Major cardiac rupture following surgical treatment for deep sternal wound infection.

To access publisher's full text version of this article, please click on the hyperlink in Additional Links field or click on the hyperlink at the top of the page marked Files. This article is open access.We report a case of an 80-year old male patient who sustained a major rupture of the right ventricle after surgical revision of an infected sternotomy wound following coronary artery bypass surgery. The rupture of the right ventricle occurred despite an early wound debridement and the use of negative pressure wound therapy on the sternum that did not provide sufficient stability to the sternum after the sternal wires were removed. The rupture resulted in a major bleeding but by establishing emergent cardiopulmonary bypass, the patient was saved

Magnetic resonance imaging of diffusion in the presence of physiological motion

Thesis (Ph. D.)--Massachusetts Institute of Technology, Dept. of Electrical Engineering and Computer Science, 1996.Includes bibliographical references (p. 167-180).by Hákon Gudbjartsson.Ph.D

Case of the monthSudden chest pain and changed voice after the use of an electronic cigarette

Tæplega tvítugur, áður hraustur, fyrrverandi reykingamaður leitaði á bráðamóttöku Landspítala vegna skyndilegra brjóstverkja. Tveimur klukkustundum áður hafði hann notað rafsígarettu sem olli kröftugu hóstakasti. Verkurinn versnaði við djúpa innöndun en hann fann einnig fyrir verkjum við hreyfingu og kyngingu, auk þess sem rödd varð rámari. Við skoðun var hann ekki bráðveikur né meðtekinn af verkjum að sjá og með eðlileg lífsmörk. Brak fannst við þreifingu efst á bringu og við háls. Lungna- og hjartahlustun var eðlileg. Tekin var röntgenmynd af lungum sem sýnd er á mynd 1. Hver er greiningin? Þarf frekari rannsóknir og í hverju er meðferð fólgin?Peer reviewe

Identification of multiple risk loci and regulatory mechanisms influencing susceptibility to multiple myeloma

Publisher's version (útgefin grein)Genome-wide association studies (GWAS) have transformed our understanding of susceptibility to multiple myeloma (MM), but much of the heritability remains unexplained. We report a new GWAS, a meta-analysis with previous GWAS and a replication series, totalling 9974 MM cases and 247,556 controls of European ancestry. Collectively, these data provide evidence for six new MM risk loci, bringing the total number to 23. Integration of information from gene expression, epigenetic profiling and in situ Hi-C data for the 23 risk loci implicate disruption of developmental transcriptional regulators as a basis of MM susceptibility, compatible with altered B-cell differentiation as a key mechanism. Dysregulation of autophagy/apoptosis and cell cycle signalling feature as recurrently perturbed pathways. Our findings provide further insight into the biological basis of MM.In the United Kingdom, Myeloma UK and Bloodwise provided principal funding. Additional funding was provided by Cancer Research UK (C1298/A8362 supported by the Bobby Moore Fund) and The Rosetrees Trust. M.W. is supported by funding from Mr Ralph Stockwell. A.S. is supported by a clinical fellowship from Cancer Research UK and charitable funds from the Royal Marsden Hospital. N.W. was supported by the National Institute of General Medical Sciences of the National Institutes of Health under Award Number P20GM125503. This study made use of genotyping data on the 1958 Birth Cohort generated by the Wellcome Trust Sanger Institute (http://www.wtccc.org.uk). We thank the High-Throughput Genomics Group at the Wellcome Trust Centre for Human Genetics (funded by Wellcome Trust grant reference 090532/Z/09/Z) for the generation of UK myeloma OncoArray data. The BCAC study would not have been possible without the contributions of the following: Manjeet K. Bolla, Qin Wang, Kyriaki Michailidou and Joe Dennis. BCAC is funded by Cancer Research UK (C1287/A10118, C1287/A16563). For the BBCS study, we thank Eileen Williams, Elaine Ryder-Mills and Kara Sargus. The BBCS is funded by Cancer Research UK and Breast Cancer Now and acknowledges NHS funding to the National Institute of Health Research (NIHR) Biomedical Research Centre (BRC), and the National Cancer Research Network (NCRN). We thank the participants and the investigators of EPIC (European Prospective Investigation into Cancer and Nutrition). The coordination of EPIC is financially supported by the European Commission (DG-SANCO) and the International Agency for Research on Cancer. The national cohorts are supported by: Ligue Contre le Cancer, Institut Gustave Roussy, Mutuelle Générale de l’Education Nationale, Institut National de la Santé et de la Recherche Médicale (INSERM) (France); German Cancer Aid, German Cancer Research Center (DKFZ), Federal Ministry of Education and Research (BMBF) (Germany); the Hellenic Health Foundation, the Stavros Niarchos Foundation (Greece); Associazione Italiana per la Ricerca sul Cancro-AIRC-Italy and National Research Council (Italy); Dutch Ministry of Public Health, Welfare and Sports (VWS), Netherlands Cancer Registry (NKR), LK Research Funds, Dutch Prevention Funds, Dutch ZON (Zorg Onderzoek Nederland), World Cancer Research Fund (WCRF), Statistics Netherlands (The Netherlands); Health Research Fund (FIS), PI13/00061 to Granada, PI13/01162 to EPIC-Murcia, Regional Governments of Andalucía, Asturias, Basque Country, Murcia and Navarra, ISCIII RETIC (RD06/0020) (Spain); Cancer Research UK (14136 to EPIC-Norfolk; C570/A16491 and C8221/A19170 to EPIC-Oxford), Medical Research Council (1000143 to EPIC-Norfolk, MR/M012190/1 to EPIC-Oxford) (UK). We thank the SEARCH and EPIC teams which were funded by a programme grant from Cancer Research UK [A16561] and supported by the UK NIHR BRC at the University of Cambridge. We thank Breast Cancer Now and The Institute of Cancer Research (ICR) for support and funding of the UKBGS, and the study participants, study staff, and the doctors, nurses and other health care providers and health information sources who have contributed to the study. We acknowledge NHS funding to the Royal Marsden/ICR NIHR BRC. UKGPCS would like to thank The Institute of Cancer Research and The Everyman Campaign for funding support. The UKGPCS acknowledges The Prostate Cancer Research Foundation, Prostate Action, The Orchid Cancer Appeal, The National Cancer Research Network UK, The National Cancer Research Institute (NCRI), the NIHR funding to the NIHR Biomedical Research data managers and consultants for their work in the UKGPCS study and urologists and other persons involved in the planning, and data collection of the CAPS study. Genotyping of the OncoArray was funded by the US National Institutes of Health (NIH) [U19 CA 148537 for ELucidating Loci Involved in Prostate cancer SuscEptibility (ELLIPSE) project and X01HG007492 to the Center for Inherited Disease Research (CIDR) under contract number HHSN268201200008I]. Additional analytic support was provided by NIH NCI U01 CA188392 (PI: Schumacher). The PRACTICAL consortium was supported by Cancer Research UK Grants C5047/A7357, C1287/A10118, C1287/A16563, C5047/A3354, C5047/A10692, C16913/A6135, European Commission’s Seventh Framework Programme grant agreement no. 223175 (HEALTH-F2-2009-223175) and The National Institute of Health (NIH) Cancer Post-Cancer GWAS initiative grant no. 1 U19 CA 148537-01 (the GAME-ON initiative). We would also like to thank the following for funding support: The Institute of Cancer Research and The Everyman Campaign, The Prostate Cancer Research Foundation, Prostate Research Campaign UK (now Prostate Action), The Orchid Cancer Appeal, The National Cancer Research Network UK, The National Cancer Research Institute (NCRI) UK. We are grateful for support of NIHR funding to the NIHR Biomedical Research Centre at The Institute of Cancer Research and The Royal Marsden NHS Foundation Trust. The APBC BioResource, which forms part of the PRACTICAL consortium, consists of the following members: Wayne Tilley, Gail Risbridger, Renea Taylor, Judith A Clements, Lisa Horvath, Vanessa Hayes, Lisa Butler, Trina Yeadon, Allison Eckert, Pamela Saunders, Anne-Maree Haynes, Melissa Papargiris. We thank the staff of the CTRU University of Leeds and the NCRI haematology Clinical Studies Group. The US GWAS was supported by a grant from the National Institutes of Health (P01CA055819). The German study was supported by the Dietmar-Hopp-Stiftung, Germany, the German Cancer Aid (110,131), the German Ministry of Education and Science (CLIOMMICS 01ZX1309), The German Research Council (DFG; Project SI 236/81, SI 236/)-1, ER 155/6-1 and the DFG CRI 216), the Harald Huppert Foundation and the Multiple Myeloma Research Foundation. The patients were collected by the GMMG and DSMM studies. The German GWAS made use of genotyping data from the population-based HNR study, which is supported by the Heinz Nixdorf Foundation (Germany). The genotyping of the Illumina HumanOmni-1 Quad BeadChips of the HNR subjects was financed by the German Center for Neurodegenerative Disorders (DZNE), Bonn. We are grateful to all investigators who contributed to the generation of this data set. The German replication controls were collected by Peter Bugert, Institute of Transfusion Medicine and Immunology, Medical Faculty Mannheim, Heidelberg University, German Red Cross Blood Service of Baden-Württemberg-Hessen, Mannheim, Germany. This work was supported by research grants from the Swedish Foundation for Strategic Research (KF10-0009), the Marianne and Marcus Wallenberg Foundation (2010.0112), the Knut and Alice Wallenberg Foundation (2012.0193), the Swedish Research Council (2012–1753), the Royal Swedish Academy of Science, ALF grants to the University and Regional Laboratories (Labmedicin Skåne), the Siv-Inger and Per-Erik Andersson Foundation, the Medical Faculty at Lund University, the Borås foundation for cancer research, and the Swedish Society of Medicine. We thank Jörgen Adolfsson, Tomas Axelsson, Anna Collin, Ildikó Frigyesi, Patrik Magnusson, Bertil Johansson, Jan Westin and Helga Ögmundsdóttir for their assistance. This work was supported by Center for Translational Molecular Medicine (BioCHIP), a clinical research grant from the European Hematology Association, an EMCR Translational Research Grant, a BMBF grant from CLIOMMICS (01ZX1309A) and FP7 grant MSCNET (LSHC-Ct-2006-037602). We thank the staff of the HOVON, as well as patients and physicians at participating sites. In addition, we also thank Jasper Koenders, Michael Vermeulen, André Uitterlinden and Nathalie van der Velde for their assistance. We are indebted to the clinicians who contributed samples to Swedish, Icelandic, Norwegian and Danish biobanks. We are indebted to the patients and other individuals who participated in the project.Peer Reviewe

Incidental detection by computed tomography is an independent prognostic factor for survival in patients operated for nonsmall cell lung carcinoma.

Efst á síðunni er hægt að nálgast greinina í heild sinni með því að smella á hlekkinnWe studied the rate of incidental detection of lung carcinomas and its effect on long-term survival in a nationwide cohort of patients operated for nonsmall cell lung cancer (NSCLC). All patients operated for NSCLC in Iceland during 1991-2010 were included. Demographic and clinicopathological features were compared in patients diagnosed incidentally using chest radiography or computed tomography (CT), and in those with symptomatic presentation. Multivariate analysis was used to evaluate prognostic factors. Out of 508 patients, 174 (34%) were diagnosed incidentally; in 26% of cases by chest radiography and in 8% by CT. The CT-detected tumours were significantly smaller than symptomatic tumours, diagnosed at earlier TNM (tumour, node and metastasis) stages and more often of adenocarcinoma histology. 5-year cancer-specific survival for symptomatic versus incidentally diagnosed patients detected by chest radiography and CT was 41%, 57% and 68%, respectively (p=0.003). After adjusting for stage, the hazard ratio (HR) for NSCLC mortality was significantly lower for incidental diagnosis by CT (HR 0.55, 95% CI 0.31‒0.98; p=0.04) compared to incidental diagnosis by chest radiography (HR 0.95, 95% CI 0.70‒1.27; p=0.71) or symptomatic diagnosis (HR 1.0). One-third of surgically treated NSCLCs were detected incidentally, with an increasing rate of incidental CT diagnosis. NSCLC patients diagnosed incidentally by CT appear to have better survival than those diagnosed incidentally by chest radiography, and particularly those who present with symptoms

Speeding up HMM algorithms for genetic linkage analysis via chain reductions of the state space

We develop an hidden Markov model (HMM)-based algorithm for computing exact parametric and non-parametric linkage scores in larger pedigrees than was possible before. The algorithm is applicable whenever there are chains of persons in the pedigree with no genetic measurements and with unknown affection status. The algorithm is based on shrinking the state space of the HMM considerably using such chains. In a two g-degree cousins pedigree the reduction drops the state space from being exponential in g to being linear in g. For a Finnish family in which two affected children suffer from a rare cold-inducing sweating syndrome, we were able to reduce the state space by more than five orders of magnitude from 250 to 232. In another pedigree of state-space size of 227, used for a study of pituitary adenoma, the state space reduced by a factor of 8.5 and consequently exact linkage scores can now be computed, rather than approximated