tbuckley/cabot-search huggingface dataset:
Brain Damage in Modern Boxers
Authors: Ira R. Casson
Journal: JAMA (1984)

Eighteen former and active boxers underwent neurological examination, EEG, computed tomographic scan of the brain, and neuropsychological testing. Eighty-seven percent of the professional boxers had definite evidence of brain damage. All the boxers had abnormal results on at least one of the neuropsychological tests. Brain damage is a frequent result of a career in professional boxing.
Specialist registration: a critical look at the proposals of the Merrison report.
Authors: M D Vickers
Journal: BMJ (1976)

In the general euphoria over the many views in the Merrison Report that the profession welcomed too little attention has been paid to what has been said about specialist registration. The report contains several basic confusions and a serious misunderstanding of the nature of specialist medical training and practice. It makes several cardinal errors in thinking that some notorious problems related to NHS staffing are also related to a lack of an effective specialist register, and it shows how the creation of such a register would largely destroy the authority of the colleges and faculties. Nowhere in the report is there any convincing argument to show that specialist registration would confer advantages sufficient to outweigh the disadvantages. To let specialist registration in the UK slip in on the irrelevant coat tails of EEC requirements would be a grave dereliction of the long-term interests of medical practice and patient care. The General Medical Council is holding a conference in which this topic is to be discussed on 24 February 1976 and it is still not too late for the profession to think again on this topic.
S129 Inflammatory Cytokines Influence Respiratory Epithelial Anti-viral Immune Responses Via Inducible Epigenetic Control Of Rig1 Expression: A Model Of Early Life Origins Of Asthma?
Authors: C. Spalluto, A. Singhania, C. Woelk, T. Sanchez-Elsner, K. Staples, T. Wilkinson
Journal: Thorax (2014)

<h3></h3> The development of asthma is linked to early life environmental exposures and the occurrence of severe viral infections. Rapid maturation of adaptive immunity from a tolerant (Th2) to an anti-infective (Th1) state occurs in the neonatal period. We hypothesised that the airway inflammatory milieu, driven by the maturing immune response to environmental exposures may have important effects on the development of anti-viral innate immunity at the level of the epithelium. We studied whether the inflammatory environment of the airway epithelium modulates gene expression via epigenetic regulation of anti-viral genes as a model of the development of a long term abnormality which is a hallmark of asthma. We optimised an <i>in-vitro</i> model using AALEB, human immortalised bronchial epithelial-derived cells which were pre-treated for 24 h with cytokines that mimic Th1 environment (IFNy, 10 ng/ml) and Th2 (IL-13, 10 ng/ml) before being infected with RSV A, MOI=2 for 48 h. Quantitative real-time PCR with Taqman primers was used to assess expression of innate genes. Cells were collected after 48 h and stored in Trizol. Chromatin Immuno Precipitation (ChIP) with antibodies against histone modifications was used to assess epigenetic controls. In order to confirm epigenetic regulation of innate genes we used a panel of HAT, HDAC and histone demethylase inhibitors. We initially studied the impact of cytokines on a range of innate anti-viral genes. RIG1 was differentially expressed and reductions in expression associated with higher viral titres. IFNy priming induced increases in RIG1 mRNA at 48 h that correlated at the promoter with enrichment of H3K9ac and RNApolII (active-promoters) and reduction of H3K9me3 (repressive-promoters). We observed a statistically significant increase of RIG1 expression by IFNγ when co-incubated with SAHA (HDAC I and II inhibitors) and JIB-04 (Pan-Jumanji histone demethylase inhibitor). No effects of Th2 priming were seen at the level of antiviral responses. This <i>in-vitro</i> study suggests the inflammatory environment of naive epithelial cells can induce epigenetic modulation of innate immune responses at the level of histone methylation and acetylation and hence potentially lead to long term impacts on anti-viral immunity. The presence of a Th1 milieu appears key to the development of effective anti-viral responses.
Carbamazepine for Hiccoughs
Authors: David A. McFarling
Journal: JAMA (1974)

<h3>To the Editor.—</h3> We have recently had under our care a patient with acute multiple sclerosis manifest by spastic paraparesis and cerebellar dysfunction. Early in hospitalization, intractable hiccoughs developed that did not respond to chlorpromazine treatment, 50 mg every six hours. Then a trial course of carbamazepine, 200 mg orally four times daily, was started. Within 24 hours, hiccoughs had disappeared. About two weeks later, severe complications followed a concurrent course of adrenocorticotropic hormone therapy, and the patient had to be transferred to the intensive care unit for 48 hours. During this time, carbamazepine was inadvertently omitted from the regimen and within 72 hours, the hiccoughs returned. Carbamazepine at the previous dosage again eliminated the hiccoughs within 24 hours. Intractable hiccoughs is a complex syndrome that probably has multiple causes, including primary disease of the central nervous system.<sup>1</sup>Many drugs have been used in the management thereof, including chlorpromazine,
Treatment of Acute and Chronic Gastritis
Authors: S. W. Patterson
Journal: BMJ (1936)

Acute GastritisAcute gastritis may be, first, to.xic, from taking poisons, such as caustic alkalis, corrosive acids, lysol, phosphorus, mercury, or arsenic.The treatment of these forms of gastritis will not be dealt with here.Secondly, gastritis may be irritative, following dietetic indiscretions, over- eating, ingestion of bad or insufficiently masticated food, or excess of alcohol.Or, finally, it may be secondary to various febrile and infectious diseases.In this last group it is necessary to treat the cause, and also to give atten- tion to dieting and medical measures for the relief of digestive symptoms. IRRITATIVE GASTRITIS
Review: Biologic agents increase short-term risk for some adverse events in conditions other than HIV or AIDS
Authors: Ami Schattner
Journal: Annals of Internal Medicine (2012)

ACP Journal Club15 May 2012Review: Biologic agents increase short-term risk for some adverse events in conditions other than HIV or AIDSAmi Schattner, MDAmi Schattner, MDHebrew University Hadassah, Jerusalem, Israel (A.S.)Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-156-10-201205150-02009 SectionsAboutFull TextPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail Source CitationSingh JA, Wells GA, Christensen R, et al. Adverse effects of biologics: a network meta-analysis and Cochrane overview. Cochrane Database Syst Rev. 2011;(2):CD008794. https://pubmed.ncbi.nlm.nih.gov/21328309Clinical Impact RatingsGIM/FP/GP: Rheumatology: Reference1 Furst DE, Keystone EC, Braun J, et al. Updated consensus statement on biological agents for the treatment of rheumatic diseases, 2011. Ann Rheum Dis. 2012;71:i2-45. [PMID: 22460137] Google Scholar Author, Article, and Disclosure InformationAffiliations: Hebrew University Hadassah, Jerusalem, Israel (A.S.)This article was published at Annals.org on 1 May 2012. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics 15 May 2012Volume 156, Issue 10Page: JC5-9KeywordsAIDSDatabasesHIVMedical conditionsNetwork analysisOpportunistic infectionsSafetySystematic reviews ePublished: 15 May 2012 Issue Published: 15 May 2012 CopyrightCopyright © 2012 by American College of Physicians. All Rights Reserved.PDF DownloadLoading ...
The 1987 US Hospital AIDS Survey
Authors: Dennis P. Andrulis
Journal: JAMA (1989)

In 1987, the National Public Health and Hospital Institute conducted a national survey of 623 acute-care hospitals to obtain information relating to inpatient and outpatient care for persons with acquired immunodeficiency syndrome (AIDS). Two hundred seventy-six hospitals reported treating persons with AIDS; the average length of stay was 16.8 days. Average costs and revenues per inpatient day were $681 and $545, respectively, with a cost per patient per year of $17 910. Estimated cost for AIDS inpatient care during 1987 was $486 million; Medicaid represented the primary payer. Regional and ownership comparisons for this year and between 1985 and 1987 indicated significant differences in utilization, payer source, and financing. Results suggest major differences in reimbursement and losses related to payer source or lack of insurance, with many hospitals that serve large numbers of low-income persons with AIDS encountering moderate to severe financial shortfalls. We conclude that increasing concentrations of persons with AIDS in relatively few hospitals in large cities may make it more difficult to secure the broader political base necessary to obtain adequate support for treatment. (<i>JAMA</i>. 1989;262:784-794)
Abstract 478: Predicting interactome networks perturbations in human cancer: application to gene fusions in acute lymphoblastic leukemia
Authors: Leon Hajingabo, Sarah Daakour, Maud Martin, Reinhard Grausenburger, Renate Panzer-Grümayer, Franck Dequiedt, Jacques Van Helden, Jean-Claude Twizere, Nicolas Simonis
Journal: Cancer Research (2014)

Abstract Genomic variations such point mutations and gene fusions are directly or indirectly associated with human diseases. They are recognized as diagnostic, prognostic markers and as therapeutic targets. However, predicting the functional impact of these genetic alterations beyond affected genes and their products is challenging because diseased phenotypes likely result in complex molecular interaction networks. Using as models three different chromosomal translocations ETV6-RUNX1 (TEL-AML1), BCR-ABL1, and E2A-PBX1 (TCF3-PBX1) frequently found in B-cell acute lymphoblastic leukemia (B-ALL), we develop an approach to extract from gene expression changes, perturbed molecular interactions. We show that the Myc and JunD transcriptional circuits are specifically deregulated following TEL-AML1 and TCF3-PBX1 gene fusions, respectively. We also identified the bulk mRNA NXF1-dependent machinery as a direct target for the TCF3-PBX1 fusion protein. Through a novel approach combining gene expression and interactome data analysis, we provide new insight into TCF3-PBX1 and TEL-AML1 acute lymphoblastic leukemia. Note: This abstract was not presented at the meeting. Citation Format: Leon Hajingabo, Sarah Daakour, Maud Martin, Reinhard Grausenburger, Renate Panzer-Grümayer, Franck Dequiedt, Jacques Van Helden, Jean-Claude Twizere, Nicolas Simonis. Predicting interactome networks perturbations in human cancer: application to gene fusions in acute lymphoblastic leukemia. [abstract]. In: Proceedings of the 105th Annual Meeting of the American Association for Cancer Research; 2014 Apr 5-9; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2014;74(19 Suppl):Abstract nr 478. doi:10.1158/1538-7445.AM2014-478
A Practical Guide to Communication Skills in Clinical Practice
Authors: Steve Allen
Journal: JAMA (1999)

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
Dangers of restocking T cells
Authors: Hema Bashyam
Journal: The Journal of Experimental Medicine (2008)

Refilling an empty niche with proliferating CD8+ T cells can cause autoimmune disease, say Tajima et al. (page 1019).






Figure 1

Autoimmune colitis (top) caused by homeostatically proliferating CD8+ T cells is resolved in mice injected with anti–IL-6 antibody (bottom).




Infusion of naive T cells into an environment where there are few native T cells—such as in patients undergoing cancer therapy—spurs two kinds of proliferation. T cells activated by non-self-peptide/MHC complexes proliferate rapidly, whereas those activated by self-peptide/MHC in the presence of cytokines such as IL-7 and IL-15 proliferate slowly. CD4+ T cells that proliferate by these methods have previously been shown to drive the inflammation seen in several autoimmune diseases.

Tajima et al. now find a new variation in homeostatic proliferation of CD8+ T cells that also induces autoimmunity. In gut lymph nodes of T cell–deficient mice, injected CD8+ T cells proliferated rapidly in response to IL-6. This inflammatory cytokine was found at high levels in these lymph nodes, perhaps due to their proximity to the bacterium-laden gut.

The mice developed a thicker gut epithelium and lost weight—signs of an autoimmune disease called colitis. T cell–injected mice treated with an IL-6–blocking antibody or with bacterium-depleting drugs, however, remained healthy.

The proliferating T cells secreted several inflammatory cytokines, including IL-17. The IL-17 alone seemed to be responsible for the colitis, as mice injected with T cells that were unable to produce IL-17 remained healthy. If these IL-17–producing CD8+ T cells are found in patients suffering from diseases such as colitis, the anti–IL-6 antibody might be a good therapeutic option.
Human Infection with the Virus of Vesicular Stomatitis during an Epizootic
Authors: Bernard N. Fields, Kathleen Hawkins
Journal: New England Journal of Medicine (1967)

IN the summer of 1965 an epizootic of vesicular stomatitis, primarily in cattle, occurred in northwest New Mexico and southwest Colorado. The disease was confirmed as the Indiana type by serologic examination of affected cattle and by isolation of the virus from vesicular lesions of cattle by Dr. E. Jenney, of the National Animal Disease Laboratory, Ames, Iowa.According to preliminary reports obtained from the Animal Health Division, United States Department of Agriculture, the epizootic began in early July in the contiguous counties of Rio Arriba (New Mexico) and La Plata (Colorado) (Fig. 1). The disease spread in an erratic . . .
ACC/AHA Guidelines for the Clinical Application of Echocardiography: Executive Summary
Authors: MD Cheitlin, JS Alpert, WF Armstrong, GP Aurigemma, GA Beller, FZ Bierman, TW Davidson, JL Davis, PS Douglas, LD Gillam, RP Lewis, AS Pearlman, JT Philbrick, PM Shah, RG Williams
Journal: Journal of the American College of Cardiology (1997)
Endotoxin accumulation prevents carcinogen-induced apoptosis and promotes liver tumorigenesis in rodents
Authors: Le-Xing Yu, He-Xin Yan, Qiong Liu, Wen Yang, Hong-Ping Wu, Wei Dong, Liang Tang, Yan Lin, Ya-Qin He, Shan-Shan Zou, Chao Wang, Hui-Lu Zhang, Guang-Wen Cao, Meng-Chao Wu, Hong-Yang Wang
Journal: Hepatology (2010)

Increasing evidence suggests that the presence of endotoxemia is of substantial clinical relevance to patients with cirrhosis, but it is unclear whether and how gut-derived LPS amplifies the tumorigenic response of the liver. We found that the circulating levels of LPS were elevated in animal models of carcinogen-induced hepatocarcinogenesis. Reduction of LPS using antibiotics regimen in rats or genetic ablation of its receptor Toll-like receptor 4 (TLR4) in mice prevented excessive tumor growth and multiplicity. Additional investigation revealed that TLR4 ablation sensitizes the liver to carcinogen-induced toxicity via blocking NF-κB activation and sensitizing the liver to reactive oxygen species (ROS)-induced toxicity, but lessens inflammation-mediated compensatory proliferation. Reconstitution of TLR4 -expressing myeloid cells in TLR4 -deficient mice restored diethylnitrosamine (DEN)-induced hepatic inflammation and proliferation, indicating a paracrine mechanism of LPS in tumor promotion. Meanwhile, deletion of gut-derived endotoxin suppressed DEN-induced cytokine production and compensatory proliferation, whereas in vivo LPS pre-challenge promotes hepatocyte proliferation. Conclusion: Our data indicate that sustained LPS accumulation represents a pathological mediator of inflammation-associated hepatocellular carcinoma (HCC) and manipulation of the gut flora to prevent pathogenic bacterial translocation and endotoxin absorption may favorably influence liver function in patients with cirrhosis who are at risk of developing HCC. (Hepatology 2010.)
CATHETER ABLATION VERSUS ANTIARRHYTHMIC DRUG THERAPY IN PAROXYSMAL AF: A COST/EFFECTIVENESS ANALYSIS
Authors: Vincenzo Santinelli, Gabriele Vicedomini, Francesca Zuffada, Enrico Frigoli, Luigi Giannelli, Andrea Petretta, Mario Baldi, Massimo Saviano, Alessia Pappone, Zarko Calovic, Carlo Pappone
Journal: Journal of the American College of Cardiology (2011)
Resolving the Scar of Pulmonary Fibrosis
Authors: Gregory P. Downey
Journal: New England Journal of Medicine (2011)

Fibrosis, or scarring, of the lung is a common consequence of certain types of pneumonias, and in such cases it is a localized and self-limited process. However, in conditions such as the complex group of disorders termed the idiopathic interstitial pneumonias, pulmonary fibrosis may be a progressive and diffuse process.1 The current classification scheme for idiopathic interstitial pneumonias is based on a combination of clinical, histopathological, and radiographic features.1 The idiopathic interstitial pneumonias may be related to an underlying connective-tissue disease, such as rheumatoid arthritis or scleroderma, or they may be caused by unknown factors, in which case the disease . . .
P1118 NO EFFECT OF FALDAPREVIR ON RENAL FUNCTION IN TREATMENT-NAIVE PATIENTS WITH CHRONIC HCV GENOTYPE-1 INFECTION: POOLED DATA FROM TWO PHASE III TRIALS
Authors: S. Zeuzem, D.M. Jensen, A. Carvalho, M. Diago, S.V. Feinman, K.V. Kowdley, J.-H. Kao, M. Maevskaya, F. Negro, P. Mantry, Y. Tanaka, D. Forton, D. Genné, S.W. Paik, E. Zehnter, M. Kuboki, W.M. Lee, C.-Y. Peng, H. Yatsuhashi, J.O. Stern, Y. Datsenko, M. Drulak, F. Voss, W. Böcher, P. Ferenci
Journal: Journal of Hepatology (2014)
The Philosophy of Medicine: The Early 18th Century
Authors: Daniel Leigh Weiss
Journal: JAMA (1978)

This is an important book, not only for its superb treatment of the philosophical bases of 18th century scientific and medical thought, but for its uncanny ability to force its 20th century reader to face his own medical-scientific assumptions. It is a rare experience to enjoy a historical treatment of our discipline that is so provocative for modern thought. Dr King has done far more than lay before us the philosophical basis of 18th century medicine. He has properly reached back in time to lay its foundations in Neoplatonic and Galenic medicine and has demonstrated the variations played on these themes until medieval theories were forced to face the new world of scientific observation. Equally interesting are his discussions of the attempts to relate past theory and new knowledge, both by accommodation by reinterpretation and by rejection of one or the other. But beyond the interplay of conflicting philosophical constructions,
Angiogenic Effects of Adrenomedullin in Ischemia and Tumor Growth
Authors: Satoshi Iimuro, Takayuki Shindo, Nobuo Moriyama, Toshihiro Amaki, Pei Niu, Norifumi Takeda, Hiroshi Iwata, Yuelan Zhang, Aya Ebihara, Ryozo Nagai
Journal: Circulation Research (2004)

Adrenomedullin (AM) is a novel vasodilating peptide involved in the regulation of circulatory homeostasis and implicated in the pathophysiology of cardiovascular disease. We tested the hypothesis that AM also possesses angiogenic properties. Using laser Doppler perfusion imaging, we found that AM stimulated recovery of blood flow to the affected limb in the mouse hind-limb ischemia model. AM exerted this effect in part by promoting expression of vascular endothelial growth factor (VEGF) in the ischemic limb, and immunostaining for CD31 showed the enhanced flow to reflect increased collateral capillary density. By enhancing tumor angiogenesis, AM also promoted the growth of subcutaneously transplanted sarcoma 180 tumor cells. However, heterozygotic AM knockout mice (AM+/-) showed significantly less blood flow recovery with less collateral capillary development and VEGF expression than their wild-type littermates. Similarly, mice treated with AM22-52, a competitive inhibitor of AM, showed reduced capillary development, and growth of sarcoma 180 tumors was inhibited in AM+/- and AM22-52-treated mice. Notably, administration of VEGF or AM rescued blood flow recovery and capillary formation in AM+/- and AM22-52-treated mice. In cocultures of endothelial cells and fibroblasts, AM enhanced VEGF-induced capillary formation, whereas in cultures of endothelial cells AM enhanced VEGF-induced Akt activation. These results show that AM possesses novel angiogenic properties mediated by its ability to enhance VEGF expression and Akt activity. This may make AM a useful therapeutic tool for relieving ischemia; conversely, inhibitors of AM could be useful for clinical management of tumor growth.
Impact of Pretransplant Anti-HLA Antibodies on Outcomes in Lung Transplant Candidates
Authors: Miae Kim, Keri R. Townsend, Isabelle G. Wood, Steve Boukedes, Indira Guleria, Steven Gabardi, Souheil El-Chemaly, Phillip C. Camp, Anil K. Chandraker, Edgar L. Milford, Hilary J. Goldberg
Journal: American Journal of Respiratory and Critical Care Medicine (2014)

The prevalence of anti-HLA antibodies in lung transplant candidates and their impact on waitlist and transplant outcomes is not known.We examined the prevalence of pretransplant anti-HLA antibodies at varying thresholds and evaluated their impact on outcomes before and after lung transplantation.We performed a single-center retrospective cohort study including all patients listed for lung transplantation between January 2008 and August 2012. Per protocol, transplant candidates were assessed by solid phase LABscreen mixed Class I and II and LABscreen Single Antigen assays.Among 224 patients, 34% had anti-HLA antibodies at mean fluorescent intensity (MFI) greater than or equal to 3,000 (group III), and 24% had antibodies at MFI 1,000 to 3,000 (group II). Ninety percent of the patients with pretransplant anti-HLA antibodies had class I antibodies, whereas only seven patients developed class II alone. Patients in group III were less likely to receive transplants than patients without any anti-HLA antibodies (group I) (45.5 vs. 67.7%, P = 0.005). Wait time to transplant was longer in group III than group I, although this difference did not meet statistical significance, and waitlist mortality was similar. Among transplant recipients, antibody-mediated rejection (AMR) was more frequent in group III than in group II (20% vs. 0%, P = 0.01) or group I (6.3%, P = 0.05).The presence of anti-HLA antibodies at the high MFI threshold (>3,000) was associated with lower transplant rate and higher rates of AMR. Screening for anti-HLA antibodies using the 3,000 MFI threshold may be important in managing transplant candidates and recipients.