tbuckley/cabot-search huggingface dataset:
Effect of visual inspection with acetic acid (VIA) screening by primary health workers on cervical cancer mortality: A cluster randomized controlled trial in Mumbai, India.
Authors: Surendra Srinivas Shastri, Indraneel Mittra, Gauravi Mishra, Subhadra Gupta, Rajesh Dikshit, Rajendra A. Badwe
Journal: Journal of Clinical Oncology (2013)

2 Background: Cervical cancer is the most common cancer among women in developing countries and is the leading cause of cancer death in Indian women. Since cytology-based screening is not easily implementable in India, there is a need to evolve simpler alternatives. Methods: We initiated a cluster-randomized controlled trial in 1998 to investigate the efficacy of VIA screening by primary health workers (PHWs) in reducing cervical cancer mortality. Women aged 35-64 years with no prior history of cancer were included. The study was designed to include 20 clusters with an average of 7,500 eligible women per cluster. Four rounds of cancer education and VIA screening were conducted by PHWs at 24-month intervals in the screening group, while cancer education was offered once at recruitment to the control group. Recruitment was completed in March 31, 2002. Although the study was planned for 16 years, we analysed the results on the advice of the DSMC at 12 years. Results: We recruited 75,360 women from 10 clusters in the screening group and 76,178 women from 10 comparable clusters in the control group. The analysis is on an intention-to-treat basis. In the screening group, we achieved 89% participation for screening and 79% compliance for post-screening diagnostic confirmation. The quality of screening by PHWs was comparable to that of an expert gynecologist (κ=0.84). The incidence of invasive cervical cancer was 26.74 per 100,000 (95%CI: 23.41-30.74) in the screening group and 27.49 per 100,000 (95%CI: 23.66-32.09) in the control group. Compliance to treatment for invasive cancer was 86.34% in screening group and 72.29% in the control group. The screening group showed a 31% reduction in cervical cancer mortality (mortality rate ratio RR=0.69; 95%CI: 0.54-0.88; p=0.003) compared to the control group. A 7% reduction was also observed in all-cause mortality (mortality rate ratio RR=0.93; 95%CI: 0.79–1.10; p=0.41). Conclusions: VIA screening conducted by PHWs significantly reduced cervical cancer mortality. VIA screening is easily implementable and could prevent 22,000 cervical cancer deaths in India and 72,600 deaths in resource poor countries annually. Clinical trial information: NCT00632047.
<i>Erratum:</i> Vol. 67, No. 7
Journal: MMWR Morbidity and Mortality Weekly Report (2018)

In the report "Self-Reported Receipt of Advice and Action Taken To Reduce Dietary Sodium Among Adults With and Without Hypertension -Nine States and Puerto Rico, 2015," on page 225, the third sentence of the second paragraph should have read "Median survey response rate for all states and territories included in this analysis was 51.3% (range = 38.6%-59.0%)(5)."
Failure of cytarabine in varicella-zoster infections
Authors: C. M. Davis
Journal: JAMA (1973)

In an effort to confirm the reported efficacy of cytarabine for the treatment of varicella-zoster (VZ), a double-blind study comparing cytarabine—150 mg/sq m of body surface for 36 hours—to dextrose in water was performed in cancer and immunosuppressed patients. One of the five cytarabine-treated patients and two of the three placebo-treated patients developed disseminated lesions. The acute phase and the time necessary for healing were the same in both groups. Until the natural course of VZ is documented in a large series of cancer patients, the benefit of medications such as cytarabine will remain in doubt.
A phase I, single-institution open-label, dose-escalation trial with an expansion cohort evaluating the safety and tolerability of AZD6244 and IMC-A12 in subjects with advanced solid malignancies.
Authors: S. R. Ahmed, D. Cosgrove, D. Ball, R. C. Donehower, B. Nelkin, E. Petito, M. Downs, H. X. Chen, A. Doyle, A. Scardina, M. A. Carducci, N. S. Azad
Journal: Journal of Clinical Oncology (2011)

TPS156 Background: IGF-1 receptor (IGF1-R) phosphorylation leads to activation of the PI3K and Raf/MEK/ERK pathways and plays a central role in the regulation of proliferation, survival, differentiation, and apoptosis. Significant crosstalk exists between the two pathways and treatment of select cell lines with a MEK inhibitor and an IGF1-R inhibitor has been shown to cause greater inhibition of growth than either agent alone. IMC-A12 (I) is a recombinant human monoclonal antibody directed IGFI-R; it blocks interaction between IGF-1R and its ligands, IGF-I and -II. I has demonstrated tumor growth inhibition in a wide range of in vitro and in vivo human cancer. AZD6244 (A) is a highly selective, non-competitive MEK 1/2 inhibitor that has had similar success in vitro and in vivo in cancer models of various solid tumors. In vivo studies have demonstrated the most potent inhibition of cell growth in cell lines harboring RAS and BRAF mutations. Phase I/II studies have shown both agents to be tolerable as single agents and suggested modest efficacy in various cancer types. Methods: A phase I, open label, dose escalation trial with I+A is currently accruing pts with advanced malignancies. The study is a standard 3+3 design with an expansion cohort of 15 pts for correlative endpoints and PK studies. Pts will be treated with A at 50 mg po BID, then 75 mg po BID; I at 12mg/kg q2week held constant. The first 2 cohorts have accrued with a single dose-limiting toxicity in cohort 2. The expansion cohort will start accrual in February 2011. Eligibility includes advanced solid tumor, good end organ function and performance status with exclusion for poorly controlled diabetes or growth hormone abnormalities. The primary objective is to determine the safety and tolerability of the combination and to determine the MTD. Secondary objectives include assessing preliminary efficacy as defined by RECIST criteria and exploration of PK/PD endpoints. Serial tumor biopsies will be evaluated for changes in signaling in the IGF pathway, including p-ERK, p-Akt and RAS. RAS and RAF mutation sites will be sequenced in order to correlate with PD endpoints and disease response.
Renal Toxicogenomic Response to Chronic Uranyl Nitrate Insult in Mice
Authors: Magali Taulan, François Paquet, Christophe Maubert, Olivia Delissen, Jacques Demaille, Marie-Catherine Romey
Journal: Environmental Health Perspectives (2004)

Although the nephrotoxicity of uranium has been established through numerous animal studies, relatively little is known about the effects of long-term environmental uranium exposure.Using a combination of conventional biochemical studies and serial analysis of gene expression (SAGE), we examined the renal responses to uranyl nitrate (UN) chronic exposure.Renal uranium levels were significantly increased 4 months after ingestion of uranium in drinking water.Creatinine levels in serum were slightly but significantly increased compared with those in controls.Although no further significant differences in other parameters were noted, substantial molecular changes were observed in toxicogenomic profiles.UN induced dramatic alterations in expression levels of more than 200 genes, mainly up-regulated, including oxidative-response-related genes, genes encoding for cellular metabolism, ribosomal proteins, signal transduction, and solute transporters.Seven differentially expressed transcripts were confirmed by real-time quantitative polymerase chain reaction.In addition, significantly increased peroxide levels support the implication of oxidative stress in UN toxicant response.This report highlights the potential of SAGE for the discovery of novel toxicant-induced gene expression alterations.Here, we present, for the first time, a comprehensive view of renal molecular events after uranium long-term exposure.
MADRID
Journal: JAMA (1926)

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
Abstract 2876: p21-activated kinase 1 is a novel therapeutic target for metastatic osteosarcoma harboring p27 mislocalization
Authors: Xiang Chen, Justin Cates, Yuchen Du, Yun Jung Sung, Xiao-nan Lo, John Hicks, Tsz-Kwong Man
Journal: Cancer Research (2019)

Abstract Lung metastasis is the leading cause of death in osteosarcoma (OS), the most common bone cancer in children and young adults. Due to a lack of biomarkers and therapeutic targets, significant progress has not been made in the treatment of metastatic OS over the past three decades. The survival of metastatic patients remains dismal. We have previously reported that the tumor suppressor protein p27 (KIP1, CDKN1B) is frequently mislocalized in the cytoplasm of OS, which promotes the motility and invasiveness of the tumor cells and the development of pulmonary metastases in mice. In this study, we showed that a higher proportion score of cytoplasmic p27 significantly correlated with metastases developed within 3- or 5-year of follow-up, and poor disease-specific and event-free survival in a large OS cohort (n=136). Using immunoprecipitation followed by mass spectrometry, we demonstrated that cytoplasmic p27 interacted with p21-activated kinase 1 (PAK1), where the two proteins co-localized in the cytoplasm of OS cells. PAK1 is a serine/threonine kinase that has been implicated in various cancers; however, its role in OS is still elusive. We showed that the phosphorylations at serine-144 and threonine-423 residues of PAK1 were higher in the p27-mislocalized cells relative to the control cells. The PAK1 phosphorylations increased actin stress fiber formation in the tumor cells. Gene silencing or therapeutic inhibition of PAK1 reduced the motility of p27-mislocalized cells in vitro. Similar results were observed in other cancer cell lines known to have the p27 mislocalization, suggesting PAK1 is a common and potential downstream effector of p27-mediated metastasis. An experimental metastasis mouse model further showed that a PAK1-silenced mutant had a significant impairment in the development of pulmonary metastasis. In summary, our study indicates that cytoplasmic p27 is a novel prognostic biomarker in OS. In the tumor cell, the mislocalization activates PAK1-mediated cell motility and metastasis. Targeting PAK1 in metastatic OS harboring the p27 mislocalization may be exploited as a potential therapeutic intervention to improve the poor outcome of the affected children. Citation Format: Xiang Chen, Justin Cates, Yuchen Du, Yun Jung Sung, Xiao-nan Lo, John Hicks, Tsz-Kwong Man. p21-activated kinase 1 is a novel therapeutic target for metastatic osteosarcoma harboring p27 mislocalization [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 2876.
South African Medical Journal, Capetown
Journal: JAMA (1964)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA HomeNew OnlineCurrent IssueFor Authors Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA journal
The Falling Death Rate and Lengthening of Life
Journal: JAMA (2016)

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
Response to Comment on Duran et al. Introduction of IADPSG Criteria for the Screening and Diagnosis of Gestational Diabetes Mellitus Results in Improved Pregnancy Outcomes at a Lower Cost in a Large Cohort of Pregnant Women: The St. Carlos Gestational Diabetes Study. Diabetes Care 2014;37:2442–2450
Authors: Alejandra Duran, María J. Torrejón, Isabelle Runkle, Alfonso L. Calle-Pascual
Journal: Diabetes Care (2015)
Observations on Typhoid or Intestinal Fever: The Pythogenic Theory
Authors: W. Budd
Journal: BMJ (1861)

So the ordinary face and view of experience is massy times satisfied by several theories and philosophies; whereas, to find the real truth, requireth another manner of sevority ancd attention." (Advancc,nwnt of Learning.)PART III.(Continued.)DOES INTESTINAL (TYPHOID) FEVER EVER ARISE SPONTANEOUSLY'?Summary of Conclusions established in precedingPapers.Their general Efect to show Typhoid Fever to be excltsively contaqious.The onty Evi- dence to the contrary Negative Evidence.If l2'phoid ZF ever originate spontaneously, by the sanze Rule Small-pox and Plants and A nimals oriqinate in the same WP`ay.First Oriqin of all these Things wrapped in impenetrable Obscurity.,Small-pox.Itch.Syphilis.Resume of the whole Arguqment.THE facts as applied to the disease of which these papers treat, stand, therefore, thus :-Cases of small- pox, like cases of fever, are constantly arising which cannot be traced to contagion.There is the strongest conceivable evidence, notwithstanding, that whatever its first origin, small-pox does not spring up de novo now.The occurrence of such cases is, therefore, no warrant for supposing that either of these diseases does so spring up.Unassailable as this argument is, it may be well, on other grounds, to cap it with another, which covers a still larger issue.I have said that, if we are to believe in the spontaneous origin of typhoid fever, * This was the case with the entozoa, especially up to a very 'recent date.Its utter untenability in regard to these types was shown by Eschricht about twenty years ago, in ani essay in which the whole question of spontaneous generation is discussed in a mas- .terlyway.Rhis essay, of which a translation appeared soon after- atards,ii 7Tmeeyn's Journal, is still well worth reading.
Gemfibrozil therapy in primary hypertriglyceridemia associated with coronary heart disease. Effects on metabolism of low-density lipoproteins
Authors: G. L. Vega
Journal: JAMA (1985)

Certain primary hypertriglyceridemias cause abnormalities in lipoproteins that seemingly predispose patients to coronary heart disease. We examined metabolism of low-density lipoproteins (LDL) in 11 men with both hypertriglyceridemia and coronary heart disease and compared them with that of controls. The LDL turnover was measured during placebo and gemfibrozil therapy. With placebo, LDL-cholesterol level usually was normal, but production and fractional clearance of LDL were high. The LDL composition also was abnormal. Gemfibrozil reduced triglycerides, lowered production and fractional clearance of LDL, and normalized LDL composition. The LDL-cholesterol level usually rose, but generally not to abnormally high levels. Therefore, normalization of LDL metabolism and marked reduction of triglycerides by gemfibrozil suggest benefit to hypertriglyceridemic patients who are at high risk for coronary heart disease. However, when LDL-cholesterol level rises excessively, gemfibrozil may not be sufficient therapy. (<i>JAMA</i>1985;253:2398-2403)
Continuing medical education
Authors: A. Osteen
Journal: JAMA (1985)

<h3>Accreditation</h3> When the Accreditation Council for Continuing Medical Education (ACCME) was established in January 1981, it recognized the intrastate accreditation programs of the medical societies of all 50 states, the District of Columbia, Puerto Rico, the Virgin Islands, and Guam.<i>A Protocol</i>was then developed in 1983 that set forth the following five criteria for ACCME continued recognition: The state society has a set of Essentials as the basis of the accreditation activities. These Essentials must be compatible with the Essentials of the ACCME but need not be identical. Each of the ACCME Essentials must be addressed. The state has a formal appeal process for any adverse accreditation decision. Appeals will not be referred to the ACCME, since the state society has the responsibility for intrastate accreditation. The state society has established and follows a set of policies regulating the accreditation process, including Essentials, procedure, and responsibilities.
In this issue
Authors: Peter Kirkpatrick, Alexandra Flemming, Charlotte Harrison, Sarah Crunkhorn, Monica Flight, Asher Mullard, Man Tse, Mariam Faruqi, Catriona Rodwell, Lucie Wootton, Isabel Woodman, Lewis Packwood, Susanne Harris, Vicky Summersby, Patrick Morgan, Kirsten Managing, Judith Shadwell, Simon Fenwick, Natalie Smith, Laura Corns, Ella Lines, Dipti Shah, Marketing Managers, Tim Redding, Nazly De, La Rosa, Peter Collins, Man Tsuey Tse
Journal: Nature Reviews Drug Discovery (2012)
The Cover
Journal: JAMA (1996)

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
New mandates? No problem for The Rockefeller University Press
Authors: Mike Rossner
Journal: The Journal of Experimental Medicine (2013)

The existing public access policy for our three journals—The Journal of Cell Biology, The Journal of Experimental Medicine, and The Journal of General Physiology—is fully compliant with new policies from the Research Councils UK (RCUK) and the Wellcome Trust. In addition to mandating public access, the new policies specify licensing terms for reuse of content by third parties, in particular for text and data mining. We question the need for these specific terms, and we have added a statement to our licensing policy stipulating that anyone, including commercial entities, is permitted to mine our published text and data.
ORIGINAL INVESTIGATIONS ON THE NATURAL HISTORY, (SYMPTOMS AND PATHOLOGY) OF YELLOW FEVER. 1854-1894.
Authors: JOSEPH JONES
Journal: JAMA (1894)

Yellow fever (vomito; vomito prieto; vomito negro,fièvre matelotte; febris flava; fièvre jaunne; gelbes fieber; febbre grilla; febris icterodes; typhus icterodes; typhus tropicus; typhus d' Amérique; fiebre amarilla; coap de banc; febris maligna biliosa Americana flava; bulam fever; hemogastric pestilence; pestilentia hemogastrica; synochus icterodes; causus; febris flava Americanorum, epanetus malignus flavus; typhus jaune; ichwaites erbrechen westendisches fieber; fiebre yialla; black vomit; malignant yellow fever; pestilential fever; epidemic yellow fever; specific yellow fever.) DEFINITION. A pestilential fever, of a continuous and specific type, originally developed in tropical and insular America; confined to definite geographical limits, and dependent in its origin and spread upon definite degrees of temperature, and capable of transportation and propagation on ships and in towns and cities in those portions of North and South America which lie between 45° N. latitude and 35° S. latitude. The disease has been limited chiefly to the coast of tropical America, rather from