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by Thomson, Scott A and Pyle, Richard L and Ahyong, Shane T and Alonso-Zarazaga, Miguel and Ammirati, Joe and Araya, Juan Francisco and Ascher, John S and Audisio, Tracy Lynn and Azevedo-Santos, Valter M and Bailly, Nicolas and Baker, William J and Balke, Michael and Barclay, Maxwell V. L and Barrett, Russell L and Benine, Ricardo C and Bickerstaff, James R. M and Bouchard, Patrice and Bour, Roger and Bourgoin, Thierry and Boyko, Christopher B and Breure, Abraham S. H and Brothers, Denis J and Byng, James W and Campbell, David and Ceríaco, Luis M. P and Cernák, István and Cerretti, Pierfilippo and Chang, Chih-Han and Cho, Soowon and Copus, Joshua M and Costello, Mark J and Cseh, Andras and Csuzdi, Csaba and Culham, Alastair and D’Elía, Guillermo and d’Udekem d’Acoz, Cédric and Daneliya, Mikhail E and Dekker, René and Dickinson, Edward C and Dickinson, Timothy A and van Dijk, Peter Paul and Dijkstra, Klaas-Douwe B and Dima, Bálint and Dmitriev, Dmitry A and Duistermaat, Leni and Dumbacher, John P and Eiserhardt, Wolf L and Ekrem, Torbjørn and Evenhuis, Neal L and Faille, Arnaud and Fernández-Triana, José L and Fiesler, Emile and Fishbein, Mark and Fordham, Barry G and Freitas, André V. L and Friol, Natália R and Fritz, Uwe and Frøslev, Tobias and Funk, Vicki A and Gaimari, Stephen D and Garbino, Guilherme S. T and Garraffoni, André R. S and Geml, József and Gill, Anthony C and Gray, Alan and Grazziotin, Felipe G and Greenslade, Penelope and Gutiérrez, Eliécer E and Harvey, Mark S and Hazevoet, Cornelis J and He, Kai and He, Xiaolan and Helfer, Stephan and Helgen, Kristofer M and van Heteren, Anneke H and Hita Garcia, Francisco and Holstein, Norbert and Horváth, Margit K and Hovenkamp, Peter H and Hwang, Wei Song and Hyvönen, Jaakko and Islam, Melissa B and Iverson, John B and Ivie, Michael A and Jaafar, Zeehan and Jackson, Morgan D and Jayat, J. Pablo and Johnson, Norman F and Kaiser, Hinrich and Klitgård, Bente B and Knapp, Dániel G and Kojima, Jun-ichi and Kõljalg, Urmas and Kontschán, Jenő and Krell, Frank-Thorsten and Krisai-Greilhuber, Irmgard and Kullander, Sven and Latella, Leonardo and Lattke, John E and Lencioni, Valeria and ...
PLoS biology, ISSN 1545-7885, 2018, Volume 16, Issue 3, p. e2005075
About the Authors: Scott A. Thomson Roles Conceptualization, Methodology, Project administration, Writing - original draft, Writing - review & editing *... 
BIOCHEMISTRY & MOLECULAR BIOLOGY | BIOLOGY | Biology | Wildlife conservation | Phenetics | Identification and classification | Methods | Endangered & extinct species | Shellfish | Taxonomy | Agricultural research | Zoology | Life sciences | Museums | Biodiversity | Reptiles & amphibians | Environmental engineering
Journal Article
Proceedings of the National Academy of Sciences - PNAS, ISSN 1091-6490, 2011, Volume 108, Issue 30, pp. 12348 - 12353
Journal Article
Journal Article
Biochemical Journal, ISSN 0264-6021, 06/2012, Volume 444, Issue 2, pp. 343 - 355
Endothelin-1 promotes cardiomyocyte hypertrophy by inducing changes in gene expression. Immediate early genes including Atf3 (activating transcription factor... 
Early growth response 1 (Egr1) | Negative feedback | Microarray | Activating transcription factor 3 (Atf3) | Hypertrophy | Immediate early gene | PROTEIN-KINASE-C | SIGNALING PATHWAYS | STIMULATION | hypertrophy | BIOCHEMISTRY & MOLECULAR BIOLOGY | early growth response 1 (Egr1) | negative feedback | microarray | ADAPTIVE-RESPONSE GENE | activating transcription factor 3 (Atf3) | CARDIAC-HYPERTROPHY | GROWTH | immediate early gene | STRESS-INDUCIBLE GENE | RAT VENTRICULAR MYOCYTES | CELL-DIFFERENTIATION | EXPRESSION | Gene Targeting - methods | Activating Transcription Factor 3 - physiology | Molecular Sequence Data | Cyclooxygenase 2 - biosynthesis | Hypertrophy, Left Ventricular - genetics | Hypertrophy, Left Ventricular - pathology | Base Sequence | Endothelin-1 - physiology | Activating Transcription Factor 3 - genetics | Animals, Newborn | Hypertrophy, Left Ventricular - metabolism | Activating Transcription Factor 3 - deficiency | Cells, Cultured | Rats | Up-Regulation - genetics | Transcriptome - drug effects | Transcriptome - genetics | Rats, Sprague-Dawley | Myocytes, Cardiac - pathology | Animals | Myocytes, Cardiac - drug effects | Early Growth Response Protein 1 - biosynthesis | Myocytes, Cardiac - metabolism | Early Growth Response Protein 1 - antagonists & inhibitors | Feedback, Physiological - drug effects | Feedback, Physiological - physiology | Early Growth Response Protein 1 - metabolism | Gapdh, glyceraldehyde-3-phosphate dehydrogenase | Il1rl1, IL1 receptor-like 1 | TLR, Toll-like receptor | IEG, immediate early gene | AdV, adenovirus | HEK, human embryonic kidney | Atf, activating transcription factor | ChIP, chromatin immunoprecipitation | ERK1 | bZIP, basic leucine zipper | SNK, Student-Newman-Keuls | CREB, CRE-binding protein | Egr1, early growth response 1 | qPCR, quantitative PCR | CRE, cAMP-response element | NF-κB, nuclear factor κB | ET-1, endothelin-1 | Areg, amphiregulin | sqPCR, semi-qPCR | 2, extracellular-signal-regulated kinase 1 | MOI, multiplicity of infection | IL, interleukin | FDR, false discovery rate | Dusp, dual specificity phosphatase | GqPCR, Gq-protein-coupled receptor | MAPK, mitogen-activated protein kinase
Journal Article
Journal Article
1995, ISBN 9780683074109, xviii, 1278
Book
The New England journal of medicine, ISSN 1533-4406, 2010, Volume 362, Issue 13, pp. 1192 - 1202
Dutasteride, an inhibitor of 5α-reductase in the prostate, was tested in a large, randomized trial to determine its ability to prevent prostate cancer. Over... 
MODELING APPROACH | MEDICINE, GENERAL & INTERNAL | DESIGN | THERAPY | 5-ALPHA-REDUCTASE INHIBITOR DUTASTERIDE | SENSITIVITY | FINASTERIDE | GRADE | HYPERPLASIA | PROGRESSION | PREVENTION TRIAL | Enzyme Inhibitors - adverse effects | Prostatic Neoplasms - pathology | Prostatic Hyperplasia - pathology | Double-Blind Method | Erectile Dysfunction - chemically induced | Humans | Middle Aged | 5-alpha Reductase Inhibitors | Male | Risk | Treatment Outcome | Azasteroids - therapeutic use | Enzyme Inhibitors - therapeutic use | Prostate-Specific Antigen - blood | Azasteroids - adverse effects | Prostate - pathology | Prostatic Neoplasms - genetics | Biopsy | Protein Isoforms | Dutasteride | Aged | Prostatic Neoplasms - prevention & control | Prostatic Hyperplasia - drug therapy | Heart Failure - chemically induced | Usage | Diagnosis | Health aspects | Prostate cancer | Risk factors | Patient safety | Age | Men | Tumors | Prostate-Specific Antigen | Erectile Dysfunction | Enzyme Inhibitors | Testosterone 5-alpha-Reductase | Prostatic Hyperplasia | Life Sciences | Prostatic Neoplasms | Azasteroids | Heart Failure | Prostate | Cancer | pathology | genetics | Urologi och njurmedicin | chemically induced | drug therapy | prevention & control | blood | adverse effects | Cancer and Oncology | Urology and Nephrology | therapeutic use | Cancer och onkologi
Journal Article
Journal of vegetation science, ISSN 1100-9233, 2014, Volume 25, Issue 5, pp. 1167 - 1180
Journal Article