tbuckley/cabot-search huggingface dataset:
FELLOWSHIP AND CITIZENSHIP
Authors: R A KERN
Journal: Annals of Internal Medicine (1958)

Article1 August 1958FELLOWSHIP AND CITIZENSHIPRICHARD A. KERN, M.D., F.A.C.P.RICHARD A. KERN, M.D., F.A.C.P.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-49-2-235 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptDistinguished guests, members of the College, ladies and gentlemen:We are gathered this evening in annual convocation for the purpose of doing honor to those who have richly deserved honor at the hands of this College. They include those who have distinguished themselves as physicians, teachers and scientists, or in the cause of Internal Medicine and of this College; also a great American who has given and is giving outstanding service to his country and to mankind. Particularly are we honoring some 349 physicians, upon their completion of a long and rigorous training and the fulfillment of the exacting requirements... This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: *Presidential Address, the Thirty-ninth Annual Convocation of The American College of Physicians, Atlantic City, New Jersey, April 30, 1958.Requests for reprints should be addressed to Richard A. Kern, M.D., 3401 North Broad Street, Philadelphia 40, Pennsylvania. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics 1 August 1958Volume 49, Issue 2Page: 235-239KeywordsFellowshipsScientists ePublished: 1 December 2008 Issue Published: 1 August 1958 Copyright & PermissionsCopyright ©, 1958, by The American College of PhysiciansPDF downloadLoading ...
FACTORS CONCERNED IN THE GENESIS OF CARDIAC ARRHYTHMIAS
Authors: A M WEDD, S M TENNEY
Journal: Annals of Internal Medicine (1954)

Article1 November 1954FACTORS CONCERNED IN THE GENESIS OF CARDIAC ARRHYTHMIASALFRED M. WEDD, M.D., F.A.C.P., STEPHEN M. TENNEY, M.D.ALFRED M. WEDD, M.D., F.A.C.P.Search for more papers by this author, STEPHEN M. TENNEY, M.D.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-41-5-935 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptThe production of delirium cordis by coronary artery ligation or electrical stimulation of the ventricle was known long before Vulpian1by faradization converted the normal systole of either auricle or ventricle into the tremulous movement which he called fibrillation. In 1887 MacWilliam2demonstrated that this phenomenon was entirely muscular and that "heightened irritability" and delayed conduction were essential to its production. Through the years there have been many theories for the genesis of cardiac arrhythmias, two of which continue to receive attention, namely, reëntry of impulses and ectopic pacemakers. Mines3showed that what he called a circulating excitation, already known...Bibliography1. Vulpian A: Sur les effets de la faradization des ventricules du coeur chez le chien, Compt. rend. Soc. de biol. 26: 394, 1874. Google Scholar2. MacWilliam JA: Fibrillar contraction of the heart, J. Physiol. 8: 296, 1887. CrossrefMedlineGoogle Scholar3. Mines GR: On dynamic equilibrium in the heart, J. Physiol. 46: 349, 1913. CrossrefMedlineGoogle Scholar4. Lewis T: Observations upon flutter and fibrillation, Heart 7: 1920. Google Scholar5. PrinzmetalCordayBrillOblathKruger MEICRWHE: The auricular arrhythmias, 1952, C. C Thomas, Springfield, Ill. Google Scholar6. TenneyWedd SMAM: Disturbances of rhythm in the cold-blooded heart under aconitine, Circ. Res. 2: 28, 1954. CrossrefMedlineGoogle Scholar7. HarrisBisteniRussellBrighamFirestone ASARAJCJE: Excitatory factors in ventricular tachycardia resulting from myocardial ischemia. Potassium a major excitant, Science 119: 200, 1954. CrossrefMedlineGoogle Scholar8. WrightColemanAdelman EBPWJ: Effect of potassium on the crustacean single motor nerve fiber, Federation Proc. 13: 168, 1954. Google Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: Rochester, N. Y.*Received for publication April 29, 1954.From the Departments of Medicine and Physiology, University of Rochester School of Medicine and Dentistry. Experimental observations cited are from work done under a grant from the National Institutes of Health, National Heart Institute. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics 1 November 1954Volume 41, Issue 5Page: 935-941KeywordsArrhythmiaAtrial fibrillationCoronary arteriesDeliriumDentistryHeartLigation assayPacemakersSystole ePublished: 1 December 2008 Issue Published: 1 November 1954 PDF downloadLoading ...
Temozolomide displays anti-migratory effects in human glioblastoma cells through neuregulin down-regulation.
Authors: Florence Lefranc, Sabine Spiegl-Kreinecker, Benjamin Haibe-Kains, Gianluca Bontempi, Christine Decaestecker, Walter Berger, Robert Kiss
Journal: Cancer Research (2008)

1174  Glioblastoma (GBM) patients have a median survival expectancy of only 14 months on the current standard treatment of surgical resection, followed by adjuvant radiotherapy plus temozolomide (TMZ). At TMZ concentrations of 100µM, cytotoxicity to GBM cells in vitro seems to be exerted through pro-autophagic processes and then late apoptosis. However, we do not believe that these effects of TMZ in vitro at 100µM can explain the significant therapeutic benefits (T/C index of ≥200%) of relatively low repeat dose (40mg/kg) p.o. or i.v. administration to athymic mice bearing orthotopic xenografts of human U373 GBM cells. The current study has investigated the: i) impact of TMZ repeat i.v. dose duration on the survival of U373 bearing mice, ii) the survival of 97 GBM patients under different regimens, including surgery + radiotherapy with and without TMZ or TMZ treatment performed following relapse or as soon as radiotherapy began, iii) effects of TMZ on human GBM cell migration and iv) genome-wide effects of TMZ on U373 cells.  Our results reveal that the U373 astrocytic 1p19q non-deleted invasive cells present a methylated MGMT promoter. No clear-cut cytotoxic effects were achieved in this study with TMZup to 100µM in vitro in several GBM cell lines, although this concentration brought a significant decrease in the wound healing process of U373 cells. The therapeutic benefits of TMZ in mouse models of human GBM was found to correlate directly to the duration of treatment. In addition, the sooner TMZ treatment began, the higher the survival rate achieved. Genomic analysis of TMZ-treated U373 cells revealed 30 genes with >2 or
Abstract 2782: Targeted Delivery of Plasmid DNA by Ultrasound Following Acute Angioplasty
Authors: Linsey Phillips, Alexander L Klibanov, Ramin Zargham, Brian R Wamhoff, John A Hossack
Journal: Circulation (2007)

Introduction : Although stents have been shown to be able to deliver therapeutic drugs to the blood vessel wall, safety issues are still a concern. FDA-approved microbubble contrast reagents can be modified to carry therapeutic reagents, as well as DNA, and visualized  in vivo  by non-invasive ultrasound. Moreover, acoustic parameters can be altered to ``burst” microbubbles and increase cell permeability and reagent penetration into the target tissue. We tested the hypothesis that a reporter gene can be delivered to the vascular wall following balloon angioplasty via ultrasound-triggered microbubble delivery.   Methods : Lipid monolayer microbubbles formed by self-assembly during ultrasonic dispersion of decafluorobutane gas in an aqueous micellar mixture of phosphatidylcholine and PEG stearate with rapamycin (0.2 mg/ml). Positively charged microbubbles were coated with plasmid DNA expressing red fluorescent protein (CMV-RFP, 4 ug/ml). Acoustic parameters were optimized  in vitro  using rat aortic SMCs and applied  in vivo  in the rat carotid artery balloon injury model.   Results : Ultrasound-triggered (8 MHz, Mechanical Index = 1.9) release of CMV-RFP resulted in effective RFP expression. Release of rapamycin (final conc. 10 ng/ml) decreased proliferation by 65% in SMCs maintained in growth media. Microbubbles and/or ultrasound alone did not result in toxicity. CMV-RFP microbubbles were infused (2x10 7  bubbles/min) into the right jugular vein of a rat that had undergone balloon injury. Microbubbles were visualized in the injured left carotid artery by non-invasive ultrasound (Sequoia, Siemens). Using the same acoustic parameters to release reagents  in vitro , focused ultrasound was delivered for 5 minutes to the injured blood vessel. 3 days after CMV-RFP delivery, the animal was euthanized and vessels were processed for frozen histological cross sectioning. RFP expression was visible by fluorescence microscopy in the inner-most SMC layer of the injured vessel and not in the contralateral vessel.   Conclusion : We demonstrate that CMV-RFP can be delivered to a blood vessel following angioplasty and that this method may be useful for clinical gene therapy as well as potential drug delivery to prevent in-stent restenosis.
STUDIES ON VENOUS PRESSURE IN HEPATIC CIRRHOSIS
Authors: L K LEVY, G E BURCH
Journal: Annals of Internal Medicine (1948)

Article1 August 1948STUDIES ON VENOUS PRESSURE IN HEPATIC CIRRHOSISLOUIS K. LEVY, M.D., GEORGE E. BURCH, M.D., F.A.C.P.LOUIS K. LEVY, M.D.Search for more papers by this author, GEORGE E. BURCH, M.D., F.A.C.P.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-29-2-274 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptThis work was undertaken to evaluate venous pressure measurements in diagnosis of cirrhosis of the liver. Only patients with classical clinical manifestations of cirrhosis were included in these studies. It is interesting that no study of pressure in the veins of the collateral circulation of the liver could be found in the medical literature.Ten normal white subjects and 10 white subjects with cirrhosis, ranging in age from 23 to 81 years, were observed (tables 1 and 2). Measurementswere obtained with the subjects in the supine position and with the use of apparatus described in earlier publications.1, 2The...Bibliography1. BURCHSODEMAN GEWA: A direct method for the measurement of venous pressure: Relationship of tissue pressure to venous pressure, Jr. Clin. Invest., 1939, xviii, 31. CrossrefGoogle Scholar2. BURCHWINSOR GET: The phlebomanometer, a new apparatus for direct measurement of venous pressure in large and small veins, Jr. Am. Med. Assoc., 1943, cxxiii, 91. CrossrefGoogle Scholar3. WINSORBURCH TGE: Use of the phlebomanometer: normal venous pressure values and a study of certain clinical aspects of venous hypertension in man, Am. Heart Jr., 1946, iii, 387. CrossrefGoogle Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: *Received for publication January 31, 1948.From the Department of Medicine, Tulane University School of Medicine and Charity Hospital of Louisiana at New Orleans.Aided by grants from the Life Insurance Medical Research Fund, A War Contract No. WD-49-007-MD-389, Helis Institute for Medical Research, and the Mrs. E. J. Caire Fund for Research in Heart Disease. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited byDie Pathophysiologie und der Pathomechanismus des Ascites bei der Lebercirrhose 1 August 1948Volume 29, Issue 2Page: 274-277KeywordsCardiovascular therapyCirrhosisHospital medicineLiverResearch fundingVeins ePublished: 1 December 2008 Issue Published: 1 August 1948 PDF downloadLoading ...
Effects of Miracil D, Amodiaquin, and a Series of Other 10-Thiaxanthenones and 4-Aminoquinolines Against a Variety of Experimental Tumors &lt;italic&gt;In Vitro&lt;/italic&gt; and &lt;italic&gt;In Vivo&lt;/italic&gt;&lt;xref ref-type="fn" rid="FN1"&gt;2&lt;/xref&gt;
Authors: Erich Hirschberg, Alfred Gellhorn, Margaret R. Murray, Edward F. Elslager
Journal: JNCI Journal of the National Cancer Institute (1959)

Miracil D, a 10-thiaxanthenone with pronounced activity as a schistosomicide, exhibits a wide spectrum of carcinostatic effectiveness against a variety of transplantable mouse tumors at nontoxic dosage levels. Sarcoma 180 and lymphoid leukemia L1210 ascites respond most readily, followed by Adenocarcinomas 755 and E0771; Glioma 26 and the Ehrlich ascites carcinoma show a marginal response at best. Oral administration of the drug appears preferable to intraperitoneal injection in some instances. Amodiaquin, a 4-aminoquinoline with potent antimalarial effects, has only borderline carcinostatic activity in the same tumor spectrum. The only tumor to respond significantly after oral administration of this agent is Adenocarcinoma 755. Seventeen other 10-thiaxanthenones and 12 other 4-aminoquinolines have been compared to these 2 compounds in terms of relative cytotoxicity in tissue cultures of human and mouse brain tumors, maximum-tolerated dose levels in the mouse, and carcinostatic activity against a variety of mouse tumors. None of the miracil analogues approaches the pronounced activity of miracil D in vivo and none of the amodiaquin analogues is superior to amodiaquin in this regard. In tissue culture, many of the 10-thiaxanthenones are more active than the parent compound; there is no correlation between activity in vivo and in vitro or between either of these indices and schistosomicidal effectiveness. About half the 4-aminoquinolines are as active as amodiaquin in the brain-tumor cultures, while the others are less active; again, there is little relationship between the effects in vivo and in vitro or between either of these and antimalarial activity.
Abstract 18901: Direct Evidence that a KCNQ1 Mutation is Linked to Familial Early-onset Atrial Fibrillation
Authors: Daniel C Bartos, Jeffrey B Anderson, Rachel Bastiaenen, Jonathan N Johnson, Michael H Gollob, David J Tester, Don E Burgess, Tessa Homfray, Elijah R Behr, Michael J Ackerman, Pascale Guicheney, Brian P Delisle
Journal: Circulation (2012)

KCNQ1 encodes the voltage-gated α-subunit of the I Ks channel complex (Kv7.1), and KCNQ1 mutations are associated with multiple arrhythmia syndromes. Over the past 12 years, hundreds of different KCNQ1 mutations have been linked to congenital long QT syndrome but only three KCNQ1 variants, each identified in only one family, are linked to familial early-onset AF (&lt;50 years of age). The scant genetic linkage between KCNQ1 and early-onset AF raises the question as to whether these KCNQ1 variants actually cause familial early-onset AF or simply unmask a latent genetic predisposition. We now report that a single KCNQ1 variant, pArg231His or R231H, is identified in five unrelated families with a high penetrance of familial early-onset AF. Whole-cell patch clamp of cells heterologously expressing the obligatory I Ks β-subunit KCNE1 with wild-type KCNQ1 (WT) or WT and R231H (to mimic the patients’ genotypes) showed that cells co-expressing R231H increased current at negative and resting membrane potentials. Additionally, currents recorded from cells using a human atrial action potential (AP) waveform at physiological temperature showed that WT is minimally activated during the atrial AP and co-expression of R231H increases current measured during the atrial AP waveform by greater than 20-fold (WT, n = 10; WT &amp; R231H, n = 12, p&lt;0.0001). Simulations using a computational model of a human atrial AP also predicted that I Ks is normally minimally activated in the atria and R231H would dramatically increase I Ks and shorten the atrial AP. We conclude that KCNQ1 mutations are capable of causing familial early-onset AF by increasing I Ks during the atrial AP and shortening atrial refractoriness.
P0063 : Sofosbuvir plus ribavirin for the treatment of severe hcv recurrence after liver transplantation: Preliminary data from a single-centre experience
Authors: S. Marco, S. Martini, S. Strona, D. Arese, D. Cocchis, S. Mirabella, G. Rizza, F. Tandoi, R. Romagnoli, A. Ottobrelli, M.R. Torrani Cerenzia, F. Balzola, M. Salizzoni, M. Rizzetto
Journal: Journal of Hepatology (2015)
Abstract 15680: Predictors of Left Ventricular Remodeling and Function After Aortic Valve Replacement in Pediatric Patients With Isolated Aortic Regurgitation
Authors: Sujatha Buddhe, Wei Du, Henry Walters, Ralph Delius, Michael Pettersen
Journal: Circulation (2011)

Purpose: There is controversy regarding the appropriate timing of surgery in asymptomatic or minimally symptomatic patients with isolated aortic regurgitation. In the pediatric age group, there are...
High Frequency of Identical Lymphoma Clones Detected in Pre-Treatment Tumor and Plasma from Untreated Patients with HIV-Associated Lymphomas: Prospective Multicenter Trial of the AIDS Malignancy Consortium (AMC 064)
Authors: Nina Wagner-Johnston, Jeannette Y. Lee, Sylvia Silver, Ariela Noy, Martha P. Mims, Francois Pepin, Martin Moorhead, Malek Faham, Richard F. Ambinder
Journal: Blood (2014)
Abstract 4329: Myocardial Protein Kinase G Activity Differs in Heart Failure with Normal and Reduced Ejection Fraction
Authors: Loek van Heerebeek, Nazha Hamdani, Martin L Handoko, Jolanda van der Velden, Ger J Stienen, Hans W Niessen, Gerrit Jan Laarman, Aernout Somsen, Onze Lieve Vrouwe Gasthuis, Walter J Paulus
Journal: Circulation (2008)

Concentric left ventricular (LV) remodeling and cardiomyocyte (CM) hypertrophy characterize heart failure with normal ejection fraction (HFNEF) whereas eccentric LV remodeling and low myofilamentary density characterize heart failure with reduced ejection fraction (HFREF). In rodents, low myocardial protein kinase G (PKG) activity has been implicated in the development of pathological CM hypertrophy induced by LV pressure-overload. The present study therefore compared LV remodeling, CM hypertrophy and myocardial PKG activity in patients (pts) with HFNEF (n=36) and HFREF (n=43). All pts had been admitted to hospital for worsening heart failure (NYHA 3–4) and were free of coronary artery disease. HFNEF pts had a LVEF &gt; 50% and a LV end-diastolic pressure &gt; 16 mmHg. HFREF pts had a LVEF &lt;45%. LV remodeling was measured by LV mass/volume ratio derived from biplane LV angiograms and 2D-echocardiograms. CM hypertrophy and myocardial PKG activity were assessed in LV endomyocardial biopsies by histomorphometry of CM diameter and by immunohistochemistry using antibodies against the specific PKG substrate vasodilator stimulated phosphoprotein (VASP) and against phosphorylated VASP ((P)-VASP). Myocardial PKG activity corresponded to the ratio of (P)-VASP/VASP. LV mass/volume ratio and CM diameter were significantly larger in HFNEF than in HFREF (Table ). As evident from (P)-VASP/VASP ratio, PKG activity was lower in HFNEF than in HFREF (Table ). Conclusion: HFNEF patients have lower myocardial PKG activity than HFREF patients. This low myocardial PKG activity could contribute to CM hypertrophy and concentric LV remodeling observed in HFNEF. Raising myocardial PKG activity by phosphodiesterase 5A inhibition could be useful to limit CM hypertrophy and concentric LV remodeling in HFNEF.
Abstract 14822: Impact of Proportional Assist Ventilation on Skeletal Muscle Reoxygenation and Central Hemodynamic During Constant Work Rate Exercise in Chronic Heart Failure
Authors: Audrey Borghi-Silva, Luiz Eduardo Nery, Dirceu R de Almeida, Jose Alberto Neder
Journal: Circulation (2014)

Introduction: Progressive chronic heart failure slows the recovery of microvascular oxygen delivery and utilization, which produce deleterious implications to exercise capacity. Respiratory muscle unloading can enhance the responses to exercise thereby allowing a closer matching between skeletal muscle oxygen delivery and utilization in patients with chronic heart failure (CHF). Hypothesis: We reasoned that noninvasive ventilation administered by proportional assisted ventilation (PAV) could accelerate skeletal muscle reoxygenation after high intensity exercise in CHF humans. To test this hypothesis, we conducted a study with 12 patients with stable CHF who were randomized to receive PAV or sham ventilation during high-intensity constant work exercise and compared the effects of these interventions on oxygen pulmonary (O2p), cardiac output and [[Unable to Display Character: &amp;#8710;]][deoxi-Hb+Mb] off kinetics. Methods: Twelve patients with CHF (NYHA class II and III and left ventricle ejection fraction= 26±9%) underwent two high-intensity, constant-work rate (80% peak) cycle ergometer tests receiving PAV or sham ventilation. Off-exercise kinetics of the primary component of oxygen uptake, an index of fractional oxygen extraction by near infrared spectroscopy (~[[Unable to Display Character: &amp;#8710;]][deoxy-Hb+Mb]) in the vastus lateralis) and cardiac output (QT) by impedance cardiography were assessed. Results: PAV significantly accelerated the recovery of O2p when compared with sham τ = 56±22 vs. 77±42s, respectively, p&lt;0.05). Interestingly, PAV was associated with faster fractional O2 extraction (~[[Unable to Display Character: &amp;#8710;]][deoxy-Hb+Mb] by near-infrared spectroscopy) (τ= 31±19 vs. 42±22s, respectively, p&lt;0.05) . In addition, kinetics of QT were significantly faster with PAV than sham (τ = 39±22 vs. 78±46s, respectively, p&lt;0.05). Conclusions: These data indicate that PAV has beneficial effects on recovery of muscle metabolism and central hemodynamics after high-intensity exercise in CHF patients. Financial Support: FAPESP 2009-01842-0
Chiropractic for low back pain
Authors: A. Breen, E. Leerberg, M. D Pedigo, G. Waddell, L. G F Giles, E Ernst, W J J Assendelft
Journal: BMJ (1999)

Taking precautions with angiotensin converting enzyme inhibitors Angiotensin converting enzyme inhibitors are not proved to cause loss of renal massEditor-We agree with Kumar et al that an awareness of the high risk of atherosclerotic renal artery stenosis is important in patients with vascular disease elsewhere, particularly if treatment with angiotensin converting enzyme inhibitors is being considered. 1 We strongly disagree with the suggestion, however, that high risk patients starting treatment with angiotensin converting enzyme inhibitors should first be screened for unilateral renal artery stenosis, for two reasons.Firstly, the assertion that angiotensin converting enzyme inhibitors cause loss of renal mass is unproved.Irreversible structural damage to kidneys with renal artery stenosis may result from hypertensive nephrosclerosis, cholesterol embolisation, ischaemia as a result of tight renal artery stenosis, and, ultimately, total occlusion. 2Angiotensin converting enzyme inhibitors cause an acute decrease in glomerular filtration rate, but in cases where this proves irreversible, the likeliest explanation is progression of the underlying disease.Renal blood flow is not specifically reduced by angiotensin converting enzyme inhibitors, 3 although any drug that lowers blood pressure might reduce renal blood flow in the presence of clinically important renal artery stenosis. 4 If screening for unilateral atherosclerotic renal artery stenosis were important, it would therefore be important for all high risk patients, not only those prescribed angiotensin converting enzyme inhibitors.Secondly, however, we do not believe that screening for unilateral atherosclerotic renal artery stenosis is worth while.The rationale for screening would presumably be to prevent end stage renal failure secondary to bilateral renal artery occlusion.Evidence is lacking that percutaneous angioplasty, with or without stenting, prevents end stage renal failure in unilateral atherosclerotic renal artery stenosis. 5 Although unilateral atherosclerotic renal artery stenosis is common and easy to find in high risk patients, current evidence does not tell us how to manage it once it is found.