tbuckley/cabot-search huggingface dataset:
Tuberculosis and Myelosclerosis with Myeloid Metaplasia
Authors: Janine André
Journal: JAMA (1961)

Three patients with myeloproliferative syndromes (polycythemia vera, myelofibrosis with myeloid metaplasia, and chronic granulocytic leukemia) with coexisting tuberculosis are described. The first patient, with myelofibrosis, was found to have tuberculosis of the spleen. He did not respond to antituberculous therapy. The second patient was found to have miliary tuberculosis. Treatment with antituberculous drugs was lifesaving. After resolution of the tuberculosis, florid chronic granulocytic leukemia appeared. The third patient, with polycythemia vera, developed cervical tuberculous adenitis which responded to isoniazid and streptomycin. Tuberculosis may be a complication of, or a cause of, myeloproliferative disease in some patients.
Effect of acute hypokalaemia on 3H-digoxin metabolism
Authors: P. F. Binnion, L. M. Morgan
Journal: Cardiovascular Research (1971)

Journal Article Effect of acute hypokalaemia on 3H-digoxin metabolism Get access Peter F. Binnion, Peter F. Binnion 2 From the Department of Physiology, Queen's University, Belfast, and Department of Biochemistry, Belfast City Hospital, Belfast 2Reprint requests: Dr. Peter F. Binnion, Division of Cardiology Pennsylvania Hospital, 8th and Spruce Streets, Philadelphia, Pa. 19107, U.S.A. Search for other works by this author on: Oxford Academic PubMed Google Scholar Leo M. Morgan Leo M. Morgan From the Department of Physiology, Queen's University, Belfast, and Department of Biochemistry, Belfast City Hospital, Belfast Search for other works by this author on: Oxford Academic PubMed Google Scholar Cardiovascular Research, Volume 5, Issue 4, October 1971, Pages 431–435, https://doi.org/10.1093/cvr/5.4.431 Published: 01 October 1971
The Monocyte: New Concepts of Function
Authors: Albert F. LoBuglio
Journal: New England Journal of Medicine (1973)

Blood monocytes are usually thought of as a minor subgroup of circulating phagocytic leukocytes that play a prominent part only in certain chronic infections such as tuberculosis. However, the role of this cell has been expanded considerably by studies in the past decade, which clarified the kinetics of the monocyte life cycle and its relation to tissue macrophages.1 Tissue macrophages, regardless of their semantic label (Kupffer cells, fixed splenic histiocytes, pulmonary alveolar macrophages, epithelioid cells, etc.), originate primarily from the bone marrow where they have a generation time of about 24 hours. They circulate as monocytes for one to three . . .
IMPACT OF PRIOR CLOPIDOGREL USE ON ISCHEMIC OUTCOMES AMONG MEDICALLY MANAGED PATIENTS WITH NON-ST-ELEVATION ACUTE CORONARY SYNDROMES: RESULTS FROM THE TRILOGY ACS TRIAL
Authors: Chee Tang Chin, William Boden, Matthew Roe, Benjamin Neely, Megan Neely, Jose Leiva-Pons, Corbalan Ramon, Jean-Pierre Bassand, Shmuel Gottlieb, Anthony Dalby, Paul Armstrong, Dorairaj Prabhakaran, Keith Fox, Harvey White, E. Magnus Ohman, Kenneth Winters, Francois Schiele
Journal: Journal of the American College of Cardiology (2014)
Observational Studies of Drug Safety — Aprotinin and the Absence of Transparency
Authors: William R. Hiatt
Journal: New England Journal of Medicine (2006)

The full safety profile of a new drug is rarely known at the time of approval by the Food and Drug Administration (FDA). Most drug-development programs designed for treatments of symptomatic indications are underpowered to detect any increased risk of rare drug reactions or change in background event rates attributable to the drug. Large, post-marketing, randomized, controlled trials provide robust data on drug safety but may be subject to multiple sources of bias. Observational studies of a drug's effects in clinical practice can offer additional information on risks. The recent discussions of aprotinin (Trasylol, Bayer) by the Cardiovascular and Renal . . .
Perinatal Exposure to Traffic-Related Air Pollution and Atopy at 1 Year of Age in a Multi-Center Canadian Birth Cohort Study
Authors: Hind Sbihi, Ryan W. Allen, Allan Becker, Jeffrey R. Brook, Piush Mandhane, James A. Scott, Malcolm R. Sears, Padmaja Subbarao, Tim K. Takaro, Stuart E. Turvey, Michael Brauer
Journal: Environmental Health Perspectives (2015)

The role of traffic-related air pollution (TRAP) exposure in the development of allergic sensitization in children is unclear, and few birth cohort studies have incorporated spatiotemporal exposure assessment.We aimed to examine the association between TRAP and atopy in 1-year-old children from an ongoing national birth cohort study in four Canadian cities.We identified 2,477 children of approximately 1 year of age with assessment of atopy for inhalant (Alternaria, Der p, Der f, cat, dog, cockroach) and food-related (milk, eggs, peanuts, soy) allergens. Exposure to nitrogen dioxide (NO2) was estimated from city-specific land use regression models accounting for residential mobility and temporal variability in ambient concentrations. We used mixed models to examine associations between atopy and exposure during pregnancy and the first year of life, including adjustment for covariates (maternal atopy, socioeconomic status, pets, mold, nutrition). We also conducted analyses stratified by time-location patterns, daycare attendance, and modeled home ventilation.Following spatiotemporal adjustment, TRAP exposure after birth increased the risk for development of atopy to any allergens [adjusted odds ratio (aOR) per 10 μg/m3 NO2 = 1.16; 95% CI: 1.00, 1.41], but not during pregnancy (aOR = 1.02; 95% CI: 0.86, 1.22). This association was stronger among children not attending daycare (aOR = 1.61; 95% CI: 1.28, 2.01) compared with daycare attendees (aOR = 1.05; 95% CI: 0.81, 1.28). Trends to increased risk were also found for food (aOR = 1.17; 95% CI: 0.95, 1.47) and inhalant allergens (aOR = 1.28; 95% CI: 0.93, 1.76).Using refined exposure estimates that incorporated temporal variability and residential mobility, we found that traffic-related air pollution during the first year of life was associated with atopy.Sbihi H, Allen RW, Becker A, Brook JR, Mandhane P, Scott JA, Sears MR, Subbarao P, Takaro TK, Turvey SE, Brauer M. 2015. Perinatal exposure to traffic-related air pollution and atopy at 1 year of age in a multi-center Canadian birth cohort study. Environ Health Perspect 123:902-908; http://dx.doi.org/10.1289/ehp.1408700.
ACUTE ABDOMINAL PAIN IN RHEUMATIC FEVER
Authors: J. D. Geissinger
Journal: JAMA (1930)

To the Editor:  —InThe Journal, February 22, page 594, I note an abstract Rheumatic Fever: Onset with Peritoneal Symptoms. In connection with this I thought it might be of interest to note a case which I reported in a paper entitled Some Acute Abdominal Conditions in Childhood Secondary to Parenteral Infections, read before the Arkansas Valley Medical Association, February 6.  A white boy, aged 5 years, had had chickenpox, measles, typhoid, parotid abscess, chronic tonsillitis with acute attacks, and, ten days before his present trouble, bilateral otitis media. January 2, both ear drums were incised and drained pus freely. At that time, too, he had nasal obstruction and pus in the nose. Just before midnight, January 9, he had severe abdominal pain. An enema was given with fair results but no relief from pain, which was still present when I saw him at 10 o'clock the following morning. The
Effects of an Anti-TSLP Antibody on Allergen-Induced Asthmatic Responses
Authors: Gail M. Gauvreau, Paul M. O'Byrne, Louis-Philippe Boulet, Ying Wang, Donald Cockcroft, Jeannette Bigler, J. Mark FitzGerald, Michael Boedigheimer, Beth E. Davis, Clapton Dias, Kevin S. Gorski, Lynn Smith, Edgar Bautista, Michael R. Comeau, Richard Leigh, Jane R. Parnes
Journal: New England Journal of Medicine (2014)

Thymic stromal lymphopoietin (TSLP) is an epithelial-cell-derived cytokine that may be important in initiating allergic inflammation. AMG 157 is a human anti-TSLP monoclonal immunoglobulin G2λ that binds human TSLP and prevents receptor interaction.In this double-blind, placebo-controlled study, we randomly assigned 31 patients with mild allergic asthma to receive three monthly doses of AMG 157 (700 mg) or placebo intravenously. We conducted allergen challenges on days 42 and 84 to evaluate the effect of AMG 157 in reducing the maximum percentage decrease in the forced expiratory volume in 1 second (FEV1). We also measured the fraction of nitric oxide in exhaled air, blood and sputum eosinophils, and airway hyperresponsiveness. The primary end point was the late asthmatic response, as measured 3 to 7 hours after the allergen challenge.AMG 157 attenuated most measures of allergen-induced early and late asthmatic responses. The maximum percentage decrease in the FEV1 during the late response was 34.0% smaller in the AMG-157 group than in the placebo group on day 42 (P=0.09) and 45.9% smaller on day 84 (P=0.02). In addition, patients receiving AMG 157 had significant decreases in levels of blood and sputum eosinophils before and after the allergen challenge and in the fraction of exhaled nitric oxide. There were 15 adverse events in the AMG-157 group, as compared with 12 in the placebo group; there were no serious adverse events.Treatment with AMG 157 reduced allergen-induced bronchoconstriction and indexes of airway inflammation before and after allergen challenge. These findings are consistent with a key role for TSLP in allergen-induced airway responses and persistent airway inflammation in patients with allergic asthma. Whether anti-TSLP therapeutics will have clinical value cannot be determined from these data. (Funded by Amgen; ClinicalTrials.gov number, NCT01405963.).
Neuropathological Findings in the Brain of Karen Ann Quinlan -- The Role of the Thalamus in the Persistent Vegetative State
Authors: Hannah C. Kinney, Julius Korein, Ashok Panigrahy, Pieter Dikkes, Robert Goode
Journal: New England Journal of Medicine (1994)

Karen Ann Quinlan had a cardiopulmonary arrest in 1975 and died 10 years later, having never regained consciousness. Her story prompted a national debate about the appropriateness of life-sustaining treatment in patients who are in a persistent vegetative state and led to the development of medicolegal guidelines for the care of such patients. This report describes the neuropathologic features of Quinlan's brain.
Gastric bicarbonate secretion in humans. Effect of pentagastrin, bethanechol, and 11,16,16-trimethyl prostaglandin E2.
Authors: M Feldman
Journal: Journal of Clinical Investigation (1983)

Although the stomach is mainly known for its ability to secrete hydrochloric acid, there is increasing evidence that the gastric mucosa also secretes bicarbonate. A simple method for simultaneous measurement of gastric HCO-3 secretion and H+ secretion was developed from a two-component model of gastric secretion. The method, which is based upon gastric juice volume, H+ concentration, and osmolality, was validated both in vitro and in vivo. In 14 healthy human beings, basal gastric HCO-3 secretion averaged 2.6 mmol/h (range, 0.7-8.7 mmol/h). Basal HCO-3 secretion was approximately 50% of basal H+ secretion and there was a significant correlation between basal HCO-3 and H+ secretion in individual subjects (r = 0.79). HCO-3 was secreted in basal nonparietal secretion at a concentration of approximately 90 mmol/liter. Intravenous pentagastrin infusion markedly stimulated H+ secretion but did not increase HCO-3 secretion. During pentagastrin infusion, the cholinergic agonist, bethanechol, significantly augmented H+ secretion (from 20.2 to 24.7 mmol/h) and increased HCO-3 secretion (from 2.2 to 4.2 mmol/h). A prostaglandin E2 analogue significantly reduced H+ secretion and increased HCO-3 secretion during pentagastrin infusion. The reduction in net gastric juice H+ output following prostaglandin E2 was due more to H+ secretory inhibition than to HCO-3 secretory stimulation. We conclude that the healthy human stomach actively secretes HCO-3 and that gastric HCO-3 secretion can be influenced by cholinergic stimulation and by prostaglandin E2.
Panniculitis-like T-cell lymphoma clinically manifested as alopecia
Authors: L. Torok, T.P. Gurbity, A. Kirschner, L. Krenacs
Journal: British Journal of Dermatology (2002)

Journal Article Panniculitis‐like T‐cell lymphoma clinically manifested as alopecia Get access L. Török, L. Török Department of Dermatology, County Hospital, Nagykörösi u. 15, 6000 Kecskemét, Hungary Dr L.Török. E‐mail: laszlo.a.torok@matavnet.hu Search for other works by this author on: Oxford Academic Google Scholar T.P. Gurbity, T.P. Gurbity Laboratory of Tumor Pathology and Molecular Diagnostics, Institute for Biotechnology, Bay Zoltan Foundation for Applied Research, Szeged, Hungary Search for other works by this author on: Oxford Academic Google Scholar Á. Kirschner, Á. Kirschner Department of Dermatology, County Hospital, Nagykörösi u. 15, 6000 Kecskemét, Hungary Search for other works by this author on: Oxford Academic Google Scholar L. Krenács L. Krenács Laboratory of Tumor Pathology and Molecular Diagnostics, Institute for Biotechnology, Bay Zoltan Foundation for Applied Research, Szeged, Hungary Search for other works by this author on: Oxford Academic Google Scholar British Journal of Dermatology, Volume 147, Issue 4, 1 October 2002, Pages 785–788, https://doi.org/10.1046/j.1365-2133.2002.04924.x Published: 01 October 2002 Article history Accepted: 14 March 2002 Published: 01 October 2002
Identical Structural and Receptor Binding Defects in Apolipoprotein E2 in Hypo-, Normo-, and Hypercholesterolemic Dysbetalipoproteinemia
Authors: Stanley C. Rall, Karl H. Weisgraber, Thomas L. Innerarity, Robert W. Mahley, Gerd Assmann
Journal: Journal of Clinical Investigation (1983)

Apolipoprotein E (apoprotein E or apo-E) from type III hyperlipoproteinemic subjects with the E2/2 homozygous phenotype displays both structural and receptor binding heterogeneity. The apo-E from all subjects thus far studied, however, has been functionally defective, though to different degrees. Although nearly every type III hyperlipoproteinemic subject has the E2/2 phenotype, 95-99% of the people with this same phenotype do not display type III hyperlipoproteinemia, nor do they have elevated plasma cholesterol levels. Consequently, it became important to determine whether the apo-E2 from hypo- and normocholesterolemic individuals with the E2/2 phenotype is also functionally abnormal. To do this, apo-E2 was isolated from two hypo-, two normo- and two hypercholesterolemic homozygous E2/2 subjects. The apo-E2 was recombined with vesicles and tested for its ability to displace (125)I-low density lipoproteins (LDL) from apo-B,E (LDL) receptors on human fibroblasts. The apo-E2 from all six subjects was found to be severely defective in receptor binding (<2% of the binding activity of normal apo-E3). In all cases, the binding activity of the apo-E2 was increased 10- to 20-fold by treating the apoproteins with cysteamine, a reagent that converts cysteine residues to positively charged lysine analogues. The cysteine content of each apo-E was determined by monitoring the change in the isoelectric focusing position of the cysteamine-treated apo-E2. Using this method, it was found that the apo-E2 from each subject contained two cysteine residues per mole. A partial sequence analysis of the cysteine-containing regions of the apo-E from three of the six subjects indicated that the two cysteine residues were at residues 112 and 158 in the amino acid sequence. The cysteine at residue 158 has previously been implicated in the severe binding defect of the apo-E2 from a type III hyperlipoproteinemic subject. Since the apo-E2 of the hypo-, normo-, and hypercholesterolemic subjects in this study all displayed a severe functional abnormality, it is apparent that factors in addition to the defective receptor binding activity of the apo-E2 are necessary for the manifestation of type III hyperlipoproteinemia.
Transient Inhibition of Interleukin 4 Signaling by T Cell Receptor Ligation
Authors: Jinfang Zhu, Hua Huang, Liying Guo, Timothy Stonehouse, Cynthia J. Watson, Jane Hu-Li, William E. Paul
Journal: The Journal of Experimental Medicine (2000)

Interleukin (IL)-4 and IL-12 together with T cell receptor (TCR) engagement are crucial for the differentiation of CD4+ T cells into T helper (Th)2 or Th1 cells, respectively. Although IL-4 receptors (IL-4Rs) but not IL-12Rs are expressed on naive CD4+ T cells, IL-4 has no apparent advantage over IL-12 in driving naive T cell differentiation when the cells are primed with both IL-4 and IL-12 in vitro. It was found that IL-4–induced phosphorylation of Janus kinases 1 and 3, IL-4Rα, signal transducer and activator of transcription 6, and insulin receptor substrate 2 was strikingly but transiently inhibited by TCR ligation both in conventional and TCR transgenic T cells. TCR engagement also blocked the expression of an IL-4–inducible gene. Signals induced by other cytokines, including IL-2, IL-6, and interferon α, but not by insulin-like growth factor 1, were also blocked by TCR engagement. The capacity of various inhibitors to reverse TCR-mediated inhibition of IL-4 signaling suggested that activation of the Ras–mitogen-activated protein kinase pathway and of the calcineurin pathway contribute to desensitizing IL-4R. IL-4 responsiveness returned at about the time (∼12 h) that IL-12–mediated signaling was first observed. Thus, through different mechanisms, neither IL-4R nor IL-12R has any clear advantage in polarizing cells; rather, the availability of cytokine is probably the limiting factor in this process.
CCR1 and CCR5 promote hepatic fibrosis in mice
Authors: Ekihiro Seki, Samuele De Minicis, Geum-Youn Gwak, Johannes Kluwe, Sayaka Inokuchi, Christina A. Bursill, Josep M. Llovet, David A. Brenner, Robert F. Schwabe
Journal: Journal of Clinical Investigation (2009)

Hepatic fibrosis develops as a response to chronic liver injury and almost exclusively occurs in a proinflammatory environment. However, the role of inflammatory mediators in fibrogenic responses of the liver is only poorly understood. We therefore investigated the role of CC chemokines and their receptors in hepatic fibrogenesis. The CC chemokines MIP-1alpha, MIP-1beta, and RANTES and their receptors CCR1 and CCR5 were strongly upregulated in 2 experimental mouse models of fibrogenesis. Neutralization of CC chemokines by the broad-spectrum CC chemokine inhibitor 35k efficiently reduced hepatic fibrosis, and CCR1- and CCR5-deficient mice displayed substantially reduced hepatic fibrosis and macrophage infiltration. Analysis of fibrogenesis in CCR1- and CCR5-chimeric mice revealed that CCR1 mediates its profibrogenic effects in BM-derived cells, whereas CCR5 mediates its profibrogenic effects in resident liver cells. CCR5 promoted hepatic stellate cell (HSC) migration through a redox-sensitive, PI3K-dependent pathway. Both CCR5-deficient HSCs and CCR1- and CCR5-deficient Kupffer cells displayed strong suppression of CC chemokine-induced migration. Finally, we detected marked upregulation of RANTES, CCR1, and CCR5 in patients with hepatic cirrhosis, confirming activation of the CC chemokine system in human fibrogenesis. Our data therefore support a role for the CC chemokine system in hepatic fibrogenesis and suggest distinct roles for CCR1 and CCR5 in Kupffer cells and HSCs.
THE ULTRASTRUCTURE OF LICHEN AMYLOIDOSUS WITH SPECIAL REFERENCE TO THE EPIDERMAL CHANGES
Authors: MARTIN M. BLACK, CHRISTOPHER J. HEATHER
Journal: British Journal of Dermatology (1972)

Summary.— The ultrastructure of lichen amyloidosus has been studied with special reference to the epidermal changes. The amyloid deposits often came into close proximity to the lower epidermis and obscured the basal lamina. Occasionally, breaks in the basal lamina occurred so that amyloid fibrils came into direct contact with the cytoplasm of basal cells. Small deposits of amyloid were sometimes seen in the inter‐cellular spaces between basal cells. Focal areas of liquefaction degeneration were observed within a number of basal cells. A few keratinocytes in the upper epidermis contained deposits of amyloid‐like fibrils. It is suggested that these amyloid‐like fibrils probably represent degenerate tonofilaments rather than true amyloid.
STUDIES ON PULMONARY EDEMA
Authors: Sidney Farber
Journal: The Journal of Experimental Medicine (1937)

1. Guinea pigs die shortly after bilateral cervical vagotomy, even when continuous artificial respiration effected through a tracheal cannula is carried out. Death is caused by severe pulmonary edema and congestion. 2. Direct observation of the lungs after bilateral vagotomy demonstrates that pulmonary edema develops gradually and increases slowly in amount and severity. Congestion precedes and accompanies the development of the edema. 3. Neuropathic pulmonary edema in the guinea pig is caused by disturbance to or abolition of the pulmonary vasomotor nerves. 4. The evidence obtained by experiments on animals suggests that neuropathic pulmonary edema in man is caused by disturbances, either central or peripheral, to the vasomotor control of the pulmonary vessels.
iNOS is a mediator of the heat stress-induced preconditioning against myocardial infarction in vivo in the rat
Authors: C ARNAUD, D GODINRIBUOT, S BOTTARI, A PEINNEQUIN, M JOYEUX, P DEMENGE, C RIBUOT
Journal: Cardiovascular Research (2003)

Objective: The inducible isoform of nitric oxide synthase (iNOS) is known to be a trigger of the heat stress (HS)-induced cardioprotection. Since iNOS also appears to mediate various forms of myocardial preconditioning, the goal of this study was to investigate its role as a mediator of the HS response. Methods and Results: Male Wistar rats were divided in six groups, subjected or not to HS (42°C internal temperature, for 15 min). Twenty-four hours later, they were treated or not with either l-NAME, a non-selective inhibitor of NO synthase isoforms, or 1400W, a selective iNOS inhibitor, 10 min before being subjected to a 30-min left coronary artery occlusion followed by a 120-min reperfusion, in vivo. The infarct size (tetrazolium staining) reducing effect conferred by heat stress (from 46.0±1.4% in sham to 26.8±3.8% in HS groups) was completely abolished by both l-NAME (53.9±3.1%) and 1400W (51.8±3.3%). Additional studies using Western blot analysis demonstrated a 3.8-fold increase in myocardial iNOS protein expression 24 h after HS. Conclusion: These results suggest an involvement of iNOS as a mediator of the protection conferred by heat stress against myocardial ischaemia.