tbuckley/cabot-search huggingface dataset:
PWE-030 Immunocytochemical assessment of intra-tumour microvessel density in oesophagogastric cancer does not have prognostic significance
Authors: R T Gray, M E O'Donnell, J A McGuigan, G M Spence
Journal: Gut (2012)

<h3>Introduction</h3> Intra-tumour microvessel density (IMD), a marker of tumour angiogenesis, correlates with metastasis and poor prognosis in many cancers. In oesophagogastric cancer however, the prognostic significance of IMD assessment remains incompletely investigated. <h3>Methods</h3> Patients undergoing surgery with curative intent, without pre-operative chemotherapy, were prospectively recruited between February 1999 and August 2000. Immunocytochemical staining of tumour microvessels was undertaken using anti-CD34 (QBEND 10 clone) antibodies. IMD (microvessels per mm<sup>2</sup>) was assessed using a validated “hot-spot” technique. Patients were followed-up over a 10-year period using the Northern Ireland Cancer Registry. The relationship between IMD and standard clinicopathological variables was assessed using the Mann–Whitney U test. Univariate survival analysis was calculated using a Cox9s proportional hazard model while survival analysis was calculated using Kaplan–Meier estimation and log rank. <h3>Results</h3> 61 patients were recruited (male=45) with a median age of 66.0 years (range 39–83). The overall 10-year survival rate was 19.7% (n=12). IMD was significantly higher in males compared to females (332.93 vs 252.44, p=0.04) and adenocarcinomas compared to squamous cell carcinomas (356.10 vs 203.66, p&lt;0.001). On univariate survival analysis only lymphovascular invasion predicted poor prognosis (HR 2.26, 95% CI 1.01 to 5.07, p=0.05). Kaplan–Meier survival analysis demonstrated no difference in long-term survival for patients with IMD levels greater or less than the median value (738 days vs 882 days, p=0.67). <h3>Conclusion</h3> Immunocytochemical analysis of IMD does not have a prognostic benefit in determining long-term survival in patients with oesophagogastric cancer. <h3>Competing interests</h3> None declared.
CLINICAL LECTURE on a CASE of LOCALISED MYELITIS, Affecting the Fifth Lumbar and the Sacral Segments of the Spinal Cord, the Result of a Slight Traumatic Injury; and a CASE of PARALYSIS of ALL FOUR LIMBS. DUE to a SPINAL INJURY: Delivered at the Edinturgh Royal Infirmary
Authors: B. Bramwell
Journal: BMJ (1898)
A clinical and immunologic phase 2 trial of Wilms tumor gene product 1 (WT1) peptide vaccination in patients with AML and MDS
Authors: Ulrich Keilholz, Anne Letsch, Antonia Busse, Anne Marie Asemissen, Sandra Bauer, Igor Wolfgang Blau, Wolf-Karsten Hofmann, Lutz Uharek, Eckhard Thiel, Carmen Scheibenbogen
Journal: Blood (2009)
Immunophenotype-defined sub-populations are common at diagnosis in childhood B-cell precursor acute lymphoblastic leukemia
Authors: N F Øbro, H V Marquart, H O Madsen, L P Ryder, M K Andersen, B Lausen, B K Albertsen, P S Wehner, J Helgestad, K Schmiegelow
Journal: Leukemia (2011)
Stress failure and high-altitude pulmonary oedema: mechanistic insights from physiology
Authors: S. R. Hopkins
Journal: European Respiratory Journal (2010)

High-altitude pulmonary oedema (HAPE) is a potentially fatal altitude illness affecting individuals within 2–4 days of rapid ascent to altitudes above 3,000 m. Although a minority of high-altitude travellers develop HAPE 1, there is some suggestion that many develop subclinical fluid accumulation without overt alveolar flooding 2. The inciting mechanism of the injury to the lung in HAPE still generates some controversy. However, there is an ever-growing body of evidence that mechanical injury to the pulmonary capillaries induced by high transmural pressures starts a cascade of events that ultimately results in the development of HAPE. This injury, termed “stress failure” described by West et al. 3, refers to mechanically induced breaks in the blood-gas barrier, and these have been suggested to be important the pathophysiology of a number of human diseases 4.

In animals, when pulmonary capillaries are subjected to increased transmural pressure, ultrastructural changes consisting of discrete areas of damage to the blood–gas barrier, with rupture of the capillary endothelium, extracellular matrix and the alveolar epithelium, interspersed with large areas of structurally intact blood–gas barrier are observed 5. Accompanying this is increased permeability of the lung to protein and red blood cells, as measured by increased concentrations in bronchoalveolar lavage fluid 6. Leukotriene (LT)B4 concentration is also increased in bronchoalveolar lavage fluid 6, perhaps representing cellular activation by exposed basement membrane. Similar findings are observed in some humans following maximal exercise in normoxia 7 where bronchoalveolar lavage fluid contains increased concentrations of red cells, protein and LTB4 thought to result from high pulmonary capillary pressures. In both of these instances, the blood–gas barrier retains sieving function for large molecular weight proteins 6. However, in established HAPE, permeability to macromolecules is increased 8, and an inflammatory response of the lung to …
Frederick Cayley Robinson's Acts of Mercy murals at the Middlesex Hospital, London
Authors: J H Baron
Journal: BMJ (1994)

wife with his symptoms after she had admitted her intentions of using it on him.Presumably his intention would not have been to kill himself but only to make himself ill.Another possibility, that of accidental ingestion of the poison, has to be considered.In this scenario we could imagine that Adelaide had shown Edwin the bottle of chloroform, confessing her intention to use it as a sexual depressant.She had left it on the mantel- piece and was either out ofthe room or fell asleep when Edwin mistakenly took the chloroform, thinking it was medicine.Perhaps he awoke from a sleep and did this; perhaps he had agreed to Adelaide helping him to sleep with a few drops of chloroform on a handerkerchief and awoke in a confused state.It would be surprising if the hot, burning taste of the chloroform had not alerted Edwin to his mistake.But his mouth and throat may have been sufficiently inflamed from his successive dental visits for the sensation in the mouth not to be as acute as it might otherwise have been.On balance, accidental ingestion seems the least likely possibility.The third possibility, that of Adelaide murdering Edwin, certainly fits some of the facts.Her motive was that, despite any outward appearance to the contrary, she saw herself happier married to Dyson than to Edwin.She procured chloroform with Dyson's help and used the vapour to make Edwin drowsy, probably with his consent as the pain of the dental treatment may have made sleep difficult.She then offered her
Gastroallergic anisakiasis: Borderline between food allergy and parasitic disease—Clinical and allergologic evaluation of 20 patients with confirmed acute parasitism by Anisakis simplex
Authors: Alvaro Daschner, Alicia Alonso-Gómez, Rosario Cabañas, José-María Suarez-de-Parga, María-Concepción López-Serrano
Journal: Journal of Allergy and Clinical Immunology (2000)
Thallium Poisoning Treated with BAL
Authors: Oscar Grunfeld
Journal: New England Journal of Medicine (1963)

THALLIUM has been used extensively as a medicament, depilatory agent, insecticide and rodenticide and in industry.1 2 3 The most frequent cause of thallotoxicosis is the accidental or suicidal ingestion of preparations containing this poison.4 5 6 7 8 9 The clinical picture is extremely variable, comprising neurologic, gastrointestinal, cardiovascular, dermatologic and endocrine manifestations.6 , 7 , 10 , 11 The clinical diagnosis may be very difficult, especially in children who present bizarre neurologic abnormalities. One of the best signs is late alopecia.12 The lethal dose for human beings varies from 0.2 to 1 gm.13 Thallium is deposited in all the tissues, especially in the liver, kidney and intestine, and is found in . . .
Ex-vivo gene therapy of human vascular bypass grafts with E2F decoy: the PREVENT single-centre, randomised, controlled trial
Authors: Michael J Mann, Anthony D Whittemore, Magruder C Donaldson, Michael Belkin, Michael S Conte, Joseph F Polak, E John Orav, Afshin Ehsan, Giorgio Dell'Acqua, Victor J Dzau
Journal: The Lancet (1999)
Integral Diagnosis of Adult Mastocytosis. Impact of the Different Clinical, Biologic, Immunophenotypic and Molecular Parameters in the Diagnosis and Classification of the disease. A Prospective Study by Spanish Network on Mastocytosis (REMA) in 191 cases
Authors: L.B. Sanchez-Muñoz, I. Alvarez, R. Nuñez, A. Prados, A.C. Garcia-Montero, M. Garcia-Cosio, M. Cuevas, M. Jara, C. Teodosio, J. Almeida, M.L. Sanchez, P.M. Hernandez-Campo, M. Mollejo, A. Orfao, L. Escribano
Journal: Journal of Allergy and Clinical Immunology (2008)
Acute Experimental Pancreatitis
Authors: Allan J. Schutt
Journal: JAMA (1965)

An antitryptic agent (Trasylol), a polyvalent proteolytic enzyme inhibitor, was used to treat four types of experimental pancreatitis. Acute hemorrhagic pancreatitis was induced in 48 dogs by injection of dilute staphylococcic toxin into the major pancreatic duct and in 15 dogs by creation of a blind duodenal loop. Mortality and severity of pancreatitis were similar for 27 untreated dogs and 36 treated dogs. Acute interstitial pancreatitis was induced in 100 rats by obstruction of the common biliary-pancreatic outflow channel. Significant reduction in mortality of treated rats was noted only when bile was excluded from the obstructed pancreas. Treatment with Trasylol may reduce mortality when the pancreatic duct is obstructed and bile is excluded from the pancreas. In these experiments Trasylol had no significant effect on the course of acute hemorrhagic pancreatitis.
Presentational skills are taught in some hospitals
Authors: D. Cummins
Journal: BMJ (1997)

Malignant cerebral glioma Modern radiotherapy can give good quality survival for six monthsEditor-We wish to correct misinformation reported by Elizabeth Davies and colleagues in their study of survival after radiotherapy for malignant cerebral glioma. 1 Contrary to their suggestion in the acknowledgements, the study had not been supported by the Medical Research Council Brain Tumour Working Party.As the poor study design indicates, the study had never been officially submitted to the Medical Research Council and had therefore not been subjected to its rigorous protocol review process.For example, Davies and colleagues report that their criteria for assessment of treatment toxicity were derived in a "pragmatic fashion after discussion" by a "process of elimination," without evidence from imaging to exclude tumour progression.This would be totally unacceptable, let alone publishable.The impression that the 105 patients represent an unselected consecutive series is difficult to believe as the seven centres should, over two years, have seen 400-800 eligible patients. 2 The reported adverse prognostic factors in patients with high grade glioma have been known for over 18 years. 3Although the authors appropriately conclude that severely disabled patients have a poor prognosis and may not be suitable for active treatment, the fact that they were considered for intensive treatment at all is surprising.Centres specialised in the treatment of patients with brain tumours would not have accepted patients with such a poor prognosis for high dose radiotherapy.Most of the patients also seemed to receive initial whole brain radiotherapy followed by a radiation boost to the tumour.Whole brain radiotherapy is nothing but toxic and has not been practised in specialist centres for many years.Given the use of outdated and often inappropriate high dose, wide field radiotherapy and the flawed assessment of morbidity from treatment, the conclusion that radiation is of little value and simply results in adverse effects seems ill advised.High grade gliomas are among the most devastating of malignancies, with few useful treatment options.Modern radiotherapy, although not curative, offers a survival benefit of about six months, 3 and for most patients without functional impairment the quality of survival is good.Without com-parative data on the quality of life, how can we decide whether prolongation of survival by six months with clinical deterioration in a small proportion of patients is worse than the alternative of progressive functional decline, which happens in all patients without treatment?Yes, we do need more effective treatments without morbidity, but to throw out a proved treatment on the basis of misinformation is a travesty to evidence based medicine, to which the BMJ claims allegiance.
Physician Must Rely on Remote-Duty Corpsman When Patient Is Deep in, or Far Across, Sea
Authors: Chris Raymond
Journal: JAMA (1989)

EVEN IF a shore-based physician wanted to make one, house calls to a submarine are not permitted during its tour of duty. And even on surface ships, "although we're not hidden from anybody, we may not want to advertise our exact position [by calling on a physician]," says CDR Steve Warlick of the Naval Undersea Medical Institute (NUMI), Groton, Conn. Nonetheless, even the hardiest sailor can fall ill or be injured. Enter the independent duty corpsman. He tackles one of the most demanding medical assignments in the military, steering a course between the unrelenting medical and health care responsibilities to fellow crew members aboard ship and the dictates of a consulting physician based on land. <h3>Independent Duty Corpsmen</h3> The Groton institute is the training site for independent duty corpsmen. About 75 men receive instruction each year to assume duties on ballistic missile and attack submarines. The exacting training includes qualifying
MITRAL VALVE PATHO-ANATOMIC PREDICTORS OF THE NUMBER OF MITRACLIP DEVICES IMPLANTED FOR PERCUTANEOUS REPAIR OF MITRAL REGURGITATION
Authors: Ehrin J. Armstrong, Christo H. Swan, Deepa Upadhyaya, Ravi Garg, Jason H. Rogers, Elyse Foster, Ted Feldman
Journal: Journal of the American College of Cardiology (2011)
Inhibition of complement-mediated opsonization and phagocytosis of Streptococcus pyogenes by D fragments of fibrinogen and fibrin bound to cell surface M protein.
Authors: E Whitnack, E H Beachey
Journal: The Journal of Experimental Medicine (1985)

The biological effects of the binding of fibrin(ogen) degradation products to M protein-bearing group A streptococci were investigated. Type 24 group A streptococci bind fibrinogen degradation products of the D family, but not fragment E. Binding appears to be mediated by M protein, since a large peptide of this molecule (pep M24) bound to fragments containing the terminal domains of the fibrinogen molecule (D, X, and Y), but not fragment E, and pep M24 inhibited the binding of digested fibrinogen to streptococcal cells. An M protein-binding site occurs on fragment D3 and, therefore, differs from several functional sites present on D1 but not D3, including the fibrin polymerization site, the two gamma chain crosslink sites, and the bindings sites for platelet fibrinogen receptor, staphylococcal clumping factor, and ionized calcium. Bound fibrinogen degradation products prevented deposition of C3 on the streptococcal cell surface, and, in consequence, prevented phagocytosis by neutrophils in nonimmune blood. The average affinity of D fragments for the streptococcal cell surface was approximately 30 times lower than that of native fibrinogen, and a terminal plasmic digest was approximately 50 times less potent in inhibiting opsonization by C3. However, physiologic concentrations of digested fibrinogen sufficed to inhibit opsonization and phagocytosis completely. Digests of crosslinked fibrin clot also inhibited opsonization, although slightly less effectively than did fibrinogen digests. The antiopsonic effect of fibrin(ogen) degradation products may be relevant to circumstances in which fibrin(ogen)olysis is occurring, e.g., exudation and suppuration.
Redox redux: protecting the ischemic myocardium
Authors: Oded N. Spindel, Bradford C. Berk
Journal: Journal of Clinical Investigation (2011)

Cardiac ischemia-reperfusion (I-R) injury occurs upon prompt restoration of blood flow to the ischemic myocardium after an acute myocardial infarction. Interestingly, many of the features of I-R injury are related to impaired mitochondrial signaling and mitochondrial dysfunction. Restoring cardiac energy bioavailability and reduction-oxidation (redox) signaling are therefore important in recovery after I-R injury. In this issue of the JCI, Yoshioka and colleagues describe an important and unexpected role for thioredoxin-interacting protein (TXNIP) in the control of mitochondrial respiration and cell energy metabolism. Their findings could open the door for development of TXNIP-targeted therapeutic approaches for the treatment of cardiac I-R injury.
Usefulness of the postexercise response of systolic blood pressure in the diagnosis of coronary artery disease.
Authors: K W Amon, K L Richards, M H Crawford
Journal: Circulation (1984)

The normal decline in systolic blood pressure (SBP) during the recovery phase of treadmill exercise does not occur in some patients with coronary artery disease (CAD). In others the recovery values of SBP exceed the peak exercise values. To examine the diagnostic value of this observation, we studied 31 normal subjects and 56 patients undergoing treadmill exercise before coronary cineangiography. Because of large differences in peak exercise pressures between the two groups, recovery ratios were derived by dividing the SBP at 1, 2, and 3 min after exercise by the peak exercise SBP. The 1, 2, and 3 min ratios in the normal subjects declined steadily from 0.85 +/- 0.07 (SD) to 0.79 +/- 0.06 and to 0.73 +/- 0.06, respectively, while the ratios in the patients with CAD remained elevated at 0.97 +/- 0.12 to 0.97 +/- 0.11 to 0.93 +/- 0.13. With use of the upper limits defined by two SDs of the normal value, recovery ratios were compared with the occurrence of angina and with ST segment depression on the exercise electrocardiogram in the patients with CAD. Abnormal ratios were more frequent in patients with CAD (53/56, 95%) than in those with ST segment depression (33/56, 59%), angina (37/56, 66%), and either ST segment depression or angina (42/56, 75%). Twenty of the patients with CAD who were on no medication underwent an additional treadmill exercise test on a separate day and no significant differences were found in the ratios from the two tests. Ten additional patients with CAD underwent treadmill exercise testing while on placebo and while on a beta-blocker.(ABSTRACT TRUNCATED AT 250 WORDS)
Open Notes: Sharing Physician Notes With Patients
Authors: David A. Nardone
Journal: Annals of Internal Medicine (2010)

Letters16 November 2010Open Notes: Sharing Physician Notes With PatientsDavid A. Nardone, MDDavid A. Nardone, MDFrom Portland Veterans Affairs Medical Center, Portland, OR 97239.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-153-10-201011160-00023 SectionsAboutFull TextPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail TO THE EDITOR:Sharing notes with our patients, as discussed by Delbanco and colleagues (1), is an important component in implementing the collaborative model of health care. I share my “problem list” as part of a summary I provide some new patients and include it in the after-visit summary given to all patients at the end of the appointment. To date, I have not received any negative feedback, including any about the sharing of a patient's mental health problems. The most frequent patient response is to clarify details and to correct any errors. I find this mutually advantageous for the ...Reference1. Delbanco T, Walker J, Darer JD, Elmore JG, Feldman HJ, Leveille SG, et al. Open notes: doctors and patients signing on. Ann Intern Med. 2010;153:121-5. [PMID: 20643992] LinkGoogle Scholar Author, Article, and Disclosure InformationAffiliations: From Portland Veterans Affairs Medical Center, Portland, OR 97239.Disclosures: None disclosed. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetailsSee AlsoOpen Notes: Doctors and Patients Signing On Tom Delbanco , Jan Walker , Jonathan D. Darer , Joann G. Elmore , Henry J. Feldman , Suzanne G. Leveille , James D. Ralston , Stephen E. Ross , Elisabeth Vodicka , and Valerie D. Weber Open Notes: Sharing Physician Notes With Patients R. Hal Baker Metrics Cited byTransparency in psychiatric care 16 November 2010Volume 153, Issue 10Page: 690KeywordsConflicts of interestElectrode recordingHealth carePsychiatry and mental health ePublished: 16 November 2010 Issue Published: 16 November 2010 Copyright & PermissionsCopyright © 2010 by American College of Physicians. All Rights Reserved.PDF downloadLoading ...
Training the Resident to Meet the Detail Men
Authors: Robert P. Ferguson
Journal: JAMA (1989)

To the Editor.—  Dr Shaughnessy 1 pointed out that the continuous exposure of residents in training to medical advertising was likely to influence their prescribing habits. Most physicians complete training unable to evaluate data on new pharmaceuticals critically, data that typically reaches the physician through advertising or via a potentially subjective presentation by a medical service representative—the detail man. Physicians who are new in practice usually are unprepared to deal with the ethical conflicts that can develop through physician incentive programs, which apparently are becoming more imaginative and played at higher stakes. 2   In September 1988, we initiated a seminar series as part of the developing University of Connecticut primary care residency program. A major part of our first seminar was devoted to pharmaceutical marketing strategies and the interaction of the physician with the medical service representative. Participants included primary care faculty at the University of Connecticut—affiliated Mount Sinai and New