tbuckley/cabot-search huggingface dataset:
Idiopathic anaphylaxis: long-term follow-up, cost, and outlook
Authors: J. Krasnick, R. Patterson, K. E. Harris
Journal: Allergy (1996)

To determine the efficacy of oral corticosteroids, antihistamines, and sympathomimetics in treating patients with idiopathic anaphylaxis, the charts of 225 patients diagnosed with idiopathic anaphylaxis from 1971 to 1990 treated at a single center were reviewed. Sixty-one patients (34 females and 27 males) were available for long-term follow-up. Ages ranged from 10 to 68 years with an average of 39 years. Patients with frequent episodes were treated with a protocol of oral corticosteroids, antihistamines, and sympathomimetics. Patients with infrequent episodes were treated for acute episodes only. The number of emergency room visits, hospitalizations, intensive care unit admissions, and length of time in remission were recorded. Sixty-five percent of patients with infrequent episodes and 91% of patients with frequent episodes of idiopathic anaphylaxis went into remission. Significant decreases in emergency room visits occurred for the idiopathic anaphylaxis-generalized-frequent group (P < 0.016), the idiopathic-anaphylaxis-generalized-infrequent group (P < 0.0001), and the idiopathic anaphylaxis-angioedema-infrequent group (P < 0.039). Significant decreases in the number of hospitalizations (P < 0.022) and intensive care unit admissions (P < 0.009) occurred for the idiopathic anaphylaxis-generalized-infrequent and frequent groups, respectively. Overall, an estimated $184 740 was saved with the treatment program, for 546 patient-years. Idiopathic anaphylaxis can be controlled and remission induced in most patients. An estimated $11 million per year can be saved for patients in the USA on the basis of the estimated prevalence in this country.
Why, Oh Why, Did He Die?
Authors: R. S. Ryan
Journal: JAMA (1964)

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
The Alexander Cancer "Cure."
Authors: Solomon Solis-Cohen
Journal: JAMA (1907)

Philadelphia, July 8, 1907.  To the Editor:  —Referring to the editorial inThe Journal, July 6, 1907, on the publication inLeslie's Weeklyof the report of an alleged clinic asserted to demonstrate the usefulness of Alexander's so-called cancer cure, I would call your attention to a reprint of the article, issued as an advertising circular, so soon after the publication you have criticised as to leave little room to doubt the commercial origin and connection of both.  The old code of ethics of the American Medical Association well said, concerning nostrums, that their proprietors must confess either to gross inhumanity or to fraudulent avarice. Surely this applies in a peculiar degree to alleged cures for cancer. If a real discovery has been made in the treatment of this sad affection, it should be published to the world, as Beard has published his experience with trypsin and amylopsin, as Jacobi
Expression of a β-Adrenergic Receptor Kinase Inhibitor Reverses Dysfunction in Failing Cardiomyocytes
Authors: Andrea D. Eckhart, Walter J. Koch
Journal: Molecular Therapy (2002)

The spontaneously hypertensive heart failure (SHHF) rat shares numerous functional and molecular characteristics of human heart failure (HF), including impairment of β-adrenergic receptor (AR) signaling with decreased βAR density and coupling to adenylyl cyclase as well as increased βAR kinase (βARK1) levels and activity. We examined the effects of βARK1 inhibition on the signaling and contractile function in failing ventricular myocytes isolated from SHHF rat hearts. This was done by adenoviral-mediated gene transfer of the carboxy-terminal 194 amino acids of βARK1 (βARKct), which acts as an in vivo βARK1 inhibitor. Basal cAMP production was reduced in cells from SHHF rat hearts (n=4) compared with that found in cells isolated from the hearts of age-matched Sprague-Dawley (SD) control rats (n=8; SHHF, 2.5±0.2% conversion [3H]adenine to cAMP, versus SD, 4.2±0.2%; P<0.01), as were cAMP responses to the β-agonist iso-proterenol (ISO; SHHF, 5.2±0.2%, versus SD, 7.2±0.4%; P<0.01). Following βARKct expression, SHHF cardiomyocytes displayed a significant increase in basal (6.6±0.6%, P<0.01) and ISO-stimulated cAMP production (8.8±0.6%, P<0.01) versus failing myocytes treated with an empty adenovirus. Concerning contractile function of these cells, βARKct expression produced significant improvement in ISO (10−6 M) stimulated (n=7 hearts) cell shortening, relaxation, and contraction compared with failing cells treated with the control empty virus (βARKct, 39±11%, 70±18%, and 70±20%, versus empty virus, 1±7%, 5±5%, and 0±7%, respectively). Thus, these data indicate that targeted βARK1 inhibition via genetic manipulation is a powerful therapeutic approach for improving the function of failing cardiomyocytes.
The relationship between proteome size, structural disorder and organism complexity
Authors: Eva Schad, Peter Tompa, Hedi Hegyi
Journal: Genome biology (2011)

Abstract Background Sequencing the genomes of the first few eukaryotes created the impression that gene number shows no correlation with organism complexity, often referred to as the G-value paradox. Several attempts have previously been made to resolve this paradox, citing multifunctionality of proteins, alternative splicing, microRNAs or non-coding DNA. As intrinsic protein disorder has been linked with complex responses to environmental stimuli and communication between cells, an additional possibility is that structural disorder may effectively increase the complexity of species. Results We revisited the G-value paradox by analyzing many new proteomes whose complexity measured with their number of distinct cell types is known. We found that complexity and proteome size measured by the total number of amino acids correlate significantly and have a power function relationship. We systematically analyzed numerous other features in relation to complexity in several organisms and tissues and found: the fraction of protein structural disorder increases significantly between prokaryotes and eukaryotes but does not further increase over the course of evolution; the number of predicted binding sites in disordered regions in a proteome increases with complexity; the fraction of protein disorder, predicted binding sites, alternative splicing and protein-protein interactions all increase with the complexity of human tissues. Conclusions We conclude that complexity is a multi-parametric trait, determined by interaction potential, alternative splicing capacity, tissue-specific protein disorder and, above all, proteome size. The G-value paradox is only apparent when plants are grouped with metazoans, as they have a different relationship between complexity and proteome size.
Medical decisions must be logically defensible
Authors: C. Dyer
Journal: BMJ (1997)

Expert witnesses will have to ensure that any conclusion they reach is logically defensible if they want the court to accept it, the House of Lords has ruled.

The court ruled that City and Hackney Health Authority in east London was not liable for brain damage suffered by a 2 year old boy with respiratory difficulties who had a cardiac arrest after a senior registrar twice failed to answer a summons from a sister. The health authority admitted negligence and accepted that the boy, Patrick Bolitho, probably would not have been brain damaged had …
Airway disease and emphysema on CT: not just phenotypes of lung pathology
Authors: Peter D Paré, Pat G Camp
Journal: Thorax (2012)

group may be an issue, demonstrating that smokers are less likely to participate in lung cancer screening programmes than ex-smokers. 18 Patel et al 3 reported on the acceptance of annual CT scans, sputum cytometry and bronchoscopy surveillance in smokers and ex-smokers with mild to moderate chronic obstructive pulmonary disease (COPD) who had already consented to take part in the Lung-SEARCH trial.Although the majority of participants found the interventions acceptable, there was evidence of doubt about the value of early detection, particularly in older patients.They also found evidence to support the hypothesis that worry is a factor that deters people from participating in screening.Such considerations clearly need to be built in to costeffectiveness analyses of any national screening programme.While it is vital we continue to push for effective screening programmes, those that use current technology are likely to be of limited benefit, costly and not likely to be implemented in the near future, at least in the UK.Strenuous efforts are also needed to find better screening methods that can eventually supersede CT scanning.We simply cannot wait and have to trialdand carefully evaluateda variety of approaches to promote earlier diagnosis in patients who already have symptoms of lung cancer.Competing interests MDP is a co-author on the paper by Simon et al, though his contribution was limited to advice on some elements of the text and the conclusions rather than the design or analysis of the study.He is also a participant in the LungSEARCH trial which is the subject of the paper by Patel et al, though he is not a co-author and has not been directly involved in this sub-study or the preparation of the paper.He is the secondary care lead for the NAEDI programme.
Head of Healthcare Commission excised figures on excess deaths from Mid Staffordshire report
Authors: C. Dyer
Journal: BMJ (2011)

The last chairman of the Healthcare Commission removed figures showing that Stafford Hospital had between 400 and 1200 excess deaths between 2005 and 2008 from the commission’s final report into the hospital’s “appalling” standards of care, against the wishes of its author.

Ian Kennedy, who chaired the commission from its beginning until it was abolished in 2009, told the public inquiry into failings at Mid Staffordshire NHS Foundation Trust that he decided to excise the figures because people did not understand the statistical concept of “excess deaths.”

He said he took the action because of his experience a decade ago …
Safety and efficacy of factor IX gene transfer to skeletal muscle in murine and canine hemophilia B models by adeno-associated viral vector serotype 1
Authors: Valder R. Arruda, Joerg Schuettrumpf, Roland W. Herzog, Timothy C. Nichols, Nancy Robinson, Yasmin Lotfi, Federico Mingozzi, Weidong Xiao, Linda B. Couto, Katherine A. High
Journal: Blood (2003)
Frusemide and renal enzyme excretion.
Authors: S Harding, A J Munro
Journal: BMJ (1978)

Changing social-class distribution of heart disease SIR,-Dr M G Marmot and others (21 October, p 1109) have reported that changes in "con- sumptions of sugar and, to a lesser extent, milk" may be related to changes in social-class mortality from heart disease (non-valvular and hypertensive)-not in prevalence, as the title of the article might suggest.Their food data from the National Food Survey Commit- tee do not take into account possible social- class differences and changes in food con- sumption outside the home.Global epidemiological evidence on total consumptions indi- cates that milk is more likely than sugar to be aetiologically implicated in ischaemic heart disease.'
Quinine-induced agranulocytosis: toxic effect of quinine bisulphate on bone marrow cultures in vitro.
Authors: R Sutherland, P C Vincent, E Raik, K Burgess
Journal: BMJ (1977)

In a case of quinine-induced agranulocytosis marrow culture studies confirmed the inhibitory effect on the patient9s cells of equivalent therapeutic plasma concentrations of quinine. Similar concentrations had no effect on normal marrow cells. Quinidine, the stereoisomer of quinine, had no effect on either cells from the patient or normal cells. The results encourage the use of in-vitro bone marrow cultures for identifying drugs responsible for agranulocytosis.
Two distinct truncated variants of ankyrin associated with hereditary spherocytosis
Authors: S. Hayette, G. Carré, M. Bozon, N. Alloisio, P. Maillet, R. Wilmotte, O. Pascal, J. Reynaud, O. Reman, J.-L. Stéphan, L. Morlé, J. Delaunay
Journal: American Journal of Hematology (1998)

We present two distinct truncated variants of ankyrin associated with mild to moderate hereditary spherocytosis. Ankyrin Saint-Etienne 1 was manifested by an additional band located between bands 2.1 and 2.2. It was associated with a nonsense mutation in exon 39: TGG-->TGA; W1721X. Ankyrin Saint-Etienne 2 appeared as two faint bands underlining bands 2.1 and 2.2. It was associated with a nonsense mutation in exon 41: CGA-->TGA; R1833X. Overall ankyrin was diminished in splenectomized patients. Messenger RNAs Saint-Etienne 1 and 2 amounted to 20 and 37% of the total ankyrin mRNA, respectively. Ankyrin molecules truncated in their C-terminal region retain some ability to bind to the membrane whereas the bulk of nonsense mutations, located in more upstream regions, result in the mere disappearance of one haploid set of ankyrin. In the present cases, it was not possible to apportion the roles of ankyrin reduction and truncation in the pathogenesis of hereditary spherocytosis.
Lung Herniation after Cardiopulmonary Resuscitation
Authors: Laura D Sprague, Filippo J Ferrigni
Journal: New England Journal of Medicine (2004)

A 63-year-old man collapsed, unresponsive and pulseless, at his workplace. Security guards, using an automated external defibrillator, delivered two shocks to his chest and performed cardiopulmonary resuscitation (CPR) until paramedics arrived and intubated the patient. After the return of spontaneous circulation, he was transported to the hospital. A high-resolution computed tomographic (CT) scan confirmed the diagnosis of pulmonary embolism. The patient, whose condition by this time was hemodynamically stable, was treated without thrombolytic agents; he received unfractionated heparin and oxygen and underwent mechanical ventilation overnight. Thirty minutes after self-extubation, the patient reported dyspnea, and subcutaneous emphysema developed, which was especially . . .
Systemic Carnitine Deficiency Presenting as Familial Endocardial Fibroelastosis
Authors: Marjorie E. Tripp, Murray L. Katcher, Henry A. Peters, Enid F. Gilbert, Sunita Arya, Richard J. Hodach, Austin L. Shug
Journal: New England Journal of Medicine (1981)

ENDOCARDIAL fibroelastosis is a cardiomyopathy of unknown origin that affects infants and young children. It is characterized by poor myocardial contractility with hypertrophy and dilatation of the heart, especially of the left ventricle. At autopsy, a milky-white thickening of the endocardium is found.1 Because similar endocardial thickening is seen in congenital cardiac anomalies complicated by subendocardial ischemia (e.g., aortic atresia), it has been suggested that endocardial fibroelastosis may be related to myocardial hypoxia.2 Familial cases suggest that the disease may result from a genetically transmitted abnormality affecting cardiac metabolism.3 The cardiac tissue in congestive cardiomyopathy contains increased numbers of mitochondria, . . .
29 The extension of LT criteria to patients with HCC ⩽5 nodules with a maximal diameter ⩽5cm does not alter 5-year survival
Authors: C. Duvoux, T. Decaens, S. Bresson-Hadni, C. Mayer, J. Gugenheim, F. Durand, Ph. Bernard, O. Boillot, K. Boudjema, Gp. Pageaux, O. Chazouillères, D. Cherqui, F. Roudot-Thoraval
Journal: Journal of Hepatology (2006)
Screening men aged over 65 for abdominal aortic aneurysms could save lives
Authors: Susan Mayor
Journal: BMJ (2007)

A meta-analysis of 42 trials of the type 2 diabetes drug rosiglitazone (Avandia) has shown a significantly raised risk of myocardial infarction and an increase in cardiovascular deaths that did not quite reach statistical significance (New England Journal of Medicine 2007 May 21 doi: 10.1056/ NEJMoa072761).The analysis by Steven Nissen and Kathy Wolski, of the Cleveland Clinic, Cleveland, Ohio, included 15 560 patients randomly assigned to regimens that included rosiglitazone, and 12 283 patients assigned to regimens that did not.The mean age of patients was 56 years, and the mean baseline glycated haemoglobin concentration was about 8.2%.Patients receiving rosiglitazone had an odds ratio for myocardial infarction of 1.43 (95% confidence interval 1.03 to 1.98, P=0.03).The odds ratio for death from cardiovascular causes was 1.64 (0.98 to 2.74, P=0.06).An editorial (doi: 10.1056/NEJMe078099) criticised the Food and Drug Administration for approving the drug on the basis of only its efficacy in glycaemic control in short term studies and also for a poor system for reporting adverse events after marketing.Bruce Psaty of the University of Washington in Seattle and Curt Furberg of Wake Forest University in Winston-Salem, North Carolina, also say that the Food and Drug Administration Revitalization Act, now moving through Congress, should be strengthened so that the FDA can follow a drug through its life cycle, with new emphasis on postmarketing.The FDA posted a safety alert on its website, cautioning patients taking the drug who have heart disease or are at high risk of a heart attack to talk to their doctors (www.fda.gov).GlaxoSmithKline said it "strongly disagrees" with the findings (www.gsk.com). Study links diabetes drug to heart deathsUK
Persistent Immunologic Abnormalities in Long-Term Survivors of Advanced Hodgkin's Disease
Authors: RICHARD I. FISHER
Journal: Annals of Internal Medicine (1980)

Immunologic studies were done on 47 long-term survivors of Hodgkin's disease who had been treated with MOPP chemotherapy (mechlorethamine, vincristine, procarbazine, and prednisone). Percentages of E rosettes and mitogen-induced lymphocyte proliferation were significantly reduced compared to those in normal control subjects. There was no tendency for these abnormalities to return to the normal range with increasing disease-free intervals. No abnormalities of B-cell number or function were detected. Long-term survivors of advanced diffuse histiocytic lymphoma treated with comparable chemotherapy, who served as a control population, had significantly higher percentages of E rosettes and no reduction in mitogen-induced lymphocyte proliferation. Thus these persistent immunologic abnormalities cannot be attributed to chemotherapy alone. The presence of similar immunologic abnormalities in untreated patients with Hodgkin's disease of all stages and in patients cured by either MOPP or radiotherapy suggests that depressed cellular immunity may be an inherent characteristic of the person in whom Hodgkin's disease develops.
Cationization of catalase, peroxidase, and superoxide dismutase. Effect of improved intraarticular retention on experimental arthritis in mice.
Authors: J Schalkwijk, W B van den Berg, L B van de Putte, L A Joosten, L van den Bersselaar
Journal: Journal of Clinical Investigation (1985)

Several enzymes and other proteins were made cationic either by coupling to polylysine or by shielding of anionic sites. These cationic proteins, all having an isoelectric point greater than 8.5 exhibited excellent retention in articular structures when injected in mouse knee joints. Autoradiography and histochemistry showed that cationic forms of catalase, superoxide dismutase, and horseradish peroxidase were firmly retained by synovial and cartilaginous tissues. The half-life of these enzymes in the joint is thus significantly extended compared with native enzymes. The native enzymes and their cationic derivatives were tested for antiinflammatory properties in mice, using antigen-induced arthritis and zymosan-induced arthritis. It was found that injection of cationic catalase or peroxidase induced a marked suppression of some parameters of the inflammatory response in both types of arthritis, as measured by 99m technetium pertechnetate uptake and leakage of 125I-labeled albumin. Native catalase and peroxidase were less, or not at all effective. Cationic superoxide dismutase or cationic nonenzyme proteins did not suppress inflammation. The observed suppression of two different types of inflammation (an immune and a nonimmune arthritis) by catalase and peroxidase suggests that elimination of peroxides contributes to the suppression of an inflammatory response. We would hypothesize that cationic enzymes offer the possibility for investigating the mechanisms of inflammation and, in addition, might be interesting from a therapeutical point of view.
Yield of Routine Annual Laboratory Tests in a Skilled Nursing Home Population
Authors: Mark R. Levinstein
Journal: JAMA (1987)

The yield of routinely performed annual panels of laboratory tests was examined among patients in the skilled nursing facility section of a large, multilevel, long-term—care institution. Of 9270 tests done as part of 336 annual panels in 121 patients over an eight-year period, 17% of the tests yielded abnormal results, and in 36% of the tests, abnormal results were new. Among the 336 panels, 56 (16.7%) had at least one abnormality that was believed to have resulted in some benefit to 30 (24.7%) of the patients. Many of the abnormalities that led to patient benefit could have been detected by periodic monitoring of chronic conditions and their treatment as opposed to true screening tests, and all such abnormalities could have been identified by a complete blood cell count, electrolyte determinations, renal and thyroid function tests, and a urinalysis. The results suggest that a modest panel of annual laboratory tests could limit the potential costs of screening and not result in the loss of potential benefits to patients in skilled nursing facilities. (<i>JAMA</i>1987;258:1909-1915)