tbuckley/cabot-search huggingface dataset:
lndium-111 WBC Splenic Bed Abscess
Authors: MICHAEL A. CAWTHON, JOHN M. BAUMAN, MICHAEL F. HARTSHORNE
Journal: Clinical Nuclear Medicine (1985)

ln-111 labeled white blood cells are currently used in the diagnosis and localization of abscess formation. The spleen is an area of normal accumulation of white blood cells. Correct current knowledge of the presence or absence of the spleen is thus required for accurate scan interpretation. A case of splenic bed abscess is presented that stresses this point.
InterLymph hierarchical classification of lymphoid neoplasms for epidemiologic research based on the WHO classification (2008): update and future directions
Authors: Jennifer J. Turner, Lindsay M. Morton, Martha S. Linet, Christina A. Clarke, Marshall E. Kadin, Claire M. Vajdic, Alain Monnereau, Marc Maynadié, Brian C.-H. Chiu, Rafael Marcos-Gragera, Adele Seniori Costantini, James R. Cerhan, Dennis D. Weisenburger
Journal: Blood (2010)
Malaria in Man
Authors: Sanford F. Kuvin
Journal: JAMA (1963)

WE KNOW THAT man acts as the normal host for four species of human malaria:Plasmodium vivax, P falciparum, P malariae, andP ovale.  The possibility of nonhuman reservoirs was not seriously considered until Eyles et al1demonstrated a fifth species ofPlasmodiumtransmissible to man, the B strain ofP cynomolgi, normally a parasite of monkeys. Four accidental infections by this simian malaria occurred amongst laboratory workers in the US between April and July of 1960, making it apparent that the B strain ofP cynomolgiwas capable of producing malaria in man.2  Initial studies with inmate volunteers infected with this parasite were carried out by Dr. Henry Beye and his associates3at the US Federal Penitentiary in Atlanta, with emphasis placed on clinical and parasitological observations. Additional clinical and physiological responses in inmate volunteers infected with this B strain ofP cynomolgiand the comparison
Raw or Pasteurized Milk
Authors: F. R. Brown
Journal: BMJ (1938)

<h3>Objectives</h3> Autoantibodies directed against cytosolic 5′-nucleotidase 1A have been identified in many patients with inclusion body myositis. This retrospective study investigated the association between anticytosolic 5′-nucleotidase 1A antibody status and clinical, serological and histopathological features to explore the utility of this antibody to identify inclusion body myositis subgroups and to predict prognosis. <h3>Materials and methods</h3> Data from various European inclusion body myositis registries were pooled. Anticytosolic 5′-nucleotidase 1A status was determined by an established ELISA technique. Cases were stratified according to antibody status and comparisons made. Survival and mobility aid requirement analyses were performed using Kaplan-Meier curves and Cox proportional hazards regression. <h3>Results</h3> Data from 311 patients were available for analysis; 102 (33%) had anticytosolic 5′-nucleotidase 1A antibodies. Antibody-positive patients had a higher adjusted mortality risk (HR 1.89, 95% CI 1.11 to 3.21, p=0.019), lower frequency of proximal upper limb weakness at disease onset (8% vs 23%, adjusted OR 0.29, 95% CI 0.12 to 0.68, p=0.005) and an increased prevalence of excess of cytochrome oxidase deficient fibres on muscle biopsy analysis (87% vs 72%, adjusted OR 2.80, 95% CI 1.17 to 6.66, p=0.020), compared with antibody-negative patients. <h3>Interpretation</h3> Differences were observed in clinical and histopathological features between anticytosolic 5′-nucleotidase 1A antibody positive and negative patients with inclusion body myositis, and antibody-positive patients had a higher adjusted mortality risk. Stratification of inclusion body myositis by anticytosolic 5′-nucleotidase 1A antibody status may be useful, potentially highlighting a distinct inclusion body myositis subtype with a more severe phenotype.
Costs of unnecessary tests.
Authors: G Sandler
Journal: BMJ (1979)

The relative importance of the history, examination, and routine and special investigations has been assessed in the diagnosis and management of 630 medical outpatients. The history was the most important factor in both diagnosis and management in cardiovascular, neurological, respiratory, urinary, and other miscellaneous problems, and decided 56% of all diagnoses and 46% of all management. Examination findings were of more limited value, accounting for only 17% of diagnostic and 17% of management decisions overall. Routine haematology and urine examinations were of minimal value, contributing to less than 1% of all diagnoses. Special investigations decided most of the diagnoses and management in alimentary and endocrine problems, but were less helpful in problems affecting all other systems. If a local survey in the Trent Region reflected the pattern of medical outpatient practice nationally, then pounds 1.25 million could be saved annually if routine investigation was discontinued on all patients whose problem had already been diagnosed on the basis of the history and the clinical examination.
Diabetes
Authors: W. Richard Ohler
Journal: New England Journal of Medicine (1950)

BECAUSE of present interest in the detection of the patient with unrecognized diabetes and more especially as a result of thirty years as chief of the Diabetic Clinic at Boston City Hospital, I should like to present a few basic considerations in relation to this disease.DiagnosisA single positive urine test does not mean diabetes, nor does a single negative test exclude it. An accurate diagnosis cannot be made without both urine and blood studies, and even then there are many cases in which the diagnosis may remain in doubt. Given the typical diabetic symptoms of weight loss, polydipsia . . .
Effect of verapamil on enzyme release after early intravenous administration in acute myocardial infarction: double blind randomised trial.
Authors: L Thuesen, J R Jorgensen, H J Kvistgaard, J A Sorensen, M Vaeth, E B Jensen, J J Jensen, L Hagerup
Journal: BMJ (1983)

convulsant treatment was never started.The patient also had severe brittle asthma and died later at home in status asthmaticus.Postmortem examination was not carried out. CommentWe believe that the temporal relation of the seizures to the administration of factor VIII on three occasions makes the factor VIII the most likely aetiological factor in precipitating the seizures.Unusual intravascular particulate material has been noted in the cerebral white matter of a haemophiliac treated with large quantities of factor VIII concentrates,' and deposition of such particles in a brain with an underlying tendency to seizures may perhaps have been sufficient stimulus to evoke these seizures.The prevalence of electroencephalographic abnormalities in adult haemophiliacs is normal2; the fact that seizures have not previously been noted after infusions of factor concentrates but were in this case may be because this patient, despite repeated warnings, occasionally injected the concentrate over a period of one to two minutes.
Collaborative Care for Adults With Congenital Heart Disease
Authors: Catherine L. Webb, Kathy J. Jenkins, Peter P. Karpawich, Ann F. Bolger, Richard M. Donner, Hugh D. Allen, Robyn J. Barst
Journal: Circulation (2002)

Section on Cardiovascular Disease in the Young T he number of adults who have survived with congenital heart disease is increasing rapidly.Although prevalence studies have not been performed, estimates of expected numbers of people reaching adulthood with congenital heart disease (CHD) can now be made because birth prevalence has been studied and mortality rates have begun to stabilize.Birth prevalence for all forms of congenital heart disease detected in the first year of life is estimated at 8.1 per thousand live births on the basis of data from the Centers for Disease Control 1 ; estimates for disease of sufficient severity to result in a catheterization, surgery, or death in the first year of life are 2.3 per thousand, using population-based data derived from the Pediatric Cardiac Care Consortium. 2 In 1990, the National Center for Health Statistics reported the number of US live births to be 4 158 212. 3 Age-specific mortality data were obtained from the complete life table for the US population 4 and from population-based death rates during hospital admission using data from 6 states in 1992.Estimates of numbers of individuals reaching adulthood born in 1990 with congenital heart disease of sufficient severity to be diagnosed or treated during the first year of life are shown in the Figure .Disregarding all patients born before 1990 and those not diagnosed in the first year and assuming stable mortality in early adulthood, by 2020, nearly 760 000 individuals will have CHD, with 200 000 in the more severe subgroup.This striking increase in the estimated number of patients with congenital heart disease who will require competent care within the next 20 years mandates careful consideration of how and by whom this care should be delivered.Pediatric and adult cardiologists who currently treat congenital heart disease in adults (ACHD) have recently begun to grapple with these issues.The Congenital Cardiac Defects Committee of the Section on Cardiovascular Disease in the Young of the American Heart Association has identified defining pathways of excellence for ACHD care as a priority.The purpose of this article is to increase awareness about this important issue and to summarize current concerns.The challenge of providing excellent care to this growing population is important and needs to be placed clearly in the spotlight.
Proposed system to detect child abuse could deter parents from seeking treatment, pressure group says
Authors: N. Hawkes
Journal: BMJ (2012)

Children who visit emergency departments or have out of hours GP consultations are to have their details logged on a national computer system in a bid to detect child abuse. 

Dan Poulter, health minister for England, said he hoped the new system, to be rolled out from 2015, would prevent cases such as those of Victoria Climbie and Baby P, two children who died as a result of abuse.

Poulter told the Times : “Doctors and nurses are often the first people to see children who are victims of abuse. Up until now, it has been hard for frontline healthcare professionals to know if a child is already listed as being at risk or if children have been repeatedly seen in different emergency …
Screening reduces all cause mortality in men
Authors: Hisato Takagi, Norikazu Kawai, Takuya Umemoto
Journal: BMJ (2007)

Pulmonary macrophages are a target for inhaled therapies. Combinations of long-acting β<sub>2</sub>-agonists (LABA) and glucocorticosteroids have been developed for asthma and chronic obstructive pulmonary disease (COPD). This study examined two LABA, salmeterol and formoterol, and the glucocorticosteroid, budesonide, on cytokine release from monocyte-derived macrophages (MDM) to determine whether anti-inflammatory effects observed in patients are due to inhibition of macrophages. MDM were incubated in the absence or presence of LABA or budesonide prior to stimulation with lipopolysaccharide (LPS). Tumour necrosis factor (TNF)-α, granulocyte macrophage-colony stimulating factor (GM-CSF) and CXC chemokine ligand (CXCL)8 were measured by ELISA. Formoterol and salmeterol inhibited LPS-stimulated release of TNF-α (mean effective concentration (EC<sub>50</sub>) 2.4±1.8 and 3.5±2.7 nM, respectively; n = 11–16), GM-CSF (EC<sub>50</sub> 24.6±2.1 and 52.4±40.8 nM, respectively, n = 11–12) but not CXCL8 from LPS-stimulated MDM. Budesonide inhibited release of all three cytokines (EC<sub>50</sub> TNF-α: 1.2±0.4 nM; GM-CSF: 0.4±0.2 nM; CXCL8: 0.4±0.1 nM; n = 3–4). Formoterol but not salmeterol elevated cAMP in these cells. These effects were attenuated by β-adrenoceptor antagonists, propranolol and ICI118551. Salmeterol (10<sup>−7</sup> M) also inhibited formoterol-induced cAMP and formoterol-mediated attenuation of cytokine release. Combining budesonide (0.3 nM) with formoterol, inhibited TNF-α release additively. LABA may inhibit inflammatory cytokine release from macrophages in a cAMP-independent manner and act additively with budesonide.
Nail-gun fatality.
Authors: J Cragg
Journal: BMJ (1967)

MemorandaJBso scopy, and perhaps a willingness to convert these patients to ureteroileal conduit at the first sign of urinary tract trouble, when a carcinoma may be fortuitously discovered as in Case 1. Probably the ureteric stump and surrounding colonic mucosa should be removed at the time of this conversion, for Gillman (1964) described a case where an adenomatous polyp developed at the site of ureterocolic anastomosis seven years after the ureters had been transplanted into the colon, and six years after removal of the associated kidney.
Pregnancy and Paresthesia of Upper Extremities
Authors: William E. Crisp
Journal: JAMA (1965)

<h3>To the Editor:—</h3> The following is in rebuttal to the remarks made by Drs. Allan W. Downie and Mark G. Lazansky (LETTERS,<i>JAMA</i><b>190</b>:689 [Nov 16] 1964) in reference to the comments of Dr. J. P. Greenhill on "Pregnancy and Paresthesia of Upper Extremities" (QUESTIONS AND ANSWERS,<i>JAMA</i><b>189</b>:592 [Aug 17] 1964). The cases that we reported in "The Hand Syndrome of Pregnancy" (<i>Obstet Gynec</i><b>23</b>:433, 1964) were mainly of ulnar-nerve distribution with only occasional thumb-median involvement. These patients were all seen by the Department of Physical Medicine. The classic definition of "carpal-tunnel syndrome" is confined to only median nerve distribution. It was the opinion of all people involved that these cases were not classic examples of carpal-tunnel syndrome. In addition, our patients improved with the prescribed exercises. Although I am well aware that carpal-tunnel syndrome does appear not infrequently in pregnancy, it was not present in
Induction of G1 arrest by down-regulation of cyclin D3 in T cell hybridomas.
Authors: S Miyatake, H Nakano, S Y Park, T Yamazaki, K Takase, H Matsushime, A Kato, T Saito
Journal: The Journal of Experimental Medicine (1995)

The relationship between activation-induced growth inhibition and regulation of the cell cycle progression was investigated in T cell hybridomas by studying the function of the cell cycle-regulating genes such as G1 cyclins and their associated kinases. Activation of T cell hybridomas by anti-T cell receptor antibody induces growth arrest at G1 phase of the cell cycle and subsequently results in activation-driven cell death. Rapid reduction of both messenger RNA and protein level of the cyclin D3 is accompanied by growth arrest upon activation. Although the residual cyclin D3 protein forms a complex with cdk4 protein, cyclin D3-dependent kinase activity is severely impaired. Stable transfectants engineered to express cyclin D3 override the growth arrest upon activation. These results imply that the activation signal through T cell receptor induces the down-regulation of cyclin D3 expression and cyclin D3-dependent kinase activity, leading to growth arrest in G1 phase of the cell cycle in T cells.
Nasopharyngeal gene expression, a novel approach to study the course of respiratory syncytial virus infection
Authors: Corné H. van den Kieboom, Inge M.L. Ahout, Aldert Zomer, Kim H. Brand, Ronald de Groot, Gerben Ferwerda, Marien I. de Jonge
Journal: European Respiratory Journal (2014)

Respiratory syncytial virus (RSV) causes mild infections in the vast majority of children. However, in some cases, it causes severe disease, such as bronchiolitis and pneumonia. Development of severe RSV infection is determined by the host response. Therefore, the main aim of this study was to identify biomarkers associated with severe RSV infection. To identify biomarkers, nasopharyngeal gene expression was profiled by microarray studies, resulting in the selection of five genes: ubiquitin D , tetraspanin 8 , mucin 13 , β-microseminoprotein and chemokine ligand 7 . These genes were validated by real-time quantitative PCR in an independent validation cohort, which confirmed significant differences in gene expression between mildly and severely infected and between recovery and acute patients. Nasopharyngeal aspirate samples are regularly taken when a viral respiratory tract infection is suspected. In this article, we describe a method to discriminate between mild and severe RSV infection based on differential host gene expression. The combination of pathogen detection and host gene expression analysis in nasopharyngeal aspirates will significantly improve the diagnosis and prognosis of respiratory tract infections.
Toll-like Receptor-7 Tolerizes Malignant B Cells and Enhances Killing by Cytotoxic Agents
Authors: Yonghong Shi, Dionne White, Liwei He, Richard L. Miller, David E. Spaner
Journal: Cancer Research (2007)

Abstract Chronic activation through Toll-like receptors (TLR) occurs in a number of pathologic settings, but has not been studied to the same extent as primary activation. TLR7, expressed by B cells and some dendritic cells, recognizes molecular patterns associated with viruses that can be mimicked by synthetic imidazoquinolines. In response to primary stimulation with the imidazoquinoline, S28690, human mononuclear cells produced tumor necrosis factor-α, but were unable to do so upon restimulation with S28690. This state of “tolerization” lasted at least 5 days. Using chronic lymphocytic leukemia B cells as a model to facilitate biochemical analysis, the tolerized state was found to be associated with altered receptor components, including down-regulated expression of TLR7 mRNA and decreased levels of interleukin-1 receptor-associated kinase 1. Tolerization was characterized by a transcriptionally regulated block in stress-activated protein kinase and nuclear factor κB activation, with relatively preserved activation of extracellular signal-regulated kinase (ERK). Tolerized chronic lymphocytic leukemia cells were found to be more sensitive to cytotoxic chemotherapeutic agents, in part through altered stress-activated protein kinase signaling pathways. This property of the TLR7-tolerized state may potentially be exploited in the treatment of B cell cancers. [Cancer Res 2007;67(4):1823–31
Cancer morbidity in British military veterans included in chemical warfare agent experiments at Porton Down: cohort study
Authors: L M Carpenter, L Linsell, C Brooks, T J Keegan, T Langdon, P Doyle, N E S Maconochie, T Fletcher, M J Nieuwenhuijsen, V Beral, K M Venables
Journal: BMJ (2009)

<b>Objective</b> To determine cancer morbidity in members of the armed forces who took part in tests of chemical warfare agents from 1941 to 1989. <b>Design</b> Historical cohort study, with cohort members followed up to December 2004. <b>Data source </b>Archive of UK government research facility at Porton Down, UK military personnel records, and national death and cancer records. <b>Participants</b> All veterans included in the cohort study of mortality, excluding those known to have died or been lost to follow-up before 1 January 1971 when the UK cancer registration system commenced: 17 013 male members of the UK armed forces who took part in tests (Porton Down veterans) and a similar group of 16 520 men who did not (non-Porton Down veterans). <b>Main outcome measures</b> Cancer morbidity in each group of veterans; rate ratios, with 95% confidence intervals, adjusted for age group and calendar period. <b>Results</b> 3457 cancers were reported in the Porton Down veterans compared with 3380 cancers in the non-Porton Down veterans. While overall cancer morbidity was the same in both groups (rate ratio 1.00, 95% confidence interval 0.95 to 1.05), Porton Down veterans had higher rates of ill defined malignant neoplasms (1.12, 1.02 to 1.22), in situ neoplasms (1.45, 1.06 to 2.00), and those of uncertain or unknown behaviour (1.32, 1.01 to 1.73). <b>Conclusion</b> Overall cancer morbidity in Porton Down veterans was no different from that in non-Porton Down veterans.
SOME NOTES ON TWO CASES OF VOLUNTARY LARYNGEAL WHISTLING.
Authors: G. HUDSON MAKUEN
Journal: JAMA (1901)

The first case that I shall speak of was a student at the Medico-Chirurgical College, and referred to me by Dr. Gleason, of Philadelphia, who also exhibited him before the Section on Laryngology and Otology at the College of Physicians, Philadelphia, where the case aroused considerable interest and discussion. The patient could whistle a tune with his mouth open as in the position for saying "ah." Owing to the absence of good light for laryngoscopic examination, the general opinion of the majority of those present was that the whistle was made in the pharynx, somewhere in the region of the palatal pillars; but that seemed to me impossible, because the pillars were not approximated sufficiently to make an aperture small enough for the production of such a sound. At Dr. Gleason's suggestion, an appointment was made with the young man at my office, where, with a little careful manipulation, he
Glucagon-induced changes in the action potential, contraction, and Na+-K+-ATPase of cardiac muscle
Authors: K. PRASAD
Journal: Cardiovascular Research (1975)

The effects of glucagon in concentrations of 0.294 times 10(-6) mol/l, 1.47 times 10(-6) mol/l; 2.94 times 10(-6) mol/l, 5.8 times 10(-6) mol/l, and 1.47 times 10(-5) mol/l on the simultaneously recorded action potentials and contractions; and microsomal and sarcolemmal Na+-tk+-atpase in the myocardium of the guinea pig, rabbit, dog, and pig were investigated. Glucagon in all the concentrations produced an inhibition of the Na+-K+-ATPase associated with an increase in the contractility and shortening of the duration of action potential in dog myocardium. The increase in contraction was concentration-dependent up to a certain concentration. Inhibition of sarcolemmal ATPase was more than that of microsomal ATPase. In none of the concentrations did glucagon produce any significant changes in the Na+-K+-ATPase. In none of the concentrations did glucagon produce any significant changes in the Na+-K+-ATPase, contractility, and action potential duration in the myocardium of guinea pig, rabbit, or pig. These results suggest that glucagon-induced positive inotropic effect might be due to an increase in the Ca++ influx as a result of inhibition of membrane Na+-K+-ATPase. Shortening of the action potential duration might also be due to an increased efflux of potassium as a result of an inhibition of Na+-K+-ATPase.