tbuckley/cabot-search huggingface dataset:
Interpretation of screening test results: Scenario does not reflect day to day practice
Authors: Mike Divers
Journal: BMJ (2006)

Editor-Gornall is correct to raise the issue of Roy Meadow's and David Southall's omission from the reference list in the Child Protection Companion. 1 2 Southall, along with others, made contributions to the sections on fabricated and induced illness and imposed airway obstruction in chapter 6 of the Companion.Considerable notice was taken of Southall's views on these topics.The editorial group discussed how to manage the references throughout the book and, for these sections, chose to reference only the two documents on fabricated and induced illness produced by the Royal College of Paediatrics and Child Health (2002) and the Department of Health (2002).We think that these documents covered the topic and referenced all the essential authors on this topic.In retrospect, however, the lack of appropriate reference to both Southall and Meadow is unsatisfactory, and their important work should have been acknowledged more fully.Unfortunately, at the time of the preparation of the content of the Companion, the two professors were involved in the disciplinary process of the General Medical Council, which has still not been concluded in relation to Meadow and which reached an unfavourable outcome with regard to Southall.We debated their difficult situation.We were concerned for them as individuals, particularly as they have both worked tirelessly in promoting the welfare and safety of children.We were also concerned about the outcome of the GMC hearings.We recognised the potential impact that an adverse outcome would have on the retention and recruitment of paediatricians into child protection and also considered any implications for the Companion, which we were in the process of producing.It is possible that had we referenced the two professors more fully, this could have provided lawyers and journalists with ammunition to undermine the value of the Companion.We were always mindful of the objectives that we had set ourselves in producing the Companion.It was never intended to be a fully referenced textbook, and many seminal papers are therefore not referenced.
REPORT OF AN OUTBREAK OF BOTULISM
Authors: CHARLES G. BEALL
Journal: JAMA (1922)

March 11, 1922, at 1 p. m., a meal was served, at the Lakeside Hospital at Kendallville, Ind., of canned salmon and canned spinach. Within from twelve to twenty-four hours nine persons, all of whom had partaken of this meal, and all of whom had certainly partaken of the spinach, developed typical symptoms of botulinus poisoning, consisting of abdominal cramps, vomiting, diplopia, ptosis, dysphagia and aphonia. All persons who ate some of the spinach developed symptoms. No one in the hospital became ill who had not partaken of the spinach, and there were four or five, though they did eat the salmon. Antibotulinus serum was requested by telegraph from Prof. Robert Graham at the University of Illinois thirty hours after the spinach was eaten. At the same time a similar telegraphic request was sent to Dr. G. W. McCoy, director of the Hygienic Laboratory, Washington, D. C. The first doses
SOME CONTRA-INDICATIONS FOR THE USE OF OPIATES.Read before the Philadelphia County Medical Society, January 27, 1892.
Authors: MARIE B. WERNER
Journal: JAMA (1892)

My object in presenting this subject before the Society to-night is manifold; I wish to show that in general practice the indications are limited for the use of opiates. We must fully realize that Ave have a broader basis for medical science than symptomatology, in order to give our patient the full benefit of our knowledge. Our position being at all times one of trust, Ave must endeavor, in helping our patient, to find the cause and remove it, rather than hide the symptoms it gives rise to by an opiate. Aside from the possible mental disturbances such a course of treatment might induce, it often materially complicates surgical efforts to relieve patients, the results of Avhich Ave have repeatedly heard discussed at these meetings. In order to discuss this drug Avith due fairness, it will be necessary to give a few moments to the consideration of its physiological action
6 SUBANALYSES OF THE TELAPREVIR LEAD-IN ARM IN THE REALIZE STUDY: RESPONSE AT WEEK 4 IS NOT A SUBSTITUTE FOR PRIOR NULL RESPONSE CATEGORIZATION
Authors: G.R. Foster, S. Zeuzem, P. Andreone, S. Pol, E.J. Lawitz, M. Diago, S. Roberts, P.J. Pockros, Z. Younossi, I. Lonjon-Domanec, R. Van Heeswijk, S. de Meyer, D. Luo, S. George, M. Beumont, G. Picchio
Journal: Journal of Hepatology (2011)
The role of alcoholism and liver disease in the appearance of serum antibodies against acetaldehyde adducts
Authors: Martin Hoerner, Ursula J. Behrens, Theresa M. Worner, Ileen Blacksberg, Lawrence F. Braly, Fenton Schaffner, Charles S. Lieber
Journal: Hepatology (1988)

We recently presented preliminary data indicating the presence of antibodies against acetaldehyde adducts in sera of over 70% of alcoholic patients. To assess the respective roles of liver disease and alcohol consumption as well as the specificity of this immune response, 141 patients in various stages of alcoholic and nonalcoholic liver diseases were tested by a hemagglutination assay. Sixty-three (73%) of 86 alcoholics had antibody titers above control levels (p &lt; 0.0001). Alcohol consumption of these individuals was significantly higher (p &lt; 0.001) than that of those alcoholics with normal titers. Twentytwo patients (39%) with nonalcoholic liver diseases also had elevated levels of antibodies against acetaldehyde adducts (p &lt; 0.0005); of these, 8 had primary biliary cirrhosis (7 in Stages III and IV), 9 had chronic active hepatitis (6 with cirrhosis) and 5 had acute (virus- or drug-induced) hepatitis. Antibody titers did not correlate with levels of transaminase or alkaline phosphatase activity, nor with bilirubin, and albumin. However, in 52 alcoholics and in nonalcoholic patients with biopsy-confirmed liver disease, the highest titers were seen in the more advanced stages of liver damage. Thus, in addition to alcohol consumption, severity of liver disease may play a role in the appearance of circulating antibodies against acetaldehyde adducts.
Origins of International Health Work
Authors: N. Howard-Jones
Journal: BMJ (1950)

MEDICAL JOURNAL~u include the substantial sums which the Unicef, in co- operation with W.H.O., has spent on child health activities.Requests for the assistance of W.H.O. in 1950 have far exceeded those in 1949.Approximately $2,000,000 is avail- able to meet these requests (roughly one-third of the total budget).Because of financial limitations and the consequent necessity for making the best possible use of the funds allotted to the advisory services, certain guiding principles for the selection of projects have been set up by the Executive Board of W.H.O.The following criteria are used:1. Programmes established by the World Health Assembly or by the United Nations and its specialized agencies.2. Recommendations of expert committees.3. The importance of the problem to the whole health pro- gramme of the requesting country, and inability of the country itself to provide the services required, as measured by the avail- ability of trained personnel, the means of training personnel, or available foreign currency.4. The probability of achieving successful and useful results. 5. Assurance of participation and co-operation on the part of the government throughout the programme, including contri- butions to the programme by meeting such costs within the country as can be met in domestic currency.6. Reasonable assurance from the government, where appropriate, that the programme will be continued, especially that the government has established, or will establish, a health organization with personnel and financial support adequate to continue the programme.7. Equitable distribution among the various countries seek-
1147-217 Do abandoned leads pose risk to implantable defibrillator patient?
Authors: orie L Martin, Michael Glikson, David O Hodge, Amy L Beeman, Win K Shen, Samual J Asirvatham, Robert F Rea, David L Hayes, Stepen C Hammill, Paul A Friedman
Journal: Journal of the American College of Cardiology (2004)
Measuring the symptom burden associated with the treatment of chronic myeloid leukemia
Authors: Loretta A. Williams, Araceli G. Garcia Gonzalez, Patricia Ault, Tito R. Mendoza, Mary L. Sailors, Janet L. Williams, Furong Huang, Aziz Nazha, Hagop M. Kantarjian, Charles S. Cleeland, Jorge E. Cortes
Journal: Blood (2013)
The homeobox gene CDX2 is aberrantly expressed in most cases of acute myeloid leukemia and promotes leukemogenesis
Authors: Claudia Scholl, Dimple Bansal, Konstanze Döhner, Karina Eiwen, Brian J.P. Huntly, Benjamin H. Lee, Frank G. Rücker, Richard F. Schlenk, Lars Bullinger, Hartmut Döhner, D. Gary Gilliland, Stefan Fröhling
Journal: Journal of Clinical Investigation (2007)

The homeobox transcription factor CDX2 plays an important role in embryonic development and regulates the proliferation and differentiation of intestinal epithelial cells in the adult. We have found that CDX2 is expressed in leukemic cells of 90% of patients with acute myeloid leukemia (AML) but not in hematopoietic stem and progenitor cells derived from normal individuals. Stable knockdown of CDX2 expression by RNA interference inhibited the proliferation of various human AML cell lines and strongly reduced their clonogenic potential in vitro. Primary murine hematopoietic progenitor cells transduced with Cdx2 acquired serial replating activity, were able to be continuously propagated in liquid culture, generated fully penetrant and transplantable AML in BM transplant recipients, and displayed dysregulated expression of Hox family members in vitro and in vivo. These results demonstrate that aberrant expression of the developmental regulatory gene CDX2 in the adult hematopoietic compartment is a frequent event in the pathogenesis of AML; suggest a role for CDX2 as part of a common effector pathway that promotes the proliferative capacity and self-renewal potential of myeloid progenitor cells; and support the hypothesis that CDX2 is responsible, in part, for the altered HOX gene expression that is observed in most cases of AML.
(24) Porphyria cutanea tarda
Authors: P.J. August, G.C. Wells
Journal: British Journal of Dermatology (1974)

Journal Article (24) Porphyria cutanea tarda Get access P.J. August, P.J. August St Thomas’Hospital, London Search for other works by this author on: Oxford Academic Google Scholar G.C. Wells G.C. Wells St Thomas’Hospital, London Search for other works by this author on: Oxford Academic Google Scholar British Journal of Dermatology, Volume 91, Issue s10, 1 July 1974, Pages 74–76, https://doi.org/10.1111/j.1365-2133.1974.tb12526.x Published: 01 July 1974
AMA Auxiliary Activities
Authors: Pat Durham
Journal: JAMA (1987)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA HomeNew OnlineCurrent IssueFor Authors Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA journal
Extracellular nucleotides and adenosine regulate microglial motility and their role in cerebral ischemia
Authors: Zehui Li, Wei Li, Qin Li, Minke Tang
Journal: Acta Pharmaceutica Sinica B (2013)

Acting as immune cells, microglia play a surveillance role in central nervous system injuries and diseases. Extracellular nucleotides such as ATP and UTP, and adenosine are reported to regulate the response of microglia to insults and disease. ATP activates P2X receptors and triggers several signal cascades, resulting in the activation of microglia. Subsequently, UDP binding to the P2Y6 receptor induces phagocytosis by microglia, while adenosine regulates process retraction in microglia. Nucleotides and adenosine leak out from dead cells and act on their corresponding receptors on microglia, stimulating the release of inflammatory factors and cytokines to provide both neurotrophic and neurotoxic effects. In this article, we review the regulatory effects of nucleotides and adenosine on microglial chemotaxis, phagocytosis, and process retraction, and summarize the activities of these cells after ischemia.
Terms of service--1805
Authors: G. R. Usmar
Journal: BMJ (1967)

<h3>Abstract</h3> Genomic mutation of the virus may impact the viral adaptation to the local environment, their transmission, disease manifestation, and the effectiveness of existing treatment and vaccination. The objectives of this study were to characterize genomic variations, non-synonymous amino acid substitutions, especially in target proteins, mutation events per samples, mutation rate, and overall scenario of coronaviruses across the country. To investigate the genetic diversity, a total of 184 genomes of virus strains sampled from different divisions of Bangladesh with sampling dates between the 10th of May 2020 and the 27<sup>th</sup> of June 2020 were analyzed. To date, a total of 634 mutations located along the entire genome resulting in non-synonymous 274 amino acid substitutions in 22 different proteins were detected with nucleotide mutation rate estimated to be 23.715 substitutions per year. The highest non-synonymous amino acid substitutions were observed at 48 different positions of the papain-like protease (nsp3). Although no mutations were found in nsp7, nsp9, nsp10, and nsp11, yet orf1ab accounts for 56% of total mutations. Among the structural proteins, the highest non-synonymous amino acid substitution (at 36 positions) observed in spike proteins, in which 9 unique locations were detected relative to the global strains, including 516E&gt;Q in the boundary of the ACE2 binding region. The most dominated variant G614 (95%) based in spike protein is circulating across the country with co-evolving other variants including L323 (94%) in RNA dependent RNA polymerase (RdRp), K203 (82%) and R204 (82%) in nucleocapsid, and F120 (78%) in NSP2. These variants are mostly seen as linked mutations and are part of a haplotype observed in Europe. Data suggest effective containment of clade G strains (4.8%) with sub-clusters GR 82.4%, and GH clade 6.4%. <h3>Highlights</h3> We have sequenced 137 and analyzed 184 whole-genomes sequences of SARS-CoV-2 strains from different divisions of Bangladesh. A total of 634 mutation sites across the SARS-CoV-2 genome and 274 non-synonymous amino acid substitutions were detected. The mutation rate of SARS-CoV-2 estimated to be 23.715 nucleotide substitutions per year. Nine unique variants were detected based on non-anonymous amino acid substitutions in spike protein relative to the global SARS-CoV-2 strains.
Modification of alternative messenger RNA splicing of fibroblast growth factor receptors in human cardiac allografts during rejection.
Authors: X M Zhao, W H Frist, T K Yeoh, G G Miller
Journal: Journal of Clinical Investigation (1994)

Accelerated coronary atherosclerosis in cardiac transplants (cardiac allograft vasculopathy, CAV) is characterized by coronary intimal hyperplasia. Acidic fibroblast growth factor (aFGF) is a potent mitogen for vascular smooth muscle cells and endothelial cells, and its expression is increased in cardiac allografts, suggesting it may play a role in the pathogenesis of CAV. The activity of aFGF is dependent on binding to transmembrane receptors. To investigate whether receptors for aFGF are also induced after transplantation, polymerase chain reaction, in situ hybridization, and immunohistochemistry were used to analyze expression of four receptors for aFGF (FGFR1-FGFR4). Expression of mRNA encoding extracellular immunoglobulin-like domains of FGFR1 was increased 35-fold in cardiac allografts compared with normal hearts and was predominantly present in cardiac myocytes and vascular structures. Alternatively spliced mRNA that encodes transmembrane forms of FGFR1, which contain the signal-transducing tyrosine kinase domains, was induced in allografts during rejection, in infiltrating cells, vascular structures, and myocytes. In vitro experiments showed that differential expression of FGF receptor isoforms was induced by aFGF, and also by IL-6 and TGF-beta, which are expressed in cardiac allografts during rejection. The results show that expression of both aFGF and its receptors is altered in cardiac allografts and suggest that these events are important in the pathogenesis of CAV.
Metabolic Syndrome and the Risk of Cardiovascular Disease in Older Adults
Authors: Javed Butler, Nicolas Rodondi, Yuwei Zhu, Kathleen Figaro, Sergio Fazio, Douglas E. Vaughan, Suzanne Satterfield, Anne B. Newman, Bret Goodpaster, Douglas C. Bauer, Paul Holvoet, Tamara B. Harris, Nathalie de Rekeneire, Susan Rubin, Jingzhong Ding, Stephen B. Kritchevsky
Journal: Journal of the American College of Cardiology (2006)
Interleukin-32 Increases Human Gastric Cancer Cell Invasion Associated with Tumor Progression and Metastasis
Authors: Chung-Ying Tsai, Chia-Siu Wang, Ming-Ming Tsai, Hsiang-Cheng Chi, Wan-Li Cheng, Yi-Hsin Tseng, Cheng-Yi Chen, Crystal D. Lin, Jun-I. Wu, Lu-Hai Wang, Kwang-Huei Lin
Journal: Clinical Cancer Research (2014)

Abstract Purpose: The proinflammatory cytokine interleukin-32 (IL-32) is a novel tumor marker highly expressed in various human carcinomas, including gastric cancer. However, its effects on prognosis of patients with gastric cancer and cancer metastasis are virtually unknown at present. The main aim of this study was to explore the clinical significance of IL-32 in gastric cancer and further elucidate the molecular mechanisms underlying IL-32–mediated migration and invasion. Experimental Design: Gastric cancer cells with ectopic expression or silencing of IL-32 were examined to identify downstream molecules and establish their effects on cell motility, invasion, and lung metastasis in vivo. Results: IL-32 was significantly upregulated in gastric cancer and positively correlated with aggressiveness of cancer and poor prognosis. Ectopic expression of IL-32 induced elongated morphology and increased cell migration and invasion via induction of IL-8, VEGF, matrix metalloproteinase 2 (MMP2), and MMP9 expression via phosphor-AKT/phospho-glycogen synthase kinase 3β/active β-catenin as well as hypoxia-inducible factor 1α (HIF-1α) signaling pathways. Conversely, depletion of IL-32 in gastric cancer cells reversed these effects and decreased lung colonization in vivo. Examination of gene expression datasets in oncomine and staining of gastric cancer specimens demonstrated the clinical significance of IL-32 and its downstream molecules by providing information on their coexpression patterns. Conclusions: IL-32 contributes to gastric cancer progression by increasing the metastatic potential resulting from AKT, β-catenin, and HIF-1α activation. Our results clearly suggest that IL-32 is an important mediator for gastric cancer metastasis and independent prognostic predictor of gastric cancer. Clin Cancer Res; 20(9); 2276–88. ©2014 AACR.
Failure of Capsule Transportation Due to Gastroparesis after Gastric Truncal Vagotomy
Authors: S. Gölder, H. Herfarth, F. Kullmann
Journal: Endoscopy (2005)

We read with interest the paper by Hollerbach et al. on ”Endoscopically assisted capsule endoscopy of the small bowel in patients with functional gastric outlet obstruction” [1].
Abstract LB-496: Low-dose aspirin targets tumor-associated inflammation and delays neuroblastoma tumor growth <i>in vivo</i>
Authors: Lena-Maria Carlson, Agnes Rasmuson, Lova Segerstrom, Baldur Sveinbjornsson, Per Kogner
Journal: Cancer Research (2012)

Abstract ABSTRACT Tumor-associated inflammation is a driving force in several adult cancers, and low doses of non-steroidal anti-inflammatory drugs (NSAIDs) such as aspirin have proven to reduce cancer incidence. Little is known about tumor-associated inflammation in pediatric neoplasms and no in vivo data exists on the effectiveness of low-dose aspirin on established tumors. Our study evaluates inflammatory patterns paralleling neuroblastoma (NB) tumor growth in vivo and low-dose aspirin as a therapeutic option for high-risk NB. Using the TH-MYCN mouse model of NB, this study demonstrates the presence and progression of tumor-associated inflammation during NB tumor growth. Ex vivo analysis of tumors revealed a transition from an adaptive immune response predominated by CD8+ T-cells in neoplastic lesions from 5 week old homozygous mice, towards an enrichment in immature cells of the innate immune system, including myeloid-derived suppressor cells (MDSCs), immature dendritic cells (DCs) and M2 tumor-associated macrophages (TAMs) during tumor progression. An ongoing M1 to M2 transition of TAMs was demonstrated, which was paralleled by a gradual deterioration of DC status. Ten days of consecutive anti-inflammatory treatment with low-dose aspirin significantly reduced tumor burden (p&amp;lt;0.01) and the presence of tumor-associated cells of the innate immune system (p&amp;lt;0.01) in homozygous mice. In conclusion, our study depicts how inflammatory pathways assist tumor progression through sculpturing of the tumor microenvironment, and for the first time demonstrates an in vivo effect of low-dose aspirin on established MYCN amplified NB tumors in a transgenic mouse model, suggesting a potential new treatment option for high-risk NB patients. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr LB-496. doi:1538-7445.AM2012-LB-496