tbuckley/cabot-search huggingface dataset:
Abstract 2780: Effects of Apadenoson, a Selective Adenosine A2a Receptor Agonist for Myocardial Perfusion Imaging, on Coronary Blood Flow Velocity in Conscious Patients
Authors: Morton J Kern, John M Hodgson, Nabil Dib, Robert S Mittleman, Paul D Crane
Journal: Circulation (2006)

Background: Apadenoson (APA) is a highly selective adenosine (ADO) A2a receptor agonist with potential utility for pharmacologic stress myocardial perfusion imaging. This study determined APA effec...
Daclizumab, a humanized anti-interleukin-2 receptor alpha chain antibody, for treatment of acute graft-versus-host disease
Authors: D. Przepiorka, N. A. Kernan, C. Ippoliti, E. B. Papadopoulos, S. Giralt, I. Khouri, J.-G. Lu, J. Gajewski, A. Durett, K. Cleary, R. Champlin, B. S. Andersson, S. Light
Journal: Blood (2000)
Abstract 16872: Levosimendan Modulates Brain Injury Pattern in a Model of Infant Cardiopulmonary Bypass
Authors: Poongundran Namachivayam, Joe Smolich, Amy Shields, Igor E Konstantinov, Sandra Rees, Lara Shekerdemian
Journal: Circulation (2011)

Introduction. Brain immaturity and cardiopulmonary bypass (CPB) are important factors in the pathophysiology of brain injury in infants undergoing cardiac surgery. However, the impact of Levosimendan (Levo), a novel inodilator, on circulatory hemodynamics and microscopic markers of brain injury have not been fully investigated. We therefore studied the effects of Levo on global and regional hemodynamics and brain immunohistochemistry in a lamb model of infant CPB. Methods. Eighteen 1-week-old and eighteen 4-week lambs were anesthetized and instrumented with vascular catheters and aortic and right carotid artery transit-time flow probes. At each age, similar numbers were allocated to one of three treatment groups: 1) Non-CPB control, 2) CPB and 3) CPB+Levo. CPB animals underwent aortic and right atrial cannulation, and all received 120 min of CPB, with 90 min of aortic cross-clamp (XC) and cardioplegic arrest. Lambs in Group 2 received dopamine, and in Group 3, dopamine plus Levo, on weaning from CPB. Hemodynamic measurements were recorded pre-CPB and at 60, 120, 180 and 240 min after XC removal. At the end of the study, brains were fixed by perfusion and prepared for immunohistochemical analysis. Data were analysed with analysis of variance and P&lt;0.05 considered significant. Results. After CPB in 1-week lambs, cardiac output fell by 25% (P&lt;0.05) and carotid artery flow by 45% (P&lt;0.05), while in the CPB+Levo group, cardiac output was preserved and carotid artery flow fell by 23% (P&lt;0.05). After CPB in 4-week lambs, cardiac output decreased by 26% (P&lt;0.05) and carotid artery flow by 32% (P&lt;0.05), but in the CPB+Levo group, both cardiac output and carotid artery flow were preserved. On brain immunohistochemistry, an increased density of microglia (P&lt;0.05) was evident in deep white matter of the CPB+Levo group in 4-week, but not 1-week lambs. Conclusion. In a model of infant CPB, Levo prevented an early post-operative fall in cardiac output after CPB. However, while Levo preserved post-CPB carotid artery blood flow in 4-week lambs, this was associated with microscopic changes suggestive of increased brain injury. The impact of Levo on cerebral hemodynamics and evolution of brain injury in the immature circulation after CPB warrants further investigation.
Cardiovascular effects of bupropion in depressed patients with heart disease
Authors: S. P. Roose, G. W. Dalack, A. H. Glassman, S. Woodring, B. T. Walsh, E. G. V. Giardina
Journal: American Journal of Psychiatry (1991)

The cardiovascular effects of therapeutic plasma levels of tricyclic antidepressants in depressed patients with and without preexisting cardiac disease have been well characterized and include orthostatic hypotension and conduction delay. Bupropion, structurally unrelated to tricyclic antidepressants, is relatively free of cardiac side effects in depressed patients without cardiac disease. However, it is unknown whether bupropion is safe for depressed patients with preexisting heart disease, so the authors studied the cardiovascular effects of bupropion in such patients.The subjects were 36 inpatients with DSM-III major depression and preexisting left ventricular impairment (N = 15), ventricular arrhythmias (N = 15), and/or conduction disease (N = 21). The patients continued their cardiac drug regimens and received bupropion for 3 weeks (mean +/- SD dose = 442 +/- 47 mg/day). Cardiovascular functioning was measured by pulse, blood pressure, high-speed ECG, 24-hour portable ECG, and radionuclide angiography.Although bupropion caused a rise in supine blood pressure, it did not cause significant conduction complications, did not exacerbate ventricular arrhythmias, had a low rate of orthostatic hypotension, and had no effect on pulse rate. However, bupropion treatment was discontinued for 14% of the patients because of adverse effects, including exacerbation of baseline hypertension in two patients.The cardiovascular profile of bupropion may make this drug a useful agent in the treatment of the depressed patient with preexisting cardiovascular disease. Further studies, with longer durations of bupropion treatment and more subjects, are needed to confirm these findings.
Dry mouth
Authors: Mark Taubert, Eleanor M R Davies, Ian Back
Journal: BMJ (2007)

A 67 year old man presents with a six week history of dry mouth (xerostomia).He has prostate cancer, which has spread to his spine, and he takes opiates for pain relief.Recently, he started taking an antidepressant.He finds having a dry mouth frustrating as it interferes with his speech and chewing and he can no longer taste his food.
Common mistakes in psychotherapy
Authors: Peter Buckley, Toksoz B. Karasu, Edward Charles
Journal: American Journal of Psychiatry (1979)

To better monitor the psychotherapy training of psychiatric residents and to understand therapist factors involved in a negative outcome to psychotherapy, the authors surveyed 20 supervisors on the frequency of mistakes made by resident therapists. Among the mistakes most commonly made were wanting to be liked by patients, premature interpretations, overuse of intellectualization, inability to tolerate patients' aggression, and avoidance of fee setting. The authors conclude that the mitigation of the most common errors requires open discussion of countertransference issues.
Phase 3 Trials of Solanezumab and Bapineuzumab for Alzheimer's Disease
Authors: Christoph Laske
Journal: New England Journal of Medicine (2014)

ezumab for this condition. The negative results of these phase 3 trials may be interpreted in two ways: either treatment was too late in the course of the disease or amyloid-beta (Aβ) alone is the wrong target for an effective treatment of Alzheimer’s disease. The first interpretation may be clarified when the results of ongoing treatment trials involving persons with preclinical Alzheimer’s disease are available. These trials include the Dominantly Inherited Alzheimer Network Trial (DIAN-TU; ClinicalTrials.gov number, NCT01760005), Alzheimer’s Prevention Initiative (API; NCT01998841), and the Anti-Amyloid Treatment in Asymptomatic Alzheimer’s Disease study (A4 Study; NCT02008357). The second interpretation has not yet been tested. Several tau-related vaccines are in advanced preclinical stages and will soon enter clinical trials. Since the pathologic process of Alzheimer’s disease is characterized by the accumulation of both amyloid plaques and neurofibrillary tangles, 3 it is reasonable to assume that a treatment strategy focusing on both targets may be more beneficial than a strategy focusing only on one.
Abstract 1865: Real-Time 3D Transesophageal Echocardiography in the Guidance of Atrial Septal Defect Closure: Comparison with Intracardiac and 2D Transesophageal Echocardiography
Authors: Joseph A Lodato, Qi Ling Cao, Lynn Weinert, Lissa Sugeng, Roberto M Lang, Ziyad M Hijazi
Journal: Circulation (2007)

Background: Intracardiac echocardiography (ICE) is the preferred method for deployment of Amplatzer septal occluder devices (ASOD) in patients with atrial septal defect (ASD). Because ICE is costly and not widely available, 2D transesophageal echocardiography (2D-TEE) is often used instead. However, ASDs can have complex oval shapes that may not be well characterized with 2D imaging. We hypothesized that a new real-time 3D TEE (RT3D-TEE) probe could provide dynamic en-face visualization of the ASD and thus allow precise assessment of ASD dimensions. Aims: To determine the feasibility of using RT3D-TEE in the guidance of ASOD deployment in patients with ASD, and to compare the size of ASD and the occluding balloon waist obtained using RT3D-TEE against ICE and 2D-TEE. Methods: 8 consecutive patients with ostium secundum ASD (age 36±11 yrs) underwent ASOD placement under general anesthesia. Biplane 2D-TEE, RT3D-TEE and ICE images were acquired (Philips iE33) sequentially throughout ASOD placement. Measurements were obtained on-line. Results: Closure was successful in all patients without complications. RT3D-TEE was feasible yielding high quality images suitable for measurements (Table). ASD size by RT3D-TEE differed by &gt;1mm from 2D-TEE and ICE in 2 and 3 patients respectively in the long axis view and in 3 and 4 patients in the short axis view. Balloon waist size was 25.5 ± 6.7 (16–37) by 3D TEE and 24.7 ± 6.5 (15–35) by ICE. Conclusions: RT3D-TEE can be used for guidance of ASOD deployment with the advantage of improved ability compared to 2D-TEE and ICE to visualize the true en-face views, from which accurate measurements of ASD dimensions can be made for device selection.
Abstract 4715: Diagnostic Accuracy of Non-invasive 64-row Computed Tomographic Coronary Angiography (CCTA) Compared with Myocardial Perfusion Imaging (MPI): The PICTURE Study, A Pospective Multicenter Trial
Authors: Matthew J Budoff, Ella A Kazerooni, Gregory S Thomas, Jennifer H Mieres, Leslee J Shaw
Journal: Circulation (2008)

Although multiple studies have shown excellent accuracy statistics for non-invasive angiography by 64-CCTA, most studies comparing nuclear imaging with CCTA were performed on patients already referred for cardiac catheterization, introducing verification and referral bias. This prospective trial evaluated the diagnostic accuracy of 64-row CCTA to detect obstructive coronary stenosis compared to MPI, using quantitative coronary angiography (QCA) as a reference standard. Methods: 12 sites prospectively enrolled 230 patients (pts) [52% male, 56.9 yrs] with chest pain who were referred for MPI to assess CAD. To date, 48 patients were clinically referred for invasive coronary angiography (ICA) for either positive MPI or abnormal CCTA. All Pts underwent both MPI and CCTA (Lightspeed VCT/Visipaque 320, GE Healthcare) prior to ICA. CCTAs were graded on a 15-segment AHA model by 2 blinded readers for presence of obstructive stenosis (≥50% or ≥70%); MPI was graded by 2 blinded readers using a 17 segment model for estimation of the % myocardium ischemic or with stress defects. ICAs were independently graded for % stenosis by QCA. Efficacy of MPI and CCTA were assessed including all vessel segments for per-patient and per-vessel analyses. Results: Prevalence of stenosis ≥50% by ICA was 52.1% (25/48). The diagnostic accuracy (per-patient analysis) of CCTA and stress MPI compared to ICA are reported in Table 1 . For ≥50% stenosis, the CTA odds ratio for ICA disease was 51.75 (95% CI=8.50–314.94). For SSS ≥5%, the odds ratio for ICA CAD was 12.73 (95% CI=2.43–66.55). Using ROC curve analysis, CCTA was better at classifying obstructive CAD when compared to MPI (Area=0.87 vs. 0.76, p&lt;0.0001). Conclusions: This study represents the first prospective multicenter data comparing 64-row CCTA to MPI, demonstrating high diagnostic accuracy of CCTA to reliably detect &gt;50% and &gt;70% stenosis in chest pain patients. Diagnostic Accuracy Statistics for Coronary Computed Tomographic Angiography (CTA) and Stress Myocardial Perfusion Imaging (MPI) SPECT in Patients Prospectively Enrolled in the PICTURE Trial
Abstract 13743: Upregulation of Nox4 by TGF{beta}1 Oxidizes SERCA the C674 Thiol and Inhibits Nitric Oxide in Arterial Smooth Muscle of the Prediabetic Zucker Rat
Authors: Xiaoyong Tong, Xiuyun Hou, David Jourd'heuil, Robert M Weisbrod, Richard A Cohen
Journal: Circulation (2010)

Background: Vascular smooth muscle cell (SMC) migration is an important pathological process in several vascular occlusive diseases, including atherosclerosis and restenosis, both of which are acce...
Fibrinolysis for Intermediate-Risk Pulmonary Embolism
Authors: Rory J Spiegel, Christopher P Nickson, Ryan P Radecki
Journal: New England Journal of Medicine (2014)

To the Editor: In the Pulmonary Embolism Thrombolysis (PEITHO) study (April 10 issue), 1 a bolus of unfractionated heparin was withheld from 303 patients because they had just received subcutaneous low-molecular-weight heparin or fondaparinux.Low-molecular-weight heparin in particular has a slow onset of action, taking 4 to 6 hours to reach full effect. 2This delay in the effect of treatment may have been unfavorable to patients not receiving tenecteplase, among whom the incidence of hemodynamic decompensation (often within the first day after randomization) was higher than that among patients receiving tenecteplase.Guidelines support the safety of low-molecularweight heparin in patients with pulmonary embolism.Caution is warranted, however, because the majority of relevant trials (10 of 12 trials in a key meta-analysis 3 ) used low-molecular-weight heparin after an initial bolus of unfractionated heparin.Omitting this bolus may be unsafe, particularly in high-risk patients such as those involved in the PEITHO study.Previous guidelines have recommended a bolus of unfractionated heparin before the administration of lowmolecular-weight heparin. 4 Later, for some reason, this recommendation disappeared.We would like to know outcome details of the subgroup of patients who did not receive an initial bolus of unfractionated heparin.If hemodynamic decompensation in the placebo group occurred primarily in this subgroup, the explanation may be a delayed onset of anticoagulant activity.
Abstract P248: The DCM-Causing D230N Tropomyosin Mutation Produces an Age-Dependent Phenotype in Mice that Is Influenced by Transgene Dosage
Authors: Lauren Tal, Jil C Tardiff
Journal: Circulation Research (2011)

A recent study in two large multigenerational families demonstrated a novel mutation in tropomyosin (Tm), Asp230Asn (D230N) that caused DCM with a unique natural history resulting in a striking bimodal disease distribution. Infants and young children with the D230N Tm mutation presented with a severe, often fatal DCM while adults developed a mild to moderate clinical phenotype. Position 230 in tropomyosin is proximal to the C-terminal unwinding of tropomyosin that is essential for the Tm-Tm overlap and for the Tm-cardiac troponin T (cTnT) interaction. We hypothesized that the age-dependent remodeling is a result of temporal isoform switches in the closely linked Tm-binding partner cTnT. To directly address this hypothesis, we used the regulated in vitro motility assay to determine the biophysical effects of the D230N Tm mutation as well as the effects of cTnT isoform changes on the regulatory function of thin filaments. We have found that both wild type and D230N Tm filaments inhibit filament sliding at low calcium indicating that the D230N mutation does not completely disrupt regulation. However in the presence of high calcium the D230N Tm mutation significantly decreases the maximal velocity of filament sliding (3.790 ± 0.1333 microns/sec, n=98) as compared to the wild type filaments (4.900 ± 0.1044, microns/sec n=76). These findings support an altered Tm-cTnT interaction because at maximal calcium concentrations, the myofilament activation at the level of cardiac troponin is not properly transmitted to tropomyosin thus decreasing the activity of myosin-ATPase. In order to extend our biophysical observations and to provide translational insight, we generated a D230N Tm transgenic mouse model. In preliminary studies we demonstrate that at two months the D230N transgenic mice have evidence for early dilatation. In addition, the differences in ventricular remodeling were highly dependent on transgene dose. At six months, we observed dilatation of the ventricle and thinning of the walls compared to non-transgenic siblings. However, the differences were not as marked as those at the two-month time point. Collectively, these findings support an age-dependent DCM phenotype that is modulated by transgene dosage.
Abstract 9277: Transplantation of Mesenchymal Stem Cells Mitigates Cardiac Electrophysiological Remodelling in a Rat Model of Myocardial Infarction
Authors: Patrick F Lai, Stephane Masse, Guangming Li, Yaoguang Zhang, Marjan Kusha, John Asta, Terrence M Yau, Kumaraswamy Nanthakumar
Journal: Circulation (2010)

Background: Cell transplantation is a promising therapy for heart failure, demonstrating modest improvements in cardiac function in clinical trials, but the underlying mechanism of the therapeutic ...
Surgical Resection First for Localized Gastric Adenocarcinoma: Are There Adjuvant Options?
Authors: Elena Elimova, Jaffer A. Ajani
Journal: Journal of Clinical Oncology (2015)

Article Tools ONCOLOGY GRAND ROUNDS Article Tools OPTIONS & TOOLS Export Citation Track Citation Add To Favorites Rights & Permissions COMPANION ARTICLES No companion articles ARTICLE CITATION DOI: 10.1200/JCO.2014.60.1765 Journal of Clinical Oncology - published online before print August 31, 2015 PMID: 26324361 Surgical Resection First for Localized Gastric Adenocarcinoma: Are There Adjuvant Options? Elena ElimovaxElena ElimovaSearch for articles by this author , Jaffer A. AjanixJaffer A. AjaniSearch for articles by this author Show More The University of Texas MD Anderson Cancer Center, Houston, TX https://doi.org/10.1200/JCO.2014.60.1765 First Page Full Text PDF Figures and Tables © 2015 by American Society of Clinical Oncology
Synergistic Blockade Of Activated B Cell-Like DLBCL Proliferation With a Selective Inhibitor Of IRAK4 In Combination With Inhibition Of The B-Cell Receptor Signaling Network
Authors: Divya Chaudhary, Nancy Wood, Donna L. Romero, Shaughnessy D. Robinson, Jeremy R Greenwood, Mee Shelley, Michael Morin, Rosana Kapeller, William F Westlin
Journal: Blood (2013)
Abstract 16798: MicroRNA 142-5p Targets Myocardial Hypertrophy and Cytokine Response
Authors: Salil Sharma, Jing Liu, Jianqin Wei, Nanette H Bishopric
Journal: Circulation (2011)

Background: p300 is a dose-dependent and limiting regulator of cardiac hypertrophy. p300 regulates hypertrophy by controlling the expression of specific microRNAs. Objective: To dissect the role of miR142 during hypertrophic growth and to verify its targets. Methods and Results: In mice with myocardial overexpression (OE) of p300 (p300tg) and in acute myocardial ischemia, we observed altered expression of microRNAs miR142-5p and -3p (miR142). Induction of myocyte hypertrophy in vitro and in vivo were associated with downregulation of miR142. Induction of miR142 by serum was sensitive to inhibitors of ERK/MAPK and JNK signaling pathways, establishing an inverse relationship between hypertrophic signaling and miR142 levels. Adenovirus-mediated OE of p300 in NRVM caused a steep reduction in miR142, while siRNA-mediated KD of p300 significantly upregulated miR142. Thus, p300 is both necessary and sufficient for miR142 downregulation. MiR142 altered the expression of many sarcomeric proteins including Tni2, Tnt2, Myh3 and Mlc1. MiR142 directly inhibited the translation of ACTN4 through a conserved 3’UTR binding site. MiR142 potently repressed multiple components of the NF-κB, TNF-α and interleukin signaling pathways and abrogated the upregulation of iNOS mRNA and NO production in myocytes exposed to cytokines. We identified IL6st/gp130 as a direct target of miR142 through paired 3’UTR 142-5p and -3p binding sites, implicating miR142 in myocyte survival signalling. Lentiviral transduction of miR142 confirmed the same gene targets in myocardium in vivo, associated with development of systolic dysfunction and extensive apoptosis at 2 months. Finally, miR142 inhibited the expression of p300 both in vitro and in vivo, through a miR142-5p 3’UTR binding site. Altered immune response gene expression in p300tg mice was restored to near-wt levels by miR142 OE, indicating that p300 and miR142 are mutually inhibitory. Conclusion: MiR142 is a potent inhibitor of myocardial cytokine signaling through repression of IL6st/gp130 expression. Induction of hypertrophy involves the MAPK-activated, p300-mediated inhibition of miR142, which removes a block to sarcomeric protein expression, gp130-mediated survival signaling, and sustained expression of p300.
Abstract 5134: Distribution of Dipyridamole in Blood Components Among Post-Stroke Patients Treated With Extended Release Formulation
Authors: Victor L Serebruany, Elena Sabaeva, Christopher Booze, Oliver Atar, Dan Hanley
Journal: Circulation (2009)

Background and Purpose - Extended release dipyridamole (ERD) is widely used in patients after ischemic stroke; however, the ability of this antithrombotic agent to be stored in different blood cells has never been explored in post-stroke patients. We hypothesized that since ERD is known to be highly lipophylic, the drug may be present not only in plasma, but also accumulated in platelets, leukocytes, and erythrocytes. Methods - Fifteen patients after documented ischemic stroke were treated with Aggrenox (ERD and low dose aspirin combination) BID for 30 days, and 12 of them completed the study. ERD concentrations in blood cells and platelet poor plasma were measured by spectrofluorimetry at Baseline, Day 14, and Day 30 after the initiation of therapy. Results - The background level of spectrofluorometry readings differs slightly among the blood components (132–211 ng/mL) due to the differences in the preparation of samples and cell isolation techniques. As expected, 2 weeks of ERD therapy produced steady state plasma concentration of dipyridamole already at Day 14 (1680±542ng/mL), followed by a slight not significant decrease at one month (1619±408). Two weeks of therapy was sufficient to achieve a consistent dipyridamole accumulation in erythrocytes (361±43), but not in platelets (244±78), or leukocytes (275±49). In fact, while blood cells continued dipyridamole intake beyond 14 days period, and this increase (398±66) was significant (p=0.02) at thirty days. Conclusion - Treatment with ERD in post-stroke patients resulted not only in the achieving of therapeutic plasma dipyridamole concentrations, but also deposition of the drug in erythrocytes and leukocytes, but not in platelets. If confirmed, these data will affect our better understanding of dipyridamole pleiotropy, and may expand future clinical indications of ERD formulation.
Frequency of Adverse Systemic Reactions after Fluorescein Angiography
Authors: Kris A. Kwiterovich, Maureen G. Maguire, Robert P. Murphy, Andrew P. Schachat, Neil M. Bressler, Susan B. Bressler, Stuart L. Fine
Journal: Ophthalmology (1991)

Intravenous fluorescein angiography is a commonly performed and extraordinarily valuable diagnostic procedure. The frequency of adverse reactions after angiography has varied considerably in previous reports. In a prospective study of 2789 angiographic procedures in 2025 patients, the authors found that the percentage of adverse reactions depended strongly on the patient's angiographic history. Overall, adverse reactions followed 4.8% of the angiographic procedures. These reactions included nausea (2.9%), vomiting (1.2%), flushing/itching/hives (0.5%), and other reactions (dyspnea, syncope, excessive sneezing) (0.2%). No cases of anaphylaxis, myocardial infarction, pulmonary edema, or seizures occurred. The percentage of reactions was 1.8% for patients who had had previous angiography without ever having had an adverse reaction. In contrast, the percentage of reactions was 48.6% for patients who had had an adverse reaction to angiography previously.