tbuckley/cabot-search huggingface dataset:
Abstract 13879: Ischemic Postconditioning Confers Cardioprotection through Adiponectin-dependent Mitochondrial STAT3 Activation in Mice
Authors: Haobo Li, Michael G Irwin, Zhengyuan Xia
Journal: Circulation (2014)

Introduction: Signal transducer and activator of transcription 3 (STAT3) plays a key role in postconditioning (IPo) mediated protection against myocardial ischemia reperfusion injury, but the mechanism by which IPo activates STAT3 is unknown. Adiponectin (APN), a protein with anti-ischemic properties, activates STAT3. We hypothesized that IPo activates mitochondrial STAT3 (MitoSTAT3) via APN signaling. Methods and Results: Wild type (WT) and APN knockout (KO) mice were either sham operated or subjected to 30 min of coronary artery occlusion followed by 2 hours of reperfusion with or without IPo (3 cycles of 10 seconds reperfusion and 10 seconds reocclusion; n=8/group). At the end of reperfusion, KO mice exhibited more severe myocardial injury evidenced as increased infarct size (% of area at risk) 49.2±2.0 vs WT 39.4±3.5, P &lt;0.01; plasma troponin I (ng/ml): KO 72.8±7.6 vs WT 45.7±4.0, P &lt;0.01; worse cardiac function (lower dP/dt max and end-systolic pressure-volume relation, P &lt;0.05); more severely impaired mitochondrial function (reductions in complex IV and complex V protein expression) and more severe reduction of MitoSTAT3 phosphorylation (activation) at site Ser727, P &lt;0.01. IPo significantly attenuated post-ischemic cardiac injury and dysfunction with a concomitant increase in phosphorylated MitoSTAT3 and attenuation of mitochondrial dysfunction in WT (all P &lt;0.05) but not in KO mice. In cultured cardiac H9C2 cells, hypoxic postconditioning (HPo, 3 cycles of 5 min hypoxia and 5 min reoxygenation) significantly attenuated hypoxia/reoxygenation (HR, 3 hours hypoxia/3 hours reoxygenation) induced cell injury (increased apoptotic cell death as % of HR): HR 100.2±0.4 vs HPo 78.2±4.8, P &lt;0.05) and reduced mitochondrial transmembrane potential (% total cells, HR 37.2±4.9 vs HPo 23.5±3.7, P &lt;0.01). APN, adiponectin receptor 1 (AdipoR1), or STAT3 gene knockdown but not AdipoR2 gene knockdown, respectively, abolished HPo cellular protection (all P &lt;0.05 vs. HPo). APN supplementation (10μg/ml) restored HPo protection in cells with APN knockdown but not in cells with AdipoR1or STAT3 gene knockdown. Conclusion: Adiponectin and AdipoR1 signaling are required for IPo to activate myocardial mitochondrial STAT3 to confer cardioprotection.
Effects of Omega-3 Fatty Acids on Cancer Risk: A Systematic Review—Correction
Authors: Catherine H. MacLean, Sydne J. Newberry, Walter A. Mojica, Puja Khanna, Amalia M. Issa, Marika J. Suttorp, Yee-Wee Lim, Shana B. Traina, Sally C. Morton
Journal: JAMA (2006)

TUDIES SHOW THAT TISSUE LEVels of arachadonic acid-and eicosopentaenoic acid (EPA)derived eicosanoids influence many physiological processes, including calcium transport across cell membranes, angiogenesis, apoptosis, cell proliferation, and immune cell function. [1]2][3][4] These processes are integral to the immune system and hence the pathogenesis of autoimmune diseases such as arthritis, systemic lupus erythematosus, and asthma, as well as cancer.0][11][12][13][14][15][16][17][18][19][20][21][22] In addition, dietary omega-3 fatty acids have been found to modulate mammary tumor formation and proliferation in rodents. 23n response to this evidence, a number of omega-3 fatty acid-containing dietary supplements have appeared on the market claiming to protect against the development of a variety of conditions including cancer.To assess the va-
Partial deficiency of DNA-PKcs increases ionizing radiation induced mutagenesis and cell killing in human cells
Authors: Ying Zhang, Junqing Zhou, Xiaofan Cao, Qinming Zhang, Susan Bailey, Howard Liber
Journal: Cancer Research (2006)

4388   The repair of DNA double strand breaks is essential to maintain the integrity of genome. Misrepaired DNA DSBs are detrimental to cells by leading to gene mutation and cancer development. Nonhomologous end-joining (NHEJ) is one of the principal rejoining processes in most higher eukaryotic cells. NHEJ is facilitated by DNA dependent protein kinase (DNA-PK), which is composed of a catalytic subunit, DNA-PKcs, and the heterodimeric DNA binding regulatory complex Ku. Null mutation of DNA-PKcs leads to immunodeficiency, chromosomal translocation, cancer predisposition in mice, and gene mutation. However, it is unknown whether the partial deficiency of DNA-PKcs that is more likely to occur in a fraction of the population influences cellular function. Using small interfering RNA transfection, we established partial deficiency of DNA-PKcs in human cells, with a range of 4-85% of control. Our results reveal that partial deficiency of DNA-PKcs leads to an increased ionizing radiation-induced mutagenesis and cell killing. Radiation mutagenesis was increased inversely with DNA-PKcs protein levels, with the most pronounced effect observed between 4 and 50% protein levels.
Class-efficacy of hyaluronan/hylan versus placebo in knee osteoarthritis: A Cochrane Review
Authors: N. Bellamy, J. Campbell, T. Gee, V. Robinson, R. Bourne, G. Wells
Journal: Annals of the Rheumatic Diseases (2005)

Background: Osteoarthritis (OA) is the most common form of chronic arthritis worldwide. Hyaluronan and hylan (HA) products provide opportunity for local treatment of individual OA knee joints.

Objectives: To evaluate the class-efficacy of HA products compared to placebo (PL) in the treatment of knee OA as part of a Cochrane review of viscosupplementation.

Methods: Electronic searches were conducted of EMBASE, MEDLINE, PREMEDLINE up to July 2003 and CENTRAL up to the 2Q of 2003. Human, randomised, controlled trials (RCTs) were included. Methodological quality was assessed using the Jadad criteria by 2 reviewers. Data on the OARSI and OMERACT core set clinical outcome measures were extracted where possible. Weighted mean differences (WMD), based on unadjusted post-test scores, and 95% confidence intervals (CI) were calculated for continuous outcomes measured on the same scale. The standardised mean difference (SMD) and 95% CI were calculated for continuous outcomes measured on different scales. Relative risk was calculated for dichotomous outcome measures. Heterogeneity was tested with chi square test; when detected a random effect (RE) model was used rather than a fixed effect model. Analysis used RevMan 4.1.1 software.

Results: 37 RCTs included comparisons of HA and PL. Statistically significant differences were detected between HA and PL at 1-4 weeks (pain on weight-bearing (100 mm VAS) WMD (RE) was -7.92 (95% CI, -11.70 to -4.14) p=0.00004, Lequesne Index (0-24) WMD (RE) was -1.21 (95% CI, -2.19 to -0.22) p=0.02), 5-13 weeks (pain on weight-bearing WMD (RE) was -12.97 (95% CI, -18.00 to -7.93) p<0.00001, WOMAC pain SMD was -0.33 (95% CI, -0.55 to -0.10) p=0.004 and WOMAC function SMD was -0.56 (95% CI, -0.89 to -0.24) p=0.0007, Lequesne Index WMD was -1.30 (95% CI, -1.93 to -0.67) p=0.00005, flexion WMD was 7.60 (95% CI, 0.46 to 14.74) p=0.04, and 14-26 weeks (pain on weight-bearing WMD (RE) was -9.04 (95% CI, -14.83 to -3.24) p=0.002, WOMAC pain (100 mm VAS) WMD was -5.66 (95% CI, -10.06 to -1.26) p=0.01) post-injection.

Conclusion: These data support the evidence for efficacy of this class of intervention on multiple efficacy variables. The beneficial effects are time and variable dependent. The pooled analyses address issues relating to class characteristics and may not be shared to the same extent by each individual HA product. The by-product analyses (data not shown) provide support for the use of those HA products for which the effect is not only statistically significant but also clinically important.
Abstract 15155: Supracardiac Type (1a) Total Anomalous Pulmonary Venous Return with Right to Left Shunt Atrial Septal Defect Diagnosed by 320 Slice CT
Authors: Nobusada Funabashi, Hiroyuki Takaoka, Koya Ozawa, Yoshio Kobayashi
Journal: Circulation (2014)

The first choice of imaging modality to evaluate complex congenital heart disease, especially in infants, is transthoracic echocardiogram (TTE) and magnetic resonance imaging. But to evaluate anatomic details of the heart, including coronary arteries with surrounding structures, CT is most useful. We experienced a patient who was diagnosed as having supracardiac type total anomalous pulmonary venous return (TAPVR) with a right to left shunt atrial septal defect (ASD) by 320 slice CT. A 63-year-old female who had palpitations and dizziness was referred to our hospital because of cardiac enlargement shown on chest X ray in a health examination. On chest X ray, enlargement of protrusion of the right first and left first aortic arches was observed. ECG revealed ectopic low part atrial rhythm, right axis deviation of the QRS wave, and incomplete right bundle branch block. On TTE, ASD with right to left shunt was observed, presence of Eisenmenger syndrome was suspected and there seemed to be no surgical indication. But on TTE, right heart configuration seemed not due to pressure load but volume load, which is not indicative of Eisenmenger syndrome. To evaluate the presence of other complications of anatomical cardiovascular heart disease, ECG-gated 320 slice CT (Aquilion ONE, Toshiba Medical) was performed. On CT, supracardiac type TAPVR with right to left shunt ASD could be accurately diagnosed. She then underwent TAPVR surgical repair from the superior approach in which total PV connected to the LA and ligated innominate vein and ASD pericardial patch closure. By this procedure, there was no blood flow from PV to the right heart, with blood from the PV flowing into the LA directly. Hemodynamics was normalized. In summary, this patient had remarkable cardiac enlargement on chest X-ray, and on TTE ASD with right-to-left shunt was detected. 320 slice CT can evaluate complex congenital heart disease as well as coronary arteries accurately and provide information on blood flow.
<i>Case Studies in Epilepsy: Common and Uncommon Presentations</i>
Authors: Gregory L. Holmes
Journal: JAMA Neurology (2013)

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 Neurology HomeNew OnlineCurrent IssueFor Authors Podcast 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 Neurology journal
Ultrastructural Changes Occurring in the Transition of the Adenocarcinoma 755 from the Solid to the Ascites Form
Authors: David Brandes, Donald P. Groth
Journal: Cancer Research (1960)

Summary  A fine structural analysis of the Adenocarcinoma 755 in the solid and ascites forms has shown that considerable alterations occur in the conversion of the solid into the ascites form and vice versa.  The cells of the ascites form displayed a pronounced polarization of the formed elements in juxtaposition with the indentations present in the nucleus.  Particles which may represent virus were detected in both solid and ascites forms, within the cavities of the endoplasmic reticulum and in the form of groups surrounded by a dense membrane.
Unusual Addison's Syndromes
Authors: A. B. Brower
Journal: Annals of Internal Medicine (1930)

Article1 August 1930Unusual Addison's SyndromesA. B. BROWER, M.D., F.A.C.P.A. B. BROWER, M.D., F.A.C.P.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-4-2-166 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail Excerpt"The leading and characteristic features of the morbid state to which I would direct attention are anemia, general languor and debility, remarkable feebleness of heart action, irritability of the stomach, and a peculiar change in color of the skin occurring in connection with diseased condition of the suprarenal capsule." This original description of adrenal insufficiency by Addison1 remains classical.If a patient presents these clinical phenomena and at autopsy shows bilateral destructive changes of the adrenals, there can be no doubt as to the diagnosis. On the other hand, if a patient presents the clinical manifestations of Addison's disease, and...References1 ADDISON T: On the Constitutional and Local Effects of Disease of the Suprarenal Capsules. London, 1855, S. Highley 43 p., 11 Pl. fol. Google Scholar2 BARKER NW: A Study of the Pathologic Anatomy of Twenty-Eight Cases of Addison's Disease. Proceedings of the Staff of the Mayo Clinic, (March 20), 1929, 4, 91. Google Scholar3 WARTHIN AS: Syphilis of the Adrenals. (Presented at the 1929 Meeting of the American College of Physicians, Boston. To appear in Ann. Int. Med.). Google Scholar4 LOEPEROLLIVER MJ: Fatty Transformation of both Suprarenals with Melanoderma. Bull. et Mem. Soc. méd. d'hôp., Paris, 1926, 50, 312. Google Scholar5 BITTORF A: Ueber die Pigmentbildung beim Morbus Addisonii. Deutsch. Arch. f. klin. Me., 1921, 136, 314. Google Scholar6 BROWN CE: Volume and Composition of the Blood in Addison's Disease. Am. J. Med. Sc., 1925, 169 47. CrossrefGoogle Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: Dayton, Ohio*From the Diagnostic Division of the Dayton Clinic, Dayton, Ohio.†Read at the Fourteenth Annual Clinical Session, American College of Physicians, Minneapolis, February 12, 1930. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics 1 August 1930Volume 4, Issue 2Page: 166-175KeywordsAnemiaAutopsyHeartStomach ePublished: 1 December 2008 Issue Published: 1 August 1930 PDF downloadLoading ...
Pseudoscleroderma associated with lung cancer: correlation of collagen type I and connective tissue growth factor gene expression
Authors: C. Querfeld, S. Sollberg, C. Huerkamp, B. Eckes, T. Krieg
Journal: British Journal of Dermatology (2000)

Abstract Pseudoscleroderma as a paraneoplastic syndrome is a rare disease. We report here a patient with lung cancer (undifferentiated squamous cell carcinoma), who developed acrosclerosis. Using in situ hybridization, marked expression of α1(I)-collagen and connective tissue growth factor (CTGF) mRNA was found in fibroblasts scattered throughout the dermis. However, transforming growth factor (TGF)-β1 expression was not detected. The pattern of CTGF gene expression and collagen synthesis was similar to that in systemic scleroderma. The absence of TGF-β1 mRNA could indicate that tumour-derived factors induce the expression of CTGF.
Review: After coronary DES placement, shorter vs longer dual- antiplatelet therapy reduces mortality
Authors: Eric R. Bates
Journal: Annals of Internal Medicine (2015)

Source Citation Palmerini T, Benedetto U, Bacchi-Reggiani L, et al. Mortality in patients treated with extended duration dual antiplatelet therapy after drug-eluting stent implantation: a pairwise and Bayesian network meta-analysis of randomised trials. Lancet. 2015;Mar 13. Epub ahead of print. 25777667
New Ischemic Stroke and Outcomes With Vorapaxar Versus Placebo
Authors: Marc P Bonaca, Benjamin M Scirica, Eugene Braunwald, Stephen D Wiviott, Shinya Goto, Vernon Bonarjee, Dennis W Nilsen, Sabina A Murphy, David A Morrow, Serge Timsit
Journal: Journal of the American College of Cardiology (2014)
Human bone marrow depleted of CD33-positive cells mediates delayed but durable reconstitution of hematopoiesis: clinical trial of MY9 monoclonal antibody-purged autografts for the treatment of acute myeloid leukemia
Authors: MJ Robertson, RJ Soiffer, AS Freedman, SL Rabinowe, KC Anderson, TJ Ervin, C Murray, K Dear, JD Griffin, LM Nadler
Journal: Blood (1992)
Abstract 1616: Intermediate Dose of Pentaglobin Eradicates Effectively Inflammation in Parvo B19 and Adenovirus Positive Myocarditis
Authors: Bernhard Maisch, Hendrik Haake, Nadine Schlotmann, Sabine Pankuweit
Journal: Circulation (2007)

152 consecutive patients with myocarditis according to the quantitative World Heart Federation Criteria (&gt; 14 infiltrating cells/mm 2 by endomyocardial biopsy(EMB)) were analysed for cardiotropic agents. In 90 pts parvoviruses B19 (59,5%) and in 36 pts adenoviruses (23,8%) were assessd by PCR as causative viral pathogens. All virus positive patients were treated with 10 g/day Pentaglobin® i. v.(enriched IgG, IgA and IgM preparation, Biotest) at day 1 and 3. After six months all patients were reevalutated clinically, 73 patients (48%) in addition by EMB. Methods: We compared the following parameters before and after therapy: left ventricular ejection fraction (LVEF), left ventricular end-diastolic diameter (LVEDD), shortening fraction (SF) by transthoracic echocardiography and LVEF or the left ventricular end-diastolic volume index (LVEDVI) using angiography. For exercise capacity we evaluated exercise ECG by treadmill test and clinical parameters according to the NYHA classification, before and after therapy. Results: After Pentaglobin therapy, all patients demonstrated a significant clinical improvement of the NYHA class, of exercise capacity and of LVEF (from 54,4 to 60,0%, p&lt;0,005) independent from the respective virus. In 52 of 73 (71%) rebiopsied pts inflammation had resolved. In 17 of the 19 rebiopsied patients (90%) with a positive PCR for ADV before therapy no more virus DNA was recovered after treatment, inflammation had resolved completely. In Parvo B 19 myocarditis inflammation had resolved in 31 of the 44 pts (70%), whereas Parvo B19 DNA was eradicated in only in 18 out of 44 pts(40%). In patients in whom both virus and inflammation were eliminated enddiastolic LV dimension decreased and EF increased significantly (p&lt;0,001). Conclusion: Treatment with an intermediate dose of Pentaglobin is highly effective in resolving myocardial inflammation independent of the underlying viral etiology, but it eradicates adenoviral much better than Parvo B19 infection.
Invasive aspergillosis in intensive care units: Underlying conditions, clinical presentation, medical imaging and mortality
Authors: Nele Brusselaers, Fabio Taccone, Pierre Bulpa, Anne-Marie Van den Abeele, George Dimopoulos, Jordi Rello, Benoit Misset, José A Paiva, K Vandewoude, Dirk Vogelaers, Stijn Blot
Journal: Intensive Care Medicine (2010)
Ventricular Arrhythmia After Cardiac Surgery
Authors: Mikhael F. El-Chami, Fadi J. Sawaya, Patrick Kilgo, William Stein, Michael Halkos, Vinod Thourani, Omar M. Lattouf, David B. Delurgio, Robert A. Guyton, John D. Puskas, Angel R. Leon
Journal: Journal of the American College of Cardiology (2012)
Abstract B27: Wnt5A-expressing melanoma cells show classical markers of senescence following radiation and therapeutic stress, but retain the ability to metastasize and proliferate at distant sites
Authors: Marie R. Webster, Mai Xu, Kathryn Kinzler, Amanpreet Kaur, Jessica Appleton, Michael P. O'Connell, Katie Marchbank, Alexander Valiga, Vanessa Dang, Michela Perego, Gao Zhang, Ana Slipicevic, Frederick Keeney, Elin Lehrmann, William Wood, Kevin Becker, Andrew V. Kossenkov, Meenhard Herlyn, Maureen Murphy, Ashani T. Weeraratna
Journal: Cancer Research (2015)

Abstract Senescence is a cytostatic cell fate that can be induced by oncogene activation, replicative stress or therapy-induced stress. Therapy-induced senescence (TIS) of tumor cells can be initiated by anti-cancer compounds or radiation. TIS is generally considered to be irreversible, and as such this process is believed to be a desirable therapeutic outcome. In this study, we show that melanomas characterized by high levels of the signaling molecule Wnt5A respond to irradiation by undergoing growth arrest, and by expressing classical markers of senescence, including positivity for senescence-associated beta-galactosidase (SA-β-gal), senescence associated heterochromatic foci (SAHF), H3K9Me chromatin marks, and PML bodies. Even though these cells are positive for classical markers of senescence, we find that they retain their ability to migrate and invade. Further, these Wnt5A-high cells are able to proliferate following metastasis and form new tumors in the lung, while expressing increased markers of senescence. Silencing Wnt5A reduces expression of these senescence markers and decreases invasiveness. Finally, Wnt5A-high melanoma cells treated with PLX4720, a BRAFV600E targeted therapy, also increase markers of a TIS response, while remaining invasive. The combined data challenge the paradigm that TIS is a desirable therapeutic endpoint. They also point to Wnt5A as a master regulator of this senescence-like stress-induced phenotype in melanoma. Citation Format: Marie R. Webster, Mai Xu, Kathryn Kinzler, Amanpreet Kaur, Jessica Appleton, Michael P. O'Connell, Katie Marchbank, Alexander Valiga, Vanessa Dang, Michela Perego, Gao Zhang, Ana Slipicevic, Frederick Keeney, Elin Lehrmann, William Wood, III, Kevin Becker, Andrew V. Kossenkov, Meenhard Herlyn, Maureen Murphy, Ashani T. Weeraratna. Wnt5A-expressing melanoma cells show classical markers of senescence following radiation and therapeutic stress, but retain the ability to metastasize and proliferate at distant sites. [abstract]. In: Proceedings of the AACR Special Conference on Advances in Melanoma: From Biology to Therapy; Sep 20-23, 2014; Philadelphia, PA. Philadelphia (PA): AACR; Cancer Res 2015;75(14 Suppl):Abstract nr B27.
Esomeprazole for Asthma
Authors: Matthew Peter Wise, Paul John Frost, Anton G. Saayman
Journal: New England Journal of Medicine (2009)

for the ERSPC Investigators 1. Draisma G, Boer R, Otto SJ, et al. Lead times and overdetection due to prostate-specific antigen screening: estimates from the European Randomized Study of Screening for Prostate Cancer. J Natl Cancer Inst 2003;95:868-78. 2. Bill-Axelson A, Holmberg L, Filen F, et al. Radical prostatectomy versus watchful waiting in localized prostate cancer: the Scandinavian Prostate Cancer Group-4 randomized trial. J Natl Cancer Inst 2008;100:1144-54. 3. Bolla M, Collette L, Blank L, et al. Long-term results with immediate androgen suppression and external irradiation in patients with locally advanced prostate cancer (an EORTC study): a phase III randomised trial. Lancet 2002;360:103-6. 4. Platz EA, Leitzmann MF, Visvanathan K, et al. Statin drugs and risk of advanced prostate cancer. J Natl Cancer Inst 2006; 98:1819-25.
Koch's Postulates and a Viral Cause of Human Cancer: Guest Editorial
Authors: Richard E. Shope
Journal: Cancer Research (1960)

The pitfalls inherent in proving conclusively that a given agent is the cause of a specific ailment were appreciated early in the bacteriological era, and for years since then investigators attempting to determine the etiology of an infectious disease have recognized the absolute necessity of relating the agent under suspicion directly to the disease it supposedly causes. When the subject of investigation was an animal disease, it was considered requisite that a suspected agent should fulfill Koch9s Postulates before an investigator reported its etiological significance. This meant that first the investigator should find the agent in every case of the disease; second, he should cultivate the agent in pure culture; third, he should reproduce the disease faithfully in experimental animals with pure cultures of the agent; and, fourth, he should recover the agent again in pure culture from the experimental animals.