tbuckley/cabot-search huggingface dataset:
Extended Follow-Up of Patients With Hairy Cell Leukemia After Treatment With Cladribine
Authors: Grant R. Goodman, Carol Burian, James A. Koziol, Alan Saven
Journal: Journal of Clinical Oncology (2003)

Hairy cell leukemia (HCL) is an uncommon, indolent, chronic B-cell lymphoproliferative disorder involving the marrow and spleen. Therapy for HCL includes splenectomy, interferon alfa-2a and alfa-2b, pentostatin, and cladribine. The purpose of this article was to report the extended follow-up of HCL patients treated with cladribine.Two hundred nine patients with HCL who were treated with cladribine had at least 7 years of follow-up. A course of cladribine constituted a 7-day continuous intravenous infusion at a dose of 0.1 mg/kg/d.Of the 207 assessable patients who had at least 7 years of follow-up, 196 (95%) achieved a complete response (CR) and 11 (5%) achieved a partial response (PR) after a single course of cladribine (overall response rate, 100%). The median first-response duration for all responders was 98 months. Seventy-six patients (37%) experienced relapse after their first course of cladribine. The median time to first relapse for all responders was 42 months. Time to treatment failure of CRs compared with PRs was statistically significant (P <.0005). The overall survival rate was 97% recorded at 108 months. Forty-seven patients developed 58 second malignancies. The observed-to-expected ratio for second malignancies was 2.03 (95% confidence interval, 1.49 to 2.71).These results confirm previous observations that single courses of cladribine administered to patients with HCL induce high response rates, the majority of which are CRs. Most patients enjoy long-lasting complete remissions, and those patients who experience relapse can be successfully re-treated with cladribine.
TREATMENT OF OCULAR METHYLROSANILINE POISONING WITH FLUORESCEIN SOLUTION
Authors: George Newton Hosford
Journal: JAMA (1952)

Accidents to the eyes from aniline pencils are so rare that many ophthalmologists have never seen a case and are unaware of the great danger to vision that such an accident may involve. The first case reported occurred in 1888, 1 and reports are not uncommon for the following 20 years; since that time they are less numerous, perhaps because such pencils are now used less, and some are probably made with less toxic dyes than formerly.  A bit of the lead of an aniline pencil in the conjunctival sac or in the tissues of the eye first stains the area around it an intense blue or purple; the longer it remains the more intense the color becomes and the more widely it spreads. Edema and hyperemia are apparent in a matter of minutes, and necrosis about the site of the injury may occur in a matter of hours. Panophthalmia,
Toxic Megacolon in Fulminating Disease
Authors: Henry J. Tumen
Journal: JAMA (1965)

Toxic megacolon, occurring in fulminating ulcerative colitis, has been called the most dreaded complication of ulcerative colitis. 1 This is a valid generalization. No complication of the disease demands prompter evaluation, more constant vigilance, and more skillful management. It results from the maximum insult to the colon by the disease and by the severe damage to the muscular coats of the colon by the active inflammatory process. Degeneration and destruction of the myenteric plexuses and ganglia of the colon have also been described so that the designation toxic megacolon has been suggested. 2 It is not certain, however, that damage to the nerve plexuses is an essential pathogenic factor. Basically, the condition is one in which there is loss of effective colonic motility. Although it is logical to assume that this results from inflammatory and degenerative changes in the colonic wall, metabolic disturbances incident to the colitis, such as hypoproteinemia
1130-219 Conus branch ischemia provokes Brugada-type ST-segment changes in patients with coronary artery disease
Authors: Masaru Yamaki, Takeshi Nishiura, Toru Kaji, Mitsuru Gima, Naoki Funayama, Katsumi Ohbori, Nobuyuki Sato, Yuichiro Kawamura, Naoyuki Hasebe, Kenjiro Kikuchi
Journal: Journal of the American College of Cardiology (2004)
Failure of APSAC Thrombolysis
Authors: Mark J. Binette
Journal: Annals of Internal Medicine (1993)

Letters1 October 1993Failure of APSAC ThrombolysisMark J. Binette, MD and Frank A. Agnone Jr., MDMark J. Binette, MDSearch for more papers by this author and Frank A. Agnone Jr., MDSearch for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-119-7_Part_1-199310010-00028 SectionsAboutFull TextPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail TO THE EDITOR:We observed a 67-year-old white woman who was hospitalized for chest pain and electrocardiographic changes consistent with a posterior myocardial infarction. She received 30 units of anisoylated plasminogen streptokinase activator complex (APSAC) intravenously over 5 minutes. She subsequently completed a myocardial infarction without evidence of reperfusion by standard criteria. No laboratory evidence of a systemic lytic state was found, and cardiac catheterization showed a 100% proximal circumflex artery occlusion with a suggestion of luminal thrombus. There were no collaterals to the infarction zone, and a ventriculogram showed akinesis of the posterior wall.On hospital day 2, the ...References1. Lew AS, Neer T, Rodriquez L, Geft I, Prediman SK, Ganz W. Clinical failure of streptokinase due to an unsuspected high titer of antistreptokinase antibody. J Am Coll Cardiol. 1984; 4:183-5. Google Scholar2. Sanjeev J, Morris G. Antistreptokinase titres after intravenous streptokinase. Lancet. 1990; 335:184-5. Google Scholar3. Brugemann J, van der Meer J, Takens BH, Hillege H, Lie KI. A systemic non-lytic state and local thrombolytic failure of anistreplase (anisoylated plasminogen streptokinase activator complex, APSAC) in acute myocardial infarction. Br Heart J. 1990; 64:355-8. Google Scholar4. Rothbard RL, Anderson JL, Fitzpatrick PG, Hakworthy RA, Sorensen SG, Marder VJ. Tolerance and complications in a multicenter trial of intravenous APSAC and intracoronary streptokinase in acute myocardial infarction. Clin Cardiol. 1990; 13(Suppl 5):V11-4, V27-32. Google Scholar Author, Article, and Disclosure InformationAffiliations: PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics 1 October 1993Volume 119, Issue 7_Part_1Page: 637KeywordsAntibodiesMyocardial infarctionPneumoniaReperfusionResearch laboratoriesSputumStreptococcal infectionsStreptococcusThoraxThrombosis Issue Published: 1 October 1993 CopyrightCopyright © 1993 by American College of Physicians. All Rights Reserved.PDF DownloadLoading ...
Clinicopathologic correlations in patients after myocardial infarction.
Authors: W R Roeske, R M Savage, R A O'Rourke, C M Bloor
Journal: Circulation (1981)

Little information is available relating the extent of coronary atherosclerosis and myocardial infarct size measured at autopsy to clinical information.We correlated data from 85 patients who died 1 day to 6 months after a myocardial infarction.Of 70 patients who had coronary artery analysis at the time of autopsy, 67 had significant (greater than 70%) occlusion of one or more major coronary arteries.The number of vessels with significant occlusion was not greater in patients with a history of hypertension, diabetes or lipid ab- normalities, but patients with these risk factors died at a younger age.The extent of atherosclerosis did not correlate with functional or clinical class, length of survival, or heart weight at autopsy.Almost all patients (84%) with a clinical history of two or more infarctions had two or more vessels with greater than 70% occlusion.Gross and microscopic myocardial infarct size was measured at autopsy.There was an inverse relation between the percentages of old and new infarct.Total infarct size was related to the number of vessels with significant occlusion in the four major coronary arteries.The total percentage of old infarct was increased in patients with a history of prior myocardial infarction.Left ventricular and septal rupture occurred in patients with a significantly greater amount of recent necrosis, whereas patients with left ventricular aneurysm had more old myocardial infarct with a smaller amount of new necrosis.We concluded that myocardial infarct size at autopsy is closely related to the number of vessels with greater than 70% occlusion.In addition, patients with a history of myocardial infarction or with left ventricular aneurysm have a greater extent of old infarct and total necrotic tissue than patients with only new infarcts, who more frequently die of left ventricular or septal rupture.CAREFUL STUDY of hearts of patients who die after acute myocardial infarction provides valuable in- formation on the pathogenesis and complications of coronary atherosclerosis.Analysis of postmortem data helps validate clinical diagnostic methods and identify areas where these methods are potentially inadequate or at variance with autopsy findings.The availability of patients with both standardized clinical and autopsy protocols in the Ischemic Heart Disease Specialized Center on Research (SCOR) program made possible the correlation of clinical and patho- logic data in patients with myocardial infarction. Methods PatientsThe study population was drawn from 327 patients admitted to the University of California at San Diego Medical Center with a diagnosis of myocardial infarc-
Efficient In Vivo Delivery of siRNA Into Brain Capillary Endothelial Cells Along With Endogenous Lipoprotein
Authors: Hiroya Kuwahara, Kazutaka Nishina, Kie Yoshida, Tomoko Nishina, Mariko Yamamoto, Yukari Saito, Wenying Piao, Masayuki Yoshida, Hidehiro Mizusawa, Takanori Yokota
Journal: Molecular Therapy (2011)

The brain capillary endothelial cell (BCEC) is a major functional component of the blood-brain barrier and is an underlying factor in the pathophysiology of various diseases, including brain ischemia, multiple sclerosis, and neurodegenerative disorders. We examined gene silencing in BCECs by using endogenous lipoprotein to introduce short-interfering RNA (siRNA) in vivo. A cholesterol-conjugated 21/23-mer siRNA targeting organic anion transporter 3 (OAT3) mRNA (Chol-siOAT3) was intravenously injected into mice after its incorporation into extracted endogenous lipoproteins. Chol-siOAT3 was not delivered to neurons or glia, but was successfully delivered into BCECs and resulted in a significant reduction of OAT3 mRNA levels when injected after its incorporation into high-density lipoprotein (HDL). Efficient delivery was not achieved, however, when Chol-siOAT3 was injected without any lipoproteins, or after its incorporation into low-density lipoprotein (LDL). Investigations in apolipoprotein E (ApoE)-deficient and LDL receptor (LDLR)-deficient mice revealed that the uptake of HDL-containing Chol-siOAT3 was mainly mediated by ApoE and LDLR in mice. These findings indicate that siRNA can be delivered into BCECs in vivo by using endogenous lipoprotein, which could make this strategy useful as a new gene silencing therapy for diseases involving BCECs.
Prognostic value of Ki67 antigen expression in basal cell carcinomas
Authors: E. HEALY, B. ANGUS, C.M. LAWRENCK, J.L. REES
Journal: British Journal of Dermatology (2006)

Journal Article Prognostic value of Ki67 antigen expression in basal cell carcinomas Get access E. HEALY, E. HEALY Department of Dermatology, Universiy of Newcastle upon type NH I 4LP, U.K. Search for other works by this author on: Oxford Academic Google Scholar B. ANGUS, B. ANGUS Pathology, Universiy of Newcastle upon type NH I 4LP, U.K. Search for other works by this author on: Oxford Academic Google Scholar C.M. LAWRENCK, C.M. LAWRENCK Department of Dermatology, Universiy of Newcastle upon type NH I 4LP, U.K. Search for other works by this author on: Oxford Academic Google Scholar J.L. REES J.L. REES Department of Dermatology, Universiy of Newcastle upon type NH I 4LP, U.K. Prof. J.L.Rees. Search for other works by this author on: Oxford Academic Google Scholar British Journal of Dermatology, Volume 133, Issue 5, 1 November 1995, Pages 737–741, https://doi.org/10.1111/j.1365-2133.1995.tb02748.x Published: 01 November 1995 Article history Accepted: 23 January 1995 Published: 01 November 1995
Adrenocortical carcinoma: What the surgeon needs to know. Case report and literature review
Authors: Giacomo Benassai, Vincenzo Desiato, Gianluca Benassai, Tommaso Bianco, Luigi Sivero, Rita Compagna, Gabriele Vigliotti, Gennaro Limite, Bruno Amato, Gennaro Quarto
Journal: International Journal of Surgery (2014)
Abstract analogies not primed by relations learned as object transformations
Authors: Steven Phillips
Journal: Behavioral and Brain Sciences (2008)

Abstract Analogy by priming learned transformations of (causally) related objects fails to explain an important class of inference involving abstract source-target relations. This class of analogical inference extends to ad hoc relationships, precluding the possibility of having learned them as object transformations. Rather, objects may be placed into momentarily corresponding, symbolic, source-target relationships just to complete an analogy.
Inhibitory effects of anticardiolipin antibodies on lymphocyte proliferation and neutrophil phagocytosis.
Authors: C L Yu, K H Sun, C Y Tsai, S R Wang
Journal: Annals of the Rheumatic Diseases (1991)

Anticardiolipin antibodies purified from serum from patients with systemic lupus erythematosus (SLE) by cardiolipin micelles were studied for their effects on lymphocytes and neutrophils. At a concentration of 160 micrograms/ml they markedly suppressed the [3H]thymidine incorporation of mononuclear cells stimulated by phytohaemagglutinin (4.9 (SEM 1.9%) of the control) and pokeweed mitogen (26.7 (10.5%) of the control). In addition, anticardiolipin antibodies changed the cell cycle of phytohaemagglutinin stimulated lymphocytes such that the S and G2+M phases were significantly diminished (G0/G1 = 64.62%, S = 20.59%, G2+M = 14.78% in the presence of normal human IgG v G0/G1 = 86.07%, S = 10.32%, G2+M = 3.59% in the presence of anticardiolipin antibodies). The suppression of lymphocyte proliferation by anticardiolipin antibodies was shown not to be caused by an alteration of T cell subpopulations. However, the interleukin 2 receptors on the cell surface and the soluble interleukin 2 receptors in the supernatant of phytohaemagglutinin stimulated mononuclear cells were decreased in the presence of anticardiolipin antibodies. On the other hand, the phagocytic activity of neutrophils was 40% inhibited at a higher concentration of anticardiolipin antibodies (300 micrograms/ml) through suppression of C3b/C4b and Fc receptors on polymorphonuclear leucocytes. These results suggest that anticardiolipin antibodies exert inhibitory effects on both lymphocytes and phagocytes in addition to the coagulation cascade. These newly found activities of anticardiolipin antibodies were mediated by the non-specific membranotropic property of the antibodies.
1-Year Risk-Adjusted Mortality and Costs of Percutaneous Coronary Intervention in the Veterans Health Administration
Authors: P. Michael Ho, Colin I. O’Donnell, Steven M. Bradley, Gary K. Grunwald, Christian Helfrich, Michael Chapko, Chuan-Fen Liu, Thomas M. Maddox, Thomas T. Tsai, Robert L. Jesse, Stephan D. Fihn, John S. Rumsfeld
Journal: Journal of the American College of Cardiology (2015)
Genetic Models of Human Vascular Disease
Authors: Victor J. Dzau, Gary H. Gibbons, Brian K. Kobilka, Richard M. Lawn, Richard E. Pratt
Journal: Circulation (1995)

Abstract The use of genetic models has greatly assisted investigations of the natural history, mechanisms, and potential therapy for human vascular disease. In the past, genetic models of vascular disease were obtained through serendipity and/or selective breeding to obtain inbred lines that express the phenotype of interest. This approach has yielded several valuable models of atherosclerosis and hypertension. In the past several years, the advent of molecular techniques has enabled investigators to produce additional novel genetic models of disease that have further enhanced the study of vascular biology and medicine. Transgenic techniques and the techniques of homologous recombination have allowed researchers to alter the genotype of an animal in a precise manner and to study the resultant change in phenotype. More recently, techniques of in vivo gene transfer have also accelerated and enhanced the development of novel models. The application of these methodologies has resulted in important breakthroughs in our understanding of the pathogenesis and treatment of vascular diseases. In this review, we compare and contrast these technologies along with examples of their use in the studies of vascular biology and medicine.
Cancer and Heart Research — They're Still Congressional Favorites
Authors: Daniel S. Greenberg
Journal: New England Journal of Medicine (1975)

The politics of biomedical research are condensed in a joke about the budgetary plight of the National Institute of General Medical Sciences (NIGMS), which, virtually alone among the institutes embraced by the National Institutes of Health, does not have a disease in its title — as, for example, the National Institute of Neurological and Communicative Disorders and Stroke. "Since no one ever died of general medical sciences," the joke goes, "GMS comes out worst in the budget."The reality of this witticism was in evidence on the floor of the Senate on September 26, when, for the first time, a . . .
Taking My Poison
Authors: Suzanne Bethard
Journal: JAMA (2006)

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
Replacement of 24-h creatinine clearance by 2-h creatinine clearance in intensive care unit patients: a single-center study
Authors: Manuel E. Herrera-Gutiérrez, Gemma Seller-Pérez, Esther Banderas-Bravo, Javier Muñoz-Bono, Miguel Lebrón-Gallardo, Juan F. Fernandez-Ortega
Journal: Intensive Care Medicine (2007)
Management of the Patient With Terminal Illness
Authors: Paul S. Rhoads
Journal: JAMA (1965)

When the physician is caring for a patient with a terminal illness, his duties go beyond doing everything that may reasonably be done to prolong life and relieve physical suffering. He has the obligation to tell the family, and usually the patient, the clinical facts and prognosis as truthfully as he knows them. Honesty often should be tempered with optimistic uncertainty. The physician must be in charge, refusing to listen to hindsight recriminations directed against colleagues, the patient, the patient's family, or himself after the final diagnosis has been made. With the patient's permission, he should enlist the help of the clergyman, if this has not already been done, and with him provide the spiritual support which the situation so urgently requires. How well he is able to do this will depend upon how well he, himself, has thought through the deeper problems of life and death.
ANTIPHTHISIN IN TUBERCULAR AFFECTIONS OF CHILDREN.
Authors: EDWIN KLEBS
Journal: JAMA (1895)

The therapeutic application of antiphthisin has thus far been limited to comparatively few practitioners, partly on account of limited production, and partly because the remedy was only furnished to such as gave us assurance that they would restrict its application to cases which were not too far advanced in the disease, and in which we could still hope for its beneficial effects. The reason for restriction is apparent by the well-known fact that specific medication can only be fully effective, when it is applied to pure uncomplicated cases, to the exclusion of those in which other pathologic processes are also present. It would certainly be unreasonable to demand that this remedy which has a specific germicidal effect upon the tubercle bacillus only, shall also remove and cause the cure of pathologic changes, which result remotely from the primary cause and, more unreasonable still, that the remedy shall also favorably influence
Effect of Cardiac Resynchronization Therapy on the Risk of First and Recurrent Ventricular Tachyarrhythmic Events in MADIT-CRT
Authors: Gregory Ouellet, David T. Huang, Arthur J. Moss, W. Jackson Hall, Alon Barsheshet, Scott McNitt, Helmut Klein, Wojciech Zareba, Ilan Goldenberg
Journal: Journal of the American College of Cardiology (2012)
Decline in Mortality Due to Varicella after Implementation of Varicella Vaccination in the United States
Authors: Huong Q. Nguyen, Aisha O. Jumaan, Jane F. Seward
Journal: New England Journal of Medicine (2005)

Varicella disease has been preventable in the United States since 1995. Starting in 1999, active and passive surveillance data showed sharp decreases in varicella disease. We reviewed national death records to assess the effect of the vaccination program on mortality associated with varicella.Data on deaths for which varicella was listed as an underlying or contributing cause were obtained from National Center for Health Statistics Multiple Cause-of-Death Mortality Data for 1990 through 2001. We calculated the numbers and rates of death due to varicella according to age, sex, race, ethnic background, and birthplace.The rate of death due to varicella fluctuated from 1990 through 1998 and then declined sharply. For the interval from 1990 through 1994, the average number of varicella-related deaths was 145 per year (varicella was listed as the underlying cause in 105 deaths and as a contributing cause in 40); it then declined to 66 per year during 1999 through 2001. For deaths for which varicella was listed as the underlying cause, age-adjusted mortality rates dropped by 66 percent, from an average of 0.41 death per 1 million population during 1990 through 1994 to 0.14 during 1999 through 2001 (P<0.001). This decline was observed in all age groups under 50 years, with the greatest reduction (92 percent) among children 1 to 4 years of age. In addition, by the period from 1999 through 2001, the average rates of mortality due to varicella among all racial and ethnic groups were below 0.15 per 1 million population, as compared with rates ranging from 0.37 per 1 million for whites to 0.66 per 1 million for other races in the period from 1990 through 1994.The program of universal childhood vaccination against varicella in the United States has resulted in a sharp decline in the rate of death due to varicella.