tbuckley/cabot-search huggingface dataset:
Radiofrequency Current Catheter Ablation of Accessory Atrioventricular Pathways in Ebstein's Anomaly
Authors: Riccardo Cappato, Michael Schlu¨ter, Christian Weiß, Matthias Antz, Dietmar H. Koschyk, Thomas Hofmann, Karl-Heinz Kuck
Journal: Circulation (1996)

In patients with Ebstein's anomaly, localization of accessory pathways (APs) may be impeded by abnormal local electrograms recorded along the atrialized right ventricle and by the presence of multiple APs. The impact of these factors on radiofrequency (RF) current catheter ablation of APs has not been evaluated yet.Twenty-one patients with Ebstein's anomaly and reentrant atrioventricular tachycardias underwent electrophysiological evaluation and subsequent attempts at RF catheter ablation. Thirty-four right-sided APs were found, with 30 located along the atrialized ventricle. Local electrograms in this region were normal in 10 patients but fragmented in 11. Fragmented electrograms prevented the clear distinction between atrial and ventricular activation potentials as well as the identification of AP potentials. Right coronary artery mapping was performed in 7 patients. Abolition of all 26 APs was achieved in the 10 patients with normal local electrograms and in 6 of 11 patients with abnormal electrograms. Right coronary artery mapping allowed AP localization and ablation in 5 patients. In the 5 patients with abnormal electrograms and a total of 8 APs, 6 APs could not be ablated. Unsuccessfully treated patients received antiarrhythmic drugs. During 22 +/- 12 months of follow-up, 5 patients had clinical recurrences, including 4 who had undergone a successful RF procedure.In patients with Ebstein's anomaly and reentrant atrioventricular tachycardias, factors likely to account for failure of RF catheter ablation include an AP located along the atrialized right ventricle and the abnormal morphology of endocardial activation potentials generated in this region.
980-90 Superior Vena Cava Versus Right Atrium Central Venous Catheter Placement Avoids Thrombosis: The Role of Transesophageal Echocardiography in Diagnosis and Evaluation — A Prospective Study
Authors: Dan Gilon, David Schechter, Azaria J.J.T. Rein, Zvi Gimon, Paul Drakos, Reuven Or, Mervyn S. Gotsman, Arnon Nagler
Journal: Journal of the American College of Cardiology (1995)
“Differentiationism” can reconcile selectionism and constructivism
Authors: G. M. Innocenti
Journal: Behavioral and Brain Sciences (1997)

Increased complexity of representations in development probably results from the differentiation of distributed neural circuits. Axonal differentiation plays a crucial role in this process. Axonal differentiation appears to be achieved in stages, each involving combinations of constructive and regressive events controlled by cell intrinsic and cell extrinsic information.
542 STATIN TREATMENT DECREASE COLLATERAL FLOW AND PORTAL PRESSURE IN CIRRHOSIS, BUT NOT IN PREHEPATIC PORTAL HYPERTENSION
Authors: J. Trebicka, S. Klein, M. Granzow, G. Ranabhat, M. Hennenberg, E. Raskopf, S. Gautsch, V. Schmitz, T. Sauerbruch
Journal: Journal of Hepatology (2010)
Patient Power: Solving America's Health Care Crisis
Authors: Jerome Arnett
Journal: JAMA (1993)

"The United States is the only country in the world where people can consume medical care almost without limit, unconstrained by market forces or by government rationing," write economists John C. Goodman and Gerald L. Musgrave. "Health-care costs are rising because, for individual patients, medical care is cheap, not expensive." <i>Patient Power: Solving America's Health Care Crisis</i>is a fascinating book, which looks at our current dilemma in three sections. The first describes the cost-plus system of health care finance and how it evolved. The second shows why this system is creating our present health care crisis. The last section describes a system that will solve the majority of our problems and how we can get to it. The book is carefully documented and richly illustrated, with 101 tables and 64 graphs. "The only way to control costs is to have someone choose between health care and money" (that is,
Prognostic impact of immunohistochemically defined germinal center phenotype in diffuse large B-cell lymphoma patients treated with immunochemotherapy
Authors: Heidi Nyman, Magdalena Adde, Marja-Liisa Karjalainen-Lindsberg, Minna Taskinen, Mattias Berglund, Rose-Marie Amini, Carl Blomqvist, Gunilla Enblad, Sirpa Leppä
Journal: Blood (2007)
Bacterial programmed cell death of cerebral endothelial cells involves dual death pathways
Authors: Daniela Bermpohl, Annett Halle, Dorette Freyer, Emilie Dagand, Johann S. Braun, Ingo Bechmann, Nicolas W.J. Schröder, Joerg R. Weber
Journal: Journal of Clinical Investigation (2005)

Major barriers separating the blood from tissue compartments in the body are composed of endothelial cells. Interaction of bacteria with such barriers defines the course of invasive infections, and meningitis has served as a model system to study endothelial cell injury. Here we report the impressive ability of Streptococcus pneumoniae, clinically one of the most important pathogens, to induce 2 morphologically distinct forms of programmed cell death (PCD) in brain-derived endothelial cells. Pneumococci and the major cytotoxins H2O2 and pneumolysin induce apoptosis-like PCD independent of TLR2 and TLR4. On the other hand, pneumococcal cell wall, a major proinflammatory component, causes caspase-driven classical apoptosis that is mediated through TLR2. These findings broaden the scope of bacterial-induced PCD, link these effects to innate immune TLRs, and provide insight into the acute and persistent phases of damage during meningitis.
Relapse risk in patients with malignant diseases given allogeneic hematopoietic cell transplantation after nonmyeloablative conditioning
Authors: Christoph Kahl, Barry E. Storer, Brenda M. Sandmaier, Marco Mielcarek, Michael B. Maris, Karl G. Blume, Dietger Niederwieser, Thomas R. Chauncey, Stephen J. Forman, Edward Agura, Jose F. Leis, Benedetto Bruno, Amelia Langston, Michael A. Pulsipher, Peter A. McSweeney, James C. Wade, Elliot Epner, Finn Bo Petersen, Wolfgang A. Bethge, David G. Maloney, Rainer Storb
Journal: Blood (2007)
Impossible to state which NSAID is safer
Authors: S. Revell, L. Fenney
Journal: BMJ (1995)

EDITOR,--In their article on recent advances in rheumatology Anthony Bradlow and Joel David state that ibuprofen is the safest non-steroidal anti-inflammatory drug when used at conventional doses.1 However, they present only the risk of serious gastrointestinal adverse events and these for only …
An Appraisal of Phenylbutazone Suppositories
Authors: C. F. Hawkins, H. T. Fawns
Journal: BMJ (1959)

BRIOnJR1.AL is 5%.An advantage of this method is that the risk of making errors of this kind is stated (Bross, 1952).In both of the methods described the number of patients needed to decide the outcome was less than would be needed, on the average, with the equivalent fixed-sample-size test.This economy in cases is a valuable feature of sequential methods.The small numbers were also determined by the comparatively high proportion of preferences required for the new drug before we were willing to recommend it.Because the procedure is so simple both methods are well suited to the trial of new drugs in a busy out-patient clinic or admission ward.Suitable patients are observed as they occur in the course of the daily work; the data
Isolated Adrenocorticotrophic Hormone Deficiency in Acute Intermittent Porphyria
Authors: ALAN D. WAXMAN
Journal: Annals of Internal Medicine (1969)

A 38-year-old white man with acute intermittent porphyria is presented. This is thought to be the first demonstrated instance of defective adrenocorticotrophic hormone (ACTH) secretion resulting from acute intermittent porphyria. He is one of three patients who have had relief of the pain associated with an attack of acute intermittent porphyria by therapy with insulin and a high carbohydrate intake.
Abstract 5662: Reductions in Atrophic E3 Ubiquitin Ligase Expression in Pulmonary Arteries Correlate With the Development of Pulmonary Hypertension
Authors: Michael L Paffett, Amie K Lund, Matthew J Campen
Journal: Circulation (2009)

Vascular remodeling in pulmonary hypertensive syndromes is driven by increased activity of nuclear factor of activated T-cells (NFAT) in smooth muscle cells. Although much is known about the regulation of NFAT activity by calcineurin, very little is known about vascular smooth muscle atrophy F-box ubiquitin E3 ligase expression, which targets calcineurin for proteosomal degradation and inhibits pathological hypertrophy. Therefore, we hypothesized the ubiquitin E3 ligases muscle atrophy F-box (MAFbx) and muscle ring finger (MuRF-1) expression would decline during the development of pulmonary hypertension. To investigate this hypothesis, rats were given a single injection of MCT (50 mg/kg i.p.) and indices of pulmonary hypertension (RVSP and RV/LVS) were measured at 0, 7, 14, 28 and 42 days post MCT injection (n=7–10/group). Left and right pulmonary arteries were harvested from each rat at the conclusion of these measures and mRNA expression was assessed by real-time multiplex PCR analysis for MAFbx and MuRF-1. Consistent with our hypothesis, pulmonary vascular smooth muscle MAFbx and MuRF-1 expression were attenuated from 14d to 42d time points compared to 0d when normalized to b-actin mRNA expression, which correlated negatively with RVSP and right ventricular hypertrophy. Interestingly, while treatment with sildenafil from days 28 – 42 reduced RVSP and RV/LVS, MAFbx expression was further compromised. These results suggest that the E3 ubiquitin ligases MAFbx and MuRF-1 may play a role in the development of MCT-induced pulmonary hypertension.
Bronchoconstriction in the Presence of Pulmonary Embolism
Authors: VICTOR GUREWICH, DUNCAN THOMAS, MYRON STEIN, STANFORD WESSLER
Journal: Circulation (1963)

In a group of seven patients with pulmonary embolism, evidence of bronchoconstriction was found. Heparin appeared to relieve partially the observed airway obstruction. A possible common mechanism for the initiation of intravascular coagulation and the production of bronchoconstriction was considered. When other causes can be eliminated, the detection of bronchoconstriction may serve as a useful index for the early recognition of pulmonary emboli.
Hemodynamic Abnormalities in Response to Mild and Intense Upright Exercise following Operative Correction of an Atrial Septal Defect or Tetralogy of Fallot
Authors: STEPHEN E. EPSTEIN, G. DAVID BEISER, ROBERT E. GOLDSTEIN, DOUGLAS R. ROSING, DAVID R. REDWOOD, ANDREW G. MORROW
Journal: Circulation (1973)

Patients are often asymptomatic after operative correction of an atrial septal defect (ASD) or tetralogy of Fallot (TF). However, the maximal functional capacity of their hearts relative to that of normal subjects has not been defined. Twelve asymptomatic patients who had ASDs closed and 10 asymptomatic patients who had total correction of tetralogy of Fallot were evaluated by catheterization studies at rest and during mild and intense treadmill exercise. Except for small right ventricular outflow gradients in the tetralogy of Fallot group (2-21 mm Hg), data recorded at rest were normal or nearly so in each subject. However, at a level of upright exercise sufficiently intense to lower pulmonary arterial oxygen saturation to 30%, cardiac output was below that attained by normal subjects (mean, 8.9 ± 0.3 liters/min/m 2 ) in seven of 12 ASD patients (mean, 6.6 ± 0.6 liters/min/m 2 ) and in eight of 10 tetralogy of Fallot patients (mean, 6.1 ± 0.3 liters/min/m 2 ). Right ventricular (RV) outflow gradients, measured during upright exercise in six TF patients, increased in each; RV systolic pressures reached levels of 75-106 mm Hg in four of the six patients studied. No outflow gradients were observed in the ASD group. Thus, patients with operative closure of an ASD and normal hemodynamic findings at rest may have impairment of their cardiac output response to intense upright exercise in the absence of residual shunts, arrhythmias, or pulmonary arterial hypertension. Although the cardiac output response in patients with corrected tetralogy of Fallot is consistently reduced, it is remarkably good considering the complicated nature of their defect and operative repair; however, the RV outflow gradient and RV systolic pressure may increase markedly with exercise. The longterm significance of these findings remains to be determined.
CHRONIC ACETANILID POISONINGWITH REPORT OF A CASE DUE TO ABSORPTION OF THE DRUG FROM AN ULCER OF THE LEG.
Authors: JAMES B. HERRICK
Journal: JAMA (1906)

It is well known that an overdose of acetanilid may produce alarming or even fatal results and that with an average dose the same untoward symptoms may follow in one who, because of idiosyncrasy, is peculiarly sensitive to the influence of the drug. There are few physicians who have used the remedy at all extensively who have not at times seen more or less pronounced cyanosis, feeble pulse, subnormal temperature, sweating, yawning, nausea, vertigo, perhaps syncope or marked symptoms of collapse, follow its administration. The literature abounds in reports of acute toxic symptoms after acetanilid. Some of these doses have been small, 1.5 to 5 grains, yet, on the other hand, large doses have been borne with impunity. I have known 30 grains at a dose to be given for the relief of pain, this amount being often repeated, yet no unpleasant results followed. Hartge<sup>1</sup>reports 30 grams (450
Blood volume prior to and following treatment of acute cardiogenic pulmonary edema.
Authors: J Figueras, M H Weil
Journal: Circulation (1978)

Following onset of acute cardiogenic pulmonary edema in 21 patients, increases in hematocrit, plasma protein concentration, and colloid osmotic pressure were associated with decreases in plasma volume. Accordingly, there was a loss of hypo-oncotic fluid into the extravascular spaces. Following treatment with oxygen, furosemide, and morphine sulfate and reversal of clinical and radiographic signs of pulmonary edema, declines in hematocrit, plasma protein concentration, and colloid osmotic pressure were associated with increases in plasma volume. Hypo-oncotic edema fluid was therefore reabsorbed into the vascular compartment. The concept that acute heeart failure with pulmonary edema is associated with an increase in intravascular volume is therefore not supported. To the contrary, there is a reduction of blood volume during acute pulmonary edema. During reversal of acute pulmonary edema with diuresis, there was re-expansion rather than contraction of blood volume.
Kenneth Fletcher Malcolm Thomson
Authors: R. Thomson, A. Thomson, A. Thomson
Journal: BMJ (2010)

Kenneth Fletcher Malcolm Thomson was educated at Westminster School and Christ Church, Oxford. After house jobs in ear, nose, and throat (ENT) surgery at St Thomas’ Hospital and Radcliffe Infirmary, Oxford, and gaining his DLO in 1953, he did national service during 1954-6 as junior specialist in ENT, mostly …
The Reaction of the Heart to Myocardial Infarction.
Authors: Sigmundur Gudbjarnason
Journal: Annals of Internal Medicine (1964)

s1 February 1964The Reaction of the Heart to Myocardial Infarction.Sigmundur Gudbjarnason, M.D., Richard J. Bing, M.D., F.A.C.P., Chiyo Chiba, M.D., Christian DeSchryver, M.D., Jiro Yamanaka, M.D.Sigmundur Gudbjarnason, M.D.Search for more papers by this author, Richard J. Bing, M.D., F.A.C.P.Search for more papers by this author, Chiyo Chiba, M.D.Search for more papers by this author, Christian DeSchryver, M.D.Search for more papers by this author, Jiro Yamanaka, M.D.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-60-2-320_3 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptMyocardial infarction was produced in dogs by ligation of branches of the coronary arteries. The rate of incorporation of a radioactive amino acid, glycine-2-C14, into heart muscle protein was studied over a period of six weeks. Three samples were analyzed from each left ventricle close to the infarcted area: normal tissue, the infarcted area, and borderline tissue.The infarcted tissue showed a rapid diminution in protein synthesis after infarction, but already on the third day, the incorporation into the infarcted tissue rose above the normal and reached a maximum after 4 days. This reflects the early destruction and the following... This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAuthors: Sigmundur Gudbjarnason, M.D.; Richard J. Bing, M.D., F.A.C.P.; Chiyo Chiba, M.D.; Christian DeSchryver, M.D.; Jiro Yamanaka, M.D.Affiliations: Detroit, Michigan PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics 1 February 1964Volume 60, Issue 2_Part_1Page: 320-321KeywordsAmino acidsCoronary arteriesHeartInfarctionLeft ventricleLigation assayMuscle proteinsMyocardial infarctionMyocardiumProtein synthesis ePublished: 1 December 2008 Issue Published: 1 February 1964 PDF downloadLoading ...
Reaction to Sulindac
Authors: I. JON RUSSELL
Journal: Annals of Internal Medicine (1980)

Letters and Corrections1 May 1980Reaction to SulindacI. JON RUSSELL, M.D.I. JON RUSSELL, M.D.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-92-5-716_3 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptTo the editor: Since sulindac was introduced in November 1978, a number of adverse reactions have been reported, including congestive heart failure, Stevens-Johnson syndrome, toxic epidermal necrolysis, bone marrow depression, thrombocytopenia, leukopenia, gastrointestinal perforation, hepatitis, nephropathy and a number of ocular disorders (1-3). The following case illustrates a reversible systemic hypersensitivity reaction due to sulindac.A 26-year-old woman complaining of arthralgias and sinus congestion was referred to the rheumatic disease section with a presumptive diagnosis of systemic lupus erythematosus. She had a 6-year history of alopecia, bimalar sun-sensitive rash, intermittent pleurisy, arthritis, biological false-positive test for syphilis, and positive antinuclear...References1. ANDERSON R. Severe reaction associated with sulinac administration. N Engl J Med. 1979;300:735-6. CrossrefMedlineGoogle Scholar2. WOLFE P. Sulindac and Jaundice. Ann Intern Med. 1979;91:656. LinkGoogle Scholar3. GOYAN J. Editorial Board Commissioner. FDA Drug Bull. 1979;9(5):29. Google Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited bySulindac-associated hepatic injury: Analysis of 91 cases reported to the food and drug administrationChanges in body temperature after administration of antipyretics, LSD, Δ9-THC and related agents: IISulindac Hepatotoxicity: A Case Report and ReviewAnaphylactic reaction associated with sulindacPeripheral Neuropathy After Concomitant Administration of Dimethyl Sulfoxide and SulindacEffects of Sulindac on in vitro immunologic function and on prostaglandin production by human peripheral blood mononuclear leukocytesSulindac Causing a Hypersensitivity Reaction with Peripheral and Mediastinal LymphadenopathyDOUGLAS JAY SPRUNG, M.D.Anti-inflammatory analgesics and drugs used in rheumatism and goutEmpirische Untersuchung zur Analyse von Erlebniswirkungen im Bereich Finanzdienstleistungen 1 May 1980Volume 92, Issue 5Page: 716-717KeywordsArthralgiaArthritisBone marrowHeart failureHepatitis AHypersensitivityLupus erythematosusRashesSyphilisSystemic lupus erythematosus Issue Published: 1 May 1980 PDF downloadLoading ...
Cidofovir for Cytomegalovirus Retinitis: Reply
Authors: Douglas A. Jabs
Journal: Annals of Internal Medicine (1997)

Letters15 September 1997Cidofovir for Cytomegalovirus Retinitis: ReplyDouglas A. Jabs, MD, Curtis L. Meinert, PhD, and Jacob P. Lalezari, MDDouglas A. Jabs, MDJohns Hopkins University School of Medicine; Baltimore, MD 21205Johns Hopkins University School of Hygiene and Public Health; Baltimore, MD 21205Quest Clinical Research; San Francisco, CA 94115Search for more papers by this author, Curtis L. Meinert, PhDJohns Hopkins University School of Medicine; Baltimore, MD 21205Johns Hopkins University School of Hygiene and Public Health; Baltimore, MD 21205Quest Clinical Research; San Francisco, CA 94115Search for more papers by this author, and Jacob P. Lalezari, MDJohns Hopkins University School of Medicine; Baltimore, MD 21205Johns Hopkins University School of Hygiene and Public Health; Baltimore, MD 21205Quest Clinical Research; San Francisco, CA 94115Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-127-6-199709150-00016 SectionsAboutFull TextPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail IN RESPONSE:Dr. Kravcik raises several issues related to the design of clinical trials evaluating promising anti-CMV therapies. Although untreated CMV retinitis spreads throughout the retina, it does so relatively slowly. Patients with small peripheral CMV retinitis lesions are not at risk for immediate loss of visual acuity and do not require immediate institution of therapy. In clinical practice, initiation of therapy may be deferred for a short period for personal reasons. “Small peripheral” retinitis studies, such as the two clinical trials of cidofovir reported in Annals, enroll only patients who are at low risk for visual loss, and they ...References1. Jabs DA. Ocular manifestations of HIV infection. Trans Am Ophthalmol Soc. 1995; 93:623-83. Google Scholar2. Drew WL, Miner RC, Busch, DF, Follansbee SE, Gullet J, Mehalko SG, et al. Prevalence of resistance in patients receiving ganciclovir for serious cytomegalovirus infection. J Infect Dis. 1991; 163:716-9. Google Scholar Author, Article, and Disclosure InformationAffiliations: Johns Hopkins University School of Medicine; Baltimore, MD 21205Johns Hopkins University School of Hygiene and Public Health; Baltimore, MD 21205Quest Clinical Research; San Francisco, CA 94115 PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics 15 September 1997Volume 127, Issue 6Page: 490-491KeywordsClinical trial reportingCytomegalovirus infectionDrug administrationDrugsLesionsRetinitisRisk managementSafetySafety studiesVisual acuity Issue Published: 15 September 1997 CopyrightCopyright © 1997 by American College of Physicians. All Rights Reserved.PDF DownloadLoading ...