tbuckley/cabot-search huggingface dataset:
The Future of Primary Care
Authors: Clair Morud
Journal: Annals of Internal Medicine (2004)

Letters6 January 2004The Future of Primary CareClair Morud, MDClair Morud, MDFrom Duluth Clinic, Ashland, WI 54806.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-140-1-200401060-00025 SectionsAboutFull TextPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail TO THE EDITOR:Thank you for your excellent series on primary care, which was summed up nicely by the editorial by Dr. Sox (1). However, I would summarize things even more concisely. I think that, above all, we are asking for respect. We want our health care executives to respect our profession enough to see us as the foundation of health care delivery. We want our academic leaders to respect us enough to recommend primary care practice to residents and students. We want our government to respect us enough to direct payment our way. We want our patients to respect ...Reference1. Sox HC. The future of primary care [Editorial]. Ann Intern Med. 2003;138:230-2. [PMID: 12558363] LinkGoogle Scholar Author, Article, and Disclosure InformationAffiliations: From Duluth Clinic, Ashland, WI 54806. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetailsSee AlsoThe Future of Primary Care Harold C. Sox The Future of Primary Care Scott A. Shipman , Jon D. Lurie , and David C. Goodman The Future of Primary Care Clifton R. Cleaveland Metrics 6 January 2004Volume 140, Issue 1Page: 69KeywordsAcademic medicineEvidence based medicineFellowshipsForecastingHealth careResidency ePublished: 6 January 2004 Issue Published: 6 January 2004 CopyrightCopyright © 2004 by American College of Physicians. All Rights Reserved.PDF DownloadLoading ...
Recurrent fixed drug eruption due to cliquinol
Authors: M. Janier, M.D. Vignon
Journal: British Journal of Dermatology (1995)

Journal Article Recurrent fixed drug eruption due to cliquinol Get access M. Janier, M. Janier Department of Dermatology, Hôpital Saint‐Louis 42 Rue Bichat, 75010, Paris, France Search for other works by this author on: Oxford Academic Google Scholar M.D. Vignon M.D. Vignon Department of Dermatology, Hôpital Saint‐Louis 42 Rue Bichat, 75010, Paris, France Search for other works by this author on: Oxford Academic Google Scholar British Journal of Dermatology, Volume 133, Issue 6, 1 December 1995, Pages 1013–1014, https://doi.org/10.1111/j.1365-2133.1995.tb06951.x Published: 01 December 1995
IMPACT OF POINT-OF-CARE PLATELET FUNCTION TESTING AMONG PATIENTS WITH AND WITHOUT ACUTE CORONARY SYNDROMES UNDERGOING PCI WITH DRUG-ELUTING STENTS: AN ADAPT-DES SUBSTUDY
Authors: Ajay J. Kirtane, Michael Rinaldi, Helen Parise, Bernhard Witzenbichler, Giora Weisz, Franz-Josef Neumann, David Metzger, Timothy Henry, David Cox, Peter Duffy, Bruce Brodie, Thomas Stuckey, Ernest Mazzaferri, Ecaterina Cristea, Roxana Mehran, Gregg Stone
Journal: Journal of the American College of Cardiology (2012)
Effect of polyunsaturated phosphatidylcholine on immune mediated hepatocyte damage.
Authors: J Neuberger, J E Hegarty, A L Eddleston, R Williams
Journal: Gut (1983)

Studies were carried out to investigate the mechanisms underlying the reduction of hepatocellular necrosis observed when polyunsaturated phosphatidylcholine was administered to patients with HBsAg negative chronic active hepatitis. After oral administration of the agent, the susceptibility of rabbit hepatocytes to both antibody dependent cell mediated cytotoxicity and mitogen induced lymphocyte cytotoxicity was substantially reduced. Short term in vitro incubation of either the hepatocytes or lymphocytes with polyunsaturated phosphatidylcholine had no effect on antibody dependent cell mediated cytotoxicity. As it has been shown that orally administered polyunsaturated phosphatidylcholine can be incorporated into the liver cell membrane, it is possible that polyunsaturated phosphatidylcholine exerts its effect by blocking the interaction between immune effector cells and hepatocytes.
Prothrombin Time: Percent vs Seconds
Authors: DAVID PRAGER
Journal: Annals of Internal Medicine (1970)

Letters and Comments1 February 1970Prothrombin Time: Percent vs SecondsDAVID PRAGER, M.D.DAVID PRAGER, M.D.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-72-2-287 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptTo the editor: The recent perspective by I. S. Wright, M.D., (1) has prompted this communication. I am surprised that Dr. Wright has emphasized the laboratory control of the Coumadin® drugs utilizing percent activity of normal instead of seconds as the unit of measurement of the Quick test. To explain further, I will describe how the value of percent activity of normal is obtained. Pooled, normal plasma that is assumed to be 100% of normal activity is diluted with any variety of diluents (barium-sulfate-adsorbed human plasma, barium-sulfate-adsorbed beef plasma, 0.85% saline, imidiazole-saline buffer). An aliquot of the pooled plasma is...References1. WRIGHT I: Recent developments in antithrombotic therapy. Ann Intern Med 71:823, 1969 LinkGoogle Scholar2. RODMANPASTORFAWCETT TBK: A comparison of laboratory methods for the control of anticoagulant therapy with prothrombinopenic agents. Amer J Med 31:547, 1961 CrossrefMedlineGoogle Scholar3. SEIDE M: Laboratory control of coumarin therapy. Ann Intern Med 57:572, 1962 LinkGoogle Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: Division of Hematology Department of Medicine Allentown Hospital Allentown, Pa. 18104 PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics 1 February 1970Volume 72, Issue 2Page: 287-287KeywordsBlood plasmaDrug regulationDrugsProthrombin timeResearch laboratories Issue Published: 1 February 1970 PDF DownloadLoading ...
Investigating allegations of research misconduct: the vital need for due process Commentary: Response from members of the Griffiths inquiry
Authors: E. Hey
Journal: BMJ (2000)

# Investigating allegations of research misconduct: the vital need for due process {#article-title-2} On 27 February 1999 the BMJ carried a news item reporting that the government had set up an inquiry into a controlled trial of neonatal ventilatory support undertaken at the North Staffordshire Hospital, in Stoke on Trent, from 1990 to 1993.1 The trial was designed to assess whether continuous negative extrathoracic pressure (CNEP) ventilation could reduce the need for, and problems associated with, tracheal intubation and positive pressure ventilation. #### Summary points We believe that almost every statement made about the design, conduct, and reporting of the neonatal continuous negative extrathoracic pressure (CNEP) trial in the Griffiths report was ill informed, misguided, or factually wrong. Errors include: A false assertion that the trial's design had not been subjected to external peer review A failure to understand the trial's statistical design, as evinced by their erroneous belief that Professor Southall was single handedly responsible for its size and shape A failure to recognise the expertise of the nurses involved in the study A false statement that some of the consent forms could not be found A false statement that it was not possible to be sure who had completed some of these forms A false statement that there was no way of checking that consent had been obtained properly An inaccurate statement that the process of consent was not managed consistently and that no system of management or documentation was in place to prove that it was A false assertion that parents were not given clear opportunities to withdraw their child from the study at any time A failure to take sufficiently into account evidence showing that parental recall of events in the newborn period can be fallible An overreliance on the evidence of the small group of parents who asked to testify to the panel at the expense of contemporaneous evidence from … Correspondence to: R Griffiths
AAV-mediated Liver-specific MPV17 Expression Restores mtDNA Levels and Prevents Diet-induced Liver Failure
Authors: Emanuela Bottani, Carla Giordano, Gabriele Civiletto, Ivano Di Meo, Alberto Auricchio, Emilio Ciusani, Silvia Marchet, Costanza Lamperti, Giulia d'Amati, Carlo Viscomi, Massimo Zeviani
Journal: Molecular Therapy (2013)

Mutations in human MPV17 cause a hepatocerebral form of mitochondrial DNA depletion syndrome (MDS) hallmarked by early-onset liver failure, leading to premature death. Liver transplantation and frequent feeding using slow-release carbohydrates are the only available therapies, although surviving patients eventually develop slowly progressive peripheral and central neuropathy. The physiological role of Mpv17, including its functional link to mitochondrial DNA (mtDNA) maintenance, is still unclear. We show here that Mpv17 is part of a high molecular weight complex of unknown composition, which is essential for mtDNA maintenance in critical tissues, i.e. liver, of a Mpv17 knockout mouse model. On a standard diet, Mpv17-/- mouse shows hardly any symptom of liver dysfunction, but a ketogenic diet (KD) leads these animals to liver cirrhosis and failure. However, when expression of human MPV17 is carried out by adeno-associated virus (AAV)-mediated gene replacement, the Mpv17 knockout mice are able to reconstitute the Mpv17-containing supramolecular complex, restore liver mtDNA copy number and oxidative phosphorylation (OXPHOS) proficiency, and prevent liver failure induced by the KD. These results open new therapeutic perspectives for the treatment of MPV17-related liver-specific MDS.
Monoclonal Antibodies and the Treatment of Gram-Negative Bacteremia and Shock
Authors: Sheldon M. Wolff
Journal: New England Journal of Medicine (1991)

It has been 40 years since the first description of bacteremia due to gram-negative rods appeared.1 It has always been assumed that the endotoxins (lipopolysaccharides) of gram-negative bacteria were responsible for the clinical manifestations of infections caused by these bacteria. This view was based on the observation that many of the characteristics of the infections could be reproduced by the infusion of endotoxin in laboratory animals and humans.2 Since the 1960s, it has been well known that the seriousness of the underlying condition was one of the most important predictors of outcome for patients with gramnegative bacteremia. Furthermore, it is . . .
Sympathomimetics and Schizophrenia
Authors: NORRIS HANSELL
Journal: JAMA (1975)

<h3>To the Editor.—</h3> Amphetamine psychosis has long been known to mimic schizophrenia.<sup>1,2</sup>Some experiences in my practice suggest that limited, continuing use of amphetamine and related substances may exert a deregulating effect on chronic schizophrenia. In particular, it appears that several sympathomimetic materials can yield subtle or dramatic exacerbations in the course of schizophrenia, the origin of which may not be visible without precise inquiry. Of a group of 575 schizophrenics under my care, and all on phenothiazine therapy, 26 are thought to have shown such exacerbations, which abated on stopping simultaneously taking a sympathomimetic material. This number is likely an understatement, because many of the events were not recognized because of our only recent appreciation of this matter. It is not mainly sympathomimetics prescribed by physicians that constitute the bulk of this problem; it is the presence of these materials in over-the-counter pharmaceuticals, particularly in diet pills and
Epidural anaesthesia and long term backache after childbirth
Authors: M. Newburn
Journal: BMJ (1990)

<h3>Abstract</h3> Intracellular Ca<sup>2+</sup> mobilization induced by second messenger IP<sub>3</sub> controls many cellular events in most of the eukaryotic groups. Despite the increasing evidence of IP<sub>3</sub>-induced Ca<sup>2+</sup> in apicomplexan parasites like <i>Plasmodium</i>, responsible for malaria infection, no protein with potential function as an IP<sub>3</sub>-receptor has been identified. The use of bioinformatic analyses based on previously known sequences of IP<sub>3</sub>-receptor failed to identify potential IP<sub>3</sub>-receptor candidates in any <i>Apicomplexa</i>. In this work, we combine the biochemical approach of an IP<sub>3</sub> affinity chromatography column with bioinformatic meta-analyses to identified potential vital membrane proteins that present binding with IP<sub>3</sub> in <i>Plasmodium falciparum</i>. Our analyses reveal that PF3D7_0523000, a gene that codes a transport protein associated with multidrug resistance, as a potential target for IP<sub>3</sub>. This work provides a new insight for probing potential candidates for IP<sub>3</sub>-receptor in <i>Apicomplexa</i>.
Sodium Intake and Hypertension: A Cause for Concern
Authors: JAMES C. HUNT
Journal: Annals of Internal Medicine (1983)

Cardiovascular disease is the leading cause of death worldwide. Hypertension--the leading cause of heart attack, stroke, and kidney failure--occurs in more than 20% of adults in most modern societies. Hypertensive patients have defective sodium metabolism. From childhood throughout adult life most acculturated peoples consume 10 to 20 g of salt daily and have more obesity. Populations with low blood pressure are more active, leaner, and consume a diet low in sodium and high in potassium; however, when members of these groups are exposed to western diets, blood pressure increases with age and hypertension occurs. Drug treatment to control blood pressure prevents deaths. Conservative management, including low-sodium, high-potassium diets, restores normal blood pressure in more than half of hypertensive patients. More information on the cause and mechanisms of this condition is needed, but our primary concern is for improved nutrition and drug treatment to prevent hypertension-related cardiovascular deaths.
Induction of mesenchymal cell phenotypes in lung epithelial cells by adenovirus E1A
Authors: A. R. Behzad, K. Morimoto, J. Gosselink, J. Green, J. C. Hogg, S. Hayashi
Journal: European Respiratory Journal (2006)

Epithelial–mesenchymal transformation is now recognised as an important feature of tissue remodelling. The present report concerns the role of adenovirus infection in inducing this transformation in an animal model of chronic obstructive pulmonary disease. Guinea pig primary peripheral lung epithelial cells (PLECs) transfected with adenovirus E1A (E1A-PLECs) were compared to guinea pig normal lung fibroblasts (NLFs) transfected with E1A (E1A-NLFs). These cells were characterised by PCR, immunocytochemistry, electron microscopy, and Western and Northern blot analyses. Electrophoretic mobility shift assays were performed in order to examine nuclear factor (NF)-κB and activator protein (AP)-1 binding activities. E1A-PLECs and E1A-NLFs positive for E1A DNA, mRNA and protein expressed cytokeratin and vimentin but not smooth muscle α-actin. Both exhibited cuboidal morphology and junctional complexes, but did not contain lamellar bodies or express surfactant protein A, B or C mRNAs. These two cell types differed, however, in their NF-κB and AP-1 binding after lipopolysaccharide stimulation, possibly due to differences in the expression of the subunits that comprise these transcriptional complexes. E1A transfection results in the transformation of peripheral lung epithelial cells and normal lung fibroblasts to a phenotype intermediate between that of the two primary cells. It is postulated that this intermediate phenotype may play a major role in the remodelling of the airways in chronic obstructive pulmonary disease associated with persistence of adenovirus E1A DNA.
The Use and Abuse of Mixtures of Active Druffs
Authors: Isaac Starr
Journal: JAMA (1962)

AN IMPORTANT PURPOSE of this annual Therapeutic Number is to provide an open forum for the discussion of general problems concerned with therapeutics—problems which, because of their fundamental character, are basic to the practice of medicine itself. During the past years no problem has taken more of the time of the Council on Drugs and none has brought out more acute divergence of opinion than the problem presented by mixtures of active drugs given to produce systemic effects. In contrast with other aspects of the Council's activities, the "mixture problem" appears to some Council members to be relatively unimportant for, despite their wide use, only rarely has there been clear evidence that any patient has been harmed by the use of a mixture. But other Council members are violently opposed in principle to the use of mixtures of active drugs. Their opposition is based not only on the occasional demonstration
PLAGUE AND THE GEOGRAPHICAL DISTRIBUTION OF RATS
Authors: B. Skinner
Journal: BMJ (1905)

THE large work by Dr. BoARDMAN REIED Of Philadelphia on D-isea8e8 of the Stomach and Intestine.94hardly needs a corre- spondingly long notice, for, although the volume, including the index, extends to over a thousand pages, it has been made up largely from istandard authoritieti whose books are well known in this country.
Glory in tandem
Authors: R. Rolls
Journal: BMJ (1990)

In the past few decades scientists have changed our way of life more drastically than any other group, yet there are many people who distrust their endeavours and regard science as more of a threat than a benefit to mankind. In its extreme this mistrust is based on an exaggerated stereotype of its protagonists?cold, dispassionate, slightly crazed men who?at least in Hollywood films?have a tendency to speak with middle European accents. Real scientists should therefore be grateful to the late Sir Peter Medawar for having done so much to dispel this image. Medawar, who is perhaps better remembered for his Nobel prize winning work on the immunological basis of tissue rejection, was a prolific author who wrote lucidly about a wide variety of topics relating to science and scientists. Under the title  Threat and the Glory David Pyke has collected and edited 23 of Peter Medawar's essays, book reviews, and broadcasts, including the 1959 Reith lectures The Future of Man. All have either escaped publication or are now out of print. Despite the diversity of subject matter there are some common themes, not least Medawar's passionate belief in the scientific method and his reverence for the philosophy of Karl Popper.  concept of pure science, devoid of any conscious search for practical solutions to
Severe hemochromatosis in a Portuguese family associated with a new mutation in the 5′-UTR of the HAMP gene
Authors: Thomas Matthes, Patricia Aguilar-Martinez, Loredana Pizzi-Bosman, Régis Darbellay, Laura Rubbia-Brandt, Emilio Giostra, Martine Michel, Tomas Ganz, Photis Beris
Journal: Blood (2004)
Serum and tissue autoantibodies to colonic epithelium in ulcerative colitis.
Authors: J A Snook, J R Lowes, K C Wu, J D Priddle, D P Jewell
Journal: Gut (1991)

Sera and colonic tissue-bound immunoglobulin extracts from patients with ulcerative colitis and disease controls were examined immunohistochemically and by killer cell cytotoxicity assay for the presence of anticolonic epithelial autoantibodies. IgG yields in the tissue extracts from patients with colitis and control subjects were similar, and the extracts were uniformly autoantibody negative. Of 41 sera from patients with inflammatory bowel disease, 9classical9 anticolon antibody was present in 41% and was commoner in patients with sclerosing cholangitis. Cytotoxic anticolon antibody was present in 20% overall and was strongly associated with disease activity; it did not correlate with the presence of 9classical9 anticolon antibody. The heterogeneous and non-universal antiepithelial autoantibody response and the failure to detect tissue bound autoantibody in vivo argue against the hypothesis that humoral autoimmunity is of major importance in the pathogenesis of ulcerative colitis.
Complementary and Alternative Medicine
Authors: Pat LePore
Journal: Annals of Internal Medicine (1998)

Medical Writings: Book Notes1 September 1998Complementary and Alternative MedicinePat LePore, JD, MPAPat LePore, JD, MPAAmerican College of Physicians-American Society of Internal Medicine, Philadelphia, PennsylvaniaSearch for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-129-5-199809010-00027 SectionsAboutFull TextPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail Complementary and Alternative Medicine; Cohen M. 180 pages. Baltimore: Johns Hopkins Univ Pr; 1998. $16.95. ISBN 0801856892. Order phone 800-537-5487.Field of medicine: Alternative medicine.Format: Softcover book.Audience: Health care professionals interested in integrating holistic medicine into their practices; lay persons interested in alternative medicine; lawyers, judges, and regulators involved in integrating holistic medical concepts into the existing biomedical framework; and insurers and providers, particularly managed care organizations, interested in integrating alternative and complementary therapies into existing health plans.Purpose: To provide a comprehensive review of the history of biomedicine and the relation of alternative therapies to conventional medicine ... Author, Article, and Disclosure InformationAffiliations: American College of Physicians-American Society of Internal Medicine, Philadelphia, Pennsylvania PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics 1 September 1998Volume 129, Issue 5Page: 431KeywordsComplementary and alternative medicineHealth careHealth care providersHistory of medicinePatientsTraditional medicine Issue Published: 1 September 1998 Copyright & PermissionsCopyright © 1998 by American College of Physicians. All Rights Reserved.PDF downloadLoading ...
Effects of residential mobility on individual versus population risk of radon-related lung cancer.
Authors: K E Warner, P N Courant, D Mendez
Journal: Environmental Health Perspectives (1995)

The U.S. Environment Protection Agency (EPA) does not consider the effects of normal patterns of residential mobility in estimating individual radon-related lung cancer risks. As a consequence, the EPA's population risk estimates may have little bearing on individual risks, and remediation of high-radon homes may have only small health benefits for the individual who remediate their homes. Through a stimulation analysis, we examine the effects of residential mobility on random exposure and lung cancer risk. Given normal mobility, only 7% of eventual radon-related mortality among current 30 year old will occur in the 5% currently living in homes above pCi/l (the EPA's action level for remediation) in contrast with you estimate of 31% of deaths when mobility's ignored. About 10 pCi/l the no-mobility assumption implies 10.3% of deaths, compared to only 0.4% when mobility taken into account. We conclude that knowledge of one's current random exposure not necessarily a useful guide to one's risk, especially for residents of the high-radon homes targeted for remediation by the EPA. The risk of such individuals is like to be substantially lower than that implied in the EPA's risk charts. If people currently living in high radon homes remediate their houses, the majority of the resulting health benefits will accrue to future occupants of their homes.