tbuckley/cabot-search huggingface dataset:
Abstract 9401: Medicare Readmission Penalties and Their Socioeconomic Correlates in Urban Hospitals
Authors: Kim A Williams, Muhammad S Hamid, Arshad A Javed, Amy M Horton
Journal: Circulation (2014)

In 2013, 2,200 U.S. hospitals forfeited more than $280 million in Medicare funds due to readmission penalties (RPs) for heart failure, pneumonia and myocardial infarction stipulated by the Affordable Care Act. This study evaluated the RPs in the hospitals of large cities, in comparison with other areas within and between states. Methods: Medicare RPs for 2013 (ranging 0 to 1%) were compared along with census and socioeconomic data for the largest city in each of 49 states in the United States, excluding Maryland due to its ongoing Medicare demonstration project. Improvements in RPs for 2014 in each urban area were tabulated. Results: There was a significant correlation between RPs and the size of the population of the cities (r = 0.37, p&lt;0.01), with larger cities receiving higher penalties. For example, Detroit, MI’s 5 hospitals and Newark, NJ’s 3 hospitals have the highest average RPs (0.9%) than the hospitals in other largest cities. The RPs correlated moderately with a higher percentage of low-educated people in the city (r=0.53, p&lt;0.001), and weakly but negatively with the percentage of high-educated people (r= -0.29, p&lt;0.05) in the city. The rate of unemployment also correlated positively and significantly with the RPs (r=0.50, p&lt;0.001). Conclusion: RPs reduce Medicare payments to inner-city hospitals, such as those in Detroit, MI and Newark, NJ, and disproportionately lower payments to large cities with poorer, underemployed and undereducated populations. This may have the unintended consequence of further reducing access care from safety-net hospitals.
Homozygous Cystathionine β-Synthase Deficiency, Combined With Factor V Leiden or Thermolabile Methylenetetrahydrofolate Reductase in the Risk of Venous Thrombosis
Authors: Leo A.J. Kluijtmans, Godfried H.J. Boers, Bert Verbruggen, Frans J.M. Trijbels, Irena R.O. Nováková, Henk J. Blom
Journal: Blood (1998)
PROLONGED REGULATION OF ALLOXAN DIABETES IN DOGS
Authors: L BAUMAN, J L R CANDELA, T MARTINO
Journal: Annals of Internal Medicine (1951)

Article1 August 1951PROLONGED REGULATION OF ALLOXAN DIABETES IN DOGSLOUIS BAUMAN, JOSE L. R. CANDELA, TERRY MARTINOLOUIS BAUMANSearch for more papers by this author, JOSE L. R. CANDELASearch for more papers by this author, TERRY MARTINOSearch for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-35-2-391 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptCan continuous careful control of diabetes prevent the degenerative complications of the disease? This controversial question, though uppermost in the minds of diabetic therapists, has never been subjected to satisfactory animal experimentation.The alloxan diabetic dog offers an approach to this problem because alloxan selectively destroys the islands of Langerhans and because the dog is best suited for this purpose.It was planned to produce the disease and then maintain the animals in metabolism cages on the proper diet and insulin dosage for an extended period of time. Unfortunately, we were limited to a small number of animals, but the...Bibliography1. ThorogoodZimmerman EB: The effects of pancreatectomy on glycosuria and ketosis in dogs made diabetic with alloxan, Endocrinology 37: 191-200, 1945. CrossrefGoogle Scholar2. Ricketts HT: Insulin and diet, J. A. M. A. 138: 353-355, 1948. CrossrefMedlineGoogle Scholar3. JacksonHardinWalkerHendricksKelly RLRCGLABHG: Degenerative changes in young diabetics in relationship to level of control, Proc. Am. Diabetes A. 9: 307-327, 1949. Google Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: *Received for publication June 30, 1950.From the Departments of Surgery and Medicine, College of Physicians and Surgeons, Columbia University, New York. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics 1 August 1951Volume 35, Issue 2Page: 391-396KeywordsDietInsulinOphthalmologySurgeonsSurgerySurgical pathology ePublished: 1 December 2008 Issue Published: 1 August 1951 PDF downloadLoading ...
Clinical Epidemiology: The Study of the Outcome of Illness.
Authors: Noel S. Weiss
Journal: Annals of Internal Medicine (1987)

1. Clinical Epidemiology: What It Is and How It Is used 2. Diagnostics and Screening Tests: Measuring Their Ability to Predict Adverse Outcome of Illness 3. Diagnostic and Screening Tests: Measuring Their Role in Improving the Outcome of Illness 4. Therapeutic Efficacy: Randomized Controlled Trials 5. Therapeutic Efficacy: Nonrandomized Studies 6. Therapeutic Safety 7. Natural History of Illness Appendix: Some Methodologic Tools Useful in the Planning and Analysis of Clinical Epidemiologic Research Index
Book: Brave New NHS?
Authors: J A Raeburn
Journal: BMJ (1999)

Jo Lenaghan Institute for Public Policy Research, £7.50, pp 135 ISBN 1 86030 065 0 Rating: ![Graphic][1]</img>![Graphic][2]</img>![Graphic][3]</img> None of us, least of all geneticists, should be denied the bitter sweet sapience prayed for by Robert Burns, “tae see ourselves as ithers see us.” The Institute for Public Policy Research report A Brave New NHS? anticipates the impact of genetics in the millennium and doesn't pull its punches: “The NHS is sleep-walking into the future.” My specialty was under examination; I felt threatened and was ready … [1]: /embed/inline-graphic-1.gif [2]: /embed/inline-graphic-2.gif [3]: /embed/inline-graphic-3.gif
Abstract 15890: Hornerin, a Multifunctional Protein Critical to Non-VEGF-Mediated Angiogenesis, Plays a Determining Role in Neovascularization of the Infarct Post-mi
Authors: Siva Sai Krishna Dasa, Michael Gutknecht, Marc Seaman, Brent A French, Kimberly A Kelly
Journal: Circulation (2014)

Introduction: Pathological angiogenesis is a hallmark of cancer and other ischemic/inflammatory diseases including remodeling after myocardial infarction (MI) and diabetic retinopathy. Inhibitors of vascular endothelial growth factor (VEGF) signaling have been tested for efficacy against various cancers in clinical trials, but have proven only moderately succesful. To identify factors other than VEGF involved in angiogenesis, we biopaned a phage display library against HUVECs in combination with negative selection against VEGF-mediated signaling. A separate phage display screen was carried out in vivo against the infarct border zone in mice at Day 4 post-MI. Methods: One of the few phage clones in common between the two screens bound to endothelium in the infarct zone at Day 4 post-MI in the mouse model. The molecular binding target of this clone was identified as hornerin (Hrnr) by means of a phage-based proteomics approach. Hornerin belongs to the S100 family, and like other proteins in this family, is relevant in wound-healing post-MI. To study its function post-MI, we performed knock-down studies using siRNA specific for Hrnr. Further, in an effort to identify the potential mechanism of hornerin-induced neovascularization, we performed in vitro proliferation and apoptosis studies using human microvasculature endothelial cells (HMVECs). Results: siRNA-mediated knock-down of Hrnr in post-MI mice prevented neovessel formation and further in vitro studies showed that Hrnr protected endothelial cells against ROS-induced apoptosis through activation of NF-kB (Fig. 1). Conclusions: Inhibitors of Hrnr hold promise as an alternative anti-angiogenic therapy for various diseases including cancer and diabetic retinopathy. The upregulation of hornerin might also serve as therapy to protect endothelial cells against oxidative stress in the healing infarct after MI.
Exercise and Risk of Breast Cancer
Authors: Richard L. Siegler
Journal: JAMA (2003)

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 5882: Myocardial Contractile Dysfunction in Heart Failure with Preserved Ejection Fraction
Authors: Barry A Borlaug, Carolyn S Lam, Veronique Roger, Richard J Rodeheffer, Margaret M Redfield
Journal: Circulation (2008)

Background Patients with heart failure and preserved ejection fraction (HFpEF) have diastolic dysfunction, but are traditionally considered to have normal left ventricular (LV) systolic function. However, ventricular remodeling can result in preservation of EF despite abnormal myocardial contractility. Methods We performed echo-Doppler characterization of LV chamber and myocardial systolic properties in a population-based study, comparing patients with HFpEF (N=244) to healthy controls (CON, N=617), and hypertensives without HF (HTN, N=719), then examined long term outcome. Results All subjects had a normal EF (&gt;50%). However, systolic chamber function, measured by wall stress-corrected endocardial fractional shortening (sc-eFS), was impaired in HFpEF (96±12%) compared to both CON (100±8%, p&lt;0.0001) and HTN (108±11%, p&lt;0.0001). Myocardial contractility, assessed by wall stress-corrected midwall shortening (sc-mFS), was also reduced in HFpEF (91±13%) compared to CON (100±10%, p&lt;0.0001) and HTN (105±12%, p&lt;0.0001). HTN had increased sc-eFS and sc-mFS compared with both HFpEF and CON (p&lt;0.0001). In HFpEF, impaired sc-mFS was associated with increased mortality, independent of age (Figure ), while EF and sc- eFS were not. Conclusions Despite preservation of EF, unselected HFpEF patients from the community have significantly impaired systolic chamber function and depressed myocardial contractility. Abnormal myocardial contractility in HFpEF is associated with increased mortality. These data suggest that myocardial systolic dysfunction contributes to the pathophysiology of HFpEF and may represent a potential therapeutic target.
Abstract MP46: Dietary Pattern and Risk of Sudden Cardiac Death in Post-Menopausal Women
Authors: Monica L Bertoia, Elizabeth W Triche, Dominique S Michaud, Ana Baylin, Joseph W Hogan, Marian L Neuhouser, Lesley F Tinker, Linda Van Horn, Molly E Waring, Wenjun Li, James M Shikany, Charles B Eaton
Journal: Circulation (2013)

Background: The Mediterranean Diet and Dietary Approaches to Stop Hypertension (DASH) diet are characterized by higher intake of fruits, vegetables, whole grains, and unsaturated fatty acids. All of these foods/nutrients may affect cholesterol, inflammation, the development of atherosclerosis, and therefore risk of sudden cardiac death (SCD). Furthermore, the DASH diet is known to lower blood pressure and hypertension is a major risk factor for SCD. Objective: To examine the association between the Mediterranean and DASH dietary patterns and risk of SCD in women. Methods: Post-menopausal women enrolled in the Women’s Health Initiative observational study (n = 93,676) completed a food frequency questionnaire at enrollment and at year three. Women enrolled at 40 clinical sites across the U.S. between 1993 and 1998, and were followed for an average of 10.5 years. We scored their diets according to how closely reported diet resembled each dietary pattern. SCD was defined as death occurring within one hour of symptom onset. We estimated risk of SCD according to quintile of dietary pattern score using hazard models with time-varying exposures. Results: A higher Mediterranean diet score was associated with a lower risk of SCD: women in the highest quintile, or who came closest to following the Mediterranean dietary pattern, had a HR of 0.62 (95% CI 0.41-0.93) compared to women in the lowest quintile, after adjustment for age, total energy, race, income, smoking, and physical activity (Table). After adjusting for other traditional coronary heart disease risk factors which are potential mediators, the association remained statistically significant: HR 0.65 (95% CI 0.43-0.99). A higher DASH diet score was not associated with reduced risk of SCD. However, sodium intake, a crucial component of the DASH dietary pattern, was not well-characterized by the FFQ. Conclusions: The Mediterranean dietary pattern may be associated with a lower risk of SCD in post-menopausal women, however there was no indication of a dose-response relationship.
Comparison of interferon-{gamma} release assays and tuberculin skin test in predicting active tuberculosis (TB) in children in the UK: a paediatric TB network study
Authors: N Bosu, R Watts, I Bajema, B Basland, T Bley, M Boers, P Brogan, L Calabrese, MC Cid, JW Cohen-Tervaert, LF Flores-Suarez, S Fujimoto, K de Groot, L Guillevin, G Hatemi, T Hauser, D Jayne, C Jennette, CG Kallenberg, S Kobayashi, MA Little, A Marh, J McLaren, PA Merkel, S Ozen, X Puechal, N Rasmussen, A Salama, C Salvarani, C Savage, DG Scott, M Segelmark, C Sunderkoetter, K Suzuki, Tesar, H Yazici, R Luqmani
Journal: Annals of the Rheumatic Diseases (2010)

Background The value of interferon-gamma release assays (IGRA) to diagnose active tuberculosis (TB) in children is not established, but these assays are being widely used for this purpose. The authors examined the sensitivity of commercially available IGRA to diagnose active TB in children in the UK compared with the tuberculin skin test (TST). Methods The authors established a paediatric tuberculosis network and conducted a retrospective analysis of data from children investigated for active TB at six large UK paediatric centres. All centres had used TST and at least one of the commercially available IGRA (T-Spot.TB or Quantiferon-Gold in Tube) in the diagnostic work-up for active TB. Data were available from 333 children aged 2 months to 16 years. The authors measured the sensitivity of TST and IGRA in definite (culture confirmed) and probable TB in children, agreement between TST and either IGRA, and their combined sensitivity. Results Of 333 children, 49 fulfilled the criteria of definite TB, and 146 had probable TB. Within the definite cohort, TST had a sensitivity of 82%, Quantiferon-Gold in tube (QFT-IT) had a sensitivity of 78% and T-Spot.TB of 66%. Neither IGRA performed significantly better than a TST with a cut-off of 15 mm. Combining the results of TST and IGRA increased the sensitivity to 96% for TST plus T-Spot.TB and 91% for TST plus QFG-IT in the definite TB cohort. Conclusions A negative IGRA does not exclude active TB disease, but a combination of TST and IGRA increases the sensitivity for identifying children with active TB.
Abstract MP71: Short Sleep Duration Modifies the Relationship Between Hypertension and All-Cause Mortality
Authors: Julio Fernandez-Mendoza, Fan He, Alexandros Vgontzas, Duanping Liao, Edward Bixler
Journal: Circulation (2015)

Introduction: Short sleep duration has been associated with increased risk of hypertension and mortality. However, previous epidemiological studies have been limited in that they used self-reported sleep measures and treated sleep duration as a sole, independent predictor of cardiometabolic morbidity or mortality. Therefore, the role of sleep duration in predicting morbidity and mortality is still not well-understood. Our current research project examines the role of objective sleep duration as an effect modifier between traditional cardiometabolic risk factors and mortality. Hypothesis: We assessed the hypothesis that objectively-measured sleep duration is a key effect modifier of the relationship between hypertension and all-cause mortality. Methods: We addressed this question in the Penn State Adult Cohort, a random, general population sample of 1,741 men and women (48.7 ± 13.5 years) who were studied in the sleep laboratory and were followed-up for 15.5 ± 4.1 years. Hypertension was defined as systoli...
Hormone Therapy and Risk of Gynecologic Cancers
Authors: Wulf H Utian
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
Partial pyruvate kinase deficiency aggravates the phenotypic expression of band 3 deficiency in a family with hereditary spherocytosis
Authors: Rob van Zwieten, Brigitte A. van Oirschot, Martijn Veldthuis, Johannes G. Dobbe, Geert J. Streekstra, Wouter W. van Solinge, Roger E.G. Schutgens, Richard van Wijk
Journal: American Journal of Hematology (2014)

In a family with mild dominant spherocytosis, affected members showed partial band 3 deficiency. The index patient showed more severe clinical symptoms than his relatives, and his red blood cells displayed concomitant low pyruvate kinase activity. We investigated the contribution of partial PK deficiency to the phenotypic expression of mutant band 3 in this family. Pyruvate kinase deficiency and band 3 deficiency were characterized by DNA analysis. Results of red cell osmotic fragility testing, the results of cell deformability obtained by the Automated Rheoscope and Cell Analyzer and the results obtained by Osmotic Gradient Ektacytometry, which is a combination of these tests, were related to the red cell ATP content. Spherocytosis in this family was due to a novel heterozygous mutation in SLC4A1, the gene for band 3. Reduced PK activity of the index patient was attributed to a novel mutation in PKLR inherited from his mother, who was without clinical symptoms. Partial PK deficiency was associated with decreased red cell ATP content and markedly increased osmotic fragility. This suggests an aggravating effect of low ATP levels on the phenotypic expression of band 3 deficiency.
Expanded polyglutamine stretches interact with TAFII130, interfering with CREB-dependent transcription
Authors: Takayoshi Shimohata, Toshihiro Nakajima, Mitsunori Yamada, Chiharu Uchida, Osamu Onodera, Satoshi Naruse, Tetsuya Kimura, Reiji Koide, Kenkichi Nozaki, Yasuteru Sano, Hiroshi Ishiguro, Kumi Sakoe, Takayuki Ooshima, Aki Sato, Takeshi Ikeuchi, Mutsuo Oyake, Toshiya Sato, Yasuyuki Aoyagi, Isao Hozumi, Toshiharu Nagatsu, Yoshihisa Takiyama, Masatoyo Nishizawa, Jun Goto, Ichiro Kanazawa, Irwin Davidson, Naoko Tanese, Hitoshi Takahashi, Shoji Tsuji
Journal: Nature Genetics (2000)
Copy number variations of the human histamine H4 receptor gene are associated with systemic lupus erythematosus
Authors: B. Yu, Y. Shao, P. Li, J. Zhang, Q. Zhong, H. Yang, X. Hu, B. Chen, X. Peng, Q. Wu, Y. Chen, M. Guan, J. Wan, W. Zhang
Journal: British Journal of Dermatology (2010)

Background Systemic lupus erythematosus (SLE) is a complex genetic disease; the histamine H4 receptor (HRH4) has been shown to be related to different kinds of autoimmune disorders; and copy number variations (CNVs) have been found to be associated with various types of diseases. Objectives To explore a possible association between HRH4 (formerly H4R) CNVs and the risk of SLE. Methods Genomic DNA and RNA from 340 patients with SLE and 392 healthy controls were extracted, and CNVs and mRNA levels of HRH4 were examined. Results The expression of HRH4 mRNA was significantly increased in patients with SLE compared with controls. Amplification of HRH4 copy numbers significantly increased the risk of SLE [P < 0·001, odds ratio (OR) 2·26, 95% confidence interval (CI) 1·50–3·40]. HRH4 amplifications also positively correlated with the incidence of arthritis (P = 0·019, OR 1·96, 95% CI 1·11–3·47), and proteinuria (P < 0·001, OR 2·95, 95% CI 1·73–5·00) and antinuclear antibody abnormalities (P < 0·001, OR 2·97, 95% CI 1·66–5·33). Deletions of HRH4 copy numbers were protective against proteinuria (P = 0·03, OR 0·50, 95% CI 0·26–0·94). Conclusion CNVs of the HRH4 gene are associated with SLE.
Polycomb Group (PcG) Proteins and Human Cancers: Multifaceted Functions and Therapeutic Implications
Authors: Wei Wang, Jiang‐Jiang Qin, Sukesh Voruganti, Subhasree Nag, Jianwei Zhou, Ruiwen Zhang
Journal: Medicinal Research Reviews (2015)

Polycomb group (PcG) proteins are transcriptional repressors that regulate several crucial developmental and physiological processes in the cell. More recently, they have been found to play important roles in human carcinogenesis and cancer development and progression. The deregulation and dysfunction of PcG proteins often lead to blocking or inappropriate activation of developmental pathways, enhancing cellular proliferation, inhibiting apoptosis, and increasing the cancer stem cell population. Genetic and molecular investigations of PcG proteins have long been focused on their PcG functions. However, PcG proteins have recently been shown to exert non-classical-Pc-functions, contributing to the regulation of diverse cellular functions. We and others have demonstrated that PcG proteins regulate the expression and function of several oncogenes and tumor suppressor genes in a PcG-independent manner, and PcG proteins are associated with the survival of patients with cancer. In this review, we summarize the recent advances in the research on PcG proteins, including both the Pc-repressive and non-classical-Pc-functions. We specifically focus on the mechanisms by which PcG proteins play roles in cancer initiation, development, and progression. Finally, we discuss the potential value of PcG proteins as molecular biomarkers for the diagnosis and prognosis of cancer, and as molecular targets for cancer therapy.