tbuckley/cabot-search huggingface dataset:
Mechanism of action of EDRF on pressurized arteries: effect on K+ conductance.
Authors: K Kauser, W J Stekiel, G Rubanyi, D R Harder
Journal: Circulation Research (1989)

Experiments were performed to study the cellular mechanism of endothelium-derived relaxing factor (EDRF) on vascular smooth muscle. Rat femoral arteries were cannulated and pressurized to 100 mm Hg. Vascular smooth muscle membrane potential (Em) and diameter responses to perfusion with 5 x 10(-6) M acetylcholine (ACh) were measured in vessels precontracted with 5 x 10(-6) M norepinephrine (NE). Hyperpolarization (-35 +/- 1.2 to -66 +/- 2.0 mV) and dilation were observed during ACh administration. Both responses were abolished on removal of the endothelium with collagenase. A bioassay was developed in which two vessel segments from the same artery were connected in series. The downstream vessel was deendothelialized while the endothelium of the upstream vessel remained intact. The protocol used was the same as in the first set of measurements. Hyperpolarization and dilation were observed in both vessels during ACh perfusion. However, when the direction of the perfusate flow in the bioassay system was reversed so that the deendothelialized vessel was upstream, only the "endothelium-intact" vessel demonstrated vascular smooth muscle hyperpolarization. To examine the ionic mechanism underlying the hyperpolarization presumably by released EDRF, the Em was measured as a function of increasing extracellular potassium ([K+]o). In the presence of ACh (but not NE) the maximum depolarization produced by a decade increase of [K+]o (10-100 mM) was 50 mV. In the deendothelialized vessel, this depolarization was decreased significantly to 39 mV. Addition to the superfusate of 10 mM tetraethylammonium, a K+ channel blocker, significantly reduced the hyperpolarization caused by ACh-induced EDRF release.(ABSTRACT TRUNCATED AT 250 WORDS)
Prognosis after myocardial infarction: results of 15 year follow up.
Authors: M A Merrilees, P J Scott, R M Norris
Journal: BMJ (1984)

A total of 271 out of 757 patients who had suffered a myocardial infarction during 1966-7 were still alive after six years; these patients were subsequently followed up 15 years after the infarction. Two hundred and sixty eight (99%) of the patients alive at six years and 519 (95%) of the 549 originally discharged from hospital were traced. A coronary prognostic index, which had predicted survival both to three years and from three to six years after recovery from the infarct also predicted survival from six to 15 years after recovery. The major factor affecting survival to 15 years was age at the time of the original infarct. Among patients aged under 60 at the time of infarction women fared better than men (p = 0.027). Factors in the coronary prognostic index that were associated with impairment of left ventricular function at the time of infarction and that had predicted mortality to three years and from three to six years also predicted mortality from six to 15 years. These factors were cardiac enlargement, pulmonary venous congestion, and the presence of infarction before the index infarct. The dominant cause of death remained coronary heart disease and its complications.
Premature Rupture of Membranes not Followed by Miscarriage.
Authors: S. P. Deahofe
Journal: JAMA (1891)

<h3>Editor Jour. Am. Med. Assoc'n:</h3> —I have just read Dr. Johnson's article inThe Journalon "Premature Rupture of Membranes not Followed by Miscarriage," and would be glad to report two similar cases—not for the purpose of reporting them only, but to offer a different diagnosis, inasmuch as I think his diagnosis is misleading to the younger members of the profession. My first case, a multipara, white, aged 30 years, pregnancy advanced to the sixth month, had a flow of quite a quantity of fluid which I at the time supposed was amniotic, but the case went on to term without any further difficulty, and I concluded that I was wrong. Shortly after I met with another case, also a multipara, white, aged 28 years; pregnancy advanced to the seventh mouth. Here again was a large flow of fluid, resembling amniotic fluid, but nothing further developed, and the woman went
Physiological patterns in early morning asthma.
Authors: M R Hetzel, T J Clark, K Houston
Journal: Thorax (1977)

Sixteen asthmatic patients who regularly showed early morning falls in peak expiratory flow rate of more than 25% were studied at 06.00 hours and 14.00 hours. At 06.00 hours considerable deterioration in static lung volumes and airways resistance occurred which was typical of an attack of acute asthma. Blood gas analysis showed less variation, with mild hypoxia and a wide alveolar-arterial oxygen tension gradient throughout the study. Diurnal variation was also seen in the response of maximal mid expiratory flow rates to the inhalation of helium/oxygen mixture in seven patients, but another seven were consistently non-responders. The overall pattern of results suggests that the calibre of both large and small airways decreased at night but improvement was more complete in large airways during the day. Despite these findings patients had few symptoms at 06.00 hours when most of them showed marked reversibility after inhaling aerosol salbutamol. This phenomenon might account for the sudden nature of some asthma deaths as these often occur in the early morning. If this is the case, the minority of patients whose early morning decline in lung function was not immediately reversible would appear to be at greatest risk.
Preconditioning protects against systemic disorders associated with hepatic ischemia-reperfusion through blockade of tumor necrosis factor–induced P-selectin up-regulation in the rat
Authors: Carmen Peralta, Leticia Fernández, Julià Panés, Neus Prats, Miquel Sans, Josep Maria Piqué, Emilio Gelpí, Joan Roselló-Catafau
Journal: Hepatology (2001)

Previous studies indicate that ischemic preconditioning protects against lung injury resulting from hepatic ischemia–reperfusion (I/R) through inhibition of tumor necrosis factor (TNF) release from Kupffer cells. The present study investigated whether this effect is limited to the lung or is a generalized systemic response and explores the molecular mechanisms involved. Hepatic I/R led to an increase in neutrophil accumulation in liver, lung, and splanchnic organs. Although preconditioning did not modify neutrophil infiltration in liver during reperfusion, it conferred protection against hepatic injury associated with I/R. In remote organs, preconditioning abrogated the increase in P–selectin up–regulation, preventing neutrophil infiltration and thus reducing the oxidative stress and microvascular disorders following hepatic I/R in these organs. Administration of Abs against P–selectin or TNF previous to ischemia had the same effects as preconditioning. The effects of preconditioning on the blockade of P–selectin up–regulation probably results from inhibition of systemic TNF release from Kupffer cells. Supplementation of TNF abolished the benefits of preconditioning, whereas the injurious effects of TNF were prevented by previous blockade of P–selectin. The results of the present study suggest that ischemic preconditioning protects the liver against I/R injury by a mechanism independent of adhesion molecule expression and neutrophil accumulation. In remote organs, however, hepatic preconditioning prevents inflammatory damage by reducing the systemic TNF release from the liver and thus preventing P–selectin up–regulation.
How We Subsidize “Offshore” Medical Schools
Authors: August G. Swanson
Journal: New England Journal of Medicine (1985)

There is a growing concern in the United States that our medical schools are graduating too many physicians and our teaching hospitals are training too many residents. Although the number of students admitted to accredited medical schools in this country stopped increasing about five years ago, freshman-class enrollments have not dropped markedly since then. In discussions about reducing class size, medical school deans point out that this will have little effect on the supply of physicians if U.S. citizens who go abroad for their medical education continue to return for postgraduate education and enter practice. In 1984, 2922 U.S. citizens . . .
Characterization of the extracellular bactericidal factors of rat alveolar lining material.
Authors: J D Coonrod, R L Lester, L C Hsu
Journal: Journal of Clinical Investigation (1984)

The surfactant fraction (55,000-g pellet) of leukocyte-free rat bronchoalveolar lavage fluid contains factors that rapidly kill and lyse pneumococci. These factors were purified and identified biochemically by using a quantitative bactericidal test to monitor fractionation procedures. 91% of the antipneumococcal activity of rat surfactant was recovered in chloroform after extraction of rat surfactant with chloroform-methanol (Bligh-Dyer procedure). After chromatography on silicic acid with chloroform, acetone, and methanol, all detectable antibacterial activity (approximately 80% of the initial activity) eluted with the neutral lipids in chloroform. When rechromatographed on silicic acid with hexane, hexane-chloroform, and chloroform, the antibacterial activity eluted with FFA. Thin-layer chromatography (TLC) established that the antibacterial activity was confined to the FFA fraction. Gas-liquid chromatography showed that the fatty acid fraction contained a mixture of long-chain FFA (C12 to C22) of which 66.7% were saturated and 32.4% were unsaturated. The quantity of TLC-purified FFA needed to kill 50% of 10(8) pneumococci under standardized conditions (one bactericidal unit) was 10.6 +/- 0.5 micrograms. Purified FFA acted as detergents, causing release of [3H]choline from pneumococcal cell walls and increased bacterial cell membrane permeability, evidenced by rapid unloading of 3-O-[3H]methyl-D-glucose. FFA acting as detergents appear to account for the bactericidal and bacteriolytic activity of rat pulmonary surfactant for pneumococci.
P241Prognostic value of heart rate in patients with acute myocardial infarction
Authors: R Vucic, O Andrejic, V Zdravkovic, M Petrovic, I Simic, V Iric Cupic, D Vulovic, V Cupurdija
Journal: Cardiovascular Research (2014)

Purpose: To evaluate prognostic value of heart rate in patients with acute myocardial infarction. Patients and method: Our retrospective study included 105 patients with acute myocardial infarction. Patients were divided in two groups: I group were patients with adverse outcome (MACE (myocardial infarction, unstable angina, cardiovascular death, revascularisation, fatal/nonfatal cerebrovascular accident, aortic event) and heart failure requiring hospitalization) during one month after myocardial infarction and II group were patients without adverse outcome. We observed the presence of the following factors: heritage, heart rate at admission and its influence on one month outcome. Results: 50 patients had STEMI and 55 NSTEMI, 65 were male. 54 patients had complications one month after myocardial infarction. There is no statistically significant difference in heritage between two groups (p=1,000; Fisher's Exact test). Average heart rate in I group was 44,50 per minute and in II group was 50,00 per minute. There was statistically significant difference between groups (p=0,008). Inquiring prognostic value of the heart rate one month after myocardial infarction we used univariate binary logistic regression: adjusted hazard ratio: 1.011; 95% confidence interval: 0,998-1,024; p= 0,098. Conclusion: Lower heart rate is present in patients with adverse outcome one month after myocardial infarction, but it can not be used as a prognostic factor.
Cholesterol and Violence: Is There A Connection?
Authors: Richard F. Weinberger
Journal: Annals of Internal Medicine (1998)

Letters15 October 1998Cholesterol and Violence: Is There A Connection?Richard F. Weinberger, MDRichard F. Weinberger, MDCase Western Reserve University School of Medicine; Cleveland, OH 44106Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-129-8-199810150-00023 SectionsAboutFull TextPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail TO THE EDITOR:Dr. Golomb's article on the possible relation between cholesterol levels and violent behavior [1] raises important issues on how our interventions to improve health can unwittingly cause harm. The article did inspire me to comment on how, I believe, some in our medical and pharmaceutical community might view these concerns. Not all problems present an opportunity.“Cholesterol and serotonin are the latest debateHow lowering the former will inevitably relateTo lowering the latter and in such a stateThe heart will be healthy, the mind full of hate.Cholesterol, cholesterol, you've been such a scourge,Lower, ...REFERENCE1. Golomb BA. Cholesterol and violence: is there a connection? Ann Intern Med. 1998; 128:478-87. Google Scholar Author, Article, and Disclosure InformationAuthors: Richard F. Weinberger, MDAffiliations: Case Western Reserve University School of Medicine; Cleveland, OH 44106 PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics 15 October 1998Volume 129, Issue 8 Page: 669 Keywords Behavior Cholesterol Diet Drugs Fats Food Heart Homicide Serotonin Suicide ePublished: 15 August 2000 Issue Published: 15 October 1998 Copyright & PermissionsCopyright © 1998 by American College of Physicians. All Rights Reserved.PDF downloadLoading ...
Adenovirus mediated intratumoral gene transfer of IP-10 and IL-12 display potent antitumor synergy and improve adoptive T-cell therapy
Authors: I. Narvaiza, G. Mazzolini, M. Barajas, M. Zaratiegui, V. Schmitz, C. Qian, I. Melero, J. Prieto
Journal: Journal of Hepatology (2000)
Abstract 21142: Electromechanical Wave Imaging for Noninvasive Mapping of the 3D Electrical Activation Sequence in vivo.
Authors: Jean Provost, Wei-Ning Lee, Kana Fujikura, Elisa E Konofagou
Journal: Circulation (2010)

Cardiac conduction abnormalities constitute a major cause of death and disability worldwide. However, as of today, no noninvasive imaging technology can directly map the electrical activation seque...
The Last Dance: Encountering Death and Dying
Authors: Dorothy M. Bernstein
Journal: JAMA (1983)

Physicians are dedicated to countering death. The new technologies of medicine focus on this end. Therefore, heart transplants, intrauterine surgery, and possible tissue transplants from fetal brains to injured brains are among issues at the frontier of medicine. The focus on finding a cure is so pervasive that the physician comes to regard death as a medical failure rather than a natural event. When Barney Clark died, his mechanical heart went on beating. This book does not focus on medicine's treatment approaches to counter death but on attitudes and social customs prevalent in regarding death. Many physicians in emphasizing technical issues are less prepared to deal with these facets. It is pointed out in the book that until the beginning of this century, death took place in the home with all family members present and participating, at times even building the coffin. The physician was almost peripheral. Today, the role
Prescription Drug Discounts
Authors: Mike Mitka
Journal: JAMA (2007)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA HomeNew OnlineCurrent IssueFor Authors Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA journal
Evidence of oxidant-induced injury to epithelial cells during inflammatory bowel disease.
Authors: S J McKenzie, M S Baker, G D Buffinton, W F Doe
Journal: Journal of Clinical Investigation (1996)

Evidence of in vivo oxidant-induced injury in inflammatory bowel disease (IBD) is largely indirect. Colon epithelial crypt cells (CEC) from paired specimens of histologically normal and inflamed bowel from IBD patients with active disease were examined for altered protein thiol redox status as an indicator of oxidative damage. When CEC preparations from 22 IBD patients were labeled with the reduced-thiol-specific probe [14C]-iodoacetamide (IAM), there was decreased labeling of a number of proteins indicating oxidation of thiol groups in CEC from inflamed mucosa compared to paired normal mucosa, especially the loss of thiol labeling of a 37-kD protein which was almost completely lost. The loss of reduced protein thiol status for the 37-kD band was paralleled by loss of epithelial cell glyceraldehyde-3-phosphate dehydrogenase (GAPDH, EC 1.2.1.12) enzyme activity, an enzyme known to contain an essential reduced cysteine (Cys149) at the active site. The identity of the 37-kD protein as GADPH monomer was confirmed by NH2-terminal amino acid sequence analysis. To examine whether this type of in vivo injury could be attributed to biologically relevant oxidants produced by inflammatory cells, CEC prepared from normal mucosa were exposed to H2O2, OCl-, nitric oxide (NO), and a model chloramine molecule chloramine T (ChT) in vitro. Dose-dependent loss of IAM labeling and GAPDH enzyme activity was observed. The efficacy (IC50) against IAM labeling was OCl- >> ChT > H2O2 > NO (52 +/- 3, 250 +/- 17, 420 +/- 12, 779 +/- 120 microM oxidant) and OCl- >> ChT > NO > H2O2 (89 +/- 17, 256 +/- 11, 407 +/- 105, 457 +/- 75 microM oxidant), respectively, for GAPDH enzyme activity. This study provides direct evidence of in vivo oxidant injury in CEC from inflamed mucosa of IBD patients. Oxidation and inhibition of essential protein function by inflammatory cells is a potential mechanism of tissue injury that may contribute to the pathogenesis of the disease and supports the exploration of compounds with antioxidant activity as new therapies for IBD.
Human recombinant erythropoietin promotes differentiation of murine megakaryocytes in vitro.
Authors: T Ishibashi, J A Koziol, S A Burstein
Journal: Journal of Clinical Investigation (1987)

To determine if erythropoietin affects megakaryocytopoiesis, we measured acetylcholinesterase (AchE) activity, a marker of the murine megakaryocytic lineage, after the addition of human recombinant erythropoietin to serumless murine bone marrow cultures. Erythropoietin increased AchE activity substantially. Moreover, when the hormone was added to serumless cultures of 426 isolated single megakaryocytes derived from megakaryocytic colonies, erythropoietin induced a significant increase in the diameters of these cells. From a Bayesian analysis of the likelihood that some megakaryocytes increased in DNA content during the culture period, we estimate that 61% of the cells increased in ploidy. These data indicate that the action of erythropoietin is not restricted to the erythroid lineage.
Abstract IA7: Translational control of cancer via eIF4E/4E-BPs
Authors: Nahum Sonenberg
Journal: Cancer Research (2013)

Abstract Control of translation initiation plays an important role in cell growth, proliferation and cancer development and progression. mRNA translation is dysregulated in many cancers via a combination of protein overexpression and defects in the pathways that signal to the translation machinery. In support of the critical function of translational control in cancer is the discovery of mutations in translational components in genetic syndromes associated with cancer susceptibility. A key regulator of translation initiation is the mRNA 5'-cap-binding protein, eIF4E. eIF4E overexpression engenders transformation of rodent and human cells and causes cancer in mice. eIF4E levels and phosphorylation are elevated in many types of human cancers. Phosphorylation of eIF4E on Ser209 is required for efficient transformation by eIF4E. We generated eIF4E ‘knock-in’ mice in which Ser209 was mutated to alanine. These mice were resistant to prostate cancer induced by PTEN deletion, or cancers induced by other means. An important downstream component of the PTEN/Akt/mTOR signaling pathway, which is strongly implicated in cancer etiology, is the translation machinery. A well-characterized target of mTOR is 4E-BP1, which binds to eIF4E and inhibits cap-dependent translation. mTOR forms two distinct complexes, mTORC1 and mTORC2. mTORC1 integrates growth factor and nutrient signals to control cell proliferation (increase in cell number) and cell growth (increase in mass). mTORC1 controls these processes by stimulating mRNA translation via phosphorylation of its two major downstream targets: the 4E-binding proteins (4E-BP1, 2 and 3) and the S6 kinases (S6K1 and 2). 4E-BPs impair the assembly of the eIF4F pre-initiation complex by competing with eIF4G for binding to eIF4E, whereas S6Ks phosphorylate a number of targets including ribosomal protein S6 and eIF4B. We showed that the 4E-BPs do not affect cell size, but strongly inhibit cell proliferation, by selectively inhibiting the translation of mRNAs encoding for proliferation-promoting proteins, and proteins involved in cell cycle progression. The hyperactivation of the mechanistic/mammalian target of rapamycin (mTOR) occurs in the majority of cancers. Therefore, targeted inhibition of mTOR is an attractive anti-cancer strategy. We show that high expression of eIF4E confers increased resistance of cells to the anti-proliferative effects of asTORi. Conversely, depletion of eIF4E levels by RNAi potentiates the anti-neoplastic effects of asTORi in vitro and in vivo. Anti-sense therapy against eIF4E is presently evaluated in clinical trials against cancers. Our data indicate that combining this strategy with targeted mTOR inhibition could have increased therapeutic benefits. Citation Format: Nahum Sonenberg. Translational control of cancer via eIF4E/4E-BPs. [abstract]. In: Proceedings of the Third AACR International Conference on Frontiers in Basic Cancer Research; Sep 18-22, 2013; National Harbor, MD. Philadelphia (PA): AACR; Cancer Res 2013;73(19 Suppl):Abstract nr IA7.
La mucosectomie colique peut-elle être effectuée en ambulatoire?
Authors: S Farhat, R Coriat, S Leblanc, B Terris, F Prat, S Chaussade
Journal: Endoscopy (2010)

Introduction: La mucosectomie endoscopique est un acte endoscopique de plus en plus pratiqué permettant la résection de lésions sessiles ou planes quelquesoit leur taille. Les patients sont souvent hospitalisés du fait du terrain (comorbidité, age, traitement anticoagulant, distance domicile – hôpital) ou du risque de complications. Ces dernières sont d'autant plus fréquentes que les polypes sont de grande taille (&gt;2cm), sessile ou plan ou situés dans le colon droit. Le but de notre travail était (1) de déterminer le% de patients ayant une mucosectomie endoscopique pouvant être prise en charge en ambulatoire, et (2) d'évaluez les critères d'hospitalisation &gt;1 jour de la mucosectomie.