tbuckley/cabot-search huggingface dataset:
Abstract 16722: Myocardial Infarction and Sudden Cardiac Death in Olmsted County, Minnesota, Before and After Smoke-Free Workplace Laws
Authors: Richard D Hurt, Susan A Weston, Jon O Ebbert, Sheila M McNallan, Ivana T Croghan, Darrell R Schroeder, Veronique L Roger
Journal: Circulation (2011)

Objective: To determine if the implementation of smoke-free workplace laws reduced the incidence of the acute coronary events including myocardial infarction (MI) and sudden cardiac death (SCD). Background: Nonsmokers chronically exposed to second-hand smoke (SHS) are at increased risk of death from heart disease. However, a nonlinear dose relationship exists between SHS exposure and coronary heart disease (CHD) such that the relative risk of CHD is 1.31 for nonsmokers and 1.78 for smokers. Reductions in admissions for MI in locales where smoke-free workplace laws have been implemented have been observed, but none have assessed SCD. On January 1, 2002, a smoke-free restaurant law (Ordinance #1) was implemented in Olmsted County, Minnesota, and on October 1, 2007, all workplaces became smoke-free (Ordinance #2). Methods: Under the auspices of the Rochester Epidemiology Project, we measured the incidence of MI and SCD during the 18-month calendar period before and after implementation of each smoke-free ordinance. All MI were validated using biomarkers, cardiac pain, and Minnesota coding of the ECG. SCD was defined as out-of-hospital deaths assigned to CHD (ICD-9 codes 410 through 414). Results: For the overall study period of the 18 months before the implementation of the smoke-free restaurant ordinance and 18 months after the implementation of the smoke-free workplace ordinance, we observed a 45% decline in the incidence for MI (p &lt;0.01) and a 50% decline in the incidence for SCD (p &lt;0.01). See Table. During this same period, the prevalence of hypertension, diabetes, hypercholesterolemia, and obesity either remained constant or increased while the prevalence of smoking among adults declined by 23% (22% to 17%). Conclusion: In the Olmsted County population, substantial declines in the incidence of MI and SCD were observed after smoke-free laws were implemented. Smoke-free workplace laws may not only be associated with a decrease in MI but SCD as well.
La Lithiase Biliaire.
Authors: Serge Erlinger
Journal: JAMA (1922)

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 Jean Delay Prize, the Okasha Award for Developing Countriesand the Geneva Prize for Human Rights in Psychiatry.
Authors: Ahmed Okasha
Journal: World Psychiatry (2004)

During the 13th World Congress of Psychiatry in Cairo, three prizes will be awarded. The Jean Delay Prize and the Okasha Award for Developing Countries will be awarded during the opening ceremony; the Geneva Prize for Human Rights in Psychiatry will be awarded during the closing ceremony.
Abstract 1214: Rational Design of a Potent Bipartite Inhibitor of Nuclear Factor of Activated T Cells (NFAT), a Key Regulator of Cardiovascular Hyperplasia
Authors: Haixiang Yu, Ilze Bot, Karen Sliedregt, Xingfu Xu, Gijs A van der Marel, Herman S Overkleeft, Theo J van Berkel, Erik A Biessen
Journal: Circulation (2007)

Purpose: Targeted intervention in calcineurin/NFAT signaling is an effective strategy in the treatment of vascular smooth muscle cell (vSMC) hyperplasia and restenosis. We have recently shown that VIVIT, a novel peptide inhibitor of NFAT, is more selective and less toxic than cyclosporine A (CsA) and holds promise in antirestenotic therapy. However, its suboptimal pharmacological features preclude direct clinical use. In this study, we sought to overcome these setbacks by stepwise optimization of VIVIT. Methods and Results: In the first stage stepwise truncation and alanine scan studies were performed to establish the critical importance of the HPVIVIT motif for NFAT inhibition. In order to create a non-toxic bipartite compound that simultaneously targets two recently identified NFAT docking sites on calcineurin, the HPVIVIT motif was conjugated to a maleimide derivative via a series of flexible spacers of 8–28 Å. One of the conjugates, maleimide conjugated HPVIVIT or MCV, was 10,000 more potent in inhibiting NFAT (IC50=1.9 nM) than the parent peptide. MCV was able to abrogate ionomycin induced nuclear translocation of NFAT1-GFP at 100 nM and this effect persisted for &gt;36h. Moreover, it profoundly inhibited platelet-derived growth factor-BB stimulated vSMC proliferation at concentrations as low as 10 nM (P=0.04; ~80%). MCV (100 nM) selectively disrupted calcineurin NFAT interaction in a GST pull-down assay but did not affect that of other binding partners (AKAP-79/Cain). It was at least equally potent as CsA in inhibiting ionomycin induced NFAT dephosphorylation in COS-1 cells. Unlike CsA however, MCV appeared to be non-toxic and did not impair the activity of calcineurin phosphatase. Moreover, in contrast to CsA MCV did not affect mitogen-activated protein kinase activity after PMA stimulation in COS-1 cells at concentrations up to 10 μM nor did it influence NFκB activity. Finally, CsA prevented nuclear accumulation of calcineurin, which remained unaffected by MCV1 (1 μM). Conclusion : The potency, chemical features and superior selectivity of the bipartite NFAT inhibitor MCV render this compound an excellent lead in the treatment of inflammatory disorders implicating NFAT activation, including myocardiac hypertrophy and restenosis.
MRI evaluation of injectable hyaluronic acid-based hydrogel therapy to limit ventricular remodeling after myocardial infarction
Authors: Shauna M. Dorsey, Jeremy R. McGarvey, Hua Wang, Amir Nikou, Leron Arama, Kevin J. Koomalsingh, Norihiro Kondo, Joseph H. Gorman, James J. Pilla, Robert C. Gorman, Jonathan F. Wenk, Jason A. Burdick
Journal: Biomaterials (2015)
Abstract 694: Ankyrin Repeat and SOCS Box Protein 4 (ASB4) is a Hydroxylation Substrate of Factor Inhibiting HIF1a (FIH) and Promotes Vascular Differentiation via an Oxygen-Dependent Mechanism
Authors: James E Ferguson, Yaxu Wu, Kevin Smith, Cam Patterson
Journal: Circulation (2007)

The molecular mechanisms of endothelial differentiation into a functional vascular network are incompletely understood. To identify novel factors in endothelial development we employed a microarray screen using differentiating embryonic stem (ES) cells that identified the previously uncharacterized Ankyrin Repeat and SOCS Box Protein 4 (ASB4) as the most highly differentially expressed gene in the vascular lineage during early differentiation. Like other SOCS box-containing proteins, ASB4 acts as the substrate recognition molecule of an Elongin-B/Elongin-C/Cullin/Roc ubiquitin ligase complex that mediates the ubiquitination and degradation of substrate protein(s). We show here that high levels of ASB4 expression in the embryonic vasculature coincide with drastic increases in oxygen tension as placental blood flow is initiated. However, as vessels mature and oxygen levels stabilize, ASB4 expression is quickly downregulated, suggesting that ASB4 may function to modulate an endothelial-specific response to increasing oxygen tension. Consistent with the hypothesis that ASB4 function is regulated by oxygen concentration, ASB4 directly interacts with Factor Inhibiting HIF1-alpha (FIH), and is a substrate for FIH-mediated hydroxylation via an oxygen-dependent mechanism. Additionally, overexpression of ASB4 in ES cells promotes differentiation into the endothelial lineage in an oxygen-dependent manner. We propose that hydroxylation of ASB4 in normoxia promotes binding to and degradation of substrate protein(s) to modulate vascular differentiation.
Virtual Histology of Colorectal Lesions Using Laser-Scanning Confocal Microscopy
Authors: M. Sakashita, H. Inoue, H. Kashida, J. Tanaka, J. Cho, H. Satodate, E. Hidaka, T. Yoshida, N. Fukami, Y. Tamegai, A. Shiokawa, S. Kudo
Journal: Endoscopy (2003)

Histological examination of gastrointestinal lesions is currently based on light-microscopic examination of thin-slice specimens, with hematoxylin and eosin staining. A study of the use of laser-scanning confocal microscopy (LCM) to obtain immediate microscopic images of untreated specimens for examining colorectal lesions was carried out. A probe-type LCM prototype endomicroscope that can be passed through the working channel of an endoscope has also been developed.The study materials consisted of colorectal lesions resected either endoscopically or surgically at Showa University Northern Yokohama Hospital. One hundred untreated specimens were examined using LCM. The histopathological findings in the lesions were seven cases of normal colonic mucosa, five hyperplastic polyps, 68 adenomas with low-grade dysplasia, 10 adenomas with high-grade dysplasia, and 10 adenocarcinomas. An argon laser beam with a wavelength of 488 nm was used for the LCM study. Observation of the resected normal colonic mucosa (in vitro) and the rectal mucosa of a healthy volunteer (in vivo) was possible using the endomicroscope. The LCM images for each specimen were compared with the hematoxylin-eosin-stained histopathological cross-sections.The LCM images corresponded well with the conventional hematoxylin-eosin light-microscopic images. The nuclei were not visualized in normal mucosa or hyperplastic polyps. In adenomas with high-grade dysplasia and carcinomas, nuclei were more often visible than in adenomas with low-grade dysplasia. The rate of visualization of nuclei was significantly different ( P < 0.01) between these two groups (60.0 % vs. 10.3 %). In LCM images using endomicroscope, it was possible to recognize the orifices of the colonic glands and goblet cells both in vitro and in vivo.Laser-scanning confocal microscopy provides immediate images that correspond well with those of hematoxylin-eosin staining. An improved probe-type LCM endomicroscope is being developed which should provide better histological images of colorectal lesions in vivo.
Cardiac Resynchronization Therapy Is More Effective in Women Than in Men
Authors: Aysha Arshad, Arthur J. Moss, Elyse Foster, Luigi Padeletti, Alon Barsheshet, Ilan Goldenberg, Henry Greenberg, W. Jackson Hall, Scott McNitt, Wojciech Zareba, Scott Solomon, Jonathan S. Steinberg
Journal: Journal of the American College of Cardiology (2011)
Abstract 2909: Determinants of Mitral Regurgitation Severity in Chronic Systolic Heart Failure. A Longitudinal and Radial Strain and Strain Rate Echocardiographic Study in 90 Consecutive Patients
Authors: Erwan Donal, Christophe Leclercq, Christian de Place, Olivier Cesari, Jean-Claude Daubert, Philippe Mabo
Journal: Circulation (2006)

Background:  Mitral regurgitation (MR) is a common finding in patients with left ventricular ( LV ) systolic dysfunction and is an independent predictor of mortality. Defining determinants remains challenging but is of crucial importance to guide treatment.   Purpose:  Assessment of the relative influence of myocardial contractilities (radial and longitudinal) and dyssynchrony on MR-severity   Methods:  91 consecutive patients referred for evaluation of their chronic heart failure (CHF) were studied by echocardiography. We measured LV volumes, diameters and geometry, left atrial and mitral annulus sizes, mitral valve tenting. We estimated filling pressures (E/Ea, E/Vp) and, myocardial contractility and dyssynchrony using a regional strain (myocardial deformation dependant in filling pressure) and strain rate (myocardial deformation independant of filling pressure) analysis with the 2D-strain software. MR was quantified using the continuity equation and the PISA method.   Results:  Table 1 displays the main parameters measured. In the bivariate regression analysis, the MR regurgitant volume was correlated with mitral annulus diameter (p   Conclusion:  MR in CHF-patients is multifactorial. Its echocardiographic evaluation has to be exhaustive. Dyssynchrony and longitudinal contractility in regard to the antero-lateral papillary muscle are determinant factors, potentially relevant in the therapeutic decision making. However we did not find any impact of radial contractility on MR-severity.
The occurrence of benign and malignant mammary lesions in rats treated with crystalline estrogen.
Authors: Milton J. Eisen
Journal: Cancer Research (1942)

The effects of slowly absorbed crystalline estrogen upon the mammary tissue of 134 Sherman rats (63 females 71 males) of known genetic constitution and aged 3-5 weeks were investigated.  Estradiol dipropionate was administered to the animals subcutaneously intramuscularly or intraperitoneally in various dosages ranging from 1-20 mg in divided doses.  Chronic diffuse alterations were observed in the genitomammary system of both sexes the most outstanding of which was a fibrocystic mammary disorder of a benign nature.  The breast lesions developed as a sequence of events characterized by considerable variability but occurring in all animals.  Initial manifestations in the epithelium consisted of proliferation chiefly of the ducts signs of functional cell activity microscopic followed by macroscopically visible enlargement of the lumina as a consequence of accumulated secretions and exhaustion of cellular activity with subsequent evidence of cell disintegration or reversion of the epithelium to a resting stage.  These lesions accounted for the succeeding changes in the stroma.  Diffuse fibrosis resulted in contraction and distortion of persisting mammary elements and resulted ultimately in a state similar to human chronic cystic mastitis.  Mammary adenocarcinoma was observed in 2 rats.  Untreated control rats did not exhibit the changes in estrogen-treated rats.  Although estrogens produced a chronic benign fibrocystic mammary lesion in this study additional factors of unknown nature possibly acting locally may be involved in the genesis of late secondary epithelial proliferations and true neoplasia.
Predictors of Permanent Pacemaker Implantation in Patients With Severe Aortic Stenosis Undergoing TAVR
Authors: George C.M. Siontis, Peter Jüni, Thomas Pilgrim, Stefan Stortecky, Lutz Büllesfeld, Bernhard Meier, Peter Wenaweser, Stephan Windecker
Journal: Journal of the American College of Cardiology (2014)
Abstract 235: Sonic Hedgehog Induces Angiogenesis via Rho Kinase-dependent MMP-9 and Osteopontin Expression
Authors: Marie-Ange Renault, Jerome Roncalli, Joern Tongers, Tina Thorne, Sol Misener, Olga V Volpert, Shanu Mehta, Aaron Burg, Corinne Luedemann, Gangjian Qin, Raj Kishore, Douglas W Losordo
Journal: Circulation (2008)

The morphogen Sonic Hedgehog (Shh) is known to promote neovascularization in adults via indirect induction of pro-angiogenic cytokine expression by fibroblasts. Direct effects of Shh on endothelial cell (EC) function and angiogenesis, however, have not been characterized. Accordingly, we performed a series of in vitro and in vivo studies to evaluate the direct effects of Shh on EC and to investigate certain mechanisms by which Shh modulates angiogenesis. Our data disclose that Shh promotes capillary morphogenesis (tube length on Matrigel ™ increased to 271±50% of the length in untreated cells), induces EC migration (191±35%) and increases EC expression of matrix metalloproteinase 9 (MMP-9) and osteopontin (OPN), which are shown to be essential for Shh-induced angiogenesis both in vitro and in vivo . Shh effects in ECs, however, occur while Gli-dependent transcription is not modulated. Furthemore, our studies show that changes in gene expression and EC migration are mediated by Shh induction of Rho. The Rho dependence of Shh-induced EC angiogenic activity is documented in vitro using dominant negative constructs for RhoA and Rho kinase (ROCK), showing that RhoA and ROCK blockade attenuates Shh induced migration and tube formation, as well as the Shh induced expression of MMP-9 and OPN. In vivo in the mouse corneal angiogenesis model pharmacologic inhibition of ROCK blocks Shh induced angiogenesis, confirming the ROCK dependence of this process. Furthermore, in MMP-9 and OPN null mice Shh induced angiogenesis also blocked, indicating that Shh induced angiogenesis is also dependent on MMP-9 and OPN expression. These data elucidate an entirely novel, “non-classical” pathway by which Shh directly modulates EC phenotype and angiogenic activity
Antipsychotic Maintenance Treatment: Time to Rethink?
Authors: Joanna Moncrieff
Journal: PLoS Medicine (2015)

Points• Existing studies of long-term antipsychotic treatment for people with schizophrenia and related conditions are too short and have ignored the impact of discontinuation-related adverse effects.• Recent evidence confirms that antipsychotics have a range of serious adverse effects, including reduction of brain volume.
Antithrombin activity during the period of percutaneous coronary revascularization
Authors: William H Matthai, Peter B Kurnik, William C Groh, William J Untereker, Jamie E Siegel
Journal: Journal of the American College of Cardiology (1999)

OBJECTIVES This study evaluated changes in antithrombin (AT) activity around the time of percutaneous transluminal coronary revascularization (PTCR) with unfractionated heparin anticoagulation and the effects these changes had on major thrombotic complications of PTCR. BACKGROUND Heparin is used during PTCR to prevent thrombosis. However, heparin, a cofactor for AT, causes AT activity to fall. AT activity <70% is associated with thrombosis. There is a prothrombotic state after heparin discontinuation that has not been well explained. METHODS Antithrombin activity was sampled at the start and end of PTCR and the next two mornings in 250 consecutive patients. We recorded occurrence of major thrombotic events, defined as 1) major thrombotic complications of PTCR; 2) major in-lab thrombus formation; or 3) subacute occlusion. Discriminant analysis was employed to evaluate the relationship of AT activity to these events. Change in AT activity and its relationship to heparin was evaluated. Evidence of restenosis at six months was obtained. RESULTS There were 14 major thrombotic events. Antithrombin activity <70% was strongly (p = 0.006) associated with these events. The AT activity fell significantly through the morning after PTCR when 21% of patients had AT activity <70%; AT activity did not normalize until >20 h after heparin discontinuation. Pre-PTCR use of heparin led to lower AT activity in proportion to duration of heparin use. There was no relationship between AT activity and restenosis. CONCLUSIONS Low AT activity may contribute to major thrombotic complications of PTCR. The way heparin is used before and after PTCR is important to development of low AT activity.
Pharmaceutical inhibition of glycogen synthetase kinase 3 beta suppresses wear debris-induced osteolysis
Authors: Dechun Geng, Jian Wu, Hongguo Shao, Shijun Zhu, Yijun Wang, Wen Zhang, Zichuan Ping, Xuanyang Hu, Xuesong Zhu, Yaozeng Xu, Huilin Yang
Journal: Biomaterials (2015)
Microarray analysis of small cell lung cancer reveals altered apoptotic imbalance and distinct expression signatures of MYC family gene amplification
Authors: Young H. Kim, Luc Girard, Craig Giacomini, Pei Wang, Tina Hernandez-Boussard, Robert Tibshirani, John D. Minna, Jonathan R. Pollack
Journal: Cancer Research (2005)

877   DNA copy number alterations (CNAs), as amplifications of oncogenes and deletions of tumor suppressor genes, frequently contribute to the development and progression of lung cancer. To identify novel such alterations in small cell lung cancer (SCLC), we performed array-based comparative genomic hybridization (aCGH) on a set of 24 SCLC cell lines using cDNA microarrays representing ∼22,000 human genes (providing an average mapping resolution of  MYC  (8q24),  MYCN  (2p24) and  MYCL1  (1p34). Other highly-localized DNA amplifications suggested candidate oncogenes not previously identified as amplified in SCLC, including the anti-apoptotic genes  TNFRSF4  (1p36),  DAD1  (14q11),  BCL2L1  (20q11) and  BCL2L2  (14q11). Likewise, newly-discovered PCR-validated homozygous deletions suggested candidate tumor suppressor genes (TSGs), including the pro-apoptotic genes  MAPK10  (4q21) and  TNFRSF6  (10q23). To characterize the effect of DNA amplification on gene expression patterns, we performed expression profiling using the same microarray platform. Among our findings, we identified sets of genes whose expression correlated with amplification of the MYC family oncogenes,  MYC ,  MYCN  and  MYCL1 , with surprisingly little overlap among gene sets.  MYC  and  MYCN  amplification were associated with increased and decreased expression of known MYC up-regulated and down-regulated targets, respectively, while  MYCL1  amplification was associated only with the latter. In summary, our findings support a role for altered apoptotic balance in the pathogenesis of SCLC, and suggest the possibility that MYC oncoproteins might effect transformation through distinct sets of targets, in particular highlighting the importance of transcriptional repression.