tbuckley/cabot-search huggingface dataset:
Abstract MP01: Association of Objectively-measured Physical Activity with Cardiovascular Risk in Mobility-limited Older Adults
Authors: Thomas W Buford, Don G Hire, Walter T Ambrosius, Stephen D Anton, Timothy S Church, John A Dodson, Anthony P Marsh, Mary M McDermott, Joe R Nocera, Daniel K White, Veronica Yank, Marco Pahor, Todd M Manini
Journal: Circulation (2014)

Introduction: In middle-aged adults, time spent being sedentary is associated with cardiovascular (CV) health risks independent of structured physical activity (PA). However, data are sparse regarding the impact of sedentary behavior on CV risk in older adults. The extent to which the absolute duration or intensity of daily PA reduces CV risk in older adults is also unknown. Objectives: Our objective was to examine the cross-sectional association between objectively-measured sedentary behavior and predicted CV risk among older adults in the Lifestyle Interventions and Independence for Elders (LIFE) study. The secondary objective was to evaluate associations between the duration/intensity of daily PA and predicted CV risk. Methods: LIFE is a randomized clinical trial to determine if regular PA prevents mobility disability among mobility-limited older adults. Activity data were collected by hip-worn accelerometer at baseline prior to participation in study interventions. Only participants with at least three days of accelerometry data (≥ 10 hrs wear time) were included. Unadjusted and adjusted linear regression was used to model the relationship between accelerometry measures and predicted 10-year Framingham risk of Hard Coronary Heart Disease (HCHD; i.e. myocardial infarction or coronary death). Adjusted models included demographic confounders (e.g. education, race, income) and health parameters (e.g. depression, cognition, arthritis) not in the risk score. Accelerometry cut-points were (in counts/min): sedentary behavior: &lt; 100; low-intensity activity: 100-499; higher intensity activity: &gt; 500. Results: Participants (n = 1170; 78.7 ± [SD] 5.3 years; 66.1% female) had a median HCHD risk of 10.3% (25 th -75 th %: 5.7-18.6). Over a mean accelerometer wear time of 8.1 ± 3.2 days, participants spent 77.0 ± 8.2% of their time sedentary. They also spent 16.6 ± 5.0% of their time in low-intensity PA and 6.4 ± 4.4% in higher-intensity PA. For all PA performed (&gt; 100 counts/min), participants achieved a median of 393.4 (337.8-473.5) counts/min. In the unadjusted model, time spent sedentary (β = 2.41; 95% CI : 1.94, 2.89), in low-intensity PA (-2.56; -3.03, -2.08), and in higher-intensity PA (-1.60; -2.09, -1.11) were all associated with HCHD risk (all p’s &lt; 0.001). These associations remained significant after adjustment. The mean intensity of daily PA was not significantly associated with HCHD risk in any model (p &gt; 0.05). Conclusions: Daily time spent being sedentary is positively associated with predicted 10-year HCHD risk among mobility-limited older adults. Duration, but not mean intensity, of daily PA is inversely associated with HCHD risk score in this population.
Abstract 15010: Disruption of Outer Mitochondrial Membrane Protein, MitoNEET, Increases Mitochondrial Iron Content in the Heart
Authors: Takaaki Furihata, Shintaro Kinugawa, Shouji Matsushima, Shingo Takada, Arata Fukushima, Wataru Mizushima, Tomoyasu Kadoguchi, Yoshihiro Masaki, Takashi Yokota, Hiroyuki Tsutsui
Journal: Circulation (2014)

Background: Iron in the mitochondria is regulated to maintain mitochondrial physiological function. A loss of mitoNEET protein located in the outer mitochondrial membrane has been shown to increase mitochondrial iron content in adipocytes. However, the role of mitoNEET in iron homeostasis has not been determined in the heart. Methods and Results: MitoNEET flox/flox (mNT f/f ) mice were generated with lox-P and homologous recombination strategies. Cardiac-specific deletion of mitoNEET was achieved using αMHC-Cre (mNT -/- ). Mice, mNT -/- (n=11) and mNT f/f (n=10), were bred for 3 months. Mitochondrial iron content, measured by colorimetric method, was significantly increased in mNT -/- mice compared to mNT f/f mice (1.13±0.09 vs. 0.58±0.07 μg/dl/μg mitochondrial protein, P&lt;0.001). In parallel, immunoblot analysis showed that mitochondrial ferritin, mitochondrial iron transporter, was significantly higher in mNT -/- than mNT f/f by 45%. Mitoferrin2, mitochondrial iron importer, and ATP-binding cassette transporter type B8, mitochondrial iron exporter, protein did not differ between groups. The activity of electron transport chain complex V, mitochondrial iron importer, was also higher in mNT -/- than mNT f/f (617±22 vs. 496±17 mM/min/mg mitochondrial protein, P&lt;0.05). In contrast, frataxin, involved in the synthesis of iron-sulfur cluster (ISC), was significantly lower in mNT -/- by 49%. ATP-binding cassette transporter type B7, mitochondrial ISC exporter, did not differ. Body weight and heart weight were comparable between groups. Left ventricular end-diastolic diameter (2.9±0.1 vs. 2.9±0.1 mm), percent fractional shortening (55±3 vs. 55±3 %), and wall thickness (0.71±0.01 vs. 0.73±0.01 mm) measured by echocardiography were also similar. Conclusions: Cardiac specific deletion of mitoNEET protein increased mitochondrial iron content in mice, in association with the increase in iron importer and transporter and the decrease in frataxin, suggesting that mitoNEET may play an important role in the regulation of mitochondrial function via iron homeostasis in the heart.
Pitfalls of Converting Practice Guidelines Into Quality Measures
Authors: Barbara B Fleming, Robert A Petzel
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 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
Combination of sPESI and cardiac troponin in the outpatient treatment of pulmoner thromboembolism
Authors: Savas Ozsu, Hayriye Bektas, Yasin Abul, Tevfik Ozlü
Journal: European Respiratory Journal (2014)

It is controversial that which patients will be taken outcome treatment in pulmonary thromboembolism. Our aim is determinantion of outpatients using sPESI and cardiac troponin in pulmonary thromboembolism.  The study was performed prospectively between 02.04.2012 and 13.09.2013. Malignite was excluded from the score of sPESI. Patients seperated into four groups according to troponin and sPESI. Group-1 was consisted with low troponin and low-risk sPESI; group-2 was negative troponin and high-risk sPESI; group-3 was high troponin and low-risk sPESI; grup-4 was high troponin and high-risk sPESI. Primary outcome was defined as all cause of mortality within 90 days. Secondary outcome was defined as recurrens or nonfatal bleeding. Patients in group-1 were treated as outpatient. Upper limit of troponin was considered as 0,04.  In our study there were 138 patients with pulmonary thromboembolism. There were 36 (%26,1) patients in group-1; 42 (%30,4) patients in group-2; 4 (%2,9) patients in group-3; 56 (%40,6) patients in group-4. There were 19 (%13,8) patients treated as outpatient . The patients %5,7 of group-1; %18,6 of group-2; %50 of group-3 and %53,6 of group-4 were died within 90 days. There were detected recurrens or nonfatal bleeding within 90 days of the patients %8,6 of group-1; %6,9 of group-2 ; %25 of group-3 and %16,1 of group-4. As a result of patients with low risk sPESI and negative troponin are thought to be safely treated as outpatients.
Antiphospholipid/antiprotein antibodies, hemostasis-related autoantibodies, and plasma homocysteine as risk factors for a first early pregnancy loss: a matched case-control study
Authors: Jean-Christophe Gris, Thomas V. Perneger, Isabelle Quéré, Eric Mercier, Pascale Fabbro-Peray, Géraldine Lavigne-Lissalde, Médéric Hoffet, Hervé Déchaud, Jean-Christophe Boyer, Sylvie Ripart-Neveu, Marie-Laure Tailland, Jean-Pierre Daurès, Pierre Marès, Michel Dauzat
Journal: Blood (2003)
Further Studies of the Immunological Properties of Polysaccharides from Serratia Marcescens (Bacillus prodigiosus) III. Passive Immunization Against the Lethal Activity of the Polysaccharides with Fractions of Mouse Antiserum Elicited by a Single Injection of Polysaccharide
Authors: Hugh J. Creech, Reed F. Hankwitz
Journal: Cancer Research (1949)

Summary  It has been found that passive immunization with relatively small amounts of the globulin fractions obtained from sera of mice either 3 or 14 days after a single injection of polysaccharides from  Serratia marcescens  afforded mice bearing sarcoma 37 pronounced protection against the lethal action of the homologous polysaccharide but not against that of the polysaccharides from a different strain of the organism.
Abstract 473: Genetic Fate Mapping Identifies Second Heart Field Epicardial Progenitor Cells as a Source of Adipocytes in Arrhythmogenic Right Ventricular Cardiomyopathy
Authors: Raffaella Lombardi, Jinjiag Dong, Gabriela Rodriguez, Achim Bell, Tack Ki Leung, Robert J Schwartz, James T Willerson, Ramon Brugada, Ali J Marian
Journal: Circulation (2008)

The pathological hallmark of arrhythmogenic right ventricular cardiomyopathy (ARVC), a genetic disease of desmosomal proteins, is fibro-adipocytic replacement of cardiac myocytes. The cellular origin of adipocytes in ARVC is an enigma. In desmosomal ARVC the impetus has to instigate from cells that express the mutant protein. Cardiac myocytes are the only cells in the heart known to express the desmosomal proteins. Adult myocytes are terminally differentiated, and hence, an unlikely source. In contrast, cardiac progenitor cells can differentiate to different lineages. Thus, we conditionally deleted Dsp, encoding desmoplakin, and concomitantly expressed enhanced yellow fluorescent protein (EYFP) using the Cre-LoxP technique, regulated by Nkx2.5, an early cardiac lineage promoter. We also screened the human hearts with ARVC for co-expression of markers of cardiac cell lineages and adipocytes. We generated Nkx-2.5-Cre:Dsp W/F and Nkx-2.5-Cre:Dsp W/F :R26-EYFP F/F mice, which showed enlarged hearts, depressed cardiac systolic function and patchy areas of fibro-adiposis, particularly at the epicardium. We detected expression of EYFP by immunoblotting (IB) and immunofluorescence (IF) and expression of cardiac progenitor cells and adipocytes markers by IF. A subset of epicardial cells in the Nkx-2.5-Cre:Dsp W/F :R26-EYFP F/F mice co-expressed adipogenic transcription factors C/EBP-α and PPAR-γ along with EYFP and the second heart field markers IsI1 and Mef2c. Likewise, we detected co-expression of C/EBP-α and IsI1 or Mef2C in the fibro-adipocytic regions in human hearts with ARVC. To determine the specific cardiac cell lineage that differentiates to adipocytes, we co-stained sections of human and lineage trace mouse hearts and detected co-expression of SM actin, a marker of smooth muscle cells (SMCs) and C/EBP-α as well as co-expression of cardiac α-actin, a marker of cardiac myocytes, and C/EBP-α but not co-expression of PECAM1, a marker of endothelial cells and C/EBP-α. We conclude excess adipocytes in desmosomal ARVC originate from second heart field epicardial SMCs/myocyte progenitor cells.
Absolut controversy: liquor ads return to network TV
Authors: Charles Marwick
Journal: BMJ (2003)

This article originally appeared in BMJ USA 

When NBC announced last December 13 that it would accept liquor advertisements on national television, the reaction was predictable. The Distillery Spirits Council of the United States, a national trade association, called the move “a positive day for the spirits industry.” The American Medical Association (AMA) called it “shockingly irresponsible.”

Advocacy groups concerned about excessive drinking criticized it. Millie I Webb, national president of Mothers Against Drunk Driving, called for “higher standards of responsibility in advertising beer, wine, and liquor.” George A Hacker, Alcohol Policies Project Director at the Center for Science in the Public Interest (CSPI), immediately described NBC's …
Structural Associations of Symptomatic Knee Osteoarthritis
Authors: Laura A. Stoppiello, Paul I. Mapp, Deborah Wilson, Roger Hill, Brigitte E. Scammell, David A. Walsh
Journal: Arthritis & Rheumatology (2014)

Objective Structural changes of osteoarthritis (OA) may occur in the absence of pain. In this study, we aimed to identify histopathologic features that are associated with symptomatic knee OA. Methods Medial tibial plateaus and synovium samples were obtained at the time of total knee replacement (TKR) surgery for OA (advanced OA group) or were obtained postmortem from subjects who had not sought medical attention for knee pain during the last year of life (non‐OA control group). To identify features of OA, we compared the patients with advanced OA with the age‐matched non‐OA controls (n = 26 per group). To identify OA features associated with symptoms, we compared two additional groups of subjects who were matched for severity of chondropathy (n = 29 per group): patients undergoing TKR for symptomatic OA (symptomatic chondropathy group) and postmortem subjects with similar severity of chondropathy who were asymptomatic during the last year of life (asymptomatic chondropathy group). The histologic features of the samples were graded, and immunoreactivities for macrophages (CD68) and nerve growth factor (NGF) in the synovium were quantified. The cellular localization of synovial NGF was determined by double immunofluorescence analysis. Results Advanced OA cases displayed more severe changes in the synovium (synovitis, increased synovial NGF, and CD68‐immunoreactive macrophages) and cartilage (loss of cartilage surface integrity, loss of proteoglycan, tidemark breaching, and alterations in chondrocyte morphology) than did the non‐OA controls. Synovial NGF was localized predominantly to fibroblasts and to some macrophages. The symptomatic chondropathy group displayed greater levels of synovitis, synovial NGF, and loss of cartilage integrity, in addition to alterations in chondrocyte morphology, than did the asymptomatic chondropathy group ( P &lt; 0.05 for each comparison). Conclusion Synovitis, increased synovial NGF, alterations in chondrocyte morphology, and loss of cartilage integrity are features of knee OA that may be associated with symptoms.
DEATH FOLLOWING STERNAL PUNCTURE: REPORT OF TWO CASES
Authors: J G FORTNER, E S MOSS
Journal: Annals of Internal Medicine (1951)

Case Reports1 March 1951DEATH FOLLOWING STERNAL PUNCTURE: REPORT OF TWO CASESJOSEPH G. FORTNER, M.D., EMMA S. MOSS, M.D., F.A.C.P.JOSEPH G. FORTNER, M.D.Search for more papers by this author, EMMA S. MOSS, M.D., F.A.C.P.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-34-3-809 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptThe relatively simple procedure of sternal puncture for marrow aspiration may be the cause of death. A review of the literature reveals four reported cases of death following this procedure.1, 2, 3 It is the purpose of this communication to record two additional cases and to comment upon the symptomatology and the mechanism of death.CASE REPORTSCase 1. A 23 year old colored female was admitted to Charity Hospital on June 25, 1948, complaining of a sore throat and tender gums of three months' duration. Hematologic studies of the peripheral blood and bone marrow revealed an acute leukemia. Aminopterin...Bibliography1. MeyerHalpern LMJ: Death following sternal puncture, Am. J. Clin. Path. 14: 247-248, 1944. CrossrefGoogle Scholar2. SchererHowe JHJS: Fatal cardiac tamponade following sternal puncture, J. Lab. and Clin. Med. 30: 450-453, 1945. Google Scholar3. Bardham PN: Death from sternal puncture, Indian M. Gaz. 82: 443-508, 1947. Google Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: New Orleans, Louisiana*Received for publication March 5, 1949.From The Department of Pathology, Charity Hospital of Louisiana at New Orleans. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited byIntraossäre Infusion beim ErwachsenenFatal Sternal PunctureThe Technique of Bone Marrow Aspiration in Children 1 March 1951Volume 34, Issue 3Page: 809-815KeywordsBloodBone marrowPharyngitis ePublished: 1 December 2008 Issue Published: 1 March 1951 PDF downloadLoading ...
409. In Vivo Comparison of Liver-Specific Enhancer-Promoter Constructs in the Context of Lentiviral Vectors
Authors: Tatiana Khakhoulina, Tuan Huy Nguyen, Catherine Fux-Cametti, Didier Trono
Journal: Molecular Therapy (2004)

Gene therapy is a promising approach for the treatment of various inherited liver disorders such as haemophilia, familial hypercholesterolemia, ornitine transcarbamylase deficiency and others. Lentiviral vectors represent a powerful tool for liver gene therapy due to their ability to transduce efficiently non-dividing hepatocytes and to govern stable transgene expression. For in vivo gene transfer protocols, it is advantageuos to restrict therapeutic gene expression to specific target cell types in order to minimize immune responses and systemic adverse effects. We characterized a series of chimeric liver-specific enhancer/promoter constructs driving GFP expression in the context of a third generation lentiviral vector. The vectors contained a self-inactivating LTR to avoid interference for the virus transcriptional elements. We identified several combinations of enhancer/promoters that governed potent and hepato-specific transgene expression when tested in hepatoma cell lines and in primary human hepatocytes. We chose the two most promising liver-specific constructs – mouse transthyretin promoter fused to a synthetic enhancer (eTTR) and human alfa1-antitrypsin promoter fused to a prothrombin enhancer (prtAAT)-for in vivo analysis after intrasplenic administration into neonatal mice and rats. We compared the GFP fluorescence intensity by FACS analysis of hepatocytes isolated from transduced animals 5 days (mice) and 23 days (rats) after vector injections. Both chimeras induced high levels of GFP expression showing no significant difference in fluorescence intensity in rat hepatocytes and an about 20% difference in favour of prtAAT in mouse cells. The cell-specificity of GFP expression in the liver was confirmed by immunochemistry: all the transduced cells exhibited the morphology of hepatocytes and no GFP-expressing endothelial cells were detected. As the spleen represents probably a most important organ in terms of immune responses against the transgene, we analysed GFP expression in splenocytes of the transduced mice 5 and 6 days after vector administration. No GFP expression was detected with the eTTR promoter-containing vector, while with the prtAAT vector some splenocytes were positive. In spite of this, GFP expression in the livers of prtAAT-transduced animals was stable for at least 2 weeks in mice and 3 weeks in rats suggesting no immune rejection of these transduced cells. Biodistribution analyses showed that the liver and the spleen were the major target organs of lentiviral transduction under this experimental procedure since no integrated proviral DNA was detected in heart, intestine and muscle. We conclude that the administration of hepatocyte-specific lentiviral vector in neonates can result in effective transcriptional targeting of transgene expression to hepatocytes thus representing an attractive approach for early intervention in cases of inherited liver disorders.
Care of Aged Persons in the United States.
Authors: Florence Evelyn Parker, Estelle M. Stewart, Mary K. Conyngton
Journal: JAMA (1930)

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
The hospital of the future: Hospital provision, activity, and productivity in England since the 1980s
Authors: M. Hensher, N. Edwards
Journal: BMJ (1999)

This is the second in a series of seven articles

The secretary of state is due to announce the results of an inquiry into beds in England. This review seems to have been in response to a perception that hospitals were experiencing increased difficulty in coping with emergency pressures and that the reduction in beds had gone too far—a fact apparently supported by a plateauing in the downward trend in the number of beds. The hospital sector, especially in the NHS, has long been a focus from all sides for rhetoric and emotive political appeals. In terms of numbers of both hospitals and beds, the NHS has been shrinking for most of its life. The bed stock of NHS in England peaked in 1957-8 and has declined since. In the more recent past, official statistics on hospital services in this country have been plentiful, yet they are rarely presented together in an easily accessible and unified form. It is the objective of this paper, therefore, to provide a concise summary of key trends and statistics in the sector that will be of use to policymakers, analysts, researchers, and practitioners. We present data on hospital provision in both the public and the private sectors, and on productivity in the NHS hospital sector. The implications of the most significant trends are discussed, and a number of lessons are suggested for audiences both within the United Kingdom and abroad The analysis starts in 1982, the year of a major administrative reorganisation within the NHS, and shortly before the Griffiths Report,1 which ushered in the concept of “general management” in the NHS NHS data reporting conventions in all areas changed in 1987, including a move in reporting from calendar years to financial years, the replacement of “deaths and discharges” with the “finished consultant …