tbuckley/cabot-search huggingface dataset:
Human papillomaviruses in anogenital warts in children: Author's reply
Authors: V A Venning
Journal: BMJ (1990)

<h3>Background</h3> Frequent attendances of the same users in emergency departments (ED) can intensify workload pressures and are common among children, yet little is known about the characteristics of paediatric frequent users in EDs. <h3>Aim</h3> To describe the volume of frequent paediatric attendance in England and the demographics of frequent paediatric ED users in English hospitals. <h3>Method</h3> We analysed the Hospital Episode Statistics dataset for April 2014–March 2017. The study included 2 308 816 children under 16 years old who attended an ED at least once. Children who attended four times or more in 2015/2016 were classified as frequent users. The preceding and subsequent years were used to capture attendances bordering with the current year. We used a mixed effects logistic regression with a random intercept to predict the odds of being a frequent user in children from different sociodemographic groups. <h3>Results</h3> One in 11 children (9.1%) who attended an ED attended four times or more in a year. Infants had a greater likelihood of being a frequent attender (OR 3.24, 95% CI 3.19 to 3.30 vs 5 to 9 years old). Children from more deprived areas had a greater likelihood of being a frequent attender (OR 1.57, 95% CI 1.54 to 1.59 vs least deprived). Boys had a slightly greater likelihood than girls (OR 1.05, 95% CI 1.04 to 1.06). Children of Asian and mixed ethnic groups were more likely to be frequent users than those from white ethnic groups, while children from black and 9other9 had a lower likelihood (OR 1.03, 95% CI 1.01 to 1.05; OR 1.04, 95% CI 1.01 to 1.06; OR 0.88, 95% CI 0.86 to 0.90; OR 0.90, 95% CI 0.87 to 0.92, respectively). <h3>Conclusion</h3> One in 11 children was a frequent attender. Interventions for reducing paediatric frequent attendance need to target infants and families living in deprived areas.
Gradation of Intensity of Cardiac Murmurs-Reply
Authors: Samuel A. Levine
Journal: JAMA (1962)

<h3>To the Editor:—</h3> The suggestions made by Dr. Samuel Waldman are ones that already have been practiced by a good many physicians. I still believe that it is desirable to have 6 gradations to indicate the different degrees of intensity of heart murmurs. Four gradations do not permit sufficient differentiation. If physicians use only 4 gradations, then the method of designation indicated by Dr. Waldman would have some use.
Serine protease activity contributes to control of Mycobacterium tuberculosis in hypoxic lung granulomas in mice
Authors: Stephen T. Reece, Christoph Loddenkemper, David J. Askew, Ulrike Zedler, Sandra Schommer-Leitner, Maik Stein, Fayaz Ahmad Mir, Anca Dorhoi, Hans-Joachim Mollenkopf, Gary A. Silverman, Stefan H.E. Kaufmann
Journal: Journal of Clinical Investigation (2010)

The hallmark of human Mycobacterium tuberculosis infection is the presence of lung granulomas. Lung granulomas can have different phenotypes, with caseous necrosis and hypoxia present within these structures during active tuberculosis. Production of NO by the inducible host enzyme NOS2 is a key antimycobacterial defense mechanism that requires oxygen as a substrate; it is therefore likely to perform inefficiently in hypoxic regions of granulomas in which M. tuberculosis persists. Here we have used Nos2-/- mice to investigate host-protective mechanisms within hypoxic granulomas and identified a role for host serine proteases in hypoxic granulomas in determining outcome of disease. Nos2-/- mice reproduced human-like granulomas in the lung when infected with M. tuberculosis in the ear dermis. The granulomas were hypoxic and contained large amounts of the serine protease cathepsin G and clade B serine protease inhibitors (serpins). Extrinsic inhibition of serine protease activity in vivo resulted in distorted granuloma structure, extensive hypoxia, and increased bacterial growth in this model. These data suggest that serine protease activity acts as a protective mechanism within hypoxic regions of lung granulomas and present a potential new strategy for the treatment of tuberculosis.
Belief not science is behind flu jab promotion, new report says
Authors: J. Lenzer
Journal: BMJ (2012)

An independent meta-analysis of vaccines against influenza has found that claims of benefit have been significantly exaggerated.

The report, released last month by the University of Minnesota’s Center for Infectious Disease Research and Policy, was based on a comprehensive review of data published from 1967 to 2012.1

Evidence for “consistent high-level protection is elusive,” the researchers concluded. Although vaccination was found to provide modest protection from infection in young healthy adults who rarely have complications of flu, the authors found that “evidence for protection in adults 65 years of age and older [who represent over 90% of deaths from flu] . . . is lacking.”

The authors also analyzed recommendations issued by the federal Advisory Committee on Immunization Practices, which provides expert advice to the US Centers for Disease Control and Prevention and which are “often considered the standard of practice . . . around the …
Erratum: Common variants in P2RY11 are associated with narcolepsy
Authors: Birgitte R Kornum, Minae Kawashima, Juliette Faraco, Ling Lin, Thomas J Rico, Stephanie Hesselson, Robert C Axtell, Hedwich Kuipers, Karin Weiner, Alexandra Hamacher, Matthias U Kassack, Fang Han, Stine Knudsen, Jing Li, Xiaosong Dong, Juliane Winkelmann, Giuseppe Plazzi, Sona Nevsimalova, Seung-Chul Hong, Yutaka Honda, Makoto Honda, Birgit Högl, Thanh G N Ton, Jacques Montplaisir, Patrice Bourgin, David Kemlink, Yu-Shu Huang, Simon Warby, Mali Einen, Jasmin L Eshragh, Taku Miyagawa, Alex Desautels, Elisabeth Ruppert, Per Egil Hesla, Francesca Poli, Fabio Pizza, Birgit Frauscher, Jong-Hyun Jeong, Sung-Pil Lee, Kingman P Strohl, William T Longstreth, Mark Kvale, Marie Dobrovolna, Maurice M Ohayon, Gerald T Nepom, H-Erich Wichmann, Guy A Rouleau, Christian Gieger, Douglas F Levinson, Pablo V Gejman, Thomas Meitinger, Paul Peppard, Terry Young, Poul Jennum, Lawrence Steinman, Katsushi Tokunaga, Pui-Yan Kwok, Neil Risch, Joachim Hallmayer, Emmanuel Mignot
Journal: Nature Genetics (2011)
Asbestos Bodies And Their Bioeffects
Authors: Robert T. P. deTreville
Journal: JAMA (1968)

<h3>To the Editor:—</h3> This letter outlines the history of the asbestos body from its discovery through a period of little clinical significance to the present day when it holds the position of being possibly one of the greatest industrial medical problems of the age. <h3>Asbestos:—</h3> Asbestos is a general term that covers a number of minerals of which four are of commercial importance: crocidolite from the Republic of South Africa, amosite also mined chiefly in the Republic of South Africa, chrysolite which occurs in many countries of the world, and anthophyllite which is mined mainly in Europe. <h3>Asbestosis:—</h3> This is a type of lung fibrosis in workers exposed to large amounts of asbestos dust. It may or may not be associated with recognizable clinical disease during life and is produced by all types of asbestos. Asbestosis was recognized as an industrial disease at the turn of the century, but at
Home Blood Pressure Determination
Authors: Stevo Julius, Charles N. Ellis, Arturo V. Pascual, Michele Matice, Lennart Hansson, Stephen N. Hunyor, Lee N. Sandler
Journal: JAMA (1974)

Self-determined home blood pressure readings taken by 112 patients with borderline hypertension were compared to values of 49 normotensive controls. Thirty percent of patients with borderline hypertensive readings in the clinic were hypertensive at home; only 28% of patients were clearly normotensive. Clinic blood pressure levels, family history, body weight, and heart rate failed as predictors of which patients were likely to be hypertensive at home. Self-determined home blood pressures are suggested for identification of individual patients with borderline hypertension who require continuous and close observation. (<i>JAMA</i>229:663-666, 1974)
Clinical Lecture on Cases of Myasthenia Gravis Pseudo-Paralytica: Delivered at the National Hospital for the Paralysed and Epileptic
Authors: T. Buzzard
Journal: BMJ (1900)

in the Hosptal an account of a cae Paralysis without Anatomical Cbanges."A girl had come to the hospital complaining weakness; she could scarcely move about, spoke slowly, showed slight strabismus.For a month she remained state, the movements of her limbs and her speech so and deliberate that the case appeared to be lethargy from want of will than a condition of At the end of this period all the symptoms became aggravated, and in three days tbey had assumed well marked bulbar paralysis.She spoke most indistinctly, with great diffIculty, and was quite unable to cough.still out of bed.Shortly afterwards increasing difficulty in respiration, and in a died.The bulb, po8t mortem, appeared quite naked eye, as well as to microscopical examination.portant observation was followed next year by a Erbof three cases in which the principal symptoms in striking paresis of muscles, especially of the neck, and of the eyes (ptosis), less in those of the tongue, and extremities.As time passed on there came accounts from other of cases manifestly belonging to the same category, terminated fatally, and, with one or two doubtful exceptions, had shown no anatomical lesions.By all the earlierobservers
Dissecting Aneurysm of the Aorta as an Unusual Cause of “Asthma” — An Anatomicopharmacologic Correlation
Authors: Kenneth C. Lasseter, Roger F. Palmer
Journal: New England Journal of Medicine (1974)

SINCE the course of acute dissecting aneurysm of the aorta has been dramatically altered by aggressive drug and surgical therapy,1 2 3 unrecognized complications may be unveiled. In the following case, profound respiratory insufficiency and bronchospasm appeared to be related to anatomic distortions caused by dissection of the aortic arch.Case ReportA 62-year-old black woman was admitted to the Jackson Memorial Hospital emergency room on January 12, 1973, with a history of recurrent severe episodes of dyspnea, nausea, vomiting, anorexia and urinary incontinence since an earlier admission 8 weeks previously, when Type 1 dissecting aneurysm of the aorta with aortic insufficiency . . .
Dysfibrinogenemia: A case with thrombosis (fibrinogen richfield) and an overview of the clinical and laboratory spectrum
Authors: Anna E. Schorer, Jasbir Singh, Michael L. Basara
Journal: American Journal of Hematology (1995)

Abstract Fibrinogen Richfield exemplifies a dysfibrinogen associated with a life‐long thrombotic tendency. The evaluation of this novel case indicates that, like similar thrombotic dysfibrinogenemias, the abnormal protein polymerizes abnormally and demonstrates impaired clot dissolution. A survey of other cases of dysfibrinogenemia indicates that the relatively common abnormalities of Fibrinopeptide A release are generally asymptomatic or associated with bleeding, polymerization abnormalities are likely to be asymptomatic or associated with thrombosis (or occasionally bleeding), and complex abnormalities or additional, independent hemostatic defects are rather common. Thrombin and Reptilase clotting times are not helpful in distinguishing between the subsets, but clinical history, fibrinopeptide release, and polymerization studies may be useful. Abnormalities of fibrinogen function tend to correlate with changes in molecular domains related to binding and hydrolysis.
Low-Methionine Diet Treatment of Homocystinuria
Authors: R. NEIL SCHIMKE
Journal: Annals of Internal Medicine (1969)

Editorial Notes1 March 1969Low-Methionine Diet Treatment of HomocystinuriaR. NEIL SCHIMKE, M.D.R. NEIL SCHIMKE, M.D.Author, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-70-3-642 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptIt has been a scant 7 years since homocystinuria was first described as an inborn error in the metabolic pathway from methionine to cystine. The genetic lesion has been established as an autosomal recessive defect in the activity of cystathionine synthase, the enzyme catalyzing the condensation of homocysteine and serine to form cystathionine. As a consequence of this metabolic block, methionine and homocystine accumulate in the plasma and urine of affected patients, and endogenous cystine is deficient. The clinical spectrum has been defined by the description of over 100 patients with this disorder and includes ectopia lentis, severe and premature...References1. SCHIMKEMCKUSICKWEILBAECHER RNVARG: Homocystinuria, in Amino Acid Metabolism and Genetic Variation, edited by NYHAN, W. L., McGraw-Hill Book Co., Inc., New York, 1967, pp. 297-314. Google Scholar2. PERRYHANSENLOVECRAWFORDTISCHLER TLSDLLEB: Treatment of homocystinuria with a low-methionine diet, supplemental cystine, and a methyl donor. Lancet 2: 474, 1968. CrossrefMedlineGoogle Scholar3. RATNOFF OD: Activation of Hageman factor by L-homocystine. Science 162: 1007, 1968. CrossrefMedlineGoogle Scholar4. BARBERSPAETH GWGL: Pyridoxine therapy in homocystinuria. Lancet 1: 337, 1967. CrossrefGoogle Scholar5. KELLYCOPELAND SW: A hypothesis on the homocystinuric's response to pyridoxine. Metabolism 17: 794. 1968. CrossrefMedlineGoogle Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: Department of Medicine University of Kansas Medical Center Kansas City, Kan. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited byMethionine restriction beyond life-span extensionMolecular Mechanisms of Cell Cycle Block by Methionine Restriction in Human Prostate Cancer CellsHomocystinuria: Challenges in diagnosis and managementMetabolic Diseases and the SkinHomocystinurieHomocystinuria: Vitamin B6 Dependent or Not?GEORGE W. FRIMPTER, M.D., F.A.C.P. 1 March 1969Volume 70, Issue 3Page: 642-643KeywordsBlood plasmaDietEnzymesGeneticsHomocystinuriaLesionsMetabolic pathwaysMethionineUrine ePublished: 1 December 2008 Issue Published: 1 March 1969 PDF downloadLoading ...
Characterization of in vitro antimurine thymocyte globulin–induced regulatory T cells that inhibit graft-versus-host disease in vivo
Authors: Melanie C. Ruzek, James S. Waire, Deborah Hopkins, Gina LaCorcia, Jennifer Sullivan, Bruce L. Roberts, Susan M. Richards, Sharon R. Nahill, John M. Williams, Abraham Scaria, John Dzuris, Srinivas Shankara, Richard D. Garman
Journal: Blood (2007)
Hydronephrosis Mimicking Metastatic Disease on a Tc-99m Sulfur Colloid Liver/Spleen Scan
Authors: RAYMOND D. DUONG, HIROSHI NISHIYAMA, DAVID T. VOLARICH, MICHAEL L. HANSLITS
Journal: Clinical Nuclear Medicine (1983)

DUONG, RAYMOND D. M.D.*; NISHIYAMA, HIROSHI M.D.†; VOLARICH, DAVID T. D.O.*; HANSLITS, MICHAEL L. M.D.* Author Information
Molecular cloning of three isoforms of the L-type voltage-dependent calcium channel beta subunit from normal human heart.
Authors: T Collin, J J Wang, J Nargeot, A Schwartz
Journal: Circulation Research (1993)

We have cloned and sequenced cDNAs for three isoforms of the L-type voltage-dependent calcium channel beta subunit isolated from a normal human heart cDNA library. One of these subunits, designated beta a, hybridized with a 3.4-kb message, and the other two, designated beta b and beta c, hybridized with a message of approximately 1.9 kb. The presence of both of these latter two messages in human heart was confirmed by polymerase chain reaction methodology. Considering the differences between beta a and beta b/beta c, we find it likely that these messages may be encoded by two different gene sequences, beta a and beta b/beta c, and that the beta b/beta c sequence can be alternatively spliced in the 209-260 region. The data suggest that the human heart presents a different pattern of beta subunit expression from that found in the rat and rabbit heart.
Functional and pathological improvements of the hearts in diabetes model by the combined therapy of bFGF-loaded nanoparticles with ultrasound-targeted microbubble destruction
Authors: Ying-Zheng Zhao, Xin-Qiao Tian, Ming Zhang, Lu Cai, Ao Ru, Xiao-Tong Shen, Xi Jiang, Rong-Rong Jin, Lei Zheng, Kyle Hawkins, Subrata Charkrabarti, Xiao-Kun Li, Qian Lin, Wen-Ze Yu, Shuping Ge, Cui-Tao Lu, Ho Lun Wong
Journal: Journal of Controlled Release (2014)
Trusts paid private firms more than 100m to treat patients waiting more than 18 weeks
Authors: H. Mooney
Journal: BMJ (2011)

<h3>ABSTRACT</h3> Analysis of the human microbiome using metagenomic sequencing data has demonstrated high ability in discriminating various human diseases. Raw metagenomic sequencing data require multiple complex and computationally heavy bioinformatics steps prior to data analysis. Such data contain millions of short sequences read from the fragmented DNA sequences and are stored as fastq files. Conventional processing pipelines consist in multiple steps including quality control, filtering, alignment of sequences against genomic catalogs (genes, species, taxonomic levels, functional pathways, etc.). These pipelines are complex to use, time consuming and rely on a large number of parameters that often provide variability and impact the estimation of the microbiome elements. Training Deep Neural Networks directly from raw sequencing data is a promising approach to bypass some of the challenges associated with mainstream bioinformatics pipelines. Most of these methods use the concept of word and sentence embeddings that create a meaningful and numerical representation of DNA sequences, while extracting features and reducing the dimensionality of the data. In this paper we present an end-to-end approach that classifies patients into disease groups directly from raw metagenomic reads: <i>metagenome2vec</i>. This approach is composed of four steps (i) generating a vocabulary of k-mers and learning their numerical embeddings; (ii) learning DNA sequence (read) embeddings; (iii) identifying the genome from which the sequence is most likely to come and (iv) training a multiple instance learning classifier which predicts the phenotype based on the vector representation of the raw data. An attention mechanism is applied in the network so that the model can be interpreted, assigning a weight to the influence of the prediction for each genome. Using two public real-life data-sets as well a simulated one, we demonstrated that this original approach reaches high performance, comparable with the state-of-the-art methods applied directly on processed data though mainstream bioinformatics workflows. These results are encouraging for this proof of concept work. We believe that with further dedication, the DNN models have the potential to surpass mainstream bioinformatics workflows in disease classification tasks.
C2 Region–Derived Peptides of β-Protein Kinase C Regulate Cardiac Ca <sup>2+</sup> Channels
Authors: Zhi-Hao Zhang, John A. Johnson, Long Chen, Nabil El-Sherif, Daria Mochly-Rosen, Mohamed Boutjdir
Journal: Circulation Research (1997)

Abstract We have previously shown that α 1 -adrenergic activation inhibited β-adrenergic–stimulated L-type Ca 2+ current ( I Ca ). To determine the role of protein kinase C (PKC) in this regulation, the inositol trisphosphate pathway was bypassed by direct activation of PKC with 4β-phorbol 12-myristate 13-acetate (PMA). To minimize Ca 2+ -induced Ca 2+ inactivation, Ba 2+ current ( I Ba ) was recorded through Ca 2+ channels in adult rat ventricular myocytes. We found that PMA (0.1 μmol/L) consistently inhibited basal I Ba by 40.5±7.4% and isoproterenol (ISO, 0.1 μmol/L)–stimulated I Ba by 48.9±7.8%. These inhibitory effects were not observed with the inactive phorbol ester analogue α-phorbol 12,13-didecanoate (0.1 μmol/L). To identify the PKC isozymes that mediate these PMA effects, we intracellularly applied peptide inhibitors of a subclass of PKC isozymes, the C2-containing cPKCs. These peptides (βC2-2 and βC2-4) specifically inhibit the translocation and function of C2-containing isozymes (α-PKC, β I -PKC, and β II -PKC), but not the C2-less isozymes (δ-PKC and ε-PKC). We first used the pseudosubstrate peptide (0.1 μmol/L in the pipette), which inhibits the catalytic activity of all the PKC isozymes, and found that PMA-induced inhibition of ISO-stimulated I Ba was reduced to 16.8±7.4% but was not affected by the scrambled pseudosubstrate peptide. The effects of PMA on basal and ISO-stimulated I Ba were then determined in the presence of C2-derived peptides or control peptides. When the pipette contained 0.1 μmol/L of βC2-2 or βC2-4, PMA-induced inhibition of basal I Ba was 26.1±4.5% and 23.6±2.2%, respectively. Similarly, ISO-stimulated I Ba was inhibited by 29.9±6.6% and 29.3±7.8% in the presence of βC2-2 and βC2-4, respectively. In contrast, there was no significant change in the effect of PMA in the presence of control peptides, scrambled βC2-4, or pentalysine. Finally, PMA-induced inhibition of basal and ISO-stimulated I Ba was almost completely abolished in cells dialyzed with both βC2-2 and βC2-4. Together, these data suggest a role for C2-containing isozymes in mediating PMA-induced inhibition of L-type Ca 2+ channel activity.
Cell Selection as Driving Force in Lung and Colon Carcinogenesis
Authors: Helmut Schöllnberger, Niko Beerenwinkel, Rudolf Hoogenveen, Paolo Vineis
Journal: Cancer Research (2010)

Abstract Carcinogenesis is the result of mutations and subsequent clonal expansions of mutated, selectively advantageous cells. To investigate the relative contributions of mutation versus cell selection in tumorigenesis, we compared two mathematical models of carcinogenesis in two different cancer types: lung and colon. One approach is based on a population genetics model, the Wright-Fisher process, whereas the other approach is the two-stage clonal expansion model. We compared the dynamics of tumorigenesis predicted by the two models in terms of the time period until the first malignant cell appears, which will subsequently form a tumor. The mean waiting time to cancer has been calculated approximately for the evolutionary colon cancer model. Here, we derive new analytic approximations to the median waiting time for the two-stage lung cancer model and for a multistage approximation to the Wright-Fisher process. Both equations show that the waiting time to cancer is dominated by the selective advantage per mutation and the net clonal expansion rate, respectively, whereas the mutation rate has less effect. Our comparisons support the idea that the main driving force in lung and colon carcinogenesis is Darwinian cell selection. Cancer Res; 70(17); 6797–803. ©2010 AACR.