tbuckley/cabot-search huggingface dataset:
VASOMOTOR RHINITIS
Authors: FRENCH K. HANSEL
Journal: JAMA (1924)

During recent years, clinicians have investigated extensively the causative factors in vasomotor rhinitis, more particularly the seasonal vasomotor rhinitis or so-called hay-fever. There is, however, a group of cases in which this type of symptoms continues throughout the year, without a definite seasonal activity. I shall review here the clinical course and the reactions to treatment in 100 cases of vasomotor rhinitis observed at the Mayo Clinic during the last two years. The cases were grouped for study according to the methods of previous observers. Particular attention was directed to the so-called reflex type of case, in which no protein sensitization factors were demonstrable. The negative skin sensitization tests in these cases do not prove that such factors are absent. There were sixty-one cases in this group; the remaining thirty-nine in which the skin reactions were positive were classified with the protein sensitization group. <h3>ETIOLOGY</h3> In studying the cause of
Expression of the hepatitis C virus genome in rat liver after cationic liposome-mediatedin vivo gene transfer
Authors: Tetsuo Takehara, Norio Hayashi, Yasuhide Miyamoto, Masato Yamamoto, Eiji Mita, Hideyuki Fusamoto, Takenobu Kamada
Journal: Hepatology (1995)

The lack of a small animal model of hepatitis C virus (HCV) infection has impeded elucidation of the pathogenesis of HCV. The aim of this study was to develop an HCV-expressing animal model by means of cationic liposome-mediated in vivo gene transfer. To examine the feasibility of this strategy, pActLacZ, an expression vector composed of the LacZ gene driven by the β-actin promoter, complexed with lipofectin, was injected retrogradely into the common bile ducts of adult rats. X-Gal histochemical staining clearly showed that the LacZ gene was expressed in hepatocytes, but not in biliary epithelial cells. Maximal expression was observed at a DNA to lipofectin ratio of 1:4. Based on this observation, pAGS3M091, an expression vector containing the full length of HCV complementary DNA (cDNA) preceded by the β-actin promoter, was evaluated. Two days after in vivo intrabiliary administration of pAGS3M091 complexed with lipofectin, polymerase chain reaction (PCR) amplification of reverse-transcribed liver RNA demonstrated the 5′ and 3′ portions of HCV transcripts derived from pAGS3M091. Immunohistochemical analysis showed the HCV core protein in a small number of hepatocytes scattered in the hepatic lobules. We conclude that the full-length HCV genome was successfully expressed in adult rat liver by means of cationic liposome-mediated in vivo gene transfer. This model will be useful for detemining the immunopathological role of HCV in vivo .
Science Fair Winners on AMA Program
Journal: JAMA (1964)

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
PROPOSED INSPECTION OF SURGICAL OPERATIONS BY THE LAITY.
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
Witchcraft and lupus erythematosus
Authors: R. A. Kirkpatrick
Journal: JAMA (1981)

THE SYMPTOMS of systemic lupus erythematosus (SLE) are as numerous as its pharmacologic treatments. Hemolytic anemia, vasculitis, synovitis, lymphadenopathy, nephritis, hepatitis, cerebritis, serositis, and rashes may respond to aspirin, corticosteroids, antimalarial and myelosuppressive alkylating agents, and a plethora of synthetic, nonsteroidal, anti-inflammatory concoctions. Apparently, however, there is another treatment. <h3>Report of a Case</h3> In early 1977, a 28-year-old Philippine-American became ill with weakness, hepatomegaly, and intermittent lymphadenopathy. Two referral clinics documented high ESRs, polyclonal gammopathy, and mild anemia. Also found were RBC and WBC casts and a moderate amount of albumin in her urine. Biopsy specimens of the liver and lymph nodes disclosed non-specific inflammatory changes, and the diagnosis of SLE was established only when antinuclear antibody and lupus erythematosus clot test results (formerly negative) became positive. The anti-DNA level was 68 units/dL (normal, &lt;10 units/dL), and the serum creatinine level was 0.7 mg/dL. Shortly after prednisone therapy, 60 mg/day,
National Cancer Institute Monograph 38, July 1973 “Chalones: Concepts and Current Researches”
Journal: JNCI Journal of the National Cancer Institute (1973)

National Cancer Institute Monograph 38, July 1973 “Chalones: Concepts and Current Researches” Get access JNCI: Journal of the National Cancer Institute, Volume 51, Issue 5, November 1973, Page 1735, https://doi.org/10.1093/jnci/51.5.1735-b Published: 01 November 1973
Marihuana and the diabetic coma
Authors: J. E. Hughes
Journal: JAMA (1970)

Marihuana ingestion by a 21-year-old man was followed by severe diabetic ketoacidosis. Following oral ingestion of marihuana, nausea, vomiting, diuresis, and an elevation of blood glucose level have previously been noted. It is speculated that when the stress of marihuana ingestion is greater than the adaptive capacity of the glucose-regulating system, diabetic ketoacidosis might evolve.
Clinical and genetic factors predict severe disease: a novel composite severity index
Authors: A. Phillips, I. Arnott, T. Heron, S. Cleary, C. Mowat, H. Clark, N. Lewin-Koh, J. Satsangi
Journal: Gut (2011)

<h3>Introduction</h3> Crohn9s disease is an incurable progressive disease with marked heterogeneity in outcome. Identifying patients at diagnosis (Dx) at high risk of poor outcomes would allow treatment stratification. Current definitions of severe disease lack discrimination. A more discriminant composite severity score would benefit clinical research and aid clinical decision making. <h3>Methods</h3> Based on a consensus of 5 clinicians, the authors designed a composite severity score, assessed over the 5 years after Dx, with a total possible score 1–16. The score was applied retrospectively in 367 CD patients who were also genotyped for 32 CD susceptibility loci. The severity score that would encompass the 50% of patients with the highest score was defined, and factors present at Dx – both clinical and genetic – were assessed by the χ<sup>2</sup> test for their ability to predict being in the more severe disease category. CD was classified according to the Montreal classification. <h3>Results</h3> 367 CD patients (median age at Dx 30.8 (IQR 22.9–46.1)) were assessed. 249 patients had full data available for the first 5 years after Dx. The mean severity score was 6.3 (95% CI 5.9 to 6.6). Patients with a score &gt;6 were defined as having more severe disease. Patients with more severe disease were younger at Dx (p=0.0004 for trend, OR A1 vs A2=4.42 (95% CI 1.4 to 13.9)) and had an ileal (p=0.0025, OR=2.2 (95% CI 1.32 to 3.68)) and upper GI location disease location at Dx (p=0.0008, OR=5.3 95% CI 1.9 to 14.7). Perianal disease at Dx approached but did not achieve statistical significance (p=0.052). Only rs9286879 (p=0.0085) and rs17582416 (p=0.0448) were observed more frequently in patients with severe disease. The need for steroids at Dx, having a first degree relative with IBD, needing surgery at Dx or smoking status at Dx did not differ between the groups. <h3>Conclusion</h3> This index discriminates more effectively between severity groups. Disease location, age at Dx and genetic markers are associated with more severe disease but validation of these factors is needed in a separate cohort.
"QUO VADIS?"
Authors: T. J. HAPPEL
Journal: JAMA (1899)

An article presented as a presidential address usually opens up a wide field for a congratulatory review of the progress of medicine in the few years immediately preceding the date at which it is read, and for painting pictures of a roseate hue of the future possibilities of surgery and gynecology. Any departure from this routine custom may be frowned upon and denounced as "not regular," but men are generally profited more by the mistakes of themselves and their friends than by their successes. A mistake made impresses an honest student of medicine and surgery—as it does workers in all other branches of life—to the extent that the same error is not likely to be committed again. The lesson has been too deeply impressed to be readily forgotten. An optimist is as dangerous in medicine as a pessimist, if not more so. The optimist, always looking for the good,
Endometriosis
Authors: David B. Redwine
Journal: JAMA (1986)

<h3>To the Editor.—</h3> I would appreciate it if Cramer et al<sup>1</sup>could clarify some points regarding the methodology and conclusions of their case-control study on endometriosis. The first question concerns their use of infertility as the main symptom to select cases, since pain may actually be a more common symptom.<sup>2</sup>Second, since cases were older than controls and since ovulatory function declines with age, it seems the study apparently did not control for possible decline in ovulation (their menstrual cycle data notwithstanding). The infertility observed might therefore in some large part be age related, not endometriosis related. Third, some of the controls may have had endometriosis, and if these were to be eliminated, this would change some of the observed risk ratios, particularly relating to their observations on height and smoking before the age of 17 years, differences that seemed less firm to begin with. Fourth, their findings
AN EXPIRING CRAZE.
Journal: JAMA (1895)

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
Mountain Fire
Journal: JAMA (2003)

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
SCIENCE AND REST.
Journal: JAMA (1903)

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
Manuscripts Approved for JNCI, May 1 to June 1, 1968
Journal: JNCI Journal of the National Cancer Institute (1968)

Manuscripts Approved for JNCI, May 1 to June 1, 1968 Get access JNCI: Journal of the National Cancer Institute, Volume 41, Issue 1, July 1968, Page 265, https://doi.org/10.1093/jnci/41.1.265-a Published: 01 July 1968
Abstract 3390: RNA interactome topology perturbation analysis reveals candidate driver mutations in cancer
Authors: Yongsheng Li, Daniel J. McGrail, Juan Xu, Junyi Li, Song Yi, Nidhi Sahni
Journal: Cancer Research (2019)

Abstract Identification of the driver genomic variants is important for precision therapy of human cancer. Interaction between RNA-binding proteins (RBPs) and RNA plays important roles in regulating cellular function. Decoding genome-wide protein-RNA regulatory networks as well as how cancer-related mutations impair RNA regulatory activities in cancer will help prioritizing candidate driver mutations. Here, we first explored the genetic alteration patterns of RBPs and found that candidate driver mutations are likely to occur on the surface of RBPs. This observations indicate that the driver mutations may perturb the RBP regulatory network in cancer. We then constructed protein-RNA interactome networks by integration of target binding screens and expression profiles. Regulatory network analysis highlights regulatory principles among interacting RBPs. In addition, somatic mutations selectively target functionally important genes (cancer genes, core fitness genes or conserved genes) in cancer. These regulatory patterns were further validated using independent data. A computational method (MERIT) and a web-based user friendly resource were further proposed to analyze the RBP-gene regulatory network perturbation induced by mutations across cancer types. Pan-cancer analysis also suggests that cancer cells selectively target "vulnerability" genes to perturb protein-RNA interactome that is involved in cancer hallmark-related functions. Based on the expression of perturbed RBP and target genes, we identified three subtypes of liver cancer with different survival rates. Specifically, we experimentally validated four pairs of RBP-gene interactions perturbed by mutations, which play critical roles in cell proliferation. Taken together, our results provide a valuable resource for characterizing somatic mutation-perturbed protein-RNA regulatory networks in cancer, yielding valuable insights into the genotype-phenotype relationships underlying human cancer, and potential biomarkers for precision medicine. Note: This abstract was not presented at the meeting. Citation Format: Yongsheng Li, Daniel J. McGrail, Juan Xu, Junyi Li, Song Yi, Nidhi Sahni. RNA interactome topology perturbation analysis reveals candidate driver mutations in cancer [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 3390.
Stuttering
Authors: Gavin Andrews
Journal: JAMA (1988)

A RECENT essay<sup>1</sup>and several letters<sup>2,3</sup>inTHE JOURNALdealing with a physician-mother's guilt about her son's stuttering suggested that there continues to be a surprising lack of understanding among some physicians about the nature of stuttering. This is unfortunate, because research findings indicate that there is now substantial empirical information about the nature, development, and management of stuttering. Readers interested in the subject could consult a recent review.<sup>4</sup> <h3>The Syndrome</h3> Developmental stuttering can begin as soon as a child starts speaking in short utterances, but most children begin to stutter between ages 3 and 5. The incidence decreases until puberty, after which the onset of developmental stuttering is rare. Syllable repetitions, especially on the first words of utterances, are the most frequent speech disruptions observed initially. Sound prolongations and tense pauses may also occur. Some children cease stuttering after a few months but in others the
Scientific Posters
Authors: Amber Dobler, Jonathan Pederson, Aaron Nathenson, Robert Snyder, Richard Allinson, Robert Fante, Michael Stanko, David Metrikin, Rainer Sundmacher, Thomas Reinhard, Christoph Althaus, Maria Susan, M Lasa, Manuel Datiles Ill, Benjamin Magno, Louella Lopez, Howard Bernstein, Henry Starr, William Clew, Siling Xiang, Washington Md, Joseph Schwartz, Kenneth Hoffer, Santa Monica, Amilia Schrier, Henry Perry, Eric Donnenfeld, ; David, Rockville Nelson
Journal: Ophthalmology (1992)
Industrial Exhibits
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 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
Opposition to the Icelandic database is based on false information
Journal: BMJ (1999)

Objective To determine the ability of montelukast, a leukotriene receptor antagonist, to allow tapering of inhaled corticosteroids in clinically stable asthmatic patients.Design Double blind, randomised, placebo controlled, parallel group study.After a single blind placebo run in period, during which (at most) two inhaled corticosteroids dose decreases occurred, qualifying, clinically stable patients were allocated randomly to receive montelukast (10 mg tablet) or matching placebo once daily at bedtime for up to 12 weeks.Setting 23 academic asthma centres in United States, Canada, and Europe.Participants 226 clinically stable patients with chronic asthma receiving high doses of inhaled corticosteroids (113 randomised to montelukast and 113 to placebo).Interventions Every 2 weeks, the inhaled corticosteroids dose was tapered, maintained, or increased (rescue) based on a standardised clinical score. Main outcome measures Last tolerated dose of inhaled corticosteroids.Results Compared with placebo, montelukast allowed significant (P = 0.046) reduction in the inhaled corticosteroid dose (montelukast 47% v placebo 30%; least square mean difference 17.6%, 95% confidence interval 0.3 to 34.8).Fewer patients on montelukast (18 (16%) v 34 (30%) placebo, P = 0.01) required discontinuation because of failed rescue.Conclusions Montelukast reduces the need for inhaled corticosteroids among patients requiring moderate to high doses of corticosteroid to maintain asthma control.