tbuckley/cabot-search huggingface dataset:
ESTROGENS IN THE TREATMENT OF ATHEROSCLEROSIS
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
Phase III randomized study of sorafenib plus doxorubicin versus sorafenib in patients with advanced hepatocellular carcinoma (HCC): CALGB 80802 (Alliance).
Authors: Ghassan K. Abou-Alfa, Donna Niedzwieski, Jennifer J. Knox, Andreas Kaubisch, James Posey, Benjamin R. Tan, Petr Kavan, Rakesh Goel, Philip Edward Lammers, Tanios S. Bekaii-Saab, Vincent Channing Tam, Lakshmi Rajdev, Robin Kate Kelley, Abby B. Siegel, Jennifer Balletti, James J. Harding, Lawrence HOWARD Schwartz, Richard M. Goldberg, Monica M. Bertagnolli, Alan P. Venook
Journal: Journal of Clinical Oncology (2016)

4003 Background: An exploratory analysis of a randomized phase II study in HCC comparing doxorubicin (D) alone to doxorubicin plus sorafenib (D+S) showed a significant improvement in overall survival favoring D+S (JAMA, 2011). The results appeared promising compared to the historic outcomes seen in the pivotal sorafenib (S) trials. CALGB 80802 was designed to determine if D+S improved survival compared to S alone. Methods: Patients with histologically proven advanced HCC, no prior systemic therapy and Child-Pugh A were randomized to receive D 60 mg/m2 every 21 days plus S 400 mg PO twice daily (D+S) or S alone. For bilirubin ≥ 1.3x normal, D and S doses were halved. D was maxed out at 360 mg/m2. The study was stratified by extent of disease (locally advanced; metastatic), the primary endpoint was overall survival (OS); and secondary endpoint progression-free survival (PFS). The final analysis was to occur when 364 events were observed among 480 total patients, with 90% power to detect a 37% increase in median OS (10.7 to 14.7 months; 1-sided α = 0.05). Results: The Alliance DSMB halted the study after accrual of 346 patients (173 on each of D+S and S) when a futility boundary was crossed at a planned interim analysis. With 107 events in each arm, median OS was 9.3 months (95%CI 7.1-12.9) for D+S, and 10.5 months (95% CI 7.4-14.3) for S with a hazard ratio (HR) 1.06 (95% CI 0.8- 1.4) for D+S vs. S. Median PFS was 3.6 (95% CI 2.8-4.6) and 3.2 months (95% CI 2.3-4.1), respectively (HR = 0.90, 95% CI 0.72-1.2). There were 38 deaths on treatment: 18 on D+S and 20 on S. Among these 8 [sepsis (1), dysphagia (1), pneumonia (1), cardiac (2), hepatic failure (2), and not otherwise specified (1)] on D+S, and 3 [fatigue (1), hepatic failure (1), and a secondary malignancy (1)] on S, were at least possibly related to treatment. A maximum grade 3 or 4 only hematologic adverse events (AE) occurred in 37.8% of patients on D+S and 8.1% of patients on S. Non-hematologic AEs were comparable, in 63.6% and 61.5% of patients, respectively. Conclusions: The addition of D to S resulted in higher toxicity and did not improve OS or PFS. The S median OS of about 10 months is consistent with previous reports. NCI Grant U10CA180821 Clinical trial information: NCT01015833.
Epidemic Legionnaires' disease. Airborne transmission down a chimney
Authors: J. D. Band
Journal: JAMA (1981)

Between June 18 and July 9, 1979, Legionnaires' disease (LD) developed in 13 persons who had visited a hotel complex in Wisconsin. All had visited the part of the hotel that contains the restaurants and meeting rooms (building A). Legionnaires' disease occurred in 1% who had been exclusively in the meeting rooms and in 0.1% who had eaten only at the hotel restaurants. Furthermore, 1.5% exposed to meeting room 1 and none of those exposed only to the other meeting rooms had LD.<i>Legionella pneumophila</i>was isolated from water in the cooling tower on top of building A. Located within 5 m downwind of the cooling-tower exhaust, a chimney with an open damper allowed cooling-tower exhaust (as demonstrated by air tracer studies) to enter meeting room 1 via the fireplace. Although cases did not occur after the cooling-tower water was treated by continuous hyperchlorination and the chimney was sealed, a seven-day lag occurred between treatment and elimination of the organism from the tower water. (<i>JAMA</i>1981;245:2404-2407)
Outcomes of Chronic Infection with Hepatitis B Virus
Journal: Annals of Internal Medicine (2001)

Summaries for Patients6 November 2001Outcomes of Chronic Infection with Hepatitis B VirusSearch for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-135-9-200111060-00002 SectionsAboutFull TextPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail What is the problem and what is known about it so far?Hepatitis B is an inflammation of the liver that is caused by a virus. The virus spreads through contact with infected body fluids. Most people who get hepatitis B recover within a few months, but some develop chronic infection. Chronic infection increases one's risk for liver failure and liver cancer. Persons with chronic infection often have viral-related protein substances in their blood (called hepatitis B surface antigens and e antigens) for many years. When e antigen is present, it usually means that the person has very active liver ... Author, Article, and Disclosure InformationAffiliations: The summary below is from the full report titled “Serologic and Clinical Outcomes of 1536 Alaska Natives Chronically Infected with Hepatitis B Virus.” It is in the 6 November 2001 issue of Annals of Internal Medicine (volume 135, pages 759-768). The authors are BJ McMahon, P Holck, L Bulkow, and M Snowball.Summaries for Patients are a service provided by Annals to help patients better understand the complicated and often mystifying language of modern medicine.Summaries for Patients are presented for informational purposes only. These summaries are not a substitute for advice from your own medical provider. If you have questions about this material, or need medical advice about your own health or situation, please contact your physician. The summaries may be reproduced for not-for-profit educational purposes only. Any other uses must be approved by the American College of Physicians-American Society of Internal Medicine. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetailsSee AlsoSerologic and Clinical Outcomes of 1536 Alaska Natives Chronically Infected with Hepatitis B Virus Brian J. McMahon , Peter Holck , Lisa Bulkow , and Mary Snowball Metrics 6 November 2001Volume 135, Issue 9Page: I-50KeywordsAntigensAntiviral therapyChronic hepatitis BHepatitis AHepatitis BHepatitis B surface antigenHepatitis B virusHepatitis EInfectious hepatitisLiver ePublished: 6 November 2001 Issue Published: 6 November 2001 Copyright & PermissionsCopyright © 2001 by American College of Physicians. All Rights Reserved.PDF downloadLoading ...
Electricity in Diseases of the Eye, Ear, Nose and Throat.
Journal: JAMA (1913)

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
Allergy and immunology
Authors: S. C. Bukantz
Journal: JAMA (1990)

The exploration of immunologic mechanisms has entered a new phase, that of molecular biology,<sup>1</sup>resulting in an improved understanding of diseases that arise from immunologic injury. From among the many basic and clinical contributions,<i>Science</i>has selected a "Molecule of the Year," the DNA polymerase, which drives the polymerase chain reaction.<sup>2</sup> The polymerase chain reaction has been used to detect proviral DNA in the peripheral blood mononuclear cells of persons infected with human immunodeficiency virus 1 who are seropositive and virus culture negative. An assay has also been developed to detect human immunodeficiency virus 1 RNA in patients with acquired immunodeficiency syndrome and acquired immunodeficiency syndrome—related complex, which raises the possibility of early detection of human immunodeficiency virus in plasma and serum through gene amplification,<sup>3</sup>of obvious benefit in blood bank screening. The long-term safety and efficacy of zidovudine therapy have been examined in 229 subjects with
Abstract 3113: Regulation of TOR complex 1 by the BRAFV600EMutant determines response and development of resistance to MEK inhibition by trametinib in glioma models
Authors: Fuyang Li
Journal: Cancer Research (2019)

Abstract Pediatric Low-Grade glioma (PLGG) is the most common brain tumor in children. Current treatment protocols, particularly those involving high dose radiation therapy are associated with neurocognitive and neuroendocrine dysfunction. Genomic studies have revealed that PLGG are characterized by activation of the MAPK cascade. Recently, the value of selumetinib, an allosteric inhibitor of MEK1/2 has been demonstrated in PLGG. However, drug resistance will inevitably limit the efficacy. Trametinib is a more potent MEK1/2 inhibitor with better brain penetration than selumetinib. Here we have attempted to identify the mechanism/s of the resistance to trametinib that PLGG developes, and to explore combination treatments that may retard or prevent emergence of trametinib resistance in animal models. In BT-40 (childhood anaplastic astrocytoma with BRAFV600E mutation) xenografts, trametinib caused complete tumor regressions, followed by tumor regrowth at the end of treatment. Trametinib treatment rapidly induced pSTAT3(Y705), that was blocked by the JAK1/2 inhibitor, ruxolitinib. Agaist BT-40 xenografts, ruxolitinib slightly enhanced the antitumor response to trametinib. The combination of trametinib with rapamycin was more active in each xenograft line than either single agent alone and in both subcutaneous and intracranial BT-40 models. In BT-40 xenografts, resistance to trametinib was consistently induced within 3 or 4 6-week cycles of treatment similar to that for the trametinib + ruxolitinib combination. In contrast, resistance to combined trametinib and rapamycin was not developed. Rapamycin prevented emergence of trametinib resistance, but did not reverse resistance to trametinib, once acquired. Inhibition of MAPK signaling by trametinib was similar in parental and trametinib-resistant BT-40 xenografts, however, trametinib reistant tumor cells failed to undergo apoptosis. Cells freshly isolated from trametinib resistant BT-40 xenografts had a higher apoptotic threshhold, whereas cells isolated from BT-40 xenografts after 3 cycles of trametinib + rapamycin, remained equally sensitive to parental BT-40 cells, as determined by BH3 profiling. This study reveals a potential new therapeutic use of rapamycin, preventing emergence of resistance to trametinib. Potentially, addition of rapamycin to MEK inhibitor therapy children with BRAF-driven low-grade glioma may be of value. Citation Format: Fuyang Li. Regulation of TOR complex 1 by the BRAFV600EMutant determines response and development of resistance to MEK inhibition by trametinib in glioma models [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 3113.
Infectious Diseases
Authors: Jerry- D. Smilack
Journal: JAMA (1983)

It has been said that there are two kinds of people: those who believe there are two kinds of people, and those who don't. Editors of infectious diseases textbooks have always had to contend with a similar dualism: should their text be oriented toward a description of syndromes and disease processes (eg, pneumonia and urinary tract infections) or strictly microorganisms? Most recent editors have elected not to make the choice, but to follow both approaches. Sanford and Luby, however, have bucked the trend and have emphasized the microorganism. This volume is the eighth in a series dealing with each subspecialty of internal medicine. The editors have assembled the work of 91 contributors into a compact package of concise, clinically oriented subjects. Except for a few introductory chapters dealing with fever, septic shock, and the like, each is devoted to diseases caused by a specific pathogen, eg,<i>Streptococcus</i>, anthrax bacillus, and
Therapeutic impact and timing of gastrointestinal malignancy genomic profiling: A single-institution experience.
Authors: Kristin Lynn Koenig, Jarred Burkart, Sameh Mikhail, Christina Sing-Ying Wu, Anne M. Noonan, Richard M. Goldberg, Tanios S. Bekaii-Saab, Kristen Keon Ciombor
Journal: Journal of Clinical Oncology (2016)

584 Background: Tumor genomic profiling has become critical in the identification of targeted therapeutic options for patients (pts) with advanced malignancies. Mutational frequencies and their therapeutic importance vary among tumor types. This analysis was undertaken to characterize the landscape of genomic alterations in gastrointestinal (GI) malignancies found in a large academic institutional practice, and to determine the frequency of alteration-specific targeted therapy selection based on genomic profiling. Methods: Adult pts with GI malignancies presenting to the Ohio State University Comprehensive Cancer Center oncology clinics were offered next generation sequencing through FoundationOne testing as part of routine clinical care. Institutional review board approval was obtained to retrospectively analyze results from FoundationOne testing performed between 2012 and 2015. Results: 265 pts with GI malignancies underwent successful genomic profiling. 1205 genomic alterations were found, with an average of 4.5 per tumor (range 0-20); 365 (30%) of these were potentially actionable and most often found in colorectal or gastroesophageal tumors. 14 pts (5.3%) had actionable alterations in MET, CDKN2A/B, FGFR2, KRAS, BRAF, or NF2 that led to enrollment in genotype-directed clinical trials or off label use of targeted therapies beyond standard of care. Pt performance status at the time of genomic alteration identification was a significant factor in precluding genotype-directed therapy. One variant of unknown significance involving FGFR2 identified at initial testing subsequently became actionable and led to pt enrollment on a clinical trial. One pt with rectal cancer was found to have a KRAS wild-type and BRAF mutant primary but KRAS mutant and BRAF wild-type liver metastasis. Conclusions: Genomic profiling of GI malignancies through next generation sequencing is feasible and can lead to genotype-directed therapy selection; however, it should be considered early in the pt’s course to optimize use of targeted therapies through clinical trials. Consideration should be given to serial tumor testing to identify emerging genomic alterations for optimal therapy selection.
WHAT IS A “COMPETENT” PHYSICIAN?
Journal: JAMA (2007)

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
Variation in patient utilities for outcomes of the management of chronic stable angina. Implications for clinical practice guidelines. Ischemic Heart Disease Patient Outcomes Research Team
Authors: R. F. Nease
Journal: JAMA (1995)

<h3>Objective.</h3> —Although practice guidelines sometimes make recommendations based on symptom severity, they rarely account for how patients feel about their symptoms. To investigate the possible importance of patient preferences in treatment of ischemic heart disease, we assessed attitudes toward symptoms in patients with angina pectoris. <h3>Design.</h3> —Case series. <h3>Setting.</h3> —Ambulatory cardiology clinics at two tertiary care medical centers. <h3>Patients.</h3> —A total of 220 subjects were selected from 589 patients with chronic stable angina referred from cardiologists to achieve patient samples balanced for sex, race, and angina severity. <h3>Main Outcome Measures.</h3> —We measured patients' attitudes toward their angina using the rating scale, time trade-off, and standard gamble utility metrics. Reliability of measurements was evaluated by repeating the assessments 2 weeks later on 50 willing patients. <h3>Results.</h3> —While the mean responses followed the expected patterns (those with more severe Canadian Cardiovascular Society scores chose lower utilities), attitudes toward symptoms varied substantially among patients with similarly severe angina. For example, there was a 33% chance that a patient with class II angina had a time trade-off utility that was lower (ie, more bothered by symptoms) than a patient with more severe angina (class III/IV). This variation in utilities was not due to random error in the assessments. <h3>Conclusions.</h3> —Angina patients with similar functional limitation vary considerably in their tolerance for their symptoms, as measured by utilities. Our findings suggest that guidelines for the management of ischemic heart disease should be based on the preferences of the individual patient rather than on symptom severity alone. (<i>JAMA</i>. 1995;273:1185-1190)
Nettleship on the Eye.
Journal: JAMA (1900)

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
Addendum: Recognition of RNA virus by RIG-I results in activation of CARD9 and inflammasome signaling for interleukin 1β production
Authors: Hendrik Poeck, Michael Bscheider, Olaf Gross, Katrin Finger, Susanne Roth, Manuele Rebsamen, Nicole Hannesschläger, Martin Schlee, Simon Rothenfusser, Winfried Barchet, Hiroki Kato, Shizuo Akira, Satoshi Inoue, Stefan Endres, Christian Peschel, Gunther Hartmann, Veit Hornung, Jürgen Ruland
Journal: Nature Immunology (2013)
Indole Production in Hartnup Disease
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
National registry of long-term dialysis patients
Authors: B. T. Burton
Journal: JAMA (1971)

The recently established National Dialysis Registry is an organ of the Artificial Kidney-Chronic Uremia Program of the National Institute of Arthritis and Metabolic Diseases of the National Institutes of Health. At present there are about 5,000 patients in irreversible kidney failure who are kept alive with the aid of long-term dialysis; a small number are awaiting renal transplants. A progressive trend from hospital-based treatment to home dialysis is discernible. The gross annual death rate (based on an observation of less than two years) is approximately 9%. The most common immediate causes of death terminating long-term dialysis are (in order of decreasing importance) cardiac disorders, cerebrovascular disease, and other vascular complications and infections.