tbuckley/cabot-search huggingface dataset:
HOST-PARASITE FACTORS IN GROUP A STREPTOCOCCAL INFECTIONS
Authors: Dennis W. Watson
Journal: The Journal of Experimental Medicine (1960)

The factors present in streptococcal lesion extracts (SLE) which enhanced the lethal and tissue-damaging properties of Gram-negative bacterial endotoxins and streptolysin O were identified with the scarlet fever group of toxins. Toxic manifestations attributed to this group of toxins included lethality, cardiotoxic and other tissue damage, enhancement of toxicity, and pyrogenicity. Of these, the measurement of febrile response in American Dutch rabbits was the most useful parameter of toxicity. In rabbits, repeated daily intravenous injections of 0.125 Lf of a purified erythrogenic toxin immunizes specifically against the pyrogenic activity; this technique was used to type the toxins and to distinguish them from exogenous and endogenous pyrogens; non-specific pyrogens, such as streptococcal endotoxin, were not found in SLE. All types of the Lancefield Group A streptococci tested produced one or or more immunologically distinct toxins in vivo in contrast to Groups B and C which did not produce them; toxins A and B, previously distinguished by neutralization of rash-inducing activity in the skin, were produced in vivo. The A toxin was the most common, as indicated by its presence in extracts prepared with Types 28, 12, 17, and 10 (NY-5); B toxin was found in 10 (NY-5) and 19. A new toxin, designated C, was obtained from a Type 18. In American Dutch rabbits, purified toxin at a concentration of 15 Lf (900,000 STD) neither gave a Dick test nor prepared the skin for the local Shwartzman reaction; by this route, however, in contrast to classical endotoxins, they enhance the lethal and tissue-damaging properties of sublethal doses of these and other toxins. These properties of the immunologic distinct exotoxins as demonstrated in American Dutch rabbits suggest by analogy their importance in the pathogenesis of streptococcal disease in man. Evidence that might implicate them in sequelae, in addition to scarlet fever, is discussed.
Consolidated research agenda needed for health economic evaluation in Europe
Authors: D. Tordrup, R. Bertollini
Journal: BMJ (2014)

The Consolidated Health Economic Evaluation Reporting Standards (CHEERS) Task Force has called on researchers, editors, and reviewers to adhere to reporting standards for health economic evaluations, recognising the importance of clearly communicated economic evidence in health policy decision making.1 Although such steps are important, it is also pertinent to consider in which technical areas the value of investing in new evidence …
Linking Geological and Health Sciences to Assess Childhood Lead Poisoning from Artisanal Gold Mining in Nigeria
Authors: Geoffrey S. Plumlee, James T. Durant, Suzette A. Morman, Antonio Neri, Ruth E. Wolf, Carrie A. Dooyema, Philip L. Hageman, Heather A. Lowers, Gregory L. Fernette, Gregory P. Meeker, William M. Benzel, Rhonda L. Driscoll, Cyrus J. Berry, James G. Crock, Harland L. Goldstein, Monique Adams, Casey L. Bartrem, Simba Tirima, Behrooz Behbod, Ian von Lindern, Mary Jean Brown
Journal: Environmental Health Perspectives (2013)

In 2010, Médecins Sans Frontières discovered a lead poisoning outbreak linked to artisanal gold processing in northwestern Nigeria. The outbreak has killed approximately 400 young children and affected thousands more.Our aim was to undertake an interdisciplinary geological- and health-science assessment to clarify lead sources and exposure pathways, identify additional toxicants of concern and populations at risk, and examine potential for similar lead poisoning globally.We applied diverse analytical methods to ore samples, soil and sweep samples from villages and family compounds, and plant foodstuff samples.Natural weathering of lead-rich gold ores before mining formed abundant, highly gastric-bioaccessible lead carbonates. The same fingerprint of lead minerals found in all sample types confirms that ore processing caused extreme contamination, with up to 185,000 ppm lead in soils/sweep samples and up to 145 ppm lead in plant foodstuffs. Incidental ingestion of soils via hand-to-mouth transmission and of dusts cleared from the respiratory tract is the dominant exposure pathway. Consumption of water and foodstuffs contaminated by the processing is likely lesser, but these are still significant exposure pathways. Although young children suffered the most immediate and severe consequences, results indicate that older children, adult workers, pregnant women, and breastfed infants are also at risk for lead poisoning. Mercury, arsenic, manganese, antimony, and crystalline silica exposures pose additional health threats.Results inform ongoing efforts in Nigeria to assess lead contamination and poisoning, treat victims, mitigate exposures, and remediate contamination. Ore deposit geology, pre-mining weathering, and burgeoning artisanal mining may combine to cause similar lead poisoning disasters elsewhere globally.
Malignant atrophic papulosis (Degos'disease)—Diffuse involvement of brain and bowel in an African patient
Authors: R.J. BARLOW, T. HEYL, I.W. SIMSON, E.J. SCHULZ
Journal: British Journal of Dermatology (1988)

We report pathognomonic skin lesions of malignant atrophic papulosis, accompanied by lethal central nervous system and gastrointestinal disease in a 22‐year‐old black man. Histopathological studies of the brain and colon showed areas of infarction and an underlying vasculitis with leukocytoclasis.
Environmental tobacco smoke is just as damaging to DNA as mainstream smoke.
Authors: E Bermúdez, K Stone, K M Carter, W A Pryor
Journal: Environmental Health Perspectives (1994)

This study demonstrates the ability of tar isolated from environmental tobacco smoke (ETS) to nick DNA in mammalian cells. Solutions of ETS tar behave similarly to aqueous solutions of cigarette tar from mainstream smoke. Both solutions contain the tar semiquinone radical, and this radical associates with the DNA in viable rat alveolar macrophages. Solutions of tar from ETS cause single-strand DNA breaks in rat thymocytes in proportion to the amount of tar present, until a plateau is reached. ETS tar solutions, like mainstream tar solutions, produce hydrogen peroxide. Hydrogen peroxide appears to be an essential component of the mechanism by which both ETS tar and mainstream tar cause DNA damage in rat thymocytes, as catalase substantially protects against DNA damage. Glutathione also protects against DNA nicking by both ETS and mainstream tar solutions by scavenging radicals and/or oxidants. The chelator diethylenetriamine pentaacetic acid also provides partial (40%) protection. The studies demonstrate that the water-soluble components of ETS tar can enter cells, associate with, and then nick DNA.
Spliceosome mutations involving <i>SRSF2</i>, <i>SF3B1</i>, and <i>U2AF35</i> in chronic myelomonocytic leukemia: Prevalence, clinical correlates, and prognostic relevance
Authors: Mrinal M. Patnaik, Terra L. Lasho, Christy M. Finke, Curtis A. Hanson, Janice M. Hodnefield, Ryan A. Knudson, Rhett P. Ketterling, Animesh Pardanani, Ayalew Tefferi
Journal: American Journal of Hematology (2012)

SRSF2, SF3B1, and U2AF35 (U2AF1) are the three most frequent genes involved with spliceosome mutations in myeloid malignancies. SF3B1 mutations are most frequent (~80%) in myelodysplastic syndromes (MDS) with ring sideroblasts (RS) but lack prognostic relevance. SRSF2 mutations are associated with shortened overall (OS) and leukemia-free survival (LFS) in both MDS and myelofibrosis. In this study of 226 patients with chronic myelomonocytic leukemia (CMML), mutational frequencies were 40% for SRSF2 (all affecting P95), 6% for SF3B1 (primarily K700E) and 9% for U2AF35 (mostly S34F and Q157P/R). These mutations were mutually exclusive and 54% of the patients displayed at least one mutation. The three mutation groups were phenotypically similar, with the exception of higher RS% (P < 0.0001) in patients with SF3B1 mutations. At a median follow-up of 15 months, 176 (78%) deaths and 32 (14%) leukemic transformations were documented. OS (median survivals of 17, 16, 17, and 20 months; P = 0.48) and LFS (leukemic transformation rates of 17, 13, 15, and 5%; P = 0.63) were similar among patients with none of the three mutations, SRSF2, SF3B1, or U2AF35 mutations, respectively. We conclude that SRSF2 is the most frequently mutated spliceosome gene in CMML but neither it nor SF3B1 or U2AF35 mutations are prognostically relevant.
Left ventricular and coronary angiographic anatomy. Relationship to ventricular irritability in the late hospital phase of acute myocardial infarction.
Authors: R A Schulze, J O Humphries, L S Griffith, H Ducci, S Achuff, M G Baird, E D Mellits, B Pitt
Journal: Circulation (1977)

Late hospital phase ventricular arrhythmias in acute myocardial infarction (MI) have been associated with a high incidence of sudden death following hospital discharge. Thirty-eight patients were studied 10-24 days following onset of symptoms of MI. Each patient had a 24-hour ambulatory ECG tape recording and left ventricular and coronary angiography performed. Patients with complicated ventricular arrhythmias (multiform, coupled, R on T VPCs or ventricular tachycardia), when compared to those with uncomplicated ventricular arrhythmias (unifocal or no VPCs), had a greater number of proximally narrowed major coronary arteries (P less than 0.001), a higher coronary "score" (P less than 0.001), a greater incidence of previous myocardial infarction (P less than 0.005), a greater percentage of abnormal left ventricular segments 86% vs 69% (P less than 0.001) and lower ejection fractions. These data suggest that late hospital phase survivors of MI with complicated ventricular arrhythmias have more extensive coronary artery disease with greater left ventricular dysfunction than survivors with uncomplicated ventricular arrhythmias. This more extensive disease may result in increased areas of ischemic myocardium and may help explain the refractoriness of these arrhythmias to pharmacologic therapy.
John Clarence Cutter and the Cutter Lectures on Preventive Medicine
Authors: John E. Gordon, Marjorie Hemming
Journal: New England Journal of Medicine (1958)

JOHN Clarence Cutter was born in the town of Warren, Massachusetts, on July 10, 1851. He graduated from the Massachusetts Agricultural College at Amherst in 1872, devoted a year to the pursuit of literature in J. B. Lippincott's publishing house, spent two years at Dartmouth Medical School and transferred to Harvard Medical School, graduating in 1877. Shortly thereafter, at the age of twenty-seven, he veered sharply away from conventional medicine and went to Japan as professor of physiology and comparative anatomy at the College of Agriculture in Sapporo. That he did not desert medicine is indicated by the fact that . . .
Vitamin B6 appears useful in treating choroid disorder
Authors: Phil Gunby
Journal: JAMA (1980)

Vitamin B<sub>6</sub>(pyridoxine) may slow down the progression of gyrate atrophy of the choroid and retina in some patients, say Oregon investigators. They caution, however, that final evidence of its efficacy is at least five years away. Gyrate atrophy is a rare autosomal recessive disorder that produces tunnel vision, night blindness, and progressive reduction of central sight until the patient goes blind, often by the age of 40 or 50 years. First described almost a century ago, it is characterized by gyrate areas of choroidal and retinal thinning in the periphery of the fundus. These round areas enlarge and merge, restricting peripheral vision. Both cones and rods are involved so night, color, and reading vision are eventually reduced. Patients usually have myopia, and cataracts often develop in mid-life. The Portland investigators have treated four such patients with vitamin B<sub>6</sub>, administered by mouth. By "a mechanism that is not
Delayed fas-mediated hepatocyte apoptosis during liver regeneration in mice: hepatoprotective role of TNF?
Authors: Tetsuo Takehara, Norio Hayashi, Eiji Mita, Tatsuya Kanto, Tomohide Tatsumi, Yutaka Sasaki, Akinori Kasahara, Masatsugu Hori
Journal: Hepatology (1998)

Fas-mediated apoptosis is one of the major death processes of hepatocytes in liver diseases. Although compensatory regeneration occurs during liver injury, it has not been determined whether regenerating hepatocytes die by the same apoptotic process as quiescent hepatocytes. To clarify this issue, the hepatocyte apoptotic process, after injection of agonistic anti-mouse Fas, was compared between sham-operated mice and two-thirds partially hepatectomized mice. The onset of hepatocyte apoptosis was retarded in hepatectomized mice, as evidenced by both morphological and biochemical observations, resulting in significantly prolonged animal survival. Flow cytometric analysis revealed similar levels of Fas expression on hepatocytes between hepatectomized mice and sham-operated mice; however, the activation of liver caspase-3-like protease after Fas stimulation was suppressed in hepatectomized mice, whereas pro-caspase-3 expression did not change with or without hepatectomy. Anti-tumor necrosis factor alfa (TNF alpha), when administered before hepatectomy, partially reversed suppression of caspase-3-like activity after Fas stimulation. Furthermore, the injection of TNF alpha into untreated mice suppressed caspase-3-like activity and prolonged animal survival after Fas stimulation. These results indicate that Fas-signaling events at the level or upstream of caspase-3-like protease are suppressed during liver regeneration, resulting in delayed hepatocyte apoptosis, and also that TNF alpha acts as one of the protective factors against Fas-mediated hepatocyte apoptosis.
TCT-263 Left anterior descending artery that wraps around the apex is associated with apical remodeling and subsequent heart failure in patients with anterior ST-Elevation MI: An INFUSE-AMI sub-study
Authors: Nobuaki Kobayashi, Akiko Maehara, Gary S. Mintz, Steven D. Wolff, Philippe Genereux, Sorin Brener, Ke Xu, Roxana Mehran, C. Michael Gibson, Gregg Stone
Journal: Journal of the American College of Cardiology (2013)
Exhaled breath condensate pH assays are not influenced by oral ammonia
Authors: K Wells
Journal: Thorax (2004)

<b>Background:</b> Measurement of pH in exhaled breath condensate (EBC) is robust and simple. Acidic source fluid (airway lining fluid) traps bases while volatilising acids, leading to EBC acidification in many lung diseases. Lower airway ammonia is one determinant of airway lining fluid pH, raising the concern that addition of the base ammonia by contamination from the mouth might confound EBC pH assays. <b>Methods:</b> Three discrete methods were used to limit oral ammonia contamination of EBC collections: endotracheal intubation, oral rinsing, and −40°C condenser temperatures. Separately, ammonia was removed from collected EBC samples by lyophilisation and resuspension. Intraweek and intraday variability of ammonia concentration was determined in 76 subjects, and ammonia and pH from a further 235 samples were graphically compared. Ammonia was assayed spectrophotometrically and pH was assessed after deaeration. <b>Results:</b> Data from 1091 samples are presented. Ammonia was reduced in EBC by all methods. Endotracheal intubation decreased EBC ammonia from a mean (SD) of 619 (124) μM to 80 (24) μM (p&lt;0.001, n = 32). Oral rinsing before collection also led to a decline in EBC ammonia from 573 (307) μM to 224 (80) μM (p = 0.016, n = 7). The colder the condensation temperature used, the less ammonia was trapped in the EBC. Lyophilisation removed 99.4 (1.9)% of ammonia. Most importantly, the pH of EBC never decreased after removal of ammonia by any of these methods. Intraweek and intraday coefficients of variation for ammonia were 64 (27)% and 60 (32)%, which is substantially more variable than EBC pH assays. <b>Conclusions:</b> Although ammonia and pH appear to correlate in EBC, the oral ammonia concentration is not an important determinant of EBC pH. No precautions need to be taken to exclude oral ammonia when EBC pH is of interest. The low pH and low ammonia found in EBC from patients with lung diseases appear to be independent effects of volatile compounds arising from the airway.
BRONCHIAL ASTHMA AND OTHER ALLERGIC MANIFESTATIONS IN PHARMACISTS
Authors: M. MURRAY PESHKIN
Journal: JAMA (1924)

There is a considerable accumulation of data in the literature on occupational idiosyncrasies, but comparatively little has been written concerning pharmacists and their tendency to acquire protein sensitization to the organic preparations that they handle. In view of the widespread interest that has been aroused by the subject of allergy and asthma in general and the ever increasing volume of literature on this subject, the scarcity of reports dealing with the subject under discussion is indeed surprising. Idiosyncrasy following the ingestion of various drugs has been observed and discussed since the early days of medical science. This paper, however, deals only with the allergic manifestations due to contact with and inhalation of drugs. In 1920, I<sup>1</sup>reported a case of true anaphylactic bronchial asthma in a pharmacist, aged 29, due to the inhalation of powdered ipecac engrafted on a recurrent seasonal bronchitis. Skin tests performed with the many drugs
Transcoronary chemical ablation of atrioventricular conduction.
Authors: P Brugada, H de Swart, J Smeets, H J Wellens
Journal: Circulation (1990)

In seven patients with symptomatic atrial fibrillation and uncontrollable ventricular rates, selective catheterization of the atrioventricular (AV) nodal artery was performed to chemically destroy the AV node. Ethanol at a concentration of 96% and a dose of 0.5-2 ml was used after selective catheterization of the AV nodal artery had demonstrated temporary AV block after the administration of isotonic iced saline. Complete AV block was produced in five patients and AV conduction was sufficiently modified to control symptoms in the remaining two patients. A minimal enzyme rise occurred in six patients. A severe complication in the remaining patient occurred when, after 2 ml ethanol in the AV nodal artery, occlusion developed in the midright coronary artery that led to an inferior wall myocardial infarction. It is concluded that the AV nodal artery can be selectively catheterized using presently available angioplasty techniques. Ethanol can be used to destroy the AV node and block AV conduction.
Trimethoprim-sulphamethoxazole in Acute Brucellosis
Authors: A. Hassan, M. M. Erian, Z. Farid, S. D. Hathout, K. Sorensen
Journal: BMJ (1971)

Eight patients with proved brucella infection were treated with trimethoprim-sulphamethoxazole. The dose varied from two to four tablets given twice daily for three weeks. Clinical response was rapid and all patients were asymptomatic and afebrile within two to seven days of starting therapy. Three patients relapsed clinically and bacteriologically within three weeks of ending treatment. There were no side effects of the treatment. It is suggested that the treatment be continued for at least six weeks to prevent relapses.
Screening for Bladder Cancer: Rationale, Limitations, Whom to Target, and Perspectives
Authors: Stéphane Larré, James W.F. Catto, Michael S. Cookson, Edward M. Messing, Shahrokh F. Shariat, Mark S. Soloway, Robert S. Svatek, Yair Lotan, Alexandre R. Zlotta, H. Barton Grossman
Journal: European Urology (2013)
Minimum alcohol pricing: a shameful episode
Authors: F. Godlee
Journal: BMJ (2014)

This time last year public health campaigners and policy makers were confident that a minimum price on a unit of alcohol would be introduced across the United Kingdom. The evidence for substantial health benefits and cost savings was clear, a public consultation on the level of the price was just closing, Scotland had introduced a minimum unit price (though now under legal challenge by the drinks industry), and the UK prime minister had given his personal commitment that England and Wales would follow suit. Then in July the government announced that the policy had been shelved.

The politics behind this sudden U-turn have been something of a mystery. The Home Office minister Jeremy Browne gave as his reason …
Renal Cortical Necrosis with Survival
Authors: J. Vernon-Parry, R. T. Williams
Journal: BMJ (1963)

NECROSIS ore FIG.1.-Right renal biopsy 28 days after onset of anuria, show- ing necrosis of glomeruli and tubules and considerable calcium deposition.(x 150.)FIG.2.-Plain radiograph of left kidney one year later, showing diffuse calcification.There is a " tramline " pattern of calcifica- tion over the medial aspect of the lower pole.FIG.3.-Intravenous pyelogram at 5 minutes showing good excretion of the dye by the left kidney.The right kidney is small and calcified, but there is no excretion of the dye at this stage.
Clinical syndromes and consequences of antiretroviral-related hepatotoxicity
Authors: Marina Núñez
Journal: Hepatology (2010)

Abstract Highly active antiretroviral therapy (HAART)-related hepatotoxicity complicates the management of patients infected with human immunodeficiency virus (HIV), increases medical costs, alters the prescription patterns, and affects the guideline recommendations. Among the clinical consequences derived from HAART-related liver toxicity, hypersensitivity reactions and lactic acidosis are recognized as acute events with potential to evolve into fatal cases, whereas there seems to be other syndromes not as well characterized but of equal concern as possible long-term liver complications. Belonging to the latter category of syndrome, HAART-related nonalcoholic steatohepatitis, liver fibrosis, portal hypertension, and nodular regenerative hyperplasia are discussed in this review. Updated information on liver toxicity of current antiretroviral drugs, including the most recently licensed, is provided. Management and prevention of liver toxicity among HIV-infected patients treated with HAART are reviewed as well.