tbuckley/cabot-search huggingface dataset:
Charter on Medical Professionalism: Putting the Charter into Practice
Authors: Neil J. Smelser
Journal: Annals of Internal Medicine (2003)

Letters20 May 2003Charter on Medical Professionalism: Putting the Charter into PracticeNeil J. Smelser, PhDNeil J. Smelser, PhDUniversity of California, Berkeley; Berkeley, CA 94704 (Smelser)Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-138-10-200305200-00024 SectionsAboutFull TextPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail IN RESPONSE:Two comments are in order in response to the very apt observations on business practices brought forward by Dr. Haskell. First, in our development of the physician charter, we operated on the general conviction that a spare constitution of basic principles is preferable to one that is detailed and exhaustive. If the charter as an enunciation of principles were to be expanded, it would certainly include honesty, integrity, and efficiency in the business practices of physicians and medical organizations. Second, given our consistent stress on social and moral commitments and responsibilities, we would have highlighted the virtues of ... Author, Article, and Disclosure InformationAffiliations: University of California, Berkeley; Berkeley, CA 94704 (Smelser) PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetailsSee AlsoMedical Professionalism in the New Millennium: A Physician CharterCharter on Medical Professionalism: Putting the Charter into Practice Donatella Lippi , GianFranco Gensini , and Andrea A. Conti Charter on Medical Professionalism: Putting the Charter into Practice Neil J. Smelser Charter on Medical Professionalism: Putting the Charter into Practice Jerome C. Arnett Jr. Charter on Medical Professionalism: Putting the Charter into Practice Sylvia L. Cruess and Richard L. Cruess Charter on Medical Professionalism: Putting the Charter into Practice Robert Feldman Charter on Medical Professionalism: Putting the Charter into Practice Walter J. McDonald Charter on Medical Professionalism: Putting the Charter into Practice Steven A. Wartman Charter on Medical Professionalism: Putting the Charter into Practice Jordan J. Cohen Charter on Medical Professionalism: Putting the Charter into Practice Yevgeniya Nusinovich Charter on Medical Professionalism: Putting the Charter into Practice Risa Lavizzo-Mourey Charter on Medical Professionalism: Putting the Charter into Practice Christopher J. Lyons Charter on Medical Professionalism: Putting the Charter into Practice Richard L. Cruess and Sylvia L. Cruess Charter on Medical Professionalism: Putting the Charter into Practice Sadeq A. Quraishi and Ayesha N. Khalid Charter on Medical Professionalism: Putting the Charter into Practice Neil J. Smelser Charter on Medical Professionalism: Putting the Charter into Practice Charles M. Haskell Metrics 20 May 2003Volume 138, Issue 10Page: 852 ePublished: 20 May 2003 Issue Published: 20 May 2003 Copyright & PermissionsCopyright © 2003 by American College of Physicians. All Rights Reserved.PDF downloadLoading ...
Coexistence of myelodysplastic syndrome and untreated chronic lymphocytic leukemia with development of acute myeloid leukemia immediately after treatment of chronic lymphocytic leukemia
Authors: Arthur W. Bracey, Anne‐Marie Maddox, Ladonna Immken, Su Ming Hsu, Michael E. Marks
Journal: American Journal of Hematology (1989)

Abstract A 72‐year‐old man originally seen for anemia and thrombocytopenia was determined to have chronic lymphocytic leukemia (CLL). Bone marrow examination at the time of CLL diagnosis revealed a small but significant population of atypical blasts. Cytogenetic analysis of the bone marrow aspirate disclosed chromosomal abnormalities (‐7, +8) suggestive of a myelodysplastic syndrome. Shortly after treatment of the CLL, there was proliferation of the previously noted blast population, which cytochemical studies demonstrated to be of the myeloid series thus indicating acute myeloid leukemia superimposed on CLL. This report presents microscopic, cytogenetic, immunophenotypic, and cytochemical evidence to document the evolution of acute myeloid leukemia in the bone marrow of a patient with CLL after one course of chemotherapy.
β1 Integrin Targeting Potentiates Antiangiogenic Therapy and Inhibits the Growth of Bevacizumab-Resistant Glioblastoma
Authors: W. Shawn Carbonell, Michael DeLay, Arman Jahangiri, Catherine C. Park, Manish K. Aghi
Journal: Cancer Research (2013)

Antiangiogenic therapies like bevacizumab offer promise for cancer treatment, but acquired resistance, which often includes an aggressive mesenchymal phenotype, can limit the use of these agents. Upregulation of β1 integrin (ITGB1) occurs in some bevacizumab-resistant glioblastomas (BRG) whereby, mediating tumor-microenvironment interactions, we hypothesized that it may mediate a mesenchymal-type resistance to antiangiogenic therapy. Immunostaining analyses of β1 integrin and its downstream effector kinase FAK revealed upregulation in 75% and 86% of BRGs, respectively, compared with pretreatment paired specimens. Furthermore, flow cytometry revealed eight-fold more β1 integrin in primary BRG cells compared with cells from bevacizumab-naïve glioblastomas (BNG). Fluorescence recovery after photobleaching of cells engineered to express a β1-GFP fusion protein indicated that the mobile β1 integrin fraction was doubled, and half-life of β1 integrin turnover in focal adhesions was reduced markedly in BRG cells compared with bevacizumab-responsive glioblastoma multiforme cells. Hypoxia, which was increased with acquisition of bevacizumab resistance, was associated with increased β1 integrin expression in cultured BNG cells. BRGs displayed an aggressive mesenchymal-like phenotype in vitro. We found that growth of BRG xenograft tumors was attenuated by the β1 antibody, OS2966, allowing a 20-fold dose reduction of bevacizumab per cycle in this model. Intracranial delivery of OS2966 through osmotic pumps over 28 days increased tumor cell apoptosis, decreased tumor cell invasiveness, and blunted the mesenchymal morphology of tumor cells. We concluded that β1 integrin upregulation in BRGs likely reflects an onset of hypoxia caused by antiangiogenic therapy, and that β1 inhibition is well tolerated in vivo as a tractable strategy to disrupt resistance to this therapy.
BESNIER'S PRURIGO: AN ECTODERMAL DEFECT.
Authors: JOHN T. INGRAM
Journal: British Journal of Dermatology (1955)

Journal Article BESNIER'S PRURIGO: AN ECTODERMAL DEFECT. Get access JOHN T. INGRAM, M.D.Lond., F.R.C.P.Lond. JOHN T. INGRAM, M.D.Lond., F.R.C.P.Lond. Physician in Charge, The Skin Department, The General Infirmary at Leeds, Lecturer on Diseases of the Skin, The University of Leeds Search for other works by this author on: Oxford Academic Google Scholar British Journal of Dermatology, Volume 67, Issue 2, 1 February 1955, Pages 43–49, https://doi.org/10.1111/j.1365-2133.1955.tb12685.x Published: 01 February 1955
Pacing-Induced Dys-Synchrony Preconditions Rabbit Myocardium Against Ischemia/Reperfusion Injury
Authors: Ward Y. Vanagt, Richard N. Cornelussen, Quincy P. Poulina, Erik Blaauw, Kevin Vernooy, Jack P. Cleutjens, Marc van Bilsen, Tammo Delhaas, Frits W. Prinzen
Journal: Circulation (2006)

Background— Because increased mechanical load induces preconditioning (PC) and dys-synchrony increases loading in late-activated regions, we investigated whether dys-synchrony induced by ventricular pacing (VP) at normal heart rate leads to cardioprotection. Methods and Results— Isolated working rabbit hearts were subjected to 35 minutes of global ischemia and 2 hours of reperfusion. Seven hearts underwent VP PC (3 periods of 5 minutes VP at the posterior left ventricular [LV] wall), 7 hearts underwent ischemic preconditioning (IPC) (3 periods of 5 minutes of global ischemia), and 9 hearts served as control (C). LV pressure and sonomicrometry were used to assess global hemodynamics and segment work (SW) and end-diastolic segment length (EDSL) in anterior and posterior LV myocardium. Myocardial release of lactate and expression of proBNP mRNA were determined to gain insight in molecular processes involved in VP PC (* P &lt;0.05). Infarct size (triphenyl tetrazolium chloride staining) was 18.3±13.0% in group C, and was uniformly reduced in the VP PC and IPC groups (1.8±0.8%*, and 3.5±3.1%*, respectively; and not significant between VP PC and IPC). LV posterior wall pacing (VP PC group) increased EDSL (by 6.3±5.8%*) and SW (to 335±207%*) in the LV anterior wall, whereas posterior wall SW decreased to negative values (−23±63%*). LV pacing did not significantly change lactate release and coronary flow but significantly increased proBNP mRNA expression in both anterior and posterior myocardium as compared with controls. Conclusions— Intermittent dys-synchrony is equally cardioprotective as “classical” IPC. Stretch-mediated signaling is a more likely trigger for VP PC than ischemia. VP PC is potentially applicable in cardiac surgery.
Decisive Factors In the Tolbutamide Controversy
Authors: John B. O'Sullivan
Journal: JAMA (1975)

No increased mortality trend attributable to tolbutamide is shown by an analysis of variance on logit-transformed data from the University Group Diabetes Program (UGDP) study. The UGDP's controversial finding of an increased rate with mortality subgrouped by "cardiovascular" causes is confirmed by the Biometric Committee's report, with reservations that failed to include overriding decisive factors. The basic problem is that inspected data set up the hypothesis (the increased cardiovascular mortality), and that the same data were used to test the hypothesis, so that resulting probability values no longer have the usual meaning. The problem was compounded by multiple testing of the data without adjusting the probability levels. When cardiovascular deaths were redefined as myocardial infarcts and sudden deaths, in an attempt to test a proposed etiologic inotropic hypothesis, no significant increase in cardiovascular mortality was found.
The Use of HIV Antibody Testing by Physicians-Reply
Authors: Renslow Sherer
Journal: JAMA (1988)

<h3>In Reply.</h3> —Dr Decker asks: Might we not unnecessarily alarm patients in whom the likelihood of HIV infection is very small with mandatory HIV antibody pretest counseling? I think not; the information contained in appropriate pretest counseling is valuable, even to those at low risk, and it may be readily accompanied by an honest expression of the physician's opinion of the unlikelihood of HIV infection. The public health value of mandating appropriate counseling and consent with HIV antibody testing is a more compelling priority than the risk of fears raised by a remote possibility of HIV infection in low-risk patients. The new Illinois law (AIDS Confidentiality Act, Public Acts 85-667 and 85-679) does indeed contain exceptions; for example, the screening of blood, blood products, and organ and semen donors, as well as appropriate HIV testing in research protocols, including blinded seroprevalence studies. Infection control policy should be directed toward implementation
Causes, Consequences, and Treatment of Inflammation of the Veins
Authors: H. Lee
Journal: BMJ (1851)

1 I have attempted to establish the following points, in reference to the Pathology and Treatment of Inflammation of the Veins.1st.That inflammation, both of the veins and of the capillary vessels, usually depends upon irritation, communicated to them through their contents.2ndly.That pus is capable of producing such irritation when de- tained in contact with the lining membrane of the veins; but that it may be conveyed along their channels, without leaving any trace of its passage.
α-Tocopherol Inhibits Aggregation of Human Platelets by a Protein Kinase C–Dependent Mechanism
Authors: Jane E. Freedman, John H. Farhat, Joseph Loscalzo, John F. Keaney
Journal: Circulation (1996)

Epidemiological studies indicate that vitamin E (alpha-tocopherol) exerts a beneficial effect on cardiovascular disease. The effect of vitamin E has generally been attributed to its antioxidant activity and the antioxidant protection of LDL. Distinct from its effect on LDL, vitamin E is also known to inhibit platelet aggregation and adhesion in vitro, but the mechanism(s) responsible for these observations are not known.Using gel-filtered platelets derived from platelet-rich plasma treated with alpha-tocopherol (500 mumol/L) or vehicle (0.5% ethanol), we found that inhibition of platelet aggregation by alpha-tocopherol was closely linked to its incorporation into platelets (r = -.78; P < .02). Platelet incorporation of alpha-tocopherol was associated with a significant reduction in platelet sensitivity to aggregation by adenosine 5'-diphosphate, arachidonic acid, and phorbol ester (PMA) by approximately, 0.15-, 2-, and 100-fold, respectively. In contrast, platelets treated similarly with butylated hydroxytoluene, another potent lipid-soluble antioxidant, did not demonstrate any change in sensitivity to these agents. Platelet incorporation of alpha-tocopherol inhibited PMA-induced stimulation of platelet protein kinase C (PKC) as determined by phosphorylation of the 47-kD PKC substrate. In 15 normal subjects, oral supplementation with alpha-tocopherol (400 to 1200 IU/d) resulted in an increase in platelet alpha-tocopherol content that correlated with marked inhibition of PMA-mediated platelet aggregation (r = .67; P < .01). Platelets derived from these subjects after supplementation also demonstrated apparent complete inhibition of PKC stimulation by PMA.These data indicate that platelet incorporation of alpha-tocopherol at levels attained with oral supplementation is associated with inhibition of platelet aggregation through a PKC-dependent mechanism. These observations may represent one potential mechanism for the observed beneficial effect of alpha-tocopherol in preventing the development of coronary artery disease.
The cGMP phosphodiesterase inhibitor zaprinast enhances the effect of nitric oxide.
Authors: K G Thusu, F C Morin, J A Russell, R H Steinhorn
Journal: American Journal of Respiratory and Critical Care Medicine (1995)

We investigated the effect of zaprinast (M&B 22948), a specific cGMP phosphodiesterase inhibitor, on pulmonary arteries isolated from lambs with persistent pulmonary hypertension following prenatal ligation of the ductus arteriosus. Relaxations to sodium nitroprusside, which donates nitric oxide inside the smooth muscle cell, were significantly decreased in pulmonary arteries from ligated lambs. Pretreatment with 3 x 10(-5) M zaprinast restored them to levels close to those observed in untreated arteries from control animals. Further studies in intact newborn lambs were then conducted under three experimental conditions: (1) NO inhalation at 6 ppm, (2) zaprinast infusion at 0.05 mg/kg/min, and (3) combination therapy of zaprinast infusion in addition to inhaled NO at 6 ppm. Combined therapy with NO and zaprinast decreased the pulmonary artery pressure (34.3 +/- 3%) and pulmonary vascular resistance (64 +/- 7%) and increased pulmonary blood flow (88 +/- 34%) and postductal PaO2 (287 +/- 34%) to a significantly greater extent than NO alone, zaprinast alone, or the sum of these two responses, indicating a true synergistic effect. Zaprinast pretreatment also markedly increased the duration of pulmonary vasodilation to nitric oxide. There was no effect on systemic blood pressure with the combined therapy. We conclude that zaprinast pretreatment significantly enhances the effect of sodium nitroprusside on isolated pulmonary arteries, as well the effect of inhaled NO at 6 ppm in newborn lambs with persistent pulmonary hypertension. We speculate that phosphodiesterase inhibition may increase the response rate to NO or allow the use of much lower inhaled concentrations of NO.
"MEDICINE AND THE COMMUNITY OF SCIENTIFIC THOUGHT"
Authors: H. E. Merriam
Journal: JAMA (1924)

<h3>To the Editor:</h3> —The editorial, March 22, on "Medicine and the Community of Scientific Thought," is to be commended. It may be of interest to you to learn how the Tompkins County Medical Society of New York State has solved the problem. By a recent change in its by-laws it established an associate membership, to which all members of the faculty of Cornell University, in sciences allied to medicine, were eligible. Many of these men have become members of the society, take an active interest, and have charge of the programs of many of the meetings. Interest has been stimulated and much benefit derived by this cooperation. Any county having the opportunity of association with men in these allied sciences would do well to establish such an associate membership.
Altered Ca2+ signalling in human neutrophils from inflammatory sites.
Authors: E V Davies, B D Williams, R J Whiston, A M Cooper, A K Campbell, M B Hallett
Journal: Annals of the Rheumatic Diseases (1994)

OBJECTIVES--To determine whether the intracellular store release of Ca2+ in neutrophils from patients with rheumatoid arthritis, other joint disease and active leg ulceration was different from normal neutrophils. METHODS--The release into the cytosol of Ca2+ from stores within individual neutrophils was determined using ratiometric imaging of fura2. The size of the elevated Ca2+ 9cloud9 and its concentration were quantified in neutrophils from the circulation of patients with rheumatoid arthritis, other joint diseases, and leg ulcers and from the joints of those with joint disease. RESULTS--In neutrophils isolated from both the synovial fluid of patients with rheumatoid arthritis and other joint conditions, and also arising from leg ulcers, the amount of the cell cytosol occupied by elevated Ca2+ was significantly increased compared with neutrophils from healthy subjects; for neutrophils from rheumatoid, non-rheumatoid joints and leg ulcers p values were 0.0006, &lt; 0.0001, 0.016 respectively (Student9s t test). There was also a significant increase in Ca2+ release from circulating neutrophils from patients with rheumatoid arthritis (p = 0.09), but not in circulating neutrophils from patients with leg ulcers or non-rheumatoid joint conditions. CONCLUSIONS--It is proposed that the increased release of free Ca2+ into the cytosol of neutrophil at inflammatory sites results in increased oxidase activation.
Prevention of post-discharge venous thromboembolism in patients with rheumatoid arthritis undergoing knee or hip arthroplasty: a continuing matter of debate
Authors: M T NURMOHAMED
Journal: Annals of the Rheumatic Diseases (2001)

Prevention of post-discharge venous thromboembolism in patients with rheumatoid arthritis undergoing knee or hip arthroplasty: a continuing matter of debate Patients undergoing major hip or knee surgery are particularly prone to postoperative venous thromboembolism (VTE)-that is, deep venous thrombosis (DVT) and pulmonary embolism (PE).Without thromboprophylaxis, the incidence of DVT in such patients is more than 50%, and fatal PE occurs in 1-6%. 1 These data are based on studies in which, predominantly, patients with osteoarthritis (OA) were investigated.It is not known whether or not there is a significant difference in the risk for developing VTE between patients with rheumatoid arthritis (RA) and those with OA undergoing major orthopaedic surgery as adequate investigations are lacking. 2 Thromboprophylaxis during hospitalisationDuring the past three decades, numerous investigations documented the eYcacy of unfractionated heparin, pneumatic compression, warfarin, and low molecular weight heparin (LMWH) in reducing the incidence of postoperative VTE.Nowadays, LMWH is the most commonly applied thromboprophylactic agent in most orthopaedic surgery units in Europe.The evidence for the eYcacy and safety of LMWH is derived from (large) trials, in which, predominantly, patients with OA were studied.Although these studies encompassed only a limited number of patients with RA, LMWH is also commonly used in patients with RA as thromboprophylaxis.However, not withstanding the use of preventive pharmacological thromboprophylaxis, there is still a considerable rate of asymptomatic DVT, approximately 15-20%, at the time of hospital discharge.
Altered spectrin dimer-dimer association and instability of erythrocyte membrane skeletons in hereditary pyropoikilocytosis.
Authors: S C Liu, J Palek, J Prchal, R P Castleberry
Journal: Journal of Clinical Investigation (1981)

Hereditary pyropoikilocytosis (HPP) is a hemolytic anemia characterized by microspherocytosis, poikilocytosis, and an unusual thermal sensitivity of erythrocytes. We have investigated the contribution of abnormal membrane skeletal assembly to these abnormal HPP erythrocyte properties. Skeletons prepared from fresh HPP ghosts with Triton X-100 were considerably more fragile than skeletons from control erythrocytes. Spectrin, the major skeleton component, extracted at 0 degrees C from normal erythrocytes, was present primarily as tetramers and high molecular weight complexes. In contrast, spectrin extracted from HPP erythrocytes under identical conditions contained a significant amount of dimers with a concomitant decrease of tetramers. Furthermore, spectrin dimers from HPP erythrocytes differed from normal spectrin dimers in their failure to reassociate into tetramers both in solution and in the membrane. Presumptive HPP carriers (asymptomatic mothers of the two patients) exhibited a mild but reproducible increase of spectrin dimers in 0 degrees C extracts and a defective reassociation of spectrin dimers of tetramers both in solution and in the membrane. We conclude that in HPP, self-association of spectrin dimers into tetramers is defective, which accounts for the instability of membrane skeletons.
Primary Pituitary Lymphoma Diagnosis by FDG-PET/CT
Authors: Kazumasa Hayasaka, Masamichi Koyama, Takashi Yamashita
Journal: Clinical Nuclear Medicine (2010)

Primary pituitary lymphoma is extremely rare. We describe a 71-year-old man who presented with appetite loss and sudden visual loss. Brain magnetic resonance imaging showed a mass at the pituitary gland that was moderately and homogeneously enhanced with contrast media. F-18 fluorodeoxyglucose positron emission tomography combined with CT (FDG-PET/CT) performed for a systemic survey revealed focal moderate FDG uptake only in the pituitary gland. The mass was histologically diagnosed as non-Hodgkin lymphoma from a biopsy of the pituitary gland.
Is fulminant viral hepatitis a systemic disease?
Authors: H. T. Ricketts
Journal: JAMA (1973)

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