tbuckley/cabot-search huggingface dataset:
Book: Germs: Biological Weapons and America's Secret War
Authors: F. Charatan
Journal: BMJ (2001)

Judith Miller, Stephen Engelberg, William Broad 

Simon and Schuster, $27, pp 382 ISBN 0 684 87158 0

Rating: 

In 1984 the Baghwan Shree cult used Salmonella typhimurium to infect salads in 10 restaurants in the small Oregon town of The Dalles. About a thousand people became ill; 751 were confirmed to have salmonella, making it the largest outbreak in Oregon's history.

Two women leaders of the cult who fled to Germany were extradited back to the United States in 1986, tried, and convicted of attempted murder by causing the salmonella outbreak. Both were released after serving four years in a federal prison, but fled again to Europe before state charges could be brought against them.

The Baghwan Shree's attack kicks off this …
Abstract P6-11-06: A phase Ib study of LCL161, an oral inhibitor of apoptosis (IAP) antagonist, in combination with weekly paclitaxel in patients with advanced solid tumors
Authors: R Dienstmann, L Vidal, EC Dees, S Chia, EL Mayer, D Porter, T Baney, S Dhuria, SK Sen, B Firestone, D Papoutsakis, S Cameron, JR Infante
Journal: Cancer Research (2012)

Abstract Background: Impaired apoptosis is a common feature of cancer cells and may contribute to chemoresistance. LCL161 is an oral small molecule antagonist of Inhibitor of Apoptosis Proteins (IAPs) that sensitizes a subset of tumors from diverse lineages to treatment with cytotoxic therapies, including paclitaxel. Multiple breast cancer models are sensitive to LCL161 as a single agent and LCL161 acts synergistically with paclitaxel in these models. A phase I study established an LCL161 dose of 1800 mg once weekly as well tolerated, with strong evidence of pharmacodynamic activity at doses ≥320 mg. This ongoing phase Ib study defines the dose limiting toxicities (DLTs), maximum tolerated dose (MTD), safety, and pharmacokinetics (PK) of LCL161 in combination with weekly paclitaxel. Methods: Patients with advanced/metastatic solid tumors were treated with paclitaxel 80 mg/m2 each week followed by escalating doses of LCL161 administered once weekly immediately following paclitaxel. PK and biomarker sampling was performed. Results: Thirty-two patients have received LCL161 doses of 600 mg (n = 3), 1200 mg (n = 5), 1500 mg (n = 4), and 1800 mg (n = 20). The most frequent adverse events considered LCL161-related included diarrhea (n = 11; 1 Grade 3), nausea (n = 8), fatigue (n = 7; 2 Grade 3), peripheral neuropathy (n = 6; 1 Grade 3), vomiting (n = 6), decreased appetite (n = 5), alopecia (n = 4), and anemia (n = 4). The principal DLTs were neutropenia, fatigue, and neuropathy. Significant cytokine release syndrome, the DLT of single-agent LCL161, has not been observed likely due to the use of dexamethasone as a premedication. No PK interaction between LCL161 and paclitaxel was observed. RECIST partial responses have been observed in 4 patients with diverse tumor types, including breast cancer. Preliminary antitumor activity in the expansion cohort with breast cancer patients will be presented. Discussion: LCL161 and paclitaxel combination therapy is well tolerated, with manageable toxicities and no evidence of a PK interaction that might interfere with the activity of either agent. Enrollment of additional patients with breast and ovarian cancer into an expansion cohort is ongoing, utilizing an approach to identify those more likely to respond to treatment with IAP antagonists. Citation Information: Cancer Res 2012;72(24 Suppl):Abstract nr P6-11-06.
The Serum Lipids in Human Atherosclerosis
Authors: J. C. PATERSON, BETTY R. CORNISH, E. C. ARMSTRONG
Journal: Circulation (1956)

An attempt is being made to determine the relation of the serum lipids to the progression of human atherosclerosis. The serum lipids are estimated serially during life and are compared with the degree of atherosclerosis found post mortem. The findings in the first 50 fatalities in the series of 800 patients are reported. The results make a poor case for the effect of derangements of the serum lipids on the disease process. Elevation of the cholesterol-phospholipid ratio has the most suggestive atherogenic effect, but this is not consistent. The total serum cholesterol and the S f 12-20 and 20-100 lipoproteins show no significant relationships.
A novel biodegradable coronary polymer stent with drug delivery capacities: Pacitaxeal loading inhibits neointimal hyperplasia in a porcine model of coronary restenosis
Authors: Felix Vogt, Andreas Stein, Goesta Rettemeier, Nicole Krott, Rainer Hoffmann, Anja-Katrin Bosserhoff, Walter Michaeli, Sasan Habibi-Naini, Ruediger Blindt
Journal: Journal of the American College of Cardiology (2003)
NIDDM, Impaired Glucose Tolerance, and Pulmonary Function in Older Adults: The Rancho Bernardo Study
Authors: Elizabeth Barrett-Connor, Catherine Frette
Journal: Diabetes Care (1996)

OBJECTIVE To determine whether NIDDM or plasma glucose level in subjects without diabetes is associated with reduced pulmonary function in 525 men and 714 women, 51–95 years of age. RESEARCH DESIGN AND METHODS The analysis was based on data from a community-based study, the Rancho Bernardo Study. Between 1984 and 1987, 82% of community-dwelling residents had an oral glucose tolerance test. Between 1988 and 1991, 80% had lung function assessed by spirometry (forced expiratory volume in 1 s [FEV1] and forced vital capacity [FVC]). RESULTS In analyses adjusted for age, height, and cigarette smoking, pulmonary function was not associated with known or newly diagnosed NIDDM in men or women. However, FEV1 and FVC were each independently reduced in men with diabetes of 10 or more years' duration. Fasting plasma glucose (FPG) levels were correlated with FEV1 and FVC in men without diabetes. No associations were found in women. CONCLUSIONS The overall absence of an association of NIDDM with pulmonary function in these older adults may reflect survival bias and the small number of subjects with severe diabetes or diabetes of prolonged duration. The apparent relation of FPG levels to FEV1 and FVC suggests that any effect of glycemia precedes diabetes and contradicts any putative causal role for duration and severity of glycemia, however. More epidemiological studies are needed to provide further information about the relationship between NIDDM and lung function.
Recent Advances in the Understanding of Small Groups, their Disorders and Treatment
Authors: J.D. Sutherland
Journal: Psychotherapy and Psychosomatics (1965)

Research Articles| February 11 2010 Recent Advances in the Understanding of Small Groups, their Disorders and Treatment Subject Area: Psychiatry and Psychology J.D. Sutherland J.D. Sutherland The Tavistock Clinic, London Search for other works by this author on: This Site PubMed Google Scholar Psychother Psychosom (1965) 13 (1-3): 110–125. https://doi.org/10.1159/000285761 Article history Published Online: February 11 2010 Content Tools Views Icon Views Article contents Figures & tables Video Audio Supplementary Data Peer Review Share Icon Share Facebook Twitter LinkedIn Email Tools Icon Tools Get Permissions Cite Icon Cite Search Site Citation J.D. Sutherland; Recent Advances in the Understanding of Small Groups, their Disorders and Treatment. Psychother Psychosom 31 December 1965; 13 (1-3): 110–125. https://doi.org/10.1159/000285761 Download citation file: Ris (Zotero) Reference Manager EasyBib Bookends Mendeley Papers EndNote RefWorks BibTex toolbar search Search Dropdown Menu toolbar search search input Search input auto suggest filter your search All ContentAll JournalsPsychotherapy and Psychosomatics Search Advanced Search Article PDF first page preview Close Modal This content is only available via PDF. 1965Copyright / Drug Dosage / DisclaimerCopyright: All rights reserved. No part of this publication may be translated into other languages, reproduced or utilized in any form or by any means, electronic or mechanical, including photocopying, recording, microcopying, or by any information storage and retrieval system, without permission in writing from the publisher.Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug.Disclaimer: The statements, opinions and data contained in this publication are solely those of the individual authors and contributors and not of the publishers and the editor(s). The appearance of advertisements or/and product references in the publication is not a warranty, endorsement, or approval of the products or services advertised or of their effectiveness, quality or safety. The publisher and the editor(s) disclaim responsibility for any injury to persons or property resulting from any ideas, methods, instructions or products referred to in the content or advertisements. You do not currently have access to this content.
Abstract 751: Synthesis of irofulven analogs
Authors: Michael J. Kelner, Trevor C. McMorris
Journal: Cancer Research (2010)

Abstract Irofulven (NSC 683863), a semi-synthetic analog of the fungal product illudin S, that has been evaluated in a variety of phase I and II clinical trials. Promising results were noted in clinical trials against a variety of solid cancers including colon, sarcoma, prostate, liver, ovarian and pancreas. Irofulven in a randomized phase IIB trial increased median overall lifespan in patients with metastatic taxane-refractory prostate cancer [HR = 0.69]. As irofulven was the first member of the acylfulvene class of agents to be created, we synthesized several hundred analogs for further testing. Modifications were specifically made to 7 sites of the irofulven molecule including the cyclopropane ring, the chiral center, the carbonyl group, the tertiary hydroxyl site, and several nucleophilic sites. Modifications at several sites completely eliminated both the cytotoxicity and antitumor activity of the analog. Analogs with modifications at one site retained cytotoxic activity, as well as in vivo toxicity in rodents, but surprisingly eliminated antitumor activity in xenograft models. Analogs in which the tertiary hydroxyl group of irofulven was replaced with specific functional groups were noted to have an increase in tumor selectivity as noted by both cell culture and xenograft studies. Specific functional groups noted to be favorable for increased activity included carbamate, sulfonamide, and urea moieties. Additional derivatives of each of these specific functional groups were synthesized and tested in a variety of cell culture and xenograft studies including multidrug resistant models. These studies identify molecular sites critical for the antitumor activity of acylfulvenes, as well as identify promising new analogs for further investigation. Note: This abstract was not presented at the AACR 101st Annual Meeting 2010 because the presenter was unable to attend. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 751.
Erythrocyte Fluorescence in Relatives of Patients With Erythropoietic Protoporphyria
Authors: Kirk D. Wuepper
Journal: JAMA (1967)

IN 1953, Kosenow and Treibs<sup>1</sup>described a new inborn error of porphyrin metabolism which Magnus et al<sup>2</sup>later termed erythropoietic protoporphyria (EPP). Porter provided evidence that EPP was due to overproduction of protoporphyrin IX in the bone marrow.<sup>3</sup>Erythrocyte and fecal protoporphyrins and, at times, coproporphyrins are increased, but urinary porphyrins are normal in affected individuals.<sup>1</sup>Erythrocytes<sup>1,4,5</sup>and their precursors<sup>6,7</sup>have been observed to fluoresce in some cases but not in others.<sup>8</sup>A dominant form of inheritance has been suggested by several authors.<sup>6,9-12</sup>Asymptomatic relatives with "latent" EPP have been previously identified by slightly increased red blood cell (RBC) protoporphyrin concentrations.<sup>6,13,14</sup>We now report increased numbers of red-fluorescing erythrocytes with<i>normal</i>RBC protoporphyrin concentrations in four asymptomatic relatives of two patients with EPP. In addition, a sibling of one of the patients was found to have elevated RBC protoporphyrin levels and
Bisalbuminemia and Diabetes?
Authors: Adrian O. Vladutiu
Journal: JAMA (1976)

To the Editor.—  Bisalbuminemia, a condition characterized by two albumin bands on electrophoresis of serum,1is hereditary-transmitted. Several cases of induced bisalbuminemia have been reported.2Despite the differences in some properties of the alloalbumin compared to normal albumin, such as binding of thyroxine, no definite pathological condition has been ascribed so far to bisalbuminemia.3  In the last few years, we found three cases of bisalbuminemia of the fast variant among hospitalized patients. All three patients had diabetes mellitus, and a family history of diabetes was found in two of them. From the description of other cases of bisalbuminemia, we could find diabetes in four other cases.1,4,5  Since the prevalence of diabetes is high in hospitalized patients, its apparent association with bisalbuminemia might be fortuitous. Association of some forms of diabetes with a genetic trait, HLA type, was described.6In our cases, as in others,5
Tauroursodeoxycholic acid for the treatment of chronic hepatitis: A dose-response study
Authors: M PODDA
Journal: Hepatology (1995)

Background: Tauroursodeoxycholic acid (TUDCA) is of potential benefit in cholestatic disorders. However, the effects of TUDCA on cytosolic free calcium [(Ca2+)i], which regulates hepatocyte secretion, are unknown. Methods: The effect of TUDCA on (Ca2+)i was investigated in groups of isolated rat hepatocytes by microspectrofluorometry and in single cells by confocal line scanning microscopy. Results: Administration of TUDCA (5–50 μmol/L) induced a nearly fourfold increase of basal levels of (Ca2+)i. After a 15 minute treatment period, the TUDCA (10 μmol/L)-induced change in (Ca2+)i was higher than that of other monodi-, and trihydroxy bile acids at equimolar concentrations. Pretreatment with TUDCA (10 μmol/L) markedly reduced or abolished increases in (Ca2+)i induced by phenylephrine (1 μmol/L), the microsomal Ca2+ translocase inhibitor 2,5-di-(tert-butyl)-1,4-benzohydroquinone (25 μmol/L), or taurolithocholic acid (10–25 μmol/L). In Ca2+-free medium, TUDCA caused only a reduced and transient increase in (Ca2+)i. TUDCA (10 μmol/L) induced Ca2+ oscillations in all single cells that responded. However, levels of inositol-1,4,5-trisphosphate (IP3) in hepatocytes were not increased by treatment with TUDCA (10 μmol/L). Conclusions: TUDCA at physiological concentrations potently modulates (Ca2+)i signals in hepatocytes by (1) mobilizing microsomal IP3-sensitive Ca2+ stores by an IP3-independent mechanism, (2) initiating Ca2+ oscillations, and (3) inducing influx of extracellular Ca2+.
Effect of vascular endothelial growth factor on hepatic regenerative activity following partial hepatectomy in rats
Authors: Nimer Assy, Gadi Spira, Melia Paizi, Larissa Shenkar, Yehudit Kraizer, Tzafra Cohen, Gera Neufeld, Butayna Dabbah, Rafael Enat, Yaacov Baruch
Journal: Journal of Hepatology (1999)
The role of inducible nitric oxide synthase in cardiac allograft rejection
Authors: P Cannon
Journal: Cardiovascular Research (1998)

Cardiac transplantation is an effective therapy for endstage heart failure with one and five year survival rates w x about 80% and 65% respectively 1 .Despite these good results, cardiac allograft rejection remains a problem which produces impaired ventricular performance and death of cardiac myocytes ultimately causing congestive heart failure, low cardiac output, hypotension and reduced pressor responses to catecholamines.Chronic allograft rejection also results in the development of transplant-associated coronary atherosclerosis, a vasculopathy that produces myocardial ischemia, infarction and sudden death and is the leading cause of death in cardiac transplant recipients after w x the first year 2 .Although there is a large body of evidence concerning the immunological interactions involved in cardiac allograft rejection, knowledge concerning the cellular and biochemical mechanisms responsible for contractile dysfunction and for death of heart muscle cells remains incomplete.Since an inflammatory reaction in the myocardium is an intrinsic component of the pathological changes observed during cardiac allograft rejection, our laboratory undertook an investigation of the participation of nitric oxide synthases, particularly the inducible Ž .nitric oxide synthase iNOS , in the manifestations of cardiac allograft rejection.
Paraquat induced pulmonary fibrosis in three survivors.
Authors: M Hudson, S B Patel, S W Ewen, C C Smith, J A Friend
Journal: Thorax (1991)

Pulmonary lesions following paraquat poisoning are believed to be almost invariably fatal. The three patients reports here survived despite persistent radiological change. One of the patients died after taking a larger dose of paraquat one year later, and at necropsy histological changes attributable to the two episodes of paraquat poisoning were apparent.
Abstract P1-01-02: Axillary Reverse Mapping: A Prospective Study on Feasibility, Oncologic Safety, and Lymphedema Prevention.
Authors: Carol S Connor, Marilee K McGinness, Joshua MV Mammen, Lori B Ranallo, Stephanie M LaFaver, Jennifer R Klemp, Fang Fan, Jonathan D Mahnken
Journal: Cancer Research (2012)

Abstract Withdrawn by Author Citation Information: Cancer Res 2012;72(24 Suppl):Abstract nr P1-01-02.
Does higher body mass index contribute to worse asthma control in an urban population?
Authors: Emmanuelle M. Clerisme-Beaty, Sabine Karam, Cynthia Rand, Cecilia M. Patino, Andrew Bilderback, Kristin A. Riekert, Sande O. Okelo, Gregory B. Diette
Journal: Journal of Allergy and Clinical Immunology (2009)
Silent cholinesterase gene: variations in the properties of serum enzyme in apparent homozygotes
Authors: H. M. Rubinstein, A. A. Dietz, L. K. Hodges, T. Lubrano, V. Czebotar
Journal: Journal of Clinical Investigation (1970)

The cholinesterase activity of the sera of 25 subjects diagnosed as homozygotes for the silent cholinesterase gene was studied by a sensitive enzymatic method employing several thiocholine esters and various inhibitors, and by disc electrophoretic, immunochemical, and chromatographic methods.(a) With one exception, the sera fell into two classes by all criteria. One class (type I, 16 cases) had no normal serum cholinesterase. The other class (type II, eight cases) had about 2% of apparently normal serum cholinesterase. The remaining serum was intermediate between the two classes in several respects. One explanation for these results is that there are several "silent" genes concerned; possibly these are allelic.(b) Normal sera and all silent sera contain small amounts of a cholinesterase activity labeled the residual cholinesterase. The enzyme(s) responsible has properties similar to those of acetylcholinesterase rather than serum cholinesterase. It is estimated that about 1% of the activity of normal serum against acetylthiocholine is due to this enzyme. The source of the residual cholinesterase is not yet known.
Differences in response of myosin isozyme transition of ordinary and specialized myocardium to overload.
Authors: K Nomoto, I Komuro, M Kuro-o, H Tsuchimochi, F Takaku, K Machii, Y Yazaki
Journal: Circulation Research (1988)

To investigate the response of myosin isozyme transition in specialized myocardium to cardiac overload, we examined immunohistochemically the distribution of myosin isozymes in sinus node cells of overloaded canine atria, using the monoclonal antibodies CMA19 and HMC14, which are specific for atrial myosin heavy chain (alpha-HC) and ventricular myosin heavy chain (beta-HC), respectively. Overloading in canine right atria was induced by artificial tricuspid valve regurgitation and pulmonary stenosis. Right atrial mean pressure rose to 15-20 mm Hg (n = 4) 2 months after surgery. In the working myocardium, cardiac overload caused redistribution of myosin isozymes, alpha-HC to beta-HC. Compared with the normal right atria, fewer myocytes were labeled with CMA19, but more were labeled with HMC14. However, the reactivity of sinus node cells with CMA19 and HMC14 was not changed between normal and overloaded right atria, indicating no redistribution of myosin heavy chain isozymes, alpha-HC to beta-HC. These results suggest that isozymes in myosin heavy chains in the specialized myocardium are protected from overload effects by their firm cytoskeletal framework or other mechanisms.
Drugs in anaesthetic practice.
Authors: James A. Krisher
Journal: JAMA (1963)

Not a general pharmacology text, this book presents many drugs ordinarily not considered anesthetic agents, but whose use may influence the course of anesthesia. Among these are the anticoagulants, enzymes, diuretics, hormones, antihistamines, cardiac glycosides, and oxytoxics. The most notable omissions are the antibiotics and cytotoxic agents. There are 23 chapters and an appendix in this moderate-size book. The printing is done on a good quality of paper in easily readable type. However, a certain monotony prevails because of the general absence of figures and charts. The first chapter is concerned with pharmacological principles, the last with fluids and electrolytes. Drugs are grouped according to principle action and each chapter is headed by a brief general discussion followed by individual drug-monographs. The latter are subdivided into sections on physical characteristics, indications, dosage, precautions, and toxic effects. The bibliography, not large and mainly from the British literature, is interposed throughout with
SYMPOSIUM ON THE TREATMENT OF ACUTE ANTERIOR POLIOMYELITIS
Authors: H. M. McCLANAHAN
Journal: JAMA (1910)

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