tbuckley/cabot-search huggingface dataset:
Diagnosing Sinusitis
Authors: John W. Williams
Journal: Annals of Internal Medicine (1993)

Letters1 July 1993Diagnosing SinusitisJohn W. Williams, Jr., MD and David L. Simel, MDJohn W. Williams, Jr., MDUniversity of Texas Health Science Center; San Antonio, TX 78284Duke University; Durham, NC 27705Search for more papers by this author and David L. Simel, MDUniversity of Texas Health Science Center; San Antonio, TX 78284Duke University; Durham, NC 27705Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-119-1-199307010-00020 SectionsAboutFull TextPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail IN RESPONSE:Drs. Cass, Cantor, and Clover's first concern is the generalizability of the study results. Although the study site is university affiliated, it serves as the primary care site (not tertiary care) for a population of primarily local residents. We agree that the study population was atypical in that only men were included; however, no known gender differences exist in the clinical presentation or clinical course of sinusitis.Their second concern is the high prevalence of sinusitis (38%) and possible misclassification by the criterion standard radiographs. The epidemiologic data Cass and colleagues use to suggest a lower prevalence of ...References1. Berg O, Carenfelt C. Analysis of symptoms and clinical signs in the maxillary sinus empyema. Acta Otolaryngol. 1988; 105:343-9. Google Scholar2. Evans FO Jr, Sydnor JB, Moore WE, Moore GR, Manwaring JL, Brill AH, et al. Sinusitis of the maxillary antrum. N Engl J Med. 1975; 293:735-9. Google Scholar3. van Duijn NP, Brouwer HJ, Lamberts H. Use of symptoms and signs to diagnose maxillary sinusitis in general practice: comparison with ultrasonography. BMJ. 1992; 305:684-7. Google Scholar4. White JA. Paranasal sinus infections. In: Ballenger JJ; ed. Diseases of the Nose, Throat, Ear, Head and Neck. Philadelphia: Lea and Febiger; 1991:184. Google Scholar Author, Article, and Disclosure InformationAffiliations: University of Texas Health Science Center; San Antonio, TX 78284Duke University; Durham, NC 27705 PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited BySystematic Review of Clinical Data with BNO-101 (Sinupret?) in the Treatment of Sinusitis 1 July 1993Volume 119, Issue 1Page: 92KeywordsAllergic rhinitisClinical epidemiologyCommon coldPrimary careSexual identityUpper respiratory tract infections Issue Published: 1 July 1993 CopyrightCopyright © 1993 by American College of Physicians. All Rights Reserved.PDF DownloadLoading ...
Egregious errors in the management of hypertension
Authors: I. H. Page
Journal: JAMA (1976)

NOW that hypertension has come of age and everyone is an expert, it is time to correct some common and often egregious errors in therapeutic management. These errors are, for the most part, simple and well known, but are frequently overlooked. The result: a considerable increase in the number of hypertensive persons is caused by false measurements and slipshod treatment of those who have hypertension. Few measurements are made more often than blood pressure, since the introduction of the auscultatory method in 1905. It is such a simple technique that results are seldom suspected of being inaccurate. We are now in the middle of a massive campaign to "identify" hypertensive persons. The federal government has pulled out all the stops, with scary statistics, threats, and importunings, to persuade our people that hypertension is the second greatest killer. "No one, not even you, is exempt." It also has racial overtones in
Rhythmic Changes in Intraocular Pressure
Journal: JAMA (1963)

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
Expression of intracellular adhesion molecule 1 by activated hepatic stellate cells
Authors: C Hellerbrand
Journal: Hepatology (1996)

The hepatic stellate cell (HSC), following a fibrogenic stimulus, is transformed from a quiescent to an activated cell. HSC activation results in numerous changes in cellular morphology, cellular metabolism, and in the pattern of gene expression. Many of the changes that are observed in activated HSCs in animal models of hepatic fibrosis are also seen when these cells are activated by culturing on plastic. These changes include morphological changes to a myofibroblast- like cell with the appearance of smooth muscle α-actin, a loss of the retinol stores, an increase in the rough endoplasmic reticulum, and increases in extracellular matrix production, including a dramatic increase in type I collagen. To identify additional genes that are induced or suppressed during HSC activation, we used the differential polymerase chain reaction (PCR) display technique. Using this technique, we isolated a complementary DNA (cDNA) fragment for the intercellular adhesion molecule 1 (ICAM-1). Northern blotting confirmed that the ICAM-1 messenger RNA (mRNA) was expressed in HSCs activated by culture, but not in quiescent, freshly isolated HSCs. The presence of ICAM-1 protein was demonstrated in culture-activated HSCs, but not in quiescent cells by Western blot analysis and immunohistochemical staining. A functional assay was performed, demonstrating that lymphocytes will adhere to activated HSCs and that treatment of these cells with tumor necrosis factor α (TNF-α) increases lymphocyte adherence. Furthermore, ICAM-1 mRNA levels were increased in HSCs activated in rats in vivo after 1 week of bile duct ligation (BDL). Together, these data indicate that ICAM-1 expression is induced following HSC activation and that the HSC may have a direct role in the transmigration of leukocytes from the hepatic sinusoid to sites of tissue damage during the inflammatory response in the liver.
Trial of vitamin E therapy for retrolental fibroplasia
Authors: Phil Gunby
Journal: JAMA (1980)

High dosages of vitamin E are being given to premature infants in an attempt to reduce the incidence and severity of retrolental fibroplasia. The study, supported by the National Eye Institute, Bethesda, Md, is to involve a total of 650 infants with a gestational age of 36 weeks or less at birth. The majority will have weighed 2,000 g or less at birth and may or may not have received oxygen therapy. The remainder will have weighed more than 2,000 g at birth and will have required oxygen therapy for at least 18 of their first 36 hours. These infants are being assigned to one of five groups on the basis of birth weight. Within a group, they are assigned randomly to treatment with vitamin E (dl-a-tocopherol) or a placebo. The vitamin or placebo is administered by infusion to those infants (about seven of ten) who already are receiving intravenous
“Failure To Thrive” in Older Adults
Authors: Catherine A. Sarkisian
Journal: Annals of Internal Medicine (1996)

The term "failure to thrive" is frequently used to describe older adults whose independence is declining.The term was exported from pediatrics in the 1970s and is used to describe older adults with various concurrent chronic diseases, functional impairments, or both. Despite this heterogeneity, failure to thrive has had its own International Classification of Diseases, Ninth Revision (ICD-9) code since 1979 and has been approached as a clinically meaningful diagnosis in many review articles. This conceptual framework, however, can create barriers to proper evaluation and management. The most worrisome of these barriers is the reinforcement of both fatalism and intellectual laziness, which need to be balanced with a deconstructionist approach, wherein the major areas of impairment are identified and quantified and have their interactions considered. Four syndromes known to be individually predictive of adverse outcomes in older adults are repeatedly cited as prevalent in patients with failure to thrive: impaired physical functioning, malnutrition, depression, and cognitive impairment. The differential diagnosis of contributors to each of these syndromes includes the other three syndromes, and multiple contributors often exist concurrently. Some of these contributors are unmodifiable, some are easily modifiable, and some are potentially modifiable but only with the use of resource-intensive strategies. Initial interventions should be directed at easily remediable contributors in the hope of improving overall functional status, because a single contributor may simultaneously influence several other syndromes that conspire to create the phenotype of failure to thrive. How aggressively should more resource-intensive strategies for less easily modifiable contributors be pursued? This is a central clinical, ethical, and policy issue in geriatric medicine that cannot be settled without better process and outcome data. This paper examines the medical etymology of failure to thrive and proposes a rational approach to evaluation and management that is based on the limited medical literature.
Dipyridamole
Authors: John A. Oates, Alastair J.J. Wood, G.A. FitzGerald
Journal: New England Journal of Medicine (1987)

DIPYRIDAMOLE (2,6-bis-diethanolamino-4,8-dipiperidinopyrimido-(5,4-d)-pyrimidine) is a pyrimidopyrimidine derivative that is among the 50 most commonly prescribed drugs in the United States.1 This review will focus on the mechanisms of action of dipyridamole and the rationale provided by clinical trials of its pharmacology for its use as an orally administered antiplatelet drug in humans.Mechanism of Action as an Antithrombotic DrugThe mechanism of action of dipyridamole as an antithrombotic drug in vivo has been a subject of controversy. Indeed, in experimental models in which the drug has been shown to prevent thrombosis, it is possible that factors other than platelet . . .
Platelets and prostaglandins in coronary artery disease. Rationale for use of platelet-suppressive drugs
Authors: J. Mehta
Journal: JAMA (1983)

THE ROLE of platelets in the genesis of atherosclerosis and its manifestations has received considerable attention. Based on the recognition of platelet "hyperactivity" in patients with coronary artery disease, several platelet-suppressive drugs have been used in a large number of patients. The purpose of this article is to review the role of platelets, the mechanisms of platelet activation, and the results of platelet-inhibitory drug trials in patients with coronary artery disease. <h3>PLATELETS AND HEMOSTASIS</h3> Platelets, small disklike cells circulating in the blood, have a primary role in hemostasis. With stress to the endothelium and its subsequent disruption, platelets adhere to the subendothelial collagen. Circulating platelets are attracted to the adhering platelets, resulting in platelet aggregation and formation of a platelet thrombus. In this thrombus, RBCs, WBCs, and other components of blood are incorporated, resulting in an occlusive clot. On activation, platelets also release potent hormones, prostaglandins, polypeptides, and other vasoactive
MYOSITIS OSSIFICANS.
Journal: JAMA (2000)

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 Journals 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
Side Effects
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
Incorrect Time in Figure
Authors: Christopher Jones
Journal: JAMA (2015)

Vivek Y. Reddy, MD; Horst Sievert, MD; Jonathan Halperin, MD; Shephal K. Doshi, MD; Maurice Buchbinder, MD; Petr Neuzil, MD, PhD; Kenneth Huber, MD; Brian Whisenant, MD; Saibal Kar, MD; Vijay Swarup, MD; Nicole Gordon, BSEE; David Holmes, MD; for the PROTECT AF Steering Committee and Investigators
906. Effective Repetitive Dystrophin Gene Transfer into Skeletal Muscle of Adult mdx Mice Using a Helper-Dependent Adenovirus Vector Expressing the Coxsackievirus and Adenovirus Receptor (CAR) and Dystrophin
Authors: Yuji Uchida, Yasushi Maeda, En Kimura, Makoto Uchino
Journal: Molecular Therapy (2006)

The helper-dependent adenovirus (HDAd) vector is less immunogenic and has a larger cloning capacity of up to 37 kb enough to carry the full-length dystrophin cDNA. However, high and long- term expression of dystrophin transduced to mature muscle still remains difficult. One of the main reasons for this is that the expression of the coxsakievirus and adenovirus receptor (CAR) is very low in mature muscle. We have constructed two different HDAd vectors. One contains the LacZ and the murine full-length dystrophin expression cassette (HDAdLacZ-dys), and the other is a new, improved vector containing the CAR and the dystrophinexpression cassette (HDAdCAR-dys).
A Fast Tissue-Dosage System for 200 Kv Arc Therapy
Journal: JAMA (1963)

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 Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More 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) 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
Molecular virology and cancer
Authors: C. R. Goodheart
Journal: JAMA (1965)

Some of the most interesting and challenging problems facing today's biologist are those related to various aspects of cellular regulation. Systems using representative cancer viruses of birds and of mammals as experimental models recently have given insights into the mechanisms of control of cellular morphology, differentiation, and growth. This is so because, when a cancer virus interacts with a cell, the malignant change that may result is manifested as a heritable alteration in these mechanisms. Therefore, better understanding of the interaction between a cancer virus and a cell is an important goal of both cancer research and more general biological research. The purpose of this review is to discuss the various known tumor viruses, the current concept of the cellular genetic apparatus, and the various ways a tumor virus might interact with a cell to cause the malignant change. Much of the information reviewed here was originally obtained from work
Heritage: A phase III safety and efficacy trial of the proposed trastuzumab biosimilar Myl-1401O versus Herceptin.
Authors: Hope S. Rugo, Abhijit Barve, Cornelius F. Waller, Miguel Hernandez-Bronchud, Jay Herson, Jinyu Yuan, Alexey Manikhas, Igor Bondarenko, Guzel Mukhametshina, Gia Nemsadze, Joseph D. Parra, Maria Luisa T. Abesamis Tiambeng, Kakhaber Baramidze, Charuwan Akewanlop, Ihor Vynnychenko, Virote Sriuranpong, Gopichand Manillapalli, Sirshendu Ray, Eduardo Patricio Yanez Ruiz, Eduardo J. Pennella
Journal: Journal of Clinical Oncology (2016)

LBA503 The full, final text of this abstract will be available at abstracts.asco.org at 2:00 PM (EDT) on Friday, June 3, 2016, and in the Annual Meeting Proceedings online supplement to the June 20, 2016, issue of the Journal of Clinical Oncology. Onsite at the Meeting, this abstract will be printed in the Monday edition of ASCO Daily News.
The Pathobiology Of Campylobacter Infections In Humans
Authors: T. Cover
Journal: Annual Review of Medicine (1989)

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the cause of coronavirus disease 2019 (COVID-19), emerged in China in December 2019 and quickly spread around the globe, killing more than 4 million people and causing a severe economic crisis. ...Read More
MINERS' NYSTAGMUS
Journal: JAMA (1926)

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
BIOM-22. EPIDERMAL GROWTH FACTOR RECEPTOR (EGFR) AS A MOLECULAR DETERMINANT OF GLIOBLASTOMA RESPONSE TO DOPAMINE RECEPTOR 2 (DRD2) INHIBITORS
Authors: Yuyu He, Jie Li, Tomoyuki Koga, Jun Ma, Sanjay Dhawan, Yuta Suzuki, Frank Furnari, Varun Prabhu, Joshua Allen, Clark Chen
Journal: Neuro-Oncology (2020)

Abstract BACKGROUND There are ongoing clinical trials exploring the efficacy of dopamine receptor 2 (DRD2) inhibition against glioblastomas, the most common primary brain tumor. Here we examine potential molecular determinants of this efficacy. METHODS The Cancer Genome Atlas (TCGA) glioblastoma database and other published mRNA profiles were used to analyze the DRD2 and EGFR expression pattern. In vitro and in vivo responses to DRD2 inhibitors were determined using patient derived xenograft (PDX) glioblastoma models. Immunohistochemical studies were performed on clinically annotated glioblastoma samples derived from patients treated with ONC201, a DRD2 inhibitor. RESULTS Analysis of clinical glioblastoma specimens derived from independent patient cohorts revealed an inverse correlation between EGFR and DRD mRNA expression, with implication that signaling mediated by these proteins shares overlapping functions. In independent panels of PDX glioblastoma lines, high EGFR expression was associated with poor in vitro and in vivo response to DRD2 inhibitors, including haloperidol and ONC201. Moreover, ectopic expression of a constitutively active EGFR, EGFRvIII, suppressed glioblastoma sensitivity to ONC201. DRD2 expression positively correlated with expression of rate-limiting enzymes for dopamine synthesis as well as dopamine secretion, suggesting contribution of autocrine DRD2 signaling. Analysis of specimens from patients treated with ONC201 (n = 15) showed an inverse correlation between the intensity of EGFR staining and clinical response. The median overall survival for patients with high and low EGFR staining was 162 and 373 days, respectively (p = 0.037). CONCLUSIONS High EGFR expression is a determinant of poor glioblastoma response to DRD2. This finding should inform future clinical trial designs.
Clinical Neurology
Authors: Terrence Riley
Journal: JAMA (1991)

This is an excellent textbook and thorough reference work in clinical neurology. Such a detailed and thorough book requires numerous contributors, as the editors point out in their preface, but they have maintained a comfortable uniformity of style and approach throughout. All chapters are quite readable and presented in a logical and orderly manner. The table of contents, index, tables, and illustrations make the book convenient to use and the abundant information easily accessible. I particularly appreciate the first brief chapter "Nosology," which properly sets the tone for the text. There is a scholarly discussion about the important interworkings and varying limitations of the sciences and clinical neurology. This text gives plenty of attention to both. Chapters blend anatomic, physiologic, diagnostic, therapeutic, and modern research topics so that all are covered in a scholarly yet readable way. As a reference work for the serious student or resident physician, it is