tbuckley/cabot-search huggingface dataset:
On Wound-Treatment
Authors: S. Gamgee
Journal: BMJ (1881)

Uan. IS, 188I.scope, is the fact that neitherto thenaked eye nor u microscopic exami- nationi did Dr. Smith find any changes worthy ofrnotice in the anterior roots; and this appears to me to l)e an argument of some weight against the supposition that thc disease in this man began at the peripheryr.*An additional evidelnce in favour of its being primarily a central affection was the early development of symptoms pointing to an implication of the nuclei of the hypoglossal, the vagus, and the spinal accessory nerves; and after a wvhile the fifth, and to some extent the seventh.As related in my report, when he first came to see me, I noticedl that his voice was husky, an(d the movement of the tip of his tongue upwards was not as free as it ought to have been.Among the clinical features presented by this case may be noted, firstly, the duration of the disease, its comparative rapidity, which can easily be accounted for by the extension of this polio-myelitis of the cervico-brachial bulb upwards to the medulla, and the involvement therefore of the resp-iratory centres ; secondly, the extreme degree of myosis, wlhich Eulenberg states (Ziermssen's Cyclopadia, vol.xiv, page 127) to be a very rare complication of progressive muscular atrophy; nas Duchenne, among several hundred cases, never once met with this l)henonmenon.\With regard to the perspiration from which Ii. E. suffered throughout his disease, its appearance in the iniLial stage, before there wvas any high degree of muscular atrophy, tells forcibly against Friedreich's explanation that it was the result of a collaterml fluxion to the cutaneouis vessels, caused by oblitera- tion of a large number of the finer muscular vessels in the rapid atrophy of the muiscles.The probability is, that it was due to the amount of disease in the cilio-spinal region.Whether there was any risc of temperature during these sweats I am unable to say.An interesting fact in connection with this case, was the absence of dribbling of saliva for the last twenty-four hours of his life.Whether or no there is an actual increase of the amount of saliva secreted in these cases or bulbar disease, authorities differ.Both Erb and Kussimaul consider that there is an increased secretion; and Schultz estimated in one case a six or eight-fold secretion.Granting, how- ever, the truLh of Cruetzner's experiments, which go to prove the existence of a cenfre of salivation in the medulla, irritation of which causes active salivation, it is difficult to understand, as Erb remarks, how, in a case of bulbar disease, there can be irritation of this centre, when all tbe other bulbar functions are paralysed.
Histocompatibility antigens controlled by the I region of the murine H-2 complex. II. K/D region compatibility is not required for I-region cell-mediated lymphocytotoxicity.
Authors: J Klein, C L Chiang, V Hauptfeld
Journal: The Journal of Experimental Medicine (1977)

In the cell-mediated lymphocytotoxicity assay, A.TH effector cells sensitized to A.TL lymphocytes lyse not only A.B10.AQR effector cells lyse B10.BR and B10.BYR target cells in addition to B10.AQR cells. These findings indicate that for CML to occur across the IA region barrier, compatibility at K or D regions is not required.
Combination chemotherapy for acute lymphoblastic leukaemia in adults.
Authors: T A Lister, J M Whitehouse, M E Beard, R L Brearley, P F Wrigley, R T Oliver, J E Freeman, R K Woodruff, J S Malpas, A M Paxton, D Crowther
Journal: BMJ (1978)

Fifty-one adults with acute lymphoblastic leukaemia were entered into a trial of intense initial chemotherapy and early "prophylaxis" of the central nervous system (CNS). Initial treatment with OPAL (Oncovin (vincristine), prednisolone, adriamycin (doxorubicin), and L-asparaginase (colaspase)) followed by craniospinal or cranial irradiation and intrathecal methotrexate produced remission in 36 patients (71%). Seventeen of these patients relapsed three to 18 months after the start of remission; the remainder had been in remission for 12 to 52 months by the end of the study. The predicted median duration of complete remission was 18.5 months. None of the four patients who initially had clinical evidence of CNS disease, three of whom also had leukaemic cells identical to those found in Burkitt's lymphoma, achieved remission. Those patients who initially had hepatomegaly or splenomegaly had a shorter remission than those without. The predicted median survival was 27 months in those who achieved complete remission, one month in those who did not, and 21 months overall. The addition of colaspase and doxorubicin to vincristine and prednisolone and the use of early CNS treatment clearly improved the remission rate among adults with acute lymphoblastic leukaemia, though the presence and length of remission was affected by the extent of disease at presentation. Burkitt-like leukaemia, which had a poor prognosis, is probably a separate disease and may benefit from a different therapeutic approach.
The clinical value of autofluorescence bronchoscopy for the diagnosis of lung cancer
Authors: B Lam, M P Wong, S L Fung, D C L Lam, P C Wong, T Y W Mok, F M Lam, M S M Ip, C G C Ooi, W K Lam
Journal: European Respiratory Journal (2006)

The aim of this study was to evaluate the role of autofluorescence bronchoscopy (AFB) in the routine work-up of lung cancer. Consecutive patients with atypical or suspicious cells in sputum or bronchial aspirate, no localising abnormality on chest radiography and nondiagnostic white-light bronchoscopic (WLB) results were recruited. WLB and AFB were performed sequentially during the same session. All abnormal areas detected by WLB, AFB or both were sampled and the biopsy specimens sent for histological examination. Sixty-two patients were recruited within the 32-month study period. Seventeen had no endobronchial lesion detected. Among the 45 patients with endobronchial lesions, 37 had lesions with a histopathological grade of mild dysplasia or less; of the eight patients who had a lesion with a histological grade of moderate dysplasia or worse, five were found to have lung cancer, two invasive lung cancer and three an intra-epithelial neoplasm (severe dysplasia). Lesions showing moderate dysplasia or worse were more commonly found in patients with suspicious cells than in those with atypical cells on sputum examination. AFB was more sensitive than WLB (91 <i>versus</i> 58%) at detecting these lesions, but less specific (26 <i>versus</i> 50%). A combination of white-light and autofluorescence bronchoscopy can increase the diagnostic yield of this invasive procedure in patients exhibiting abnormal sputum cytology.
Intrinsically defective skin barrier function in children with atopic dermatitis correlates with disease severity
Authors: Jayanta Gupta, Emilie Grube, Mark B. Ericksen, Michelle D. Stevenson, Anne W. Lucky, Anita P. Sheth, Amal H. Assa'ad, Gurjit K. Khurana Hershey
Journal: Journal of Allergy and Clinical Immunology (2008)
Oscillation between B-lymphoid and myeloid lineages in Myc-induced hematopoietic tumors following spontaneous silencing/reactivation of the EBF/Pax5 pathway
Authors: Duonan Yu, David Allman, Michael H. Goldschmidt, Michael L. Atchison, John G. Monroe, Andrei Thomas-Tikhonenko
Journal: Blood (2003)
European experts differ on neonatal intensive care
Authors: A. Tuffs
Journal: BMJ (2003)

Experts from Germany and Switzerland clashed last week on whether or not babies born before the 25th week of pregnancy should be automatically considered for intensive care. The doctors were discussing the matter at an international symposium on neonatology in Heidelberg, Germany.

The guidelines of the German Society for Neonatal and Paediatric Intensive Care state that every preterm infant, regardless of immaturity, must be considered for treatment. The decision should be taken according to each baby's prognosis. Doctors should not refuse treatment …
L’amorce du processus thérapeutique en psychiatrie infantile
Authors: G. Basecqz
Journal: Psychotherapy and Psychosomatics (1978)

Research Articles| February 16 2010 L’amorce du processus thérapeutique en psychiatrie infantile Subject Area: Psychiatry and Psychology G. Basecqz G. Basecqz Unite de Psychiatrie de la famille et de l’enfant, Université d’Ottawa, Ottawa, Ont. Search for other works by this author on: This Site PubMed Google Scholar Psychother Psychosom (1978) 29 (1-4): 228–230. https://doi.org/10.1159/000287132 Article history Published Online: February 16 2010 Content Tools Views Icon Views Article contents Figures & tables Video Audio Supplementary Data Peer Review Share Icon Share Facebook Twitter LinkedIn Email Tools Icon Tools Get Permissions Cite Icon Cite Search Site Citation G. Basecqz; L’amorce du processus thérapeutique en psychiatrie infantile. Psychother Psychosom 31 December 1978; 29 (1-4): 228–230. https://doi.org/10.1159/000287132 Download citation file: Ris (Zotero) Reference Manager EasyBib Bookends Mendeley Papers EndNote RefWorks BibTex toolbar search Search Dropdown Menu toolbar search search input Search input auto suggest filter your search All ContentAll JournalsPsychotherapy and Psychosomatics Search Advanced Search Article PDF first page preview Close Modal This content is only available via PDF. 1978Copyright / Drug Dosage / DisclaimerCopyright: All rights reserved. No part of this publication may be translated into other languages, reproduced or utilized in any form or by any means, electronic or mechanical, including photocopying, recording, microcopying, or by any information storage and retrieval system, without permission in writing from the publisher.Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug.Disclaimer: The statements, opinions and data contained in this publication are solely those of the individual authors and contributors and not of the publishers and the editor(s). The appearance of advertisements or/and product references in the publication is not a warranty, endorsement, or approval of the products or services advertised or of their effectiveness, quality or safety. The publisher and the editor(s) disclaim responsibility for any injury to persons or property resulting from any ideas, methods, instructions or products referred to in the content or advertisements. You do not currently have access to this content.
Intestinal Bacteria Modify Lymphoma Incidence and Latency by Affecting Systemic Inflammatory State, Oxidative Stress, and Leukocyte Genotoxicity
Authors: Mitsuko L. Yamamoto, Irene Maier, Angeline Tilly Dang, David Berry, Jared Liu, Paul M. Ruegger, Jiue-in Yang, Phillip A. Soto, Laura L. Presley, Ramune Reliene, Aya M. Westbrook, Bo Wei, Alexander Loy, Christopher Chang, Jonathan Braun, James Borneman, Robert H. Schiestl
Journal: Cancer Research (2013)

Abstract Ataxia-telangiectasia is a genetic disorder associated with high incidence of B-cell lymphoma. Using an ataxia-telangiectasia mouse model, we compared lymphoma incidence in several isogenic mouse colonies harboring different bacterial communities, finding that intestinal microbiota are a major contributor to disease penetrance and latency, lifespan, molecular oxidative stress, and systemic leukocyte genotoxicity. High-throughput sequence analysis of rRNA genes identified mucosa-associated bacterial phylotypes that were colony-specific. Lactobacillus johnsonii, which was deficient in the more cancer-prone mouse colony, was causally tested for its capacity to confer reduced genotoxicity when restored by short-term oral transfer. This intervention decreased systemic genotoxicity, a response associated with reduced basal leukocytes and the cytokine-mediated inflammatory state, and mechanistically linked to the host cell biology of systemic genotoxicity. Our results suggest that intestinal microbiota are a potentially modifiable trait for translational intervention in individuals at risk for B-cell lymphoma, or for other diseases that are driven by genotoxicity or the molecular response to oxidative stress. Cancer Res; 73(14); 4222–32. ©2013 AACR.
Letter: Renal lesions in a case of septicaemia.
Authors: M F Dixon
Journal: BMJ (1976)

the UK ?In many countries the cost of alcohol-induced problems exceeds the revenue raised from alcohol taxation.7Let not anyone, even members of Parlia- ment, be surprised that if you give more of a drug you get a greater response.Whatever special aetiological factor-for example, genetic -there may be in alcoholism, this overall doseresponse relationship with alcohol and its effects on society are established with a high degree of probability.I do not think that the experiment that the legislators seemed poised to carry out would pass any hospital ethical committee; it's been done before and the risk of a high incidence of adverse effects is too great.
Cytokine stimulated vascular cell adhesion molecule-1 (VCAM-1) ectodomain release is regulated by TIMP-3
Authors: R SINGH, J MASON, E LIDINGTON, D EDWARDS, R NUTTALL, R KHOKHA, V KNAUPER, G MURPHY, J GAVRILOVIC
Journal: Cardiovascular Research (2005)

Vascular cell adhesion molecule-1 (VCAM-1) is a cell surface adhesion molecule involved in the recruitment of leukocytes to endothelial cells on arterial walls during the pathogenesis of atherosclerosis. The soluble ectodomain of VCAM-1 (sVCAM-1) is proteolytically released from the cell surface into the circulation, a process which is up-regulated in patients with cardiovascular or inflammatory disease. Here we investigate mechanisms involved in sVCAM-1 generation in response to cytokine stimulation.VCAM-1 ectodomain release into the conditioned media of MCEC-1 murine endothelial cells and cells grown from primary aortic explants from timp3-/- mice and wild-type littermates was measured by sandwich ELISA and Western blot after stimulation with tumor necrosis factor alpha (TNFalpha), interleukin-1beta (IL-1beta), or the phorbol ester PMA. Protease expression was inhibited (knocked down) with siRNA and validated using real-time PCR.Proinflammatory cytokines IL-1beta and TNFalpha up-regulated VCAM-1 ectodomain release from the MCEC-1 cells, and this was dependant on p38 and mitogen-activated protein kinases (MAP kinases) and inhibited by the matrix metalloproteinase (MMP) inhibitor BB94 and tissue inhibitor of metalloproteinase (TIMP)-3, but not TIMP-1 or TIMP-2. Timp-3-/- cells exhibited greater VCAM-1 ectodomain release following cytokine stimulation than TIMP-3-expressing cells. Additionally, cytokine stimulation of MCEC-1 cells was shown to cause down-regulation of TIMP-3 expression. Knockdown of the metalloproteinase ADAM17, but not ADAM10 or ADAM12, gene expression reduced cytokine-stimulated VCAM-1 shedding.TIMP-3 regulates the release of sVCAM-1 from cytokine-stimulated endothelial cells, which is mediated by ADAM17.
Gene recombination in postmitotic cells. Targeted expression of Cre recombinase provokes cardiac-restricted, site-specific rearrangement in adult ventricular muscle in vivo.
Authors: R Agah, P A Frenkel, B A French, L H Michael, P A Overbeek, M D Schneider
Journal: Journal of Clinical Investigation (1997)

Mouse models of human disease can be generated by homologous recombination for germline loss-of-function mutations. However, embryonic-lethal phenotypes and systemic, indirect dysfunction can confound the use of knock-outs to elucidate adult pathophysiology. Site-specific recombination using Cre recombinase can circumvent these pitfalls, in principle, enabling temporal and spatial control of gene recombination. However, direct evidence is lacking for the feasibility of Cre-mediated recombination in postmitotic cells. Here, we exploited transgenic mouse technology plus adenoviral gene transfer to achieve Cre-mediated recombination in cardiac muscle. In vitro, Cre driven by cardiac-specific alpha-myosin heavy chain (alphaMyHC) sequences elicited recombination selectively at loxP sites in purified cardiac myocytes, but not cardiac fibroblasts. In vivo, this alphaMyHC-Cre transgene elicited recombination in cardiac muscle, but not other organs, as ascertained by PCR analysis and localization of a recombination-dependent reporter protein. Adenoviral delivery of Cre in vivo provoked recombination in postmitotic, adult ventricular myocytes. Recombination between loxP sites was not detected in the absence of Cre. These studies demonstrate the feasibility of using Cre-mediated recombination to regulate gene expression in myocardium, with efficient induction of recombination even in terminally differentiated, postmitotic muscle cells. Moreover, delivery of Cre by viral infection provides a simple strategy to control the timing of recombination in myocardium.
Modification of Hemoglobin H Disease by Sickle Trait
Authors: Katherine K. Matthay, William C. Mentzer, Andree M. Dozy, Yuet Wai Kan, Dorothy F. Bainton
Journal: Journal of Clinical Investigation (1979)

The rarity of hemoglobin (Hb) H disease in combination with sickle trait may be due in part to the absence of actual Hb H in individuals who, nonetheless, have inherited the deletion of three α-globin genes. We describe here a boy with persistent microcytic, hypochromic anemia despite adequate iron stores, who exhibited splenomegaly with a normal reticulocyte count and only rare inclusions in circulating erythrocytes. Starch gel electrophoresis and isoelectric focusing at age 5 yr showed 21% Hb S, persistent Hb Bart's, but no Hb H. Recticulocyte α/non-α globin chain synthesis ratio was 0.58 at age 5. The mother (Asian) had laboratory evidence of α-thalassemia trait and the father (Black) had sickle trait. The nature of α-thalassemia in this patient was investigated both by liquid hybridization and by the Southern method of gene mapping, in which DNA is digested with restriction endonucleases and the DNA fragments that contained the α-globin structural gene identified by hybridization with complementary DNA. The patient had only one α-globin structural gene, located in a DNA fragment shorter than that found in normal or α-thalassemia trait individuals, but similar to that present in other patients with Hb H disease. Morphologic studies of bone marrow by light and electron microscopy revealed erythroid hyperplasia with inclusions in polychromatic and orthochromatic erythroblasts, suggesting early precipitation of an unstable hemoglobin. The lack of demonstrable Hb H may be the result of both diminished amounts of βA available for Hb H formation (since one β-globin gene is βS) and the greater affinity of α-chains for βA than βS-globin chains leading to the formation of relatively more Hb A than Hb S. The presence of a βS gene may thus modify the usual clinical expression of Hb H disease.
Red Snapper or Crab?
Authors: Paul B. Cornia, Benjamin A. Lipsky, Gurpreet Dhaliwal, Sanjay Saint
Journal: New England Journal of Medicine (2004)

A 68-year-old man originally from the Philippines presented with a three-month history of increasing dyspnea on exertion and orthopnea. He also reported an unintentional weight loss of 7 kg (15 lb), night sweats, and abdominal bloating.
Large Trials vs Meta-analysis of Smaller Trials
Authors: Mark A. Klebanoff
Journal: JAMA (1997)

<h3>To the Editor.</h3> —Dr Cappelleri and colleagues<sup>1</sup>concluded that unexplained clinically important differences between the results of large trials and meta-analyses of small trials are extremely uncommon. We have several concerns with this conclusion. First, the authors based it on the results of a random effects model. While both fixed and random effects models can be useful, the interpretation of results when these models disagree is the subject of much debate.<sup>2</sup>However, the authors note that a fixed effects model reported more disagreement between small and large studies than a random effects model. This is to be expected by the very nature of the way these 2 models address heterogeneity between studies.<sup>2</sup>Since the a priori belief of the authors was that large trials usually support the results of meta-analyses of small trials, it appears self-serving to emphasize the results of random effects models. Second, the authors
Cross-linking of fibronectin to collagen by blood coagulation Factor XIIIa.
Authors: D F Mosher, P E Schad
Journal: Journal of Clinical Investigation (1979)

Soluble fibronectin is found in body fluids and media of adherent cultured cells and binds to fibrin and collagen. Insoluble fibronectin is found in tissue stroma and in extracellular matrices of cultured cells. Fibronectin is a substrate for Factor XIIIa (plasma transglutaminase) and can be cross-linked by Factor XIIIa to itself and the the alpha-chain of fibrin. We used sodium dodecyl sulfate-polyacrylamide gel electrophoresis to investigate Factor XIIIa-mediated crosslinking of fibronectin to collagen. At O degrees or 37 degrees C, fibronectin could be cross-linked to iodinated cyanogen bromide fragment 7 of the alpha 1(I) chain. At 22 degrees or 37 degrees C, fibronectin could be cross-linked to isolated alpha 1(I) chains of type I collagen. Fibronectin could also be crosslinked to types I and III collagen, but only at 37 degrees C. alpha 1(I)-CB7, alpha 1(I) collagen chains, type I collagen, type III collagen, and fibrin all blocked cross-linking between 125I-alpha 1 (I)-CB7 and fibronectin. alpha 1(I)-CB7 blocked cross-linking between fibronectin and fibrin. These results indicate that the determinants of fibronectin-fibrin and fibronectin-collagen binding and cross-linking are similar. Cross-linking of fibronectin to collagen likely occurs in vivo and may be important for normal wound healing, collagen fibrillogenesis, and embryogenesis.
EPIDERMAL CHANGES IN ERYTIIROFOIETIC PROTOPORPHYRIA AFTER IRRADIATION WITH GLASS-FILTERED MERCURY LIGHT
Authors: E. H. BAART FAILLE-KUYPER, P. B. ROTTIER, H. BAART FAILLE
Journal: British Journal of Dermatology (1968)

SUMMARY.— Histochemical studies of 3 patients with erythropoietic protoporphyria revealed the presence of lipid droplets in and around small subepidermal blood vessels and also in the epidermis. Lipid droplets were found only after irradiation with visible light.