The duration of pregnancy is influenced by fetal and maternal genetic and non-genetic factors. Here we report a fetal genome-wide association meta-analysis of gestational duration, and early preterm, preterm, and postterm birth in 84,689 infants. One locus on chromosome 2q13 is associated with gestational duration; the association is replicated in 9,291 additional infants (combined P = 3.96 × 10-14). Analysis of 15,588 mother-child pairs shows that the association is driven by fetal rather than maternal genotype. Functional experiments show that the lead SNP, rs7594852, alters the binding of the HIC1 transcriptional repressor. Genes at the locus include several interleukin 1 family members with roles in pro-inflammatory pathways that are central to the process of parturition. Further understanding of the underlying mechanisms will be of great public health importance, since giving birth either before or after the window of term gestation is associated with increased morbidity and mortality. ; We are grateful for the cooperation of the EGG Consortium and the iPSYCH-BROAD Working Group. Lists of members of the EGG Consortium and collaborators in the iPSYCH-BROAD Working Group are given in the Supplementary Notes 1 and 2, respectively. For study-specific acknowledgements, please see Supplementary Note 3. B.F. received support from an Oak Foundation fellowship, a Novo Nordisk Foundation grant (12955), and a Bill and Melinda Gates Foundation subward (137097); X.L. received support from the Nordic Center of Excellence in Health-Related e-Sciences; D.H., V.A., A.J.S., R.N., T.M.W., and A.D.B. recieved funding from the Lundbeck Foundation (R102-A9118, R155-2014-1724, R248-2017-2003); L.S. reports funding from a Carlsberg Foundation postdoctoral fellowship (CF15-0899); R.M.F. is a Sir Henry Dale Fellow (Wellcome and Royal Society grant: WT104150); R.N.B. is funded by Wellcome and Royal Society (grant: WT104150); M.C.B. and D.A.L. work in a unit that receives UK MRC funding (MC_UU_00011/6); M.C.B. is supported by the MRC Skills Development Fellowship MR/P014054/1; D.A.L.'s contribution to this work was funded by grants from the US NIH and European Research Council under the European Union's Seventh Framework Programme (FP/2007–2013)/ERC Grant Agreement (Grant number 669545; DevelopObese) and European Union's Horizon 2020 research and innovation programme under grant agreement 733206 (LIFECYCLE); D.A.L. is also an NIHR senior investigator (NF-SI-0611-10,196); F.R. received partial funding from the Netherlands Organization for Health Research and Development (VIDI 016.136.367); J.F.F. and V.W.V.J. received partial funding from the European Union's Horizon 2020 research and innovation programme under grant agreements 733206 (LIFECYCLE) and 633595 (DynaHEALTH); V.W.V.J. received partial funding from the Netherlands Organization for Health Research and Development (VIDI 016.136.361) and the European Research Council (ERC Consolidator Grant, ERC-2014-CoG-648916); I.K. reports funding from Sigrid Juselius Foundation and Biomendicum Foundation postdoctoral fellowship; L.J.M. was supported by the March of Dimes Prematurity Research Center Ohio Collaborative, NICHD HD 091527, and the Bill and Melinda Gates Foundation (OPP1113966); M.T.W. was supported by NIH R01 NS099068, NIH R01 GM055479-19A1, a Lupus Research Alliance Novel Approaches award, CCRF Endowed Scholar, a CCHMC CpG Pilot study award, and a CCHMC Trustee award; K.K.R. received support from March of Dimes (21-FY13-19); C.P. was supported by the NIHR Great Ormond Street Hospital Biomedical Research Centre; M.I.M. is a Wellcome Senior Investigator and a NIHR Senior Investigator. His work is supported by Wellcome (090532, 093831, 203141, 106130) and by the NIH (U01DK105535). The views expressed in this article are those of the authors and not necessarily those of the NHS, the NIHR, or the Department of Health. For study-specific funding, please see Supplementary Note 4.
BACKGROUND: The role of inflammation in mood disorders has received increased attention. There is substantial evidence that cytokine therapies, such as interferon alpha (IFN-alpha), can induce depressive symptoms. Indeed, proinflammatory cytokines change brain function in several ways, such as altering neurotransmitters, the glucocorticoid axis, and apoptotic mechanisms. This study aimed to evaluate the impact on mood of initiating IFN-alpha and ribavirin treatment in a cohort of patients with chronic hepatitis C. We investigated clinical, personality, and functional genetic variants associated with cytokine-induced depression. METHODS: We recruited 344 Caucasian outpatients with chronic hepatitis C, initiating IFN-alpha and ribavirin therapy. All patients were euthymic at baseline according to DSM-IV-R criteria. Patients were assessed at baseline and 4, 12, 24, and 48 weeks after treatment initiation using the Patient Health Questionnaire (PHQ), the Hospital Anxiety and Depression Scale (HADS), and the Temperament and Character Inventory (TCI). We genotyped several functional polymorphisms of interleukin-28 (IL28B), indoleamine 2,3-dioxygenase (IDO-1), serotonin receptor-1A (HTR1A), catechol-O-methyl transferase (COMT), glucocorticoid receptors (GCR1 and GCR2), brain-derived neurotrophic factor (BDNF), and FK506 binding protein 5 (FKBP5) genes. A survival analysis was performed, and the Cox proportional hazards model was used for the multivariate analysis. RESULTS: The cumulative incidence of depression was 0.35 at week 24 and 0.46 at week 48. The genotypic distributions were in Hardy-Weinberg equilibrium. Older age (p = 0.018, hazard ratio [HR] per 5 years = 1.21), presence of depression history (p = 0.0001, HR = 2.38), and subthreshold depressive symptoms at baseline (p = 0.005, HR = 1.13) increased the risk of IFN-induced depression. So too did TCI personality traits, with high scores on fatigability (p = 0.0037, HR = 1.17), impulsiveness (p = 0.0200 HR = 1.14), disorderliness (p = 0.0339, HR = 1.11), and low scores on extravagance (p = 0.0040, HR = 0.85). An interaction between HTR1A and COMT genes was found. Patients carrying the G allele of HTR1A plus the Met substitution of the COMT polymorphism had a greater risk for depression during antiviral treatment (HR = 3.83) than patients with the CC (HTR1A) and Met allele (COMT) genotypes. Patients carrying the HTR1A CC genotype and the COMT Val/Val genotype (HR = 3.25) had a higher risk of depression than patients with the G allele (HTR1A) and the Val/Val genotype. Moreover, functional variants of the GCR1 (GG genotype: p = 0.0436, HR = 1.88) and BDNF genes (Val/Val genotype: p = 0.0453, HR = 0.55) were associated with depression. CONCLUSIONS: The results of the study support the theory that IFN-induced depression is associated with a complex pathophysiological background, including serotonergic and dopaminergic neurotransmission as well as glucocorticoid and neurotrophic factors. These findings may help to improve the management of patients on antiviral treatment and broaden our understanding of the pathogenesis of mood disorders. ; This study was funded by the following Spanish grants: Instituto de Carlos III, Fondo de Investigaciones Sanitarias PSICOCITVHC-P110/01827 and PSIGEN-VHC-EC08/00201 (Dr MartínSantos). It was co-financed by the ERDF, European Union "One way to make Europe," Ministerio de Economía y Competitividad (MTM2012-38067-C02-01), and the support of the Generalitat de Catalunya (SGR2009/1435/SGR2014/1411; Dr Martín-Santos). Dr Grande has received a research grant from Río Hortega Contract (CM12/00062), Instituto de Salud Carlos III, Spanish Ministry of Economy and Competiveness.
Using targeted NMR spectroscopy of 227 fasting serum metabolic traits, we searched for novel metabolic signatures of renal function in 926 type 2 diabetics (T2D) and 4838 non-diabetic individuals from four independent cohorts. We furthermore investigated longitudinal changes of metabolic measures and renal function and associations with other T2D microvascular complications. 142 traits correlated with glomerular filtration rate (eGFR) after adjusting for confounders and multiple testing: 59 in diabetics, 109 in non-diabetics with 26 overlapping. The amino acids glycine and phenylalanine and the energy metabolites citrate and glycerol were negatively associated with eGFR in all the cohorts, while alanine, valine and pyruvate depicted opposite association in diabetics (positive) and non-diabetics (negative). Moreover, in all cohorts, the triglyceride content of different lipoprotein subclasses showed a negative association with eGFR, while cholesterol, cholesterol esters (CE), and phospholipids in HDL were associated with better renal function. In contrast, phospholipids and CEs in LDL showed positive associations with eGFR only in T2D, while phospholipid content in HDL was positively associated with eGFR both cross-sectionally and longitudinally only in non-diabetics. In conclusion, we provide a wide list of kidney function-associated metabolic traits and identified novel metabolic differences between diabetic and non-diabetic kidney disease. ; TwinsUK was funded by the Wellcome Trust; European Community's Seventh Framework Programme (FP7/2007–2013). The study also receives support from the National Institute for Health Research (NIHR) Clinical Research Facility at Guy's & St Thomas' NHS Foundation Trust and NIHR Biomedical Research Centre based at Guy's and St Thomas' NHS Foundation Trust and King's College London. TS is holder of an ERC Advanced Principal Investigator award. CB and the Genodiab-Mar cohort is supported by a grant from the Institute Carlos III (FIS-FEDER PI16/00620) and RedinRen RD16/0013/0009. CM is funded by the MRC AimHy (MR/M016560/1) project grant. The KORA study was initiated and financed by the Helmholtz Zentrum München – German Research Center for Environmental Health, which is funded by the German Federal Ministry of Education and Research (BMBF) and by the State of Bavaria. Furthermore, KORA research has been supported within the Munich Center of Health Sciences (MC-Health), Ludwig-Maximilians-Universität, as part of LMUinnovativ. The research leading to these results has received funding from the European Union Seventh Framework Programme under grant agreement [n°313010] (Large-scale prospective cohort studies - BBMRI-LPC; www.bbmri-lpc.org), [n°305280] (Methods for Integrated analysis of multiple Omics datasets – MIMOmics; http://www.mimomics.eu/) and under grant agreements [n°603288] (Systems Biology to Identify Molecular Targets for Vascular Disease Treatment – SysVasc; http://www.sysvasc.eu/). The Young Finns Study has been financially supported by the Academy of Finland: grants 286284, 134309 (Eye), 126925, 121584, 124282, 129378 (Salve), 117787 (Gendi), and 41071 (Skidi); the Social Insurance Institution of Finland; Competitive State Research Financing of the Expert Responsibility area of Kuopio, Tampere and Turku University Hospitals (grant X51001); Juho Vainio Foundation; Paavo Nurmi Foundation; Finnish Foundation for Cardiovascular Research; Finnish Cultural Foundation; Tampere Tuberculosis Foundation; Emil Aaltonen Foundation; Yrjö Jahnsson Foundation; Signe and Ane Gyllenberg Foundation; and Diabetes Research Foundation of Finnish Diabetes Association. MAK was supported by the Sigrid Juselius Foundation, Finland. MAK works in a Unit that is supported by the University of Bristol and UK Medical Research Council (MC_UU_12013/1). PW is funded by the Academy of Finland (312476 & 312477), and the Novo Nordisk Foundation Competing Interests.
Background: Few studies have investigated traffic-related air pollution as a risk factor for respiratory infections during early childhood. Objectives: We aimed to investigate the association between air pollution and pneumonia, croup, and otitis media in 10 European birth cohorts—BAMSE (Sweden), GASPII (Italy), GINIplus and LISAplus (Germany), MAAS (United Kingdom), PIAMA (the Netherlands), and four INMA cohorts (Spain)—and to derive combined effect estimates using meta-analysis. Methods: Parent report of physician-diagnosed pneumonia, otitis media, and croup during early childhood were assessed in relation to annual average pollutant levels [nitrogen dioxide (NO2), nitrogen oxide (NOx), particulate matter ≤ 2.5 μm (PM2.5), PM2.5 absorbance, PM10, PM2.5–10 (coarse PM)], which were estimated using land use regression models and assigned to children based on their residential address at birth. Identical protocols were used to develop regression models for each study area as part of the ESCAPE project. Logistic regression was used to calculate adjusted effect estimates for each study, and random-effects meta-analysis was used to calculate combined estimates. Results: For pneumonia, combined adjusted odds ratios (ORs) were elevated and statistically significant for all pollutants except PM2.5 (e.g., OR = 1.30; 95% CI: 1.02, 1.65 per 10-μg/m3 increase in NO2 and OR = 1.76; 95% CI: 1.00, 3.09 per 10-μg/m3 PM10). For otitis media and croup, results were generally null across all analyses except for NO2 and otitis media (OR = 1.09; 95% CI: 1.02, 1.16 per 10-μg/m3). Conclusion: Our meta-analysis of 10 European birth cohorts within the ESCAPE project found consistent evidence for an association between air pollution and pneumonia in early childhood, and some evidence for an association with otitis media. ; The research leading to these results was funded by the European Community's Seventh Framework Program (FP7/2007–2011) under grant 211250. The BAMSE study was supported by the Swedish Research Council FORMAS (for Environment, Agricultural Sciences and Spatial Planning), the Stockholm County Council, the Swedish Foundation for Health Care Sciences and Allergy Research, and the Swedish Environmental Protection Agency. The GINIplus study was supported for the first 3 years by the Federal Ministry for Education, Science, Research and Technology, Germany (interventional arm) and Helmholtz Zentrum München, Germany (former GSF; National Research Center for Environment and Health) (observational arm). The LISAplus study was supported by grants from the Federal Ministry for Education, Science, Research and Technology, Germany; Helmholtz Zentrum München, Germany (former GSF); Helmholtz Centre for Environmental Research–UFZ, Germany; Marien-Hospital Wesel, Germany; and Pediatric Practice, Bad Honnef, Germany. The PIAMA study is supported by The Netherlands Organization for Health Research and Development; The Netherlands Organization for Scientific Research; The Netherlands Asthma Fund; The Netherlands Ministry of Spatial Planning, Housing, and the Environment; and The Netherlands Ministry of Health, Welfare, and Sport. MAAS was supported by an Asthma UK Grant (04/014); the JP Moulton Charitable Foundation, UK; and the James Trust and Medical Research Council, UK (G0601361). INMA was funded by grants from the Spanish Ministry of Health-Instituto de Salud Carlos III (Red INMA G03/176, CB06/02/0041, FISPI041436, FIS-PI081151, FIS-PI042018, FIS-PI09/02311, FIS-PI06/0867, FIS-PS09/00090, FIS-FEDER 03/1615, 04/1509, 04/1112, 04/1931, 05/1079, 05/1052, 06/1213, 07/0314, and 09/02647); Generalitat de Catalunya-CIRIT, Spain (1999SGR 00241); Conselleria de Sanitat Generalitat Valenciana, Spain; Universidad de Oviedo, Obra social Cajastur, Spain; Department of Health of the Basque Government, Spain (2005111093 and 2009111069); Provincial Government of Gipuzkoa (DFG06/004 and DFG08/001), Spain; and Fundación Roger Torné, Spain. GASPII was funded by The Italian Ministry of Health (ex art.12 D.Lgs 502/92, 2001)
In: The Howard Journal of Criminal Justice, Band 3, Heft 2, S. 103-128
ISSN: 1468-2311
Book reviewed in this article:MORE ABOUT ELIZABETH FRY. Elizabeth Fry's Journeys on the Continent, 1840–41. From a Diary kept by her niece, Elizabeth Gurney.SCIENCE AND THE CRIMINAL. Psychopathology. By Bernard Hart, M.D., F.R.C.P., Cambridge, 1929.SCIENCE AND THE CRIMINAL. The Natural History of a Delinquent Career. By Clifford R. Shaw, Research Sociologist and Head of the Department of Research Sociology, Institute for Juvenile Research and Behaviour Research Fund, in collaboration with Maurice E. Moore, Assistant in Sociology, Institute for Juvenile Research, formerly Boys' Worker, Juvenile Protective Association. (Behavior Research Fund Monograph.SCIENCE AND THE CRIMINAL. Crime as Destiny. By Professor Dr. Johannes Lange. With a Foreword by Professor J. B. S. Haldane.SCIENCE AND THE CRIMINAL. Criminology. By Fred. E. Haynes.CAPITAL PUNISHMENT. The Death Penalty Enquiry. The Evidence Reviewed. By E. Roy Calvert.TRIALS NOTABLE AND FAMOUS. The Trial of Alfred Arthur Rouse. Edited by Helena Normanton. Notable British Trials.TRIALS NOTABLE AND FAMOUS. The Trial of Alfred Arthur Rouse. Edited by Sydney Tremayne. Famous Trials Series.TRIALS NOTABLE AND FAMOUS. The Trial of William Henry Podmore. Edited by the Hon. H. Fletcher Moulton and W. Lloyd Woodland. Famous Trials Series.THE POLICEMAN'S HANDBOOK. Sir Howard Vincent's Police Code. Seventeenth Edition. Revised by the Commissioner of Police of the Metropolis.ON PUNISHMENT. The Crime of Punishment. By Margaret Wilson. (Jonathan Cape. Pp. 309. 10s. 6d. net.)ON PUNISHMENT. The Story of Punishment. By Harry Elmer Barnes.THE YOUNG OFFENDER. Boys in Trouble. By L. Le Mesurier.THE YOUNG OFFENDER. Fifty‐five "Bad" Boys. By S. W. Hartwell, M.D.THE YOUNG OFFENDER. Children's Behaviour Problems. By Luton Ackerson.FRENCH GUIANA. Terre de Bagne. By Charles Péan, Officier de l'Armée du Salut, with an Introduction by Albin Peyron, Commissaire Général de l'Armée du Salut en France and Preface by Pierre Hamp.FRENCH GUIANA. Devil's Island: Revelations of the Penal Settlements in French Guiana. By W. E. Allison‐Booth.FRENCH GUIANA. The Horrors of Cayenne. Edited by Karl Bartz. (Constable. Pp. 206. 6s. net.)FRENCH GUIANA. French Justice. By M. M. Valdes.PRISONS AND PRISONERS. Prisoner at the Bar. By Arthur R. L. Gardner.FRENCH GUIANA. Life in London's Great Prisons. By T. Whyte Mountain. (Methuen. 5/‐. Pp. 180.)FRENCH GUIANA. The Prisoner and the Prison. By Sir Sidney J. Pocock, J.P.FROM AMERICA. The Education of Adult Prisoners.FROM AMERICA. Reformatories for Women in the United States. By Eugenia C. Lekkerkerker.FROM AMERICA. Report of the Royal Commission on Public Welfare of Ontario.FROM AMERICA. Taming the Criminal. By John L. Gillin, Ph.D.FROM AMERICA. Education, Crime and Social Progress. By William C. Bagley.FROM AMERICA. The Criminal: A Study. By Henry A. Geisert.A LAWYER ON LAW REFORM. In Quest of Justice. By Claud Mullins.OTHER REVIEWS. Harron Lectures on Education. Edited by T. F. Coade.OTHER REVIEWS. Prisons de Femmes. Francis Carco.OTHER REVIEWS. Receil de Documents en Matiere Pénale et Pénitentiaire. 7.50 frs. Pp. 142. March, 1931.OTHER REVIEWS. Martyrdom in our Times. An introductory essay to Prison and Punishment. By A. Mitchell Innes.OTHER REVIEWS. The Personality of Criminals. By Albert Warren Stearns, M.D., Dean of Tufts College Medical School, Boston; Commissioner of Correction, Commonwealth of Massachusetts; formerly Psychiatrist of Massachusetts State Prison.OTHER REVIEWS. The Elements of Crime (psycho‐social interpretation). By Boris Brasol, M.A., former Prosecuting Attorney, St. Petersburg Supreme Court; member Columbia University Law School Criminological Survey; member of the Académie Internationale de Criminalistique. With Introductions by John H. Wigmore, Professor of Law in North‐western University, and William A. White. M.D., Superintendent Saint Elizabeth's Hospital, Washington, D.C. Second edition, 1931 (first edition, 1927).
ADRESSBUCH DER RESIDENZSTADT CASSEL SOWIE DER ORTSCHAFTEN HARLESHAUSEN, IHRINGSHAUSEN, NIEDERVELLMAR, NIEDERZWEHREN, OBERZWEHREN, SANDERSHAUSEN, WALDAU, WILHELMSHÖHE, WOLFSANGER, GARTENSTADT BRASSELSBERG UND GUTSBEZIRK FASANENHOF Adreßbuch von Kassel und Umgebungen (-) Adreßbuch der Residenzstadt Cassel sowie der Ortschaften Harleshausen, Ihringshausen, Niedervellmar, Niederzwehren, Oberzwehren, Sandershausen, Waldau, Wilhelmshöhe, Wolfsanger, Gartenstadt Brasselsberg und Gutsbezirk Fasanenhof (Jg. 80.1913) ( - ) Einband ( - ) Titelblatt ( - ) Vorwort ( - ) Inhalt ( - ) Königl. Haus, Landgr. Hess. Haus, Allgemeines ( - ) Königliches Haus ( - ) Landgräfliches Haus Hessen (4) Aus der Geschichte Cassels ([5]) Sehenswürdigkeiten, Theater, Konzerte (8) Flächenangaben (12) Höhenangaben (12) Bevölkerung (12) Standesamtliches (15) Städtische indirekte Steuern (16) Höhe des Schulgeldes in der Stadt Cassel (21) Auszug aus den Bedingungen für den Bezug von Gas, Wasser und Elektrizität aus den städtischen Anstalten (22) Ordnung für die Erhebung einer Hundesteuer in der Residenzstadt Cassel (24) Ortsstatut betreffend Einschränkung der Arbeit an Sonn- und Festtagen im Handelsgewerbe in der Residenzstadt Cassel (26) Schuldbuch der Residenzstadt Cassel (27) Städtische Sparkasse (27) Städt. Wannen- und Brause-Bäder (28) Städtische Desinfektionsanstalt (28) Beerdigungswesen (28) Familien-Begräbnisplätze (29) Polizei-Verordnungen (30) Verkehrswesen (34) Krankenpflege (42) Feuerlöschwesen (44) Behörden, Öffentliche Anstalten und Institute, Vereine ( - ) Behörden der Königl. Hofverwaltung ( - ) Reichsbehörden ( - ) Königl. preuss. Zivilbehörden (3) Königl. preuss. Justizbehörden (16) Königl. preuss. Militärbehörden (25) Königl. preuss. Militär-Verwaltungsbehörden (28) Provinzial- u. Kommunal-Verwaltung (29) Städtische Behörden (32) Öffentlicher Gottesdienst (40) Öff. Unterrichts- u. Erzieh.-Anstalten (49) Waisenhäuser und Hospitäler (55) Stiftungen (56) Vereine (58) Anzeigen ( - ) Alphabetisches Verzeichnis der Casseler Einwohner ( - ) Buchstabe A ( - ) Buchstabe B (11) Buchstabe C (49) Buchstabe D (54) Buchstabe E (70) Buchstabe F (82) Buchstabe G (96) Buchstabe H (119) Buchstabe I / J (158) Buchstabe K (166) Buchstabe L (203) Buchstabe M (222) Buchstabe N (247) Buchstabe O (254) Buchstabe P (259) Buchstabe Q (271) Buchstabe R (272) Buchstabe S (295) Buchstabe T (357) Buchstabe U (365) Buchstabe V (367) Buchstabe W (374) Buchstabe Z (400) Verzeichnis der in Cassel wohnenden inaktiven Offiziere ([406]) Nachtrag zum Casseler Adreßbuch 1913 ( - ) Alphabetisches Strassenverzeicnis nebst Bewohner jedes einzelnen Hauses der Residenzstadt Cassel ( - ) Achenbach-Straße bis Schöne Aussicht ( - ) Bach-Straße bis Buttlar-Straße (7) Christoph-Straße bis Corbacher Straße (20) Dalwigk-Straße bis Druselplatz (20) An den Eichen bis Eulenburg-Straße (24) Fahrt-Gasse bis Fuldahafen (29) Gabelsberger-Str. bis Gutenberg-Straße (45) Habichtswalder Straße bis Hutten-Straße (59) Jäger-Straße bis Julien-Straße (89) Kaiserplatz bis Kurze Straße (95) Landau-Straße bis Luther-Straße (132) Magazin-Straße bis Hinter dem Museum (146) Nahl-Straße bis Nürnberger Straße (168) Oberste Gasse bis Otto-Straße (171) Packhof-Straße bis Prinzen-Straße (179) Quellhöfe bis Querallee (189) Raabe-Straße bis Du Ry-Straße (190) Sack bis Süd-Straße (198) Tannenhecker Weg bis Turm-Gasse (219) Ufer-Straße bis Uhland-Straße (222) Vellmarsche Straße bis Vogelsang (223) Alt-Walershausen bis Wolfsschlucht (225) York-Straße bis Ysenburg-Straße (259) Zedlitz-Straße bis Zwehrener Weg (261) Alphabetisches Verzeichnis der Einwohner: Harleshausen, Ihringshausen, Niedervellmar, Niederzwehren, Oberzwehren, Sandershausen, Waldau, Wilhelmshöhe, Wolfsanger, Gartenstadt Brasselsberg, Gutsbezirk Fasanenhof ( - ) Harleshausen ( - ) Ihringshausen (6) Niedervellmar (10) Niederzwehren (13) Oberzwehren (23) Sandershausen (26) Waldau (29) Wilhelmshöhe (31) Wolfsanger (32) Gartenstadt Brasselsberg (36) Gutsbezirk Fasanenhof (36) Genossenschafts- und Handelsregister ( - ) Verzeichnis der Casseler Geschäfte nach den Geschäftszweigen geordnet ( - ) Abreiß-Kalender für Reklame-Zwecke bis Autotypien ( - ) Backpulver-Fabrik bis Bureau-Einrichtungen (5) Cafés bis Cliché-Fabrik (12) Dachdecker bis Dütenfabriken (13) Eierhandlungen bis Essig- u. Senffabriken (15) Fabrikschornstein- und Feuerungsanlagen bis Futterstoffe für Schneiderei (17) Gärtner u. Blumenhandlungen bis Gypswände (20) Haferkakaofabrik bis Hutwäschereien und -Färbereien (25) Jalousiefabrik bis Jutespinnerei (28) Spezial-Käsefabrik bis Kuranstalten (30) Lackfabriken bis Lotterie-Einnehmer, Königliche (35) Mal- und Zeichen-Utensilien bis Musikalienhandlungen (38) Nähmaschinenlager bis Nährmittelfabriken (43) Obst- u. Gemüsehandlg. bis Orthopäd. Heilanstalten (43) Papierfabriken bis Putzmacherinnen (44) Rabitz-Arbeiten bis Roßschlachtereien (47) Sachverständiger (gerichtlicher) f. Maschinenbau u. Elektrotechnik bis Stukkateure (48) Tabak- und Zigarrenfabriken bis Turn-, Sport- u. Spielgeräte (56) Uhrketten und Taschenuhren en gros. bis Uniformfabriken (59) Verbandstoff-Fabriken und -Handlungen bis Vogelhandlung (60) Waagengeschäfte bis Wollwäschereien (66) Xylographen bis Zuschneideschule (68) Werbung ( - ) Plan des Königlichen Theaters zu Cassel ( - ) Farbkeil ( - ) Einband ( - )
Objective To identify the genetic determinants of fracture risk and assess the role of 15 clinical risk factors on osteoporotic fracture risk. DESIGN Meta-analysis of genome wide association studies (GWAS) and a two-sample mendelian randomisation approach. Setting 25 cohorts from Europe, United States, east Asia, and Australia with genome wide genotyping and fracture data. Participants A discovery set of 37 857 fracture cases and 227 116 controls; with replication in up to 147 200 fracture cases and 150 085 controls. Fracture cases were defined as individuals (>18 years old) who had fractures at any skeletal site confirmed by medical, radiological, or questionnaire reports. Instrumental variable analyses were performed to estimate effects of 15 selected clinical risk factors for fracture in a twosample mendelian randomisation framework, using the largest previously published GWAS meta-analysis of each risk factor. Results Of 15 fracture associated loci identified, all were also associated with bone mineral density and mapped to genes clustering in pathways known to be critical to bone biology (eg, SOST, WNT16, and ESR1) or novel pathways (FAM210A, GRB10, and ETS2). Mendelian randomisation analyses showed a clear effect of bone mineral density on fracture risk. One standard deviation decrease in genetically determined bone mineral density of the femoral neck was associated with a 55% increase in fracture risk (odds ratio 1.55 (95% confidence interval 1.48 to 1.63; P=1.5×10?68). Hand grip strength was inversely associated with fracture risk, but this result was not significant after multiple testing correction. The remaining clinical risk factors (including vitamin D levels) showed no evidence for an effect on fracture. Con clusions This large scale GWAS meta-analysis for fracture identified 15 genetic determinants of fracture, all of which also influenced bone mineral density. Among the clinical risk factors for fracture assessed, only bone mineral density showed a major causal effect on fracture. Genetic predisposition to lower levels of vitamin D and estimated calcium intake from dairy sources were not associated with fracture risk. ; Funding: This research and the Genetic Factors for Osteoporosis (GEFOS) consortium have been funded by the European Commission (HEALTH-F2-2008-201865-GEFOS). AGES: NIH contract N01- AG-12100 and NIA Intramural Research Program, Hjartavernd (the Icelandic Heart Association), and Althingi (the Icelandic Parliament). Icelandic Heart Association. Anglo-Australasian Osteoporosis Genetics Consortium (AOGC): National Health and Medical Research Council (Australia) (grant reference 511132). Australian Cancer Research Foundation and Rebecca Cooper Foundation (Australia). National Health and Medical Research Council (Australia). National Health and Medical Research Council (Australia) Career Development Award (569807). Medical Research Council New Investigator Award (MRC G0800582). Health Research Council of New Zealand. Sanofi-Aventis, Eli Lilly, Novartis, Pfizer, Proctor & Gamble Pharmaceuticals and Roche. National Health and Medical Research Council, Australia. Australian National Health and Medical Research Council, MBF Living Well foundation, the Ernst Heine Family Foundation and from untied educational grants from Amgen, Eli Lilly International, GE-Lunar, Merck Australia, Novartis, Sanofi-Aventis Australia and Servier. Medical Research Council UK and Arthritis Research UK. The Victorian Health Promotion Foundation and the Geelong Region Medical Research Foundation, and the National Health and Medical Research Council, Australia (project grant 628582). Action Research UK. DME is supported by an Australian Research Council Future Fellowship (FT130101709). This work was supported by a Medical Research Council programme grant (MC_UU_12013/4). B-Vitamins for the PRevention Of Osteoporotic Fractures (BPROOF) study: supported and funded so far by The Netherlands Organisation for Health Research and Development (ZonMw, grant 6130.0031), The Hague; unrestricted grant from NZO (Dutch Dairy Association), Zoetermeer; Orthica, Almere; Netherlands Consortium Healthy Ageing (NCHA) Leiden/Rotterdam; Ministry of Economic Affairs, Agriculture and Innovation (project KB-15-004-003), The Hague; Wageningen University, Wageningen; VUmc, Amsterdam; Erasmus Medical Center, Rotterdam. Cardiovascular Health Study (CHS): National Heart Lung and Blood Institute (NHLBI) contracts HHSN268201200036C, HHSN268200800007C, N01HC55222, N01HC85079, N01HC85080, N01HC85081, N01HC85082, N01HC85083, N01HC85086; and NHLBI grants U01HL080295, R01HL087652, R01HL105756, R01HL103612, R01HL120393, and R01HL130114 with additional contribution from the National Institute of Neurological Disorders and Stroke (NINDS). Additional support was provided through R01AG023629 from the National Institute on Ageing (NIA). Genotyping supported in part by the National Center for Advancing Translational Sciences, CTSI grant UL1TR000124, and the National Institute of Diabetes and Digestive and Kidney Disease Diabetes Research Center (DRC) grant DK063491 to the Southern California Diabetes Endocrinology Research Center. deCODE Genetics. EPIC-Norfolk: Medical Research Council G9321536 and G9800062, MAFF AN0523, EU FP5 (QLK6-CT-2002-02629), Food Standards Agency N05046, GEFOS EU FP7 Integrated Project Grant Reference: 201865, The UK's National Institute for Health Research (NIHR) Biomedical Research Centre Grant to Cambridge contributed to the costs of genotyping. Estonian Genome Center University of Tartu (EGCUT): This study was supported by EU H2020 grants 692145, 676550, 654248, Estonian Research Council Grant IUT20-60, NIASC and EIT—Health and EU through the European Regional Development Fund (project No 2014-2020.4.01.15-0012 GENTRANSMED). Erasmus Rucphen Family Study (ERF): Netherlands Organisation for Scientific Research (NWO), Erasmus University Medical Centre, the Centre for Medical Systems Biology (CMSB1 and CMSB2) of the Netherlands Genomics Initiative (NGI). Framingham Osteoporosis Study (FOS): National Institute for Arthritis, Musculoskeletal and Skin Diseases and National Institute on Ageing (R01 AR41398; DPK and R01 AR 050066; DK National Heart, Lung, and Blood Institute's Framingham Heart Study (N01-HC-25195) and its contract with Affymetrix for genotyping services (N02-HL-6-4278). The Gothenburg Osteoporosis and Obesity Determinan Study (GOOD): Swedish Research Council (K2010-54X-09894-19-3, 2006-3832 and K2010-52X-20229-05-3), Swedish Foundation for Strategic Research, ALF/LUA research grant in Gothenburg, Lundberg Foundation, Torsten and Ragnar Söderberg's Foundation, Västra Götaland Foundation, Göteborg Medical Society, Novo Nordisk Foundation, and European Commission grant HEALTH-F2-2008- 201865-GEFOS. Health Aging and Body Composition Study (HealthABC): the Intramural Research Program of the National Institute of Health (NIH), National Institute on Ageing. US National Institute of Ageing (NIA) contracts N01AG62101, N01AG62103, and N01AG62106. NIA grant 1R01AG032098. The Center for Inherited Disease Research (CIDR). National Institutes of Health contract number HHSN268200782096C. Hong Kong Osteoporosis Study (HKOS): Hong Kong Research Grant Council (HKU 768610M); Bone Health Fund of HKU Foundation; KC Wong Education Foundation; Small Project Funding (201007176237); Matching Grant, Committee on research and conference (CRCG) Grant and Osteoporosis and Endocrine Research Fund; and the Genomics Strategic Research Theme of the University of Hong Kong. The Osteoporotic Fractures in Men (MrOS) Study is supported by National Institutes of Health funding. The following institutes provide support: National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS), National Institute on Ageing (NIA), National Center for Research Resources (NCRR), and National Institute of Health (NIH) Roadmap for Medical Research under the following grant numbers: U01 AR45580, U01 AR45614, U01 AR45632, U01 AR45647, U01 AR45654, U01 AR45583, U01 AG18197, U01-AG027810, and UL1 RR024140. Prospective study of pravastatin in the elderly at risk (PROSPER): European Union's Seventh Framework Programme (FP7/2007-2013) under grant agreement No HEALTH-F2-2009-223004 PHASE. Rotterdam study I, Rotterdam study II, Rotterdam study III: Netherlands Organisation of Scientific Research (NWO) Investments (No 175.010.2005.011, 911-03-012); Research Institute for Diseases in the Elderly (014-93-015; RIDE2); Netherlands Genomics Initiative/Netherlands Consortium for Healthy Ageing (050-060-810); German Bundesministerium fuer Forschung und Technology under grants #01 AK 803 A-H and # 01 IG 07015 G. the Netherlands Organisation for Health Research and Development ZonMw VIDI 016.136.367 (funding FR, CM-G, KT). Study of Osteoporotic Fractures (SOF): supported by National Institutes of Health funding. The National Institute on Ageing (NIA) and the National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS) provides support under the following grant numbers: R01 AG005407, R01 AR35582, R01 AR35583, R01 AR35584, R01 AG005394, R01 AG027574, R01 AG027576, and R01 AG026720. TwinsUK1, TwinsUK2: NIHR Biomedical Research Centre (grant to Guys' and St Thomas' Hospitals and King's College London); Chronic Disease Research Foundation; Wellcome Trust; Canadian Institutes of Health Research, Canadian Foundation for Innovation, Fonds de la Recherche en Santé Québec, Lady Davis Institute, Jewish General Hospital, and Ministère du Développement économique, de l'Innovation et de l'Exportation du Quebec. UK Biobank: This research has been conducted using the UK Biobank Resource (application No 12703). Access to the UK Biobank study data was funded by a University of Queensland Early Career Researcher Grant (2014002959). Access to the UK Biobank study data was funded by University of Queensland Early Career Researcher Grant (2014002959) and University of Western Australia-University of Queensland Bilateral Research Collaboration Award (2014001711). NMW is supported by a National Health and Medical Research Council Early Career Fellowship (APP1104818). Women's Genome Health Study (WGHS): HL 043851 and HL69757 from the National Heart, Lung, and Blood Institute and CA 047988 from the National Cancer Institute, the Donald W Reynolds Foundation, and the Fondation Leducq Amgen. Women's Health Initiative (WHI) program is funded by the National Heart, Lung, and Blood Institute, National Institutes of Health, US. Department of Health and Human Services through contracts N01WH22110, 24152, 32100-2, 32105-6, 32108-9, 32111-13, 32115, 32118-32119, 32122, 42107-26, 42129-32, and 44221. Young Finns study (YFS): has been financially supported by the Academy of Finland: grants 286284 (TL), 134309 (Eye), 126925, 121584, 124282, 129378 (Salve), 117787 (Gendi), and 41071 (Skidi); the Social Insurance Institution of Finland; Competitive State Research Financing of the Expert Responsibility area of Tampere, Turku and Kuopio University Hospitals (grant X51001); Juho Vainio Foundation; Paavo Nurmi Foundation; Finnish Foundation for Cardiovascular Research; Finnish Cultural Foundation; Tampere Tuberculosis Foundation; Emil Aaltonen Foundation; Yrjö Jahnsson Foundation; Signe and Ane Gyllenberg Foundation; and Diabetes Research Foundation of Finnish Diabetes Association; and EU Horizon 2020 (grant 755320 for TAXINOMISIS). Barcelona cohort osteoporosis (BARCOS): Red de Envejecimiento y fragilidad RETICEF, CIBERER, Instituto Carlos III. Fondos FEDER. Fondo de Investigación Sanitaria (FIS PI13/00116). Spanish MINECO (SAF2014-56562-R), Catalan Government (2014SGR932). Austrios-A, Austrios-B: was supported by BioPersMed (COMET K project 825329), and the Competence Center CBmed (COMET K1 centre 844609), funded by the Austrian Federal Ministry of Transport, Innovation and Technology (BMVIT) and the Austrian Federal Ministry of Economics and Labour/ the Federal Ministry of Economy, Family and Youth (BMWA/BMWFJ) and the Styrian Business Promotion Agency (SFG). Cantabria-Camargo study (Cabrio-C), Cantabria osteoporosis case-control study (Cabrio-CC): Instituto de Salud Carlos III-Fondo de Investigaciones Sanitarias Grants PI 06/34,PI09/539, PI12/615 and PI15/521 (that could be cofunded by European Union-FEDER funds). Calcium Intake Fracture Outcome Study (CAIFOS): Healthway Health Promotion Foundation of Western Australia, Australasian Menopause Society and the Australian National Health and Medical Research Council Project Grant (254627, 303169 and 572604). Canadian Multicentre Osteoporosis Study (CaMos): was supported by a grant from the Canadian Institutes for Health Research (CIHR) (grant No MOP111103). JBR and JAM are funded by the Canadian Institutes of Health Research, Fonds du Recherche Québec Santé, and Jewish General Hospital. Edinburgh Osteoporosis Study (EDOS): was supported by a grant from Arthritis Research UK (grant number 15389). European Prospective Osteoporosis Study (EPOS): EU Biomed 1 (BMHICT920182, CIPDCT925012, ERBC1PDCT 940229, ERBC1PDCT930105), Medical Research Council G9321536 and G9800062, Wellcome Trust Collaborative Research Initiative 1995, MAFF AN0523,EU FP5 (QLK6-CT-2002-02629), Food Standards Agency N05046, GEFOS EU FP7 Integrated Project Grant Reference: 201865. The UK's National Institute for Health Research (NIHR) Biomedical Research Centre Grant to Cambridge contributed to the costs of genotyping. Geelong Osteoporosis Study (GEOS): Canadian Institutes for health research operating grant funding reference #86748. Genetic analysis of osteoporosis in Greece (GROS): University of Athens, Greece (Kapodistrias 2009). Hertfordshire Cohort Study (HCS): supported by Medical Research Council UK; Arthritis Research UK; National Institute for Health Research (NIHR) Musculoskeletal BRU Oxford; National Institute for Health Research (NIHR) Nutrition BRC Southampton. Hong Kong: The projects have been supported by The Hong Kong Jockey Club Charities Trust, VC discretionary fund of The Chinese University of Hong Kong, and Research Grants Council Earmarked Grant CUHK4101/02M. Korean osteoporosis study in Asan Medical Center (KorAMC): a grant of the Korea Health Technology R&D Project, the Ministry of Health and Welfare, Republic of Korea (project No HI14C2258); a grant of the Korea Health Technology R&D Project, the Ministry of Health and Welfare, Republic of Korea (project No HI15C0377). Longitudinal Aging Study Amsterdam (LASA): largely supported by a grant from the Netherlands Ministry of Health Welfare and Sports, Directorate of Long term Care. MINOS study was supported by a grant from the Merck-Sharp-Dohme Chibret company. Malta osteoporotic fracture study (MOFS): financial support was received from the European Union Strategic Educational Pathways Scholarhip scheme (STEPS). The Osteoporotic Fractures in Men (MrOS) Sweden: financial support was received from the Swedish Research Council (K2010- 54X-09894-19-3, 2006-3832), Swedish Foundation for Strategic Research, ALF/LUA research grant in Gothenburg, Lundberg Foundation, Torsten and Ragnar Söderberg's Foundation, Västra Götaland Foundation, Göteborg Medical Society, Novo Nordisk foundation, and European Commission grant HEALTH-F2-2008- 201865-GEFOS. Odense androgen study (OAS): World Anti-Doping Agency, Danish Ministry of Culture, Institute of Clinical Research of the University of Southern Denmark. Prevalence of osteoporosis in Slovenia (Slo-preval): was created as part of projects financially supported by the Slovenian research agency: P3-298 Geni, Hormoni in osebnostne spremembe pri hormonskih motnjah; Z1-3238: Genski in okoljski dejavniki tveganja za razvoj motnje pri remodellaciji kosti; J2-3314 Genetski faktorji in hormoni pri presnovnih boleznih; and J3-2330 Genetski dejavniki pri osteoporozi. TWINGENE: supported in part by the Ragnar Söderberg Foundation (E9/11); the National Science Foundation (EArly Concept Grants for Exploratory Research: "Workshop for the Formation of a Social Science Genetic Association Consortium," SES-1064089) as supplemented by the National Institutes of Health's (NIH) Office of Behavioural and Social Sciences Research; and the National Institute on Ageing/NIH through Grants P01-AG005842, P01-AG005842-20S2, P30-AG012810, and T32-AG000186-23 to the National Bureau of Economic Research. The Swedish Twin Registry is supported by the Swedish Department of Higher Education, European Commission European Network for Genetic and Genomic Epidemiology (ENGAGE: 7th Framework Program (FP7/2007-2013)/Grant agreement HEALTH-F4-2007-201413; and GenomEUtwin: 5th Framework program "Quality of Life and Management of the Living Resources" Grant QLG2-CT-2002-01254); NIH (DK U01-066134); Swedish Research Council (M-2005-1112 and 2009-2298); Swedish Foundation for Strategic Research (ICA08-0047); Jan Wallander and Tom Hedelius Foundation; and Swedish Council for Working Life and Social Research. The Umeå Fracture and Osteoporosis Study (UFO) is supported by the Swedish Research Council (K20006- 72X-20155013), Swedish Sports Research Council (87/06), Swedish Society of Medicine, Kempe-Foundation (JCK-1021), and by grants from the Medical Faculty of Umeå University (ALFVLL:968:22-2005, ALFVL:-937-2006, ALFVLL:223:11-2007, ALFVLL:78151-2009) and county council of Västerbotten (SpjutspetsanslagVLL:159:33-2007). GRW and JHDB were funded by the Wellcome Trust (Strategic Award grant No 101123; Joint Investigator Award No 110141; project grant No 094134). DPK was funded by a grant from the National Institute on Arthritis Musculoskeletal and Skin Diseases R01 AR041398. The funding agencies had no role in the study design, analysis, or interpretation of data; the writing of the manuscript; or in the decision to submit the article for publication.
This open access book focuses on the public health crisis of youth suicide and provides a review of current research and prevention practices. It addresses important topics, including suicide epidemiology, suicide risk detection in school and medical settings, critical cultural considerations, and approaches to lethal means safety. This book offers cutting-edge research on emerging discoveries in the neurobiology of suicide, psychopharmacology, and machine learning. It focuses on upstream suicide prevention research methods and details how cost-effective approaches can mitigate youth suicide risk when implemented at a universal level. Chapters discuss critical areas for future research, including how to evaluate the effectiveness of suicide prevention and intervention efforts, increase access to mental health care, and overcome systemic barriers that undermine generalizability of prevention strategies. Finally, this book highlights what is currently working well in youth suicide prevention and, just as important, which areas require more attention and support. Key topics include: The neurobiology of suicide in at-risk children and adolescents. The role of machine learning in youth suicide prevention. Suicide prevention, intervention, and postvention in schools. Suicide risk screening and assessment in medical settings. Culturally informed risk assessment and suicide prevention efforts with minority youth. School mental health partnerships and telehealth models of care in rural communities. Suicide and self-harm prevention and interventions for LGBTQ+ youth. Risk factors associated with suicidal behavior in Black youth. Preventing suicide in youth with autism spectrum disorder (ASD) and intellectual disability (ID). Youth Suicide Prevention and Intervention is a must-have resource for policy makers and related professionals, graduate students, and researchers in child and school psychology, family studies, public health, social work, law/criminal justice, sociology, and all related disciplines.
Krankheit in digitalen Spielen hat viele Facetten - egal ob psychisch oder somatisch. Ihre Darstellung fußt dabei auf Prozessen, die gesellschaftliches Wissen zu Krankheiten aufgreifen und gemäß der Eigenlogik digitaler Spiele verändern. Ästhetik, Narration und Spielmechanik partizipieren so an Kämpfen um Deutungshoheiten zwischen der Tradierung stigmatisierender Krankheitsvorstellungen einerseits und selbstreflexivem Empowerment andererseits. Die Beiträger*innen dieses ersten Sammelbandes zum Thema widmen sich theoretischen, analytischen und praktischen Fragestellungen rund um die Bedeutungsvielfalt von Krankheitskonstruktionen in digitalen Spielen aus interdisziplinärer Perspektive.
"In der Altenpflege steht einem steigenden Bedarf ein sinkendes Angebot gegenüber. In der qualifizierten Pflege und Betreuung wird das fehlende Angebot vielfach unter dem Begriff 'Pflegenotstand' problematisiert und mit der mangelnden Attraktivität der Altenpflege als Beruf sowie den wenig attraktiven Arbeitsbedingungen dort begründet. Der Beitrag fokussiert auf das Forschungsfeld der professionellen, qualifizierten Langzeitpflege und -betreuung aus sozialwissenschaftlicher Perspektive und untersucht vor dem Hintergrund theoretischer Ansätze zur Definition und Abgrenzung des Begriffs der 'Pflege' auf der Basis von leitfadengestützten Interviews die Arbeitsbedingungen, die die hier tätigen Personen vorfinden. Ziel ist es, zur Entwicklung und Diskussion von Ansatzpunkten zur adäquaten Bewertung von Pflege und Betreuungsarbeit beizutragen und damit auch Inputs für die längst fällige Intensivierung der Qualitätsdiskussion zur Pflege zu erbringen." (Autorenreferat)
In diesem Artikel stellen wir eine ethnografische Forschung in ethnopsychoanalytischer Tradition vor, in der eine bestimmte Therapieform, die in Frankreich entwickelt wurde, untersucht wird: die transkulturellen Therapien im "multikulturellen Gruppensetting". Wir beschreiben die Konstruktion des methodischen Zugangs, der auf der Grundlage der französischen und der schweizerischen Tradition ethnopsychoanalytischer Forschung entwickelt wurde. Wir versuchen zu zeigen, dass das Herstellen eines therapeutischen Arbeitsbündnisses, die Mediation und das Schaffen neuer Bedeutungen zentral für diese Art der therapeutischen Arbeit sind. Und wir beschreiben das therapeutische Setting als einen Ort, in dem äußerst kreative Begegnungen stattfinden und neue Bedeutungen geschaffen werden, die auch die Perspektive marginalisierter Teile der französischen Gesellschaft widerspiegeln.
"Neben der Dezentralisierung der Tarifpolitik in den Industriebranchen und der geringen Tarifbindung in den privaten Dienstleistungssektoren hat die Liberalisierung und Privatisierung öffentlicher Dienstleistungen als ein dritter, bisher zu wenig berücksichtigter Faktor die Erosion des deutschen Flächentarifvertragssystems befördert. Der Beitrag zeigt, dass es mit der Privatisierung und Schaffung neuer Märkte im Bereich der öffentlichen Daseinsvorsorge in zahlreichen Dienstleistungssektoren zur Abkopplung vom Tarifgefüge des öffentlichen Dienstes gekommen ist. Im Bereich von Telekommunikation, Post, Bahn, öffentlichem Personennahverkehr, Entsorgungswirtschaft und Krankenhäusern entstanden keine neuen Branchentarifverträge, sondern fragmentierte Tariflandschaften mit ausgeprägter Tarifkonkurrenz zwischen öffentlichen und neuen privaten Unternehmen sowie einer erheblichen Ausdifferenzierung von Arbeitsbedingungen innerhalb einzelner Unternehmen. Der Beitrag endet mit einer Diskussion, wie es heute gelingen kann, in den liberalisierten Märkten einheitliche Branchen(mindest)standards durchzusetzen, die den Wettbewerb um niedrige Lohn- und Arbeitskosten begrenzen." (Autorenreferat)
