tbuckley/cabot-search huggingface dataset:
FIBRO-ADENOMA OF THE LACHRYMAL GLAND.
Authors: LYMAN SKEEN
Journal: JAMA (1904)

<h3>Patient.</h3> —Mr. J. A. T., aged 82, came to me in July, 1904, with a tumor the size of a hazel nut at the outer canthus of left eye. <h3>History.</h3> —A history of gradual development with no pain was obtained. The patient had been told that cancer existed and the sun glass and<i>x</i>-rays had been used as treatment. One operation on the under surface of the lid had been done before I saw the case. <h3>Examination.</h3> —The tumor was pressing on the eyeball and interfered with its movement; a portion of the growth presented below the border of the upper eyelid. A clear fluid was discharged from a sinus near the outer edge of the orbit. <h3>Diagnosis.</h3> —Benign tumor of the lachrymal gland. <h3>Operation.</h3> —Under general anesthesia the entire mass was removed<i>en masse</i>through an incision along the eyebrow. On microscopic examination it proved to be a fibro-adenoma of the lachrymal gland. The
Diastolic coronary resistance in the isolated rabbit heart during and after ischaemia: contribution of extravascular forces
Authors: G. FLEETWOOD, P. A POOLE-WILSON
Journal: Cardiovascular Research (1986)

Coronary blood flow is influenced by contraction of the myocardium. The contribution of extravascular forces to coronary resistance during and after a period of low pressure perfusion or hypoxia and after a period of global ischaemia was studied in experiments on rabbit hearts perfused by the Langendorff method. End diastolic flow, perfusion pressure, developed tension, and resting tension were measured. Under control conditions the relation between end diastolic flow and perfusion pressure was almost linear (r>0.92). There was an initial fall in coronary resistance on initiation of hypoxia or low pressure perfusion, but subsequently coronary resistance increased concomitantly with the rise in resting tension. After 60 min total global ischaemia and 30 min reperfusion coronary resistance increased by 410(99)% and resting tension by 382(92)%. Increasing the potassium concentration of the perfusate to 19.2 mmol·litre−1 under control conditions caused the coronary resistance to increase by 336(74)%, whereas resting tension was unchanged. The increase in resistance with potassium could be reduced but not abolished by adenosine (1.87 × 10−5 mol·litre−1), indicating that the effect was largely attributable to vasoconstriction. Increased stimulation frequency (30 Hz) raised coronary resistance by 37(10)% and resting tension by 303(53)%. Perfusion with carbonyl cyanide p-trifluoromethoxyphenylhydrazone (1 × 10−6 mol·litre−1) increased coronary resistance by 169(27)% and resting tension by 782(11)6% and relaxed isolated epicardial coronary arteries. The effects of carbonyl cyanide p-trifluoromethoxyphenylhydrazone and increased stimulation frequency on coronary resistance were due to myocardial contracture. Myocardial contracture can increase coronary resistance and contributes to the increase in resistance seen during hypoxia or low pressure perfusion. But on reperfusion after global ischaemia the major cause of the increase in coronary resistance is increased obstruction in the vascular bed; extravascular factors have only a minor effect.
Adrenergically mediated variations in the energy required to defibrillate the heart: observations in closed-chest, nonanesthetized dogs.
Authors: R Ruffy, K Schechtman, E Monje, J Sandza
Journal: Circulation (1986)

The day-to-day variations in epicardial defibrillation threshold (DFT) were examined in closed-chest, unanesthetized dogs. In 11 animals, DFT decreased from 15.8 +/- 2.1 J (mean +/- SE) at the beginning of the study (day 1), to 7.4 +/- 1.7 J on day 2 (p less than .0001). DFT measured daily for 5 consecutive days in seven dogs decreased from 22.1 +/- 3.1 J on day 1 to 9.3 +/- 2.3 J on day 2 (p less than .01) and remained stable from day 2 to day 5. Transcardiac impedance, measured in six dogs, decreased from 112 +/- 6 omega on day 1 to 100 +/- 6 omega on day 2 (p = NS). Propranolol given on day 2 in 14 dogs increased DFT from 12.0 +/- 2.2 to 18.0 +/- 3.1 J (p less than .05). The effects on DFT of sequential administration of isoproterenol and propranolol were examined in 10 dogs. Isoproterenol decreased DFT from 10.0 +/- 1.9 to 5.5 +/- 1.5 J when given before propranolol (p less than .001, n = 10), and from 11.7 +/- 3.0 to 9.7 +/- 3.1 J when given after propranolol (p less than .05, n = 9). Propranolol increased DFT from 10.6 +/- 3.0 to 14.6 +/- 3.9 J when given before isoproterenol (p less than .02, n = 9), and from 10.7 +/- 1.4 to 14.4 +/- 1.5 J when given after isoproterenol (p less than .01, n = 10). These experiments demonstrate a sustained cardiac effect of epicardial defibrillation reflected by a decrease in DFT that is partially reversible by propranolol.(ABSTRACT TRUNCATED AT 250 WORDS)
A Suggestion for the Next Meeting.
Authors: Edward A. Tracy
Journal: JAMA (1897)

Boston, Aug. 18, 1897. <h3>To the Editor:</h3> —Permit me to make a suggestion. If it be carried out I think it will add to the interest of our annual meetings. Some of us in theAssociationare engaged upon original work. This work can be presented to our brother members in two ways: by reading a paper about it, and (when it concerns something concrete) presenting the thing itself. The combination method at present employed could be improved on without infringing on the practical work of the Section. Instead of the momentary presentation of instruments, etc., in conjunction with the reading of a paper, would it not be well to have such devices and objects placed where the members could examine them at their leisure? Such an exhibit could be conveniently made in the rear of the hall where the Section meets, or in a reserved space in the usual
MODERATE ALCOHOL CONSUMPTION PREVENTS CARDIOVASCULAR EVENTS AMONG SMOKERS IN JAPANESE MEN
Authors: Takahisa Kondo, Shigeki Osugi, Keiko Shimokata, Haruo Honjo, Kengo Maeda, Takashi Muramatsu, Kentaro Yamashita, Satoshi Shintani, Kunihiro Matsushita, Toyoaki Muroahra
Journal: Journal of the American College of Cardiology (2011)
Right ventricular outflow tract tachycardia due to a somatic cell mutation in G protein subunitalphai2.
Authors: B B Lerman, B Dong, K M Stein, S M Markowitz, J Linden, D F Catanzaro
Journal: Journal of Clinical Investigation (1998)

Idiopathic ventricular tachycardia is a generic term that describes the various forms of ventricular arrhythmias that occur in patients without structural heart disease and in the absence of the long QT syndrome. Many of these tachycardias are focal in origin, localize to the right ventricular outflow tract (RVOT), terminate in response to beta blockers, verapamil, vagal maneuvers, and adenosine, and are thought to result from cAMP-mediated triggered activity. DNA was prepared from biopsy samples obtained from myocardial tissue from a patient with adenosine-insensitive idiopathic ventricular tachycardia arising from the RVOT. Genomic sequences of the inhibitory G protein Galphai2 were determined after amplification by PCR and subcloning. A point mutation (F200L) in the GTP binding domain of the inhibitory G protein Galphai2 was identified in a biopsy sample from the arrhythmogenic focus. This mutation was shown to increase intracellular cAMP concentration and inhibit suppression of cAMP by adenosine. No mutations were detected in Galphai2 sequences from myocardial tissue sampled from regions remote from the origin of tachycardia, or from peripheral lymphocytes. These findings suggest that somatic cell mutations in the cAMP-dependent signal transduction pathway occurring during myocardial development may be responsible for some forms of idiopathic ventricular tachycardia.
Can Molecular Markers Predict When to Implement Treatment with Aromatase Inhibitors in Invasive Breast Cancer?
Authors: Sian Tovey, Barbara Dunne, Caroline J. Witton, Amanda Forsyth, Timothy G. Cooke, John M.S. Bartlett
Journal: Clinical Cancer Research (2005)

Resistance to tamoxifen is linked to overexpression of HER2, and aromatase inhibitors show particular benefit in progesterone receptor (PR)-negative patients. We previously reported reduced survival in patients overexpressing HER1, HER2, and HER3. We now show that both HER1-3 and PR status predicts for early relapse in estrogen receptor (ER)-positive tamoxifen-treated breast cancer patients.Tissue microarray technology was used to analyze 402 ER-positive tamoxifen-treated patients. Immunohistochemistry using epidermal growth factor receptor, HER2, HER3, HER4, and PR antibodies was done. Kaplan-Meier life table and Cox Regression analysis (log-rank testing of differences in breast cancer-related relapse on tamoxifen) was done.HER1-3 (but not HER4) overexpression predicted for early relapse on tamoxifen (P = 0.0060). PR-negative cases were also significantly more likely to relapse while on tamoxifen (P= 0.017). HER1-3-positive and/or PR-negative patients combined as a "high-risk" group were significantly more likely to relapse on tamoxifen in univariate (P < 0.0001) and Cox's multivariate analysis (P = 0.0069). However, this applied to early relapse on tamoxifen only, as any disease relapse after 3 years of tamoxifen was unrelated to PR/HER status.We show that HER1-3 and PR status can identify time-dependent de novo tamoxifen resistance with risk declining markedly after 3 years of tamoxifen treatment. These results parallel data from the ATAC and Intergroup Exemastane Study trials which suggest that whereas PR-negative patients derive greater benefit from initial aromatase inhibitor treatment, PR status has no effect on response when given as delayed treatment to those disease free on tamoxifen after 3 years.
HOW MUCH OUGHT A SMALL CITY TO PAY ITS HEALTH OFFICER?
Authors: HENRY B. BAKER
Journal: JAMA (1891)

[From advance sheets of "Proceedings of a Sanitary Convention held at Negaunee, Michigan," August, 1891.] I presume that the reason why each city is required by law to have a health officer, is that sentiments of common humanity dictate that proper effort shall be made, constantly, by the officers of every locality, for the best possible protection of human life and health within their jurisdiction. But in this paper I propose to go a step further, and to point out the fact that this high humanitarian position which the law contemplates, when it requires cities to guard the health of their inhabitants, and to contribute facts and statistics for the general welfare of the people of the State, that all this from a financial stand-point, pays the people of each city and of each locality. I propose to speak especially of the city of Negaunee, but the same principle which
An epidemic of pseudomembraneous colitis or simply a nosocomial case clustering.
Authors: M Tvede, F Trautner, J Rask-Madsen
Journal: Gut (1988)

with disseminated carcinoma to respond to the LAK process, and indicates the requirement for tech- niques to increase lymphocyte cellular renewal in such patients.Lymphokine activated killer source cannot simply be explained on the basis of cell type, but surely represents a functional disruption of a down regulated networks when performed outside the body.This results in large numbers of effector lymphocytes derived from those cell types, both T-cell and NK cell, in which anti-tumour activity can be augmented.
HETEROGENETIC ANTIBODIES IN ACUTE HEPATITIS
Authors: Monroe D. Eaton, William D. Murphy, V. Lee Hanford
Journal: The Journal of Experimental Medicine (1944)

A heterogenetic antibody showing fixation of complement with human liver and agglutination of sheep erythrocytes was found in certain cases of acute infective hepatitis. The antigen concerned in these reactions was apparently heat stable and alcohol soluble. Differences from other heterogenetic antigen-antibody systems have been noted. The possible relation of the heterogenetic antibody to liver damage was considered.
Chronic lymphocytic leukaemia skin infiltrates affecting prominent parts of the face and the scalp
Authors: Z.F. Jasim, N. Cooke, J.E. Somerville, R.J. Hay
Journal: British Journal of Dermatology (2006)

Chronic lymphocytic leukaemia (CLL) infiltrating the skin is uncommon and can present in different forms. We report a case of CLL infiltrating the prominent parts of the face and the scalp. A 63‐year‐old male with a 10‐year history of CLL presented with plum‐coloured swelling of the skin of the ears, eyebrows, tip of the nose and the scalp. Histopathology showed dense sheets of lymphoid infiltrate of the dermis which stained positive with B‐cell markers CD20 and CD5 in keeping with the infiltrate of CLL.
A novel heparin-dependent processing pathway for human tryptase. Autocatalysis followed by activation with dipeptidyl peptidase I.
Authors: K Sakai, S Ren, L B Schwartz
Journal: Journal of Clinical Investigation (1996)

Tryptase is the major protein constituent of human mast cells, where it is stored within the secretory granules as a fully active tetramer. Two tryptase genes (alpha and beta) are expressed by human mast cells at the level of mRNA and protein, each with a 30 amino acid leader sequence. Recombinant precursor forms of human alpha- and beta-tryptase were produced in a baculovirus system, purified, and used to study their processing. Monomeric beta-protryptase first is shown to be intermolecularly autoprocessed to monomeric beta-pro'tryptase at acid pH in the presence of heparin by cleavage between Arg-3 and Val-2 in the leader peptide. The precursor of alpha-tryptase has an Arg-3 to Gln-3 mutation that precludes autoprocessing. this may explain why alpha-tryptase is not stored in secretory granules, but instead is constitutively secreted by mast cells and is the predominant form of tryptase found in blood in both healthy subjects and those with systemic mastocytosis under nonacute conditions. Second, the NH2-terminal activation dipeptide on beta-pro'tryptase is removed by dipeptidyl peptidase I at acid pH in the absence of heparin to yield an inactive monomeric form of tryptase. Conversion of the catalytic portion of beta-tryptase to the active homotetramer at acid pH requires heparin. Thus, beta-tryptase homotetramers probably account for active enzyme detected in vivo. Also, processing of tryptase to an active form should occur optimally only in cells that coexpress heparin proteoglycan, restricting this pathway to a mast cell lineage.
Iron Therapy for Hepatic Dysfunction in Erythropoietic Protoporphyria
Authors: Victor R. Gordeuk, Gary M. Brittenham, Curtis W. Hawkins, Hasan Mukhtar, David R. Bickers
Journal: Annals of Internal Medicine (1986)

Erythropoietic protoporphyria, caused by an inherited deficiency of ferrochelatase, results in increased free protoporphyrin concentrations in erythrocytes and plasma. Cutaneous photosensitivity is the primary clinical manifestation, but in some patients, protoporphyrin accumulation in the liver may lead to fatal hepatic failure. No treatment exists for this lethal complication. We report the case of a patient with erythropoietic protoporphyria and abnormal results of liver function tests in whom oral iron therapy led to a substantial decrease in free erythrocyte and stool protoporphyrin levels with return of liver function to normal. Iron therapy should be considered for preventing potentially fatal hepatic failure in patients with erythropoietic protoporphyria.
Regulation of cellular proliferation and intimal formation following balloon injury in atherosclerotic rabbit arteries.
Authors: R D Simari, H San, M Rekhter, T Ohno, D Gordon, G J Nabel, E G Nabel
Journal: Journal of Clinical Investigation (1996)

Injury to atherosclerotic arteries induces the expression of growth regulatory genes that stimulate cellular proliferation and intimal formation. Intimal expansion has been reduced in vivo in nonatherosclerotic balloon-injured arteries by transfer of genes that inhibit cell proliferation. It is not known, however, whether vascular cell proliferation can be inhibited after injury in more extensively diseased atherosclerotic arteries. Accordingly, the purpose of this study was to investigate whether expression of recombinant genes in atherosclerotic arteries after balloon injury could inhibit intimal cell proliferation. To test this hypothesis, we examined the response to balloon injury in atherosclerotic rabbit arteries after gene transfer of herpesvirus thymidine kinase gene (tk) and administration of ganciclovir. Smooth muscle cells from hyperlipidemic rabbit arteries infected with adenoviral vectors encoding tk were sensitive to ganciclovir, and bystander killing was observed in vitro. In atherosclerotic arteries, a human placental alkaline phosphatase reporter gene was expressed in intimal and medial smooth muscle cells and macrophages, identifying these cells as targets for gene transfer. Expression of tk in balloon-injured hyperlipidemic rabbit arteries followed by ganciclovir treatment resulted in a 64% reduction in intimal cell proliferation 7 d after gene transfer (P = 0.004), and a 35-49% reduction in internal area 21 d after gene transfer, compared with five different control groups (P < 0.05). Replication of smooth muscle cells and macrophages was inhibited by tk expression and ganciclovir treatment. These findings indicate that transfer of a gene that inhibits cellular proliferation limits the intimal area in balloon-injured atherosclerotic arteries. Molecular approaches to the inhibition of cell proliferation in atherosclerotic arteries constitute a possible treatment for vascular proliferative diseases.
Saphenous Vein Graft Failure After Coronary Artery Bypass Surgery
Authors: Connie N. Hess, Renato D. Lopes, C. Michael Gibson, Rebecca Hager, Daniel M. Wojdyla, Brian R. Englum, Michael J. Mack, Robert M. Califf, Nicholas T. Kouchoukos, Eric D. Peterson, John H. Alexander
Journal: Circulation (2014)

Background— Coronary artery bypass grafting success is limited by vein graft failure (VGF). Understanding the factors associated with VGF may improve patient outcomes. Methods and Results— We examined 1828 participants in the Project of Ex Vivo Vein Graft Engineering via Transfection IV (PREVENT IV) trial undergoing protocol-mandated follow-up angiography 12 to 18 months post–coronary artery bypass grafting or earlier clinically driven angiography. Outcomes included patient- and graft-level angiographic VGF (≥75% stenosis or occlusion). Variables were selected by using Fast False Selection Rate methodology. We examined relationships between variables and VGF in patient- and graft-level models by using logistic regression without and with generalized estimating equations. At 12 to 18 months post–coronary artery bypass grafting, 782 of 1828 (42.8%) patients had VGF, and 1096 of 4343 (25.2%) vein grafts had failed. Demographic and clinical characteristics were similar between patients with and without VGF, although VGF patients had longer surgical times, worse target artery quality, longer graft length, and they more frequently underwent endoscopic vein harvesting. After multivariable adjustment, longer surgical duration (odds ratio per 10-minute increase, 1.05; 95% confidence interval, 1.03–1.07), endoscopic vein harvesting (odds ratio, 1.41; 95% confidence interval, 1.16–1.71), poor target artery quality (odds ratio, 1.43; 95% confidence interval, 1.11–1.84), and postoperative use of clopidogrel or ticlopidine (odds ratio, 1.35; 95% confidence interval, 1.07–1.69) were associated with patient-level VGF. The predicted likelihood of VGF in the graft-level model ranged from 12.1% to 63.6%. Conclusions— VGF is common and associated with patient and surgical factors. These findings may help identify patients with risk factors for VGF and inform the development of interventions to reduce VGF. Clinical Trial Registration— URL: http://www.clinicaltrials.gov . Unique identifier: NCT00042081.
Anti-A Autoantibody with Severe Intravascular Hemolysis
Authors: Irma O. Szymanski, Phillip L. Roberts, Richard E. Rosenfield
Journal: New England Journal of Medicine (1976)

Anti-A autoantibody manifested itself clinically in fatal hemolysis and kidney failure in the following case. Case Report A 73-year-old man suddenly experienced severe bilateral lumbar pain associa...
Smoking cessation services: use them or lose them
Authors: J Britton
Journal: Thorax (2004)

Medical professionals in the UK need to engage more in smoking cessation services

Of the 120 000 people who die from smoking each year in the UK, more than half die from a respiratory disease. In 1997 deaths from lung cancer, chronic obstructive pulmonary disease (COPD), and pneumonia caused by smoking totalled over 63 000,1 all of which were potentially avoidable. These figures show that preventing smoking is more relevant to respiratory medicine than any other speciality. In this issue of Thorax Abdullah and Husten2 review the priorities for tobacco control in the developing world and summarise the difficulties of developing smoking cessation in countries already severely challenged by generally low levels of health service funding and infrastructure, by competing public health priorities such as HIV, by low levels of public awareness of smoking as a dangerous behaviour, and other issues. However, one of the problems they identify that is especially relevant in the UK is the need to engage medical professionals in smoking cessation.

The National Health Service (NHS) approach to smoking cessation in the UK has changed radically in the past 5 years. Although the effectiveness of behavioural support and nicotine replacement therapy (NRT) for smoking cessation had been …
Clinical Anticoagulant Therapy
Authors: William J. Harrington
Journal: JAMA (1965)

In the topic of anticoagulant therapy, uncritical and overly enthusiastic appraisals have often diluted the worthwhile contributions of two generations of investigators. Dr. Vigran has succeeded in distinguishing between the good and the poor literature on anticoagulants. He has divided his book into 13 chapters, which include such areas as blood coagulation; thrombosis, embolism, and atherosclerosis; the chemistry and pharmacology of anticoagulant drugs; contraindications to use; and laboratory controls. He goes on with detailed consideration of various forms of vascular disease, as well as the complications of treatment.  Each chapter he introduces with a biographical sketch of a man whose efforts have paced the progress that has been made. This provides a design which might well be copied by other authors of similar reviews.  The volume contains a well-annotated documentation of the present status of anticoagulant therapy and provides an excellent readable summary of its indications. If there is any