tbuckley/cabot-search huggingface dataset:
Passage of dietary antigens into the blood of children with coeliac disease. Quantification and size distribution of absorbed antigens.
Authors: S Husby, N Foged, A Host, S E Svehag
Journal: Gut (1987)

The uptake of ovalbumin (OA) from egg and beta-lactoglobulin (BLG) from cow9s milk into the blood was investigated for seven hours after a test meal in five children with coeliac disease on a gluten free diet and after gluten challenge, and in five children with normal jejunal mucosa. Ovalbumin was detectable by ELISA in three of five coeliac children (maximal concentrations 8-178 ng/ml serum) and in five of five controls (maximal 4-91 ng/ml serum). Beta-lactoglobulin was detected in three of five coeliac children (maximal 0.6-6 ng/ml serum) and in two of five controls (maximal 0.5 and 50 ng/ml serum). No clear relationship was seen between maximal antigen concentrations and titres of serum IgG or IgA antibodies determined by ELISA, or as percentage antigen binding in a Farr type radioimmunoassay. Ovalbumin and beta-lactoglobulin was seen in serum of all coeliac patients and controls by HPLC fractionation in combination with ELISA, either in high MW fractions, or at the Mr of native OA and BLG, respectively. In one control degradation products (about 17 kD) of BLG were detectable in serum. The serum concentrations of OA and BLG were increased on gluten challenge in four or five coeliac children, indicating increased macromolecular passage through the gut mucosa in untreated coeliac disease.
Lincoln-Marfan Debate...
Authors: A. M. Gordon
Journal: JAMA (1964)

<h3>To the Editor:—</h3> I was delighted to learn that my contention identifying Abraham Lincoln with the Marfan syndrome (<i>J Kentucky Med Assoc</i><b>60</b>:249 [March] 1962) has now been confirmed by Dr. Harold Schwartz (<i>JAMA</i><b>187</b>:473 [Feb 15] 1964). My address to the Kentucky State Medical Association on Sept 21, 1961, is the first reference to appear anywhere associating Lincoln with the Marfan syndrome. I also know that since 1961 many physicians have asked patients with the syndrome, "Are you by chance related to Abraham Lincoln?" and since there are thousands of living Americans who claim such kinship, I predict the appearance of many more reports similar to the recentJournalcommunication. I carefully read the Schwartz communication and aside from his case reports I could not find that he has added anything new to my earlier report. The image of Nancy Hanks fits the Marfan syndrome. This cannot
Localization and Resection of Insulinomas and Gastrinomas
Authors: Douglas L. Fraker
Journal: JAMA (1988)

<h3>SELECTED CASES</h3><h3>Case 1</h3> A 45-YEAR-OLD woman with a threeyear history of epigastric pain was treated initially with cimetidine and then with ranitidine hydrochloride and antacids, with only mild relief. Her fasting serum gastrin level was elevated at 496 ng/L (496 pg/mL) (normal, &lt;100 ng/L [&lt;100 pg/mL]). Her basal acid output was 32 mEq/h (normal, &lt;15 mEq/h). The results of her secretin stimulation test were abnormal, with a rise in the serum gastrin level from 239 ng/L (239 pg/mL) at baseline to 825 ng/L (825 pg/mL) (abnormal increment, &gt;200 ng/L [&gt;200 pg/mL]). Ultrasound, computed tomographic (CT) scan, and selective angiogram all failed to demonstrate a gastrinoma. Selective venous sampling was performed and a marked step-up in gastrin levels was found in the superior pancreaticoduodenal vein (Fig 1). The patient underwent an exploratory laparotomy, and intraoperative ultrasound demonstrated a lesion in the posterior head of the pancreas (Fig 2). After enucleation,
Relationship of Aspirin Use With Age-Related Macular Degeneration: Association or Causation?
Authors: Sanjay Kaul, George A. Diamond
Journal: JAMA Internal Medicine (2013)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA Internal Medicine HomeNew OnlineCurrent IssueFor Authors Podcast Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA Internal Medicine journal
Where, Oh Where Has the MB Gone?
Authors: Robert Roberts
Journal: New England Journal of Medicine (1985)

In 1959 Ebashi et al. reported that plasma creatine kinase activity was elevated in patients with skeletal-muscle injury,1 and in 1960 Dreyfus et al. reported similar findings in patients with acute myocardial infarction.2 The increased diagnostic specificity for myocardial infarction afforded by assay of the MB isoenzyme was appreciated by Van der Ween and Willebrands in 1966.3 Measurement of plasma MB creatine kinase every 8 to 12 hours for 24 to 48 hours after a suspected myocardial infarction is now more commonly performed than the traditional daily measurements of lactic dehydrogenase, serum aspartate aminotransferase and total creatine kinase. Plasma MB . . .
Teen With Lesion on Nasal Sidewall
Authors: Tara Bronsnick, A. Yasmine Kirkorian, Jisun Cha
Journal: JAMA Pediatrics (2013)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA Pediatrics HomeNew OnlineCurrent IssueFor Authors Podcast Journals JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2024 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA Pediatrics journal
21 The selective cyclooxygenase-2 inhibitor SC-236 reduces experimental liver fibrosis by inactivating kupffer cells and acting as a peroxisome proliferator-activated receptor gamma ligand
Authors: A. Planagumà, J. Clària, M. López-Parra, E. Titos, R. Miquel, J.L. Masferrer, V. Arroyo, J. Rodés
Journal: Journal of Hepatology (2004)
Further Experiences with Severe Allergic Reactions to Insect Stings
Authors: Harry Louis Mueller
Journal: New England Journal of Medicine (1959)

A PREVIOUS report1 on allergic reactions to bee and wasp stings emphasized the seriousness of these reactions and the importance of specific treatment. Up to the present, I have seen 101 such patients, and Dr. Lewis W. Hill and I have studied a total of over 120 cases. The additional experience and information gained in the testing and treatment of these patients has seemed to be of such importance as to warrant this publication.Our experience, and frequent public press reports, indicate that severe reactions to insect stings occur more commonly than is generally supposed. In fact, it is possible . . .
Is the Governance of the Medical Schools Adequate to Meet the New Demands?
Authors: John Z. Bowers
Journal: JAMA (1968)

Governance is defined in<i>Webster's New International Dictionary, Second Edition</i>, as "Act, manner, office, or power of governing; government.... Method or system of government or regulation." If we apply this definition to medical schools we are not concerned solely with the dean. We include the trustees or regents; the president and his staff; vice presidents, the dean, department chairmen, faculty and external agencies, federal and private, that influence the decision-making process. My assignment is to present the reasons why the Macy Foundation became interested in the problems of governance, what we have done, and what we plan to do in the future. The medical schools have undergone what it is not an overstatement to call wrenching changes in the last 20 years. First, there has been an explosive growth in the variety and scale of programs. Second, there have been rapid changes in the character of the medical schools. They
Activation of cultured vascular endothelial cells by antiphospholipid antibodies.
Authors: R Simantov, J M LaSala, S K Lo, A E Gharavi, L R Sammaritano, J E Salmon, R L Silverstein
Journal: Journal of Clinical Investigation (1995)

Circulating antiphospholipid antibodies (aPL) are associated with a syndrome of thrombosis, recurrent fetal loss, and thrombocytopenia. We have demonstrated the activation of cultured human umbilical vein endothelial cells (HUVEC) by IgG from patients with anticardiolipin antibodies (aCL). Incubation of HUVEC for 4 h with purified IgG (100 micrograms/ml) from patients with high-titer aCL induced a 2.3-fold increase in monocyte adhesion over that seen in HUVEC incubated with IgG's from normal subjects. The effect of aCL was not attributable to LPS contamination, Fc receptors, or immune complexes. Monocyte adhesion was not induced when the aCL were added in serum-free media but was restored by the addition of purified beta 2GP1, previously described as a necessary cofactor for aCL reactivity. Purified rabbit polyclonal IgG raised against beta 2GP1 also induced monocyte adhesion when incubated with HUVEC. Preadsorption of patient serum with cardiolipin reduced monocyte adhesion by 60%. Immunofluorescent microscopy demonstrated that endothelial cells incubated with patient IgG expressed cell adhesion molecules, including E-selectin, vascular cell adhesion molecule-1, and intracellular adhesion molecule-1. These data support the hypothesis that aPL activate vascular endothelial cells, thereby leading to a pro-thrombotic state.
Use of Esophageal Gastric Tube Airway
Authors: Robert R. Fluck
Journal: JAMA (1984)

<h3>To the Editor.—</h3> I refer to the article on use of the EGTA in the prehospital setting. At first it seemed a convincing condemnation of EGTA use. However, a closer perusal revealed three problems. First, no one has yet addressed temporal changes in arterial blood gases (ABG) in the patient who has suffered full cardiopulmonary arrest. Ventilation-perfusion matching would be very poor at first, with widespread atelectasis. As proper resuscitation proceeds, it seems reasonable to assume that ABG values would improve as ventilation-perfusion matching improves. This uncontrolled variable could, therefore, account for some of the improvement that occurred when the patients were intubated. Second, in their discussion of results, the authors point out that only nine victims had ABG values within their criterion limits (Pao<sub>2</sub>≥80 mm Hg, Paco<sub>2</sub>≤55 mm Hg) when ventilated with EGTA. What they fail to point out is that after endotracheal intubation, 14
Donald James Grubb
Authors: H. Murray
Journal: BMJ (2002)

Former consultant anaesthetist Royal Hospital for Sick Children, Edinburgh, 1964-96 (b 1931; q St Andrews 1950; FFA), died from complications of vascular disease and carcinoma on 4 December 2001.

He rapidly progressed in his chosen specialty, becoming consultant anaesthetist in 1963 at the early age of 32. He was much involved in the development of innovative techniques in anaesthesia and among many other firsts he administered the anaesthetic for the first bypass operation carried out at the Royal Hospital for Sick Children, Edinburgh, in 1974. He leaves a wife, Val; and three sons.
Instance-based manifesto?
Authors: Márk Jelasity
Journal: Behavioral and Brain Sciences (2000)

Page's definition of localism is inspired by the instance-based paradigm. However, the locality of representations is not necessary for a model to be instance-based and, on the other hand, explicit featural representations are generally considered local. The important distinction is between instance-based and noninstance-based paradigms and not between distributed and local representations as Page claims.
Effects of Low-Dose Heparin Infusion on Arterial Endothelin-1 Release in Humans
Authors: P.M. Piatti, L.D. Monti, G. Valsecchi, M. Conti, R. Nasser, B. Guazzini, E. Fochesato, C.V. Phan, A.E. Pontiroli, G. Pozza
Journal: Circulation (1996)

Background The aim of this study was to evaluate the effect of low-dose heparin infusion on arterialized endothelin-1 (ET-1) release in the presence of fasting or high insulin levels in healthy humans. Methods and Results Eleven normal subjects underwent two tests in random order lasting 240 minutes. A primed (250 IU), continuous heparin (600 IU/h) infusion was performed in test 1; saline was infused in test 2 as control. At 120 minutes, a euglycemic hyperinsulinemic clamp (25 mU·kg −1 ·h −1 ) was started that lasted 2 hours in both tests. Two hours after heparin infusion (test 1), ET-1 levels decreased by 32% (3.52±0.60 to 3.02±0.73 pg/mL), while nitric oxide (NO) and forearm blood flow increased by 29% and 14%, respectively. During saline infusion, ET-1, nitric oxide, and forearm blood flow remained unchanged. There was a significant interaction between the effect of decreasing ET-1 levels and the heparin treatment ( F , 4.06; df , 3.30; P &lt;.01). The decrease in ET-1 levels was significantly correlated with the increase in forearm blood flow in test 1 ( r =.74; P &lt;.01) but not in test 2. During the heparin/insulin period, ET-1 increased by 25%, returning to fasting values; nitric oxide levels increased by 12%; and forearm blood flow remained unchanged. Conclusions The present study showed that it is possible to decrease ET-1 levels by use of low-dose heparin infusion in humans. This effect seems mediated by a simultaneous increase in nitric oxide levels and is completely reversed by a mild increase in insulin concentrations.
Immunofluorescence studies in primary localized cutaneous amyloidosis
Authors: D.M. MacDONALD, M.M. Black, N. Ramnarain
Journal: British Journal of Dermatology (1977)

Immunofluorescence studies were carried out on 47 patients with primary localized cutaneous amyloidosis. The majority had the macular, maculopapular or papular forms of lichen amyloidosus, although 3 patients had the nodular type. All biopsies fluoresced positively for immunoglobulins or complement, particularly IgM and C3. Staining for kappa and lambda light chains was positive. The consistent immunofluorescent patterns observed were similar in some respects to lichen planus, suggesting that colloid bodies and amyloid may share similar properties in acting as a filamentous sponge on to which immunoglobulins and complement are absorbed. The pathogenesis of lichen amyloidosus is compared with that of lichen planus.
Double-edged Sword?
Authors: Prescott G. Woodruff
Journal: JAMA Internal Medicine (2013)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA Internal Medicine HomeNew OnlineCurrent IssueFor Authors Podcast Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA Internal Medicine journal
Personality traits associated with different chest pains after myocardial infarction.
Authors: R. R. Lovell, A. Verghese
Journal: BMJ (1967)

Most patients who have had an acute myocardial infarction later experience pain in the chest of one sort or another. Angina pectoris is the commonest pain, and one in or including the left anterior chest is the next commonest single entity. The factors which determine post-infarction pain are complex. Clinical observation suggests that they include mental ones. Angina pectoris is often induced by emotion, and left chest pain in patients with heart disease has long been associated with anxiety. If mental factors associated with pain after myo cardial infarction could be defined, more might be learnt of the mechanisms causing the pains and it might be possible to prevent some of them.
Knowing too much
Authors: Sofie Zermansky, Adam Zermansky
Journal: BMJ (2008)

“There’s something wrong with her eye, it doesn’t seem to abduct past the midline. I think she has a sixth nerve palsy.”⇓





Twenty four hours after undergoing an emergency caesarean section, I was not in the mood for my husband (a neurology registrar) to be overdiagnosing my newborn baby. “There’s nothing wrong with her eye,” I replied, “she …
Demonstration of an abnormality of C apoprotein of very low density lipoprotein in patients with gout.
Authors: D G Macfarlane, C A Midwinter, P A Dieppe, C H Bolton, M Hartog
Journal: Annals of the Rheumatic Diseases (1985)

The very low density (VLDL) apolipoproteins of 12 male patients with gout have been studied by analytical isoelectric focusing. The relative percentage distribution of the C apolipoproteins was calculated and compared with that from 12 normolipidaemic and 12 9lipid-matched9 controls. In the gout patients apolipoprotein CII (apo CII) represented 19.6% of the VLDL C proteins and the CII/CIII2 ratio was 0.57. In the normolipidaemic controls apo CII represented 28.8% and in the lipid-matched controls 33.1% of VLDL apo C, and the CII/CIII2 ratio approached one in each control group. These differences were significant. This suggests that a reduction in VLDL apo CII may predispose to the hypertriglyceridaemia that is commonly found in patients with gout.
In vivo effects of PUVA on lymphocyte function
Authors: WARWICK L. MORISON, JOHN A. PARRISH, KURT J. BLOCH, JOEL I. KRUGLAR
Journal: British Journal of Dermatology (1981)

Whole-body exposure to erythemogenic doses of PUVA in normal volunteer subjects resulted in a decrease in the proportion of circulating sheep erythrocyte rosette-forming and surface membrane immunoglobulin-positive lymphocytes and an increase in the proportion of null cells. Doses of PUVA resulting in minimal or no erythema had similar but less marked effects on lymphocytes. The changes appeared 30 min after exposure, were maximal at 12–16 h and returned to pre-treatment levels by 72 h post-irradiation. The response of lymphocytes to stimulation with phytohaemagglutinin was unaffected. No alteration occurred in the absolute numbers of circulating lymphocytes or poly-morphonuclear leukocytes.
Early diagnosis of acute myocardial infarction based on assay for subforms of creatine kinase-MB.
Authors: P R Puleo, P A Guadagno, R Roberts, M V Scheel, A J Marian, D Churchill, M B Perryman
Journal: Circulation (1990)

Thrombolytic therapy for patients with acute myocardial infarction (AMI) has produced the need for an accurate early diagnostic marker. We previously developed and assessed an assay for the creatine kinase (CK)-MB subforms; assay time is 25 minutes. Plasma MB2 (tissue subform) activity, MB1 (plasma-modified subform) activity, and MB2/MB1 ratio in 56 healthy individuals were 0.61 +/- 0.33 units/l, 0.63 +/- 0.33 units/l, and 0.94 +/- 0.39, respectively. Only one individual had both an MB2 activity greater than 1.0 units/l and an MB2/MB1 ratio of more than 1.5. Similar results were obtained in 50 hospitalized patients without cardiac disease; two of these patients had both an MB2 activity and an MB2/MB1 ratio greater than the cutoff values. Among 49 patients with AMI, MB2 activity and the MB2/MB1 ratio began to increase 2 hours after AMI; the ratio reached a plateau of 3.1 by 4-6 hours. The first available plasma sample was abnormal by the subform assay in 67% of patients and by a conventional MB assay in 27% of patients. Assay sensitivities in samples collected at 2-4, 4-6, and 6-8 hours after AMI were 59%, 92%, and 100% for the subform assay and 23%, 50%, and 71% for the conventional assay (p less than 0.03 versus subform assay at each time interval). False-negative results were obtained by the subform and conventional assays in 15 and 45 samples at a mean of 2.3 and 5.8 hours, respectively. Subform assay provides rapid and reliable diagnosis of AMI within 4-6 hours after the onset of symptoms, which is 6 hours before conventional CK-MB assays are accurate.
A Personalized Approach to Assessing and Managing Pain in Patients With Cancer
Authors: David Hui, Eduardo Bruera
Journal: Journal of Clinical Oncology (2014)

Pain is one of the most common and distressing symptoms in patients with cancer. In this review, we discuss an evidence-based approach to personalized pain assessment and management. Recent insights into the pain expression pathway have led to a paradigm shift in pain management, allowing clinicians to deliver personalized treatments tailored to the individual's needs. Personalized pain management begins with systematic screening, followed by comprehensive pain assessment. Impeccable characterization of pain informs its etiology and the mechanism to guide treatment choices. Identification of modulators of pain expression such as psychological distress, alcoholism, substance use, and delirium allow clinicians to further tailor treatment recommendations. Documentation of a personalized pain goal provides an individualized response criterion. A multidimensional treatment plan is then formulated targeting the pain mechanism, etiologic factors, and modulators. Finally, longitudinal monitoring customized to the individual's needs allows clinicians to improve adherence and, ultimately, to optimize pain control over time.