tbuckley/cabot-search huggingface dataset:
Abstract P408: Plasma Alkylresorcinol, A Biomarker of Whole-Grain Intake, Is Not Associated With Progression of Coronary Artery Atherosclerosis In Postmenopausal Women With Coronary Artery Disease
Authors: Nicola M McKeown, Adela Hruby, Rikard Landberg, David M Herrington, Alice H Lichtenstein
Journal: Circulation (2014)

Background: Higher whole-grain intake has been associated with lower risk of cardiovascular disease in prospective observational studies. Few observational studies have incorporated biomarkers of whole-grain intake to confirm self-reported diet-disease associations. Plasma alkylresorcinols (AR) have been used as biomarkers for whole-grain wheat and rye intake. Objective: To assess the relationship between plasma AR concentrations and atherosclerotic progression over a 3-y period. Methods: Plasma AR concentrations were measured by gas chromatography mass spectrometry in baseline samples from 163 post-menopausal women (aged 49-78 y; median BMI: 29.0 kg/m2) with established coronary artery disease (CAD) who participated in the Estrogen Replacement and Atherosclerosis Study (enrolled 1995-1996) and had baseline food frequency questionnaire (FFQ), baseline and follow-up angiography measures, and complete covariate data. Dietary fiber intake was estimated by FFQ and energy-adjusted. Atherosclerosis progression, defined as change in mean minimum coronary artery diameter (MCAD, mm) and change in percent stenosis (%ST), was regressed on plasma AR in mixed models accounting for within-person correlations of coronary segments, and adjusted for the baseline measure, treatment allocation, clinic, age, race, BMI and follow-up time. Results: Median plasma AR was 16.1 nmol/L (interquartile range: 10.9-25.7). Over 3.1±0.7 years of follow-up, MCAD decreased by approximately 0.09±0.02 mm, while %ST increased by approximately 3.2±0.7%. No significant association was observed between AR and change in MCAD or %ST: a 10% increment in AR was associated with a -0.0002±0.0008 mm (P=0.76) change in MCAD and a 0.008±0.03 change in %ST (P=0.79). Further adjustment for lifestyle and risk factors did not materially change these results. As expected, AR correlated with FFQ- derived intake of cereal fiber (Spearman r=0.27, P&lt;0.001) and whole grains (Spearman r=0.28, P&lt;0.001). Of note, this cohort reported low whole-grain and cereal fiber intakes (9.5 servings/wk and 5.3 g/d, respectively). Conclusions: Plasma AR concentrations were not significantly associated with coronary narrowing over a 3-y period in postmenopausal women with CAD. We cannot rule out that large measurement errors in the biomarker, owing to low intake and short half-life may explain the findings.
Essentials of Pediatric Nursing.
Authors: Theresa Kyle, Susan Carman
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
Abstract 17746: Telecinobufagin, a Novel Cardiotonic Steroid, Promotes Myocardial and Renal Fibrosis via Na/K-ATPase Profibrotic Signalling Pathways
Authors: David J Kennedy, Malory E Weber, Anuradha Guggilam, Kristen M Westfall, Brendan Agatisa-Boyle, Philip Bucur, Jerry B Lingrel, W. H. Wilson Tang
Journal: Circulation (2014)

Cardiotonic steroids (CTS) are Na/K-ATPase (NKA) ligands that are elevated in volume-expanded states and associated with cardiac and renal dysfunction in both clinical and experimental settings. We recently discovered significantly elevated levels of a novel CTS, telocinobufagin (TCB), in patients with heart failure. We tested the hypothesis that TCB promotes cardiac and renal dysfunction in a process involving signaling through the NKA-α-1 in the following studies. First, we infused TCB (4 weeks at 10 ug/Kg/day) or vehicle into mice expressing wild type NKA-α-1 (WT), as well as mice with a genetic reduction of NKA-α-1 (NKA+/-) or transgenic human NKA-α-1 (NKA-Tg), which renders them more sensitive to CTS. TCB infusion resulted in impairment of cardiac structure (36% increase in heart weight/body weight ratio, 18% increase in diastolic Left Ventricular Internal Dimension vs. vehicle, p&lt;0.05) in WT mice which was significantly attenuated in NKA+/- mice. TCB infusion also resulted increased proteinuria and cystatin C in WT mice which was significantly attenuated in NKA+/- mice (all p&lt;0.05) despite similar increases in blood pressure. In NKA-Tg mice, TCB infusion resulted in increased myocardial (Fig 1A) and renal (Fig 1B) fibrosis vs. WT (all p&lt;0.05). In a series of in vitro experiments, 24 hour treatment of HK2 renal proximal tubular cells with TCB resulted in significant dose dependent increases in both Collagen 1 and 3 mRNA (2 fold increases at 10 nM, 5 fold increases at 100 nM, p&lt;0.05). TCB treatment (100 nM) of SYF fibroblasts reconstituted with cSrc resulted in a 1.5 fold increase in Collagen 1 and 3 mRNA (p&lt;0.05) as well as increases in both Transforming Growth factor beta (TGFb, 1.5 fold, p&lt;0.05) and Connective Tissue Growth Factor (CTGF, 2 fold, p&lt;0.05), while these effects were absent in SYF cells without Src kinase. These studies suggest that the pro-fibrotic effects of TCB are mediated though the NKA-Src kinase signaling pathway.
Corticotropin-releasing hormone promotes blastocyst implantation and early maternal tolerance
Authors: A. Makrigiannakis, E. Zoumakis, S. Kalantaridou, C. Coutifaris, A. N. Margioris, G. Coukos, K. C. Rice, A. Gravanis, G. P. Chrousos
Journal: Nature Immunology (2001)
Abstract 3719: Mechanisms of resistance to the second-generation alk inhibitor ap26113 in human npm-alk-positive anaplastic large cell lymphoma cells
Authors: Monica Ceccon, Luca Mologni, Giovanni Giudici, Rocco Piazza, Alessandra Pirola, Diletta Fontana, Carlo Gambacorti-Passerini
Journal: Cancer Research (2014)

Abstract ALK is a tyrosine kinase receptor involved in a broad range of solid and haematological tumors. It has been shown that about 70-80% of ALK+ Anaplastic Large Cell Lymphoma (ALCL) cases, an aggressive Non Hodgkin T-cell lymphoma, are characterized by the traslocation t(2;5), originating the functional, aberrant oncogenic fusion protein NPM-ALK. Crizotinib was the first clinically relevant ALK inhibitor, now approved for the treatment of late stage and metastatic cases of lung cancer. Several patients soon developed Crizotinib resistance, mainly due to the appearance of new point mutations located in ALK kinase domain. Currently, other ALK inhibitors are available and already in clinical trial, hopefully representing the second line therapy able to overcome Crizotinib resistance. In this work we focused our attention on the more potent phase I/II dual ALK/EGFR inhibitor AP26113 (Ariad Pharm.), able to overcome the Crizotinib-resistant gatekeeper mutation L1196M. Two NPM-ALK+ human cell lines, KARPAS-299 and SUP-M2, were grown in four independent flasks in the presence of increasing doses of AP26113, so that eight cell lines able to grow in the presence of high AP26113 doses were selected. All cell lines show an AP26113 50% inhibitory concentration (IC50) value substantially higher than the one observed in parental cells, with a 130 to 1000-fold increase. All KARPAS-299 populations resistant to AP26113 show NPM-ALK overexpression, due to oncogene amplification, as the main cause of resistance, while SUP-M2 cells proliferating in the presence of the drug harbour several point mutations spanning the entire ALK kinase domain. In particular, we identified the following aminoacid substitutions: L1122V, , L1196M, S1206C and a double F1174V+L1198F mutation. The knowledge of the possible appearance of new clinically relevant mechanisms of drug resistance is a useful tool for the management of new TKI resistant cases. Citation Format: Monica Ceccon, Luca Mologni, Giovanni Giudici, Rocco Piazza, Alessandra Pirola, Diletta Fontana, Carlo Gambacorti-Passerini. Mechanisms of resistance to the second-generation alk inhibitor ap26113 in human npm-alk-positive anaplastic large cell lymphoma cells. [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 3719. doi:10.1158/1538-7445.AM2014-3719
414. Design of an HIV Vector for Site-Specific Gene Insertion
Authors: Gilles Michel, Ying Yu, Jiing-Kuan Yee
Journal: Molecular Therapy (2004)

Top of pageAbstract
Pluripotent hematopoietic stem cells (HSCs) give rise to all lineages of mature blood cells, and serve as an important gene therapy target. While vectors derived from murine leukemia virus (MLV) are widely used to deliver genes into HSCs in various human gene therapy trials, their transduction efficiency of HSCs is rather low. This could be partly due to the quiescent nature of HSCs. Vectors derived from human immunodeficiency virus (HIV) are developed to circumvent the problem of low transduction efficiency of quiescent cells by the MLV vector. However, since both vectors integrate randomly into the host genome, it can lead to gene disruption or unanticipated gene activation through the enhancer or the promoter element present in the vector. The leukemia incidence induced by MLV vector integration near an oncogene in severe combined immunodeficiency (SCID) patients and recent discoveries of preferential integration by MLV and HIV near or within active genes underscore the importance of designing strategies for site-specific gene insertion. To address this issue, we have incorporated the Cre-loxP system into an HIV vector. We generated a human cell line containing a unique loxP site in the genome to serve as a target for gene insertion. A targeting vector containing the loxP site was produced from 293T cells and used to transduce the loxP-containing cell line. Transduced cells were pooled and the genomic DNA was prepared. PCR analysis of the genomic DNA showed site-specific insertion of the gene carried by the targeting vector into the loxP site in the host genome. From the number of the transduced cells, the efficiency of site-specific gene insertion was determined to be in the range between 0.04% and 0.004%. If we enriched for the site-specific gene insertion event by using an HIV vector deficient in integrase, the efficiency was increased to 0.7%. Our approach demonstrates the first step of designing HIV vectors for therapeutic gene targeting.
Initial Cost of Primary Angioplasty for Acute Myocardial Infarction11This work was supported by The Permanente Medical Group.All editorial decisions for this article, including selection of referees, were made by a Guest Editor. This policy applies to all articles with authors from the University of California, San Francisco.
Authors: TRACY A. LIEU, ROBERT J. LUNDSTROM, G.THOMAS RAY, BRUCE H. FIREMAN, R.JAN GURLEY, WILLIAM W. PARMLEY
Journal: Journal of the American College of Cardiology (1996)
The New Generation: The Intimate Problems of Modern Parents and Children.
Authors: Victor Francis Calverton, Samuel Daniel Schmalhausen
Journal: JAMA (1931)

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
<i>Annals</i> Graphic Medicine - One in a Million
Authors: Yehuda Z. Cohen, Saul Haber
Journal: Annals of Internal Medicine (2015)

Web Exclusives7 July 2015Annals Graphic Medicine - One in a MillionYehuda Z. Cohen, MD and Saul HaberYehuda Z. Cohen, MDSearch for more papers by this author and Saul HaberSearch for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/G14-0001 SectionsAboutFull TextPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail Download figure Download PowerPoint Download figure Download PowerPoint Download figure Download PowerPoint Download figure Download PowerPoint Download figure Download PowerPoint Author, Article, and Disclosure InformationAffiliations: Acknowledgment: Dedicated to Jonathan “Vinny” Weinberg, 1981–2013. Special thanks to Jonathan's family for permission to share this story.Disclosures: Authors have disclosed no conflicts of interest. Forms can be viewed at www.acponline.org/authors/icmje/ConflictOfInterestForms.do?msNum=G14-0001.Author and Illustrator Information: Yehuda Z. Cohen, MD, was, at the time of submission, at Beth Israel Deaconess Medical Center in Boston and is now an Instructor in Clinical Investigation at The Rockefeller University in New York City. Saul Haber is a freelance illustrator based in New York City (www.comicbookman.com).Corresponding Author: Yehuda Z. Cohen, MD, The Rockefeller University, 1230 York Avenue, Box 220, New York, NY 10065; e-mail, [email protected]com.Author Contributions: Conception and design: Y.Z. Cohen, S. Haber.Drafting of the article: Y.Z. Cohen, S. Haber.Final approval of the article: Y.Z. Cohen. Previousarticle Advertisement FiguresReferencesRelatedDetails Metrics 7 July 2015Volume 163, Issue 1Page: W129-W134KeywordsConflicts of interestDisclosureHealth care ePublished: 7 July 2015 Issue Published: 7 July 2015 Copyright & PermissionsCopyright © 2015 by American College of Physicians. All Rights Reserved.PDF downloadLoading ...
Abstract #2308: Radiosensitization of cancer cells by \#946;-lapachone
Authors: Guang-Zhi Dong, Eun-Taex Oh, Hyemi Lee, Dos Santos Troy, Chang W Song, Heon Joo Park
Journal: Cancer Research (2009)

The purpose of the present study was to elucidate the radiosensitization caused by \#946;-lapachone, a novel anti-cancer drug. FSaII fibrosarcoma of C3H mice and A549 human lung cancer cells were used. Cells were exposed to a single or split-dose irradiation with or without \#946;-lapachone treatment and the clonogenic cell survival was determined. The effect of \#946;-lapachone on the radiation-induced DNA double strand breaks was studied with \#947;-H2AX method, and that on the radiation induced activation of NF-kB was determined. Molecular signals involved in cell death were studied with western blot analysis. Treating the cells with \#946; -lapachone for 2 h, starting immediately before irradiation, markedly increased the radiosensitivity of the cells as indicated by significant change in the shoulder and the slop of the radiation survival curve of the cells. \#946;-Lapachone suppressed the repair of sublethal radiation damage, as determined with split-dose irradiation method. Upon an exposure to 2 Gy irradiation, \#947;-H2AX expression, hallmark of DNA double strand breaks, marked increased till 2 h post-irradiation and declined, and \#946;-Lapachone significantly delayed the decay of \#947;-H2AX, indicating that \#946;-lapachone inhibited the repair of radiation-induced DNA double strand breaks. \#946;-lapachone inhibited the radiation-induced phosphorylation of IkB-\#945;, thereby inhibiting the activation of NF-kB. Phosphorylation of JNK by combination of \#946;-lapachone and irradiation was significantly greater than that caused by either of them alone. All these interaction between \#946;-lapachone and radiation could be reduced when cells were transfected with shNQO1, demonstrating that NQO1 plays critical role in the radiosensitization caused by \#946; -lapachone. Conclusion: \#946; -lapachone sensitizes cancer cells to radiation by inhibiting repair of DNA double strand breaks in NQO1 dependent manner. Acknowledgments: This work supported by grants of National Nuclear Technology Program (2007) from KOSEF, the Korea Health 21 RD 2009 Apr 18-22; Denver, CO. Philadelphia (PA): AACR; 2009. Abstract nr 2308.
Abstract P318: Risk factors for 10-year coronary artery calcium progression in the Multi-Ethnic Study of Atherosclerosis
Authors: Amanda J Gassett, Lianne Sheppard, Robyn L McClelland, Richard A Kronmal, Matthew J Budoff, Michael J Blaha, Joel D Kaufman
Journal: Circulation (2014)

Coronary artery calcium (CAC) progression has previously been observed to predict coronary events above and beyond its association with baseline CAC. Prior studies show associations between CAC progression and risk factors, but were limited by short follow-up or restriction to individuals with advanced disease. We examined the relationship between risk factors for clinical events and the progression of CAC in MESA, a prospective cohort study. Participants were 6810 adults without CVD at recruitment in 2000-2002. Agatston scores for extent of calcification were assessed 1-4 times (mean 2.5) over a 10-year period with interim exams spaced at approximately 2-4 years. Mean follow-up time for those with at least 2 scans was 5.0 years. An innovative approach to mixed effects models jointly modeled the associations between risk factors and CAC both at baseline and with CAC progression rate. This method is less biased than controlling for baseline CAC, since the same risk factors are associated with both baseline and progression. Hence, time-varying factors can adjust progression rate, and data from participants with varying follow-up time and number of measurements_even those measured only at baseline_are incorporated. Mean CAC progression rate was 25 CAC units/year. All models were adjusted for age, sex, site, and race/ethnicity. Strong effects were observed for age, male sex, hypertension, and diabetes. Effects for statins likely reflect poor health status, rather than a causal effect of medication. Simultaneous adjustment for all risk factors produced similar results except the effect of statin use was not observed. See table for estimates and confidence intervals. In conclusion, CAC progression is associated with risk factors for clinical coronary events, confirming that processes involved in CAC progression mirror development of clinical atherosclerosis. The methods applied for the analysis of repeated continuous noninvasive measures of atherosclerosis extent can also be applied to evaluating novel risk factors.
Provocation tests as measure of efficacy and dosage
Authors: F. de Blay
Journal: Allergy (2011)

Provocation and challenge tests have been used to understand the pathobiology of asthma, to facilitate diagnosis and to assess therapeutic efficacy and dosage. Current challenge tests expose the patient to 'natural conditions', for example, in an allergen chamber. For determining drug efficacy in asthma, allergen challenge has a moderate positive predictive value and an excellent negative predictive value. The best challenge tests are standardized, and the best bronchial challenge tests use a large allergen particle size. Allergen provocation tests are safe when performed by experienced investigators.
Sarcoidosis or primary Sjogren's syndrome?
Authors: Jorge Ferrer, Francisco Javier Bosch Aparici, Ricard Cervera i Segura, Josep Font Franco, Miguel Ingelmo Morín
Journal: Annals of the Rheumatic Diseases (1988)

studies.5-FU remains an unproved treatment for scleroderma and its use outside properly conducted clinical studies is strongly discouraged.The report of Malaviya et al emphasises that no matter how promising a new treatment appears it must be critically evaluated before patients are subjected to its potentially harmful effects.
New Oral Anticoagulants Show Promise
Authors: Tracy Hampton
Journal: JAMA (2006)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA HomeNew OnlineCurrent IssueFor Authors 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