tbuckley/cabot-search huggingface dataset:
SURVEY OF EXECUTIVE GOVERNMENT WITH VIEW TO REORGANIZATION
Journal: JAMA (1920)

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
Derivation and validation of a clinical diagnostic model for chlamydial cervical infection in university women
Authors: B. A. Johnson
Journal: JAMA (1990)

We developed and prospectively tested a logistic regression model for chlamydial cervical infection. Study subjects included 2271 women receiving gynecologic care in our student health clinic. Clinical data were collected in a standardized fashion. We identified cell culture—isolated Chlamydia trachomatis from 133 (9%) of 1458 subjects in the derivation set and 73 (10%) of 729 subjects in the validation set. Model variables included a new sexual partner within 2 months or more than one sexual partner within 6 months; cervical ectopy; cervical friability; at least 20 polymorphonuclear leukocytes per high-power field in cervical secretions; white blood cells in vaginal secretions; and use of an antibiotic active against C trachomatis within a month. This model can distinguish women with low, medium, and high risks of chlamydial infection (on derivation set: receiver operating characteristic curve area, 0.710; SE, 0.026; on validation set: area, 0.698; SE, 0.035) using simple clinical information obtained in the office. (<i>JAMA</i>. 1990;264:3161-3165)
Randomised phase III trial of enzalutamide in androgen deprivation therapy (ADT) with radiation therapy for clinically localised, high risk, or node-positive prostate cancer: ENZARAD (ANZUP 1303).
Authors: Scott Williams, Ian D. Davis, Christopher Sweeney, Martin R. Stockler, Andrew James Martin, Wendy Hague, Xanthi Coskinas, Sonia Yip, Emily Tu, Nicola Jane Lawrence, Ray McDermott, Paul J. Kelly, Olwyn Deignan, Simon Hughes, Valerie Fonteyne, Bertrand F. Tombal, Paul L. Nguyen
Journal: Journal of Clinical Oncology (2017)

TPS5096 Background: Adjuvant ADT with an LHRH analog (LHRHA) given before, during and after radiotherapy (RT) is standard of care for high risk localised prostate cancer (PC). Enzalutamide is more effective in metastatic disease than conventional non-steroidal anti-androgens (NSAA). We hypothesize that addition of enzalutamide to adjuvant ADT and RT will improve outcomes. The aim is to determine the efficacy of enzalutamide compared with NSAA as part of adjuvant ADT with LHRHA in men planned for RT for localized high risk or node-positive PC. Methods: DESIGN: Open label, randomised, phase 3 trial including ANZ, USA, UK, Ireland and Europe. ENDPOINTS: OS (primary), cause-specific survival, PSA PFS, clinical PFS, time to subsequent hormonal therapy, time to castration-resistant disease (PCWG2 criteria), metastasis free survival, adverse events and HRQOL. Tertiary objectives: identification of prognostic/predictive biomarkers from archival tumour tissue and 4 serial fasting bloods. 800 target participants with 5.5 yrs minimum follow-up. 80% power to detect 33% reduction in the hazard of death assuming 5-year survival rate of 76% amongst controls. TREATMENT: Participants are randomised 1:1 to enzalutamide 160mg daily for 24 months versus conventional NSAA for 6 months. All participants receive LHRHA for 24 months and RT starting after week 16. RT delivered as 78Gy in 39 Fx or 46Gy in 23 Fx plus brachytherapy (nodal RT optional for N0, mandatory for N1). ASSESSMENTS: Baseline, then every 8 weeks until year 2, then 3-4 monthly until year 5, 6-monthly until year 7, then annually. CT/MRI and bone scan at baseline, PSA progression, 6 monthly until re-initiation of ADT, when PCWG2 criteria for CRPC are met and then 3 monthly until evidence of metastases. As of 1 st February 2017, 55 of 67 sites open with 398 patients recruited. EORTC sites expected to open from Quarter 1 2017. ENZARAD is an investigator-initiated cooperative group trial led by ANZUP Cancer Trials Group with funds and product from Astellas. ANZUP is supported by Cancer Australia and previously CI NSW. ClinicalTrials.gov: NCT02446444, ANZCTR: ACTRN12614000126617 Clinical trial information: NCT02446444.
Growth factors in breast cancer
Authors: R. B. Dickson
Journal: Endocrine Reviews (1995)

A. Hormonal control of mammary development, proliferation, and lactational defferentation DEVELOPMENT of the normal breast, carcinogenesis of its epithelium breast, and progression of breast cancer are regulated by hormonal factors. The best defined of these factors are the endocrine steroids, peptides, and other molecules produced by the secretory cells of the ovaries, pituitary, endocrine pancreas, thyroid, and adrenal cortex. After their initial interaction with either nuclear or cell surface receptors, these hormones regulate cellular function. In addition, normal and malignant mammary tissues are able to synthesize locally acting hormone-like substances. One class of these factors is known as the paracrine hormones, factors released by one cell type which then modulate the function of neighboring cells of the same or different mammary cell type. A recently described variation on this theme is the class of juxtacrine factors. These factors are growth-regulatory molecules that remain exposed on a cell surface and modulate adjacent cells by contact. A third general class of local factors is that of the autocrine (or intracrine) hormones, soluble molecules synthesized by one cell type that act back on the same cell type through surface or intracellular receptors. It is of considerable interest that after their synthesis, polypeptide factors may be routed either to a cell surface receptor or to a nuclear site.
BST-236
Authors: Tsila Zuckerman, Ron Ram, Ruth Ben Yakar, Stela Gengrinovitch, Liat Flaishon, Jacob Rowe
Journal: Journal of Clinical Oncology (2017)

e18520 Background: Cytarabine, the first-line treatment for acute myeloid leukemia (AML), is associated with severe toxicity and high treatment-related mortality (TRM), especially in older patients. Hence, while AML incidence increases with age, advanced age and comorbidities limit cytarabine administration. BST-236 is a new cytarabine pro-drug, enabling delivery of high dose cytarabine to leukemia cells with lower systemic exposure to the free drug. The aim of this study was to evaluate the safety and optimal BST-236 dose in acute leukemia patients. Methods: A Phase I/IIa prospective open label study enrolled adult relapsed/refractory or newly-diagnosed acute leukemia patients. Patients are enrolled into 6 BST-236 escalating-dose cohorts (0.3 – 6 g/m 2 /d). Treatment was administered as 1-hour daily infusion for 6 days. To date, 18 patients, median age 77 (27-90), were treated with up to 4.5 g/m 2 /day: 6 relapsed/refractory AML patients, median age 64 (27-81), and 12 newly-diagnosed, unfit for standard chemotherapy patients (7 secondary AML; 5 de novo AML/ALL), median age 79 (70-90). Results: BST-236 treatment was well-tolerated. Only 6 SAEs were assessed as possibly/probably related to BST-236, all “on-target” hematological toxicity events or bacterial infections. The 8-weeks TRM (including from disease progression) in the newly-diagnosed population was 16%. No neurological events or &gt; grade 2 typical cytarabine events such as mucositis, diarrhea, or alopecia were reported during treatment or within 30 days of follow up. Response to the treatment was observed in 6 of the 12 newly-diagnosed patients, including 4 complete remissions (CR), with increased overall survival (OS). No response was reached in the relapse/refractory patients. Conclusions: BST-236 is safe and very well tolerated, enabling delivery of high dose cytarabine to old patients, resulting in overall response and CR rates of 50% and 33%, respectively and increased OS. Notably, 67% of the responding patients had secondary AML, refractory to hypomethylating agents. A phase II study is planned to confirm these encouraging results. Clinical trial information: NCT02544438.
Notes on Pathological and Operative Obstetrics.
Authors: J Human, Physiology By, C Douglas, F John', J Priestly, Christopher Welch
Journal: JAMA (1925)

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
How to Organize Group Health Plans
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 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
PHENOCOLL HYDROCHLORIDE AS A LOCAL APPLICATION.
Journal: JAMA (1893)

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
Underdosing the Antidote for Acetaminophen
Authors: Martin J. Smilkstein
Journal: JAMA (1993)

<h3>To the Editor.</h3> —We would like to inform your readers of a disturbing pattern in the treatment of acetaminophen overdoses. The Oregon Poison Center serves a population of 2.5 million people and, like all poison centers, it frequently deals with acetaminophen overdoses. In the last 6 months we have noted three instances in which physicians treating patients with acetaminophen overdoses discontinued acetylcysteine therapy on the basis of serial acetaminophen assays and did not complete the standard course of treatment. When questioned, they stated that the package insert recommended cessation of acetylcysteine therapy when acetaminophen levels were no longer detectable. We believe that this potentially dangerous practice is the result of ambiguous wording. The outcomes for these patients are unknown because after hospital discharge they were not available for follow-up. The package inserts for at least two available acetylcysteine preparations (Mucosil and Mucomyst) state: "The maintenance dose is then repeated at
Atezolizumab + bevacizumab versus sorafenib in patients with unresectable hepatocellular carcinoma: safety results from the Phase III IMbrave150 study
Authors: Michel Ducreux, Andrew Zhu, Shukui Qin, Masafumi Ikeda, Tae-You Kim, Ho Yeong Lim, Masatoshi Kudo, Valeriy Breder, Philippe Merle, Ahmed Kaseb, Daneng Li, Wendy Verret, Zhen Xu, Sairy Hernandez, Juan Liu, Hui Shao, Chen Huang, Ann-LII Cheng, Richard Finn, Peter Galle
Journal: Journal of Hepatology (2020)
Use of Arterenol in the Treatment of Patients with Myocardial Infarction Complicated by Collapse
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
Annals of Thoracic Surgery, Boston
Journal: JAMA (1970)

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
Molecular characterization and dynamics of hepatitis C virus replication in human fetal hepatocytes infected in vitro.
Authors: S Iacovacci
Journal: Hepatology (1997)

The molecular features of hepatitis C virus (HCV) replication in human fetal hepatocytes (HFHs) were addressed in this study. Using a competitive reverse-transcription polymerase chain reaction (RT-PCR) assay for the quantitation of HCV-RNA molecules, the highest level of viral replication was detected 30 days' postinfection. At this time point, viral particles of 41 to 45 nm in diameter accumulated in the cell cytoplasm. Their density in cell extracts and culture medium was distributed between heavy (1.180-1.360 g/cm3) and light fractions (1.105-1.050 g/cm3) of a sucrose gradient, while, in the serum inoculum, they had a positive fraction at 1.180 g/cm3. In infected HFHs, minus-strand HCV RNA was observed in fractions displaying a sedimentation coefficient of 28 S to 18 S, while plus-strand HCV RNA showed a peak restricted to the 21 S fraction; the HCV RNA of serum inoculum had a sedimentation coefficient of 38 to 40 S, which revealed the presence of HCV RNA of unique positive polarity. The 21 S RNA fraction of cell extracts was resistant to 20 minutes of RNase I digestion, while the same incubation time totally inactivated a comparable amount of HCV RNA purified from the serum inoculum, revealing the presence of completely and/or partially double-stranded HCV-RNA molecules in the infected cells. Detection in HFHs of replicative forms and replicative intermediates suggests that the dynamic profile of HCV replication in these cells is similar to that described in other flaviviruses. (Hepatology 1997 Nov;26(5):1328-37)
Inactivation of MAP kinase signalling in Myc transformed cells and rescue by LiCl inhibition of GSK3.
Authors: Osama Al-Assar, Dorothy H Crouch
Journal: Molecular Cancer (2005)

c-Myc oncogene is an important regulator of cell cycle and apoptosis, and its dysregulated expression is associated with many malignancies. Myc is instrumental in directly or indirectly regulating the progression through the G1 phase and G1/S transition, and transformation by Myc results in perturbed cell cycle. Also contributory to the control of G1 is the Ras effector pathway Raf/MEK/ERK MAP kinase. Together with GSK3, ERK plays an important role in the critical hierarchical phosphorylation of S62/T58 controlling Myc protein levels. Therefore, our main aim was to examine the levels of MAPK in Myc transformed cells in light of the roles of ERK in cell cycle and control of Myc protein levels. We found that active forms of ERK were barely detectable in v-Myc (MC29) transformed cells. Furthermore, we could only detect reduced levels of activated ERK in c-Myc transformed cells compared to the non-transformed primary chick embryo fibroblast cells. The addition of LiCl inhibited GSK3 and successfully restored the levels of ERK in v-Myc and c-Myc transformed cells to those found in non-transformed cells. In addition, LiCl stabilised Myc protein in the non-transformed and c-Myc transformed cells but not in v-Myc transformed cells. These results can provide an important insight into the role of MAPK in the mechanism of Myc induced transformation and carcinogenesis.
Erratum: Capacitively coupled arrays of multiplexed flexible silicon transistors for long-term cardiac electrophysiology
Authors: Hui Fang, Ki Jun Yu, Christopher Gloschat, Zijian Yang, Enming Song, Chia-Han Chiang, Jianing Zhao, Sang Min Won, Siyi Xu, Michael Trumpis, Yiding Zhong, Seung Won Han, Yeguang Xue, Dong Xu, Seo Woo Choi, Gert Cauwenberghs, Matthew Kay, Yonggang Huang, Jonathan Viventi, Igor R. Efimov, John A. Rogers
Journal: Nature Biomedical Engineering (2017)
Heart Failure
Authors: Audrey Wu
Journal: Annals of Internal Medicine (2018)

Letters20 November 2018Heart FailureAudrey Wu, MDAudrey Wu, MDUniversity of Michigan, Ann Arbor, Michigan (A.W.)Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/L18-0464 SectionsAboutFull TextPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail IN RESPONSE:I agree with Dr. Trainor and colleagues that recognizing and managing iron deficiency in patients with CHF is important. Given the limited space allotted for my article, I gave preference to therapies or interventions that are class I recommendations (for example, guideline-directed medical therapy with angiotensin-converting enzyme inhibitors or β-blockers), especially those with a definitive effect on survival. I also included therapies that did not meet this criterion but have long been and still are widely used in the treatment of heart failure (particularly digoxin and diuretics). In addition, I discussed practices that are not definitively associated with ...References1. Yancy CW, Jessup M, Bozkurt B, Butler J, Casey DE, Colvin MM, et al. 2017 ACC/AHA/HFSA focused update of the 2013 ACCF/AHA guideline for the management of heart failure: a report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines and the Heart Failure Society of America. Circulation. 2017;136:e137-61. [PMID: 28455343] doi:10.1161/CIR.0000000000000509 CrossrefMedlineGoogle Scholar2. Ponikowski P, Voors AA, Anker SD, Bueno H, Cleland JGF, Coats AJS, et al; ESC Scientific Document Group. 2016 ESC guidelines for the diagnosis and treatment of acute and chronic heart failure: the Task Force for the Diagnosis and Treatment of Acute and Chronic Heart Failure of the European Society of Cardiology (ESC) developed with the special contribution of the Heart Failure Association (HFA) of the ESC. Eur Heart J. 2016;37:2129-200. [PMID: 27206819] doi:10.1093/eurheartj/ehw128 CrossrefMedlineGoogle Scholar Author, Article, and Disclosure InformationAffiliations: University of Michigan, Ann Arbor, Michigan (A.W.)Disclosures: The author has disclosed no conflicts of interest. The form can be viewed at www.acponline.org/authors/icmje/ConflictOfInterestForms.do?msNum=M18-0070. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetailsSee AlsoHeart Failure Audrey Wu Heart Failure Róisín Trainor , Eamon P. McCarron , Shiva Sreenivasan , and Monica Monaghan Metrics Cited byHierro e insuficiencia cardiacaIron and heart failure 20 November 2018Volume 169, Issue 10Page: 738KeywordsDisclosureDiureticsEjection fractionExerciseExercise therapyHeart failureIron deficiencyIron deficiency anemiaQuality of lifeTreatment guidelines ePublished: 20 November 2018 Issue Published: 20 November 2018 Copyright & PermissionsCopyright © 2018 by American College of Physicians. All Rights Reserved.PDF downloadLoading ...