tbuckley/cabot-search huggingface dataset:
The Do-Not-Resuscitate Order
Authors: DAVID BAR-OR
Journal: Annals of Internal Medicine (1982)

Letters and Corrections1 August 1982The Do-Not-Resuscitate OrderDAVID BAR-OR, M.D.DAVID BAR-OR, M.D.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-97-2-280 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptTo the editor: I read with interest the article on the do-not-resuscitate order (1), and there are a few points I would like to raise.The word policy—even in its broadest and most lenient sense—seems inappropriate. The word suggests a rigid framework that cannot yield to the needs of both patients and physicians. General guidelines that can be adapted to the changing circumstances would serve better.The author's statement, "Do-not-resuscitate orders are compatible to maximal therapeutic care," is unrealistic. The issue of resuscitation usually is raised in cases of terminally ill patients where maximum therapeutic care will only prolong suffering....References1. MILESCRANFORDSCHULTZ SRA. The do-not-resuscitate order in a teaching hospital: considerations and a suggested policy. Ann Intern Med. 1982;97:660-4. LinkGoogle Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: 775 Kearney Street; Denver, CO 80220 PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics 1 August 1982Volume 97, Issue 2Page: 280-280KeywordsDo not resuscitate ordersResuscitation Issue Published: 1 August 1982 PDF DownloadLoading ...
Long‐term left ventricular reverse remodelling with cardiac resynchronization therapy: results from the CARE‐HF trial
Authors: Stefano Ghio, Nick Freemantle, Laura Scelsi, Alessandra Serio, Giulia Magrini, Michele Pasotti, Aparna Shankar, John G.F. Cleland, Luigi Tavazzi
Journal: European Journal of Heart Failure (2009)
Abstract 2354: A neural origin for intracranial germ cell tumors
Authors: Chris Tan
Journal: Cancer Research (2012)

Abstract Intracranial germ cell tumours (GCTs) are thought to arise from germ cells that aberrantly migrate to the brain during embryogenesis. In normal development, germ cells migrate from the hindgut towards the gonads. GCTs are found in several regions outside of the gonads and all of these are all thought to be midline structures. Therefore, the observation that GCTs occur in midline structures, and that normal germ cells migrate along the midline forms the basis of the current hypothesis for their formation. All GCTs regardless of location also share similar histology. Intracranial GCTs often occur in the ventral midline, such as the pineal and suprasellar regions. However, we challenge this model. We suggest that intracranial GCTs arise from endogenous neural progenitors in the brain rather than from misplaced germ cell progenitors. Neural stem cells have the potential to become pluripotent when Oct4 is activated. When these cells are transplanted into SCID mice they form teratomas, a type of GCT. We postulate that if only one gene is required to trigger formation of a GCT from a brain cell, that it is reasonable to suggest this as a more likely mechanism for GCT development. Oct4 is expressed in the brain until E13.5, so a delay in Oct4 silencing may allow pluripotent cells to form these tumours. Using doxycycline-dependent Oct4-expressing transgenic mice, we have shown that expression of Oct4 allows neural tissue to form teratomas. We have also surveyed the current literature which reveals that many GCTs also occur in all regions of the brain. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 2354. doi:1538-7445.AM2012-2354
Benchmarking the Physician Workforce-Reply
Authors: Steven A. Schroeder
Journal: JAMA (1997)

<h3>In Reply.</h3> —Dr Floch argues that the intrinsic uncertainties in workforce projections should persuade us to preserve the status quo—ie, to leave the current level of funding for GME unchanged. It is an argument to delight the purist, since at some level all social science research is imprecise. Nevertheless, the implications of the status quo are too significant to ignore. For example, the numbers of filled residency positions in the United States—supported by federal and tax dollars—have expanded from about 18 000 in 1980 to almost 25 000 in 1995, including nearly 7000 that are filled by IMGs.<sup>1</sup> The study by Dr Goodman and colleagues,<sup>2</sup>in which the national supply of both generalist and specialist physicians exceed 3 different benchmarks, is but the latest in a series of reports, beginning with the 1980 GMENAC report,<sup>3</sup>that predict an oversupply of physicians.<sup>2</sup>Floch is correct that GMENAC badly underestimated
Early Outcome of Mitral Valve Repair for Mitral Regurgitation
Authors: Selim İsbir, Koray Ak, Halil Ünal, Murat Sünbül, Emre Elçi, Kürşat Tigen, Yaşar Birkan, Yelda Başaran, Osman Yeşildağ, Sinan Arsan
Journal: Journal of the American College of Cardiology (2013)
Effect of Left Ventricular Hypertrophy Secondary to Chronic Pressure Overload on Transmural Myocardial 2-Deoxyglucose Uptake
Authors: Jianyi Zhang, Dirk J. Duncker, Xu Ya, Yi Zhang, Todd Pavek, Horan Wei, Hellmut Merkle, Kâmil Ugurbil, Arthur H. L. From, Robert J. Bache
Journal: Circulation (1995)

This study tested the hypothesis that 31P nuclear magnetic resonance (NMR)-detectable 2-deoxyglucose (2DG) uptake is increased in chronically pressure-overloaded hypertrophied left ventricular myocardium.31P NMR spectroscopy was used to determine the transmural distribution of high-energy phosphate levels and 2-deoxyglucose-6-phosphate (2DGP) accumulation during intracoronary infusion of 2DG (15 mumol.kg body wt-1.min-1) in eight normal dogs and in eight dogs with severe left ventricular hypertrophy (LVH) produced by ascending aortic banding. The ratio of LV weight to body weight was 8.25 +/- 0.65 g/kg in the LVH group compared with 4.35 +/- 0.11 g/kg in the normal group (P < .01). Myocardial ATP content was decreased by approximately 40% and phosphocreatine (PCr) by approximately 60% in LVH hearts. ATP values were transmurally uniform in LVH and normal hearts, whereas PCr was lower in the subendocardium (Endo) than the subepicardium (Epi) of both groups. The PCr/ATP ratio was lower in LVH hearts (1.72 +/- 0.05, 1.64 +/- 0.07, and 1.53 +/- 0.10 in Epi, midwall, and Endo, respectively) compared with normal hearts (2.36 +/- 0.05, 2.09 +/- 0.06, and 1.96 +/- 0.06; each P < .01 normal versus LVH). Arterial blood levels of glucose, insulin, and free fatty acids were comparable between groups, whereas arterial lactate and norepinephrine levels were significantly higher in the LVH group. 2DG infusion did not affect systemic hemodynamics or myocardial high-energy phosphate or inorganic phosphate levels in either group. At the end of 60 minutes of 2DG infusion, there was no detectable accumulation of 2DGP in the normal hearts. However, seven of the eight LVH hearts showed time-dependent accumulation of 2DGP, which was linearly related to the severity of hypertrophy (r = .90 for subendocardial 2DGP versus LV weight/body weight). A transmural gradient of 2DGP was present, with greatest accumulation in the subendocardium (3.3 +/- 1.6, 5.8 +/- 2.3, and 7.9 +/- 2.2 mumol/g in Epi, midwall, and Endo of the LVH hearts, respectively; P < .05 Epi versus Endo).The pressure-overloaded hypertrophied left ventricle demonstrated increased accumulation of 2DGP detected with 31P NMR spectroscopy. Accumulation of 2DGP was positively correlated with the degree of hypertrophy and was most marked in the subendocardium.
1323 THE EFFECT OF HOST IL28B GENOTYPE ON EARLY VIRAL KINETICS DURING INTERFERON-FREE TREATMENT IN PATIENTS WITH CHRONIC HEPATITIS C (CHC)
Authors: T. Chu, R. Kulkarni, E.J. Gane, S.K. Roberts, C. Stedman, P. Angus, B. Ritchie, X.Y. Lu, D. Ipe, U. Lopatin, S. Germer, V. Iglesias, R. Elston, M.M. Berrey, P.F. Smith, N.S. Shulman
Journal: Journal of Hepatology (2011)
Obstruction of the Renal Artery Producing Malignant Hypertension
Authors: Irving Imber, Robert H. Clymer
Journal: New England Journal of Medicine (1955)

ONE of the most important recognized factors in the pathogenesis of hypertension is the role of the kidney. In spite of tremendous effort the mechanism by which hypertension is produced in renal disease has remained obscure. It is our purpose to report a case in which malignant hypertension was caused by an extrinsic compression of the right renal artery and permanently relieved by removal of the right kidney. We consider this case worth adding to those already reported because the arterial obstruction was demonstrated by aortography before operation and because severe functional impairment of the contralateral kidney, which existed at . . .
TCT-440 Two-year Clinical Outcomes Of Primary Stenting Of Totally Occluded Native Coronary Arteries III (PRISON III): A Randomized Comparison Of Sirolimus-Eluting Stent Implantation With Zotarolimus-Eluting Stent Implantation For The Treatment Of Total Coronary Occlusions
Authors: Koen Teeuwen, Ben Van den Branden, Jacques Koolen, Jose Henriques, Jan Tijssen, Hans Kelder, René Van der Schaaf, Paul Vermeersch, Benno Rensing, Maarten j. Suttorp
Journal: Journal of the American College of Cardiology (2012)
Insulin-Like Growth Factor I — An Important Intrauterine Growth Factor
Authors: Jaime Guevara-Aguirre
Journal: New England Journal of Medicine (1996)

The importance of insulin-like growth factor I (IGF-I) in regulating the effects of growth hormone on postnatal growth and development is well established, but its role during the prenatal period is not. Postnatally, the synthesis and release of IGF-I and its carriers — the IGF-binding proteins — are induced by the binding of growth hormone to its receptors in the liver. IGF-II, on the other hand, is not dependent on growth hormone. IGF-I acts by means of receptors for IGF-I and perhaps insulin, and IGF-II acts by means of a mannose-6-phosphate receptor. An understanding of how the system functions prenatally . . .
Obesity, Hypertension, and Cardiovascular Disease
Authors: L. H. Kuller
Journal: JAMA (1987)

To the Editor.—  The article entitled Does Obesity Protect Hypertensives Against Cardiovascular Disease? 1 in the Dec 5,1986, issue of JAMA purports to show results inconsistent with previous studies that suggested differences in outcome between obese and non-obese hypertensives.  Table 2 in this article clearly shows no relationship between obesity and either cardiovascular deaths or coronary heart disease deaths among the normotensives, and a possible weak relationship among hypertensives, with coronary heart disease and total cardiovascular deaths primarily limited to stratum 1 only. Missing from Table 2 is the group Other cardiovascular disease  found by subtracting coronary heartdisease deaths from the total cardiovascular disease deaths. The Table is a revised version of Table 2 from the original article. There is a very strong inverse relationship between obesity and other cardiovascular diseases, in terms of both total disease and deaths, among the hypertensives. Those hypertensives in the lowest weight
Diferentially expressed adenylyl cyclase isoforms mediate secretory functions in cholangiocyte subpopulation
Authors: Mario Strazzabosco, Romina Fiorotto, Saida Melero, Shannon Glaser, Heather Francis, Carlo Spirli, Gianfranco Alpini
Journal: Hepatology (2009)

Abstract Cyclic adenosine monophosphate (cAMP) is generated by adenylyl cyclases (ACs), a group of enzymes with different tissue specificity and regulation. We hypothesized that AC isoforms are heterogeneously expressed along the biliary tree, are associated with specific secretory stimuli, and are differentially modulated in cholestasis. Small duct and large duct cholangiocytes were isolated from controls and from lipopolysaccharide-treated or α-naphthylisothiocyanate–treated rats. AC isoform expression was assessed via real-time polymerase chain reaction. Secretion and cAMP levels were measured in intrahepatic bile duct units after stimulation with secretin, forskolin, HCO 3 − /CO 2 , cholinergic agonists, and β-adrenergic agonists, with or without selected inhibitors or after silencing of AC8 or soluble adenylyl cyclase (sAC) with small interfering RNA. Gene expression of the Ca 2+ -insensitive isoforms (AC4, AC7) was higher in small duct cholangiocytes, whereas that of the Ca 2+ -inhibitable (AC5, AC6, AC9), the Ca 2+ /calmodulin-stimulated AC8, and the soluble sAC was higher in large duct cholangiocytes. Ca 2+ /calmodulin inhibitors and AC8 gene silencing inhibited choleresis and cAMP production stimulated by secretin and acetylcholine, but not by forskolin. Secretion stimulated by isoproterenol and calcineurin inibitors was cAMP-dependent and γ-aminobutyric acid–inhibitable, consistent with activation of AC9. Cholangiocyte secretion stimulated by isohydric changes in [HCO 3 − ] i was cAMP-dependent and inhibited by sAC inhibitor and sAC gene silencing. Treatment with lipopolysaccharide or α-naphthylisothiocyanate increased expression of AC7 and sAC but decreased expression of the other ACs. Conclusion: These studies demonstrate a previously unrecognized role of ACs in biliary pathophysiology. In fact: (1) AC isoforms are differentially expressed in cholangiocyte subpopulations; (2) AC8, AC9, and sAC mediate cholangiocyte secretion in response to secretin, β-adrenergic agonists, or changes in [HCO 3 − ] i , respectively; and (3) AC gene expression is modulated in experimental cholestasis. (Hepatology 2009)
Withdrawal Reaction to Diazepam
Authors: Arthur Rifkin
Journal: JAMA (1976)

<h3>To the Editor.—</h3> Major withdrawal reactions were evoked experimentally in patients taking larger than usual therapeutic doses of benzodiazepines for several weeks and who suddenly had the drug withdrawn.<sup>1</sup> Covi et al<sup>2</sup>studied the effects of abrupt withdrawal of chlordiazepoxide, 15 mg three times per day, when given for 20 weeks or longer. They found only minor abstinence symptoms. We wish to report a severe withdrawal reaction on a therapeutic dose of diazepam. <h3>Report of a Case.—</h3> The patient was a healthy, 23-year-old man who suffered from moderate anticipatory anxiety mainly related to fear of poor performance at work. Treatment with diazepam, 10 mg three times per day, brought considerable relief. After three months of drug treatment he went to an army base to fulfill his reserve duty obligation. At this time, he abruptly discontinued use of diazepam. Five days later he had two grand mal convulsions within
415. Evaluating Polyethylene Glycol (PEG) Modified Adenoviral Vectors for Cell Targeting and Detargeting and Reducing Vector Toxicity
Authors: Hoyin Mok, Michael A. Barry
Journal: Molecular Therapy (2005)

Adenovirus type 5 (Ad5) are robust gene delivery vectors in vivo, but are limited by the number of clinically relevant tissues they can transduce effectively, mostly due to the low expression of coxsackie and adenoviral receptor (CAR) in most tissues. In order to improve gene transfer to tissues that express low level of CAR, vectors are detargeted to remove the inherent tropism, reduce non-specific uptake, and add new cell-specific ligands. Towards this goal, we have chemically engineered vectors polyethylene glycol (PEG) to detarget the vector as well as add new ligands by cross-linking. We demonstrate that PEGylation detargets CAR binding and non-specific uptake by macrophages and Kupffer cells while retaining in vivo hepatocyte transduction due to physiological forces that drive the vectors onto cells expressing heparan sulfate proteoglycan and integrins. To engineer a targeted vector, we have conjugated a wide array of ligands (peptides, growth factors, antibodies) onto adenoviruses using PEG crosslinkers. We demonstrate enhanced transduction of 1) epidermal, breast and prostate cancer using Ad-PEG-EGF, 2) enhanced transduction of chronic myelogenous leukemia with Ad-PEG-anti-CD59 antibodies to target receptors expressed on acute myeloid leukemia (AML). In general, PEGylation was most effective using ligands already displaying reduced cysteines for conjugation to the maleimide group of NHS-PEG-maleimide, particularly if these cysteines were well away from the receptor binding domain of the ligand. Conjugation of antibody ligands was substantially difficult wherein great care needs to be taken to selectively disrupt select disulfide bonds or to cysteinate the molecules to provide free cysteines for conjugation without destroying ligand function.
CAMPYLOBACTER PYLORI IN ABATTOIR WORKERS: IS IT A ZOONOSIS?
Authors: D. Vaira, J. Holton, M. Londei, E. Beltrandi, P.R. Salmon, Clelia D'Anastasio, J.F. Dowsett, F. Bertoni, P. Grauenfels, L. Gandolfi
Journal: The Lancet (1988)
Postmortem urinary alcohol is unreliable in diabetes
Authors: W. Alexander
Journal: BMJ (1998)

<h3>Abstract</h3> Ste5 is a prototype of scaffold proteins that regulate activation of mitogen-activated protein kinase (MAPK) cascades in all eukaryotes. Ste5 associates with many proteins including Gβγ (Ste4), Ste11 MAPKKK, Ste7 MAPKK, Fus3 and Kss1 MAPKs, Bem1, Cdc24. Here we show that Ste5 also associates with heat shock protein 70 chaperone (Hsp70) Ssa1 and that Ssa1 and its ortholog Ssa2 are together important for Ste5 function and efficient mating responses. The majority of purified overexpressed Ste5 associates with Ssa1. Loss of Ssa1 and Ssa2 has deleterious effects on Ste5 abundance, integrity, and localization particularly when Ste5 is expressed at native levels. The status of Ssa1 and Ssa2 influences Ste5 electrophoresis mobility and formation of high molecular weight species thought to be phosphorylated, ubiquitinylated and aggregated and lower molecular weight fragments. A Ste5 VWA domain mutant with greater propensity to form punctate foci has reduced predicted propensity to bind Ssa1 near the mutation sites and forms more punctate foci when Ssa1 Is overexpressed, supporting a dynamic protein quality control relationship between Ste5 and Ssa1. Loss of Ssa1 and Ssa2 reduces activation of Fus3 and Kss1 MAPKs and <i>FUS1</i> gene expression and impairs mating shmoo morphogenesis. Surprisingly, <i>ssa1</i>, <i>ssa2</i>, <i>ssa3</i> and <i>ssa4</i> single, double and triple mutants can still mate, suggesting compensatory mechanisms exist for folding. Additional analysis suggests Ssa1 is the major Hsp70 chaperone for the mating and invasive growth pathways and reveals several chaperone-network proteins required for mating morphogenesis.
Biotherapeutic Targets for the Treatment of Allergic Airway Disease
Authors: ANTHONY J. COYLE, CLARE M. LLOYD, JOSE-CARLOS GUTIERREZ-RAMOS
Journal: American Journal of Respiratory and Critical Care Medicine (2000)

Section:ChooseTop of pageAbstract <<CYTOKINES AND CYTOKINE RE...ANTI-IgE MONOCLONAL ANTIB...CHEMOKINES AND CHEMOKINE ...MEMBERS OF THE IL-1 RECEP...COSTIMULATORY SIGNALS: CD...CONCLUSIONReferencesCITING ARTICLES
IL-6 trans-signaling promotes pancreatitis-associated lung injury and lethality
Authors: Hong Zhang, Patrick Neuhöfer, Liang Song, Björn Rabe, Marina Lesina, Magdalena U. Kurkowski, Matthias Treiber, Thomas Wartmann, Sara Regnér, Henrik Thorlacius, Dieter Saur, Gregor Weirich, Akihiko Yoshimura, Walter Halangk, Joseph P. Mizgerd, Roland M. Schmid, Stefan Rose-John, Hana Algül
Journal: Journal of Clinical Investigation (2013)

Acute lung injury (ALI) is an inflammatory disease with a high mortality rate. Although typically seen in individuals with sepsis, ALI is also a major complication in severe acute pancreatitis (SAP). The pathophysiology of SAP-associated ALI is poorly understood, but elevated serum levels of IL-6 is a reliable marker for disease severity. Here, we used a mouse model of acute pancreatitis–associated (AP-associated) ALI to determine the role of IL-6 in ALI lethality. Il6-deficient mice had a lower death rate compared with wild-type mice with AP, while mice injected with IL-6 were more likely to develop lethal ALI. We found that inflammation-associated NF-κB induced myeloid cell secretion of IL-6, and the effects of secreted IL-6 were mediated by complexation with soluble IL-6 receptor, a process known as trans-signaling. IL-6 trans-signaling stimulated phosphorylation of STAT3 and production of the neutrophil attractant CXCL1 in pancreatic acinar cells. Examination of human samples revealed expression of IL-6 in combination with soluble IL-6 receptor was a reliable predictor of ALI in SAP. These results demonstrate that IL-6 trans-signaling is an essential mediator of ALI in SAP across species and suggest that therapeutic inhibition of IL-6 may prevent SAP-associated ALI.
Pediatric Chest Roentgenology: Recognizing the Abnormal
Authors: J. S. Dunbar
Journal: JAMA (1980)

It is evident that the author has had a large experience in pediatric chest roentgenology, is interested in teaching, and has a knack of imparting information and explaining concepts about radiology, ie, he is a good teacher. This book, as the author points out, is intended for the general radiologist or the pediatrician. It is an effort, for the most part successful, to explain to these groups how chest x-ray films of children are made, and how they should be interpreted. The emphasis is on distinguishing normal from abnormal and on identifying common abnormalities. Residents in general diagnostic radiology training programs might well be added to the list of those to whom the book is directed. The book has the advantage of an easy conversational style that makes it pleasant and readable. Further advantages are large, clear type and an almost complete absence of typographical errors. There are inevitably a
Demonstration of the Ascending Colon on Tc-99m MDP Skeletal Imaging
Authors: SHIGERU KOSUDA, SHINAKO KATAGIRI, WEI JEY KA, SHINICHI TOMINAGA, SHOICHI KUSANO
Journal: Clinical Nuclear Medicine (2000)

Bone scintigraphy unexpectedly revealed increased accumulation of tracer in the ascending colon. This accumulation was proved to be swallowed urine containing tracer.
Wide Access Protocols for Breast Implants Approved
Authors: Stuart L. Nightingale
Journal: JAMA (1992)

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