tbuckley/cabot-search huggingface dataset:
Preventing Firearm Violence
Authors: William C. Waters IV
Journal: Annals of Internal Medicine (1995)

Letters15 November 1995Preventing Firearm ViolenceWilliam C. Waters IV, MDWilliam C. Waters IV, MDDoctors for Integrity in Policy Research; Atlanta, GA 30339Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-123-10-199511150-00032 SectionsAboutFull TextPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail TO THE EDITOR:In reviewing the College's position paper on preventing firearm violence [1], we are struck by the fact that although it is written by persons with careers in science, it lacks the attributes of a scientific approach to problem solving. The most basic strategy in science is to collect and analyze all available facts and data. This was simply not done; for every controversial assertion in the position paper, there is an egregious lack of balancing argument.In their haste to link guns causally to the deaths of young black males, the authors did not mention that the ...References1. American College of Physicians. Preventing firearm violence: a public health imperative. Ann Intern Med. 1995; 122:311-3. Google Scholar2. Kleck G. Point Blank: Guns and Violence in America. Hawthorne, NY: Aldine de Gruyter; 1993. Google Scholar3. Kleck G, Gertz M. Armed resistance to crime: the prevalence and nature of self-defense with a gun. Journal of Criminology and Criminal Law. 1995; 86:[In press]. Google Scholar4. Kates DB, Schaffler HE, Lattimer JK, Murray GB, Cassem EH. Guns and public health: epidemic of violence or pandemic of propaganda? University of Tennessee Law Review. Summer 1995. Google Scholar5. Accident Facts: 1992 edition. Chicago: National Safety Council; 1992. Google Scholar Author, Article, and Disclosure InformationAffiliations: Doctors for Integrity in Policy Research; Atlanta, GA 30339 PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics 15 November 1995Volume 123, Issue 10Page: 813-813KeywordsCrimeDeath ratesFirearm injuriesHomicidePlaguePrevention, policy, and public healthProblem solvingScientistsSports Issue Published: 15 November 1995 Copyright & PermissionsCopyright © 1995 by American College of Physicians. All Rights Reserved.PDF downloadLoading ...
Hemodynamic Factors Affecting the Fate of Valvular Bioprosthesis
Authors: Alain Carpentier
Journal: Circulation (2010)

Ce qui est simple est faux mais ce qui ne l'est pas est inutilisable.-Paul Vale ´ry S ince their introduction in 1969, valvular bioprostheses (ie, glutaraldehyde-processed animal valves) 1 have experienced a surprising increase in use as a result of progress in valve processing 2 and growing patient desire for nonthrombogenic valve surgery. 3However, the persistent risk of structural valve deterioration, particularly in the young population, remains a major concern.The 2 main causes of valve failure are valve degeneration and calcification.Among the numerous factors influencing the fate of a bioprosthesis, hemodynamic factors are addressed more rarely than biological factors.In this issue of Circulation, Flameng and colleagues 4 add important information to the understanding of how hemodynamic factors play a role in structural valve failure.To do so, they revive an old debate on the practical significance of prosthesis-patient mismatch.First introduced by Rahimtoola in 1978 5 and having fed numerous discussions for many years, this paradigm led to the simple conclusion that, in aortic valve replacement, the larger the valve is, the better the hemodynamics and therefore the clinical result are.Accordingly, surgeons were advised to carefully measure the aortic valve orifice and to select a valve by fitting the aortic valve orifice in correlation to body size.This recommendation is still valid today.A mismatch is defined by the authors as an orifice area index Ͻ0.85 cm 2 /m 2 , which is within the range of Rahimtoola's 6 moderately severe stenosis.It creates significant transvalvular gradient, residual clinical symptoms, and arrhythmias.The originality of this article lies in the fact that the authors make a distinction between 2 simple categories of valve structural deterioration, depending on whether the valve is stenotic or regurgitant as assessed by echocardiography.
Characterizing DNA methylation alterations from The Cancer Genome Atlas
Authors: Daniel J. Weisenberger
Journal: Journal of Clinical Investigation (2014)

The Cancer Genome Atlas (TCGA) Research Network is an ambitious multi-institutional consortium effort aimed at characterizing sequence, copy number, gene (mRNA) expression, microRNA expression, and DNA methylation alterations in 30 cancer types. TCGA data have become an extraordinary resource for basic, translational, and clinical researchers and have the potential to shape cancer diagnostic and treatment strategies. DNA methylation changes are integral to all aspects of cancer genomics and have been shown to have important associations with gene expression, sequence, and copy number changes. This Review highlights the knowledge gained from DNA methylation alterations in human cancers from TCGA.
Effect of Dietary Vitamin E on Spontaneous or Nitric Oxide Donor-Induced Mutations in a Mouse Tumor Model
Authors: J. K. Sandhu
Journal: JNCI Journal of the National Cancer Institute (2000)

Background: Vitamin E, an antioxidant, has been investigated for its effect on cancer incidence in humans, but no firm conclusions about a protective effect can be drawn from these studies. Recently, we reported a statistically significant correlation in the Mutatect mouse tumor model between the number of neutrophils and the frequency of mutation at the hypoxanthine phosphoribosyltransferase (hprt) locus. We have now used this model to investigate vitamin E's effect on the hprt mutation rate. Methods: Mutatect cells were grown in mice as subcutaneous tumors for 2–3 weeks, the tumor cells were recovered, and 6-thioguanine-resistant (i.e., hprt mutant) colonies were scored. Myeloperoxidase activity was used as a measure of neutrophil infiltration. Vitamin E (2 IU/kg body weight) was provided in the diet for 3–4 weeks. In some experiments, glyceryl trinitrate (100 mg/kg body weight) was also administered as a source of nitric oxide. All statistical tests were two-sided. Results: Mouse tumors from the Mutatect MN-11 cell line exhibited a 3.2-fold higher median mutation frequency than the same cells in culture (P<.0001); vitamin E reduced this frequency by 24.9% (P = .01). Mutatect TM-28-derived tumors (which secrete interleukin 8) were heavily infiltrated with neutrophils and had a correspondingly high mutation frequency; in two separate experiments, vitamin E reduced the median mutation frequency by 68.9% (P = .0019) and 84.1% (P = .011) and myeloperoxidase levels by 75.3% (P = .0002) and 75.5% (P = .026), respectively. Glyceryl trinitrate increased the mutation frequency in MN-11 tumors, and vitamin E reduced the median frequency by 61.4% (P = .058). Conclusions: Dietary vitamin E afforded strong protection against both spontaneously arising and nitric oxide-induced mutations. Two separate protective mechanisms by vitamin E may be operating: scavenging of a nitric oxide-related genotoxic species and altering the infiltration of neutrophils into tumors.
Endothelial derived relaxing factor controls renal hemodynamics in the normal rat kidney.
Authors: C Baylis, P Harton, K Engels
Journal: Journal of the American Society of Nephrology (1990)

These studies were conducted in the conscious, chronically catheterized rat to determine whether the endothelial derived relaxing factor (EDRF) controls renal function in the normal state. Administration of the EDRF synthesis inhibitors N-monomethyl-L-arginine (NMA; 100 mg/kg body weight) or N-nitro-L-arginine methylester (NAME; 10 mg/kg body wt) led to a large, sustained rise in blood pressure, a large rise in renal vascular resistance, a fall in renal plasma flow, a relatively slight reduction in glomerular filtration rate, and a consequent rise in filtration fraction. In addition, a marked natriuresis occurred because of a reduction in the fractional reabsorption of sodium. In separate studies, a continuous infusion of excess L-arginine (300 mg/kg body wt bolus followed by 50 mg/kg body wt per min) attenuated the NMA- or NAME-induced rise in blood pressure and reversed the renal hemodynamic effects such that a significant rise in renal plasma flow was seen. L-Arginine alone produced a selective renal vasodilation and large increases in sodium excretion. These observations support earlier suggestions that tonic release of EDRF controls the basal blood pressure and also show that renal function in the normal unstressed rat is markedly influenced by EDRF. These studies suggest that, in addition to controlling renal plasma flow, EDRF may have other, complex actions at the glomerulus. The natriuresis seen after acute inhibition of EDRF with NMA or NAME was probably the result of a pressure natriuretic response to the abrupt rise in blood pressure and also, perhaps, reflects removal of an EDRF influence to directly enhance sodium reabsorption somewhere in the nephron.
Increased exhaled nitric oxide precedes lung fibrosis in a murine model of systemic sclerosis
Authors: Thong Hua-Huy, Nhat-Nam Le-Dong, Sy Duong-Quy, Yihua Bei, Sébastien Rivière, Kiet-Phong Tiev, Carole Nicco, Frédéric Batteux, Anh Tuan Dinh-Xuan
Journal: European Respiratory Journal (2012)

Background:  Exhaled nitric oxide (eNO) increased in patients with systemic sclerosis (SSc) and interstitial lung disease. Reactive oxygen species (ROS) and bleomycin induced skin and lung fibrosis in mice, mimicking the SSc in humans.  Objectives:  This study aimed to validate eNO measurement method in mice and to study the evolution of lung inflammatory and fibrotic processes in mice injected with HOCl or bleomycin.  Methods:  C57BL/6 mice were randomized into 3 groups receiving subcutaneous injections of HOCl, bleomycin, or PBS for 2, 4, or 6 weeks. Exhaled NO was measured at the end of each injection period and after 2 resting weeks without injection (8 weeks). Mice were then sacrificed to obtain skin and lung tissues for NO synthases (NOS) expression analysis.  Results:  Increased exhaled NO, inducible NOS and 3-nitrotyrosine expression in bronchial epithelium, lung neutrophils and macrophages were observed at early phases (2 and 4 weeks) in HOCl- and bleomycin-treated mice. Inversely, lung vascular endothelial NOS expression decreased significantly at 6th and 8th week. Skin fibrosis was significantly increased from the 4th week and lung fibrosis from 6th week.  Conclusions:  Exhaled NO can be used as a sensitive biomarker of lung inflammation in these murine models in which inflammation precedes fibrotic processes in skin and lungs. Mechanisms linking inflammation and fibrosis remain to be clarified.
Influence of Familial Risk on Diabetes Risk–Reducing Behaviors Among U.S. Adults Without Diabetes
Authors: Man-huei Chang, Rodolfo Valdez, Renée M. Ned, Tiebin Liu, Quanhe Yang, Ajay Yesupriya, Nicole F. Dowling, James B. Meigs, Michael S. Bowen, Muin J. Khoury
Journal: Diabetes Care (2011)

To test the association of family history of diabetes with the adoption of diabetes risk-reducing behaviors and whether this association is strengthened by physician advice or commonly known factors associated with diabetes risk.We used cross-sectional data from the 2005-2008 National Health and Nutrition Examination Survey (NHANES) to examine the effects of family history of diabetes on the adoption of selected risk-reducing behaviors in 8,598 adults (aged ≥20 years) without diabetes. We used multiple logistic regression to model three risk reduction behaviors (controlling or losing weight, increasing physical activity, and reducing the amount of dietary fat or calories) with family history of diabetes.Overall, 36.2% of U.S. adults without diabetes had a family history of diabetes. Among them, ~39.8% reported receiving advice from a physician during the past year regarding any of the three selected behaviors compared with 29.2% of participants with no family history (P < 0.01). In univariate analysis, adults with a family history of diabetes were more likely to perform these risk-reducing behaviors compared with adults without a family history. Physician advice was strongly associated with each of the behavioral changes (P < 0.01), and this did not differ by family history of diabetes.Familial risk for diabetes and physician advice both independently influence the adoption of diabetes risk-reducing behaviors. However, fewer than half of participants with familial risk reported receiving physician advice for adopting these behaviors.
Activated Nrf2 impairs liver regeneration in mice by activation of genes involved in cell-cycle control and apoptosis
Authors: Ulrike A. Köhler, Svitlana Kurinna, Dominik Schwitter, Andrea Marti, Matthias Schäfer, Claus Hellerbrand, Tobias Speicher, Sabine Werner
Journal: Hepatology (2013)

The nuclear factor erythroid-derived 2, like 2 (Nrf2) transcription factor is a key regulator of the antioxidant defense system, and pharmacological activation of Nrf2 is a promising strategy for prevention of toxin-induced liver damage. However, the consequences of Nrf2 activation on liver regeneration (LR) have not been determined. To address this question, we generated mice expressing a constitutively active Nrf2 (caNrf2) mutant in hepatocytes. Expression of the transgene did not affect liver homeostasis. Surprisingly, however, there was no beneficial effect of Nrf2 activation on CCl4 -induced liver injury and fibrosis. Most important, LR after partial hepatectomy was impaired in caNrf2-transgenic mice as a result of delayed hepatocyte proliferation and enhanced apoptosis of these cells after liver injury. Mechanistically, this involved up-regulation of the cyclin-dependent kinase inhibitor p15 and the proapoptotic protein Bcl2l11 (Bim). Using chromatin immunoprecipitation, we show that the p15 and Bcl2l11 genes are direct targets of Nrf2, which are activated under hyperproliferative conditions in the liver. Activated Nrf2 delays proliferation and induces apoptosis of hepatocytes in the regenerating liver. These negative effects of Nrf2 activation on LR should be considered when Nrf2-activating compounds are used for prevention of liver damage.
GRENZ-RAY TREATMENT OE FAMILIAL BENIGN CHRONIC PEMPHIGUS
Authors: I. SARKANY
Journal: British Journal of Dermatology (1959)

British Journal of DermatologyVolume 71, Issue 7 p. 247-252 GRENZ-RAY TREATMENT OE FAMILIAL BENIGN CHRONIC PEMPHIGUS I. SARKANY, I. SARKANY King's College Hospital, London, S.E.5.Search for more papers by this author I. SARKANY, I. SARKANY King's College Hospital, London, S.E.5.Search for more papers by this author First published: July 1959 https://doi.org/10.1111/j.1365-2133.1959.tb13419.xCitations: 21AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinked InRedditWechat Citing Literature Volume71, Issue7July 1959Pages 247-252 RelatedInformation
The Relative Contribution of Point Mutations and Genomic Rearrangements in <i>BRCA1</i> and <i>BRCA2</i> in High-Risk Breast Cancer Families
Authors: Maurizia Dalla Palma, Susan M. Domchek, Jill Stopfer, Julie Erlichman, Jill D. Siegfried, Jessica Tigges-Cardwell, Bernard A. Mason, Timothy R. Rebbeck, Katherine L. Nathanson
Journal: Cancer Research (2008)

The demand for BRCA1 and BRCA2 mutation screening is increasing as their identification will affect medical management. However, both the contribution of different mutation types in BRCA1 and BRCA2 and whom should be offered testing for large genomic rearrangements have not been well established in the U.S. high-risk population. We define the prevalence and spectrum of point mutations and genomic rearrangements in BRCA genes in a large U.S. high-risk clinic population of both non-Ashkenazi and Ashkenazi Jewish descent, using a sample set representative of the U.S. genetic testing population. Two hundred fifty-one probands ascertained through the University of Pennsylvania high-risk clinic, all with commercial testing for BRCA1 and BRCA2, with an estimated prevalence of BRCA mutation >or=10% using the Myriad II model and a DNA sample available, were studied. Individuals without deleterious point mutations were screened for genomic rearrangements in BRCA1 and BRCA2. In the 136 non-Ashkenazi Jewish probands, 36 (26%) BRCA point mutations and 8 (6%) genomic rearrangements (7 in BRCA1 and 1 in BRCA2) were identified. Forty-seven of the 115 (40%) Ashkenazi Jewish probands had point mutations; no genomic rearrangements were identified in the group without mutations. In the non-Ashkenazi Jewish probands, genomic rearrangements constituted 18% of all identified BRCA mutations; estimated mutation prevalence (Myriad II model) was not predictive of their presence. Whereas these findings should be confirmed in larger sample sets, our data suggest that genomic rearrangement testing be considered in all non-Ashkenazi Jewish women with an estimated mutation prevalence >or=10%.
Carboplatin and Paclitaxel in Combination With Either Vorinostat or Placebo for First-Line Therapy of Advanced Non–Small-Cell Lung Cancer
Authors: Suresh S. Ramalingam, Michael L. Maitland, Paul Frankel, Athanassios E. Argiris, Marianna Koczywas, Barbara Gitlitz, Sachdev Thomas, Igor Espinoza-Delgado, Everett E. Vokes, David R. Gandara, Chandra P. Belani
Journal: Journal of Clinical Oncology (2009)

PURPOSE Vorinostat, a histone deacetylase inhibitor, exerts anticancer effects by both histone and nonhistone-mediated mechanisms. It also enhances the anticancer effects of platinum compounds and taxanes in non-small-cell lung cancer (NSCLC) cell lines. This phase II randomized, double-blinded, placebo-controlled study evaluated the efficacy of vorinostat in combination with carboplatin and paclitaxel in patients with advanced-stage NSCLC. PATIENTS AND METHODS Patients with previously untreated stage IIIB (ie, wet) or IV NSCLC were randomly assigned (2:1) to carboplatin (area under the curve, 6 mg/mL x min) and paclitaxel (200 mg/m(2) day 3) with either vorinostat (400 mg by mouth daily) or placebo. Vorinostat or placebo was given on days 1 through 14 of each 3-week cycle to a maximum of six cycles. The primary end point was comparison of the response rate. Results Ninety-four patients initiated protocol therapy. Baseline patient characteristics were similar between the two arms. The median number of cycles was four for both treatment arms. The confirmed response rate was 34% with vorinostat versus 12.5% with placebo (P = .02). There was a trend toward improvement in median progression-free survival (6.0 months v 4.1 months; P = .48) and overall survival (13.0 months v 9.7 months; P = .17) in the vorinostat arm. Grade 4 platelet toxicity was more common with vorinostat (18% v 3%; P < .05). Nausea, emesis, fatigue, dehydration, and hyponatremia also were more frequent with vorinostat. CONCLUSION Vorinostat enhances the efficacy of carboplatin and paclitaxel in patients with advanced NSCLC. HDAC inhibition is a promising therapeutic strategy for treatment of NSCLC.
Optimum anti-emetic therapy for cisplatin induced emesis over repeat courses: Ondansetron plus dexamethasone compared with metoclopramide, dexamethasone plus lorazepam
Authors: D. Cunningham, M. Dicato, J. Verweij, R. Crombez, P. de Mulder, A. du Bois, A. Stewart, J. Smyth, P. Selby, D. van Straelen, R. Parideans, B. McQuade, J. McRae
Journal: Annals of Oncology (1996)
Central Nervous System Dysfunction Following Open-Heart Surgery
Authors: Henry M. Tufo
Journal: JAMA (1970)

A prospective study of the conditions of 100 open-heart surgery patients elicited more precise information about incidence, characteristics, and causes of central nervous system dysfunctions after surgery. Neurological, psychometric, and behavioral observations were made preoperatively and postoperatively. Half the sample developed neurological damage following recovery from anesthesia. Forty-three percent of survivors developed behavioral abnormalities preceded by focal neurological damage; intellectual functions were depressed in all such patients. In most patients neurological signs and mental symptoms disappeared and mental status normalized by discharge. However, 15% of survivors had signs of cerebral damage at discharge. Cerebral damage was significantly related to increasing age and depression of arterial pressure. In patients with cerebral dysfunction, arterial pressure fell to levels which did not support adequate cerebral perfusion. Older patients were especially vulnerable to such effects. Neuropathological findings suggested cerebral ischemia.
PHYTOHEMAGGLUTININ MITOGENIC PROTEINS
Authors: J. Bruce Miller, Claudia Noyes, Robert Heinrikson, Henry S. Kingdon, Stanley Yachnin
Journal: The Journal of Experimental Medicine (1973)

The phytohemagglutinin (PHAP) glycoproteins derived from Phaseolus vulgaris consist of five isomitogens that are tetrameric structures made up of two different glycoprotein subunits. Although identical in size (mol wt = 34,000), the subunits differ in their isoelectric points and amino acid sequences for six of the first seven amino-terminal residues, but are identical in primary structure from the 8th through the 24th amino acid residue. The isomitogen containing four L subunits (L-PHAP) is a potent leukoagglutinin and mitogen that lacks hemagglutinating properties. The isomitogen made up of four R subunits (4R H-PHAP) is a potent hemagglutinin. The hybrid isomitogens consisting of varying proportions of the two subunits (3L-1R, 2L-2R, 1L-3R) are capable of causing mixed erythrocyte-lymphocyte agglutination. These studies provide a structural basis for explaining the differences in biological activities of the various PHAP isomitogens.