tbuckley/cabot-search huggingface dataset:
Acute Hemodynamic Effects of Pacing in Patients With Fontan Physiology
Authors: Brent J. Barber, Anjan S. Batra, Grant H. Burch, Irving Shen, Ross M. Ungerleider, John W. Brown, Mark W. Turrentine, Motomi Mori, Yi-Ching Hsieh, Seshadri Balaji
Journal: Journal of the American College of Cardiology (2005)
Röntgentherapie in Tabellenform
Authors: Emmerich Markovits
Journal: JAMA (1934)

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Combinatorial cancer therapy using a pharmacological inhibitor of indoleamine 2,3-dioxygenase (IDO), a target of the cancer suppression gene Bin1
Authors: Alexander J. Muller, James B. Duhadaway, Erika Sutanto-Ward, Scott Donover, George C. Prendergast
Journal: Cancer Research (2004)

4589   Mutations produce a dynamic substratum from which modifier genes and the stromal microenvironment act to facilitate the development of a fully malignant state. Previous studies of Myc interactions identified Bin1 as a candidate suppressor or negative modifier gene in cancer. Bin1 encodes a set of alternately spliced adapter proteins implicated in nuclear processes but also actin-membrane dynamics. Expression of Bin1 is often attenuated in breast and prostate cancers; its restoration in cancer cells can stanch proliferation and facilitate cell death. Here we report that Bin1 loss also promotes tumor formation by facilitating escape from host anti-tumor immunity, and ongoing mechanistic investigations have identified a unique pharmacological strategy to correct this. We have found that homozygous deletion of the Bin1 gene enhances tumor formation by Myc+Ras-transformed murine fibroblasts and skin epithelial cells. Unexpectedly, the benefits conferred by Bin1 loss are reduced in immunocompromised hosts, suggesting cell autonomous effects on anti-tumor immunity. A candidate mediator of this effect has been identified in indoleamine 2,3-dioxygenase (IDO), an oxidoreductase found to interact genetically with Bin1. The classical function of IDO is to catalyze tryptophan degradation in the first step towards biosynthesis of the metabolic regulator NAD. However, more recently, catabolism of tryptophan by IDO has been shown to attenuate local activation of T cells. Bin1−/− cells exhibit superinducible IDO, possibly explaining the more aggressive growth of Bin1−/− isografts in immunocompetent hosts. We have tested whether IDO blockade may have therapeutic benefit in MMTV-neu transgenic mice (a model of breast cancer where Bin1 is epigenetically attenuated), using the competitive bioactive IDO inhibitor 1-methyl-tryptophan (1MT). By itself 1MT had little effect on tumor growth. In contrast, 1MT elicited massive cell death and tumor regression when combined with cytotoxic agents that alone were inefficacious in the model. No synergy occurred in tumors engrafted into nude mice, supporting the expectation that combinatorial efficacy is immune-based. Results of additional studies examining mechanism, PK/PD, and survival in response to treatment will be presented. Our findings 1) support the concept of Bin1 as a cancer suppression gene, 2) link Bin1 deficiency to a pharmaceutically tractable enzyme that may control tumor metabolism and immunity, and 3) identify IDO/cytotoxic combination therapy as a promising new strategy to treat cancer. One radical implication of this work is that combining immunotherapy and chemotherapy to treat cancer, which may seem counterintuitive in principle, may prove to be unexpectedly effective in practice.
Abstract 704: The Omega-3 Fatty Acid Docosahexaenoate Attenuates Vascular Inflammation Reducing Endothelial Cyclooxygenase-2 Induction through the Inhibition of Both NADP(H) Oxidase and PKC{varepsilon}
Authors: Marika Massaro, Egeria Scoditti, Maria Annunziata Carluccio, Carlo Storelli, Alessandro Distante, Raffaele De Caterina
Journal: Circulation (2006)

Background and Aims. A high intake of the omega-3 fatty acid docosahexaenoate (DHA) has been associated with systemic anti-inflammatory effects and cardiovascular protection, but the molecular basi...
Abstract 1417: Combined Assessment of Left Ventricular Strain and Rotation - A Novel Approach for Assessment of Function in Infarcted Myocardium and its Border Zones
Authors: Thomas Helle-Valle, Espen Remme, Erik Lyseggen, Trond Vartdal, Eirik Pettersen, Hans Jørgen Smith, Nael F Osman, Ketil Lunde, Thor Edvardsen, Otto A Smiseth
Journal: Circulation (2007)

Background : LV circumferential strain and rotation are markers of myocardial function, but the two measures dissociate in the ischemic LV. This study investigates the mechanism and clinical significance of this dissociation. Methods : In healthy subjects (n=15) and patients with LAD-related myocardial infarction (n=15), LV apical rotation and strain were measured from apical short-axis recordings by STE and MRI tagging. Infarct extent was determined by contrast MRI. To define mechanisms of the dissociation between strain and rotation we used a finite element model. Results : Mean apical rotation and strain by STE were lower in the patients than in healthy subjects (13±4 vs. 10±5° and −24±2 vs. −12±10%, respectively, P &lt;0.05). In patients, segmental strain was reduced in proportion to extent of infarction (r=0.84, P &lt;0.0001). Maximum and minimum rotation, however, were found at the infarct borders; maximum rotation at the border in direction of rotation (counter-clockwise) and minimum rotation at the opposite infarct border (Figure ). The simulation study reproduced the clinical findings and indicated that the dissociation was mainly caused by mechanical interactions between infarcted and viable myocardium transmitted along circumferentially oriented LV fibers. Conclusions : Systolic strain reflects regional myocardial function and infarct extent, while systolic rotation defines infarct borders. Strain and rotation provides complementary information in assessment of myocardial dysfunction and infarct extent.
Abstract 14748: Protective Role of Cardiac-Specific alpha1A-AR Overexpression in Chronic Myocardial Infarction Through Improved Blood Flow
Authors: Xin Zhao, Lin Yan, Grace J Lee, Dorothy E Vatner, Robert M Graham, Stephen F Vatner
Journal: Circulation (2013)

Relatively few transgenic (TG) cardiomyocyte (CM)-specific overexpression models reduce infarct size and afford protection from chronic permanent coronary artery occlusion (CAO). This is because, in the absence of collateral blood flow or angiogenesis, it is unlikely that infarct size would be reduced following permanent CAO, given that transgene overexpression is CM specific and does not occur in blood vessels. The goal of this investigation was to determine if the α 1A -adrenergic receptor (AR) protects against permanent CAO-induced chronic ischemia and to elucidate the underlying mechanisms in α 1A -TG rats with CM-specific receptor overexpression. Four weeks after permanent left anterior descending CAO, LV ejection fraction was greater, p 1A -TG rats (55±3.6%) than in non-TG littermates (NTLs) (35±3.1%), whereas LV systolic wall stress was lower, p 2 ). In addition, our hypothesis was that there was improved blood flow to the ischemic zone, which would diminish the scar by providing more blood flow. Indeed, at 1 week after permanent CAO, there was more viable tissue within the risk area, assessed by picrosirius red staining (34±1.8 vs. 17±1.8%, p 1A -overexpression shows protection from chronic permanent CAO, which is due to an enhanced coronary circulation that maintains blood flow within the area at risk better than in NTLs, resulting in improved cardiac performance.
Abstract 15253: Effect of Carbohydrate, Unsaturated Fats and Protein Intake on Measures of Insulin Sensitivity: Results From the OmniHeart Trial
Authors: Meghana D Gadgil, Cheryl Anderson, Frank M Sacks, Edwina Yeung, Lawrence J Appel, Edgar R Miller
Journal: Circulation (2011)

Background: Impaired insulin sensitivity increases the risk of cardiovascular disease. The optimal macronutrient intake to increase insulin sensitivity is unknown. The purpose of this study is to d...
Abstract 3943: Adrenomedullin Induces Lymphangiogenesis and Ameriolates Secondary Lymphedema
Authors: DongHao Jin, Kenich Yamahara, Kazuhiko Harada, Shunsuke Ohnishi, Kenji Kangawa, Noritoshi Nagaya
Journal: Circulation (2008)

Background: Adrenomedullin (AM) stimulates angiogenesis by activation of extracellular signal-regulated kinase (ERK) and Akt in vascular endothelial cells (EC). Vascular endothelial growth factor C and D were major lymphangiogenesis factors, which enhance lymphatic EC activity via ERK and Akt pathways. Therefore, we investigated whether AM promotes lymphangiogenesis through activation of lymphatic EC and improves secondary lymphedema. Methods and Results: RT-PCR analysis revealed that human lymphatic microvascular EC (HLMVEC) expressed mRNAs of all AM receptor complexes including calcitonin-receptor-like receptor (CRLR) and receptor-activity-modifying proteins (RAMP) 1–3. AM (10 −9 -10 −7 M) significantly enhanced proliferation of HLMVEC (MTS assay; 194 ± 4% in 10 −7 M, P &lt; 0.05) with accumulation of intracellular cAMP in a dose dependent manner. Transwell migration assay revealed that AM (10 −9 -10 −7 M) enhanced the chemotactic activity of HLMVEC (204 ± 7% in 10 −7 M, P &lt; 0.05). Proliferation of HLMVEC induced by AM (10 −7 M) or a cAMP agonist, 8-Br-cAMP (10 −4 M) was significantly inhibited by mitogen-activated protein kinase kinase (MEK) inhibitors, PD98059 (5 × 10 −6 M) and U0126 (10 −6 M). Western blot analysis revealed that AM (10 −7 M) and 8-Br-cAMP (10 −4 M) induced the phosphorylation of ERK in HLMVEC. A mouse model of tail lymphedema was developed in 8 –10 weeks old male BALB/c mice, and human AM (0.05 μg/kg/min) was delivered for 14 days using an osmotic minipump, which was subcutaneously implanted. AM significantly decreased the tail thicknesses at day 14 to 16 postoperation (Tail diameter at day 14; control vs. AM treatment, 4.19 ± 0.13 vs. 3.79 ± 0.08 mm, P = 0.023). Immunohistological analysis of injury sites using anti-LYVE-1 and anti-vWF antibodies revealed that AM treatment increased the number of lymphatic vessels (104 ± 15 vs. 188 ± 15 / mm 2 , P = 0.007) and vascular vessels (230 ± 11 vs. 315 ± 15 / mm 2 , P = 0.003). Conclusions: AM enhanced proliferation and migration of lymphatic EC through activation of cAMP/MEK/ERK pathway. Infusion of AM induced lymphangiogenesis and improved secondary lymphedema in the mouse model of tail lymphedema. These results indicate that AM might represent a novel therapeutic strategy for treatment of lymphedema.
Abstract 204: Intracranial Pressure During Compression-Only and Compression-Ventilation CPR in a Porcine Model of Ventricular Fibrillation
Authors: Anatolij Truhlar, Zdenek Turek, Vladimir Cerny
Journal: Circulation (2010)

Introduction: Recent guidelines recommend compression-only CPR for bystander response to adults who experience sudden cardiac arrest. However, gasping/apnea is known to cause hypercapnia which incr...
Hepatic Arterial Infusion Chemotherapy for Colorectal Cancer Metastasis to the Liver
Authors: Lee M. Ellis, Judy Chase, Yehuda Patt, Steven A. Curley
Journal: Liver Cancer (1998)

The liver is the most common site of distant organ metastasis in patients with colorectal carcinoma. Of the 160,000 patients who develop colorectal carcinoma each year in the United States, half develop a recurrence at some point in their lifetimes, with the liver being the most common site (70%). 1 Although we have developed a better understanding of the molecular determinants that lead to colorectal cancer progression and metastasis, little progress has been made in therapy for metastatic disease. Fewer than 10% of patients who develop liver metastasis can undergo potentially curative resection.2 Despite advances in surgical technology and imaging techniques, at least half of the patients who undergo liver resection for metastatic colorectal cancer suffer a recurrence. Systemic chemotherapy for liver metastasis from colorectal cancer results in only one-third of patients obtaining a partial response, with complete responses being anecdotal.3,4
Abstract 9913: Different Impacts of Body Fat Composition and Computed-Tomography-Determined Visceral Fat on Left Ventricular Mass, Geometry and Left Atrial Structural Alteration
Authors: Yau-Huei Lai, Chun-Ho Yun, Yih-Jer Wu, Jen-Yuan Kuo, Hung-I Yeh, Cheng-Ho Tsai, Chung-Lieh Hung
Journal: Circulation (2011)

Background The adverse effects of body fat distribution on left ventricular (LV) mass and geometry has recently been recognized. Excessive visceral fat deposition, specifically those surrounding the heart and central aorta, was associated with adverse cardiovascular events. We sought to examine the impact of body fat composition and visceral adipose tissue on cardiac structure and geometry. Methods We studied 1,063 subjects (age: 49.5±10.5, 39.4% female) without angina or heart failure symptoms. Cardiac structures and LV geometry parameters including LV mass index (LVMI), relative wall thickness (RWT) and mass-to-volume ratio were all determined by echocardiography. Body fat composition (both fat and fat-free mass) was assessed by Tanita foot-to-foot bioimpedance analysis. A subgroup of 361 subjects further underwent multidetector computed tomography (MDCT) for three-dimensional, volume-based epicardial adipose tissue (EAT) and thoracic peri-aortic adipose tissue (TAT) quantification. Results Both fat and fat-free mass were positively related to LV mass (β coef: 0.42 &amp; 0.31, both p&lt;0.001) after multivariate adjustment for age, gender, blood pressure and medical histories. However, only fat mass (β coef: 0.15, p&lt;0.001) contributed independently to concentric remodeling (RWT&gt;0.42). For each standard-deviation increase of EAT and TAT volume, there was an observed increase of LVMI (β coef: 0.14 &amp; 0.15, both p&lt;0.05) after multivariate adjustment. In addition, left atrial dimension was also positively related to both EAT and TAT even after adjusting for severity of mitral regurgitation (β coef: 0.16 &amp; 0.12, both p&lt;0.05). Conclusions While both fat and fat-free mass exert their independent effect on ventricular mass increase, only fat mass had independent impact on ventricular geometry. Our data also suggested that epicardial adipose tissue may further impact LA dimension, possibly mediated by impeding ventricular diastolic filling.
Abstract 010: Population-wide Weight Loss and Regain in Relation to Diabetes and Cardiovascular Disease Mortality: Cuba 1980-2010
Authors: Usama Bilal, Manuel Franco, Pedro Orduñez, Mikhail Benet, Alain Morejon, Benjamin Caballero, Joan F Kennelly, Richard S Cooper
Journal: Circulation (2013)

INTRODUCTION The Cuban economic crisis in the early 1990’s led to weight loss of about 4-5 kg in the entire population, leading to a sharp drop in diabetes and cardiovascular mortality. Following modest economic recovery (1996-2012) body weight was regained as adequate food sources became available and public transportation was restored. Our objective was to evaluate the association of these population-wide body weight changes with mortality trends from diabetes and cardiovascular disease, cancer, and all-causes. HYPOTHESIS We hypothesize that the previously observed mortality improvements in diabetes and cardiovascular disease due to population-wide weight loss will be reversed following the population-wide weight rebound. METHODS Changes in daily energy intake, physical activity, and body weight were tracked from 1980 to 2010 using national and regional surveys from Cuba. Body weight data was measured in four local surveys in the city of Cienfuegos in 1991(n=1657), 1995(n=1351), 2001(n=1667), and 2011(n=1492). Diabetes prevalence and incidence trends were obtained from population-based registries. Mortality trends were modeled using national vital statistics over the period 1980-2010. RESULTS A rebound in population-wide body weight was observed starting in 1996 and by 2011 obesity prevalence had already exceeded pre-crisis levels. The upward weight trend was accompanied by a 140% increase in diabetes incidence (from 1 per 10000 in 1997 to 2.4 per 10000 in 2003), a 47% increase in diabetes mortality (from 9.3 per 10000 in 2002 to 13.9 per 10000 in 2010) and a deceleration in the rate of mortality decline in coronary heart disease. CONCLUSIONS This unique, 30-year natural experiment demonstrates the strong association at the population level of weight reduction on diabetes and cardiovascular mortality and the contrary effect of weight regain. Moderate and healthy weight loss, affecting the totality of contemporary populations, could yield significant public health benefits.
Abstract 5885: Impacts of Renal Insufficiency on the Prevalence of Heart Failure With Preserved Ejection Fraction in Hypertensive Patients
Authors: Tomohito Ohtani, Toshiaki Mano, Yasushi Sakata, Mayu Nishio, Yasuharu Takeda, Daisuke Kamimura, Shunsuke Tamaki, Yosuke Omori, Kazuhiro Yamamoto
Journal: Circulation (2008)

Renal insufficiency is a predictor of hospitalization for heart failure in hypertensive patients. However, the onset of heart failure in patients with kidney diseases is principally attributed to left ventricular systolic dysfunction induced by myocardial infarction or long-term hypertension, and the effects of renal insufficiency on the prevalence of symptomatic heart failure stage without systolic dysfunction remain unclear. This study aimed to assess the effects of renal insufficiency on the prevalence of heart failure with preserved ejection fraction. Out of 650 hypertensive outpatients with ejection fraction≥50%, 191 patients met the Framingham heart failure criteria. The multiple logistic regression analysis revealed that obese, female, estimated glomerular filtration rate (eGFR) &lt;60 ml/min/1.73m 2 and a ratio of transmitral E velocity to early diastolic mitral annular velocity (E/E′) &gt;15 were independent predictors of the prevalence of heart failure (Table ). To assess the effect of the renal insufficiency, the patients were divided into three groups as follow; CKD-A: eGFR≥75 (n=158), CKD-B: 60≤eGFR&lt;75 (n=207), CKD-C: eGFR&lt;60ml/min/1.73m 2 (n=285). The patients in CKD-B group represented higher E/E′ ratio and lower E′ velocity than those in CKD-A group. These indices were not different between the patients in CKD-B and CKD-C group. Hemoglobin concentration was significantly decreased and brachial-ankle pulse wave velocity was significantly elevated in the patients in CKD-C group compared to the other groups. Left ventricular diastolic dysfunction and renal insufficiency are independent risk factors for the prevalence of heart failure with preserved ejection fraction in hypertensive patients. Renal insufficiency exerts its effects through the modulation of extracardiac factors such as anemia and arterial stiffening rather than through the promotion of diastolic dysfunction. Table. Multivariate analysis of determinants of heart failure with EF≥50%
Antiplatelet and Anticoagulant Agents in Heart Failure
Authors: Paul A. Gurbel, Udaya S. Tantry
Journal: JACC Heart Failure (2014)

There has been a 3-fold increase in hospital discharges for heart failure (HF) and also significantly increased mortality rate in HF patients in recent years. A major focus of HF research has been in the area of neurohormonal control and resynchronization therapy. There is a great urgency in better understanding the pathophysiology underlying the exceedingly high mortality and a need for exploration of therapeutic strategies beyond those that influence neurohormonal pathways. The decision to treat patients with HF with antiplatelet therapy remains largely influenced by the presence or absence of concomitant arterial disease. Antithrombotic therapy has been shown to be effective in many forms of cardiac disease, including patients with HF and atrial fibrillation. Although it is clear that platelet activation and hypercoagulability are present in HF, and there is evidence that stroke is reduced by warfarin therapy in the HF patient, the available data suggest that the risk of major bleeding overshadows the antithromboembolic benefit in HF patients in sinus rhythm. The utility of oral anticoagulant and/or antiplatelet therapy has never been evaluated in an adequately powered dedicated clinical trial of HF patients in sinus rhythm. In this state-of-the art paper we explore the evidence for targeting the inhibition of platelet function and coagulation to improve outcomes in the HF patient.
Abstract 258: Emergency Department Involvement Reduces Subjectivity for Hypothermia
Authors: Heather M Ross, Roger Elias, David Harriman, Anna Andreozzi, Eric M Grubman
Journal: Circulation (2011)

Background: Therapeutic hypothermia (TH) is an effective adjunctive therapy to standard post-resuscitation care for neurologically unresponsive survivors of cardiac arrest. TH has been demonstrated to improve survival and functional outcomes in this vulnerable patient population in a variety of academic and community hospital settings. We have previously reported that with an ICU-centered protocol in a community setting, patients who were subjectively deemed healthy prior to cardiac arrest received TH significantly more often than other patients who met TH protocol criteria. Methods: A TH protocol was initiated in the intensive care unit (ICU) setting for comatose survivors of cardiac arrest in our 511-bed community teaching hospital for 12 months, January-December 2009. Based on initial outcomes data, the protocol was modified to include Emergency Department (ED) stakeholders beginning January 2010. With IRB approval, we conducted a retrospective chart review to evaluate TH application and outcomes for appropriate patients according to the Utstein style to identify whether ED involvement impacted patient selection for TH from January-December 2010. Results: Five of 22 eligible patients received TH under the ICU-only protocol, and 5 of 20 eligible patients received TH under the ICU+ED protocol (p=NS). Comparing baseline assessments of “healthy” prior to cardiac arrest, significantly more healthy patients received TH under the ICU-only protocol (p=.02), whereas there was no significant difference in baseline assessments of healthy for patients receiving TH under the ICU+ED protocol (p=NS). Conclusion: In a community teaching hospital with an ICU-centered TH protocol, adding ED stakeholder involvement to the TH protocol did not significantly influence the application of TH to eligible patients. However, this system-wide integration reduced the impact of a subjective assessment of a “healthy” pre-arrest state as an influencing factor for patients to receive TH. These findings warrant further investigation to identify means to better implement TH for appropriate patients, regardless of subjective pre-arrest health assessments.