tbuckley/cabot-search huggingface dataset:
<i>In vitro</i> and <i>In vivo</i> Evidence of Metallopanstimulin-1 in Gastric Cancer Progression and Tumorigenicity
Authors: Yun-wei Wang, Ying Qu, Jian-fang Li, Xue-hua Chen, Bing-ya Liu, Qin-long Gu, Zheng-gang Zhu
Journal: Clinical Cancer Research (2006)

Abstract Purpose: The metallopanstimulin-1 (MPS-1) gene is a growth factor–inducible gene, which is highly expressed in many human cancers and may be involved in the progression towards tumor malignancy. However, it is unclear whether MPS-1 plays any role in gastric cancer development or progression. Our studies were designed to clarify the MPS-1 expression pattern and to explore its potential role in gastric cancer. Experimental Design: The expression pattern of MPS-1 was determined in primary gastric cancer specimens and gastric cancer cell lines via immunohistochemistry and Western blotting. To investigate the functional significance of MPS-1 expression, three small interfering RNA (siRNA) expression plasmids were constructed and transfected into gastric cancer cell line SGC7901. The stable cell lines transfected with the siRNA targeting MPS-1 mRNA plasmids were selected and the biological features of these cells were examined. Results: MPS-1 was overexpressed in 86% of the gastric cancer tissues and all gastric cancer cells. In addition, MPS-1 expression was significantly increased and corresponded with the tumor-node-metastasis clinical stage, and was significantly higher in the late stage (P &amp;lt; 0.01). The MPS-1 expression level was significantly decreased in the transfected cells with MPS-1-specific siRNA expression plasmid pRNAT-133. Furthermore, the stable transfected cancer cells exhibited an increase in the incidence of spontaneous apoptosis and a decrease in growth ability and tumorigenicity in nude mice. Conclusions: These results provide strong evidence that MPS-1 plays an important role in gastric cancer cell proliferation and development, and suggests that MPS-1 is a promising target for gastric cancer treatment.
Vitamin Discoveries and Disasters: History, Science, and Controversies
Authors: Judy A. Driskell
Journal: JAMA (2010)

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
Abstract 17: Bcl-2 is a downstream target of ATF5 that mediates ATF5's pro-survival function in a cell type-dependent manner
Authors: Douglus Dluzen, Guangfu Li, Diana Tacelosky, Matthew Moreau, David X. Liu
Journal: Cancer Research (2011)

Abstract The activating transcription factor 5 (ATF5) is a member of the ATF/CREB family of basic zipper (bZIP) proteins. Recent reports showed that ATF5 loss-of-function causes apoptotic cell death in glioblastoma and breast cancer cells but not in non-transformed astrocytes and human breast epithelial cells. The mechanism for ATF5's cell type-dependent survival function is unknown. We report here that the anti-apoptotic factor Bcl-2 is a downstream target that mediates ATF5-promoted cancer-cell survival in C6 glioma cells and MCF-7 breast cancer cells. ATF5 binds to an ATF5-specific regulatory element (ARE) that is downstream of and adjacent to the negative regulatory element (NRE) in the Bcl-2 P2 promoter, stimulating Bcl-2 expression. Highlighting the importance of Bcl-2 in ATF5-dependent cancer-cell survival, expression of Bcl-2 blocks death of C6 and MCF-7 cells induced by d/nATF5 and depletion of Bcl-2 impairs ATF5-promoted cell survival. Moreover, we found that Bcl-2 expression is not regulated by ATF5 in non-transformed rat astrocytes, MEFs, and human breast epithelial cells (HBEC), where knock-down of Bcl-2 but not that of ATF5 evokes cell death. These findings identify Bcl-2 as an essential mediator for ATF5's cancer-specific cell survival function in glioblastoma and breast cancer cells and provide direct evidence that the cell type-specific function of ATF5 derives from the differential regulation of downstream targets by ATF5 in different types of cells. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 17. doi:10.1158/1538-7445.AM2011-17
Magnification and Chromoscopy with the Acetic Acid Test
Authors: H. B. Kaufman, D. M. Harper
Journal: Endoscopy (2004)

Transferring knowledge and techniques that have been learned from decades of the use of acetic acid in colposcopy to the field of digestive endoscopy is a noteworthy objective. However, to be accurate, the fundamental mechanism involved in the whitening of cervical tissue after the application of acetic acid - the process known as ”acetowhitening” - has not yet been definitively clarified. In a recent paper in Endoscopy, Lambert et al. claim that ”Cytokeratins are the major cause of the acetowhite reaction, due to their filamentous architecture” [1]. This hypothesis does not explain other acetowhitening phenomena observed in nonneoplastic tissue. For example, crypt openings (resulting in so-called ”cuffed gland openings”), borders of the transformation zone, and immature metaplasia can all display whitening characteristics similar to the whitening observed with tissue classified as cervical intraepithelial neoplasia (CIN) grades I, II, and III. In fact, since nonneoplastic tissue can acetowhiten and mimic neoplastic tissue, there is a need for improved diagnostic training and/or new techniques to improve the accuracy of classifying whitened tissue when observed colposcopically.
Mandating Public Service
Authors: Eugene M. Bozymski
Journal: Annals of Internal Medicine (1994)

Letters1 April 1994Mandating Public ServiceEugene M. Bozymski, MDEugene M. Bozymski, MDUniversity of North Carolina; Chapel Hill, NC 27599Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-120-7-199404010-00022 SectionsAboutFull TextPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail TO THE EDITOR:In medicine and health care, it is, to quote Dickens, “the best of times and it is the worst of times”—a time of unsettling change, challenge, and opportunity. Yet, it is and always will be a privilege to be a physician and have the opportunity to prevent illness and to care for the sick. I have read and heard much about the problems in our profession and its decreased attractiveness among young persons. Yet, more and more people are applying to medical schools. New physicians will not be hampered by preconceived notions of the “good old days” ... Author, Article, and Disclosure InformationAuthors: Eugene M. Bozymski, MDAffiliations: University of North Carolina; Chapel Hill, NC 27599 PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics 1 April 1994Volume 120, Issue 7Page: 621KeywordsEngineersGraduate medical educationHealth care ePublished: 15 August 2000 Issue Published: 1 April 1994 Copyright & PermissionsCopyright © 1994 by American College of Physicians. All Rights Reserved.PDF downloadLoading ...
Detection and Characterization of Early Prostate Cancer by Six Systematic Biopsies and Fine Needle Aspiration Cytology in Prostates from Bladder Cancer Patients
Authors: Stefan Conrad, Stefan H. Hautmann, Rolf P. Henke, Andreas Erbersdobler, J&ouml;rg Simon, Michael Straub, Markus Graefen, Richard E. Hautmann, Hartwig Huland
Journal: European Urology (2001)
Response to Acute Lung Infection with Mucoid <b><i>Pseudomonas aeruginosa</i></b> in Cystic Fibrosis Mice
Authors: Anna M. van Heeckeren, Mark D. Schluchter, Wei Xue, Pamela B. Davis
Journal: American Journal of Respiratory and Critical Care Medicine (2005)

Cystic fibrosis is caused by defects in the cystic fibrosis transmembrane conductance regulator gene, which codes for a chloride channel, but the role of this chloride channel in inflammation induced by lung infection with Pseudomonas aeruginosa remains to be defined.We tested the hypothesis that loss of this chloride channel alone is sufficient to cause excessive inflammation in response to inflammatory stimuli.We investigated the response of cystic fibrosis and wild-type mice to mucoid P. aeruginosa administered by insufflation.The host responses measured included survival, weight change, lung morphometry, bacterial clearance, and inflammatory mediators, and cell counts were assessed in bronchoalveolar lavage fluid.Depending on the dose administered and frequency of dosing, cystic fibrosis mice experienced significantly higher mortality rates, greater weight loss, higher lung pathology scores, and higher inflammatory mediator and neutrophil levels compared with wild-type mice, even after the bacteria had been cleared. Surprisingly, bacteria were cleared just as rapidly in cystic fibrosis mice as in wild-type mice, and sepsis was not observed. Chronic lung infections could not be established with mucoid P. aeruginosa in either cystic fibrosis or wild-type mice.Absence of this chloride channel alone appears sufficient for exaggerated inflammation and excess mortality compared with wild-type controls in the face of mucoid P. aeruginosa lung infection. To establish chronic infection, additional factors such as bacterial trapping or poor clearance may be required.
Beat-to-Beat QT Interval Variability
Authors: Ronald D. Berger, Edward K. Kasper, Kenneth L. Baughman, Eduardo Marban, Hugh Calkins, Gordon F. Tomaselli
Journal: Circulation (1997)

Dilated cardiomyopathy (DCM) is associated with a high incidence of malignant ventricular arrhythmias and sudden death. Abnormalities in repolarization of ventricular myocardium have been implicated in the development of these arrhythmias. Spatial heterogeneity in repolarization has been studied in DCM, but temporal fluctuations in repolarization in this setting have been largely ignored. We sought to test the hypothesis that beat-to-beat QT interval variability is increased in DCM patients compared with control subjects.Eighty-three patients with ischemic and nonischemic DCM and 60 control subjects served as the study population. Beat-to-beat QT interval variability was measured by automated analysis on the basis of 256-second records of the surface ECG. A QT variability index (QTVI) was calculated for each subject as the logarithm of the ratio of normalized QT variance to heart rate variance. The coherence between heart rate and QT interval fluctuations was determined by spectral analysis. In patients, ejection fractions were assessed by echocardiography or ventriculography, and spatial QT dispersion was determined from the standard 12-lead ECG. DCM patients had greater QT variance than control subjects (60.4+/-63.1 versus 25.7+/-24.8 ms2, P<.0001) despite reduced heart rate variance (6.7+/-7.8 versus 10.5+/-10.4 bpm2, P=.01). The QTVI was higher in DCM patients than in control subjects, with a high degree of significance (-0.43+/-0.71 versus -1.29+/-0.51, P<10[-12]). QTVI did not correlate with ejection fraction or spatial QT dispersion but did depend on New York Heart Association functional class. QTVI did not differ between DCM patients with ischemic and those with nonischemic origin. Coherence between heart rate and QT interval fluctuations at physiological frequencies was lower in DCM patients compared with control subjects (0.28+/-0.14 versus 0.39+/-0.18, P<.0001).DCM is associated with beat-to-beat fluctuations in QT interval that are larger than normal and uncoupled from variations in heart rate. QT interval variability increases with worsening functional class but is independent of ejection fraction. These data indicate that DCM leads to temporal lability in ventricular repolarization.
Medical Futility: Its Meaning and Ethical Implications
Authors: Lawrence J. Schneiderman
Journal: Annals of Internal Medicine (1990)

The notion of medical futility has quantitative and qualitative roots that offer a practical approach to its definition and application. Applying these traditions to contemporary medical practice, we propose that when physicians conclude (either through personal experience, experiences shared with colleagues, or consideration of published empiric data) that in the last 100 cases a medical treatment has been useless, they should regard that treatment as futile. If a treatment merely preserves permanent unconsciousness or cannot end dependence on intensive medical care, the treatment should be considered futile. Unlike decision analysis, which defines the expected gain from a treatment by the joint product of probability of success and utility of outcome, our definition of futility treats probability and utility as independent thresholds. Futility should be distinguished from such concepts as theoretical impossibility, such expressions as "uncommon" or "rare," and emotional terms like "hopelessness." In judging futility, physicians must distinguish between an effect, which is limited to some part of the patient's body, and a benefit, which appreciably improves the person as a whole. Treatment that fails to provide the latter, whether or not it achieves the former, is "futile." Although exceptions and cautions should be borne in mind, we submit that physicians can judge a treatment to be futile and are entitled to withhold a procedure on this basis. In these cases, physicians should act in concert with other health care professionals, but need not obtain consent from patients or family members.
Silver Nanoparticles Compromise Neurodevelopment in PC12 Cells: Critical Contributions of Silver Ion, Particle Size, Coating, and Composition
Authors: Christina M. Powers, Appala R. Badireddy, Ian T. Ryde, Frederic J. Seidler, Theodore A. Slotkin
Journal: Environmental Health Perspectives (2010)

Silver exposures are rising because of the increased use of silver nanoparticles (AgNPs) in consumer products. The monovalent silver ion (Ag+) impairs neurodevelopment in PC12 cells and zebrafish.We compared the effects of AgNPs with Ag+ in PC12 cells for neurodevelopmental end points including cell replication, oxidative stress, cell viability, and differentiation. First, we compared citrate-coated AgNPs (AgNP-Cs) with Ag+, and then we assessed the roles of particle size, coating, and composition by comparing AgNP-C with two different sizes of polyvinylpyrrolidone-coated AgNPs (AgNP-PVPs) or silica nanoparticles.In undifferentiated cells, AgNP-C impaired DNA synthesis, but to a lesser extent than an equivalent nominal concentration of Ag+, whereas AgNP-C and Ag+ were equally effective against protein synthesis; there was little or no oxidative stress or loss of viability due to AgNP-C. In contrast, in differentiating cells, AgNP-C evoked robust oxidative stress and impaired differentiation into the acetylcholine phenotype. Although the effects of AgNP-PVP showed similarities to those of AgNP-C, we also found significant differences in potencies and differentiation outcomes that depended both on particle size and coating. None of the effects reflected simple physical attributes of nanoparticles, separate from composition or coating, as equivalent concentrations of silica nanoparticles had no detectable effects.AgNP exposure impairs neurodevelopment in PC12 cells. Further, AgNP effects are distinct from those of Ag+ alone and depend on size and coating, indicating that AgNP effects are not due simply to the release of Ag+ into the surrounding environment.
Management of Septic Arthritis
Authors: D. Barry Lotman
Journal: JAMA (1982)

<h3>To the Editor.—</h3> I would be remiss in not adding my comments to those that are sure to be made on the article by Ho and Su. As an orthopedic surgeon familiar with the ravages caused by pus in a joint, I do not believe in the medical management of septic arthritis. I believe that most orthopedic surgeons consider a purulent joint to be a "surgical" emergency that requires prompt evacuation, lest irretrievable damage be done to the articular cartilage.
Association between cutaneous melanoma incidence rates among white US residents and county-level estimates of solar ultraviolet exposure
Authors: Thomas B. Richards, Christopher J. Johnson, Zaria Tatalovich, Myles Cockburn, Melody J. Eide, Kevin A. Henry, Sue-Min Lai, Sai S. Cherala, Youjie Huang, Umed A. Ajani
Journal: Journal of the American Academy of Dermatology (2011)
Accumulation of Fetal Fibronectin mRNAs After Balloon Denudation of Rabbit Arteries
Authors: Christophe Bauters, Francoise Marotte, Martial Hamon, Patricia Oliviéro, Farah Farhadian, Valérie Robert, Jane Lyse Samuel, Lydie Rappaport
Journal: Circulation (1995)

Background Fibronectin (FN), a component of the extracellular matrix, influences cellular migration and differentiation. It is a prominent component of the extracellular matrix of normal arteries and is thought to play an important role in the pathogenesis of restenosis after angioplasty. FN exists in multiple forms that arise from a single RNA transcript that can be alternatively spliced. EIIIA- and EIIIB-containing FN mRNAs predominate in the embryo, whereas in the adult, most of the normal tissue FN lacks these domains. Since few data were available concerning pattern of expression of the different alternatively spliced forms of FN mRNA in arteries after endoluminal injury, we analyzed the expression of EIIIA and EIIIB FN isoforms at different times after experimental angioplasty. Methods and Results The spatial and temporal alterations in FN expression were studied in an in vivo model of endothelial denudation in the rabbit aorta and iliac artery by a combination of immunochemistry and in situ hybridization methods. Alternatively spliced forms of FN EIIIA and EIIIB were detected in the media and the adventitia of both types of vessels 24 to 48 hours after injury. Two weeks after injury, EIIIA and EIIIB mRNAs were found to accumulate within the luminal layers of the neointima. The cellular form of FN protein was not found until 2 weeks after the injury and accumulated in the inner part of the neointima. Conclusions These data demonstrate that FN upregulation is an early and long-lasting process after arterial injury. These results suggest that the induction of the embryonic FN isoforms may be involved in the restenotic process that follows balloon denudation of arteries.
PREDICTORS OF EARLY, LATE AND VERY LATE STENT THROMBOSIS FROM THE SPIRIT II, SPIRIT III, SPIRIT IV AND COMPARE POOLED DATA BASE
Authors: Pieter Smits, Dean Kereiakes, Martin Fahy, Elvin Kedhi, Helen Parise, Gregg Stone, Maasstad Ziekenhuis
Journal: Journal of the American College of Cardiology (2011)
Secreted Gaussia luciferase as a sensitive reporter gene for in vivo and ex vivo studies of airway gene transfer
Authors: Uta Griesenbach, Catarina C. Vicente, Megan J. Roberts, Cuixiang Meng, Samia Soussi, Stefania Xenariou, Peter Tennant, Alison Baker, Eilidh Baker, Catherine Gordon, Christina Vrettou, Dominique McCormick, Rebecca Coles, Anne-Marie Green, Anna E. Lawton, Stephanie G. Sumner-Jones, Seng H. Cheng, Ronald K. Scheule, Stephen C. Hyde, Deborah R. Gill, David D. Collie, Gerry McLachlan, Eric W.F.W. Alton
Journal: Biomaterials (2011)
CORRECTION IN SURGICAL PROGRAM IN SPAIN
Authors: Alton Ochsner
Journal: JAMA (1952)

<h3>To the Editor:—</h3> I would like to correct a statement in the May 3rd issue ofThe Journal, page 81, concerning the Congress of Surgery in Spain, in which it was stated that I was going to be on the program. I have never been on the program of the congress and do not intend to be on it, nor to attend the meeting.
Mannitol Infusion
Authors: Kevin G. Barry, Ann R. Berman
Journal: New England Journal of Medicine (1961)

MANNITOL is the reduced form of the 6-carbon sugar mannose. It is a time-honored osmotic diuretic for research purposes, but has received only sporadic and limited clinical attention.1 2 3 4 5 Urea and other clinically popular osmotic diuretics are composed of small particles that are freely filtered across the glomerulus into the lumen of the renal tubule.6 Urinary excretion of the particles, with their obligatory water, constitutes an osmotic diuresis. The diuretic effectiveness of urea and similar agents per mol administered is limited by their rapid diffusion from the blood stream into the extravascular fluids and their reabsorption from the tubular lumen of . . .