tbuckley/cabot-search huggingface dataset:
Clinical efficacy of antitachycardia pacing in patients with ventricular tachyarrhythmias with implanted third-generation cardioverter-defibrillators
Authors: Ryszard B. Krol, Sanjeev Saksena, Nicholas G. Tullo, Amarkanth Sarena, Rajesh Sam Suri, Margaret Gordon, Edward Burkhardt, Debbie Hibbard, John Neglia
Journal: Journal of the American College of Cardiology (1991)
Mammographic Screening in Women Younger Than 50 Years
Authors: Daniel B. Kopans
Journal: JAMA (1995)

<h3>To the Editor.</h3> —<i>JAMA</i>'s 500-word limit for Letters to the Editor is insufficient to address the incomplete understanding of the breast cancer screening trials that has characterized recent analyses of the data and the recent Editorial by Drs Davis and Love.<sup>1</sup> The authors stated "mammographic screening in women under 50 years of age does not reduce deaths." This is simply not true. They based their conclusions about screening on a meta-analysis that used outdated information. The Gothenburg trial<sup>2</sup>recently revealed a 40% decrease in breast cancer deaths for screened women aged 40 to 49 years whose cancers were detected in their 40s and not, as some have suggested, because they had reached the magical age of 50 years. The preliminary results of a new meta-analysis of the seven trials with similar design demonstrate a statistically significant mortality reduction (at the 95% confidence level using a two-tailed
Intermittent claudication: factors determining outcome.
Authors: W G Hughson, J I Mann, D J Tibbs, H F Woods, I Walton
Journal: BMJ (1978)

Two groups of patients were followed up for four to eight years after first referral or admission to hospital for intermittent claudication (IC) in a study of the natural history of the disease and of factors determining its outcome. In one series of 60 patients, those who stopped or reduced smoking after referral had a much improved prognosis. Thus even after the diagnosis of IC it is extremely important that patients should be encouraged to stop smoking, since this correctable factor appears to be of greater importance in determining outcome than other medical risk factors for the disease that are less amenable to treatment. In the second study, 160 patients were followed up for eight years after first hospital admission. They had a total of 480 hospital admissions and had spent 11 190 days in hospital; their life expectancy after the age of 60 was about half that of the general population. Age, coronary artery disease, cerebrovascular disease, and diabetes were associated with an adverse outcome.
Evaluating treatment effects reliably
Authors: M. J Landray
Journal: BMJ (2002)

The introduction, more than half a century ago, of properly randomised trials in which the treatment allocation was rigorously concealed was a watershed in the evaluation of treatment effects.1 But this major advance did not come out of the blue: as was highlighted at a recent conference in Oxford (Beating biases in therapeutic research: historical perspectives, www.wuhmo.ox.ac.uk/docs/BeatingBiases.html), attempts to combat bias in therapeutic evaluation had in fact been made during the preceding few centuries.2–4

In the 18th century, the traditional practice of claiming therapeutic achievement on the basis of pathophysiological theories and anecdotal “successes” started to be challenged by medical non-conformists who wrote careful, prospective, analytical accounts of medical treatments, some of which included comparison with a control group.4 These “arithmetic observationists and experimentalists”4 recognised the need …
Selective induction of an embryonic fibronectin isoform in the rat aorta in vitro.
Authors: M Hosoi, I Takasaki, A Pavlova-Rezakova, H Himeno, A V Chobanian, P Brecher
Journal: Circulation Research (1993)

The temporal changes in the expression of fibronectin and other extracellular matrix genes were studied in rat aortic rings incubated in vitro in a serum-free medium. Changes in all forms of fibronectin mRNA increased progressively during the 24-hour incubation period, although an increase in the alternatively spliced form of fibronectin designated EIIIA was most pronounced. Both collagen and elastin mRNA levels decreased markedly during the 24-hour interval, as did alpha-actin mRNA. The increase in the relative amount of the EIIIA isoform after a 24-hour incubation was also shown using ribonuclease protection assays. In situ hybridization showed the distribution of the induced fibronectin mRNA to be within all cell types, including endothelial cells, medial smooth muscle cells, and adventitial fibroblasts. Localization in the media was not uniform and was clearly identified mainly in clusters of cells distributed throughout the media. The early induction of fibronectin mRNA was inhibited by genistein, implicating tyrosine kinase activation as a causative factor in fibronectin expression. The in vitro changes reported may reflect a phenotypic change in vascular cell types that is both similar to and different from the changes reported in vivo under conditions in which vascular injury and repair occur.
THE TREATMENT OF BURNS IN WARTIME
Authors: HENRY N. HARKINS
Journal: JAMA (1942)

The problem of thermal injuries is as old as recorded history. Even before fire had been harnessed to man's use the danger of burns from molten lava, forest fires and hot springs was constantly present. More recently the accidents of wartime have greatly increased the importance of thermal injuries. It is reported that 60 per cent of the casualties at Pearl Harbor were burns.  The treatment of war burns requires an adequate knowledge of the management of peacetime injuries coupled with an understanding of several of the distinguishing features of wartime burns. The present conflict has produced several unusual injuries not previously seen in large numbers, e. g. the airman's burn, the phosphorus burn and the burn contaminated by oil and sea water. These special types will be discussed later in more detail.  The adequate management of any burn includes a careful cooperative effort in two directions, namely (1) the
Most people would be willing to take part in clinical research
Authors: J. Wise
Journal: BMJ (2014)

Nine in 10 people would be willing to take part in clinical research if they had a medical condition diagnosed, a National Institute for Health Research survey has found.

The survey of 3000 people in England found that 89% would be happy to take part in a research study if they had a diagnosed disease or condition, and just 3% said that they would not consider it …
Mutation analysis of PTEN/MMAC1 in acute myeloid leukemia
Authors: Ta-Chih Liu, Pai-Mei Lin, Jan-Gowth Chang, Jing-Ping Lee, Tyen-Po Chen, Sheng-Fung Lin
Journal: American Journal of Hematology (2000)

Recently, a putative tumor suppressor gene, PTEN/MMAC1, has been identified at chromosome 10q23.3, which encodes a 403 amino acid dual-specificity phosphatase containing a region of homology to tensin and auxillin. Somatic mutations of the PTEN/MMAC1 gene have been identified in a number of cancer cell lines and primary cancers. Mutations in PTEN/MMAC1 are most frequently found in advanced cancers. To evaluate the role of the PTEN/MMAC1 gene in leukemia, bone marrow and/or peripheral blood from 62 acute myeloid leukemia (AML) patients, 5 hemopoietic cell lines (HL60, U937, Raji, KG-1, K562), and 30 normal controls were analyzed. The results showed aberrant PTEN/MMAC1 transcripts in 15 of the 62 (24%) AML patients, 4 of the 5 cell lines (80%), and 4 of the 30 (13%) normal controls. As in our previous study of TSG101, the abnormal transcripts may result from aberrant RNA splicing as evidenced by the presence of both these aberrant transcripts and normal full length transcripts in all specimens examined. Loss of heterozygosity (LOH) analysis and PCR-SSCP of the entire coding region showed that none of the AML cases had LOH or mutation. Only one frameshift mutation at codon 130 (insertion of CCCG) with premature termination of coding sequence was observed in the U937 cell line. Our results indicate that the PTEN/MMAC1 gene may play a role in a small percentage of AML, but its significance needs to be further evaluated.
US bill on pain relief bars doctor assisted suicide
Authors: F. Charatan
Journal: BMJ (2000)

The bipartisan Pain Relief Promotion Act introduced by Oklahoma Republican senator Don Nickles will be voted on soon in the US Senate as part of a much larger year-end tax bill.

The proposed new law reaffirms doctors' ability to use controlled substances to manage patients' pain and discomfort aggressively, especially among terminally ill patients. It provides for education and research into palliative care. However, it bars the use of drugs …
Queries and Minor Notes.
Authors: E. S. Goodhue
Journal: JAMA (1900)

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
Relation between bone erosions and rheumatoid factor isotypes.
Authors: J A Arnason, T Jonsson, A Brekkan, K Sigurjonsson, H Valdimarsson
Journal: Annals of the Rheumatic Diseases (1987)

Total rheumatoid factor (RF) activity and individual RF isotypes were measured in 62 patients with rheumatic diseases. Retrospective analysis of available x rays showed an association between IgA RF and the occurrence of periarticular bone erosions in hands. In contrast, IgG RF and IgM RF did not show any significant association with erosions. Furthermore, a close correlation was observed between the RF isotype levels in simultaneously drawn serum and synovial fluid samples. The possible significance of IgA RF in the pathogenesis of bone erosions is discussed.
The Practice of Reform in Health, Medicine and Science, 1500-2000
Authors: David Hughes
Journal: BMJ (2006)

H ealthcare reform has become a global phenomenon. Countries around the world are reshaping their health systems. The modified systems are often based on Western models and are subject to terms of “conditionality” imposed by supranational funding bodies. Many European countries seem to be locked into a continuous cycle of reform akin to Maostyle permanent revolution. Reform has become routine, and “reform fatigue” is widespread. Eds Margaret Pelling, Scott Mandelbrote Ashgate, £55, pp 376 ISBN 0 7546 3933 9 Rating: ![Graphic][1]</img>![Graphic][2]</img>![Graphic][3]</img>![Graphic][4]</img> A major health policy conference to be held in Israel later this year is entitled “Are we … [1]: /embed/inline-graphic-1.gif [2]: /embed/inline-graphic-2.gif [3]: /embed/inline-graphic-3.gif [4]: /embed/inline-graphic-4.gif
The Interleukin 2 and 4-Inducible Protein Phosphatase 5 (PP5) Abrogates Phosphorylation of Glucocorticoid Receptor and Induction of Dual Specificity Phosphatase 1 (DUSP1) in Eosinophils
Authors: K. Pazdrak, C. Straub, L. Richmond, K. Soman, A. Kurosky
Journal: Journal of Allergy and Clinical Immunology (2011)
Follistatin-like 1 Suppresses Sensory Afferent Transmission by Activating Na+,K+-ATPase
Authors: Kai-Cheng Li, Fang-Xiong Zhang, Chang-Lin Li, Feng Wang, Ming-Yan Yu, Yan-Qing Zhong, Kai-Hua Zhang, Ying-Jin Lu, Qiong Wang, Xiao-Li Ma, Jun-Ru Yao, Jin-Yuan Wang, Li-Bo Lin, Mei Han, Yu-Qiu Zhang, Rohini Kuner, Hua-Sheng Xiao, Lan Bao, Xiang Gao, Xu Zhang
Journal: Neuron (2011)
Prognostic role of troponin T and troponin I in patients with acute coronary syndromes: Meta-analysis of 20 studies
Authors: Dmitriy N Feldman, Michael Farkouh, Roxana Mehran, Eve D Aymong, Martin Fahy, Eugenia Nikolsky, Andrea S Abizaid, Alexandre A Abizaid, George Dangas
Journal: Journal of the American College of Cardiology (2003)
The Role of Tumor-Infiltrating Immune Cells and Chronic Inflammation at the Tumor Site on Cancer Development, Progression, and Prognosis: Emphasis on Non-small Cell Lung Cancer
Authors: Roy M. Bremnes, Khalid Al-Shibli, Tom Donnem, Rafael Sirera, Samer Al-Saad, Sigve Andersen, Helge Stenvold, Carlos Camps, Lill-Tove Busund
Journal: Journal of Thoracic Oncology (2010)
Abstract LB-122: LY2835219, a selective inhibitor of CDK4 and CDK6, inhibits growth in preclinical models of human cancer.
Authors: Jack A. Dempsey, Edward M. Chan, Teresa F. Burke, Richard P. Beckmann
Journal: Cancer Research (2013)

Abstract Cell growth is regulated by the activity of certain cyclin-dependent kinases (CDKs), including CDK4 and CDK6 (hereafter CDK4/6), which specifically regulate cell cycle progression through the G1 restriction point. These CDKs act with the D-type cyclins to phosphorylate and inactivate the retinoblastoma (Rb) tumor suppressor protein, which in turn enables cell cycle progression from G1 to S phase. LY2835219 is a selective inhibitor of CDK4/6 with IC50 of 2 and 10 nM for CDK4 and CDK6, respectively. The current study evaluates the activity of LY2835219 in preclinical models of human cancer including non-small cell lung cancer (NSCLC), melanoma, mantle cell lymphoma (MCL), and ovarian cancer. A secondary focus of this study is to identify potential predictive biomarkers for response to LY2835219 in NSCLC, melanoma, and other cancers. For NSCLC, increased sensitivity to LY2835219 is associated both in vitro and in vivo with KRAS mutations. For established melanoma cell lines, similar levels of in vitro sensitivity are observed in different genetic subtypes. Accordingly, LY2835219 shows single-agent activity in the A375 melanoma xenograft model with daily oral dosing at 45 or 90 mg/kg. For MCL, durable growth inhibition of subcutaneously implanted xenografts is achieved with daily oral dosing at 50mg/kg. Finally, in an intra-peritoneal model that recapitulates clinical features of human ovarian cancer, LY2835219 not only inhibits tumor growth but also increases survival. These studies suggest that LY2835219 may have potential therapeutic application in the treatment of human cancers with specific molecular alterations. Citation Format: Jack A. Dempsey, Edward M. Chan, Teresa F. Burke, Richard P. Beckmann. LY2835219, a selective inhibitor of CDK4 and CDK6, inhibits growth in preclinical models of human cancer. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr LB-122. doi:10.1158/1538-7445.AM2013-LB-122
Prevention of Venous Thrombosis With Small, Subcutaneous Doses of Heparin
Authors: Alexander S. Gallus
Journal: JAMA (1976)

The effect of low-dose heparin prophylaxis on venous thrombosis and bleeding after major elective surgery was studied in a prospective controlled study of 820 patients. The total incidence of venous thrombosis detected with leg-scanning using fibrinogen labeled with radioactive iodine (125I) was reduced from 16.0% in the control group to 4.2% in treated patients. More important, the incidence of popliteal or femoral vein thrombosis was reduced from 2.9% to 1.0%. Prophylaxis resulted in a slight increase in bleeding-minor wound hematoma, mean volume of blood transfused, and a post-operative hematocrit fall in treated patients. However, increased bleeding was clinically minor, and prophylaxis was well tolerated.
Abstract 1335: Lack of casein kinase 1 delta induces DNA damage, inhibition of mTORC1 signaling and nucleophagy
Authors: Yoshimi Endo Greer, Bo Gao, Yingzi Yang, Jeffrey S. Rubin
Journal: Cancer Research (2014)

Abstract Casein kinase 1 delta (CK1δ) is a conserved serine/threonine protein kinase that regulates diverse cellular processes including vesicle trafficking, cell cycle progression, chromosomal segregation, DNA repair, circadian rhythm, neurite outgrowth and ciliogenesis. CK1δ has been reported to phosphorylate Mdm2, the E3 ubiquitin ligase for p53, resulting in Mdm2 ubiquitination/degradation and concomitant accumulation of p53, the latter functioning as a mediator of cell cycle checkpoints and DNA repair. Mice that lack Csnk1d exhibit a perinatal lethal phenotype and typically weigh 30-50% less than their wild type littermates. The exact causes of death and small size are unknown. We hypothesized that the absence of CK1δ initiates cellular stresses that adversely affect cell survival. To examine this idea, we collected mouse embryonic fibroblasts (MEFs) from mice homozygous for a Csnk1d floxed allele, and generated MEF Csnk1d null cells by infection with adenovirus expressing Cre. Endogenous p53 protein level was significantly lower in MEF Csnk1d null cells relative to MEF Ctl cells infected with adenovirus-GFP. Substantial DNA damage also was detected in MEF Csnk1d null cells, as measured by γ-H2AX staining. Flow cytometric analysis revealed that early passage (P3) MEF Csnk1d null cells exhibited a larger sub-G0 fraction (64%) than MEF Ctl cells (34%). The sub-G0 fraction decreased sharply with increasing passage number, becoming negligible by P10. In addition to the decline in sub-G0 fraction, we observed a transient population of MEF Csnk1d null cells with multiple DAPI-stained micronuclei containing both γ-H2AX and membranes positive for the autophagosomal marker LC3 and lysosomal marker LAMP1. These features were preceded by and coincided with mTORC1 pathway inactivation, as indicated by low concentrations of phospho-Akt, phospho-mTOR and phospho-S6K, consistent with the view that mTORC1 inhibition facilitates the induction of autophagy. Subsequently, these differences between MEF Csnk1d null and MEF Ctl cells subsided. Our findings demonstrate that loss of CK1δ expression in proliferating MEF cells results in DNA damage and initially a large sub-G0 peak, followed by a wave of nucleophagy and ultimately cell survival in culture. Ongoing investigation will explore whether similar processes occur in embryonic tissues from Csnk1d null mice and contribute to their pathologic phenotype. Citation Format: Yoshimi Endo Greer, Bo Gao, Yingzi Yang, Jeffrey S. Rubin. Lack of casein kinase 1 delta induces DNA damage, inhibition of mTORC1 signaling and nucleophagy. [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 1335. doi:10.1158/1538-7445.AM2014-1335
Work and School Phobias: A Family Approach to Treatment
Authors: FRANK S. PITTMAN, DONALD G. LANGSLEY, CAROL D. DEYOUNG
Journal: American Journal of Psychiatry (1968)

The authors describe the syndrome of work phobia, which is not a classical phobia but separation anxiety associated with leaving home to go to work. Differentiated from work inhibition and success neurosis, work phobia is considered to be the adult form of school phobia. It occurs most often in former school phobics and, like school phobia, responds to helping the wife or mother to firmly allow the man to separate. The authors feel that such crisis family therapy is more successful than long-term individual therapy in the treatment of this syndrome.
Bell Palsy and Herpes Simplex Virus
Authors: Shingo Murakami
Journal: Annals of Internal Medicine (1996)

Letters15 October 1996Bell Palsy and Herpes Simplex VirusShingo Murakami, MD and Naoaki Yanagihara, MDShingo Murakami, MDEhime University School of Medicine, Ehime, 791-02 JapanSearch for more papers by this author and Naoaki Yanagihara, MDEhime University School of Medicine, Ehime, 791-02 JapanSearch for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-125-8-199610150-00024 SectionsAboutFull TextPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail IN RESPONSE:Since the ischemic hypothesis was first proposed by Kettel in 1947 [1], ischemia has been widely accepted as having one of the most important roles in the pathogenesis of Bell palsy. However, direct evidence supporting this hypothesis was lacking. Dr. Devriese [2] was the first to clearly show that increasing pressure and subsequent ischemia of the facial nerve could produce facial palsy. The results apparently substantiated Kettel's hypothesis and were repeatedly presented as having a role in the pathogenesis of Bell palsy at the Third (Zurich, 1976) and Fourth (Los Angeles, 1980) International Symposium on the Facial Nerve. ...References1. Kettel K. Bell's palsy: pathology and surgery. A report concerning fifty patients who were operated on after the methods of Ballance and Duel. Arch Otolaryngol. 1947; 46:427-72. Google Scholar2. Devriese PP. Compression and ischaemia of the facial nerve. Acta Otolaryngol (Stockholm). 1974; 77:108-18. Google Scholar3. Furuta Y, Takasu T, Sata KC, Fukuda S, Inuyama, Nagashima K. Latent herpes simplex virus type 1 in human geniculate ganglia. Acta Neuropathol. 1992; 84:39-44. Google Scholar4. Murakami S, Hato N, Mizubuchi M, Doi T, Yanagihara N. Role of herpes simplex virus infection in the pathogenesis of facial paralysis in mice. Ann Otol Rhinol Laryngol. 1996; 105:49-53. Google Scholar5. Hunt JR. On herpetic inflammations of the geniculate ganglion. A new syndrome and its complications. J Nerv Ment Dis. 1907; 34:73-96. Google Scholar Author, Article, and Disclosure InformationAffiliations: Ehime University School of Medicine, Ehime, 791-02 Japan PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics 15 October 1996Volume 125, Issue 8Page: 698-699KeywordsAnimal modelsCellsEdemaFacial nerveGangliaHerpes simplexIschemiaNervesParalysisPathogenesis ePublished: 15 August 2000 Issue Published: 15 October 1996 Copyright & PermissionsCopyright © 1996 by American College of Physicians. All Rights Reserved.PDF downloadLoading ...
Ovarian Hyperstimulation Syndrome Due to a Mutation in the Follicle-Stimulating Hormone Receptor
Authors: Guillaume Smits, Olufemi Olatunbosun, Anne Delbaere, Roger Pierson, Gilbert Vassart, Sabine Costagliola
Journal: New England Journal of Medicine (2003)

The overproduction of endogenous chorionic gonadotropin during pregnancy has been associated with spontaneous ovarian hyperstimulation syndrome. Yet the syndrome has been observed in women with normal levels of chorionic gonadotropin. This Brief Report defines a mutation in the follicle-stimulating hormone (FSH) receptor that is associated with recurrent, spontaneous ovarian hyperstimulation syndrome. In this instance, the mutant receptor responded both to chorionic gonadotropin and to thyrotropin.