tbuckley/cabot-search huggingface dataset:
Abstract 2786: Downregulated expression of hepatoma-derived growth factor (HDGF) reduces glioma cancer cell tumor growth and angiogenesis
Authors: Li-Feng Liu, Shu-Shong Hsu, Chih-Hao Chen
Journal: Cancer Research (2014)

Abstract Hepatoma derived growth factor (HDGF) is a mitogenic growth factor in the progression of human glioma. In this paper, we study the gliomagenesis role of HDGF in syngenic glioma rat model by Lenti-virus sh-HDGF (LV-shHDGF) infection. The tumor inhibition of HDGF depletion in rat glioma C6 cells was measured by MRI scanning. We found all glioma tumors growth after implanting but only HDGF knock down tumors had a significant reduction in the tumor size at the 4th-week MRI-scanning. After tumor volume was quantified on serial brain section, we found a 10-folds of reduction in the tumor size was observed in HDGF knock down tumors than scrambles (p&amp;lt;0.005). By survival analysis, rats with gliomas had a less median survival of 25 days and the HDGF knock down group was still alive from the time point of implanting. According to the pathological analysis, the HDGF knock down tumors presented a significant cell apoptosis and reduction in the Ki67 mitotic index, CD31 angiogenesis index, and ANG-4 that exhibited markedly reduced tumor growth and blood vessel formation than controls. In addition, Western blot analysis showed exogenous HDGF increased the expression of PI3K, phospho-Akt, phospho-FAK, phospho-MDM2, PCNA and transcription factors of Iκ-B, NF-κB, cFos, ANG-4, and HIF-α in a dose-dependent manner; however, these tumorigenesis moleculars were significantly decreased in HDGF knock down cells. We concluded that HDGF is a mitogenic growth factor in the progression of glioma and it can be a useful therapeutic target for clinical management of glioma in the future. Note: This abstract was not presented at the meeting. Citation Format: Li-Feng Liu, Shu-Shong Hsu, Chih-Hao Chen. Downregulated expression of hepatoma-derived growth factor (HDGF) reduces glioma cancer cell tumor growth and angiogenesis. [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 2786. doi:10.1158/1538-7445.AM2014-2786
Charles Oberling 1895–1960
Authors: W. Bernhard
Journal: Cancer Research (1960)

Charles Oberling passed away March 11, struck by the enemy he had fought all his life. The Institute for Cancer Research at Villejuif has lost its great director; France, one of her dominating figures in Medical Science. His friends are mourning an extraordinary man whom they loved. He was so much alive, it is still difficult to believe that he is no more. It seems, world traveler that he was, that he could as well be absent for awhile in some distant place, soon to return and recount his adventures and discoveries, as he always did.  Charles Oberling was born in Metz (Lorraine) in 1895, the son of an humble postman. Soon afterwards, the family moved to Strasbourg, and it is there that Charles attended school, started his University career and founded his family. He had two sons, Jean-Jacques and Pierre.
Abstract 14689: Regional Aortic Wall Shear Stress Mapping Implicates Hemodynamics in Human Bicuspid Aortopathy
Authors: David G Guzzardi, Pim van Ooij, Alex J Barker, Giampaolo Martufi, Katherine E Olsen, Elena S Di Martino, Yong-Xiang Chen, Michael Markl, Patrick M McCarthy, S C Malaisrie, Jyothy J Puthumana, Darrell D Belke, Edward R O’Brien, Holly E Mewhort, Daniyil A Svystonyuk, James Carr, Robert O Bonow, Paul W Fedak
Journal: Circulation (2014)

Introduction: A suspected genetic cause for bicuspid aortic valve (BAV) aortopathy has led to aggressive resection strategies. Using 4D flow MRI, we documented increased regional wall shear stress (WSS) in BAV patients. Local hemodynamics may exacerbate extracellular matrix (ECM) degradation leading to disease progression. If validated, preoperative regional hemodynamic assessment could be used to guide more targeted patient-specific aortic resection. For the first time, we correlated regional WSS with aortic tissue remodeling in BAV patients. Methods &amp; Results: BAV patients (N=11) undergoing ascending aortic resection received preoperative 4D flow MRI with regional WSS differences mapped. Paired aortic wall samples (from same-patient with elevated WSS paired to normal WSS regions) were collected during surgery and compared using histology (pentachrome), biomechanics (biaxial mechanical testing), and ECM regulation (protein expression). Patient mean age: 49±18 years; mean aortic diameter: 4.6±0.7cm (range: 3.6 - 6.3cm); 55% had R+L fusion pattern; 36% had severe aortic stenosis. All patients had heterogeneous WSS patterns with regions of elevated WSS adjacent to those of normal WSS. By histology, regions of increased WSS showed greater medial elastin fragmentation, fibrosis, and cystic medial necrosis compared to adjacent areas of normal WSS. Regions of increased WSS showed increased elastic modulus (fold change±SD: 1.53±0.68; P=0.06, N=5) and collagen stiffness (1.37±0.49; P=0.07, N=5) compared to normal WSS regions suggesting altered distensibility. Multiplex protein analyses of ECM regulatory molecules revealed an increase in transforming growth factor β-1 (1.49±0.71, P=0.02), MMP-1 (1.62±0.84; P=0.01), MMP-2 (1.49±1.00; P=0.06), MMP-3 (1.23±0.36; P=0.02), MMP-7 (1.57±0.75; P=0.02), and TIMP-2 (1.26±0.33; P=0.01) in elevated WSS regions suggesting ECM dysregulation consistent with aortic remodeling. Conclusions: In BAV aorta, regional WSS corresponds with local histologic abnormalities, altered biomechanics, and ECM dysregulation. These novel data strongly implicate local hemodynamics as a mediator of BAV aortopathy. With further validation, 4D flow MRI could be used to guide personalized resection strategies.
How to measure renal function in clinical practice
Authors: Mark S MacGregor
Journal: BMJ (2006)

Bhandari suggests an estimated glomerular filtration rate (eGFR) <60 ml/min/1.73 m2 may be normal in patients older than 70,1. The study he cites as evidence showed a decline in creatinine clearance at 0.75 ml/min/year reaching a mean of 107 (SD 22) ml/min in the …
<i>SF3B1</i> mutations in patients with myelodysplastic syndromes: The mutation is stable during disease evolution
Authors: Chien‐Chin Lin, Hsin‐An Hou, Wen‐Chien Chou, Yuan‐Yeh Kuo, Shang‐Ju Wu, Chieh‐Yu Liu, Chien‐Yuan Chen, Mei‐Hsuan Tseng, Chi‐Fei Huang, Fen‐Yu Lee, Ming‐Chih Liu, Chia‐Wen Liu, Jih‐Luh Tang, Ming Yao, Shang‐Yi Huang, Szu‐Chun Hsu, Bor‐Sheng Ko, Woei Tsay, Yao‐Chang Chen, Hwei‐Fang Tien
Journal: American Journal of Hematology (2014)

The SF3B1 mutation can be detected in patients with myelodysplastic syndrome (MDS), but the report regarding the association of this mutation with other genetic alterations and its stability during disease progression is limited. In this study, SF3B1 mutations were identified in 10% of total cohort of 479 MDS patients and 61.8% of 34 patients with refractory anemia with ring sideroblasts (RARS). SF3B1 mutations were closely associated with older age, higher platelet counts, lower lactate dehydrogenase levels, good‐risk cytogenetics, and mutations of DNMT3A , but inversely related to ASXL1 mutations. Most SF3B1‐ mutated patients had concurrent other genetic alterations, including DNMT3A and RUNX1 mutations. There was no prognostic difference between patients with SF3B1 mutations and those without. Sequential studies in 417 samples from 142 patients demonstrated that all SF3B1 ‐mutated patients retained the same mutations during disease evolution with the exception of two patients who lost the mutation after allogeneic hematopoietic stem cell transplantation, whereas none of the SF3B1 ‐wild patients acquired a novel mutation during clinical follow‐ups. In conclusion, the patients with SF3B1 mutations had distinct clinic‐biologic features. SF3B1 mutations, accompanied with other genetic alterations, especially DNMT3A mutations, may play a role in the development of MDS, but have little role in disease progression. Am. J. Hematol. 89:E109–E115, 2014. © 2014 Wiley Periodicals, Inc.
Erectile Dysfunction in Obese Men
Authors: Michael Bursztyn
Journal: JAMA (2004)

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 13044: Serum Vascular Endothelial Growth Factor-C Levels are Inversely Associated with the Risk of Cardiac and Cerebrovascular Events Following Drug-eluting Stent Implantation
Authors: Takashi Unoki, Hiromichi Wada, Masaharu Akao, Shuichi Ura, Akira Yamada, Kensuke Takabayashi, Yugo Yamashita, Yasuhiro Hamatani, Nobutoyo Masunaga, Mitsuru Ishii, Moritake Iguchi, Hisashi Ogawa, Daisuke Takagi, Noriko Satoh-Asahara, Akira Shimatsu, Koji Hasegawa
Journal: Circulation (2014)

Background: Vascular endothelial growth factor-C (VEGF-C) plays a key role in lymphangiogenesis. Recently, we demonstrated that VEGF-C is closely associated with dyslipidemia and atherosclerosis. However, the prognostic value of VEGF-C levels after drug-eluting stent (DES) implantation is unknown. Methods and Results: We performed a prospective cohort study involving a total of 443 patients (age, 71.7±9.0 y [SD]; male, 73.8%; number of lesions, 1.6±0.8) who underwent successful DES implantation. Patients were recruited between January 2010 and October 2013, and were followed up over 3 years. The primary outcome was major adverse cardiac and cerebrovascular events (MACCE) defined as cardiovascular death, hospitalization due to acute coronary syndrome, stroke, heart failure, and coronary revascularization. The median follow-up was 617 (inter-quartile range, 320-937) days. Pre-procedural serum levels of high-sensitivity C-reactive protein (hsCRP), vascular endothelial growth factor-A (VEGF-A), and VEGF-C were measured. During the follow-up period, MACCE developed in a total of 106 patients (23.9%). Patients were divided into two groups based on the median of each biomarker. In Kaplan-Meier analyses, low-VEGF-C (P=0.0005 by log-rank test), but not high-hsCRP (P=0.3) or high-VEGF-A (P=0.3), was significantly associated with the risk of MACCE. Multivariate Cox proportional hazard analyses revealed that levels of VEGF-C (hazard ratio [HR], 0.77 per 1-SD increase; 95% confidence interval [CI], 0.62-0.94; P=0.011), but not hsCRP (HR, 1.05; 95% CI, 0.86-1.25; P=0.6) or VEGF-A (HR, 1.04; 95% CI, 0.86-1.23; P=0.6), were inversely and significantly associated with MACCE after adjustment for age, gender, and established risk factors, the number of lesions, and type of DES. Finally, we performed stepwise multivariate Cox proportional hazard analysis including data on age, gender, established risk factors, the number of lesions, type of DES, and VEGF-C levels. Notably, the only independent predictor of MACCE was the VEGF-C level (HR, 0.74 per 1-SD increase; 95% CI, 0.61-0.91; P=0.0042), followed by diabetes (HR, 1.47; 95% CI, 0.98-2.21; P=0.060). Conclusions: A low VEGF-C value may serve as a predictor of MACCE after DES implantation.
Abstract 18615: Subclinical Thyroid Dysfunction, Rather than Low-T3 Syndrome, is an Independent Predictor of Adverse Cardiac Events in Patients with Acute Decompensated Heart Failure
Authors: Tomohiro Hayashi, Takuya Hasegawa, Hideaki Kanzaki, Akira Funada, Makoto Amaki, Takahiro Ohara, Yasuo Sugano, Satoshi Yasuda, Hisao Ogawa, Toshihisa Anzai
Journal: Circulation (2014)

Background: Altered thyroid hormone metabolism characterized by low triiodothyronine (T3) levels is a common finding in patients with severe systemic diseases, called low T3 syndrome (LT3-S). Additionally, subclinical thyroid dysfunction, defined as abnormal thyroid-stimulation hormone (TSH) and normal thyroxine (T4) levels, causes left ventricular dysfunction. However, the prevalence and prognostic impact of LT3-S and subclinical thyroid dysfunction in patients with acute decompensated heart failure (ADHF) have not been investigated. Methods: We examined consecutive 287 patients with ADHF who received thyroid function tests and no thyroid medications at admission (age 69±15 years, 166 male). Thyroid dysfunction was defined as follows: LT3-S as free T3&lt; 4.0 pmol/L; euthyroidism as TSH of 0.45 to 4.49 mIU/L; subclinical hypothyroidism (Sc-hypo) as TSH of 4.5 to 19.9 mIU/L; subclinical hyperthyroidism (Sc-hyper) as TSH&lt; 0.45mIU/L with normal free T4 levels for the last two. We sought to investigate the impact of the indices of thyroid function and the thyroid disorders above to predict cardiac death and re-hospitalization for heart failure after discharge. Results: At admission for ADHF, 155 patients (54%) showed LT3-S, and 62 (22%) Sc-hypo, and 5 (2%) Sc-hyper, and 196 (68%) euthyroidism. Cox proportional hazards model analysis revealed that TSH and fT4, not fT3, were independent predictors of adverse cardiac events among variables including age, sex, estimated glomerular filtration rate, left ventricular ejection fraction and B-type natriuretic peptide. Indeed, Sc-hypo was an independent predictor (HR 2.21, 95% CI 1.41-3.43, p&lt; 0.001), whereas LT3-S and SC-hyper was not (p = 0.49 and 0.24, respectively). Conclusion: Although LT3-S was observed in about half of ADHF patients, the presence of LT3-S did not indicate poor prognosis after discharge. Meanwhile, Sc-hypo at admission was an independent predictor of adverse cardiac events in ADHF patients.
Abstract 19313: MicroRNA-146a Augments Vascular Smooth Muscle Cell Proliferation and Neointima Formation
Authors: Rebecca Teske, Jan-Marcus Daniel, Jochen Dutzmann, Johann Bauersachs, Daniel Sedding
Journal: Circulation (2014)

Background: Micro RNAs (miRNAs) are implicated to regulate mRNA levels in a post transcriptional manner, comprising key regulators for cellular function including proliferation, differentiation and apoptosis. Up to now, the role of miRNAs for vascular smooth muscle cell function remains elusive.

Hypothesis: The aim of this study was to evaluate the regulation and impact of miR 146a for smooth muscle cell function during the development of neointimal lesions in vitro and in vivo.

Methods/Results: Neointima formation was induced in C57BL6/N by dilation of the femoral artery and miRNA was isolated 10 and 21 days after injury. Using microarray analysis, miR-146a was found to be one of the most strongly up-regulated miRNAs during neointima formation. Further expression analysis in isolated primary vascular cell types revealed that miR-146a, besides in monocytes/macrophages and in endothelial cells, was highly expressed in vascular smooth muscle cells. In vitro, the upregulation of miR-146a could be attributed to the inflammatory stimulus Il-1β. IRAK1, a key adapter molecule in TLR- and IL-1 receptor signaling cascades, was identified as a molecular target of 146a. Indeed, IRAK1 was found down-regulated on the mRNA and protein level after transfection of SMC with miR-146a mimics and could be confirmed as direct target using luciferase reporter assays. To further assess the functional role of miR-146a, smooth muscle cells were transfected with miR-146a inhibitors. miR-146a inhibition resulted in a significantly decreased total cell count and migration of smooth muscle cells. In complementing in vivo experiments, the inhibition of miR-146a in injured murine femoral arteries significantly reduced the proliferation of neointimal smooth muscle cells as assessed by Ki67 staining. Moreover, morphometric analysis revealed a significantly attenuated neointima formation following 146a inhibition.

Conclusion: These findings reveal a pivotal role of miR-146a for function in vascular smooth muscle cells, especially under conditions of pathological vascular remodeling processes. Thus, modulating miR-146a expression may represent a novel approach for the prevention and treatment of vascular proliferative diseases.
RECURRENT HEART FAILURE WITH TAMPONADE DUE TO PERICARDIAL EFFUSION; IMPROVEMENT FOLLOWING PLEURAL-PERICARDIAL FENESTRATION
Authors: F A SILVERSTONE
Journal: Annals of Internal Medicine (1955)

Case Reports1 April 1955RECURRENT HEART FAILURE WITH TAMPONADE DUE TO PERICARDIAL EFFUSION; IMPROVEMENT FOLLOWING PLEURAL-PERICARDIAL FENESTRATIONFELIX A. SILVERSTONE, M.D.FELIX A. SILVERSTONE, M.D.Author, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-42-4-937 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptThe management of heart failure due to pericardial effusion involves two general phases. When cardiac tamponade is the pressing problem, the patient can be immediately benefited by a pericardial tap, which also affords diagnostic data. Otherwise treatment is directed at the underlying cause, be it inflammatory, traumatic, neoplastic, nutritional or metabolic, in an attempt to prevent re-accumulation of fluid. While this regimen usually suffices, an occasional instance will arise where repeated re-accumulation of fluid cannot be controlled in this way. The outlook then becomes unfavorable unless another means can be devised to prevent cardiac tamponade, with its attendant diminished cardiac... This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: Baltimore, Maryland*Received for publication May 14, 1954.Presented in the Program Clinics at the Annual Session of the American College of Physicians, New York, New York, March 29, 1949.From the Kings County Hospital, Brooklyn, N. Y.†Present address: Section on Gerontology, National Heart Institute, Baltimore City Hospital, Baltimore, Maryland. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited byCardiac tamponade and hypothyroidismCholesterol pericarditis and cardiac tamponade with congenital hypothyroidism in adulthoodCardiac tamponade in medical patients.Subxiphoid pericardial windowSubxiphoid pericardial windowChronic idiopathic pericardial effusion.Chronic Exudative Pericarditis Treated by Pleuro-pericardial FenestrationErkrankungen des PerikardChronic Idiopathic Pericardial Effusion without TamponadeSyndrome of chronic massive pericardial effusion 1 April 1955Volume 42, Issue 4Page: 937-941KeywordsGeriatricsHeartHeart failureNutrition ePublished: 1 December 2008 Issue Published: 1 April 1955 PDF downloadLoading ...
Der Effekt der ersten Untersuchungsnacht auf die Erektionen im Schlaf
Authors: Uros J. Jovanovic
Journal: Psychotherapy and Psychosomatics (1969)

Research Articles| February 12 2010 Der Effekt der ersten Untersuchungsnacht auf die Erektionen im Schlaf Subject Area: Psychiatry and Psychology Uros J. Jovanovic Uros J. Jovanovic Universitäts-Nervenklinik und Poliklinik, Würzburg (Direktor: Professor Dr. H. Scheller) Search for other works by this author on: This Site PubMed Google Scholar Psychother Psychosom (1969) 17 (5-6): 295–308. https://doi.org/10.1159/000286045 Article history Published Online: February 12 2010 Content Tools Views Icon Views Article contents Figures & tables Video Audio Supplementary Data Peer Review Share Icon Share Facebook Twitter LinkedIn Email Tools Icon Tools Get Permissions Cite Icon Cite Search Site Citation Uros J. Jovanovic; Der Effekt der ersten Untersuchungsnacht auf die Erektionen im Schlaf. Psychother Psychosom 31 December 1969; 17 (5-6): 295–308. https://doi.org/10.1159/000286045 Download citation file: Ris (Zotero) Reference Manager EasyBib Bookends Mendeley Papers EndNote RefWorks BibTex toolbar search Search Dropdown Menu toolbar search search input Search input auto suggest filter your search All ContentAll JournalsPsychotherapy and Psychosomatics Search Advanced Search Article PDF first page preview Close Modal This content is only available via PDF. 1969Copyright / Drug Dosage / DisclaimerCopyright: All rights reserved. No part of this publication may be translated into other languages, reproduced or utilized in any form or by any means, electronic or mechanical, including photocopying, recording, microcopying, or by any information storage and retrieval system, without permission in writing from the publisher.Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug.Disclaimer: The statements, opinions and data contained in this publication are solely those of the individual authors and contributors and not of the publishers and the editor(s). The appearance of advertisements or/and product references in the publication is not a warranty, endorsement, or approval of the products or services advertised or of their effectiveness, quality or safety. The publisher and the editor(s) disclaim responsibility for any injury to persons or property resulting from any ideas, methods, instructions or products referred to in the content or advertisements. You do not currently have access to this content.
1044. Growth Hormone Releasing Hormone Plasmid Administration Decreases Tumor Growth and Enhances Immune Function in Nude Mice
Authors: Amir S. Khan, Ingrid W. Anscombe, Kathleen K. Cummings, Melissa A. Pope, Louis C. Smith, Ruxandra Draghia-Akli
Journal: Molecular Therapy (2004)

Recent studies have shown that growth hormone releasing hormone (GHRH) has immune stimulatory effects, both through stimulation of the GH axis and direct actions as an immune-modulator. We have investigated the effects of plasmid-mediated GHRH supplementation on tumor growth and immune function in nude mice implanted with two different tumor cell lines, NCI-H358 human bronchioalveolar carcinoma and MDA-MB-468 human breast adenocarcinoma. Plasmid-mediated, physiologic GHRH supplementation did not increase tumor progression in tumor-bearing nude mice. We observed a clear sexual dimorphism for tumor growth and immunological outcome. Male animals implanted with the NCI-H358 tumor cell line and treated with GHRH-expressing plasmid exhibited a 40% decrease in the size of the tumors (p < 0.02), 48% increase in white blood cells (p < 0.025), 300% increase in monocyte count (p < 0.0001), as well as an increase in numbers of intratumoral activated CD3+ and CD4+ cells, as compared to control animals. There was a trend towards reduction of tumor growth in treated females; however, these effects did not attain statistical significance. No adverse findings were found in animals that received the GHRH-plasmid treatment. The findings in the present study suggest that physiological stimulation of the GHRH-GH-IGF-I axis in patients with cancer may enhance their immune function and reduce tumor growth.