tbuckley/cabot-search huggingface dataset:
Local antibodies against Pneumocystis carinii in bronchoalveolar lavage fluid
Authors: AL Laursen, BN Jensen, PL Andersen
Journal: European Respiratory Journal (1994)

Pneumocystis carinii pneumonia (PCP) is a frequent cause of pneumonia among human immunodeficiency virus (HIV)-infected patients. Little is known, however, about the role played by humoral immunity to control the infection. This study was undertaken to elucidate the role played by local antibodies. Bronchoalveolar lavage (BAL) fluids from 18 acquired immune deficiency syndrome (AIDS) patients with PCP, 20 HIV-antibody positive patients without PCP, and 20 lung cancer patients were examined for antibodies against P. carinii by the indirect immunofluorescence method. The ratio of albumin concentration in BAL fluid to serum was used to standardize the lavage fluids. Immunoglobulin G (IgG) antibodies against P. carinii occurred less frequently, and immunoglobulin M (IgM) antibodies more frequently, in PCP patients than in other groups. Immunoglobulin A (IgA) antibodies against pneumocysts were found with the same frequency in all three groups, although the median titre was lower among HIV-antibody positive patients without PCP, compared with the other groups. When indexed (antibody titre in BAL fluid x albumin concentration in serum/antibody titre in serum x albumin concentration in BAL fluid) to express locally produced antibodies, IgG indices were significantly higher in HIV-infected patients without PCP, whereas IgM and IgA indices were significantly higher in PCP patients. These findings suggest that the local IgG response is impaired in patients with PCP, whereas the local IgA and, to some extent, the IgM responses are preserved.
BACTERIAL GROWTH AND MULTIPLICATION AS DISCLOSED BY MICRO MOTION PICTURES
Authors: Ralph W. G. Wyckoff
Journal: The Journal of Experimental Medicine (1934)

Using a micro motion picture technique for making records, studies covering several thousand hours of observation have been made of the growth of a number of bacteria. On the basis of these experiments a discussion is offered of bacterial division and its influence on gross colony appearance, of different kinds of pleomorphism that have been observed, and of the nature of the internal structure that is seen in some bacteria. Several of the microorganisms chosen for examination are ones that have been thought to give evidence of life cycle phenomena. The present pictures, however, contain no evidence of a bacterial cycle in the commonly accepted meaning of the term.
Urinary 1-Hydroxypyrene as a Biomarker of PAH Exposure in 3-Year-Old Ukrainian Children
Authors: Amy Pelka Mucha, Daniel Hryhorczuk, Andrij Serdyuk, Joseph Nakonechny, Alexander Zvinchuk, Serap Erdal, Motria Caudill, Peter Scheff, Elena Lukyanova, Zoreslava Shkiryak-Nyzhnyk, Natalia Chislovska
Journal: Environmental Health Perspectives (2005)

Urinary 1-hydroxypyrene (1-OHP) is a biomarker of polycyclic aromatic hydrocarbon (PAH) exposure. We measured urinary 1-OHP in 48 children 3 years of age in Mariupol, Ukraine, who lived near a steel mill and coking facility and compared these with 1-OHP concentrations measured in 42 children of the same age living in the capital city of Kiev, Ukraine. Children living in Mariupol had significantly higher urinary 1-OHP and creatinine-adjusted urinary 1-OHP than did children living in Kiev (adjusted: 0.69 vs. 0.34 micromol/mol creatinine, p < 0.001; unadjusted: 0.42 vs. 0.30 ng/mL, p = 0.002). Combined, children in both cities exposed to environmental tobacco smoke in their homes had higher 1-OHP than did children not exposed (0.61 vs. 0.42 micromol/mol creatinine; p = 0.04; p = 0.07 after adjusting for city). In addition, no significant differences were seen with sex of the children. Our sample of children in Mariupol has the highest reported mean urinary 1-OHP concentrations in children studied to date, most likely due to their proximity to a large industrial point source of PAHs.
Detection of a Pedunculated Right Atrial Tumor by Radionuclide Imaging
Authors: A. BARSOTTI, R. MARIOTTI, W. BENCIVELLI, G. PUCCINI, A. BALBARINI, G. TARTARINI, M. MARIANI
Journal: Clinical Nuclear Medicine (1981)

BARSOTTI, A.; MARIOTTI, R.; BENCIVELLI, W.; PUCCINI, G.; BALBARINI, A.; TARTARINI, G.; MARIANI, M. Author Information
Sickle-Cell Trait: Benign or Malignant?
Authors: ROBERT M. COOPER
Journal: Annals of Internal Medicine (1972)

Editorial Notes1 December 1972Sickle-Cell Trait: Benign or Malignant?ROBERT M. COOPER, M.D., JAMES F. TOOLE, M.D.ROBERT M. COOPER, M.D.Search for more papers by this author, JAMES F. TOOLE, M.D.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-77-6-997 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptDespite the specificity of the molecular defect in hemoglobin S, the consequences of having this abnormal hemoglobin may show extreme variations in clinical expression in the same patient as well as among different affected individuals. Hemolysis is consistently present, but infarction and thrombosis are occasional or intermittent phenomena. Additional factors must coexist with the hemoglobin S to modify its phenotypic expression.Even greater variability in clinical expression is found in individuals heterozygous for hemoglobin S, in whom the percentage of abnormal hemoglobin ranges from 22% to 45%, with an average of 40% (1). Sickle-cell trait was once considered to be...References1. NECHELESALLENFINKEL TDH: Clinical Disorders of Hemoglobin Structure and Synthesis. New York, Appleton-Century-Crofts, 1967, p. 32 Google Scholar2. JONESBINDERDONOWHO SRE: Sudden death in sickle-cell trait. N Engl J Med 282:323-325, 1970 CrossrefMedlineGoogle Scholar3. SCHENK E: Sickle cell trait and superior longitudinal sinus thrombosis. Ann Intern Med 60:465-470, 1964 LinkGoogle Scholar4. GREENWALD J: Stroke, sickle cell trait, and oral contraceptives (letter). Ann Intern Med 72:960, 1970 LinkGoogle Scholar5. BENNETTHESLOPMEYNELL MRM: Massive hematuria associated with sickle-cell trait. Br Med J 1:677-679, 1967 CrossrefMedlineGoogle Scholar6. OSUNTOKUNOSUNTOKUN BO: Complicated migraine and haemoglobin AS in Nigerians. Br Med J 2:621-622, 1972 CrossrefMedlineGoogle Scholar7. COCHRANE A: Background to Migraine: Third Migraine Symposium. New York, Springer Verlag, 1970 Google Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: The Bowman Gray School of Medicine of Wake Forest University Winston-Salem, N.C. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited byStabilities of hemoglobins A and S in dried blood spots stored under controlled conditionsAn autopsy case of sudden death in a patient with sickle cell diseaseThe risk of sudden death in sickle cell trait: Noninvasive assessment of cardiac response to exerciseThe morbidity of sickle cell trait 1 December 1972Volume 77, Issue 6Page: 997-998KeywordsHemoglobinInfarctionSpecificityThrombosis Issue Published: 1 December 1972 PDF downloadLoading ...
Extemporaneous vs Commercial Formulations of Steroids for Topical Usage
Authors: Ernst Epstein
Journal: JAMA (1970)

<h3>To the Editor.—</h3> Considering all the published admonishments to avoid errors in logic when evaluating the efficacy of drugs, I am truly amazed that the communication on "Extemporaneous Formulation of Corticosteroids for Topical Usage" by Burdick et al was published (<b>211</b>:462, 1970). I should like to point out that the article is completely misleading and engages in several elementary errors of logic which, however, may escape detection by those unfamiliar with some of the facets determining the activity of topically administered steroids. When comparing two pharmacologic preparations, it is important that they differ in only one significant factor. Burdick et al in comparing extemporaneously pharmacistcompounded steroids for topical use with commercially formulated steroids imply that the difference in activity is the result of dispersion of the active substance and show impressive photographs of the different ointment bases, graphs, etc. All this is hokum! The simple fact is that the
Progressive Multifocal Leukoencephalopathy after Natalizumab Therapy for Crohn's Disease
Authors: Gert Van Assche, Marc Van Ranst, Raf Sciot, Bénédicte Dubois, Séverine Vermeire, Maja Noman, Jannick Verbeeck, Karel Geboes, Wim Robberecht, Paul Rutgeerts
Journal: New England Journal of Medicine (2005)

The prior diagnosis of fatal astrocytoma in a 60-year-old man with Crohn's disease treated with natalizumab, a monoclonal antibody against alpha4 integrins, was reclassified as JC virus-related progressive multifocal leukoencephalopathy (PML). Analysis of frozen serum samples showed that JC virus DNA had appeared in the serum three months after the initiation of open-label natalizumab monotherapy and two months before the appearance of symptomatic PML. There was staining of the brain lesion for polyomavirus. This case report, along with two others, suggests that anti-alpha4-integrin therapy can result in JC virus-induced PML.
Does coronary artery bypass surgery restore normal maximal coronary flow reserve? The effect of diffuse atherosclerosis and focal obstructive lesions.
Authors: R F Wilson, C W White
Journal: Circulation (1987)

Aortocoronary vein bypass surgery might not restore normal maximal coronary flow reserve to bypassed coronary vessels because residual diffuse coronary atherosclerosis might limit maximal hyperemia. To investigate the effect of diffuse atherosclerosis and a focal stenosis at the graft-coronary anastomosis, we measured coronary flow reserve with an extensively validated subselective Doppler catheter in 24 patients with 35 bypass grafts perfusing angiographically normal coronary vessels. The Doppler catheter was positioned in the midportion of the graft, and coronary flow reserve was measured as the peak/resting velocity ratio after selective graft injection of a maximally vasodilating dose of papaverine. Luminal dimensions of the bypass graft, graft-coronary insertion, and bypassed coronary vessel were measured by quantitative coronary angiography (Brown/Dodge method). Measurements of coronary flow reserve and coronary dimensions of vein bypass grafts were compared with similar measurements obtained from 13 patients with normal coronary vessels and normal myocardium. Seventeen of the 35 bypass grafts perfused unobstructed coronary-vein graft anastomoses (less than 50% area stenosis) and normal myocardium. The coronary flow reserve of these 17 bypass grafts was normal (5.0 +/- 0.4, mean +/- SEM) and not significantly different from that measured in normal arteries (5.1 +/- 0.6), even though the cross-sectional area of the native coronary artery just distal to the bypass insertion was 40% smaller than in matched normal vessels. Bypass grafts perfusing hypertrophied (n = 2) or infarcted (n = 6) myocardium had significantly reduced coronary flow reserve compared with normal vessels (2.7 +/- 0.3; p less than .01), even when the infarcted wall had only minimal hypokinesis.(ABSTRACT TRUNCATED AT 250 WORDS)
Splenic Repair in Agnogenic Myeloid Metaplasia
Authors: Juan F. Jaramillo
Journal: JAMA (1980)

LACERATION of the spleen in a patient with agnogenic myeloid metaplasia (AMM) was successfully treated with splenorrhaphy. Splenectomy is hazardous in AMM, and repair should be a useful alternative. <h3>Report of a Case</h3> A 57-year-old woman was admitted on Oct 21, 1977, to St Mary's Hospital, Saginaw, Mich, after sustaining trauma to the chest and abdomen in a car accident. The patient's condition had previously been diagnosed as AMM. On admission, blood pressure was 100/60 mm Hg; pulse rate, 84 beats per minute; temperature, 36.7 °C. The patient was alert and complained of left upper quadrant pain radiating to the left shoulder. Deep palpation elicited tenderness in the left upper quadrant of the abdomen, with no demonstrable splenomegaly. Laboratory data included the following values: WBCs, 19,400/cu mm, with 43% polymorphonuclear leukocytes, 31% band forms, 15% metamyelocytes, 4% lymphocytes, and 2% monocytes; hemoglobin, 10.5 g/dL; platelets, 309,000/cu mm; prothrombin time, 12.8
Academic medicine: time for reinvention: Wholesale review of research and teaching is required
Authors: L. G Morrison
Journal: BMJ (2004)

Editor—The BMJ of 1 November and Clark and Smith in their editorial focus on the crisis in academic medicine with the tagline “Medicine's capacity to research, think, and teach is collapsing.”1 I do not disagree, but I am concerned that all of the articles predominantly emphasise research and those who are employed as medical academics.

To focus mainly on those with a formal academic contract of employment and particularly on those who do substantive research is to look at only part of the problem.

Many consultants and others employed by the NHS have important teaching and research responsibilities, and clinical teaching is often delivered largely by “non-academics.” An assumption prevails that these areas are largely the province of medical academics, and the BMJ seems to be perpetuating this view. Good research and good teaching are somehow assumed to go together, when that is not necessarily the case. Neither are they mutually exclusive.​exclusive.




Figure 1




The problem is that across medicine doctors are struggling to maintain a commitment to research and teaching as well as an ever increasing commitment to service delivery. The new consultant contracts in England, Scotland, and Wales may help to better define the non-clinical duties of NHS and academic staff alike, but they are also in danger of being squeezed out in favour of delivering services and meeting targets.

Nothing short of a wholesale review of the way research and teaching are delivered will address these problems. Sorting out research, and only research done by medical academics, is at best papering over the cracks.
CEREBRAL SPASTIC PARALYSIS
Authors: M. E. BLAHD
Journal: JAMA (1918)

The syndrome known as Little's disease was first brought to the attention of the profession by Little of London, who, in 1843, in a lecture before the London Orthopedic Institute, reported several cases of the disease, which since has borne his name. 1 For a great number of years, this syndrome was erroneously classified as a medical entity, without any regard for the numerous causative factors. Since its etiology has been more completely recognized, it has been found that instead of its being a single medical entity, there are a great number of conditions with various etiologic factors, all producing the same end-results classified as Little's disease.  Cerebral spastic paralysis, or hemiplegie cerebrale infantile, seems a better term by which to express the manifestations of these various etiologic factors. The latter have been well classified by Grossman 2 into three groups: 1. intra-uterine, or prenatal; (2) natal, or intrapartum, and
Linear IgA dermatosis with IgA antibodies to type VII collagen
Authors: G. Zambruno, J. Kanitakis
Journal: British Journal of Dermatology (1996)

Journal Article Linear IgA dermatosis with IgA antibodies to type VII collagen Get access G. Zambruno, G. Zambruno Istituto Dermopatico dell'Immacolata, Via dei Monti di Creta 104, 00167 Roma, Italy Search for other works by this author on: Oxford Academic Google Scholar J. Kanitakis J. Kanitakis Department of Dermatology, Hôspital Ed. Herriot (Pav. R). 69437 Lyon cx 03, France Search for other works by this author on: Oxford Academic Google Scholar British Journal of Dermatology, Volume 135, Issue 6, 1 December 1996, Page 1004, https://doi.org/10.1111/j.1365-2133.1996.tb07394.x Published: 01 December 1996
Evaluation of a Laboratory System Intended for Use in Physicians' Offices
Authors: Richard Belsey
Journal: JAMA (1987)

The accuracy and precision of the Kodak DT-60 tabletop chemistry analyzer were evaluated in the clinical laboratory at the Portland (Ore) Veterans Administration Medical Center, and its operational throughput and cost were estimated. All DT-60 tests that were studied exhibited clinically acceptable precision and, except for the glucose method, accuracy. The accuracy of the glucose method was indeterminate with the available data. Throughput under field conditions was found to be less than half of the manufacturer's claim. The estimated supply cost per test could vary from $1.20 to $5.49 per test, depending on the test type and the number of assays expected to be performed daily. The instrument seems to be accurate, precise, and generally reliable when operated by professional medical technologists. (<i>JAMA</i>1987;258:353-356)
Genetic Disorders and the Fetus: Diagnosis, Prevention, and Treatment
Authors: Theodore Kushnick
Journal: JAMA (1987)

It was a great pleasure for me to examine a definitive work in the field of fetal genetic disorders, which has been written in an easily readable and literate style. The majority of the chapters are thorough in the treatment of particular subjects. All follow the format of an excellent, complete but succinct review of previous literature in a style reminiscent of the<i>Lancet</i>. Subsequently, there are extensive and lucid (ie, no inbred technical jargon) descriptions of the basic techniques utilized, be they cytogenetic, biochemical, molecular, or ultrasonographic. For the most part, the sections are followed by discussions of clinical applications of these techniques for prenatal diagnosis and the limitations of such use. Most of the book is devoted to the diagnosis of fetal genetic disorders rather than the limited available measures for treatment, but there is excellent coverage in the few areas where prevention and treatment other than pregnancy
Macrophages Inhibit Neovascularization in a Murine Model of Age-Related Macular Degeneration
Authors: Rajendra S Apte, Jennifer Richter, John Herndon, Thomas A Ferguson
Journal: PLoS Medicine (2006)

Background Age-related macular degeneration (AMD) is the leading cause of blindness in people over 50 y of age in at least three continents. Choroidal neovascularization (CNV) is the process by which abnormal blood vessels develop underneath the retina. CNV develops in 10% of patients with AMD but accounts for up to 90% of the blindness from AMD. Although the precise etiology of CNV in AMD remains unknown, the macrophage component of the inflammatory response, which has been shown to promote tumor growth and support atherosclerotic plaque formation, is thought to stimulate aberrant angiogenesis in blinding eye diseases. The current theory is that macrophage infiltration promotes the development of neovascularization in CNV. Methods and Findings We examined the role of macrophages in a mouse model of CNV. IL-10−/− mice, which have increased inflammation in response to diverse stimuli, have significantly reduced CNV with increased macrophage infiltrates compared to wild type. Prevention of macrophage entry into the eye promoted neovascularization while direct injection of macrophages significantly inhibited CNV. Inhibition by macrophages was mediated by the TNF family death molecule Fas ligand (CD95-ligand). Conclusions Immune vascular interactions can be highly complex. Normal macrophage function is critical in controlling pathologic neovascularization in the eye. IL-10 regulates macrophage activity in the eye and is an attractive therapeutic target in order to suppress or inhibit CNV in AMD that can otherwise lead to blindness.
Anticardiolipin Antibodies From Patients With the Antiphospholipid Antibody Syndrome Recognize Epitopes in Both β <sub>2</sub> -Glycoprotein 1 and Oxidized Low-Density Lipoprotein
Authors: Sohvi Hörkkö, Tsaiwei Olee, Lian Mo, D. Ware Branch, Virgil L. Woods, Wulf Palinski, Pojen P. Chen, Joseph L. Witztum
Journal: Circulation (2001)

Background —We recently suggested that many anticardiolipin antibodies bind only to oxidized cardiolipin (OxCL) and/or to OxCL–β 2 -glycoprotein 1 (β 2 GP1) adducts but not to a “reduced” cardiolipin that is unable to undergo oxidation. To test this hypothesis, we investigated 24 sera, 4 protein A–purified IgG fractions, and 3 human monoclonal antibodies that were all isolated from patients with antiphospholipid antibody syndrome (APS); testing was also performed in 7 controls. Two monoclonal antibodies (IS3 and IS4) were selected for binding to CL and one was selected for binding to β 2 GP1 (LJB8). Methods and Results —By chemiluminescent immunoassay, all APS sera samples bound only to OxCL and not to reduced CL, and the binding was inhibited &gt;95% by OxCL but not reduced CL. All purified IgG fractions bound to β 2 GP1 but only when the β 2 GP1 was plated on microtiter wells coated with OxCL. All 3 monoclonal antibodies bound only to OxCL. On Western blots, IS4 and LJB8 bound to β 2 GP1 as well as to delipidated apoB of oxidized LDL but not to native apoB. IS3 also bound to oxidized apoB on Western blot. Covalent modification of β 2 GP1 with oxidation products of CL made it more antigenic for APS serum samples, for purified IgG fractions, and for the monoclonal antibodies. Conclusions —These data support the hypothesis that oxidation of CL is needed to generate epitopes for many anticardiolipin antibodies and that some of these epitopes are covalent adducts of OxCL with β 2 GP1 or apoB.
Alcohol Potentiates Orthostatic Hypotension
Authors: Krzysztof Narkiewicz, Ryan L. Cooley, Virend K. Somers
Journal: Circulation (2000)

Background —Alcohol consumption may be linked to syncopal events. The mechanisms by which alcohol may induce syncope are unknown. Impairment of the response to orthostatic stress may be involved. Using a double-blind, randomized, placebo-controlled study, we tested the hypothesis that short-term alcohol intake causes orthostatic hypotension because of an impairment in the vasoconstrictor response to orthostatic stress. Methods and Results —We examined the effects of alcohol on blood pressure, heart rate, and forearm vascular resistance (FVR) during orthostatic stress achieved by stepwise increases in lower-body negative pressure (LBNP) in 14 healthy young volunteers. During the placebo session, blood pressure did not change significantly during LBNP at −5, −10, and −20 mm Hg. A significant decrease in blood pressure was evident only at −40 mm Hg. In contrast, blood pressure fell significantly at all levels of LBNP during the alcohol session. Compared with placebo, alcohol potentiated the hypotensive responses to LBNP, particularly at −40 mm Hg, when the decrease in systolic blood pressure after alcohol intake (−14 mm Hg) was double that after placebo intake (−7 mm Hg). FVR increased with LBNP after placebo. However, after alcohol intake, FVR did not increase during LBNP despite the potentiated decrease in blood pressure. FVR responses during LBNP were reduced during alcohol compared with placebo consumption ( P =0.04). Conclusions —Short-term alcohol consumption elicits hypotension during orthostatic stress because of impairment of vasoconstriction. These findings have implications for the understanding of the hemodynamic effects of alcohol and, in particular, for understanding syncopal events that occur in association with alcohol intake.
4 Pharmacokinetic boosting of VX-950, an inhibitor of HCV protease, by co-dosing with ritonavir
Authors: D.J. Kempf, H.-J. Chen, C.M. Yeung, J.T. Randolph, Y.Y. Lau, L.E. Chovan, T.M. Turner, P.J. Dandliker, L.L. Klein, K.C. Marsh
Journal: Journal of Hepatology (2006)