tbuckley/cabot-search huggingface dataset:
Much Cheaper, Almost as Good: Decrementally Cost-Effective Medical Innovation
Authors: Aaron L. Nelson, Joshua T. Cohen, Dan Greenberg, David M. Kent
Journal: Annals of Internal Medicine (2009)

Under conditions of constrained resources, cost-saving innovations may improve overall outcomes, even when they are slightly less effective than available options, by permitting more efficient reallocation of resources. The authors systematically reviewed all MEDLINE-cited cost–utility analyses written in English from 2002 to 2007 to identify and describe cost- and quality-decreasing medical innovations that might offer favorable "decrementally" cost-effective tradeoffs—defined as saving at least $100 000 per quality-adjusted life-year lost. Of 2128 cost-effectiveness ratios from 887 publications, only 9 comparisons (0.4% of total) described 8 innovations that were deemed to be decrementally cost-effective. Examples included percutaneous coronary intervention (instead of coronary artery bypass graft) for multivessel coronary disease, repetitive transcranial magnetic stimulation (instead of electroconvulsive therapy) for drug-resistant major depression, watchful waiting for inguinal hernias, and hemodialyzer sterilization and reuse. On a per-patient basis, these innovations yielded savings from $122 to almost $12 000 but losses of 0.001 to 0.021 quality-adjusted life-years (approximately 8 hours to 1 week). These findings demonstrate the rarity of decrementally cost-effective innovations in the medical literature.
What Should Be Done About the Uninsured Poor?
Authors: Vicente Navarro
Journal: JAMA (1989)

<h3>To the Editor.—</h3> Dr Blendon's<sup>1</sup>article entitled "What Should Be Done About the Uninsured Poor?" outlines a proposal to cover the uninsured poor that the author believes would enjoy popular support. Dr Blendon calls for employermandated coverage with federal subsidization of the premiums of low-income wage earners and the nonworking poor. Dr Blendon, however, dismisses another proposal to resolve the problems of the uninsured poor, the establishment of national health insurance. The reasons he gives are that (1) people are not willing to pay the higher taxes that such a program would entail to cover the costs of expanding health benefits coverage to the whole population and (2) people are not convinced that they personally would benefit from such a universal insurance program, since the majority already have access to health insurance coverage. In support of the first proposition, Dr Blendon quotes polls that show that while the majority
Physician-Run Health Plans and Antitrust
Authors: Michael Werner
Journal: Annals of Internal Medicine (1997)

Letters1 February 1997Physician-Run Health Plans and AntitrustMichael Werner, JDMichael Werner, JDAmerican College of Physicians, Washington, DC 20005Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-126-3-199702010-00024 SectionsAboutFull TextPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail IN RESPONSE:On 28 August 1996, the U.S. Federal Trade Commission and the U.S. Department of Justice issued new guidelines that will give physicians greater leeway to form networks and to integrate their practices under the antitrust laws [1]. By making it easier for physicians to band together, these guidelines address many of the concerns outlined by Dr. Duvall.The guidelines were originally published in 1993 by the federal antitrust enforcement agencies to help physicians, hospitals, and other health providers understand the application of the antitrust laws to the health care market. In December 1995, the agencies announced that they ...References1. Statements of Antitrust Enforcement Policy in Health Care. Washington, DC: U.S. Department of Justice and the Federal Trade Commission; 1996. Google Scholar2. Pear R. U.S. issues guidelines to help doctors form health networks. The New York Times. 29 August 1996:A1. Google Scholar Author, Article, and Disclosure InformationAuthors: Michael Werner, JDAffiliations: American College of Physicians, Washington, DC 20005 PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics 1 February 1997Volume 126, Issue 3 Page: 253 Keywords Health care Health care providers Health care sector Quality improvement Safety ePublished: 15 August 2000 Issue Published: 1 February 1997 Copyright & PermissionsCopyright © 1997 by American College of Physicians. All Rights Reserved.PDF downloadLoading ...
Abstract LB-79: PRC2 loss amplifies Ras-driven transcription and sensitizes cancers to bromodomain inhibitor-based combination therapies
Authors: Thomas D. Raedt, Eline Beert, Eric Pasmant, Armelle Luscan, Hilde Brems, Nicolas Ortonne, Kristian Helin, Victor Mautner, Hildegard Kehrer-Sawatski, Wade Clapp, James Bradner, Meena Upadhyaya, Michel Vidaud, Eric Legius, Karen Cichowski
Journal: Cancer Research (2014)

Abstract The polycomb repressive complex 2 (PRC2) exerts oncogenic effects in many tumor types. However, loss-of-function mutations in PRC2 components occur in a subset of hematopoietic malignancies, suggesting that this complex plays a dichotomous and poorly understood role in cancer. Our genomic, cellular, and mouse modeling data demonstrates that the polycomb group gene SUZ12 functions as tumor suppressor in PNS tumors, glioblastomas, and melanomas by cooperating with mutations in NF1. NF1 encodes a Ras GTPase-activating protein and its loss drives cancer by activating Ras. We show that SUZ12-loss potentiates the effects of NF1 mutations by amplifying Ras-driven transcription. Importantly however, SUZ12-inactivation also triggers an epigenetic switch that sensitizes these cancers to bromodomain inhibitors. Collectively, these studies not only reveal an unexpected connection between the PRC2 complex, NF1, and Ras, but also identify a promising epigenetic-based therapeutic strategy that may be exploited for a variety of cancers. Citation Format: Thomas De Raedt, Eline Beert, Eric Pasmant, Armelle Luscan, Hilde Brems, Nicolas Ortonne, Kristian Helin, Victor Mautner, Hildegard Kehrer-Sawatski, Wade Clapp, James Bradner, Meena Upadhyaya, Michel Vidaud, Eric Legius, Karen Cichowski. PRC2 loss amplifies Ras-driven transcription and sensitizes cancers to bromodomain inhibitor-based combination therapies. [abstract]. In: Proceedings of the 105th Annual Meeting of the American Association for Cancer Research; 2014 Apr 5-9; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2014;74(19 Suppl):Abstract nr LB-79. doi:10.1158/1538-7445.AM2014-LB-79
Fenway Guide to Lesbian, Gay, Bisexual and Transgender Health
Authors: Michael A. Horberg
Journal: Annals of Internal Medicine (2008)

Medical Writings: Book Notes2 September 2008Fenway Guide to Lesbian, Gay, Bisexual and Transgender HealthMichael A. Horberg, MD, MASMichael A. Horberg, MD, MASFrom Kaiser Permanente, Oakland, California.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-149-5-200809020-00030 SectionsAboutFull TextPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail Fenway Guide to Lesbian, Gay, Bisexual and Transgender HealthMakadon HJ, Mayer KH, Potter J, Goldhammer H, eds. Philadelphia: American Coll of Physicians; 2007. $59.95. ISBN 9781930513952. Order at www.acponline.org.Field of medicine: Lesbian, gay, bisexual, and transgender (LGBT) health.Format: Softcover book.Audience: Primary care physicians who care for adolescent or adult LGBT patients.Purpose: To provide primary care clinicians with a comprehensive handbook on the appropriate approach to the health issues of LGBT patients and offer practical guidance for their routine health care.Content: As background, the text provides a historical context for LGBT health care and its ... Author, Article, and Disclosure InformationAffiliations: From Kaiser Permanente, Oakland, California. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited byRevisiting Gendered Web Forms: An Evaluation of Gender Inputs with (Non-)Binary People 2 September 2008Volume 149, Issue 5Page: 368KeywordsAdolescentsBisexualsHealth careHealth care providersPatientsSexual identitySexually transmitted diseasesSoftware tools ePublished: 2 September 2008 Issue Published: 2 September 2008 Copyright & PermissionsCopyright © 2008 by American College of Physicians. All Rights Reserved.PDF downloadLoading ...
Tom MacDonald replies to Marisa de Andrade
Authors: T. MacDonald
Journal: BMJ (2009)

Thank you for allowing me to respond to Ms Andrade’s article about the Standard Care versus Celecoxib Outcome Trial (SCOT).1

SCOT was designed by me with Professor C J Hawkey (Nottingham University) and Professor Ian Ford (Glasgow University). The protocol is the property of Dundee University (the study sponsor) and was formally approved by the European Medicines Evaluation Agency (EMEA), as well as other regulatory bodies. The aim of the study is to assess the long term drug safety of non-steroidal anti-inflammatory drugs (NSAIDs) and is funded by Pfizer USA. In general the pharmaceutical industry does not see such safety studies as attractive commercially, which is why SCOT is led by an independent investigator (me) and …
Emergency medical admissions: taking stock and planning for winter
Authors: O. Blatchford, S. Capewell
Journal: BMJ (1997)

Emergency medical admissions have risen by 50% since 1984 and now account for almost half of all NHS admissions.1 Through recurrent winter bed crises, disrupted elective admissions, growing waiting lists, and highly publicised interhospital transfers of seriously ill patients this continuing rise threatens the future of the NHS. Has anything changed since we last reviewed this problem?2

We now understand better the epidemiology of emergency medical admissions. Winter peaks principally reflect respiratory and cardiovascular illness.3 Nevertheless, twofold variations exist between individual hospitals in both admission rates and increases in rates.4 Whereas the proportion of the total population using inpatient hospital services has remained almost constant,5 the number of patients readmitted four or more times in a five year period doubled between 1981 and 1994.

Age and deprivation take their toll. People aged over 65 account for only 15% of the Scottish population but 37% of emergency admissions.1 This proportion may have …
Three Cases of Severe Subfulminant Hepatitis in Heart–Transplanted Patients After Nosocomial Transmission of A Mutant Hepatitis B Virus
Authors: Lieven Stuyver, Sija De Gendt, Jean Fran Cadranel, Caroline Van Geyt, Georges Van Reybroeck, Richard Dorent, Iranj Gandjbachkh, Michel Rosenheim, Frederic Charlotte, Pierre Opolon, Jean Marie Huraux, Françoise Lunel
Journal: Hepatology (1999)

Fulminant and severe viral hepatitis are frequently associated with mutant hepatitis B virus (HBV) strains. In this study, the genetic background of a viral strain causing severe subfulminant outcome in heart–transplanted patients was studied and compared with viral hepatitis B strains that were not linked to severe liver disease in the same setting. A total of 46 patients infected nosocomially with HBV genotype A were studied. Five different viral strains were detected, infecting 3, 9, 5, 24, and 5 patients, respectively. Only one viral strain was found to be associated with the subfulminant outcome and 3 patient deaths as a consequence of severe liver disease. The remaining 43 patients with posttransplantation HBV infection did not show this fatal outcome. Instead, symptoms of hepatitis were generally mild or clinically undiagnosed. Comparison of this virus genome with the four other strains showed an accumulation of mutations in the basic core promoter, a region that influences viral replication, but also in hepatitis B X protein (HBX) (7 mutant motifs), core (10 mutant motifs), the preS1 region (5 mutant motifs), and the HBpolymerase open reading frame (17 motifs). Some of these variations, such as those in the core region, were located on the tip of the protruding spike of the viral capsid (codons 60 to 90), also known in part as an important HLA class II-restricted epitope region. These mutations might therefore influence the immune–mediated response. The viral strain causing subfulminant hepatitis was, in addition, the only strain with a preCore stop codon mutation and, thus, hepatitis B e antigen (HBeAg) expression was never observed. The combination of these specific viral factors is thought to be responsible for the fatal outcome in these immune–suppressed heart–transplant recipients.
The Use of In-Hospital Physician Services for Acute Myocardial Infarction
Authors: Eric Sawitz
Journal: JAMA (1988)

Changes between 1972 and 1982 in the use of in-hospital services were studied for 164 patients admitted with acute myocardial infarction. Resource use was measured in constant 1982 dollars adjusted for differences in clinical severity of the patients. Although average length of stay decreased by almost 40% during this period, the number of physician services doubled and total physician costs increased almost threefold. The increase in physician costs was due primarily to the use of complex diagnostic technologies and to the provision of coronary artery bypass graft surgery. The results of this study suggest that as hospital costs are constrained by prospective payment, physician costs may continue to rise as new diagnostic and therapeutic services are introduced into practice and as more care is shifted to the outpatient setting.
P118 The role of the retinoic acid pathway in human lung regeneration
Authors: J. P. Ng-Blichfeldt, M. Griffiths, U. Griesenbach, B. Allen, M. Hind
Journal: Thorax (2011)

Recent studies into retinoic acid (RA)-induced alveolar regeneration in rodent models of emphysema and bronchopulmonary dyplasia strongly suggest a latent regenerative potential of the adult mammalian lung. RA signalling is known to have an important role during alveolar formation in the developing lung in rodents and man. However, critical differences between animal and human physiology and development qualify the relevance of animal models of regeneration. Here we explore the role of RA signalling in human lung regeneration. Using RT-PCR with primers specific to RA signalling genes, we confirm expression of the RA synthesising enzymes Raldh1, 2 and 3, RA degrading enzymes Cyp26 A1, B1 and C1, retinoic acid receptors RAR-α, β, γ and retinoid binding proteins CRBPI and II, and CRABP I and II in normal, human peripheral lung tissue. To determine which cell types of peripheral lung are involved in RA signalling we have isolated primary alveolar type 2 epithelial cells and primary vascular endothelial cells and confirm expression of RA signalling genes. We have developed an high performance liquid chromatography (HPLC) method to identify and quantify endogenous human lung retinoids and demonstrate the ability to separate known standard retinoids by characteristic elution times. Finally, using precision cut lung slices we are developing an experimental system to determine the effects of retinoids in an architecturally complex human tissue model. Future work will include characterisation and optimisation of a primary human type 2 alveolar epithelial cell wound healing model and the effects of various selective retinoic acid receptor agonists and antagonists.
Evidence that prostacyclin modulates the vascular actions of calcium in man.
Authors: J L Nadler, M McKay, V Campese, J Vrbanac, R Horton
Journal: Journal of Clinical Investigation (1986)

Increases in extracellular calcium (Ca++) can alter vascular tone, and thus may result in increased blood pressure (Bp) and reduced renal blood flow (RBF). Ca++ can stimulate prostaglandin E2 (PGE2) and/or prostacyclin (PGI2) release in vitro, which may modulate Ca++ vascular effects. However, in man, the effect of Ca++ on PG release is not known. To study this, 14 volunteers received low-dose (2 mg/kg Ca++ gluconate) or high-dose (8 mg/kg) Ca++ infusions. The low-dose Ca++ infusion did not alter systemic or renal hemodynamics, but selectively stimulated PGI2, as reflected by the stable metabolite 6-keto-PGF1 alpha in urine (159 +/- 21-244 +/- 30 ng/g creatinine, P less than 0.02). The same Ca++ infusion given during cyclooxygenase blockade with indomethacin or ibuprofen was not associated with a rise in PGI2 and produced a rise in Bp and fall in RBF. However, sulindac, reported to be a weaker renal PG inhibitor, did not prevent the Ca++ -induced PGI2 stimulation (129 +/- 33-283 +/- 90, P less than 0.02), and RBF was maintained despite similar increases in Bp. The high-dose Ca++ infusion produced an increase in mean Bp without a change in cardiac output, and stimulated urinary 6-keto-PGF1 alpha to values greater than that produced by the 2-mg/kg Ca++ dose (330 +/- 45 vs. 244 +/- 30, P less than 0.05). In contrast, urinary PGE2 levels did not change. A Ca++ blocker, nifedipine, alone had no effect on Bp or urinary 6-keto-PGF1 alpha levels, but completely prevented the Ca++ -induced rise in Bp and 6-keto-PGF1 alpha excretion (158 +/- 30 vs. 182 +/- 38, P greater than 0.2). However, the rise in 6-keto-PGF1 alpha was not altered by the alpha 1 antagonist prazosin (159 +/- 21-258 +/- 23, P less than 0.02), suggesting that calcium entry and not alpha 1 receptor activation mediates Ca++ pressor and PGI2 stimulatory effects. These data indicate a new vascular regulatory system in which PGI2 modulates the systemic and renal vascular actions of calcium in man.
Dopamine producing cells cloned to treat Parkinson's disease
Authors: A. Berger
Journal: BMJ (1998)

Scientists in Colorado have succeeded in cloning dopamine producing cells that could one day be used to treat Parkinson's disease.

Transplantation of dopamine cells into the brains of people with Parkinson's disease has been under trial as a treatment for the disease for several years. Traditionally, the dopamine containing cells have been retrieved from human embryos, but this source is limited and raises ethical dilemmas, so alternative molecular options are being explored.

Now, Curt Freed and his colleagues at the University of …
An Atlas of Pelvic Operations
Authors: John H. Wulsin
Journal: JAMA (1969)

The second edition of this established atlas (first edition, 1953) is excellent, as one might expect. The chief changes lie in the format. The atlas is now fatter and heavier and less portable, but it opens along the long dimension, a definite advantage in durability. Miss Codding's splendid drawings are arranged on the right-hand page with the corresponding legends and editorial comment on the adjacent left-hand page. While esthetically superior to the first edition, this layout requires more traveling of the eye between drawing and legend and wastes considerable blank paper on the legend pages.  The authors have excluded from this edition some little-used gynecologic procedures and have considerably expanded the number of drawings alloted to extensive procedures for cancer, such as radical vulvectomy with groin dissection and Wertheim hysterectomy. A detailed and lengthy section on pelvic exenterations, total, anterior, and posterior, has been added, a particularly valuable feature of
Reduced intensity conditioning is superior to nonmyeloablative conditioning for older chronic myelogenous leukemia patients undergoing hematopoietic cell transplant during the tyrosine kinase inhibitor era
Authors: Erica Warlick, Kwang Woo Ahn, Tanya L. Pedersen, Andrew Artz, Marcos de Lima, Michael Pulsipher, Gorgun Akpek, Mahmoud Aljurf, Jean-Yves Cahn, Mitchell Cairo, Yi-Bin Chen, Brenda Cooper, Abhinav Deol, Sergio Giralt, Vikas Gupta, H. Jean Khoury, Holbrook Kohrt, Hillard M. Lazarus, Ian Lewis, Richard Olsson, Joseph Pidala, Bipin N. Savani, Matthew Seftel, Gerard Socié, Martin Tallman, Celaettin Ustun, Ravi Vij, Lars Vindeløv, Daniel Weisdorf
Journal: Blood (2012)
Res ipsa loquitur. 7. General surgery
Authors: A. R. Holder
Journal: JAMA (1972)

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
Social and Physical Environments and Disparities in Risk for Cardiovascular Disease: The Healthy Environments Partnership Conceptual Model
Authors: Amy J. Schulz, Srimathi Kannan, J. Timothy Dvonch, Barbara A. Israel, Alex Allen, Sherman A. James, James S. House, James Lepkowski
Journal: Environmental Health Perspectives (2005)

The Healthy Environments Partnership (HEP) is a community-based participatory research effort investigating variations in cardiovascular disease risk, and the contributions of social and physical environments to those variations, among non-Hispanic black, non-Hispanic white, and Hispanic residents in three areas of Detroit, Michigan. Initiated in October 2000 as a part of the National Institute of Environmental Health Sciences' Health Disparities Initiative, HEP is affiliated with the Detroit Community–Academic Urban Research Center. The study is guided by a conceptual model that considers race-based residential segregation and associated concentrations of poverty and wealth to be fundamental factors influencing multiple, more proximate predictors of cardiovascular risk. Within this model, physical and social environments are identified as intermediate factors that mediate relationships between fundamental factors and more proximate factors such as physical activity and dietary practices that ultimately influence anthropomorphic and physiologic indicators of cardiovascular risk. The study design and data collection methods were jointly developed and implemented by a research team based in community-based organizations, health service organizations, and academic institutions. These efforts include collecting and analyzing airborne particulate matter over a 3-year period; census and administrative data; neighborhood observation checklist data to assess aspects of the physical and social environment; household survey data including information on perceived stressors, access to social support, and health-related behaviors; and anthropometric, biomarker, and self-report data as indicators of cardiovascular health. Through these collaborative efforts, HEP seeks to contribute to an understanding of factors that contribute to racial and socioeconomic health inequities, and develop a foundation for efforts to eliminate these disparities in Detroit.