tbuckley/cabot-search huggingface dataset:
A first-in-human, first-in-class phase I trial of the anti-CD47 antibody Hu5F9-G4 in patients with advanced cancers.
Authors: Branimir I. Sikic, Sujata Narayanan, A. Dimitrios Colevas, Sukhmani Kaur Padda, George A. Fisher, Dana Supan, Heather A. Wakelee, Rhonda Aoki, Mark D. Pegram, Victor Manuel Villalobos, Jie Liu, Mark Chao, Jens-Peter Volkmer, Ravindra Majeti, Irving L Weissman
Journal: Journal of Clinical Oncology (2016)

3019 Background: Hu5F9-G4 is a humanized monoclonal antibody that binds to CD47 and blocks its anti-phagocytic "don't-eat-me" signal, leading to tumor phagocytosis and cross-presentation to T cells. CD47 is highly expressed on red blood cells (RBCs) and many human cancers, and less on normal tissues. Inhibition of CD47-SIRPα signaling by Hu5F9-G4 has broad antitumor activity in human tumor xenografts. In primate toxicology, Hu5F9-G4 caused a transient anemia that was mitigated by a single low Priming Dose enabling subsequent higher Maintenance Doses. Methods: Adults with solid tumors were enrolled in this two part dose-escalation study: Part A to determine the optimal Priming Dose and Part B to determine the optimal Maintenance Dose. Primary objectives were to assess safety and tolerability; secondary objectives were to assess PK and pharmacodynamics (PD). CD47 receptor occupancy was evaluated as a PD marker on peripheral blood RBCs. Results: To date, 16 patients have been enrolled, 11 in Part A and 5 in Part B. In Part A, 0.1, 0.3, and 1 mg/kg doses were well-tolerated. 2/2 pts at 3 mg/kg had G3 DLTs: G3 abdominal pain; and G1 RBC hemagglutination [H] with G2 headache. The 1 mg/kg dose resulted in a mean RBC CD47 receptor occupancy of 91% ± 3% [95% CI 86 – 93%], indicating target saturation with no G3 anemia, and was selected as the Priming Dose. In Part B, the 1 mg/kg Priming Dose followed by 3 mg/kg Maintenance Dose was well tolerated. The study is ongoing with the current cohort at 1 mg/kg followed by 10 mg/kg weekly. Hu5F9-G4-related AEs include anemia (11 G1, 5 G2), hyperbilirubinemia (5 G1, 3 G2, 1 G3), headache (9 G1, 1 G2), H on peripheral blood smears (9 G1), nausea (3 G1), and retinal toxicity on serial retinal imaging (1 G2 cotton wool spot). Most adverse events were associated with the Priming Dose and were reversible. Mean peak Cmax levels were 78 ± 32 μg/mL on the 3 mg/kg Maintenance Dose. Two patients (adenoid cystic ca) receiving weekly doses in Part A (0.1 mg/kg and 1 mg/kg) had stable disease for 16 and 8 months on continuous weekly drug dosing, respectively. Conclusions: Hu5F9-G4 was well tolerated at 3 mg/kg weekly, with a 1 mg/kg Priming Dose. No G3 anemia has occurred. Testing of higher Maintenance Doses is ongoing. Clinical trial information: NCT02216409.
Psychiatric illness among British Afro-Caribbeans
Authors: R. Littlewood, M. Lipsedge
Journal: BMJ (1988)

Healthy citiesWe are concerned lest the letter by Drs F L R Williams and 0 H Lloyd (14 May, p 1399) deflects attention from the main aim of the Healthy Cities project, which is a major opportunity for health authorities, district councils, regional authorities, and all who work with populations in a social or medical context to come together to improve the health of the community.The aim is to achieve measurable reductions in morbidity and mortality.Populations exhibit considerable heterogeneity of lifestyle, and this allows the prospect of success in an international project."Health for all" is relevant to everyone, but comparison between large urban areas and small towns can be mis- leading.The interpretation of comparative health statistics for towns and cities of widely different populations requires caution.Professor Martin J Gardner and Mr Douglas G Altman (30 April, p 1210) emphasise the importance of giving confidence intervals when rates are reported.Excesses of mortality in small areas, therefore, may not mean what they seem.Even if a town is at the top of a league table once, or even twice, this may not be of significance.Drs Williams and Lloyd state that over the period 1979-83 Glasgow had an excess mortality (compared with Scotland as a whole) of 15%.This statistic conceals the fact that the 20% of the population of Glasgow living in the most dis- advantaged areas has an excess mortality of 48%, whereas the 20% living in the least disadvantaged areas has a standardised mortality rate 8% below that of Scotland.In fact, the most disadvantaged communities in Glasgow have standardised mortality rates up to 70% greater than those for Scotland.The publication of data for Glasgow as a whole, rather than for its constituent communities, obscures this fact.It is, therefore, inappropriate to compare cities the size of Glasgow with smaller communities without recognising such internal variations.
THE BEHAVIOR OF ETHER IN THE BODY
Journal: JAMA (1924)

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
Methoxyflurane Nephrotoxicity
Authors: Michael J. Cousins
Journal: JAMA (1973)

Dose-related abnormalities in renal function occurred in ten of 18 patients following administration of methoxyflurane (Penthrane) with the usual anesthetic adjuvants. Eight control patients anesthetized with halothane (Fluothane) showed no abnormalities in renal function. Subclinical toxicity occurred following methoxyflurane at minimum alveolar concentration (MAC) for 2.5 to 3 hours, that is 2.5 to 3 MAC hours (serum inorganic fluoride, &gt;50 micromols/liter), while clinical toxicity was present in all patients at dosages greater than five MAC hours (serum inorganic fluoride, &gt;90 micromols/liter). Superimposed on the dose-response relationship were other factors that probably increased nephrotoxicity. These were as follows: individual variations in metabolism of methoxyflurane; increased sensitivity to the nephrotoxic effects of inorganic fluoride; presence of enzyme induction; and interaction of methoxyflurane with other nephrotoxic drugs. The use of methoxyflurane in clinical anesthesia should be restricted to situations where it offers specific advantages and where dosages less than 2.5 MAC hours can be attained.
Programma de Resuscitation Cardiac in Morte Subite a Causa de Morbo del Arteria Coronari
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
Erratum
Journal: JNCI Journal of the National Cancer Institute (2008)

Some of the age-specifi c rates for invasive breast cancer, h 1 ( t ), were given on page 1786 and in a footnote to Table 4 as 176 .2,212.4,226.2, 267.4,286.8, 298.3, 289.5, and 265.3 per 10 5 women-years.These rates should have been, respectively, 179.7, 216.6, 230.7, 272.7, 292.5, 304.2, 295.2, and 270.6.Other rates on page 1786 and in the footnote to Table 4 were correct.The correct rates were used in all the calculations in the paper and in the revised National Cancer Institute Breast Cancer Risk Assessment Tool.Thus, none of the results in the paper are changed, but this erratum corrects the documentation.
BOOK REVIEW
Authors: E. H. ROSENBAUM
Journal: JNCI Journal of the National Cancer Institute (1993)

BOOK REVIEW Get access Breast Cancer: The Complete Guide Yashar Hirshaut , Peter I. Pressman . New York : Bantam Books , 1992 . 322 pp., illus. $24.50. ISBN 0-553-08960-9 ERNEST H. ROSENBAUM, M.D. ERNEST H. ROSENBAUM, M.D. San Francisco Hematology-Oncology, Medical Group1515 Scott St., San Francisco, CA 94115 Search for other works by this author on: Oxford Academic PubMed Google Scholar JNCI: Journal of the National Cancer Institute, Volume 85, Issue 4, 17 February 1993, Page 324, https://doi.org/10.1093/jnci/85.4.324 Published: 17 February 1993
Upper GI/clinical
Authors: J Mella, E Roschmann, K Maier
Journal: Gut (1994)

3rd UEGWOslo 1994 the animal's treatment status.C. Ethanol blood clearance and hepatocellular necrosis: 20 rats were administered an LD50-IP dose of ethanol and thirty minutes afterwards saline or ZS (50 mcg/kg) were IP injected.Two animals from each group were hourly sacrificed in order to measure blood ethanol levels by gas chromatography and the extent of hepatocellular necrosis by a pathologist who was unaware of the animal's treatment status.Results: A. A reduction in mortality was observed in rats receiving ZS.The strongest protective effect was observed with a dose of 50 mcg/kg (36% vs 83%, p < 0.05).B. ZS shortened the narcotic period.The strongest effect was observed 4 hrs after intoxication (2.4 vs 1.9 Majchrowicz Index, p < 0.05).C. Finally ZS significantly decreased the extent of hepatocellular necrosis 3 and 5 hrs after intoxication (1% and 5% in ZS vs 20% and 15% in controls).Blood ethanol levels were lower with ZS than with saline.Conclusions: ZS in physiological dose was shown to have a protective effect on acute ethanol intoxication.The precise mechanism of action remains to be elucidated.
Urology
Authors: Mark S. Litwin
Journal: JAMA (1995)

The medical outcomes and practice guidelines movements profoundly affected the field of urology in 1994 with the long-awaited publication of the<i>Clinical Practice Guideline for Benign Prostatic Hyperplasia</i>(BPH) from the US Agency for Health Care Policy and Research.<sup>1</sup>Intended for use by primary care providers as well as urologists, the guideline provides a straightforward algorithm for the diagnosis and treatment of obstructive urinary symptoms in men older than 50 years. It is an evidence-based guideline, developed by a multidisciplinary panel of experts during several years of work.<sup>2</sup> In the guideline, diagnostic evaluation relies heavily on the patient's own symptom assessment using the American Urological Association Symptom Index, a seven-item questionnaire that focuses on incomplete emptying, weak or intermittent stream, urgency, hesitancy, and nocturia.<sup>3</sup>This questionnaire is a psychometrically valid and reliable self-administered instrument that scores obstructive voiding symptoms on a scale from 0 to 35, with
The science of anthropogenic climate change: what every doctor should know
Journal: BMJ (2014)

In Figure 6 the key to the curves had RCP2.6 and RCP8.5 the wrong way round (RCP2.6 should have been represented by the green dotted curve), and the mean values at the right-hand side of the illustration should have read, left to right, RCP2.6,RCP4.5, RCP6.0, and RCP8.5.The same errors occurred in Figures 10 and11.Additionally, in Figure 11 the curves in the graph for RCP2.6 and RCP8.5 were transposed, as well as the labels in the key.
Abstract A2-25: Identification of RASA1 as a novel melanoma tumor suppressor gene
Authors: Hyeran Sung, Krishna L. Kanchi, Jane Messina, Ji-Hyun Lee, Youngchul Kim, Li Ding, Richard K. Wilson, Jeffrey S. Weber, Minjung Kim
Journal: Cancer Research (2015)

Abstract Hyperactivation of the Ras-Raf-Mitogen-activated protein kinase (MAPK) pathway has been commonly observed in melanoma via frequent activating mutations in NRAS and BRAF. Novel mutations in other components of this pathway such as MEK1, MEK2, MAP3K5, and MAP3K9 have been reported recently by high-throughput sequencing efforts. In addition, NF1 (neurofibromatosis type 1), one of the Ras GTPase activating proteins (RasGAPs) that negatively regulate Ras, has been shown to be mutated or suppressed in melanoma. However, importance of other RasGAPs has not been addressed in melanoma. To obtain a comprehensive view of melanoma genomes, we conducted whole genome sequencing (WGS) of 15 metastatic melanomas and matched normal PBMC genomes from 13 melanoma patients. All melanoma genomes from these 13 patients contained at least one mutation in genes of Ras-Raf-MAPK pathway (MAPK1, MAP3K1, MAP4K2, MAP3K14, NRAS, and BRAF). In addition, we identified two novel, clustered somatic missense mutations (p.Tyr472His and p.Leu481Phe) in RASA1 (RAS p21 protein activator 1, p120RasGAP). In this study, we addressed functional roles of RASA1 in melanoma tumorigenesis. The RNAi-mediated down-regulation of RASA1 promoted, while ectopic expression of wild type RASA1 decreased, anchorage-independent colony formation, tumor growth, and RAS activation. Interestingly, RASA1 Y472H mutant enhanced soft agar colony formation and tumor growth, while RASA1 L481F mutant lost its tumor suppressive activity. Mechanistically, RASA1 required RasGAP activity to suppress colony formation and showed higher activity toward R-Ras (related RAS viral (r-ras) oncogene homolog) isoform among the Ras superfamily of small GTPases. In addition, RASA1 suppressed Ral-A among Ras downstream effectors. Interestingly, RASA1 expression was frequently down-regulated in metastatic melanoma samples (11.4% (4/35) of lymph node metastasis and 3.4% (1/29) of distal metastases) compared to primary melanomas (33.3% (21/63)) and dysplastic nevi (44.1% (15/34)). We also observed significantly shorter overall survival of melanoma patients with BRAF mutations when RASA1 mRNA expression is low. Thus, these data support that RASA1 is a novel melanoma tumor suppressor that is inactivated by suppressed expression or by mutation. Citation Format: Hyeran Sung, Krishna L. Kanchi, Jane Messina, Ji-Hyun Lee, Youngchul Kim, Li Ding, Richard K. Wilson, Jeffrey S. Weber, Minjung Kim. Identification of RASA1 as a novel melanoma tumor suppressor gene. [abstract]. In: Proceedings of the AACR Special Conference on Translation of the Cancer Genome; Feb 7-9, 2015; San Francisco, CA. Philadelphia (PA): AACR; Cancer Res 2015;75(22 Suppl 1):Abstract nr A2-25.
A Randomized Comparison of Pioglitazone to Inhibit Restenosis After Coronary Stenting in Patients With Type 2 Diabetes
Authors: K. Nishio
Journal: Diabetes Care (2006)

OBJECTIVE—Recent studies have demonstrated that the treatment with thiazolidinediones reduces in-stent restenosis. The aim of this study was to elucidate the mechanism of the efficacy of pioglitazone for preventing in-stent restenosis in type 2 diabetic patients.
INTERNATIONAL MEDICAL MISSIONARY INSTITUTE, NEW YORK.
Journal: JAMA (1894)

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
MEDICINE AND THE CULTURAL ENVIRONMENT
Journal: JAMA (1965)

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
Carbamazepine Overdosage
Authors: Samuel Livingston
Journal: JAMA (1975)

<h3>To the Editor.—</h3> Salcman and Pippenger (231:915, 1975) presented the case history of a 16-year-old boy in whom an encephalopathy developed secondary to a massive overdosage of carbamazepine (Tegretol). On the basis of this single and rather unremarkable episode, Salcman and Pippenger rejected the findings of several hundred published investigations and 15 years' experience relative to the use of carbamazepine in epilepsy by stating, "The widely held belief that carbamazepine is an innocuous drug is clearly unwarranted." We believe it is ludicrous to classify a drug as dangerous or unsafe because it produces toxic effects when taken in a dosage that greatly exceeds the conventional or therapeutic range. We are perplexed as to how one can attempt to evaluate the relative safety or toxicity of a drug on the basis of massive overdosage, since even the most benign medication may cause serious or fatal results when ingested in enormous amounts.
Therapy of Psoriasis 1975
Authors: Eugene J. Van Scott
Journal: JAMA (1976)

EVER a subject for perennial reports of "breakthroughs," psoriasis recently has indeed been the recipient of several therapeutic developments that promise to provide new options to patients and their physicians harassed by this vexing disease. Among the new entries are triacetyl azauridine, with New Drug Application recently approved; mycophenolic acid, still under an Investigational New Drug application; and long-wave ultraviolet light (UV) and methoxsalen phototherapy, now scheduled for multiinstitutional evaluation over the next year. At this time it is uncertain which of the new introductions will provide solutions and which might provide additional haunting problems. <h3>Burden to Patients</h3> The issue of what constitutes appropriate therapy of psoriasis has been repetitiously controversial with each new treatment advanced over the years. The recurrent controversy seems to have its foundations in the choice of adjectives through which the disease is characterized in divergent points of view. Thus, it is seen as ei<b>See</b>
JHEP at a glance (July 2018)
Authors: Gonzalo Crespo, Núria Trota, Maria-Carlota Londoño, Jaume Tort, Xavier Forns, Miquel Navasa, Salvatore Petta, Luigi Adinolfi, Anna Ludovica Fracanzani, Luca Valenti, Silvia Fargion, Antonio Craxì, Zhenfeng Zhang, Christina Filzmayer, Yi Ni, Florian Vondran, Ralf Bartenschlager, Stephan Urban, Sumeet Asrani, Giovanna Saracino, Jacqueline O'leary, Greg Mckenna, Goran Klintmalm, James Trotter, Wai-Kay Seto, Siu-King Mak, Keith Chiu, Ka-Shing Cheung, Man-Fung Yuen, Wai Leung
Journal: Journal of Hepatology (2018)
Bone Involvement After Vaccination Against Smallpox
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
Thrombocytopenia
Authors: David Y. Graham
Journal: JAMA (1974)

The mechanism of thrombocytopenia associated with mumps was investigated in a case proved by virus isolation. Although an immune mechanism for the thrombocytopenia has been postulated, platelet agglutinins, clot retraction inhibitors, complement-fixing platelet antibodies, or stimulation of platelet factor 3 availability could not be demonstrated in either the presence or absence of mumps-specific antigens. These results suggest that thrombocytopenia is not a consequence of antibodies directed against normal platelets nor against mumps antigen adsorbed to platelets. Rather, it appears that in this disorder, thrombocytopenia may result from a direct action of the virus or a viral antigen-antibody complex on platelets.
An Address Delivered at the Opening of the Section of Public Medicine
Authors: A. Hill
Journal: BMJ (1890)

Among the causes of insanity in women, heredity, intemperance, and the vicissitudes of female life are said to be the most frequent; and it has long occurred to me, as I know it has to others, that in regard to the latter element as a cau3e, much good might result if every case in which there was the least doubt were thoroughly overhauled and investigated by an experienced gynee- -cologist.Every one knows that occasionally, although rarely, a cse of