tbuckley/cabot-search huggingface dataset:
Notes on Chronic Otorrhœa with Especial Reference to the Use of Zinc Ionization in the Treatment of Selected Cases.
Journal: JAMA (1929)

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
Highlights
Journal: JAMA Neurology (2015)

Lim and colleagues indicate that the risk of early recurrent stroke after transient ischemic attack (TIA) may be modifiable by optimal treatment.They determine the rate of early recurrent stroke after TIA and its neuroimaging predictors.They find that a total of 500 patients (mean age, 64 years; male, 291 [58.2%]; median ABCD 2 score, 4) completed 90-day follow-up with guidelinebased management: antiplatelets (457 [91.4%]), anticoagulants (74 [14.8%]), and statins (345 [69.0%]).Recurrent stroke occurred in 25 patients (5.0%) and was associated with cerebral microbleeds.
Modern Practice in Tuberculosis. Volumes I and II
Journal: JAMA (1952)

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
Guillaume de Baillou (1538-1616) clinician and epidemiologist
Journal: JAMA (1966)

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
Beta-Adrenergic Receptor Blocking Drugs
Authors: Stephen E. Epstein, Eugene Braunwald
Journal: New England Journal of Medicine (1966)

Cardiac ArrhythmiasShortly after their development, attempts were made to determine the effects of beta-adrenergic receptor blocking agents on variovis types of experimentally induced cardiac arrhythmias. It was soon found that the drugs effectively antagonized arrhythmias induced by catecholamines65 66 67 68 and digitalis69 70 71 72 73 in laboratory animals. The first clinical report on the use of beta-adrenergic blocking drugs in the treatment of cardiac arrhythmias was in 1963, when Stock and Dale74 observed that pronethalol effectively slowed the ventricular rate in patients with atrial fibrillation and suppressed several types of arrhythmias caused by digitalis toxicity.Digitalis-Induced ArrhythmiasThere appears to be little doubt that . . .
"FIRST AID" DANGERS.
Journal: JAMA (1902)

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
FEEBLEMINDEDNESS AND HEREDITY
Journal: JAMA (1942)

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
Solitary lesion of femur
Authors: R. F. Rider
Journal: JAMA (1970)

Dr. Richard M. Heller: This is the first admission to Massachusetts General Hospital for a 20-year-old white man who complained of pain in the left hip for six months. The findings of physical examination were normal, and results of the laboratory tests were completely normal. Roentgenograms of the hip were done at the time of admission. (Fig 1). <h3>Discussion</h3> Dr. Laurence L. Robbins: Dr. Otto, would you comment on this case, please. Dr. William J. Otto: There is a solitary lesion in the left proximal femur involving the greater trochanter and intertrochanteric area extending into the femoral neck. The cortex appears intact, and there is no soft-tissue mass visible. There are a few sclerotic lines crossing the lesion which seem to be true septa rather than scalloping of the inner cortex. The margins of the lesion are not very sharp. There is no sclerosis in the surrounding bone and no
Tricyclic Overdose
Authors: John B. Marshall
Journal: JAMA (1980)

<h3>To the Editor.—</h3> Tricyclic antidepressant (TCA) overdose is common and associated with substantial mortality; rates as high as 7% to 10% have been reported in some series.<sup>1,2</sup>The cause of death is primarily cardiovascular, generally due to arrhythimias or hypotension. The best clinical correlate to the severity of the overdose is QRS prolongation on ECG (238:135, 1977). A prolonged QRS duration of 100 ms or greater has a substantial likelihood of being associated with a plasma TCA level greater than 1,000 ng/mL, implying a severe overdose. In a study by Biggs et al (238:135, 1977), all patients with plasma TCA levels greater than 1,000 ng/mL had a maximum QRS duration of 100 ms or longer. We recently saw a patient with a TCA overdose who had an exceedingly high plasma TCA level (1,765 ng/mL) whose ECG showed a normal QRS duration. <h3>Report of a Case.—</h3> A 28-year-old man was
Mutagenesis after Cancer Therapy
Authors: Karl T. Kelsey, Michele Caggana, Peter M. Mauch, C. Norman Coleman, John R. Clark, Howard L. Liber
Journal: Environmental Health Perspectives (1993)

A subset of Hodgkin's disease (HD) and breast cancer patients have been reported to have elevated hprt mutant frequencies in peripheral blood lymphocytes after cessation of therapy.A subset of these patients are also known to develop second therapy-related malignancies.Therefore, it is clearly important to determine if these elevations in mutant frequency represent true, persistently elevated mutation frequencies.As a follow-up to our study of patients previously treated for HD, we recruited for a prospective study six previously treated HD patients and five patients who had been treated for squamous cell carcinoma of the head and neck.These individuals were studied several times over a 6-7 months.The results confirmed that a subset of patients have persistently high mutant frequencies when compared to 71 previously studied controls.The study was designed to determine if the elevated mutant frequencies of treated patients represented independent mutations or resulted from the in vivo expansion of single mutant cells.We used the polymerase chain reaction to examine DNA single strand conformation polymorphisms at the T-cell receptor-y locus of individual mutant clones.This analysis showed that 20.1% of the mutants from Hodgkin's disease patients and 17.5% of the mutants from squamous cell carcinoma patients were siblings.The sibling mutants generally did not persist over time.However, one patient had one mutant clone that persisted, but slowly decreased in prevalence over a 7 month sampling period.The data demonstrate that treatments for cancer result in persistently elevated mutation frequencies at the hprt locus in some, but not all, patients.In addition, our results confirm previous studies indicating that it is not always appropriate to assume equality between mutant and mutation frequencies when studying individuals exposed to significant doses of known mutagens or carcinogens.
Arsenic
Authors: Frederick A. J. Kingery
Journal: JAMA (1966)

Administration of arsenical compounds for therapeutic or criminal purposes has lost its popularity. Arsenic intoxication is nevertheless encountered occasionally, recognizable by the presence of a few subtle but distinctive cutaneous changes. Chemical identification of arsenic in the hair, nails, or urine provides proof of exposure. Chronic arsenic poisoning usually develops from the ingestion of an inorganic compound such as arsenic trioxide (As<sub>2</sub>O<sub>3</sub>) or one of its salts. These are found in some pesticides and rat poisons (Fig 1 and 2), and also are used in the paint and dye industries. Contaminated well water in areas where fruit or tobacco has been treated with an arsenical spray, such as Paris green, accounts for most cases of chronic intoxication (Fig 3). Malicious introduction of "white arsenic" (As<sub>2</sub>O<sub>3</sub>) into food or drink provides a small but constant number of victims. The poison has the advantages of being
Mucous Membrane of Respiratory Epithelium
Authors: Lynne M. Reid, Rosemary Jones
Journal: Environmental Health Perspectives (1980)

Of the eight epithelial cell types of the airway surface epithelium three are secretory, the mucous, serous and Clara cells: the first two are also found in the submucosal glands. Organ culture results indicate that the pattern of control of the surface cells is different from that of the glands. Our recent studies show that in the surface epithelium Clara and serous cells can quickly convert to mucous as do nonsecretory undifferentiated cells. The balance between the various cell types changes with airway level. The type of glycoprotein within the secretory granules is neutral or acid, sialylated or sulfated, and also shows a regional pattern. Homeostasis is maintained in the normal but the equilibrium is quickly upset by a variety of irritants, infection of drugs. Change in pattern of glycoprotein synthesis depends largely on change of granules. The granules at the cell apex change first. The nature and distribution of the various receptor binding sites is significant in patterns of control. This lability occurs in an intact epithelium and whether or not mitotic activity is increased. With irritation tolerance to stimulus develops. Antiinflammatory agents can protect against some of these cellular and intracellular events. Our organ culture studies and biochemical analysis of secretion complement the tissue studies. Recent studies show that isoproterenol and salbutamol (a nonselective beta agonist and a selective beta 2, respectively) alter the normal mix of cell types and quickly, but that they have different regional specificity.
Paralysed hemidiaphragm and shingles.
Authors: Natalie Haywood, Katherine Bridge #, Cheukyau Luk #, Nele Warmke, Katie Simmons, Michael Drozd, Amy Moran, Sam Straw, Jason Scragg, Jessica Smith, Sunti Limumpornpetch, Claire Ozber, Chloe Wilkinson, Anna Skromna, Natallia Makava, Andrew Walker, Nicole Watt, Romana Mughal, Kathryn Griffin, Hema Viswambharan, Nadira Yuldasheva, David Beech, Antonio Vidal- Puig, Klaus Witte, Stephen Wheatcroft, Richard Cubbon, Mark Kearney
Journal: BMJ (1970)

There are at least two distinct types of thermogenic adipocyte in mammals: a pre-existing form established during development, termed classical brown adipocytes and an inducible form, 'beige' adipocytes [1][2][3] .Various environmental cues can stimulate a process frequently referred to as 'beiging' of white adipose tissue (WAT), leading to enhanced thermogenesis and obesity resistance 4,5 .Whilst beiging of WAT as a therapeutic goal for obesity and obesity-related complications has attracted much attention [6][7][8][9] ; therapeutics stimulating beiging without deleterious side-effects remain elusive 10 .The endothelium lines all blood vessels and is therefore in close proximity to all cells.Many studies support the possibility that the endothelium acts as a paracrine organ [11][12][13][14] .We explored the potential role of endothelial insulin-like growth factor-1 receptor (IGF-1R) as a paracrine modulator of WAT phenotype.Here we show that a reduction in endothelial IGF-1R expression in the presence of nutrient excess leads to white adipocyte beiging, increases whole-body energy expenditure and enhances insulin sensitivity via a non-cell autonomous paracrine mechanism.We demonstrate that this is mediated by endothelial release of malonic acid, which we show, using prodrug analogues, has potentially therapeutically-relevant properties in the treatment of metabolic disease.
Abstract 1588: Germline variation in DNA repair genes and risk of Barrett's esophagus and esophageal adenocarcinoma
Authors: Matthew F. Buas, Li Yan, Xuan Peng, Qianya Qi, Jianhong Chen, Aaron Thrift, Qianchuan He, Lynn Onstad, Puya Gharahkhani, Stuart MacGregor, Thomas L. Vaughan, Margaret M. Madeleine
Journal: Cancer Research (2019)

Abstract Incidence of esophageal adenocarcinoma (EA) has risen substantially in Western countries over recent decades. Established risk factors for EA and its precursor lesion, Barrett’s esophagus (BE), include reflux, obesity, and tobacco smoking. Inherited genetic variation also influences disease risk, although only a limited number of susceptibility loci have been identified. Genomic analyses of EA tumors have revealed a distinctive mutational signature, high mutational burden, and extensive somatic chromosome alterations, features also observed in high-risk BE tissue. To explore whether germline variation in DNA repair-related genes may be associated with altered disease susceptibility, we analyzed data from a recent meta-analysis of genome-wide association studies (GWAS) encompassing 4,112 EA cases, 6,167 BE cases, and 17,159 controls, representing the largest sample size assembled for these conditions. Using a gene-based testing approach (VEGAS2), we assessed 263 DNA repair-related genes and found that variation in NEIL2, a mediator of base excision repair (BER), was significantly associated with risk of BE (P=1.4×10-5, q&amp;lt;0.05). No other gene-level associations with BE or EA survived correction for multiple comparisons. SNP-level analysis of 239 polymorphisms at the NEIL2 locus revealed six variants strongly associated with altered risk of BE (P&amp;lt;5×10-5, q&amp;lt;0.01), with the index SNP classified as an intronic eQTL for NEIL2 in esophageal tissue. Four of these SNPs were also associated with risk of EA (P&amp;lt;0.05), with odds ratios in the same direction and of similar magnitude. Our results provide evidence that germline genetic variation in a DNA glycosylase enzyme (NEIL2) may influence risk of BE/EA, and suggest a potential novel biological role for altered BER in BE/EA pathogenesis. Citation Format: Matthew F. Buas, Li Yan, Xuan Peng, Qianya Qi, Jianhong Chen, Aaron Thrift, Qianchuan He, Lynn Onstad, Puya Gharahkhani, Stuart MacGregor, Thomas L. Vaughan, Margaret M. Madeleine. Germline variation in DNA repair genes and risk of Barrett's esophagus and esophageal adenocarcinoma [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2019; 2019 Mar 29-Apr 3; Atlanta, GA. Philadelphia (PA): AACR; Cancer Res 2019;79(13 Suppl):Abstract nr 1588.
Maternal diethylstilbestrol a time bomb for child?
Authors: K. S. Huss
Journal: JAMA (1971)

Clear-cell carcinomas or adenocarcinomas of the vagina, which are appearing in teen-agers and young adults whose mothers received diethylstilbestrol or other synthetic estrogens during pregnancy, recently have assumed great scientific importance. During the late 1940s and early 1950s, estrogen therapy was believed indicated for maintaining pregnancies considered to be at high risk because of bleeding or previous pregnancy loss. Adenocarcinoma of the vagina previously was considered a rare tumor, especially in young women (<i>Cancer</i><b>25</b>:745-757, 1970). Between the years 1966 and 1969, this tumor was diagnosed in eight patients ranging from 15 to 22 years of age, who were treated in two Boston hospitals (seven in one hospital). Medical advice was sought by these adolescent girls and young women because of abnormal bleeding, and hormonal therapy was administered in most cases since the irregular bleeding was assumed to be due to anovulation. Vaginal smears were made in six cases,
11P Pharmacokinetic/pharmacodynamic (PK/PD) exposure-response characterization of GSK3359609 (GSK609) from INDUCE-1, a phase I open-label study
Authors: E. Angevin, S. Groenland, T. Bauer, D. Rischin, I. Gardeazabal, V. Moreno, J.M. Trigo, M. Chisamore, J. Shaik, F. Rigat, C. Ellis, H. Chen, R. Gagnon, S.J. Scherer, D. Turner, S. Yadavilli, M. Ballas, A. Hoos, M. Maio
Journal: Annals of Oncology (2020)
A Mechanism-Mediated Model for Carcinogenicity: Model Content and Prediction of the Outcome of Rodent Carcinogenicity Bioassays Currently Being Conducted on 25 Organic Chemicals
Authors: Rich Purdy
Journal: Environmental Health Perspectives (1996)

A hierarchical model consisting of quantitative structure-activity relationships based mainly on chemical reactivity was developed to predict the carcinogenicity of organic chemicals to rodents.The model is comprised of quantitative structure-activity relationships, QSARs based on hypothe- sized mechanisms of action, metabolism, and partitioning.Predictors included octanol/water partition coefficient, molecular size, atomic partial charge, bond angle strain, atomic acceptor delocalizibility, atomic radical superdelocalizibility, the lowest unoccupied molecular orbital (LUMO) energy of hypothesized intermediate nitrenium ion of primary aromatic amines, differ- ence in charge of ionized and unionized carbon-chlorine bonds, substituent size and pattern on polynuclear aromatic hydrocarbons, the distance between lone electron pairs over a rigid struc- ture, and the presence of functionalities such as nitroso and hydrazine.The model correctly classified 96% of the carcinogens in the training set of 306 chemicals, and 90% of the carcinogens in the test set of 301 chemicals.The test set by chance contained 84% of the positive thio- containing chemicals.A QSAR for these chemicals was developed.This posttest set modified model correctly predicted 94% of the carcinogens in the test set.This model was used to predict the carcinogenicity of the 25 organic chemicals the U.S.