tbuckley/cabot-search huggingface dataset:
Cardiac signs for students: the wheat and the chaff.
Authors: J K Finlayson, A C Kenmure, D S Short
Journal: BMJ (1978)

Cardiology has undergone some of the greatest transitions of any branch of medicine in recent years. Not only has technologi cal improvement increased the therapeutic possibilities but the pattern of disease has also changed greatly since the beginning of the century. Nevertheless, the teaching of clinical cardiology has remained remarkably static through the years, and students are still often encumbered with unreliable methods and outdated physical signs that have little relevance to most of the patients they will encounter in practice. Moreover, there is a conspicuous lack of uniformity about the teaching of physical signs and their meaning not only among different medical schools but even among different clinics in the same hospital. There is an urgent need to re-examine our teaching methods and reach agreement about what should and should not be taught. The following proposals are presented as a basis for dis cussion. They are founded on our combined experience of over 60 years of teaching and examining students, and they have been tested by the discipline of a weekly consultative clinic at which we compare our findings after examining the patients and before we know the results of the investigations.
Effects of Stroke on Medical Resource Use and Costs in Acute Myocardial Infarction
Authors: Chen Y. Tung, Christopher B. Granger, Michael A. Sloan, Eric J. Topol, J. David Knight, W. Douglas Weaver, Kenneth W. Mahaffey, Harvey White, Nancy Clapp-Channing, Maarten L. Simoons, Joel M. Gore, Robert M. Califf, Daniel B. Mark
Journal: Circulation (1999)

Stroke occurs concurrently with myocardial infarction (MI) in approximately 30 000 US patients each year. This number is expected to rise with the increasing use of thrombolytic therapy for MI. However, no data exist for the economic effect of stroke in the setting of acute MI (AMI). The purpose of this prospective study was to assess the effect of stroke on medical resource use and costs in AMI patients in the United States.Medical resource use and cost data were prospectively collected for 2566 randomly selected US GUSTO I patients (from 23 105 patients) and for the 321 US GUSTO I patients who developed non-bypass surgery-related stroke during the baseline hospitalization. Follow-up was for 1 year. All costs are expressed in 1993 US dollars. During the baseline hospitalization, stroke was associated with a reduction in cardiac procedure rates and an increase in length of stay, despite a hospital mortality rate of 37%. Together with stroke-related procedural costs of $2220 per patient, the baseline medical costs increased by 44% ($29 242 versus $20 301, P<0.0001). Follow-up medical costs were substantially higher for stroke survivors ($22 400 versus $5282, P<0.0001), dominated by the cost of institutional care. The main determinant for institutional care was discharge disability status. The cumulative 1-year medical costs for stroke patients were $15 092 higher than for no-stroke patients. Hemorrhagic stroke patients had a much higher hospital mortality rate than non-hemorrhagic stroke patients (53% versus 15%, P<0.001), which was associated with approximately $7200 lower mean baseline hospitalization cost. At discharge, hemorrhagic stroke patients were more likely to be disabled (68% versus 46%, P=0.002).In this first large prospective economic study of stroke in AMI patients, we found that strokes were associated with a 60% ($15 092) increase in cumulative 1-year medical costs. Baseline hospitalization costs were 44% higher because of longer mean lengths of stay. Stroke type was a key determinant of baseline cost. Follow-up costs were more than quadrupled for stroke survivors because of the need for institutional care. Disability level was the main determinant of institutional care and thus of follow-up costs.
The Importance of Bence-Jones Albumosuria in Diagnosis
Authors: E. S. Reynolds
Journal: BMJ (1926)

r T475original haemorrhage than -a recuirrence.One, aged 35, lhad a recurrence after eight months and became normal; two (aged 32 and 37) after a year and became normal; one (aged 38) recurred after four months; anid onie -(aged 39) after seven months.
Stimulus specificity of the generation of leukotrienes by dog mastocytoma cells.
Authors: E J Goetzl, M J Phillips, W M Gold
Journal: The Journal of Experimental Medicine (1983)

Isolated dog mastocytoma cells sensitized with dog anti-ragweed IgE and challenged with ragweed antigen or incubated with ionophore A23187 or the carboxy-terminal dodecapeptide of platelet factor 4, PF4(59-70), release histamine and concurrently generate leukotrienes B4, C4, and D4. In contrast, the exposure of mastocytoma cells to 0.1-3 micrograms/ml of 15-hydroxyeicosatetraenoic acid (15-HETE) stimulates selectively the generation of leukotrienes, in the absence of histamine release, while 0.1-1 micrograms/ml of compound 48/80 releases histamine without enhancing the generation of leukotrienes. That natural stimuli are capable of selectively activating one synthetic or secretory compartment of mast cells suggests that separate subsets of receptors as well as different biochemical events may serve to mobilize each class of mediators.
Benzene Metabolite 1,2,4-Benzenetriol Induces Halogenated DNA and Tyrosines Representing Halogenative Stress in the HL-60 Human Myeloid Cell Line
Authors: Takuro Nishikawa, Emiko Miyahara, Masahisa Horiuchi, Kimiko Izumo, Yasuhiro Okamoto, Yoshichika Kawai, Yoshifumi Kawano, Toru Takeuchi
Journal: Environmental Health Perspectives (2011)

Although benzene is known to be myelotoxic and to cause myeloid leukemia in humans, the mechanism has not been elucidated.We focused on 1,2,4-benzenetriol (BT), a benzene metabolite that generates reactive oxygen species (ROS) by autoxidation, to investigate the toxicity of benzene leading to leukemogenesis.After exposing HL-60 human myeloid cells to BT, we investigated the cellular effects, including apoptosis, ROS generation, DNA damage, and protein damage. We also investigated how the cellular effects of BT were modified by hydrogen peroxide (H2O2) scavenger catalase, hypochlorous acid (HOCl) scavenger methionine, and 4-aminobenzoic acid hydrazide (ABAH), a myeloperoxidase (MPO)-specific inhibitor.BT increased the levels of apoptosis and ROS, including superoxide (O2•-), H2O2, HOCl, and the hydroxyl radical (•OH). Catalase, ABAH, and methionine each inhibited the increased apoptosis caused by BT, and catalase and ABAH inhibited increases in HOCl and •OH. Although BT exposure increased halogenated DNA, this increase was inhibited by catalase, methionine, and ABAH. BT exposure also increased the amount of halogenated tyrosines; however, it did not increase 8-oxo-deoxyguanosine.We suggest that BT increases H2O2 intracellularly; this H2O2 is metabolized to HOCl by MPO, and this HOCl results in possibly cytotoxic binding of chlorine to DNA. Because myeloid cells copiously express MPO and because halogenated DNA may induce both genetic and epigenetic changes that contribute to carcinogenesis, halogenative stress may account for benzene-induced bone marrow disorders and myeloid leukemia.
Abstract LB-261: Maintenance of aerobic glycolysis provides selective protection from apoptosis upon loss of growth signals or inhibition of BCR-Abl through suppression of p53 activation
Authors: Emily F. Mason, Yuxing Zhao, Pankuri Goraksha-Hicks, Jonathan L. Coloff, Hugh Gannon, Stephen N. Jones, Jeffrey C. Rathmell
Journal: Cancer Research (2011)

Abstract Healthy cells require input from growth factor signaling pathways to maintain cell metabolism and survival. In contrast, cancer cells can maintain growth factor-independent glycolysis and survival through expression of oncogenic kinases, such as BCR-Abl. While disruption of these growth signals through targeted kinase inhibition can promote cancer cell death, therapeutic resistance frequently develops, and further mechanistic understanding is needed. Cell metabolism may play a central role in this cell death pathway, as we have shown that growth factor deprivation leads to decreased glycolysis that promotes apoptosis via p53 activation and induction of the pro-apoptotic protein Puma. However, it has remained unclear how cell metabolism regulates p53 activation. To investigate this, we have utilized a system in which stable overexpression of the glucose transporter Glut1 and hexokinase 1 in hematopoietic cells drives growth factor-independent glycolysis. This system allows us to examine the effects of altered glucose metabolism in the absence of other signaling events activated downstream of growth factor receptors or oncogenic kinases. Here, we extend our findings to demonstrate that elevated glucose metabolism, characteristic of cancer cells, can suppress Protein Kinase C delta-dependent p53 activation to maintain cell survival after growth factor withdrawal. In contrast, DNA damage-induced p53 activation was independent of Protein Kinase C delta and was not metabolically sensitive. Both stresses required phosphorylation of p53 at serine 18 for maximal activity, but each led to a unique pattern of p53 target gene expression, demonstrating distinct activation and response pathways for p53 that were differentially regulated by metabolism. Consistent with oncogenic kinases acting to replace growth factors, treatment of BCR-Abl-expressing cells with the kinase inhibitor imatinib led to reduced glycolysis and p53- and Puma-dependent cell death. Accordingly, maintenance of glucose metabolism inhibited p53 activation and promoted imatinib resistance. Furthermore, inhibition of glycolysis enhanced imatinib sensitivity in BCR-Abl-positive cells expressing wild type p53 but had little effect on p53-null cells. These data demonstrate that distinct pathways regulate p53 after DNA damage and metabolic stress and that inhibition of glucose metabolism may enhance the efficacy of and overcome resistance to targeted molecular cancer therapies. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr LB-261. doi:10.1158/1538-7445.AM2011-LB-261
Management and treatment of chronic hepatitis B virus infection in HIV positive and negative patients: The EPIB 2008 study
Authors: Lionel Piroth, Stanislas Pol, Karine Lacombe, Patrick Miailhes, Agathe Rami, David Rey, Veronique Loustau-Ratti, Philippe Morlat, Isabelle Goderel, Damien Sene, Eric Rosenthal, Fabrice Carrat, Patrice Cacoub
Journal: Journal of Hepatology (2010)
The Allocation and Rationing of High-Cost Services-Reply
Authors: William A. Knaus
Journal: JAMA (1986)

<h3>In Reply.—</h3> I appreciate Dr Ashley's support of my editorial. I urge him, however, to reread it, going beyond my deliberately provocative statement suggesting that rationing of ICU services, if it consisted only of refusing occasional patients who were too healthy to require intensive care, could be viewed as painless. In the remainder of the editorial, I explain why such "painless" rationing decisions are ineffective in saving costs. They simply do not lead to a reduction in a total allocation of hospital resources allocated to intensive care. I then emphasize how the more difficult and painful decisions, those that truly reduce expenditures, are not yet being made. Both points are illustrated well by the letter from Franklin and colleagues. They describe how, in response to an increased demand for ICU services at Cook County Hospital, they responded by almost doubling the size of the ICU! Such investments may temporarily avoid
Letter: Kidneys from living donors.
Authors: R Shackman
Journal: BMJ (1974)

revealed antibody and therefore a state of inm unity.The seronegative cases have re- main.dseronegaFive after Ig prophylaxis and have delivered normal children with no increased levels of IgM in the cord sample.On the other hand if seroconversion had occurred following the administration of Ig the patient and her medical practitioner could be advised accordingly, but this has not occurred in our experience.It would probably be preferable, as suggested by Drs.Forrest and Menser, to have an Ig preparation with a high antibody titre, but as this is not generally available and becaus,e there is some variation in the antibody titre of the normal pooled Ig product, we have used a large dose of 3 g administered in two separate doses.Though this is considerably greater than what is advocated we think it is justifiable in the circumtances.-Iam, etc.,
Biological Antithrombin III Levels
Authors: Rodger L. Bick
Journal: JAMA (1978)

To the Editor.—  The MEDICAL NEWS article Automated Test Measures Functional Antithrombin, Coagulation Enzymes (report of Jayed Fareed, PhD, and Harry L. Mesmore, MD) confirms my observations 1 and those of others 2,3 that there is poor correlation between immunological (total) and functional antithrombin III levels in disease states. Fareed and Mesmore point out that at Loyola University Stritch School of Medicine antithrombin III assay by chromogenic substrates (still an investigational procedure) is being used to identify three groups of patients: hereditary thrombophiliacs, patients with hypercoagulable states, and patients who may be resistant to heparin therapy. Clearly, a fourth area where this test may be indicated is in women ingesting oral contraceptives; 13 of 14 international studies have provided data showing that women with an increased predisposition to thromboembolic phenomena while ingesting oral contraceptives have decreased antithrombin III levels after ingesting the agents. 4   One caution is that chromogenic substrates
EPIDEMIC STREPTOCOCCUS SORE THROAT —ITS SYMPTOMS, ORIGIN AND TRANSMISSION
Authors: JOSEPH A. CAPPS
Journal: JAMA (1913)

Epidemics of streptococcus sore throat have recently sprung up as a scourge, so new that they receive no mention even in the latest editions of our text-books. Within two years three extensive and alarming epidemics have occurred, which have no counterpart in American medical history. In some respects they call to mind the first severe invasion of influenza, but the latter disease spread everywhere throughout the country, whereas each of the streptococcus sore throat outbreaks was confined to a single community. It is quite probable, however, that many of our local tonsillitis epidemics, loosely designated as "grip," have in reality been due to streptococcus. In England comparatively small outbreaks of "septic sore throat" have been described<sup>1</sup>in seventeen localities, and a probable relationship to the milk-supply has been recognized; but in few instances were careful bacteriologic investigations carried out. The streptococcus was first demonstrated in cultures obtained from cases
Physicians Married to Physicians
Authors: Cynda Ann Johnson
Journal: Annals of Internal Medicine (1994)

Letters15 April 1994Physicians Married to PhysiciansCynda Ann Johnson, MD and Bruce E. Johnson, MDCynda Ann Johnson, MDUniversity of Kansas Medical Center; Kansas City, KS 66160Search for more papers by this author and Bruce E. Johnson, MDUniversity of Kansas Medical Center; Kansas City, KS 66160Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-120-8-199404150-00031 SectionsAboutFull TextPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail TO THE EDITOR:We read with interest the editorial [1] on dual-physician marriages because, as you note, “soon nearly half of all young physicians will be married to each other.” As a married physician couple with two children whose academic jobs carry heavy clinical responsibility, we have found it difficult to study the uniqueness of this relationship here.However, during a sabbatical in England, we studied the phenomenon of married doctor couples there [2, 3]. Although many of our findings also apply to married doctor couples in the United States, the system of postgraduate training in the United Kingdom usually ...References1. Fletcher RH, Fletcher SW. Here come the couples (Editorial). Ann Intern Med. 1993; 119:628-30. Google Scholar2. Johnson CA. Impact of the structure of medicine in Britain on the careers of women physicians. J Am Med Wom Assoc. 1993; 48:108-13. Google Scholar3. Johnson CA, Johnson BE, Liese BS. Dual-doctor marriages: career development. Fam Med. 1992; 24:205-8. Google Scholar Author, Article, and Disclosure InformationAffiliations: University of Kansas Medical Center; Kansas City, KS 66160 PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics 15 April 1994Volume 120, Issue 8Page: 697KeywordsChildrenResidency Issue Published: 15 April 1994 CopyrightCopyright © 1994 by American College of Physicians. All Rights Reserved.PDF DownloadLoading ...
Effect of an inhaled adenosine A<sub>2A</sub> agonist on the allergen‐induced late asthmatic response
Authors: B. Luijk, M. Van Den Berge, H. A. M. Kerstjens, D. S. Postma, L. Cass, A. Sabin, J.‐W. J. Lammers
Journal: Allergy (2007)

Background: Adenosine receptor activation is suggested to play a role in asthmatic airway inflammation. Inhibition of adenosine receptors may have an effect on the late asthmatic response (LAR) after allergen inhalation and this mechanism could offer a potential new treatment in asthma. Methods: We evaluated the effect of an inhaled adenosine‐ 2A (A 2A )‐receptor agonist (GW328267X), 25 μg, in 15 nonsmoking atopic asthmatics who underwent an inhaled allergen challenge following twice daily treatment for 1 week in a double‐blind, placebo‐ and fluticasone propionate (250 μg) controlled study. Results: In contrast to fluticasone, treatment with the A 2A ‐receptor agonist neither significantly protect against the allergen‐induced early and late asthmatic reaction, nor the accompanying inflammatory response as measured by sputum total cell counts, number of EG2+ cells, and the concentration of interleukin‐8 and eosinophil cationic protein. Conclusion: The inhaled A 2A ‐receptor agonist, GW328267X, 25 μg does not affect the allergen‐induced LAR or the associated inflammatory response in asthma.
Edward Lorden Trickey
Authors: J N Wilson
Journal: BMJ (2002)

Former consultant orthopaedic surgeon London (b China 1920; q King's College, London, 1944; FRCS), d 17 April 2002.

Although he always remained a generalist, Lorden Trickey was one of the leading knee surgeons of his day. In 1957 he was made a consultant orthopaedic surgeon at Ashton-under-Lyne, returning to London in 1960, when he was invited to set up an orthopaedic and traumatic service at Edgware General Hospital, combined with a consultant post at the Royal National Orthopaedic Hospital and Institute of Orthopaedics, Stanmore. In the late 1960s he introduced arthroscopy to the Royal National Orthopaedic Hospital, taking himself off to Canada to learn the technique. He retired from the NHS in 1985, but continued as dean of the Institute of Orthopaedics until 1987.
Nasal potential difference measurements in patients with atypical cystic fibrosis
Authors: M. Wilschanski, H. Famini, N. Strauss-Liviatan, J. Rivlin, H. Blau, H. Bibi, L. Bentur, Y. Yahav, H. Springer, M.R. Kramer, A. Klar, A. Ilani, B. Kerem, E. Kerem
Journal: European Respiratory Journal (2001)

The diagnosis of cystic fibrosis (CF) is based on characteristic clinical and laboratory findings. However, a subgroup of patients present with an atypical phenotype that comprises partial CF phenotype, borderline sweat tests and one or even no common cystic fibrosis transmembrane conductance regulator (CFTR) mutations. The aim of this study was to evaluate the role of nasal potential difference (PD) measurements in the diagnosis of CF patients with an atypical presentation and in a population of patients suspected to have CF. Nasal PD was measured in 162 patients from four different groups: patients with classical CF (n=31), atypical phenotype (n=11), controls (n=50), and patients with questionable CF (n=70). The parameter, or combination of nasal PD parameters was calculated in order to best discriminate all CF patients (including atypical CF) from the non-CF group. The patients with atypical CF disease had intermediate values of PD measurements between the CF and non-CF groups. The best discriminate model that assigned all atypical CF patients as CF used: e (response to chloride-free and isoproterenol/response to amiloride) with a cut-off &gt;0.70 to predict a CF diagnosis. When this model was applied to the group of 70 patients with questionable CF, 24 patients had abnormal PD similar to the atypical CF group. These patients had higher levels of sweat chloride concentration and increased rate of CFTR mutations. Nasal potential difference is useful in diagnosis of patients with atypical cystic fibrosis. Taking into account both the sodium and chloride transport elements of the potential difference allows for better differentiation between atypical cystic fibrosis and noncystic fibrosis patients. This calculation may assist in the diagnostic work-up of patients whose diagnosis is questionable.
Critical Role of Reactive Oxygen Species and Mitochondrial Permeability Transition in Microcystin-Induced Rapid Apoptosis in Rat Hepatocytes
Authors: Wen-Xing Ding, Han-Ming Shen, Choon-Nam Ong
Journal: Hepatology (2000)

Microcystin-LR (M-LR) is a specific hepatotoxin. At present, the exact toxic mechanism of its action remains unclear though apoptosis is believed to be involved. This study was designed to investigate the role of reactive oxygen species (ROS) and mitochondrial permeability transition (MPT) in the M-LR-induced apoptotic process. Morphologic changes such as cell shrinkage, externalization of cell membrane phosphatidylserine, DNA fragmentation, and nuclear condensation suggest that M-LR causes rapid apoptosis in hepatocytes. Confocal microscopy revealed that M-LR exposure led to the onset of MPT and mitochondrial depolarization, evidenced by (1) redistribution of calcein fluorescence from cytosol to mitochondria, and (2) loss of mitochondrial tetramethyrhodamine methyl ester (TMRM) fluorescence; both occurred before apoptosis. Moreover, there was a significant and rapid increase of ROS level before the onset of MPT and loss of MMP, indicating a critical role of ROS in M-LR-induced apoptosis. Deferoxamine (DFO), an iron chelator, prevented the increase of ROS production, delayed the onset of MPT, and, subsequently, cell death. In addition, a specific MPT inhibitor, cyclosporin A (CsA), blocked the M-LR-induced ROS formation, onset of MPT, and mitochondrial depolarization as well as cell death. Thus, we conclude that the M-LR-induced ROS formation leads to the onset of MPT and apoptosis.
Cancer of the Breast: Amputation and After-treatment by Secondary X-rays of Known Quality: A Suggestion
Authors: W. Mitchell
Journal: BMJ (1910)

Thank you for your interest in spreading the word about The BMJ.NOTE: We only request your email address so that the person you are recommending the page to knows that you wanted them to see it, and that it is not junk mail. We do not capture any email address. Username * Your Email * Send To * You are going to email the following Cancer of the Breast: Amputation and After-treatment by Secondary X-rays of Known Quality: A Suggestion Your Personal Message CAPTCHA This question is for testing whether or not you are a human visitor and to prevent automated spam submissions.