboration document is intended to enhance the use, understanding, and dissemination of the STROBE Statement. The meaning and rationale for each checklist item are presented. For each item, one or several published examples and, where possible, references to relevant empirical studies and methodological literature are provided. Examples of useful flow diagrams are also included. The STROBE Statement, this document, and the associated web site (http://www.strobe-statement.org) should be helpful resources to improve reporting of observational research.
2,020 citations
TL;DR: Men and women of the same ability differ in their selection into a competitive environment as discussed by the authors, and this gender gap in tournament entry is not explained by performance, and factors such as risk and feedback aversion only play a negligible role.
Abstract: We examine whether men and women of the same ability differ in their selection into a competitive environment. Participants in a laboratory experiment solve a real task, first under a noncompetitive piece rate and then a competitive tournament incentive scheme. Although there are no gender differences in performance, men select the tournament twice as much as women when choosing their compensation scheme for the next performance. While 73 percent of the men select the tournament, only 35 percent of the women make this choice. This gender gap in tournament entry is not explained by performance, and factors such as risk and feedback aversion only playa negligible role. Instead, the tournament-entry gap is driven by men being more overconfident and by gender differences in preferences for performing in a competition. The result is that women shy away from competition and men embrace it.
National Institutes of Health1, Imperial College London2, Aarhus University3, University of Oxford4, University of Wisconsin-Madison5, University of Toronto6, University of California, Los Angeles7, Columbia University8, National Institute of Radiological Sciences9, University of Michigan10, University of Copenhagen11, University of Turku12, VU University Amsterdam13, Brookhaven National Laboratory14, Pfizer15, Washington University in St. Louis16, Indiana University – Purdue University Indianapolis17, University of Pittsburgh18, University of British Columbia19, Emory University20, Johns Hopkins University21, Yale University22
TL;DR: An international group of experts in pharmacokinetic modeling recommends a consensus nomenclature to describe in vivo molecular imaging of reversibly binding radioligands.
Abstract: An international group of experts in pharmacokinetic modeling recommends a consensus nomenclature to describe in vivo molecular imaging of reversibly binding radioligands.
TL;DR: It is demonstrated that ATG16L1 is expressed in intestinal epithelial cell lines and that functional knockdown of this gene abrogates autophagy of Salmonella typhimurium, and these findings suggest thatAutophagy and host cell responses to intracellular microbes are involved in the pathogenesis of Crohn disease.
Abstract: We present a genome-wide association study of ileal Crohn disease and two independent replication studies that identify several new regions of association to Crohn disease. Specifically, in addition to the previously established CARD15 and IL23R associations, we identified strong and significantly replicated associations (combined P < 10(-10)) with an intergenic region on 10q21.1 and a coding variant in ATG16L1, the latter of which was also recently reported by another group. We also report strong associations with independent replication to variation in the genomic regions encoding PHOX2B, NCF4 and a predicted gene on 16q24.1 (FAM92B). Finally, we demonstrate that ATG16L1 is expressed in intestinal epithelial cell lines and that functional knockdown of this gene abrogates autophagy of Salmonella typhimurium. Together, these findings suggest that autophagy and host cell responses to intracellular microbes are involved in the pathogenesis of Crohn disease.
TL;DR: The studies provide evidence that word-level knowledge has consequences for word meaning processes in comprehension, and large-scale correlational results show the general interdependence of comprehension and lexical skill while identifying disassociations that allow focus on comprehension-specific skill.
Abstract: The lexical quality hypothesis (LQH) claims that variation in the quality of word representations has consequences for reading skill, including comprehension. High lexical quality includes well-specified and partly redundant representations of form (orthography and phonology) and flexible representations of meaning, allowing for rapid and reliable meaning retrieval. Low-quality representations lead to specific word-related problems in comprehension. Six lines of research on adult readers demonstrate some of the implications of the LQH. First, large-scale correlational results show the general interdependence of comprehension and lexical skill while identifying disassociations that allow focus on comprehension-specific skill. Second, word-level semantic processing studies show comprehension skill differences in the time course of form-meaning confusions. Studies of rare vocabulary learning using event-related potentials (ERPs) show that, third, skilled comprehenders learn new words more effectively and sho...
TL;DR: Patients with squamous-cell carcinoma of the head and neck who received docetaxel plus cisplatin and fluorouracil induction chemotherapy plus chemoradiotherapy had a significantly longer survival than did patients who received cisPlatin and fluoride induction chemotherapyplus cheMoradiotherapy.
Abstract: Background A randomized phase 3 trial of the treatment of squamous-cell carcinoma of the head and neck compared induction chemotherapy with docetaxel plus cisplatin and fluorouracil (TPF) with cisplatin and fluorouracil (PF), followed by chemoradiotherapy. Methods We randomly assigned 501 patients (all of whom had stage III or IV disease with no distant metastases and tumors considered to be unresectable or were candidates for organ preservation) to receive either TPF or PF induction chemotherapy, followed by chemoradiotherapy with weekly carboplatin therapy and radiotherapy for 5 days per week. The primary end point was overall survival. Results With a minimum of 2 years of follow-up (≥3 years for 69% of patients), significantly more patients survived in the TPF group than in the PF group (hazard ratio for death, 0.70; P=0.006). Estimates of overall survival at 3 years were 62% in the TPF group and 48% in the PF group; the median overall survival was 71 months and 30 months, respectively (P=0.006). There...
Wake Forest University1, Mount Sinai St. Luke's and Mount Sinai Roosevelt2, Harvard University3, Johns Hopkins University4, Pennington Biomedical Research Center5, Miriam Hospital6, American Indian Center7, Baylor College of Medicine8, University of Southern California9, University of Texas Health Science Center at San Antonio10, University of Colorado Denver11, University of Tennessee Health Science Center12, University of Pittsburgh13, University of Alabama at Birmingham14, University of Pennsylvania15
TL;DR: At 1 year, ILI resulted in clinically significant weight loss in people with type 2 diabetes and was associated with improved diabetes control and CVD risk factors and reduced medicine use in ILI versus DSE.
Abstract: Objective: The effectiveness of intentional weight loss in reducing cardiovascular disease (CVD) events in type 2 diabetes is unknown. This report describes one-year changes in CVD risk factors in a trial designed to examine the long-term effects of an intensive lifestyle intervention on the incidence of major CVD events. Research Design and Methods: A multi-centered randomized controlled trial of 5,145 individuals with type 2 diabetes, aged 45-74 years, with body mass index >25 kg/m2 (>27 kg/m2 if taking insulin). An Intensive Lifestyle Intervention (ILI) involving group and individual meetings to achieve and maintain weight loss through decreased caloric intake and increased physical activity was compared to a Diabetes Support and Education (DSE) condition. Results: Participants assigned to ILI lost an average 8.6% of their initial weight versus 0.7% in DSE group (p Conclusions: At 1 year, ILI resulted in clinically significant weight loss in persons with type 2 diabetes. This was associated with improved diabetes control and CVD risk factors and reduced medicine use in ILI versus DSE. Continued intervention and follow-up will determine whether these changes are maintained and will reduce CVD risk. Trial Registration: clinicaltrials.gov Identifier: NCT00017953
McMaster University1, University of Toronto2, Dalhousie University3, Pennsylvania State University4, Nationwide Children's Hospital5, University of Iowa6, University of Miami7, University of South Carolina8, University of Paris9, Pasteur Institute10, University of Gothenburg11, Icahn School of Medicine at Mount Sinai12, Stanford University13, Vanderbilt University14, Johns Hopkins University15, University of North Carolina at Chapel Hill16, University of California, Los Angeles17, University of Pennsylvania18, Washington University in St. Louis19, University of Chicago20, Harvard University21, Emory University22, George Washington University23, Yale University24, University of Utah25, University of Washington26, University of Pittsburgh27, University of California, Irvine28, Veterans Health Administration29, University of Rochester30, University of Toulouse31, German Cancer Research Center32, Goethe University Frankfurt33, National and Kapodistrian University of Athens34, University of Bologna35, Utrecht University36, Guy's Hospital37, King's College London38, University of Cambridge39, University of Manchester40, Newcastle University41, University of Oxford42, University of Illinois at Chicago43, University of Michigan44, Centre Hospitalier Universitaire de Toulouse45, McGill University46, Autism Speaks47
TL;DR: Linkage and copy number variation analyses implicate chromosome 11p12–p13 and neurexins, respectively, among other candidate loci, highlighting glutamate-related genes as promising candidates for contributing to ASDs.
Abstract: Autism spectrum disorders (ASDs) are common, heritable neurodevelopmental conditions. The genetic architecture of ASDs is complex, requiring large samples to overcome heterogeneity. Here we broaden coverage and sample size relative to other studies of ASDs by using Affymetrix 10K SNP arrays and 1,181 [corrected] families with at least two affected individuals, performing the largest linkage scan to date while also analyzing copy number variation in these families. Linkage and copy number variation analyses implicate chromosome 11p12-p13 and neurexins, respectively, among other candidate loci. Neurexins team with previously implicated neuroligins for glutamatergic synaptogenesis, highlighting glutamate-related genes as promising candidates for contributing to ASDs.
TL;DR: Findings support the hypothesis that NMDA receptor hypofunction, which has been implicated in the pathophysiology of schizophrenia, diminishes the inhibitory control of PFC output neurons and may be critical for treatment of schizophrenia.
Abstract: NMDA receptors mediate excitatory postsynaptic potentials throughout the brain but, paradoxically, NMDA receptor antagonists produce cortical excitation in humans and behaving rodents. To elucidate a mechanism for these diverging effects, we examined the effect of use-dependent inhibition of NMDA receptors on the spontaneous activity of putative GABA interneurons and pyramidal neurons in the prefrontal cortex of awake rats. We find that inhibition of NMDA receptors predominately decreases the activity of putative GABA interneurons but, at a delayed rate, increases the firing rate of the majority of pyramidal neurons. Thus, NMDA receptors preferentially drive the activity of cortical inhibitory interneurons suggesting that NMDA receptor inhibition causes cortical excitation by disinhibition of pyramidal neurons. These findings support the hypothesis that NMDA receptor hypofunction, which has been implicated in the pathophysiology of schizophrenia, diminishes the inhibitory control of PFC output neurons. Reducing this effect may be critical for treatment of schizophrenia.
TL;DR: Cell death mechanisms have been studied across a broad spectrum of models of oxidative stress, including H2O2, nitric oxide and derivatives, endotoxin-induced inflammation, photodynamic therapy, ultraviolet-A and ionizing radiations, and cigarette smoke.
Abstract: Reactive oxygen or nitrogen species (ROS/RNS) generated endogenously or in response to environmental stress have long been implicated in tissue injury in the context of a variety of disease states. ROS/RNS can cause cell death by nonphysiological (necrotic) or regulated pathways (apoptotic). The mechanisms by which ROS/RNS cause or regulate apoptosis typically include receptor activation, caspase activation, Bcl-2 family proteins, and mitochondrial dysfunction. Various protein kinase activities, including mitogen-activated protein kinases, protein kinases-B/C, inhibitor-of-I-κB kinases, and their corresponding phosphatases modulate the apoptotic program depending on cellular context. Recently, lipid-derived mediators have emerged as potential intermediates in the apoptosis pathway triggered by oxidants. Cell death mechanisms have been studied across a broad spectrum of models of oxidative stress, including H2O2, nitric oxide and derivatives, endotoxin-induced inflammation, photodynamic therapy, ultraviole...
TL;DR: It is found that polypharmacy continues to increase and is a known risk factor for important morbidity and mortality, and health care professionals should be aware of the risks and fully evaluate all medications at each patient visit to prevent polypharacy from occurring.
Abstract: Background: Polypharmacy (ie, the use of multiple medications and/or the administration of more medications than are clinically indicated, representing unnecessary drug use) is common among the elderly. Objective: The goal of this research was to provide a description of observational studies examining the epidemiology of polypharmacy and to review randomized controlled studies that have been published in the past 2 decades designed to reduce polypharmacy in older adults. Methods: Materials for this review were gathered from a search of the MEDLINE database (1986-June 2007) and International Pharmaceutical Abstracts (1986-June 2007) to identify articles in people aged >65 years. We used a combination of the following search terms: polypharmacy, multiple medications, polymedicine, elderly, geriatric , and aged . A manual search of the reference lists from identified articles and the authors' article files, book chapters, and recent reviews was conducted to identify additional articles. From these, the authors identified those studies that measured polypharmacy. Results: The literature review found that polypharmacy continues to increase and is a known risk factor for important morbidity and mortality. There are few rigorously designed intervention studies that have been shown to reduce unnecessary polypharmacy in older adults. The literature review identified 5 articles, which are included here. All studies showed an improvement in polypharmacy. Conclusions: Many studies have found that various numbers of medications are associated with negative health outcomes, but more research is needed to further delineate the consequences associated with unnecessary drug use in elderly patients. Health care professionals should be aware of the risks and fully evaluate all medications at each patient visit to prevent polypharmacy from occurring.
University of Alberta1, Harvard University2, Johns Hopkins University3, University of Manitoba4, Mayo Clinic5, University of Pittsburgh6, University of Maryland, Baltimore7, University of California, San Diego8, Katholieke Universiteit Leuven9, Washington University in St. Louis10, National Institutes of Health11, Hannover Medical School12, University of Basel13, University of Sydney14, University of North Carolina at Chapel Hill15, John Radcliffe Hospital16, Saint Louis University17, Scripps Research Institute18, University of Barcelona19, Royal London Hospital20, University of Amsterdam21
TL;DR: The 8th Banff Conference on Allograft Pathology was held in Edmonton, Canada, 15–21 July 2005, and major outcomes included the elimination of the non‐specific term ‘chronic allograft nephropathy’ (CAN) and the recognition of the entity of chronic antibody‐mediated rejection.
Posted Content•
TL;DR: This paper examined the moderating influence of the extent to which a brand's social initiatives are integrated into its competitive positioning (i.e., a CSR positioning) on consumer reactions to CSR and found that positive CSR beliefs held by consumers are associated with greater purchase likelihood and longer-term loyalty and advocacy behaviors.
Abstract: This research examines the moderating influence of the extent to which a brand's social initiatives are integrated into its competitive positioning (i.e., a CSR positioning) on consumer reactions to CSR. We find that positive CSR beliefs held by consumers are associated not only with greater purchase likelihood but also with longer-term loyalty and advocacy behaviors. More importantly, we find that not all CSR initiatives are created equal: a brand that positions itself on CSR, integrating its CSR strategy with its core business strategy, is more likely than brands that merely engage in CSR to reap a range of CSR-specific benefits in the consumer domain.
TL;DR: It is shown that deficiency of dectin-1, the myeloid receptor for β-glucan, rendered mice susceptible to infection with Candida albicans, and a signaling non–Toll-like pattern-recognition receptor required for the induction of protective immune responses is established.
Abstract: Beta-Glucan is one of the most abundant polysaccharides in fungal pathogens, yet its importance in antifungal immunity is unclear. Here we show that deficiency of dectin-1, the myeloid receptor for -glucan, rendered mice susceptible to infection with Candida albicans. Dectin-1-deficient leukocytes demonstrated significantly impaired responses to fungi even in the presence of opsonins. Impaired leukocyte responses were manifested in vivo by reduced inflammatory cell recruitment after fungal infection, resulting in substantially increased fungal burdens and enhanced fungal dissemination. Our results establish a fundamental function for Beta-glucan recognition by dectin-1 in antifungal immunity and demonstrate a signaling non–Toll-like pattern-recognition receptor required for the induction of protective immune responses.
TL;DR: Polaritons are created in a harmonic potential trap analogous to atoms in optical traps and observe a number of signatures of Bose-Einstein condensation: spectral and spatial narrowing, a peak at zero momentum in the momentum distribution, first-order coherence, and spontaneous linear polarization of the light emission.
Abstract: We have created polaritons in a harmonic potential trap analogous to atoms in optical traps. The trap can be loaded by creating polaritons 50 micrometers from its center that are allowed to drift into the trap. When the density of polaritons exceeds a critical threshold, we observe a number of signatures of Bose-Einstein condensation: spectral and spatial narrowing, a peak at zero momentum in the momentum distribution, first-order coherence, and spontaneous linear polarization of the light emission. The polaritons, which are eigenstates of the light-matter system in a microcavity, remain in the strong coupling regime while going through this dynamical phase transition.
Medical University of South Carolina1, University of Massachusetts Medical School2, Johns Hopkins University3, University of Washington4, University of Texas Health Science Center at San Antonio5, Baylor College of Medicine6, University of Pittsburgh7, Columbia University8, University of Texas Southwestern Medical Center9, Pennsylvania State University10, Cystic Fibrosis Foundation11, Dartmouth College12
TL;DR: New guidelines are provided for the appropriate application of drug therapies used in the maintenance of pulmonary function to improve and extend the lives of all individuals with cystic fibrosis.
Abstract: The natural history of cystic fibrosis lung disease is one of chronic progression with intermittent episodes of acute worsening of symptoms frequently called acute pulmonary exacerbations These exacerbations typically warrant medical intervention. It is important that appropriate therapies are recommended on the basis of available evidence of efficacy and safety. The Cystic Fibrosis Foundation therefore established a committee to define the key questions related to pulmonary exacerbations, review the clinical evidence using an evidence-based methodology, and provide recommendations to clinicians. It is hoped that these guidelines will be helpful to clinicians in the treatment of individuals with cystic fibrosis.
TL;DR: The brain activation of a group of high-functioning autistic participants was measured using functional magnetic resonance imaging during the performance of a Tower of London task, in comparison with a control group matched with respect to intelligent quotient, age, and gender to suggest underconnectivity in the group with autism.
Abstract: The brain activation of a group of high-functioning autistic participants was measured using functional magnetic resonance imaging during the performance of a Tower of London task, in comparison with a control group matched with respect to intelligent quotient, age, and gender. The 2 groups generally activated the same cortical areas to similar degrees. However, there were 3 indications of underconnectivity in the group with autism. First, the degree of synchronization (i.e., the functional connectivity or the correlation of the time series of the activation) between the frontal and parietal areas of activation was lower for the autistic than the control participants. Second, relevant parts of the corpus callosum, through which many of the bilaterally activated cortical areas communicate, were smaller in cross-sectional area in the autistic participants. Third, within the autism group but not within the control group, the size of the genu of the corpus callosum was correlated with frontal--parietal functional connectivity. These findings suggest that the neural basis of altered cognition in autism entails a lower degree of integration of information across certain cortical areas resulting from reduced intracortical connectivity. The results add support to a new theory of cortical underconnectivity in autism, which posits a deficit in integration of information at the neural and cognitive levels.
TL;DR: A case where lean principles were adapted for the process sector for application at a large integrated steel mill is described, and a simulation model is developed to contrast the “before” and “after” scenarios in detail.
TL;DR: Pittsburgh Compound B PET findings match histopathologic reports of β-amyloid (Aβ) distribution in aging and dementia, and suggest that Aβ may influence the development of dementia with Lewy bodies, and therefore strategies to reduce A β may benefit this condition.
Abstract: I read the article by Rowe et al.1 with interest. Diagnosing Alzheimer disease (AD) in a preclinical phase would enable early implementation of therapeutic interventions which might have long-term benefits.
PET technology by using the Pittsburgh compound (PiB) allows detection of amyloid deposits in the brain.1,2 Pathologic studies indicate that amyloid deposition is present in cortical regions of all patients with AD even before the onset of dementia.3 One application of PiB-PET may be all that is necessary to identify the neuropathologic changes of AD in clinically normal individuals prior to the development of cognitive changes. These individuals would be considered to have preclinical AD.
PET studies performed with PiB in cognitively intact subjects have shown that between 15 and 22% of them had abnormal scans.1,2 The objective is to determine who and when someone will become demented. It is and will be unclear because the proportion of subjects with cerebral amyloid deposits is, and will be, higher than the proportion of people with clinical AD.
Otherwise, it is impossible to understand pathologic observations which indicate that more than 30% of older persons over age 75 die without any clinical evidence of dementia despite showing amyloid deposits and pathologic changes characteristic of AD.3 Presumably all of them would have abnormal PiB-PET scans. Amyloid deposition is not synonymous with clinical AD unless we assume that everyone with an abnormal PiB-PET scan would develop AD.
Even in this case, many of them (70% according to pathologic data and prevalence estimates of AD) will die without dementia in the …
TL;DR: This work provides a systems-oriented approach to interpreting the function of the dopamine system, its modulation of limbic-cortical interactions and how disruptions within this system might underlie the pathophysiology of schizophrenia and drug abuse.
TL;DR: MSCs protect lung tissue from BLM-induced injury by blocking TNF-α and IL-1, two fundamental proinflammatory cytokines in lung, which may provide a novel cellular vector for treating chronic inflammatory diseases in humans.
Abstract: Mesenchymal stem cells (MSCs) have been exploited as cellular vectors to treat a wide array of diseases but the mechanisms responsible for their therapeutic effect remain indeterminate. Previously, we reported that MSCs inhibit bleomycin (BLM)-induced inflammation and fibrosis within the lungs of mice. Interrogation of the MSC transcriptome identified interleukin 1 receptor antagonist (IL1RN) as a potential mediator of this effect. Fractionation studies indicated that MSCs are the principal source of IL1RN in murine bone marrow and that its expression is restricted to a unique subpopulation of cells. Moreover, MSC-conditioned media was shown to block proliferation of an IL-1α-dependent T cell line and inhibit production of TNF-α by activated macrophages in vitro. Studies conducted in mice revealed that MSC administration was more effective than recombinant IL1RN delivered via adenoviral infection or osmotic pumps in inhibiting BLM-induced increases in TNF-α, IL-1α, and IL1RN mRNA in lung, IL1RN protein in bronchoalveolar lavage (BAL) fluid, and trafficking of lymphocytes and neutrophils into the lung. Therefore, MSCs protect lung tissue from BLM-induced injury by blocking TNF-α and IL-1, two fundamental proinflammatory cytokines in lung. Identification of IL1RN-expressing human MSC subpopulations may provide a novel cellular vector for treating chronic inflammatory diseases in humans.