292 research outputs found

    Infarct vessel status after intravenous tissue plasminogen activator and acute coronary angioplasty: Prediction of clinical outcome

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    To determine the risk of arterial reocclusion or recurrent ischemia after acute intervention in myocardial infarction, we analyzed the results of coronary arteriography performed acutely and at 1 week in 50 consecutive patients who received acute intervention. Successful recanalization of the infarct vessel was achieved in 46 (92%) patients after therapy with intravenous tissue plasminogen activator, percutaneous coronary angioplasty, or both. Follow-up angiography in 44 showed early reocclusion in 10 patients (23%). Intermittent patency during acute arteriography was always associated with reocclusion; suboptimal (Thrombolysis in Myocardial Infarction [TIMI] class 2) flow was associated with a 50% rate of reocclusion. Although residual stenosis of >50% alone was not predictive of rethrombosis, 90% of all reocclusions were associated with either stenosis >50%, TIMI 2 flow, or intermittent patency. Absence of these angiographic risk factors predicted a 95% patency rate at follow-up. In-hospital cardiac complications occurred in 17 of 23 (74%) patients with residual stenosis of >50% (death in four, ischemia in 13), and late revascularization was required in 53% of survivors. Only 15% of the group with p =50% appears to predict a high incidence of negative in-hospital clinical outcomes and the need for subsequent revascularization.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/27437/1/0000475.pd

    A magnetic field diagnostic for sonoluminescence

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    This study is motivated by the extraordinary process of single bubble sonoluminescence (SBSL), where an acoustically driven spherical shock is thought to power the emitted radiation. We propose new experiments using an external magnetic field which can induce anisotropies in both the shock propagation and radiation pattern. The effects will depend on the temperature, conductivity, and size of the radiating region. Our predictions suggest that such a laboratory experiment could serve as an important diagnostic in placing bounds on these parameters and understanding the physics of sonoluminescence.Comment: Latex File, Two .eps files, 5 pages, submitted to PR

    Correction: Mucosal Healing and Fibrosis after Acute or Chronic Inflammation in Wild Type FVB-N Mice and C57BL6 Procollagen α1(I)-Promoter-GFP Reporter Mice

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    BackgroundInjury and intestinal inflammation trigger wound healing responses that can restore mucosal architecture but if chronic, can promote intestinal fibrosis. Intestinal fibrosis is a major complication of Crohn’s disease. The cellular and molecular basis of mucosal healing and intestinal fibrosis are not well defined and better understanding requires well characterized mouse models.MethodsFVB-N wild type mice and C57BL6 procollagen α1(I)-GFP reporter mice were given one (DSS1) or two (DSS2) cycles of 3% DSS (5 days/cycle) followed by 7 days recovery. Histological scoring of inflammation and fibrosis were performed at DSS1, DSS1+3, DSS1+7, DSS2, DSS2+3, and DSS2+7. Procollagen α1(I)-GFP activation was assessed in DSS and also TNBS models by whole colon GFP imaging and fluorescence microscopy. Colocalization of GFP with α-smooth muscle actin (α-SMA) or vimentin was examined. GFP mRNA levels were tested for correlation with endogenous collagen α1(I) mRNA.ResultsMales were more susceptible to DSS-induced disease and mortality than females. In FVB-N mice one DSS cycle induced transient mucosal inflammation and fibrosis that resolved by 7 days of recovery. Two DSS cycles induced transmural inflammation and fibrosis in a subset of FVB-N mice but overall, did not yield more consistent, severe or sustained fibrosis. In C57BL6 mice, procollagen α1(I)-GFP reporter was activated at the end of DSS1 and through DSS+7 with more dramatic and transmural activation at DSS2 through DSS2+7, and in TNBS treated mice. In DSS and TNBS models GFP reporter expression localized to vimentin+ cells and much fewer α-SMA+ cells. GFP mRNA strongly correlated with collagen α1(I) mRNA.ConclusionsOne DSS cycle in FVB-N mice provides a model to study mucosal injury and subsequent mucosal healing. The procollagen α1(I)-GFP transgenic provides a useful model to study activation of a gene encoding a major extracellular matrix protein during acute or chronic experimental intestinal inflammation and fibrosis

    Incidence and predictors of early recurrent ischemia after successful percutaneous transluminal coronary angioplasty for acute myocardial infarction

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    Two hundred forty consecutive patients with acute myocardial infarction treated within 48 hours by successful percutaneous transluminal coronary angioplasty (PTCA) were analyzed to determine the incidence and predictors of recurrent ischemic events during hospitalization. Thirty-nine patients had recurrent ischemia: 20 patients had chest pain or electrocardiographic changes requiring repeat PTCA or bypass surgery, or resulting in a second creatine kinase elevation suggestive of myocardial infarction; 12 had total occlusion of the dilated artery on follow-up angiography; and 7 had exercise-induced ischemia and >= 70% diameter stenosis that required PTCA or bypass surgery before hospital discharge. In-hospital mortality was 15% in the recurrent ischemia group, compared to 1% in the group without recurrent myocardial ischemia (p 25 mm Hg (p = 0.001), dissection (p = 0.01) and post-PTCA Thrombolysis in Myocardial Infarction 2 flow pattern (p = 0.016). However, even in the absence of these risk factors recurrent ischemic events occurred in 13% of patients. Post-PTCA percent diameter stenosis (whether assessed by objective or visual assessment), degree of the early systemic fibrinolytic state, post-PTCA residual minimal diameter and concomitant use of thrombolytic agents were not predictive. Thus, recurrent ischemia after successful PTCA for acute myocardial infarction occurs in 16 to 20% of patients, is significantly more common with post-PTCA translesional gradient >= 25 mm Hg, dissection or Thrombolysis in Myocardial Infarction 2 flow, but may also occur unpredictably.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/28072/1/0000515.pd

    Evaluating The National Land Cover Database Tree Canopy and Impervious Cover Estimates Across the Conterminous United States: A Comparison with Photo-Interpreted Estimates

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    The 2001 National Land Cover Database (NLCD) provides 30-m resolution estimates of percentage tree canopy and percentage impervious cover for the conterminous United States. Previous estimates that compared NLCD tree canopy and impervious cover estimates with photo-interpreted cover estimates within selected counties and places revealed that NLCD underestimates tree and impervious cover. Based on these previous results, a wall-to-wall comprehensive national analysis was conducted to determine if and how NLCD derived estimates of tree and impervious cover varies from photo-interpreted values across the conterminous United States. Results of this analysis reveal that NLCD significantly underestimates tree cover in 64 of the 65 zones used to create the NCLD cover maps, with a national average underestimation of 9.7% (standard error (SE) = 1.0%) and a maximum underestimation of 28.4% in mapping zone 3. Impervious cover was also underestimated in 44 zones with an average underestimation of 1.4% (SE = 0.4%) and a maximum underestimation of 5.7% in mapping zone 56. Understanding the degree of underestimation by mapping zone can lead to better estimates of tree and impervious cover and a better understanding of the potential limitations associated with NLCD cover estimates

    The Integrated Medical Model: A Risk Assessment and Decision Support Tool for Human Space Flight Missions

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    This slide presentation reviews the Integrated Medical Model (IMM) and its use as a risk assessment and decision support tool for human space flight missions. The IMM is an integrated, quantified, evidence-based decision support tool useful to NASA crew health and mission planners. It is intended to assist in optimizing crew health, safety and mission success within the constraints of the space flight environment for in-flight operations. It uses ISS data to assist in planning for the Exploration Program and it is not intended to assist in post flight research. The IMM was used to update Probability Risk Assessment (PRA) for the purpose of updating forecasts for the conditions requiring evacuation (EVAC) or Loss of Crew Life (LOC) for the ISS. The IMM validation approach includes comparison with actual events and involves both qualitative and quantitaive approaches. The results of these comparisons are reviewed. Another use of the IMM is to optimize the medical kits taking into consideration the specific mission and the crew profile. An example of the use of the IMM to optimize the medical kits is reviewed

    Validation of the Integrated Medical Model Using Historical Space Flight Data

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    The Integrated Medical Model (IMM) utilizes Monte Carlo methodologies to predict the occurrence of medical events, utilization of resources, and clinical outcomes during space flight. Real-world data may be used to demonstrate the accuracy of the model. For this analysis, IMM predictions were compared to data from historical shuttle missions, not yet included as model source input. Initial goodness of fit test-ing on International Space Station data suggests that the IMM may overestimate the number of occurrences for three of the 83 medical conditions in the model. The IMM did not underestimate the occurrence of any medical condition. Initial comparisons with shuttle data demonstrate the importance of understanding crew preference (i.e., preferred analgesic) for accurately predicting the utilization of re-sources. The initial analysis demonstrates the validity of the IMM for its intended use and highlights areas for improvement

    Long Term Stabilization of Expanding Aortic Aneurysms by a Short Course of Cyclosporine A through Transforming Growth Factor-Beta Induction

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    Abdominal aortic aneurysms (AAAs) expand as a consequence of extracellular matrix destruction, and vascular smooth muscle cell (VSMC) depletion. Transforming growth factor (TGF)-beta 1 overexpression stabilizes expanding AAAs in rat. Cyclosporine A (CsA) promotes tissue accumulation and induces TGF -beta1 and, could thereby exert beneficial effects on AAA remodelling and expansion. In this study, we assessed whether a short administration of CsA could durably stabilize AAAs through TGF-beta induction. We showed that CsA induced TGF-beta1 and decreased MMP-9 expression dose-dependently in fragments of human AAAs in vitro, and in animal models of AAA in vivo. CsA prevented AAA formation at 14 days in the rat elastase (diameter increase: CsA: 131.9±44.2%; vehicle: 225.9±57.0%, P = 0.003) and calcium chloride mouse models (diameters: CsA: 0.72±0.14 mm; vehicle: 1.10±0.11 mm, P = .008), preserved elastic fiber network and VSMC content, and decreased inflammation. A seven day administration of CsA stabilized formed AAAs in rats seven weeks after drug withdrawal (diameter increase: CsA: 14.2±15.1%; vehicle: 45.2±13.7%, P = .017), down-regulated wall inflammation, and increased αSMA-positive cell content. Co-administration of a blocking anti-TGF-beta antibody abrogated CsA impact on inflammation, αSMA-positive cell accumulation and diameter control in expanding AAAs. Our study demonstrates that pharmacological induction of TGF-beta1 by a short course of CsA administration represents a new approach to induce aneurysm stabilization by shifting the degradation/repair balance towards healing

    Developed in collaboration with and endorsed by the Heart Rhythm Society (HRS), the American College of Cardiology (ACC), the American Heart Association (AHA), and the Association for European Paediatric and Congenital Cardiology (AEPC). Endorsed by the Asia Pacific Heart Rhythm Society (APHRS), the Indian Heart Rhythm Society (IHRS), and the Latin American Heart Rhythm Society (LAHRS).

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    AbstractIn view of the increasing complexity of both cardiovascular implantable electronic devices (CIEDs) and patients in the current era, practice guidelines, by necessity, have become increasingly specific. This document is an expert consensus statement that has been developed to update and further delineate indications and management of CIEDs in pediatric patients, defined as ≀21 years of age, and is intended to focus primarily on the indications for CIEDs in the setting of specific disease categories. The document also highlights variations between previously published adult and pediatric CIED recommendations and provides rationale for underlying important differences. The document addresses some of the deterrents to CIED access in low- and middle-income countries and strategies to circumvent them. The document sections were divided up and drafted by the writing committee members according to their expertise. The recommendations represent the consensus opinion of the entire writing committee, graded by class of recommendation and level of evidence. Several questions addressed in this document either do not lend themselves to clinical trials or are rare disease entities, and in these instances recommendations are based on consensus expert opinion. Furthermore, specific recommendations, even when supported by substantial data, do not replace the need for clinical judgment and patient-specific decision-making. The recommendations were opened for public comment to Pediatric and Congenital Electrophysiology Society (PACES) members and underwent external review by the scientific and clinical document committee of the Heart Rhythm Society (HRS), the science advisory and coordinating committee of the American Heart Association (AHA), the American College of Cardiology (ACC), and the Association for European Paediatric and Congenital Cardiology (AEPC). The document received endorsement by all the collaborators and the Asia Pacific Heart Rhythm Society (APHRS), the Indian Heart Rhythm Society (IHRS), and the Latin American Heart Rhythm Society (LAHRS). This document is expected to provide support for clinicians and patients to allow for appropriate CIED use, appropriate CIED management, and appropriate CIED follow-up in pediatric patients
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