tbuckley/cabot-search huggingface dataset:
MEDICAL FALLACIES.
Journal: JAMA (2006)

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 Across the Seas
Authors: E. J. H.
Journal: Annals of Internal Medicine (1966)

Editorials1 June 1966ANNALS Across the SeasE. J. H.E. J. H.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-64-6-1361 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptFrom time to time the American College of Physicians gets requests for free distribution of the ANNALSto hospitals and medical schools abroad that are unable to afford the high cost of subscriptions to even a fraction of currently important journals. Some and perhaps all such needs for the ANNALSmight be met by a redistribution of one kind of "surplus" copies. Some members of the College may regularly see the ANNALSin their hospital libraries or on their partners' desks and hence do not need personal copies. These members might like to have their own copies sent directly to... This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics 1 June 1966Volume 64, Issue 6Page: 1361-1361KeywordsLibraries ePublished: 1 December 2008 Issue Published: 1 June 1966 PDF downloadLoading ...
Endpiece: Every knock
Authors: Fred Charatan
Journal: BMJ (2003)

AIMS--To determine the value of the red cell distribution width (RDW) and erythrocyte zinc protoporphyrin (ZPP) concentration in discriminating between iron deficiency, and beta and alpha thalassaemia in a mixed urban Asian population. METHODS--The RDW and ZPP concentrations were measured in 1412 subjects attending for outpatient phlebotomy, with classification into diagnostic groups on the basis of haemoglobin, mean cell haemoglobin, ferritin, HbA2 and haemoglobin electrophoresis. RESULTS--Non-parametric 95% reference ranges for RDW were 11.7-15.7% and for ZPP 38-104 mumol/mol haem. Both RDW and zinc protoporphyrin rose with increasing severity of iron deficiency, but were also raised in significant numbers of subjects with beta and probable alpha thalassaemia. CONCLUSIONS--Measurements of RDW and ZPP do not differentiate between alpha or beta thalassaemia trait and moderate degrees of iron deficiency (hypochromasia without anaemia). ZPP is a more accurate indicator of iron deficiency than RDW and concentrations above 150 mumol/mol haem strongly suggest iron deficiency, usually with anaemia, rather than thalassaemia.
Books Received
Journal: JAMA (1985)

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
A Pilot Study Evaluating the Safety and Efficacy of AMD3100 for the Mobilization and Transplantation of HLA-Matched Sibling Donor Hematopoietic Stem Cells in Patients with Advanced Hematological Malignancies.
Authors: Steven M. Devine, Leslie Andritsos, Laura Todt, Ravi Vij, Jesper Bonde, David Hess, Jan Nolta, Dan Link, Gary Bridger, Gary Calandra, John F. DiPersio
Journal: Blood (2005)
MUTANT IDH1-DRIVEN CELLULAR TRANSFORMATION INCREASES RAD51-MEDIATED HOMOLOGOUS RECOMBINATION AND TEMOZOLOMIDE (TMZ) RESISTANCE.
Authors: R. O. Pieper, S. Ohba, J. Mukherjee
Journal: Neuro-Oncology (2014)

BACKGROUND: IDH1 mutation is noted in roughly 75% of all lower-grade glioma and is considered to be an early and driving event in the genesis of these tumors. In clinical studies IDH1 mutation correlates with increased overall survival, progression-free survival, and upfront response to TMZ implying that mutant IDH1 directly contributes to drug sensitivity. IDH1 mutant gliomas, however, have a different underlying biology than comparable IDH1 WT glioma, complicating any analysis of the contribution of IDH1 mutation to drug sensitivity. To more accurately determine if and how IDH1 mutation alters drug sensitivity, we employed a system widely for the study of cellular transformation and IDH biology. In this system normal human astrocytes immortalized by introduction of virally-encoded E6, E7 and hTERT can be transformed by additional expression of oncogenic H-Ras or by mutant IDH1, the latter of which induces epigenetic changes similar to those noted in lower-grade glioma. We therefore used these cells to determine if mutant IDH1 expression and/or the transformative events it sets in place were sufficient to alter TMZ sensitivity. METHODS: E6/E7/hTERT-immortalized, untransformed human astrocytes, and the same cells transformed by prior introduction of oncogenic V12H-Ras, were infected with lentiviral constructs encoding WT or mutant (R132H) IDH1, then monitored for transformation status and, following TMZ exposure (100 uM, 3hrs), for DNA damage and repair, cell cycle response, and TMZ sensitivity. RESULTS: The TMZ-sensitive immortalized, untransformed parental cells exhibited DNA damage (H2AX foci) and a prolonged G2 cell cycle arrest that began 2 days after TMZ exposure and persisted for 5 days. The same cells transformed by mutant IDH1 exhibited the same levels of initial DNA damage and cell cycle arrest as controls, although both events resolved significantly faster in the IDH1 mutant cells in association with increased clonagenic survival. The increases in DNA damage processing, cell cycle progression, and clonagenicity were unique to cells transformed by mutant IDH1, and were not noted following introduction of mutant IDH1 into Ras-transformed or established GBM cells. The changes were, however, associated with increased homologous recombination (HR) and could be reversed by the genetic suppression of Rad51, the rate limiting protein in HR. CONCLUSIONS: Mutant IDH1 drives a unique set of transformative events that indirectly enhance HR and increase repair of TMZ-induced DNA damage and TMZ resistance. Inhibitors of HR may therefore be a viable means to further enhance TMZ response in IDH1 mutant glioma. SECONDARY CATEGORY: Preclinical Experimental Therapeutics.
Software
Authors: David Behar
Journal: JAMA (1988)

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
Sensitive Periods of Susceptibility to Auditory Trauma in Mammals
Authors: James C. Saunders, Chia-Shong Chen
Journal: Environmental Health Perspectives (1982)

Evidence is presented to support the hypothesis that the cochleae of young animals are more susceptible to auditory trauma than the cochleae of the adult. A sensitive period of heightened susceptibility to acoustic trauma from noise exposure has been demonstrated in three mammalian species. The cochlear pathology associated with this trauma is severe damage to the outer hair cell system. Abnormal growth of auditory evoked responses recorded in central auditory nuclei accompanies the receptor damage during the sensitive period. There is evidence of a similar sensitive period of susceptibility to cochlear insult from ototoxic drugs. The time frame of the sensitive period may be different for drug or noise insult to the cochlea, but the principal pathology of outer hair cell loss remains the same in both cases. The implication of these sensitive periods to auditory trauma, for human development is considered.
Acute Reduction in Intracranial Pressure as a Mechanism of Postural Syncope
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
Essentials of Refraction and of Diseases of the Eye.
Journal: JAMA (1901)

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
Caffeine during pregnancy: grounds for concern?
Authors: B. Eskenazi
Journal: JAMA (1993)

Is caffeine consumption safe during pregnancy? Caffeine, the most widely used psychotropic drug, is consumed by at least 75% of pregnant women via caffeinated beverages.<sup>1</sup>In spite of its widespread use, the safety of this habit during pregnancy is unresolved. See also p 2940. In the last year,<i>JAMA</i>has published two excellent studies that assessed the safety of caffeine consumption during pregnancy. The conclusions of these studies somewhat conflict. In February, Mills and colleagues,<sup>2</sup>in a prospective cohort study of 431 pregnant women, reported that moderate caffeine consumption of less than 300 mg/d (or about three cups of coffee) did not increase the risk for spontaneous abortion (SAB), intrauterine growth retardation (IUGR), or microcephaly. Although the heavy consumption group was small and the power limited, caffeine consumption above 300 mg/d did appear to be related to IUGR.<sup>3,4</sup>In this issue of<i>JAMA</i>, Infante-Rivard and colleagues<sup>5</sup>
Dose dense gemcitabine/epirubicin (GE) followed sequentially by dose dense docetaxel (Doc) as primary systemic therapy (PST) of patients (pts) with early breast cancer (BC): First results of a phase I/II trial
Authors: A. Schneeweiss, C. Rudlowski, H.-P. Sinn, F. Beldermann, D. Von Fournier, G. Bastert
Journal: Journal of Clinical Oncology (2004)

734
P44.01 WITHDRAWN
Authors: T Umeda, H Minemura, Y Tanino, K Hirai, T Koizumi, T Nikaido, Y Sato, R Togawa, T Kawamata, N Watanabe, H Tomita, M Rikimaru, J Morimoto, Y Suzuki, M Uematsu, N Fukuhara, A Fukuhara, J Saito, K Kanazawa, Y Shibata
Journal: Journal of Thoracic Oncology (2021)
From the authors
Authors: R. Pellegrino, G. Viegi, P. Levy, V. Brusasco
Journal: European Respiratory Journal (2008)

values in Europe are still those implemented by the European Coal and Steel Community (ECSC) [2] and the ERS [3].The ATS/ERS Task Force has not commented on newer reference values for spirometry derived from the Swiss Study on Air Pollution and Lung Disease in Adults (SAPALDIA) [4, 5].
Barbiturates and fractures.
Journal: BMJ (1977)

sented, with 4 ' overall and none in the 2 pm-10 pm group.This at first sight implies that barbiturates protect against daytime fractures, but this would be ridiculous.Non- barbiturate hypnotics were under-represented in the nocturnal group and over-represented in the day groups with 216 cases (79 %).If the
Long-term corrections of bilirubin glucuronidation defect in Gunn rats by ex vivo gene therapy using conditionally immortalized autologous hepatocytes . Dept. of Medicine, Marion Bessin Liver Research Center, Albert Einstein College of Medicine, Bronx, NY; 2Dept. of Transplantation Surgery, University of Nebraska, Omaha, NE; 3Dept. of Gastroenterology and Liver Diseases, Academic Medical Center, Amsterdam, The Netherlands
Journal: Hepatology (1995)
Community Hygiene
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
Effects of methylprednisolone on human myeloid leukemic cells in vitro
Authors: Namık Özbek, Esra Erdemli, Gönül Hiçsönmez, Hamza Okur, Meral Tekelioğlu
Journal: American Journal of Hematology (1999)

We have demonstrated previously that high-dose methylprednisolone treatment induces differentiation and apoptosis of leukemic cells in patients with different morphological subtypes of acute myeloblastic leukemia (AML) in vivo.In the present study, we investigated the in vitro effects of high (10 -3 M) and low (10 -6 M) concentrations of methylprednisolone (MP) on freshly isolated bone marrow leukemic cells from nine newly diagnosed patients with AML by light and electron microscopy (EM) and agarose gel electrophoresis.A marked increase in MP-induced apoptosis of leukemic cells, with a maximum effect at 24 hr of exposure to both low and high concentrations of MP (10 -6 M and 10 -3 M), was demonstrated by light microscopy in cultures of four (three with AML-M1 and one with AML-M7) of the nine patients.In three cases, the increase in the number of apoptotic cells induced by high-concentration MP was approximately twice that observed when the lower concentration was used.A few apoptotic cells were detected in the cultures from the other five patients.However, a typical DNA ladder pattern of apoptosis was observed on gel electrophoresis of MP-treated leukemic cells from one patient (AML-M1) after 2 hr of incubation with both high-and low-MP concentrations.In two patients, a nonspecific DNA smear was observed only when high-concentration MP was used.The increase in differentiated leukemic cells induced by MP was also dose dependent, and was observed in cultures from all but one patient.Morphological features of apoptosis and differentiation were also confirmed by EM studies.The results of the present study, together with our previous clinical experience, suggest that MP, especially at high doses, could have a significant role in the treatment of some AML patients by inducing apoptosis and differentiation of leukemic cells.Am.
Correction to: PIK3CA mutations are associated with reduced pathological complete response rates in primary HER2-positive breast cancer: pooled analysis of 967 patients from five prospective trials investigating lapatinib and trastuzumab
Authors: S. Loibl, I. Majewski, V. Guarneri, V. Nekljudova, E. Holmes, E. Bria, C. Denkert, C. Schem, C. Sotiriou, S. Loi, M. Untch, P. Conte, R. Bernards, M. Piccart, G. von Minckwitz, J. Baselga
Journal: Annals of Oncology (2018)

Ann Oncol 2016; 27: 1519–1525 (doi: 10.1093/annonc/mdw197) In the original article, the following funding information was omitted: This research was funded in part through the NIH/NCI Cancer Center Support Grant P30 CA008748. This has now been added. PIK3CA mutations are associated with reduced pathological complete response rates in primary HER2-positive breast cancer: pooled analysis of 967 patients from five prospective trials investigating lapatinib and trastuzumabAnnals of OncologyVol. 27Issue 8PreviewThe predictive value of PIK3CA mutations in HER2 positive (HER2+) breast cancer treated with neoadjuvant anti-HER2 and chemotherapy has been reported, but the power for subgroup analyses was lacking. Full-Text PDF Open Archive
Phase 1 with expansion cohorts in a study of NEO-201 in adults with chemo-resistant solid tumors.
Authors: Maria Pia Morelli, Justin M. David, Nicole D. Houston, Stan Lipkowitz, Jung-min Lee, Alexandra Dos Santos Zimmer, Farah Z. Zia, Irene Ekwede, Erin Nichols, Mira Pavelova, Rebecca Trupp, Stephen M. Hewitt, Massimo Fantini, Philip M. Arlen, Kwong Y. Tsang, Christina M. Annunziata
Journal: Journal of Clinical Oncology (2019)

TPS2645 Background: NEO-201 is a novel humanized IgG1 monoclonal antibody (mAb) generated against the Hollinshead allogenic colorectal cancer vaccine platform. Briefly, tumor-associated antigens (TAA) derived from tumor membrane fractions pooled from colorectal cancer surgical specimens were screened for delayed-type hypersensitivity and evaluated in clinical trials. The original vaccine was used to generate monoclonal antibodies, one of which is NEO-201. In preclinical data generated in our laboratory, we have demonstrated that NEO-201 exert anti-tumor activity by natural killer (NK)-mediated antibody-dependent cytotoxicity (ADCC) against several tumor type including colorectal and pancreatic cancer models (Fantini, et al. 2018). We have identified NEO-201 antigen as a glycosylated form of CEACAM-5 and -6, which is expressed by tumor tissue but is not present in the surrounding healthy tissue (David, et al. 2018). This could result in a specific anti-tumor activity without significant normal tissue toxicity. Nevertheless, toxicity was further assessed in non-human primates and transient neutropenia was the only adverse event observed. Based on this data we designed a first in human phase I trial to evaluate the safety, maximum-tolerated dose (MTD), pharmacokinetics (PK) and pharmacodynamics (PD) of the humanized monoclonal antibody NEO-201. Methods: This is a first-in-human phase 1 study with expansion cohort to determine the maximum tolerated dose (MTD) and recommended phase II dose (RP2D) of NEO-201 in adults with advanced solid tumors that have high likelihood pof expression NEO201 antigen and have progressed to standard of treatments and have a PS0-2 ECOG. Study design is a classic Fibonacci (3+3) dose escalation, with a cohort expansion at the MTD. NEO-201 is administered intravenously every two weeks, and four different dose levels will be explored (DL1 = 1mg/kg, DL2 = 2mg/kg, DL3 = 4mg/kg and DL4 = 6mg/kg). No intra-patient dose escalation is allowed. Patients will be evaluated for safety every two weeks, with weekly laboratory testing, according to CTCAEv4.0. and with a DLT window of 28 days (cycle 1). Response will be assessed every 8 weeks (2 cycles of treatment) according to RECISTv1.1. Additionally, biological samples will be collected to understand NEO-201 pharmacokinetic, the effect on the immune process and their correlation with treatment toxicity and response. As of February 2019 we have completed enrollment in the first DL and are evaluating for DLT. Clinical trial information: NCT03476681.