98 results on '"Koulu, L"'
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2. New insights into the genetic etiology of Alzheimer's disease and related dementias
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Bellenguez, C., Küçükali, F., Jansen, I. E., Kleineidam, L., Moreno-Grau, S., Amin, N., Naj, A. C., Campos-Martin, R., Grenier-Boley, B., Andrade, V., Holmans, P. A., Boland, A., Damotte, V., van der Lee, S. J., Costa, M. R., Kuulasmaa, T., Yang, Q., de Rojas, I., Bis, J. C., Yaqub, A., Prokic, I., Chapuis, J., Ahmad, S., Giedraitis, V., Aarsland, D., Garcia-Gonzalez, P., Abdelnour, C., Alarcón-Martín, E., Alcolea, D., Alegret, M., Alvarez, I., Álvarez, V., Armstrong, N. J., Tsolaki, A., Antúnez, C., Appollonio, I., Arcaro, M., Archetti, S., Pastor, A. A., Arosio, B., Athanasiu, L., Bailly, H., Banaj, N., Baquero, M., Barral, S., Beiser, A., Pastor, A. B., Below, J. E., Benchek, P., Benussi, L., Berr, C., Besse, C., Bessi, V., Binetti, G., Bizarro, A., Blesa, R., Boada, M., Boerwinkle, E., Borroni, B., Boschi, S., Bossù, P., Bråthen, G., Bressler, J., Bresner, C., Brodaty, H., Brookes, K. J., Brusco, L. I., Buiza-Rueda, D., Bûrger, K., Burholt, V., Bush, W. S., Calero, M., Cantwell, L. B., Chene, G., Chung, J., Cuccaro, M. L., Carracedo, Á., Cecchetti, R., Cervera-Carles, L., Charbonnier, C., Chen, H. -H., Chillotti, C., Ciccone, S., Claassen, J. A. H. R., Clark, C., Conti, E., Corma-Gómez, A., Costantini, E., Custodero, C., Daian, D., Dalmasso, M. C., Daniele, A., Dardiotis, E., Dartigues, J. -F., de Deyn, P. P., de Paiva Lopes, K., de Witte, L. D., Debette, S., Deckert, J., del Ser, T., Denning, N., Destefano, A., Dichgans, M., Diehl-Schmid, J., Diez-Fairen, M., Rossi, P. D., Djurovic, S., Duron, E., Düzel, E., Dufouil, C., Eiriksdottir, G., Engelborghs, S., Escott-Price, V., Espinosa, A., Ewers, M., Faber, K. M., Fabrizio, T., Nielsen, S. F., Fardo, D. W., Farotti, L., Fenoglio, C., Fernández-Fuertes, M., Ferrari, R., Ferreira, C. B., Ferri, E., Fin, B., Fischer, P., Fladby, T., Fließbach, K., Fongang, B., Fornage, M., Fortea, J., Foroud, T. M., Fostinelli, S., Fox, N. C., Franco-Macías, E., Bullido, M. J., Frank-García, A., Froelich, L., Fulton-Howard, B., Galimberti, D., García-Alberca, J. M., García-González, P., Garcia-Madrona, S., Garcia-Ribas, G., Ghidoni, R., Giegling, I., Giorgio, G., Goate, A. M., Goldhardt, O., Gomez-Fonseca, D., González-Pérez, A., Graff, C., Grande, G., Green, E., Grimmer, T., Grünblatt, E., Grunin, M., Gudnason, V., Guetta-Baranes, T., Haapasalo, A., Hadjigeorgiou, G., Haines, J. L., Hamilton-Nelson, K. L., Hampel, H., Hanon, O., Hardy, J., Hartmann, A. M., Hausner, L., Harwood, J., Heilmann-Heimbach, S., Helisalmi, S., Heneka, M. T., Hernández, I., Herrmann, M. J., Hoffmann, P., Holmes, C., Holstege, H., Vilas, R. H., Hulsman, M., Humphrey, J., Biessels, G. J., Jian, X., Johansson, C., Jun, G. R., Kastumata, Y., Kauwe, J., Kehoe, P. G., Kilander, L., Ståhlbom, A. K., Kivipelto, M., Koivisto, A., Kornhuber, J., Kosmidis, M. H., Kukull, W. A., Kuksa, P. P., Kunkle, B. W., Kuzma, A. B., Lage, C., Laukka, E. J., Launer, L., Lauria, A., Lee, C. -Y., Lehtisalo, J., Lerch, O., Lleó, A., Longstreth, W., Lopez, O., de Munain, A. L., Love, S., Löwemark, M., Luckcuck, L., Lunetta, K. L., Ma, Y., Macías, J., Macleod, C. A., Maier, W., Mangialasche, F., Spallazzi, M., Marquié, M., Marshall, R., Martin, E. R., Montes, A. M., Rodríguez, C. M., Masullo, C., Mayeux, R., Mead, S., Mecocci, P., Medina, M., Meggy, A., Mehrabian, S., Mendoza, S., Menéndez-González, M., Mir, P., Moebus, S., Mol, M., Molina-Porcel, L., Montrreal, L., Morelli, L., Moreno, F., Morgan, K., Mosley, T., Nöthen, M. M., Muchnik, C., Mukherjee, S., Nacmias, B., Ngandu, T., Nicolas, G., Nordestgaard, B. G., Olaso, R., Orellana, A., Orsini, M., Ortega, G., Padovani, A., Paolo, C., Papenberg, G., Parnetti, L., Pasquier, F., Pastor, P., Peloso, G., Pérez-Cordón, A., Pérez-Tur, J., Pericard, P., Peters, O., Pijnenburg, Y. A. L., Pineda, J. A., Piñol-Ripoll, G., Pisanu, C., Polak, T., Popp, J., Posthuma, D., Priller, J., Puerta, R., Quenez, O., Quintela, I., Thomassen, J. Q., Rábano, A., Rainero, I., Rajabli, F., Ramakers, I., Real, L. M., Reinders, M. J. T., Reitz, C., Reyes-Dumeyer, D., Ridge, P., Riedel-Heller, S., Riederer, P., Roberto, N., Rodriguez-Rodriguez, E., Rongve, A., Allende, I. R., Rosende-Roca, M., Royo, J. L., Rubino, E., Rujescu, D., Sáez, M. E., Sakka, P., Saltvedt, I., Sanabria, Á., Sánchez-Arjona, M. B., Sanchez-Garcia, F., Juan, P. S., Sánchez-Valle, R., Sando, S. B., Sarnowski, C., Satizabal, C. L., Scamosci, M., Scarmeas, N., Scarpini, E., Scheltens, P., Scherbaum, N., Scherer, M., Schmid, M., Schneider, A., Schott, J. M., Selbæk, G., Seripa, D., Serrano, M., Sha, J., Shadrin, A. A., Skrobot, O., Slifer, S., Snijders, G. J. L., Soininen, H., Solfrizzi, V., Solomon, A., Song, Y. E., Sorbi, S., Sotolongo-Grau, O., Spalletta, G., Spottke, A., Squassina, A., Stordal, E., Tartan, J. P., Tárraga, L., Tesí, N., Thalamuthu, A., Thomas, T., Tosto, G., Traykov, L., Tremolizzo, L., Tybjærg-Hansen, A., Uitterlinden, A., Ullgren, A., Ulstein, I., Valero, S., Valladares, O., Broeckhoven, C. V., Vance, J., Vardarajan, B. N., van der Lugt, A., Dongen, J. V., van Rooij, J., van Swieten, J., Vandenberghe, R., Verhey, F., Vidal, J. -S., Vogelgsang, J., Vyhnalek, M., Wagner, M., Wallon, D., Wang, L. -S., Wang, R., Weinhold, L., Wiltfang, J., Windle, G., Woods, B., Yannakoulia, M., Zare, H., Zhao, Y., Zhang, X., Zhu, C., Zulaica, M., Laczo, J., Matoska, V., Serpente, M., Assogna, F., Piras, F., Ciullo, V., Shofany, J., Ferrarese, C., Andreoni, S., Sala, G., Zoia, C. P., Zompo, M. D., Benussi, A., Bastiani, P., Takalo, M., Natunen, T., Laatikainen, T., Tuomilehto, J., Antikainen, R., Strandberg, T., Lindström, J., Peltonen, M., Abraham, R., Al-Chalabi, A., Bass, N. J., Brayne, C., Brown, K. S., Collinge, J., Craig, D., Deloukas, P., Fox, N., Gerrish, A., Gill, M., Gwilliam, R., Harold, D., Hollingworth, P., Johnston, J. A., Jones, L., Lawlor, B., Livingston, G., Lovestone, S., Lupton, M., Lynch, A., Mann, D., Mcguinness, B., Mcquillin, A., O’Donovan, M. C., Owen, M. J., Passmore, P., Powell, J. F., Proitsi, P., Rossor, M., Shaw, C. E., Smith, A. D., Gurling, H., Todd, S., Mummery, C., Ryan, N., Lacidogna, G., Adarmes-Gómez, A., Mauleón, A., Pancho, A., Gailhajenet, A., Lafuente, A., Macias-García, D., Martín, E., Pelejà, E., Carrillo, F., Merlín, I. S., Garrote-Espina, L., Vargas, L., Carrion-Claro, M., Marín, M., Labrador, M., Buendia, M., Alonso, M. 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E., Mars, N., Pelkonen, M., Kauppi, P., Kankaanranta, H., Harju, T., Close, D., Greenberg, S., Chen, H., Betts, J., Ghosh, S., Salomaa, V., Niiranen, T., Juonala, M., Metsärinne, K., Kähönen, M., Junttila, J., Laakso, M., Pihlajamäki, J., Sinisalo, J., Taskinen, M. -R., Tuomi, T., Challis, B., Peterson, A., Chu, A., Parkkinen, J., Muslin, A., Joensuu, H., Meretoja, T., Aaltonen, L., Mattson, J., Auranen, A., Karihtala, P., Kauppila, S., Auvinen, P., Elenius, K., Popovic, R., Schutzman, J., Loboda, A., Chhibber, A., Lehtonen, H., Mcdonough, S., Crohns, M., Kulkarni, D., Kaarniranta, K., Turunen, J. A., Ollila, T., Seitsonen, S., Uusitalo, H., Aaltonen, V., Uusitalo-Järvinen, H., Luodonpää, M., Hautala, N., Loomis, S., Strauss, E., Podgornaia, A., Hoffman, J., Tasanen, K., Huilaja, L., Hannula-Jouppi, K., Salmi, T., Peltonen, S., Koulu, L., Harvima, I., Wu, Y., Choy, D., Pussinen, P., Salminen, A., Salo, T., Rice, D., Nieminen, P., Palotie, U., Siponen, M., Suominen, L., Mäntylä, P., Gursoy, U., Anttonen, V., Sipilä, K., Davis, J. W., Quarless, D., Petrovski, S., Wigmore, E., Chen, C. -Y., Bronson, P., Tsai, E., Huang, Y., Maranville, J., Shaikho, E., Mohammed, E., Wadhawan, S., Kvikstad, E., Caliskan, M., Chang, D., Bhangale, T., Pendergrass, S., Holzinger, E., Chen, X., Hedman, Å., King, K. S., Wang, C., Xu, E., Auge, F., Chatelain, C., Rajpal, D., Liu, D., Xia, T. -H., Brauer, M., Kurki, M., Karjalainen, J., Havulinna, A., Jalanko, A., Palta, P., della Briotta Parolo, P., Zhou, W., Lemmelä, S., Rivas, M., Harju, J., Lehisto, A., Ganna, A., Llorens, V., Laivuori, H., Rüeger, S., Niemi, M. E., Tukiainen, T., Reeve, M. P., Heyne, H., Palin, K., Garcia-Tabuenca, J., Siirtola, H., Kiiskinen, T., Lee, J., Tsuo, K., Elliott, A., Kristiansson, K., Hyvärinen, K., Ritari, J., Koskinen, M., Pylkäs, K., Kalaoja, M., Karjalainen, M., Mantere, T., Kangasniemi, E., Heikkinen, S., Laakkonen, E., Sipeky, C., Heron, S., Karlsson, A., Jambulingam, D., Rathinakannan, V. S., Kajanne, R., Aavikko, M., Jiménez, M. G., della Briotta Parola, P., Kanai, M., Kaunisto, M., Kilpeläinen, E., Sipilä, T. 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Uitterlinden, A, Ullgren, A, Ulstein, I, Valero, S, Valladares, O, Broeckhoven, C, Vance, J, Vardarajan, B, van der Lugt, A, Dongen, J, van Rooij, J, van Swieten, J, Vandenberghe, R, Verhey, F, Vidal, J, Vogelgsang, J, Vyhnalek, M, Wagner, M, Wallon, D, Wang, L, Wang, R, Weinhold, L, Wiltfang, J, Windle, G, Woods, B, Yannakoulia, M, Zare, H, Zhao, Y, Zhang, X, Zhu, C, Zulaica, M, Andreoni, S, Ferrarese, C, Sala, G, Zoia, C, Farrer, L, Psaty, B, Ghanbari, M, Raj, T, Sachdev, P, Mather, K, Jessen, F, Ikram, M, de Mendonça, A, Hort, J, Tsolaki, M, Pericak-Vance, M, Amouyel, P, Williams, J, Frikke-Schmidt, R, Clarimon, J, Deleuze, J, Rossi, G, Seshadri, S, Andreassen, O, Ingelsson, M, Hiltunen, M, Sleegers, K, Schellenberg, G, van Duijn, C, Sims, R, van der Flier, W, Ruiz, A, Ramirez, A, Lambert, J, VU University medical center, Amsterdam Neuroscience - Neurodegeneration, Neurology, Human genetics, Amsterdam Neuroscience - Complex Trait Genetics, Amsterdam Neuroscience - Compulsivity, 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Sachdev, Perminder [0000-0002-9595-3220], Mather, Karen [0000-0003-4143-8941], Ikram, M Arfan [0000-0003-0372-8585], Tsolaki, Magda [0000-0002-2072-8010], Pericak-Vance, Margaret A [0000-0001-7283-8804], Amouyel, Philippe [0000-0001-9088-234X], Williams, Julie [0000-0002-4069-0259], Frikke-Schmidt, Ruth [0000-0003-4084-5027], Seshadri, Sudha [0000-0001-6135-2622], Andreassen, Ole A [0000-0002-4461-3568], Sleegers, Kristel [0000-0002-0283-2332], van Duijn, Cornelia M [0000-0002-2374-9204], Sims, Rebecca [0000-0002-3885-1199], van der Flier, Wiesje M [0000-0001-8766-6224], Ramirez, Alfredo [0000-0003-4991-763X], Lambert, Jean-Charles [0000-0003-0829-7817], Apollo - University of Cambridge Repository, Complex Trait Genetics, Clinical sciences, Neuroprotection & Neuromodulation, Pathologic Biochemistry and Physiology, Clinical Biology, Epidemiology, Internal Medicine, Psychiatrie & Neuropsychologie, RS: MHeNs - R1 - Cognitive Neuropsychiatry and Clinical Neuroscience, MUMC+: MA Med Staf Spec Psychiatrie (9), UAM. Departamento de Biología Molecular, University of Helsinki, Department of Neurosciences, HUS Internal Medicine and Rehabilitation, Timo Strandberg / Principal Investigator, Department of Medicine, Clinicum, HUS Neurocenter, Neurologian yksikkö, Centre of Excellence in Complex Disease Genetics, HUS Abdominal Center, Institut Pasteur, Institut National de la Santé et de la Recherche Médicale (France), European Commission, LabEx DISTALZ, Pérez-Tur, Jordi, University Children’s Hospital Basel (Suiza), INSERM (Francia), Lille Métropole Communauté Urbaine, Government of France (Francia), EADB, GR@ACE, DEGESCO, EADI, GERAD, Demgene, FinnGen, ADGC, CHARGE, Holmans, Peter A. [0000-0003-0870-9412], van der Lee, Sven J. [0000-0003-1606-8643], Costa, Marcos R. [0000-0002-4928-2163], Bis, Joshua C. [0000-0002-3409-1110], Brookes, Keeley J. [0000-0003-2427-2513], Bush, William S. [0000-0002-9729-6519], de Witte, Lot D. [0000-0002-7235-9958], del Ser, Teodoro [0000-0001-9806-7083], Fox, Nick C. [0000-0002-6660-657X], Bullido, María J. [0000-0002-6477-1117], Goate, Alison M. [0000-0002-0576-2472], Herrmann, Martin J. [0000-0001-9970-2122], Jun, Gyungah R. [0000-0002-3230-8697], Kehoe, Patrick G. [0000-0002-7542-1139], Kosmidis, Mary H. [0000-0001-8790-1220], Lunetta, Kathryn L. [0000-0002-9268-810X], MacLeod, Catherine A. [0000-0002-9314-7380], Nöthen, Markus M. [0000-0002-8770-2464], Nordestgaard, Børge G. [0000-0002-1954-7220], Pineda, Juan A. [0000-0002-3751-0296], Real, Luis M. [0000-0003-4932-7429], Reinders, Marcel J. T. [0000-0002-1148-1562], Satizabal, Claudia L. [0000-0002-1115-4430], Schott, Jonathan M. [0000-0003-2059-024X], Shadrin, Alexey A. [0000-0002-7467-250X], Farrer, Lindsay A. [0000-0001-5533-4225], Psaty, Bruce M. [0000-0002-7278-2190], Ikram, M. Arfan [0000-0003-0372-8585], Pericak-Vance, Margaret A. [0000-0001-7283-8804], Andreassen, Ole A. [0000-0002-4461-3568], van Duijn, Cornelia M. [0000-0002-2374-9204], van der Flier, Wiesje M. [0000-0001-8766-6224], and Molecular Neuroscience and Ageing Research (MOLAR)
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tau Proteins/genetics ,Alzheimer`s disease Donders Center for Medical Neuroscience [Radboudumc 1] ,Neurologi ,MED/03 - GENETICA MEDICA ,45/43 ,Medizin ,Stress-related disorders Donders Center for Medical Neuroscience [Radboudumc 13] ,genetics [Alzheimer Disease] ,Genome-Wide Association Study ,Humans ,tau Proteins ,Alzheimer Disease ,Cognitive Dysfunction ,VARIANTS ,pathology [Alzheimer Disease] ,Tau Proteins ,Settore BIO/13 - Biologia Applicata ,Cognitive Dysfunction/psychology ,692/699/375/365/1283 ,IMPUTATION ,article ,1184 Genetics, developmental biology, physiology ,Biología y Biomedicina / Biología ,AMYLOID-BETA ,Settore MED/26 - NEUROLOGIA ,Neurology ,psychology [Cognitive Dysfunction] ,Medical Genetics ,Human ,Neuroscience(all) ,631/208/205/2138 ,All institutes and research themes of the Radboud University Medical Center ,SDG 3 - Good Health and Well-being ,ddc:570 ,Genetics ,Genetic Predisposition to Disease ,GENOME-WIDE ASSOCIATION ,METAANALYSIS ,Medicinsk genetik ,MED/26 - NEUROLOGIA ,Alzheimer Disease/genetics ,neurology ,tau Protein ,NECROSIS-FACTOR-ALPHA ,RISK LOCI ,genetics [tau Proteins] ,PREDICTION MODELS ,Human medicine ,GENERATION ,RESPONSES - Abstract
25 páginas, 6 figuras, 2 tablas, Characterization of the genetic landscape of Alzheimer's disease (AD) and related dementias (ADD) provides a unique opportunity for a better understanding of the associated pathophysiological processes. We performed a two-stage genome-wide association study totaling 111,326 clinically diagnosed/'proxy' AD cases and 677,663 controls. We found 75 risk loci, of which 42 were new at the time of analysis. Pathway enrichment analyses confirmed the involvement of amyloid/tau pathways and highlighted microglia implication. Gene prioritization in the new loci identified 31 genes that were suggestive of new genetically associated processes, including the tumor necrosis factor alpha pathway through the linear ubiquitin chain assembly complex. We also built a new genetic risk score associated with the risk of future AD/dementia or progression from mild cognitive impairment to AD/dementia. The improvement in prediction led to a 1.6- to 1.9-fold increase in AD risk from the lowest to the highest decile, in addition to effects of age and the APOE ε4 allele., This work was funded by a grant (EADB) from the EU Joint Programme – Neurodegenerative Disease Research. INSERM UMR1167 is also funded by the INSERM, Institut Pasteur de Lille, Lille Métropole Communauté Urbaine and French government’s LABEX DISTALZ program (development of innovative strategies for a transdisciplinary approach to AD). Full consortium acknowledgements and funding are in the Supplementary Not
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- 2022
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3. Uniting biobank resources reveals novel genetic pathways modulating susceptibility for atopic dermatitis
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Sliz, E. (Eeva), Huilaja, L. (Laura), Pasanen, A. (Anu), Laisk, T. (Triin), Reimann, E. (Ene), Mägi, R. (Reedik), F. (FinnGen), E. B. (Estonian Biobank Research Team), Hannula-Jouppi, K. (Katariina), Peltonen, S. (Sirkku), Salmi, T. (Teea), Koulu, L. (Leena), Tasanen, K. (Kaisa), Kettunen, J. (Johannes), Sliz, E. (Eeva), Huilaja, L. (Laura), Pasanen, A. (Anu), Laisk, T. (Triin), Reimann, E. (Ene), Mägi, R. (Reedik), F. (FinnGen), E. B. (Estonian Biobank Research Team), Hannula-Jouppi, K. (Katariina), Peltonen, S. (Sirkku), Salmi, T. (Teea), Koulu, L. (Leena), Tasanen, K. (Kaisa), and Kettunen, J. (Johannes)
- Abstract
Background: Atopic dermatitis (AD) is a common chronic inflammatory skin disease with high heritability. Previous genome-wide association studies have identified several loci predisposing to AD. These findings explain approximately 30% of the variance in AD susceptibility, suggesting that further work is required to fully understand the genetic underpinnings. Objectives: We sought to gain additional understanding of the genetic contribution to AD risk by using biobank resources. Methods: We completed a genome-wide meta-analysis of AD in 796,661 individuals (Ncases = 22,474) from the FinnGen study, the Estonian Biobank, and the UK Biobank. We further performed downstream in silico analyses to characterize the risk variants at the novel loci. Results: We report 30 loci associating with AD (P < 5 × 10-8 ), 5 of which are novel. In 2 of the novel loci, we identified missense mutations with deleterious predictions in desmocollin 1 and serpin family B member 7, genes encoding proteins crucial to epidermal strength and integrity. Conclusions: These findings elucidate novel genetic pathways involved in AD pathophysiology. The likely involvement of desmocollin 1 and serpin family B member 7 in AD pathogenesis may offer opportunities for the development of novel treatment strategies for AD in the future.
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- 2022
4. Psoriasis Causes Significant Economic Burden to Patients
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Mustonen, A., Mattila, K., Leino, M., Koulu, L., and Tuominen, R.
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- 2014
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5. Chromosome Xq23 is associated with lower atherogenic lipid concentrations and favorable cardiometabolic indices
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Natarajan, P. (Pradeep), Pampana, A. (Akhil), Graham, S. E. (Sarah E.), Ruotsalainen, S. E. (Sanni E.), Perry, J. A. (James A.), de Vries, P. S. (Paul S.), Broome, J. G. (Jai G.), Pirruccello, J. P. (James P.), Honigbere, M. C. (Michael C.), Aragam, K. (Krishna), Wolford, B. (Brooke), Brody, J. A. (Jennifer A.), Antonacci-Fulton, L. (Lucinda), Arden, M. (Moscati), Aslibekyan, S. (Stella), Assimes, T. L. (Themistocles L.), Ballantyne, C. M. (Christie M.), Bielak, L. F. (Lawrence F.), Bisl, J. C. (Joshua C.), Cade, B. E. (Brian E.), Do, R. (Ron), Doddapaneni, H. (Harsha), Emery, L. S. (Leslie S.), Hung, Y.-J. (Yi-Jen), Irvin, M. R. (Marguerite R.), Khan, A. T. (Alyna T.), Lange, L. (Leslie), Lee, J. (Jiwon), Lemaitre, R. N. (Rozenn N.), Martin, L. W. (Lisa W.), Metcalf, G. (Ginger), Montasser, M. E. (May E.), Moon, J.-Y. (Jee-Young), Muzny, D. (Donna), Connell, J. R. (Jeffrey R. O.), Palmer, N. D. (Nicholette D.), Peralta, J. M. (Juan M.), Peyser, P. A. (Patricia A.), Stilp, A. M. (Adrienne M.), Tsai, M. (Michael), Wang, F. F. (Fei Fei), Weeks, D. E. (Daniel E.), Yanek, L. R. (Lisa R.), Wilson, J. G. (James G.), Abecasis, G. (Goncalo), Arnett, D. K. (Donna K.), Becker, L. C. (Lewis C.), Blangercy, J. (John), Boerwinkle, E. (Eric), Bowden, D. W. (Donald W.), Chang, Y.-C. (Yi-Cheng), Chen, Y. I. (Yii-Der, I), Choi, W. J. (Won Jung), Correa, A. (Adolfo), Curran, J. E. (Joanne E.), Daly, M. J. (Mark J.), DutcherE, S. K. (Susan K.), Ellinor, P. T. (Patrick T.), Fornage, M. (Myriam), Freedman, B. I. (Barry, I), Gabriel, S. (Stacey), Germer, S. (Soren), Gibbs, R. A. (Richard A.), He, J. (Jiang), Hveem, K. (Kristian), Jarvik, G. P. (Gail P.), Kaplan, R. C. (Robert C.), Kardia, S. L. (Sharon L. R.), Kennyn, E. (Eimear), Kim, R. W. (Ryan W.), Kooperberg, C. (Charles), Laurie, C. C. (Cathy C.), Lee, S. (Seonwook), Lloyd-Jones, D. M. (Don M.), Loos, R. J. (Ruth J. F.), Lubitz, S. A. (Steven A.), Mathias, R. A. (Rasika A.), Martinez, K. A. (Karine A. Viaud), McGarvey, S. T. (Stephen T.), Mitche, B. D. (Braxton D.), Nickerson, D. A. (Deborah A.), North, K. E. (Kari E.), Palotie, A. (Aarno), Park, C. J. (Cheol Joo), Psat, B. M. (Bruce M. Y.), Rao, D. C. (D. C.), Redline, S. (Susan), Reiner, A. P. (Alexander P.), Seo, D. (Daekwan), Seo, J.-S. (Jeong-Sun), Smith, A. V. (Albert, V), Tracy, R. P. (Russell P.), Kathiresan, S. (Sekar), Cupples, L. A. (L. Adrienne), Rotten, J. I. (Jerome, I), Morrison, A. C. (Alanna C.), Rich, S. S. (Stephen S.), Ripatti, S. (Samuli), Wilier, C. (Cristen), Peloso, G. M. (Gina M.), Vasan, R. S. (Ramachandran S.), Abe, N. (Namiko), Albert, C. (Christine), Almasy, L. (Laura), Alonso, A. (Alvaro), Ament, S. (Seth), Anderson, P. (Peter), Applebaum-Bowden, D. (Deborah), Arking, D. (Dan), Ashley-Koch, A. (Allison), Auer, P. (Paul), Avramopoulos, D. (Dimitrios), Barnard, J. (John), Barnes, K. (Kathleen), Barr, R. G. (R. Graham), Barron-Casella, E. (Emily), Beaty, T. (Terri), Becker, D. (Diane), Beer, R. (Rebecca), Begum, F. (Ferdouse), Beitelshees, A. (Amber), Benjamin, E. (Emelia), Bezerra, M. (Marcos), Bielak, L. (Larry), Blackwel, T. (Thomas), Bowler, R. (Russell), Broecke, U. (Ulrich), Bunting, K. (Karen), Burchard, E. (Esteban), Buth, E. (Erin), Cardwel, J. (Jonathan), Carty, C. (Cara), Casaburi, R. (Richard), Casella, J. (James), Chaffin, M. (Mark), Chang, C. (Christy), Chasman, D. (Daniel), Chavan, S. (Sameer), Chen, B.-J. (Bo-Juen), Chen, W.-M. (Wei-Min), Chol, M. (Michael), Choi, S. H. (Seung Hoan), Chuang, L.-M. (Lee-Ming), Chung, M. (Mina), Conomos, M. P. (Matthew P.), Cornell, E. (Elaine), Crapo, J. (James), Curtis, J. (Jeffrey), Custer, B. (Brian), Damcott, C. (Coleen), Darbar, D. (Dawood), Das, S. (Sayantan), David, S. (Sean), Davis, C. (Colleen), Daya, M. (Michelle), de Andrade, M. (Mariza), DeBaunuo, M. (Michael), Duan, Q. (Qing), Devine, R. D. (Ranjan Deka Dawn DeMeo Scott), Duggirala, Q. R. (Qing Ravi), Durda, J. P. (Jon Peter), Dutcher, S. (Susan), Eaton, C. (Charles), Ekunwe, L. (Lynette), Farber, C. (Charles), Farnaml, L. (Leanna), Fingerlin, T. (Tasha), Flickinger, M. (Matthew), Franceschini, N. (Nora), Fu, M. (Mao), Fullerton, S. M. (Stephanie M.), Fulton, L. (Lucinda), Gan, W. (Weiniu), Gao, Y. (Yan), Gass, M. (Margery), Ge, B. (Bruce), Geng, X. P. (Xiaoqi Priscilla), Gignoux, C. (Chris), Gladwin, M. (Mark), Glahn, D. (David), Gogarten, S. (Stephanie), Gong, D.-W. (Da-Wei), Goring, H. (Harald), Gu, C. C. (C. Charles), Guan, Y. (Yue), Guo, X. (Xiuqing), Haessler, J. (Jeff), Hall, M. (Michael), Harris, D. (Daniel), Hawle, N. Y. (Nicola Y.), Heavner, B. (Ben), Heckbert, S. (Susan), Hernandez, R. (Ryan), Herrington, D. (David), Hersh, C. (Craig), Hidalgo, B. (Bertha), Hixson, J. (James), Hokanson, J. (John), Hong, E. (Elliott), Hoth, K. (Karin), Hsiung, C. A. (Chao Agnes), Huston, H. (Haley), Hwu, C. M. (Chii Min), Jackson, R. (Rebecca), Jain, D. (Deepti), Jaquish, C. (Cashell), Jhun, M. A. (Min A.), Johnsen, J. (Jill), Johnson, A. (Andrew), Johnson, C. (Craig), Johnston, R. (Rich), Jones, K. (Kimberly), Kang, H. M. (Hyun Min), Kaufman, L. (Laura), Kell, S. Y. (Shannon Y.), Kessler, M. (Michael), Kinney, G. (Greg), Konkle, B. (Barbara), Kramer, H. (Holly), Krauter, S. (Stephanie), Lange, C. (Christoph), Lange, E. (Ethan), Laurie, C. (Cecelia), LeBoff, M. (Meryl), Lee, S. S. (Seunggeun Shawn), Lee, W.-J. (Wen-Jane), LeFaive, J. (Jonathon), Levine, D. (David), Levy, D. (Dan), Lewis, J. (Joshua), Li, Y. (Yun), Lin, H. (Honghuang), Lin, K. H. (Keng Han), Lin, X. (Xihong), Liu, S. (Simin), Liu, Y. (Yongmei), Lunetta, K. (Kathryn), Luo, J. (James), Mahaney, M. (Michael), Make, B. (Barry), Manichaikul, A. (Ani), Mansonl, J. (JoAnn), Margolin, L. (Lauren), Mathai, S. (Susan), McArdle, P. (Patrick), Mcdonald, M.-L. (Merry-Lynn), McFarland, S. (Sean), McHugh, C. (Caitlin), Mei, H. (Hao), Meyers, D. A. (Deborah A.), Mikulla, J. (Julie), Min, N. (Nancy), Minear, M. (Mollie), Minster, R. L. (Ryan L.), Musani, S. (Solomon), Mwasongwe, S. (Stanford), Mychaleckyj, J. C. (Josyf C.), Nadkarni, G. (Girish), Naik, R. (Rakhi), Naseri, T. (Take), Nekhai, S. (Sergei), Nelson, S. C. (Sarah C.), Nickerson, D. (Deborah), Connell, J. O. (Jeff O.), Connor, T. O. (Tim O.), Ochs-Balcom, H. (Heather), Pankow, J. (James), Papanicolaou, G. (George), Parkerl, M. (Margaret), Parsa, A. (Afshin), Penchey, S. (Sara), Perez, M. (Marco), Peters, U. (Ulrike), Phillips, L. S. (Lawrence S.), Phillips, S. (Sam), Pollin, T. (Toni), Post, W. (Wendy), Becker, J. P. (Julia Powers), Boorgula, M. P. (Meher Preethi), Preuss, M. (Michael), Prokopenko, D. (Dmitry), Qasba, P. (Pankaj), Qiao, D. (Dandi), Rafaels, N. (Nicholas), Raffield, L. (Laura), Rasmussen-Torvik, L. (Laura), Ratan, A. (Aakrosh), Reed, R. (Robert), Reganl, E. (Elizabeth), Reupena, M. S. (Muagututi Sefuiva), Rice, K. (Ken), Roden, D. (Dan), Roselli, C. (Carolina), Ruczinski, I. (Ingo), Russel, P. (Pamela), Ruuska, S. (Sarah), Ryan, K. (Kathleen), Sabino, E. C. (Ester Cerdeira), Sakornsakolpatl, P. (Phuwanat), Salzberg, S. (Steven), Sandow, K. (Kevin), Sankaran, V. G. (Vijay G.), Scheller, C. (Christopher), Schmidt, E. (Ellen), Schwander, K. (Karen), Schwartz, D. (David), Sciurba, F. (Frank), Seidman, C. (Christine), Seidman, J. (Jonathan), Sheehan, V. (Vivien), Shetty, A. (Amol), Shetty, A. (Aniket), Sheu, W. H. (Wayne Hui-Heng), Shoemaker, M. B. (M. Benjamin), Silver, B. (Brian), Silvermanl, E. (Edwin), Smith, J. (Jennifer), Smith, J. (Josh), Smith, N. (Nicholas), Smith, T. (Tanja), Smoller, S. (Sylvia), Snively, B. (Beverly), Soferlm, T. (Tamar), Streeten, E. (Elizabeth), Su, J. L. (Jessica Lasky), Sung, Y. J. (Yun Ju), Sylvia, J. (Jody), Sztalryd, C. (Carole), Taliun, D. (Daniel), Tang, H. (Hua), Taub, M. (Margaret), Taylor, K. D. (Kent D.), Taylor, S. (Simeon), Telen, M. (Marilyn), Thornton, T. A. (Timothy A.), Tinker, L. (Lesley), Tirschwel, D. (David), Tiwari, H. (Hemant), Vaidya, D. (Dhananjay), VandeHaar, P. (Peter), Vrieze, S. (Scott), Walker, T. (Tarik), Wallace, R. (Robert), Waits, A. (Avram), Wan, E. (Emily), Wang, H. (Heming), Watson, K. (Karol), Weir, B. (Bruce), Weiss, S. (Scott), Weng, L.-C. (Lu-Chen), Williams, K. (Kayleen), Williams, L. K. (L. Keoki), Wilson, C. (Carla), Wong, Q. (Quenna), Xu, H. (Huichun), Yang, I. (Ivana), Yang, R. (Rongze), Zaghlou, N. (Norann), Zekavat, M. (Maryam), Zhang, Y. (Yingze), Zhao, S. X. (Snow Xueyan), Zhao, W. (Wei), Zni, D. (Degui), Zhou, X. (Xiang), Zhu, X. (Xiaofeng), Zody, M. (Michael), Zoellner, S. (Sebastian), Daly, M. (Mark), Jacob, H. (Howard), Matakidou, A. (Athena), Runz, H. (Heiko), John, S. (Sally), Plenge, R. (Robert), McCarthy, M. (Mark), Hunkapiller, J. (Julie), Ehm, M. (Meg), Waterworth, D. (Dawn), Fox, C. (Caroline), Malarstig, A. (Anders), Klinger, K. (Kathy), Call, K. (Kathy), Mkel, T. (Tomi), Kaprio, J. (Jaakko), Virolainen, P. (Petri), Pulkki, K. (Kari), Kilpi, T. (Terhi), Perola, M. (Markus), Partanen, J. (Jukka), Pitkranta, A. (Anne), Kaarteenaho, R. (Riitta), Vainio, S. (Seppo), Savinainen, K. (Kimmo), Kosma, V.-M. (Veli-Matti), Kujala, U. (Urho), Tuovila, O. (Outi), Hendolin, M. (Minna), Pakkanen, R. (Raimo), Waring, J. (Jeff), Riley-Gillis, B. (Bridget), Liu, J. (Jimmy), Biswas, S. (Shameek), Diogo, D. (Dorothee), Marshall, C. (Catherine), Hu, X. (Xinli), Gossel, M. (Matthias), Schleutker, J. (Johanna), Arvas, M. (Mikko), Hinttala, R. (Reetta), Kettunen, J. (Johannes), Laaksonen, R. (Reijo), Mannermaa, A. (Arto), Paloneva, J. (Juha), Soininen, H. (Hilkka), Julkunen, V. (Valtteri), Remes, A. (Anne), Klviinen, R. (Reetta), Hiltunen, M. (Mikko), Peltola, J. (Jukka), Tienari, P. (Pentti), Rinne, J. (Juha), Ziemann, A. (Adam), Waring, J. (Jeffrey), Esmaeeli, S. (Sahar), Smaoui, N. (Nizar), Lehtonen, A. (Anne), Eaton, S. (Susan), Landenper, S. (Sanni), Michon, J. (John), Kerchner, G. (Geoff), Bowers, N. (Natalie), Teng, E. (Edmond), Eicher, J. (John), Mehta, V. (Vinay), Gormle, P. Y. (Padhraig Y.), Linden, K. (Kari), Whelan, C. (Christopher), Xu, F. (Fanli), Pulford, D. (David), Frkkil, M. (Martti), Pikkarainen, S. (Sampsa), Jussila, A. (Airi), Blomster, T. (Timo), Kiviniemi, M. (Mikko), Voutilainen, M. (Markku), Georgantas, B. (Bob), Heap, G. (Graham), Rahimov, F. (Fedik), Usiskin, K. (Keith), Maranville, J. (Joseph), Lu, T. (Tim), Oh, D. (Danny), Kalpala, K. (Kirsi), Miller, M. (Melissa), McCarthy, L. (Linda), Eklund, K. (Kari), Palomki, A. (Antti), Isomki, P. (Pia), Piri, L. (Laura), Kaipiainen-Seppnen, O. (Oili), Lertratanaku, A. (Apinya), Bing, D. C. (David Close Marla Hochfeld Nan), Gordillo, J. E. (Jorge Esparza), Mars, N. (Nina), Laitinen, T. (Tarja), Pelkonen, M. (Margit), Kauppi, P. (Paula), Kankaanranta, H. (Hannu), Harju, T. (Terttu), Greenberg, S. (Steven), Chen, H. (Hubert), Betts, J. (Jo), Ghosh, S. (Soumitra), Salomaa, V. (Veikko), Niiranen, T. (Teemu), Juonala, M. (Markus), Metsrinne, K. (Kaj), Khnen, M. (Mika), Junttila, J. (Juhani), Laakso, M. (Markku), Pihlajamki, J. (Jussi), Sinisalo, J. (Juha), Taskinen, M.-R. (Marja-Riitta), Tuomi, T. (Tiinamaija), Laukkanen, J. (Jari), Challis, B. (Ben), Peterson, A. (Andrew), Chu, A. (Audrey), Parkkinen, J. (Jaakko), Muslin, A. (Anthony), Joensuu, H. (Heikki), Meretoja, T. (Tuomo), Aaltonen, L. (Lauri), Auranen, A. (Annika), Karihtala, P. (Peeter), Kauppila, S. (Saila), Auvinen, P. (Pivi), Elenius, K. (Klaus), Popovic, R. (Relja), Schutzman, J. (Jennifer), Loboda, A. (Andrey), Chhibber, A. (Aparna), Lehtonen, H. (Heli), McDonough, S. (Stefan), Crohns, M. (Marika), Kulkarni, D. (Diptee), Kaarniranta, K. (Kai), Turunen, J. (Joni), Ollila, T. (Terhi), Seitsonen, S. (Sanna), Uusitalo, H. (Hannu), Aaltonen, V. (Vesa), Uusitalo-Jrvinen, H. (Hannele), Luodonp, M. (Marja), Hautala, N. (Nina), Strauss, E. (Erich), Chen, H. (Hao), Podgornaia, A. (Anna), Hoffman, J. (Joshua), Tasanen, K. (Kaisa), Huilaja, L. (Laura), Hannula-Jouppi, K. (Katariina), Salmi, T. (Teea), Peltonen, S. (Sirkku), Koulu, L. (Leena), Harvima, I. (Ilkka), Wu, Y. (Ying), Choy, D. (David), Jalanko, A. (Anu), Kajanne, R. (Risto), Lyhs, U. (Ulrike), Kaunisto, M. (Mari), Davis, J. W. (Justin Wade), Quarless, D. (Danjuma), Petrovski, S. (Slav), Chen, C.-Y. (Chia-Yen), Bronson, P. (Paola), Yang, R. (Robert), Chang, D. (Diana), Bhangale, T. (Tushar), Holzinger, E. (Emily), Wang, X. (Xulong), Chen, X. (Xing), Auro, K. (Kirsi), Wang, C. (Clarence), Xu, E. (Ethan), Auge, F. (Franck), Chatelain, C. (Clement), Kurki, M. (Mitja), Karjalainen, J. (Juha), Havulinna, A. (Aki), Palin, K. (Kimmo), Palta, P. (Priit), Parolo, P. D. (Pietro Della Briotta), Zhou, W. (Wei), Lemmel, S. (Susanna), Rivas, M. (Manuel), Harju, J. (Jarmo), Lehisto, A. (Arto), Ganna, A. (Andrea), Llorens, V. (Vincent), Karlsson, A. (Antti), Kristiansson, K. (Kati), Hyvrinen, K. (Kati), Ritari, J. (Jarmo), Wahlfors, T. (Tiina), Koskinen, M. (Miika), Pylkäs, K. (Katri), Kalaoja, M. (Marita), Karjalainen, M. (Minna), Mantere, T. (Tuomo), Kangasniemi, E. (Eeva), Heikkinen, S. (Sami), Laakkonen, E. (Eija), Kononen, J. (Juha), Loukola, A. (Anu), Laiho, P. (Pivi), Sistonen, T. (Tuuli), Kaiharju, E. (Essi), Laukkanen, M. (Markku), Jrvensivu, E. (Elina), Lhteenmki, S. (Sini), Mnnikk, L. (Lotta), Wong, R. (Regis), Mattsson, H. (Hannele), Hiekkalinna, T. (Tero), Jimnez, M. G. (Manuel Gonzlez), Donner, K. (Kati), Prn, K. (KaIle), Nunez-Fontarnau, J. (Javier), Kilpelinen, E. (Elina), Sipi, T. P. (Timo P.), Brein, G. (Georg), Dada, A. (Alexander), Awaisa, G. (Ghazal), Shcherban, A. (Anastasia), Sipil, T. (Tuomas), Laivuori, H. (Hannele), Kiiskinen, T. (Tuomo), Siirtola, H. (Harri), Tabuenca, J. G. (Javier Gracia), Kallio, L. (Lila), Soini, S. (Sirpa), Pitknen, K. (Kimmo), and Kuopio, T. (Teijo)
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Cardiovascular genetics ,Genome-wide association studies - Abstract
Autosomal genetic analyses of blood lipids have yielded key insights for coronary heart disease (CHD). However, X chromosome genetic variation is understudied for blood lipids in large sample sizes. We now analyze genetic and blood lipid data in a high-coverage whole X chromosome sequencing study of 65,322 multi-ancestry participants and perform replication among 456,893 European participants. Common alleles on chromosome Xq23 are strongly associated with reduced total cholesterol, LDL cholesterol, and triglycerides (min P = 8.5 × 10−72), with similar effects for males and females. Chromosome Xq23 lipid-lowering alleles are associated with reduced odds for CHD among 42,545 cases and 591,247 controls (P = 1.7 × 10−4), and reduced odds for diabetes mellitus type 2 among 54,095 cases and 573,885 controls (P = 1.4 × 10−5). Although we observe an association with increased BMI, waist-to-hip ratio adjusted for BMI is reduced, bioimpedance analyses indicate increased gluteofemoral fat, and abdominal MRI analyses indicate reduced visceral adiposity. Co-localization analyses strongly correlate increased CHRDL1 gene expression, particularly in adipose tissue, with reduced concentrations of blood lipids.
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- 2021
6. Pro-inflammatory and Th2-type cytokine responses in PBMC in infants are associated with parental smoking
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Linnamaa, P., Nieminen, K., Koulu, L., Tuomasjukka, S., Kallio, H., Yang, B., Tahvonen, R., and Savolainen, J.
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- 2012
- Full Text
- View/download PDF
7. Blackcurrant seed oil for prevention of atopic dermatitis in newborns: a randomized, double-blind, placebo-controlled trial
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Linnamaa, P., Savolainen, J., Koulu, L., Tuomasjukka, S., Kallio, H., Yang, B., Vahlberg, T., and Tahvonen, R.
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- 2010
- Full Text
- View/download PDF
8. Iän tuomat iho-ongelmat
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Sinikumpu, S.-P. (Suvi-Päivikki), Horn, J. (Johannes), and Koulu, L. (Leena)
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integumentary system - Abstract
Tiivistelmä Ikääntyminen aiheuttaa rakenteellisia ja toiminnallisia muutoksia eri elimiin, myös ihoon. Monien ihosairauksien esiintyvyys kasvaa ikääntyessä (1). Nykyiselläänkin ihotaudit aiheuttavat kuolemaan johtamattomista sairauksista neljänneksi eniten tautitaakkaa sairauden vuoksi menetettyinä toimintakykyisinä elinvuosina mitaten (disability adjusted life years, DALY) (2). Väestön vanhetessa tämä taakka lisääntyy. Väestötason tutkimuksia ikäihmisten ihosairauksien yleisyydestä on niukasti. Noin 4 000 potilaan sairaalarekisteristä tehdyn tutkimuksen mukaan yleisimpiä olivat ekseemat, ihoinfektiot, kutina ja ihosyövät (3). Myös hyvänlaatuisten ihokasvainten, kuten seborrooisten keratoosien (rasvaluomien), kirsikkaluomien ja lentigojen, määrä lisääntyy iän karttuessa (4). Tässä katsauksessa käsittelemme tavanomaisia iän tuomia iho-ongelmia. Krooniset alaraajahaavat sekä lääkeaineihottumat on jätetty katsauksesta pois. Abstract Skin problems in the elderly Aging causes many structural changes in the skin and affects its functionality. Therefore, many skin diseases are more common in the older population. Measured on the DALY index (disability adjusted life years), skin diseases are the fourth most common disease group causing disability. The most common skin diseases in older adults are eczemas, skin infections, pruritus and malignant diseases. Skin aging can be divided into chronological aging and photoaging. Smoking, air pollutants and exposure to ultraviolet radiation are the most significant factors in skin aging. Dry skin is the most common cause of pruritus in the elderly but sometimes systemic diseases can be the cause and they must be excluded. Asteatotic eczema is a common skin disease found particularly in the elderly population. It is caused by structural changes in the skin and excessive washing with soap. It can be prevented by applying moisturizing cream daily. Sometimes corticosteroid creams or ultraviolet light treatment are needed. Seborrhoeic dermatitis is most common in older people and possibly caused by a weakened immune system. As many as half of the elderly population are estimated to have dermatitis in skinfolds. The term MASD (moistureassociated skin damage) is used when moisture and chemicals break the skin’s protective barrier. It is treated with washing and careful drying of the skinfolds. Sometimes local antimycotics are needed because of secondary infection. Skin infections caused by bacteria, viruses and fungi are common in the elderly because of their weakened immune system. Malignant and premalignant lesions are becoming more common due to aging of the population. The prevalence of actinic keratosis varies according to age, skin phototype and residence. Some actinic keratoses evolve to Bowen’s disease and eventually to squamous cell carcinoma. Diagnosis is confirmed by biopsy. Actinic keratoses with mild dysplasia can be treated topically. Otherwise treatment by a dermatologist is needed. Patients’ ability to function must be considered when treating older patients.
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- 2020
9. Validation of psoriasis diagnoses recorded in Finnish biobanks
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Haverinen, S. (Suvi), Vihervaara, A. (Armi), Löyttyniemi, E. (Eliisa), Peltonen, S. (Sirkku), Koulu, L. (Leena), Tasanen, K. (Kaisa), Huilaja, L. (Laura), Haverinen, S. (Suvi), Vihervaara, A. (Armi), Löyttyniemi, E. (Eliisa), Peltonen, S. (Sirkku), Koulu, L. (Leena), Tasanen, K. (Kaisa), and Huilaja, L. (Laura)
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- 2020
10. Susceptibility of xeroderma pigmentosum keratinocytes from different complementation groups to ultraviolet B-induced apoptosis
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PETIT-FRÈRE, C., CAPULAS, E., LOWE, J. E., KOULU, L., MARTTILA, R. J., JASPERS, N. G.J., CLINGEN, P. H., GREEN, M. H.L., and ARLETT, C. F.
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- 2000
11. Genetic architecture of human plasma lipidome and its link to cardiovascular disease
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Tabassum, R. (Rubina), Ramo, J. T. (Joel T.), Ripatti, P. (Pietari), Koskela, J. T. (Jukka T.), Kurki, M. (Mitja), Karjalainen, J. (Juha), Palta, P. (Priit), Hassan, S. (Shabbeer), Nunez-Fontarnau, J. (Javier), Kiiskinen, T. T. (Tuomo T. J.), Soderlund, S. (Sanni), Matikainen, N. (Niina), Gerl, M. J. (Mathias J.), Surma, M. A. (Michal A.), Klose, C. (Christian), Stitziel, N. O. (Nathan O.), Laivuori, H. (Hannele), Havulinna, A. S. (Aki S.), Service, S. K. (Susan K.), Salomaa, V. (Veikko), Pirinen, M. (Matti), Jauhiainen, M. (Matti), Daly, M. J. (Mark J.), Freimer, N. B. (Nelson B.), Palotie, A. (Aarno), Taskinen, M.-R. (Marja-Riitta), Simons, K. (Kai), Ripatti, S. (Samuli), Jalanko, A. (Anu), Kaprio, J. (Jaakko), Donner, K. (Kati), Kaunisto, M. (Mari), Mars, N. (Nina), Dada, A. (Alexander), Shcherban, A. (Anastasia), Ganna, A. (Andrea), Lehisto, A. (Arto), Kilpelainen, E. (Elina), Brein, G. (Georg), Awaisa, G. (Ghazal), Harju, J. (Jarmo), Parr, K. (Kalle), Parolo, P. D. (Pietro Della Briotta), Kajanne, R. (Risto), Lemmela, S. (Susanna), Sipila, T. P. (Timo P.), Sipila, T. (Tuomas), Lyhs, U. (Ulrike), Llorens, V. (Vincent), Niiranen, T. (Teemu), Kristiansson, K. (Kati), Mannikko, L. (Lotta), Jimenez, M. G. (Manuel Gonzalez), Perola, M. (Markus), Wong, R. (Regis), Kilpi, T. (Terhi), Hiekkalinna, T. (Tero), Jarvensivu, E. (Elina), Kaiharju, E. (Essi), Mattsson, H. (Hannele), Laukkanen, M. (Markku), Laiho, P. (Paivi), Lahteenmaki, S. (Sini), Sistonen, T. (Tuuli), Soini, S. (Sirpa), Ziemann, A. (Adam), Lehtonen, A. (Anne), Lertratanakul, A. (Apinya), Georgantas, B. (Bob), Riley-Gillis, B. (Bridget), Quarless, D. (Danjuma), Rahimov, F. (Fedik), Heap, G. (Graham), Jacob, H. (Howard), Waring, J. (Jeffrey), Davis, J. W. (Justin Wade), Smaoui, N. (Nizar), Popovic, R. (Relja), Esmaeeli, S. (Sahar), Waring, J. (Jeff), Matakidou, A. (Athena), Challis, B. (Ben), Close, D. (David), Petrovski, S. (Slave), Karlsson, A. (Antti), Schleutker, J. (Johanna), Pulkki, K. (Kari), Virolainen, P. (Petri), Kallio, L. (Lila), Mannermaa, A. (Arto), Heikkinen, S. (Sami), Kosma, V.-M. (Veli-Matti), Chen, C.-Y. (Chia-Yen), Runz, H. (Heiko), Liu, J. (Jimmy), Bronson, P. (Paola), John, S. (Sally), Landenpera, S. (Sanni), Eaton, S. (Susan), Zhou, W. (Wei), Hendolin, M. (Minna), Tuovila, O. (Outi), Pakkanen, R. (Raimo), Maranville, J. (Joseph), Usiskin, K. (Keith), Hochfeld, M. (Marla), Plenge, R. (Robert), Yang, R. (Robert), Biswas, S. (Shameek), Greenberg, S. (Steven), Laakkonen, E. (Eija), Kononen, J. (Juha), Paloneva, J. (Juha), Kujala, U. (Urho), Kuopio, T. (Teijo), Laukkanen, J. (Jari), Kangasniemi, E. (Eeva), Savinainen, K. (Kimmo), Laaksonen, R. (Reijo), Arvas, M. (Mikko), Ritari, J. (Jarmo), Partanen, J. (Jukka), Hyvarinen, K. (Kati), Wahlfors, T. (Tiina), Peterson, A. (Andrew), Oh, D. (Danny), Chang, D. (Diana), Teng, E. (Edmond), Strauss, E. (Erich), Kerchner, G. (Geoff), Chen, H. (Hao), Chen, H. (Hubert), Schutzman, J. (Jennifer), Michon, J. (John), Hunkapiller, J. (Julie), McCarthy, M. (Mark), Bowers, N. (Natalie), Lu, T. (Tim), Bhangale, T. (Tushar), Pulford, D. (David), Waterworth, D. (Dawn), Kulkarni, D. (Diptee), Xu, F. (Fanli), Betts, J. (Jo), Gordillo, J. E. (Jorge Esparza), Hoffman, J. (Joshua), Auro, K. (Kirsi), McCarthy, L. (Linda), Ghosh, S. (Soumitra), Ehm, M. (Meg), Pitkanen, K. (Kimmo), Makela, T. (Tomi), Loukola, A. (Anu), Joensuu, H. (Heikki), Sinisalo, J. (Juha), Eklund, K. (Kari), Aaltonen, L. (Lauri), Farkkila, M. (Martti), Carpen, O. (Olli), Kauppi, P. (Paula), Tienari, P. (Pentti), Ollila, T. (Terhi), Tuomi, T. (Tiinamaija), Meretoja, T. (Tuomo), Pitkaranta, A. (Anne), Turunen, J. (Joni), Hannula-Jouppi, K. (Katariina), Pikkarainen, S. (Sampsa), Seitsonen, S. (Sanna), Koskinen, M. (Miika), Palomaki, A. (Antti), Rinne, J. (Juha), Metsarinne, K. (Kaj), Elenius, K. (Klaus), Pirila, L. (Laura), Koulu, L. (Leena), Voutilainen, M. (Markku), Juonala, M. (Markus), Peltonen, S. (Sirkku), Aaltonen, V. (Vesa), Loboda, A. (Andrey), Podgornaia, A. (Anna), Chhibber, A. (Aparna), Chu, A. (Audrey), Fox, C. (Caroline), Diogo, D. (Dorothee), Holzinger, E. (Emily), Eicher, J. (John), Gormley, P. (Padhraig), Mehta, V. (Vinay), Wang, X. (Xulong), Kettunen, J. (Johannes), Pylkas, K. (Katri), Kalaoja, M. (Marita), Karjalainen, M. (Minna), Hinttala, R. (Reetta), Kaarteenaho, R. (Riitta), Vainio, S. (Seppo), Mantere, T. (Tuomo), Remes, A. (Anne), Huhtakangas, J. (Johanna), Junttila, J. (Juhani), Tasanen, K. (Kaisa), Huilaja, L. (Laura), Luodonpaa, M. (Marja), Hautala, N. (Nina), Karihtala, P. (Peeter), Kauppila, S. (Saila), Harju, T. (Terttu), Blomster, T. (Timo), Soininen, H. (Hilkka), Harvima, I. (Ilkka), Pihlajamaki, J. (Jussi), Kaarniranta, K. (Kai), Pelkonen, M. (Margit), Laakso, M. (Markku), Hiltunen, M. (Mikko), Kiviniemi, M. (Mikko), Kaipiainen-Seppanen, O. (Oili), Auvinen, P. (Paivi), Kalviainen, R. (Reetta), Julkunen, V. (Valtteri), Malarstig, A. (Anders), Hedman, A. (Asa), Marshal, C. (Catherine), Whelan, C. (Christopher), Lehtonen, H. (Heli), Parkkinen, J. (Jaakko), Linden, K. (Kari), Kalpala, K. (Kirsi), Miller, M. (Melissa), Bing, N. (Nan), McDonough, S. (Stefan), Chen, X. (Xing), Hu, X. (Xinli), Wu, Y. (Ying), Auranen, A. (Annika), Jussila, A. (Airi), Uusitalo-Jarvinen, H. (Hannele), Kankaanranta, H. (Hannu), Uusitalo, H. (Hannu), Peltola, J. (Jukka), Kahonen, M. (Mika), Isomaki, P. (Pia), Laitinen, T. (Tarja), Salmi, T. (Teea), Muslin, A. (Anthony), Wang, C. (Clarence), Chatelain, C. (Clement), Xu, E. (Ethan), Auge, F. (Franck), Call, K. (Kathy), Klinger, K. (Kathy), Crohns, M. (Marika), Gossel, M. (Matthias), Palin, K. (Kimmo), Rivas, M. (Manuel), Siirtola, H. (Harri), and Tabuenca, J. G. (Javier Gracia)
- Subjects
lipids (amino acids, peptides, and proteins) - Abstract
Understanding genetic architecture of plasma lipidome could provide better insights into lipid metabolism and its link to cardiovascular diseases (CVDs). Here, we perform genome-wide association analyses of 141 lipid species (n = 2,181 individuals), followed by phenome-wide scans with 25 CVD related phenotypes (n = 511,700 individuals). We identify 35 lipid-species-associated loci (P
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- 2019
12. Validation of Psoriasis Diagnoses Recorded in Finnish Biobanks
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Haverinen, S, primary, Vihervaara, A, additional, Löyttyniemi, E, additional, Peltonen, S, additional, Koulu, L, additional, Tasanen, K, additional, Huilaja, L, additional, and investigators, f, additional
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- 2020
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13. A review of studies on the effects of ultraviolet irradiation on the resistance to infections: evidence from rodent infection models and verification by experimental and observational human studies
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Termorshuizen, F, Garssen, J, Norval, M, Koulu, L, Laihia, J, Leino, L, Jansen, C.T, De Gruijl, F, Gibbs, N.K, De Simone, C, and Van Loveren, H
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- 2002
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14. Genetic architecture of human plasma lipidome and its link to cardiovascular disease
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Tabassum, R, Ramo, JT, Ripatti, P, Koskela, JT, Kurki, M, Karjalainen, J, Palta, P, Hassan, S, Nunez-Fontarnau, J, Kiiskinen, TTJ, Soderlund, S, Matikainen, N, Gerl, MJ, Surma, MA, Klose, C, Stitziel, NO, Laivuori, H, Havulinna, AS, Service, SK, Salomaa, V, Pirinen, M, Jauhiainen, M, Daly, MJ, Freimer, NB, Palotie, A, Taskinen, M-R, Simons, K, Ripatti, S, Jalanko, A, Kaprio, J, Donner, K, Kaunisto, M, Mars, N, Dada, A, Shcherban, A, Ganna, A, Lehisto, A, Kilpelainen, E, Brein, G, Awaisa, G, Harju, J, Parr, K, Parolo, PDB, Kajanne, R, Lemmela, S, Sipila, TP, Sipila, T, Lyhs, U, Llorens, V, Niiranen, T, Kristiansson, K, Mannikko, L, Jimenez, MG, Perola, M, Wong, R, Kilpi, T, Hiekkalinna, T, Jarvensivu, E, Kaiharju, E, Mattsson, H, Laukkanen, M, Laiho, P, Lahteenmaki, S, Sistonen, T, Soini, S, Ziemann, A, Lehtonen, A, Lertratanakul, A, Georgantas, B, Riley-Gillis, B, Quarless, D, Rahimov, F, Heap, G, Jacob, H, Waring, J, Davis, JW, Smaoui, N, Popovic, R, Esmaeeli, S, Matakidou, A, Challis, B, Close, D, Petrovski, S, Karlsson, A, Schleutker, J, Pulkki, K, Virolainen, P, Kallio, L, Mannermaa, A, Heikkinen, S, Kosma, V-M, Chen, C-Y, Runz, H, Liu, J, Bronson, P, John, S, Landenpera, S, Eaton, S, Zhou, W, Hendolin, M, Tuovila, O, Pakkanen, R, Maranville, J, Usiskin, K, Hochfeld, M, Plenge, R, Yang, R, Biswas, S, Greenberg, S, Laakkonen, E, Kononen, J, Paloneva, J, Kujala, U, Kuopio, T, Laukkanen, J, Kangasniemi, E, Savinainen, K, Laaksonen, R, Arvas, M, Ritari, J, Partanen, J, Hyvarinen, K, Wahlfors, T, Peterson, A, Oh, D, Chang, D, Teng, E, Strauss, E, Kerchner, G, Chen, H, Schutzman, J, Michon, J, Hunkapiller, J, McCarthy, M, Bowers, N, Lu, T, Bhangale, T, Pulford, D, Waterworth, D, Kulkarni, D, Xu, F, Betts, J, Gordillo, JE, Hoffman, J, Auro, K, McCarthy, L, Ghosh, S, Ehm, M, Pitkanen, K, Makela, T, Loukola, A, Joensuu, H, Sinisalo, J, Eklund, K, Aaltonen, L, Farkkila, M, Carpen, O, Kauppi, P, Tienari, P, Ollila, T, Tuomi, T, Meretoja, T, Pitkaranta, A, Turunen, J, Hannula-Jouppi, K, Pikkarainen, S, Seitsonen, S, Koskinen, M, Palomaki, A, Rinne, J, Metsarinne, K, Elenius, K, Pirila, L, Koulu, L, Voutilainen, M, Juonala, M, Peltonen, S, Aaltonen, V, Loboda, A, Podgornaia, A, Chhibber, A, Chu, A, Fox, C, Diogo, D, Holzinger, E, Eicher, J, Gormley, P, Mehta, V, Wang, X, Kettunen, J, Pylkas, K, Kalaoja, M, Karjalainen, M, Hinttala, R, Kaarteenaho, R, Vainio, S, Mantere, T, Remes, A, Huhtakangas, J, Junttila, J, Tasanen, K, Huilaja, L, Luodonpaa, M, Hautala, N, Karihtala, P, Kauppila, S, Harju, T, Blomster, T, Soininen, H, Harvima, I, Pihlajamaki, J, Kaarniranta, K, Pelkonen, M, Laakso, M, Hiltunen, M, Kiviniemi, M, Kaipiainen-Seppanen, O, Auvinen, P, Kalviainen, R, Julkunen, V, Malarstig, A, Hedman, A, Marshal, C, Whelan, C, Lehtonen, H, Parkkinen, J, Linden, K, Kalpala, K, Miller, M, Bing, N, McDonough, S, Chen, X, Hu, X, Wu, Y, Auranen, A, Jussila, A, Uusitalo-Jarvinen, H, Kankaanranta, H, Uusitalo, H, Peltola, J, Kahonen, M, Isomaki, P, Laitinen, T, Salmi, T, Muslin, A, Wang, C, Chatelain, C, Xu, E, Auge, F, Call, K, Klinger, K, Crohns, M, Gossel, M, Palin, K, Rivas, M, Siirtola, H, Tabuenca, JG, Tabassum, R, Ramo, JT, Ripatti, P, Koskela, JT, Kurki, M, Karjalainen, J, Palta, P, Hassan, S, Nunez-Fontarnau, J, Kiiskinen, TTJ, Soderlund, S, Matikainen, N, Gerl, MJ, Surma, MA, Klose, C, Stitziel, NO, Laivuori, H, Havulinna, AS, Service, SK, Salomaa, V, Pirinen, M, Jauhiainen, M, Daly, MJ, Freimer, NB, Palotie, A, Taskinen, M-R, Simons, K, Ripatti, S, Jalanko, A, Kaprio, J, Donner, K, Kaunisto, M, Mars, N, Dada, A, Shcherban, A, Ganna, A, Lehisto, A, Kilpelainen, E, Brein, G, Awaisa, G, Harju, J, Parr, K, Parolo, PDB, Kajanne, R, Lemmela, S, Sipila, TP, Sipila, T, Lyhs, U, Llorens, V, Niiranen, T, Kristiansson, K, Mannikko, L, Jimenez, MG, Perola, M, Wong, R, Kilpi, T, Hiekkalinna, T, Jarvensivu, E, Kaiharju, E, Mattsson, H, Laukkanen, M, Laiho, P, Lahteenmaki, S, Sistonen, T, Soini, S, Ziemann, A, Lehtonen, A, Lertratanakul, A, Georgantas, B, Riley-Gillis, B, Quarless, D, Rahimov, F, Heap, G, Jacob, H, Waring, J, Davis, JW, Smaoui, N, Popovic, R, Esmaeeli, S, Matakidou, A, Challis, B, Close, D, Petrovski, S, Karlsson, A, Schleutker, J, Pulkki, K, Virolainen, P, Kallio, L, Mannermaa, A, Heikkinen, S, Kosma, V-M, Chen, C-Y, Runz, H, Liu, J, Bronson, P, John, S, Landenpera, S, Eaton, S, Zhou, W, Hendolin, M, Tuovila, O, Pakkanen, R, Maranville, J, Usiskin, K, Hochfeld, M, Plenge, R, Yang, R, Biswas, S, Greenberg, S, Laakkonen, E, Kononen, J, Paloneva, J, Kujala, U, Kuopio, T, Laukkanen, J, Kangasniemi, E, Savinainen, K, Laaksonen, R, Arvas, M, Ritari, J, Partanen, J, Hyvarinen, K, Wahlfors, T, Peterson, A, Oh, D, Chang, D, Teng, E, Strauss, E, Kerchner, G, Chen, H, Schutzman, J, Michon, J, Hunkapiller, J, McCarthy, M, Bowers, N, Lu, T, Bhangale, T, Pulford, D, Waterworth, D, Kulkarni, D, Xu, F, Betts, J, Gordillo, JE, Hoffman, J, Auro, K, McCarthy, L, Ghosh, S, Ehm, M, Pitkanen, K, Makela, T, Loukola, A, Joensuu, H, Sinisalo, J, Eklund, K, Aaltonen, L, Farkkila, M, Carpen, O, Kauppi, P, Tienari, P, Ollila, T, Tuomi, T, Meretoja, T, Pitkaranta, A, Turunen, J, Hannula-Jouppi, K, Pikkarainen, S, Seitsonen, S, Koskinen, M, Palomaki, A, Rinne, J, Metsarinne, K, Elenius, K, Pirila, L, Koulu, L, Voutilainen, M, Juonala, M, Peltonen, S, Aaltonen, V, Loboda, A, Podgornaia, A, Chhibber, A, Chu, A, Fox, C, Diogo, D, Holzinger, E, Eicher, J, Gormley, P, Mehta, V, Wang, X, Kettunen, J, Pylkas, K, Kalaoja, M, Karjalainen, M, Hinttala, R, Kaarteenaho, R, Vainio, S, Mantere, T, Remes, A, Huhtakangas, J, Junttila, J, Tasanen, K, Huilaja, L, Luodonpaa, M, Hautala, N, Karihtala, P, Kauppila, S, Harju, T, Blomster, T, Soininen, H, Harvima, I, Pihlajamaki, J, Kaarniranta, K, Pelkonen, M, Laakso, M, Hiltunen, M, Kiviniemi, M, Kaipiainen-Seppanen, O, Auvinen, P, Kalviainen, R, Julkunen, V, Malarstig, A, Hedman, A, Marshal, C, Whelan, C, Lehtonen, H, Parkkinen, J, Linden, K, Kalpala, K, Miller, M, Bing, N, McDonough, S, Chen, X, Hu, X, Wu, Y, Auranen, A, Jussila, A, Uusitalo-Jarvinen, H, Kankaanranta, H, Uusitalo, H, Peltola, J, Kahonen, M, Isomaki, P, Laitinen, T, Salmi, T, Muslin, A, Wang, C, Chatelain, C, Xu, E, Auge, F, Call, K, Klinger, K, Crohns, M, Gossel, M, Palin, K, Rivas, M, Siirtola, H, and Tabuenca, JG
- Abstract
Understanding genetic architecture of plasma lipidome could provide better insights into lipid metabolism and its link to cardiovascular diseases (CVDs). Here, we perform genome-wide association analyses of 141 lipid species (n = 2,181 individuals), followed by phenome-wide scans with 25 CVD related phenotypes (n = 511,700 individuals). We identify 35 lipid-species-associated loci (P <5 ×10-8), 10 of which associate with CVD risk including five new loci-COL5A1, GLTPD2, SPTLC3, MBOAT7 and GALNT16 (false discovery rate<0.05). We identify loci for lipid species that are shown to predict CVD e.g., SPTLC3 for CER(d18:1/24:1). We show that lipoprotein lipase (LPL) may more efficiently hydrolyze medium length triacylglycerides (TAGs) than others. Polyunsaturated lipids have highest heritability and genetic correlations, suggesting considerable genetic regulation at fatty acids levels. We find low genetic correlations between traditional lipids and lipid species. Our results show that lipidomic profiles capture information beyond traditional lipids and identify genetic variants modifying lipid levels and risk of CVD.
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- 2019
15. Effect of a single UVB or PUVA exposure on immediate and delayed skin hypersensitivity reactions in humans: Correlation to erythemal response and langerhans cell depletion
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Kalimo, K., Koulu, L., and Jansén, C. T.
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- 1983
- Full Text
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16. Epidermal langerhans cell number and morphology during oral retinoid treatment
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Koulu, L. and Jansén, C. T.
- Published
- 1981
- Full Text
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17. Neurological symptoms and natural course of xeroderma pigmentosum
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Anttinen, A., primary, Koulu, L., additional, Nikoskelainen, E., additional, Portin, R., additional, Kurki, T., additional, Erkinjuntti, M., additional, Jaspers, N. G. J., additional, Raams, A., additional, Green, M. H. L., additional, Lehmann, A. R., additional, Wing, J. F., additional, Arlett, C. F., additional, and Marttila, R. J., additional
- Published
- 2008
- Full Text
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18. Urocanic Acid Concentration and Photoisomerization in Caucasian Skin Phototypes
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Snellman, E., primary, Jansén, C T., additional, Laihia, J. K., additional, Milán, T., additional, Koulu, L., additional, Leszczynski, K., additional, and Pasanen, P., additional
- Published
- 1997
- Full Text
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19. <em>In vivo</em> PUVA and UVB sensitivity of various human epidermal Langerhans cell markers (ATPase, HLA-DR and T6)--Dose-response and time-sequence studies.
- Author
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Koulu, L. and Jansén, C. T.
- Subjects
- *
LANGERHANS cells , *ULTRAVIOLET radiation , *DOSE-response relationship in biochemistry , *TIME series analysis , *CELL surface antigens - Abstract
To form a comprehensive view of the UV-sensitivity of human epidermal Langerhans cells (LC), the time-sequence and dose-response effects of single doses of UVB or 8-methoxypsoralen plus UVA (PUVA) radiation on three different LC surface markers were studied with histochemical and immunohistochemical staining. An increasing PUVA dose from 1 to 10 J/cm[SUP2] caused an almost linear decrease in the surface enzyme (ATPase) positive LC count, whereas the cell surface antigens (HLA-DR and T6) were rather more resistant, up to PUVA dose of 5 J/cm[SUP2]. A single dose of 5 J/cm[SUP2] of PUVA induced an LC depletion that was similar during the 21 days of observation, irrespective of where the cells were visualized with ATPase staining or with monoclonal antibodies against the cell surface antigens HLA-DR or T6. In each case, the nadir was reached 14 days after irradiation; the average residual LC count was then 57%. The cell counts 21 days after PUVA irradiation were still only approximately 74% of the nontreated skin counts. Langerhans cell depletion induced by an erythemagenic dose of UVA irradiation was swifter and more pronounced than that induced by 5 J/cm[SUP2] of PUVA but, again, a similar time schedule was recorded with ATPase, HLA-DR and T6 staining. [ABSTRACT FROM AUTHOR]
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- 1988
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20. Human autoantibodies against a desmosomal core protein in pemphigus foliaceus.
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Koulu, L, Kusumi, A, Steinberg, M S, Klaus-Kovtun, V, and Stanley, J R
- Abstract
Pemphigus foliaceus (PF) is a human autoimmune disease in which antibodies are directed against the cell surface of epidermal cells with resultant blister formation. The histopathology of these blisters indicates that cells have detached from each other, and electron microscopy of early blisters shows diminished numbers, to complete loss, of desmosomes as well as abnormalities of the tonofilament-desmosome complex. In this study we demonstrate that autoantibodies from certain PF patients bind to a desmosomal core glycoprotein called desmoglein (DG) I. Proteins in extracts of normal human epidermis were separated by sodium dodecyl sulfate (SDS) polyacrylamide gel electrophoresis (PAGE), then transferred to nitrocellulose or 2-aminophenylthioether paper for immunoperoxidase staining. Results of these immunoblots indicated that sera from 6 of 13 PF patients specifically and intensely stained an approximately 160,000 mol wt polypeptide, "PF antigen". Such staining was not seen with normal human sera or sera from patients with pemphigus vulgaris or bullous pemphigoid, two autoimmune blistering skin diseases that are clinically, histologically, and immunochemically distinct from PF. However, rabbit antiserum directed against DGI, that was isolated from bovine muzzle desmosomes, stained a polypeptide band which co-migrated with PF antigen. Furthermore, when proteins from extracts of normal human epidermis were electrophoresed in two dimensions (isoelectric focusing, then SDS-PAGE) before transfer to nitrocellulose for immunoperoxidase staining, PF antibodies and antibodies to DGI stained identical spots. Finally, PF sera as well as PF IgG that was affinity purified with PF antigen from normal human epidermis, both selectively bound to DGI extracted from bovine muzzle desmosomes. These studies demonstrate that the human autoantibodies from certain patients with PF, a disease of epidermal cell adhesion, are directed against a desmosomal core protein.
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- 1984
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21. Epidermal langerhans cell number and morphology during oral retinoid treatment.
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Koulu, L. and Jansén, C.
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- 1982
- Full Text
- View/download PDF
22. Skin photosensitizing and Langerhans´ cell depleting activity of topical (bath) PUVA therapy: comparison of trimethylpsoralen and 8-methoxypsoralen
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Koulu, L., primary and Jansén, CT., additional
- Published
- 1983
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23. Incorporation and distribution of eicosanoid precursor fatty acids in murine fibroblasts in culture
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PUNNONEN, K., primary, PUUSTINEN, T., additional, KOULU, L., additional, and JANSÉN, C. T., additional
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- 1987
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24. A monoclonal antibody to the desmosomal glycoprotein desmoglein I binds the same polypeptide as human autoantibodies in pemphigus foliaceus.
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Stanley, J R, primary, Koulu, L, additional, Klaus-Kovtun, V, additional, and Steinberg, M S, additional
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- 1986
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25. Distinction between epidermal antigens binding pemphigus vulgaris and pemphigus foliaceus autoantibodies.
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Stanley, J R, primary, Koulu, L, additional, and Thivolet, C, additional
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- 1984
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26. In vivo PUVA and UVB sensitivity of various human epidermal Langerhans cell markers (ATPase, HLA-DR and T6)-Dose-response and time-sequence studies
- Author
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KOULU, L., primary and JANSEN, C.T., additional
- Published
- 1988
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27. Cancer incidence among Finnish psoriasis patients treated with 8-methoxypsoralen bath PUVA
- Author
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Hannuksela-Svahn, A., Pukkala, E., Koulu, L., Jansen, C.T., and Karvonen, J.
- Abstract
Background: Long-term oral 8-methoxypsoralen (8-MOP) and UVA (PUVA) therapy increases the risk of nonmelanoma skin cancer and possibly also of cutaneous malignant melanoma. Topical application of 8-MOP PUVA induces malignant tumors in rodent skin, but little is known about its carcinogenicity in human skin. Objective: Our purpose was to investigate the carcinogenicity of 8-MOP bath PUVA in humans. Methods: This was a cohort study of 158 patients with psoriasis, for whom 8-MOP bath PUVA had been initiated during 1979 to 1992. The average number of 8-MOP bath PUVA treatments was 36 (range, 6 to 204) and the mean cumulative UVA dose was 92 J/cm^2 (range, 3 to 884 J/cm^2) by the end of 1995. The patients were not treated with any other forms of PUVA. Cancer incidence subsequent to 8-MOP bath PUVA up to the end of 1995 was determined by linking the cohort with the records of the Finnish Cancer Registry. The standardized incidence ratios (SIR) were calculated for skin cancer and some common internal cancers, using the expected numbers of cases based on the regional cancer incidence rates. Results: There was one case of basal cell carcinoma, but no cases of other types of skin cancer. A total of 6 noncutaneous cancers were observed (SIR, 1.3; 95% confidence interval, 0.5 to 2.8). Conclusion: No association between cutaneous cancer and 8-MOP bath PUVA was found, but the statistical power of this study alone is not adequate to warrant definite conclusions. The results can be used in a meta-analysis as soon as other studies on the carcinogenicity of 8-MOP bath PUVA are published.(J Am Acad Dermatol 1999;40:694-6.)
- Published
- 1999
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28. Treatment Preferences in Young Adults with Moderate to Severe Psoriasis: A Qualitative Study from the Nordic Countries.
- Author
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Balieva FN, Catton L, Claréus BW, Danielsen K, Fierens F, Iversen L, Koulu L, Osmanecevic A, Pasternack R, and Skov L
- Abstract
Introduction: The purpose of this study is to explore treatment preferences and identify patient characteristics in young bio-naive adults with moderate to severe psoriasis in the Nordic countries (Norway, Finland, Sweden, and Denmark)., Methods: Patients were 18-45 years old and bio-naive but referred for biologic treatment of moderate to severe psoriasis. Patients were included at eight Nordic dermatology clinics. Patients with significant comorbidity or psoriatic arthritis were excluded. The Psoriasis Area and Severity Index (PASI) and Dermatology Life Quality Index (DLQI) were assessed along with basic patient information. A semistructured interview guide was used in individual qualitative interviews, asking patients about their treatment preferences and reasons, disease journey, and disease management. The interviews were analyzed using thematic content analysis. Twenty-four patients sufficed to reach saturation in this qualitative study., Results: The patient sample characteristics represented a qualitative variation in age, sex, symptoms, duration of disease, and country. We included a total of 12 male and 12 female patients. The mean age was 34 years (range 18-45 years), the mean age at diagnosis was 20 years (range 6-34 years), the mean ± standard deviation (SD) time since diagnosis was 13 ± 8 years, PASI was 9.5 ± 4.7, and DLQI was 15.2 ± 6.4. Interviews suggested that both the burden of disease as well as the burden of treatment influenced patient preferences regarding treatment attributes, hence getting alleviation from symptoms did not alone influence patient preferences. Time, effort, and inconvenience related to psoriasis treatments also influenced patient preferences., Conclusions: This first in-depth, qualitative study in young bio-naive adults with psoriasis suggests that patient preferences are focusing not only on symptom relief but also on alleviating the burden of psoriasis treatment. Understanding the reasons for patient preferences and the perspectives of young adults is needed to guide individual shared decision-making in psoriasis management., (© 2023. The Author(s).)
- Published
- 2023
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29. Uniting biobank resources reveals novel genetic pathways modulating susceptibility for atopic dermatitis.
- Author
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Sliz E, Huilaja L, Pasanen A, Laisk T, Reimann E, Mägi R, Hannula-Jouppi K, Peltonen S, Salmi T, Koulu L, Tasanen K, and Kettunen J
- Subjects
- Biological Specimen Banks, Genetic Predisposition to Disease, Genome-Wide Association Study, Humans, Polymorphism, Single Nucleotide, Dermatitis, Atopic genetics, Desmocollins genetics, Serpins genetics
- Abstract
Background: Atopic dermatitis (AD) is a common chronic inflammatory skin disease with high heritability. Previous genome-wide association studies have identified several loci predisposing to AD. These findings explain approximately 30% of the variance in AD susceptibility, suggesting that further work is required to fully understand the genetic underpinnings., Objective: We sought to gain additional understanding of the genetic contribution to AD risk by using biobank resources., Methods: We completed a genome-wide meta-analysis of AD in 796,661 individuals (N
cases = 22,474) from the FinnGen study, the Estonian Biobank, and the UK Biobank. We further performed downstream in silico analyses to characterize the risk variants at the novel loci., Results: We report 30 loci associating with AD (P < 5 × 10-8 ), 5 of which are novel. In 2 of the novel loci, we identified missense mutations with deleterious predictions in desmocollin 1 and serpin family B member 7, genes encoding proteins crucial to epidermal strength and integrity., Conclusions: These findings elucidate novel genetic pathways involved in AD pathophysiology. The likely involvement of desmocollin 1 and serpin family B member 7 in AD pathogenesis may offer opportunities for the development of novel treatment strategies for AD in the future., (Copyright © 2021 The Authors. Published by Elsevier Inc. All rights reserved.)- Published
- 2022
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30. Influence of Psoriasis on Household Chores and Time Spent on Skin Care at Home: A Questionnaire Study.
- Author
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Leino M, Mustonen A, Mattila K, Koulu L, and Tuominen R
- Abstract
Introduction: Previous studies have shown that psoriasis has a significant effect on patients' health-related quality of life. The impact of psoriasis on household chores and the need for assistance with such tasks are not well documented. The aim of this study was to estimate the impact of psoriasis on the ability to carry out household chores, the time spent on skin care at home and the assistance that patients with psoriasis require with these activities., Methods: In a questionnaire study 262 patients with moderate-to-severe psoriasis, visiting a tertiary level dermatological clinic during a 1-year study period, listed household chores which they considered were particularly affected by psoriasis. This was done without a predefined list of chores. Questions on their ability to perform household chores as well as time spent on skin care at home were asked. The need for outside assistance with household chores and help received were also determined., Results: More than half of the patients (57.8%) reported difficulties with household chores because of psoriasis. Psoriasis affected a wide range of everyday household activities, with physically demanding tasks and those involving contact with water mentioned most often. Most of the patients (84.6%) reported that they have increased the time spent on skin care because of psoriasis, on average by 87 min per week. A quarter of patients received assistance in household chores. Women received more assistance than men (p < 0.01). The need for additional assistance was reported by a fifth of patients, women more often than men (p < 0.05)., Conclusion: When estimating the overall burden of psoriasis, considering only the economic and productivity consequences may underestimate the impact of the disease. The impact on everyday life events such as the ability to perform household chores should also be taken into account., Funding: This study was supported by unconditional grants from the research funds of the Hospital District of Southwest Finland. Hospital District of Southwest Finland's research permission K44/10/EVO13043.
- Published
- 2015
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31. How much of the productivity losses among psoriasis patients are due to psoriasis.
- Author
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Mustonen A, Mattila K, Leino M, Koulu L, and Tuominen R
- Subjects
- Adult, Costs and Cost Analysis, Employment economics, Female, Humans, Male, Middle Aged, Presenteeism economics, Surveys and Questionnaires, Absenteeism, Psoriasis economics, Sick Leave economics
- Abstract
Background: In previous studies, productivity losses have been measured specifically due to psoriasis or generally due to health problems in psoriasis patients. There is no information on the proportion of health related productivity losses that are due to psoriasis. The aim of this study was to estimate the proportion of productivity losses due to psoriasis and due to other medical problems among employed psoriasis patients., Methods: Patients visiting a tertiary level dermatological clinic during a one-year period due to psoriasis or psoriasis arthritis, who were employed, were selected to the study. A questionnaire was used to assess productivity losses during the previous month., Results: Psoriasis accounted for 38% of the total lost productivity costs. One fifth of patients had been on sick leave (absenteeism) due to psoriasis and a third of patients worked despite being sick with psoriasis (presenteeism). Men had higher costs of presenteeism, but the costs of absenteeism due to psoriasis were lower for men than for women., Conclusions: Productivity losses should be assessed disease specifically to avoid overestimations of the role of the disease on indirect costs. Our study shows that about a third of the lost productivity costs are due to psoriasis.
- Published
- 2015
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32. Treatment costs of psoriasis in a tertiary-level clinic.
- Author
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Mustonen A, Leino M, Mattila K, Koulu L, and Tuominen R
- Subjects
- Female, Hospitalization economics, Humans, Linear Models, Male, Medical Records, Middle Aged, Psoriasis therapy, Tertiary Care Centers, Health Expenditures, Phototherapy economics, Psoriasis economics
- Abstract
Background: The costs of psoriasis to a tertiary-level clinic vary considerably depending on the country of study and methods used. Hospitalisation and phototherapy have been significant cost components. This study was performed to estimate the distribution and relative magnitude of the costs of psoriasis to a tertiary-level clinic., Methods: Based on 233 patients, outpatient and phototherapy visits and the days hospitalised were collected from the treatment provider's records. The visit costs represented true costs, used to charge the final payers. Patients were analysed according to their treatment modalities., Results: On average, hospitalised patients (3.4%) had 31-fold higher total costs than non-hospitalised patients (p < 0.0001). The costs of hospitalisations formed 45% of all the treatment costs to the entire study population. Phototherapy accumulated 19% of the overall treatment costs. Patients receiving biological drugs or both phototherapy and traditional systemic therapy had the highest costs of treatment., Conclusions: The current study indicates that a small percentage of all psoriasis patients generate a large proportion of the overall costs to a tertiary-level hospital. Treatment modality has a significant effect on the costs to a tertiary-level hospital.
- Published
- 2014
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33. Perceived impact of psoriasis on leisure-time activities.
- Author
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Leino M, Mustonen A, Mattila K, Koulu L, and Tuominen R
- Subjects
- Cross-Sectional Studies, Female, Humans, Male, Middle Aged, Surveys and Questionnaires, Attitude to Health, Leisure Activities, Psoriasis psychology
- Abstract
Background: Psoriasis has an influence on various aspects of patients' everyday life. When estimating the total burden of the disease, the influence on leisure-time should also be taken into account., Objectives: To evaluate the perceived impact of psoriasis on leisure-time activities., Material and Methods: The questionnaire study was based on 262 patients with psoriasis. The patients were asked to list their leisure-time activities, any activities they had reduced or given up completely because of psoriasis, the time spent on current leisure-time activities and the time they would have spent in a hypothetical situation if they did not have psoriasis. Using a visual analogue scale (VAS) of 0-100, the patients assessed how well they could currently perform their leisure-time activities and how well in a hypothetical situation without psoriasis. The difference between the VAS scores depicted the level of disadvantage caused by psoriasis., Results: More than half the patients (51.9%) had reduced or completely given up at least one leisure-time activity. The disadvantage score (VAS) of psoriasis was 16.9. Younger age was associated with higher disadvantage (r = 0.154, p<0.05). Sports activities were completely given up by 30.2% and reduced by 23.7%. Social activities and those which could be expected to cause embarrassment were given up by 29.0% and reduced by 21.4% of the patients., Conclusion: A majority of patients with psoriasis reduce or give up leisure-time activities because of their condition, so the influence of psoriasis on leisure-time is considerable.
- Published
- 2014
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34. [UV radiation, tanning and DNA damage].
- Author
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Koulu L
- Subjects
- Humans, Risk Factors, DNA Damage, Skin Neoplasms etiology, Sunbathing injuries, Ultraviolet Rays adverse effects
- Abstract
Excessive exposure to UV radiation is the most significant known risk factor for skin cancer. Solarium devices produce UVA radiation that is 5 to 10 times stronger than that produced by the sun. All wavelengths of UV radiation cause DNA damage to skin cells and cause tanning. Tanning protects skin cells from further damage. The DNA damages caused by UVA and UVB radiation, however, differ from each other. The protective capacity of tanning caused by UVA radiation seems to be lower than that caused by UVB radiation.
- Published
- 2014
35. The costs of psoriasis medications.
- Author
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Mustonen A, Mattila K, Leino M, Koulu L, and Tuominen R
- Abstract
Introduction: Psoriasis is a chronic disease, which contributes to the economic burden on health care. The distribution of psoriasis medication costs and the quality of life in these patients has been estimated to be around 20% of total costs., Objectives: To estimate the economic distribution of medications and the impact of multiple treatment options on a patient's quality of life., Materials and Methods: The study was based on 236 Finnish psoriasis patients. The Finnish Social Insurance Institution had databases for all psoriasis related medications purchased. Each purchase, during the 1-year study period (1 October 2009-30 September 2010), was recorded and analyzed. The dermatological quality-of-life index was collected from the medical records., Results: Total medication costs were
1,083 per year per patient. Topical treatments were the most often purchased medication and they comprised 18% of the total medication costs. Ten percent of the patients needed 3 or more medication changes during the 1-year study period. Biologics were used only by 5% of patients, but they produced 67% of total medication costs. Patients needing various treatments had higher medication costs and a poorer quality of life., Conclusion: A small number of patients generated a great sum of medication costs partly due to the need to change medications. These patients had the worst quality-of-life index scores. Biologics formed a major cost component. - Published
- 2013
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36. Black currant seed oil supplementation of mothers enhances IFN-γ and suppresses IL-4 production in breast milk.
- Author
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Linnamaa P, Nieminen K, Koulu L, Tuomasjukka S, Kallio H, Yang B, Tahvonen R, and Savolainen J
- Subjects
- Breast Feeding, Dermatitis, Atopic immunology, Dietary Supplements, Female, Finland, Follow-Up Studies, Gene Expression Regulation drug effects, Gene Expression Regulation immunology, Humans, Infant, Infant, Newborn, Interferon-gamma genetics, Interferon-gamma immunology, Interleukin-4 genetics, Interleukin-4 immunology, Milk, Human immunology, Mothers, Plant Oils administration & dosage, Pregnancy, Ribes, Seeds, Th1-Th2 Balance drug effects, Dermatitis, Atopic therapy, Diet Therapy, Interferon-gamma metabolism, Interleukin-4 metabolism, Milk, Human metabolism
- Abstract
Background: The first year of infancy is crucial for the development of atopic immune response. Inadequate early Th1 and Treg responses and increased production of Th2 cytokines are associated with atopy. Breast milk contains several immunomodulatory cytokines and other factors that might influence the maturation of the infant's immune system. We assessed the cytokines in breast milk of mother of newborn infants and their associations with black currant seed oil (BCSO) supplementation during pregnancy, mother's atopic status and the development of infant's atopic dermatitis., Methods: Mothers and infants from an intervention study by black currant seed oil (n = 31) or olive oil as placebo (n = 30) were included in the study. Breast milk samples were collected during the first 3 months of breastfeeding. Breast milk levels of IL-4, IL-5, IL-10, IL-12, IFN-γ and TNF were measured by Luminex technology., Results: BCSO intervention group had decreased level of IL-4 (p = 0.044) and elevated level of IFN-γ (p = 0.014) in breast milk as compared to olive oil group. No significant differences were observed in IL-5, IL-10, IL-12 and TNF levels between the BCSO and olive oil groups. Mothers who had atopic dermatitis had significantly decreased levels of IL-10 (p = 0.044) in breast milk. Breast milk of the mothers of the children who developed atopic dermatitis had lower levels of IFN-γ (p = 0.039) as compared to the breast milk of the mothers of the children without dermatitis., Conclusion: Dietary intervention with BCSO had immunomodulatory effects on breast milk cytokine production towards Th2 to Th1 immunodeviation., (© 2013 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.)
- Published
- 2013
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37. Influence of psoriasis on work.
- Author
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Mattila K, Leino M, Mustonen A, Koulu L, and Tuominen R
- Subjects
- Adult, Aged, Female, Finland, Humans, Male, Middle Aged, Occupations, Retirement, Sick Leave, Surveys and Questionnaires, Work, Absenteeism, Efficiency, Employment, Psoriasis economics
- Abstract
Background: Previous research indicates that psoriasis has an impact on early retirement, sick leave days and reduced work performance., Objectives: To evaluate the disadvantages at work caused by psoriasis., Material and Methods: The sample was based on patients visiting the dermatology outpatient clinic in Turku University Hospital. 262 returned a mailed questionnaire. The subjects were asked how many hours they were on a sick leave (absenteeism) and working while sick (presenteeism) due to psoriasis and other health reasons., Results: Of the retired, 17.0% felt they were retired due to psoriasis. Those in the active work force reported on average 4.5 hours absenteeism and 8.3 hours of presenteeism due to psoriasis during the last 4 weeks. Psoriasis caused 27.0% of the total absenteeism and 39.0% of presenteeism. More than a quarter (28.9%) had been forced to modify their work due to psoriasis, most frequently to make the work less irritating for the skin., Conclusion: Psoriasis has a negative effect on patients' work in many ways, causing early retirement from work, sick leave days, change of occupation and work modifications.
- Published
- 2013
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38. Cutaneous lupus erythematosus after treatment with paclitaxel and bevacizumab for metastatic breast cancer: a case report.
- Author
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Vihinen P, Paija O, Kivisaari A, Koulu L, and Aho H
- Abstract
Introduction: The monoclonal anti-vascular endothelial growth factor antibody bevacizumab is increasingly used in the treatment of several malignant tumors. The usual side effects of this drug are hypertension and proteinuria. Paclitaxel is widely used in the treatment of breast cancer and head and neck carcinomas. Neither of these two drugs typically causes skin disorders. Paclitaxel-related cutaneous lupus erythematosus has been described before, but in earlier cases patients had a history of autoimmune disease., Case Presentation: We report a case of a 65-year-old Caucasian woman who presented with cutaneous lupus erythematosus after receiving paclitaxel-bevacizumab combination treatment as first-line therapy for metastatic breast cancer. Her cutaneous symptoms and increased serum anti-SSA and anti-SSB antibodies disappeared shortly after the discontinuation of therapy., Conclusion: We conclude that cutaneous lupus erythematosus can also be seen in patients without earlier anamnesis of autoimmune disorders and that, furthermore, bevacizumab might cause atypical cutaneous side effects.
- Published
- 2011
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39. [How is hyposensitization executed?].
- Author
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Pallasaho P, Pelkonen A, Numminen J, Koulu L, and Valovirta E
- Subjects
- Humans, Immunoglobulin E immunology, Skin Tests, Allergens immunology, Desensitization, Immunologic methods, Hypersensitivity therapy
- Abstract
Hyposensitization alleviates the symptoms of allergic rhinitis, eye symptoms and asthma by attenuating the underlying allergic inflammation. In the treatment of hymenoptera allergy, hyposensitization may be life-saving. The need for anti-allergic medication decreases markedly with successful hyposensitization. The decision about the initiation of hyposensitization is made by a doctor specialized in allergies together with the patient. Before the treatment decision, the IgE-mediated nature of the allergic symptoms is confirmed by skin-prick or blood tests. With the development of new sublingual hyposensitizations the availability of hyposensitization will improve and its application become more common.
- Published
- 2011
40. [Treatment of skin psoriasis].
- Author
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Koulu L
- Subjects
- Arthritis, Psoriatic therapy, Health Status, Humans, Psoriasis therapy
- Abstract
Partly similar inflammatory mediators are functioning in the disease process of psoriasis and its associated diseases. An overall improvement in patient's health status is likely to result in a better control of the comorbidities as well. Arthropathic psoriasis should be suspected, if arthritis and psoriasis occur simultaneously. Dermatitis can be only rarely rendered symptomless. Skin psoriasis with mild symptoms requires no treatment, provided that it doesn't disturb the patient. Most patients will manage moderately with topical therapy. Internal treatment of skin psoriasis will be initiated and monitored by a specialized dermatologist.
- Published
- 2010
41. [Nevi, sun and the risk of melanoma].
- Author
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Snellman E, Koulu L, and Rantanen T
- Subjects
- Dysplastic Nevus Syndrome complications, Dysplastic Nevus Syndrome pathology, Humans, Melanoma etiology, Nevus pathology, Nevus, Pigmented complications, Nevus, Pigmented pathology, Patient Education as Topic, Prognosis, Risk Factors, Skin Neoplasms etiology, Sunburn prevention & control, Ultraviolet Rays adverse effects, Melanoma diagnosis, Melanoma prevention & control, Nevus complications, Skin Neoplasms diagnosis, Skin Neoplasms prevention & control, Sunburn complications
- Published
- 2002
42. [Atopic eczema--an allergy or not?].
- Author
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Kalimo K, Turjanmaa K, and Koulu L
- Subjects
- Dermatitis, Atopic genetics, Dermatitis, Atopic pathology, Humans, Risk Factors, Skin pathology, Dermatitis, Atopic immunology
- Published
- 2001
43. Ultraviolet-B-induced apoptosis and cytokine release in xeroderma pigmentosum keratinocytes.
- Author
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Petit-Frère C, Capulas E, Lowe JE, Koulu L, Marttila RJ, Jaspers NG, Clingen PH, Green MH, and Arlett CF
- Subjects
- Apoptosis radiation effects, Cells, Cultured, Cytokines metabolism, Enzyme-Linked Immunosorbent Assay, Fibroblasts radiation effects, Humans, In Situ Nick-End Labeling, Infant, Newborn, Interleukin-6 metabolism, Keratinocytes radiation effects, Male, Tumor Necrosis Factor-alpha metabolism, Keratinocytes cytology, Ultraviolet Rays, Xeroderma Pigmentosum pathology
- Abstract
We have assessed the ability of xeroderma pigmentosum and normal keratinocytes grown out from skin biopsies to undergo apoptosis after irradiation with ultraviolet B. Keratinocytes have been studied from xeroderma pigmentosum complementation groups A (three biopsies), C (three biopsies), D (one biopsy), xeroderma pigmentosum variant (two biopsies), and Cockayne syndrome (one biopsy). The three xeroderma pigmentosum group A and the xeroderma pigmentosum group D samples were at least six times more sensitive than normal cells to ultraviolet B-induced apoptosis. The xeroderma pigmentosum variant samples showed intermediate susceptibility. Xeroderma pigmentosum group C samples proved heterogeneous: one showed high sensitivity to apoptosis, whereas two showed near normal susceptibility. The Cockayne syndrome sample showed the high susceptibility of xeroderma pigmentosum groups A and D only at a higher fluence. These results suggest that the relationships between repair deficiency, apoptosis, and susceptibility to skin cancer are not straightforward. Ultraviolet B-induced skin cancer is also thought to be due in part to ultraviolet B-induced impairment of immune responses. The release of the inflammatory cytokines interleukin-6 and tumor necrosis factor-alpha from cultured xeroderma pigmentosum keratinocytes tended to occur at lower fluences than in normals, but was less extensive, and was more readily inhibited at higher fluences of ultraviolet B.
- Published
- 2000
- Full Text
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44. Systemic suppression of human peripheral blood phagocytic leukocytes after whole-body UVB irradiation.
- Author
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Leino L, Saarinen K, Kivistö K, Koulu L, Jansen CT, and Punnonen K
- Subjects
- Adult, Cell Adhesion immunology, Cell Adhesion radiation effects, Female, Hematopoietic Stem Cells radiation effects, Humans, Interleukin-10 pharmacology, Macrophage-1 Antigen biosynthesis, Male, Neutrophils immunology, Phagocytosis immunology, Phagocytosis radiation effects, Receptors, Complement 3b biosynthesis, Receptors, IgG biosynthesis, Recombinant Proteins pharmacology, Immunosuppression Therapy adverse effects, Neutrophils radiation effects, Ultraviolet Rays adverse effects, Whole-Body Irradiation adverse effects
- Abstract
We examined systemic effects of whole-body UVB irradiation on human peripheral blood phagocytes. We found that 24 h after a single erythemal dose of UVB radiation two phagocyte functions, adhesion and phagocytosis, were reduced by 50%. This functional suppression was accompanied by a significant decrease in the expression of complement receptors (CR1 and CR3) and IgG Fc receptors (FcRII and FcRIII). The greatest reduction (47%) was observed in CR3, which is important for both adhesion and phagocytosis. A kinetic analysis showed that both CR1 and CR3 levels started to decrease 15 min after the UVB exposure, reaching the lowest levels at 4.5- and 24-h time points, respectively. The down-modulation of CRs after whole-body UVB exposure was not due to a defective receptor synthesis or translocation from internal stores to plasma membrane because the maximal CR levels in stimulated cells were not affected by UVB. No change in the serum soluble ICAM-1 was detected after UVB, which rules out CD1 1b epitope masking by sICAM-1. UVB did not release low-receptor-density myeloid progenitor cells from storage pools into circulation. Interleukin 10, a mediator of UVB-induced immunosuppression, was unable to modulate CR expression in vitro. When seven suberythemal whole-body UVB exposures were given repeatedly within 2 weeks, a significant decrease in CR expression was seen, which was greatest after three irradiations. Our data suggest that an exposure to UVB has systemic effects in humans which, possibly due to the down-modulation of preexisting cell-surface receptors, suppress some important functions of circulating phagocytic cells.
- Published
- 1999
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45. Regulation of CD44v6-containing isoforms during proliferation of normal and malignant epithelial cells.
- Author
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Soukka T, Salmi M, Joensuu H, Häkkinen L, Sointu P, Koulu L, Kalimo K, Klemi P, Grénman R, and Jalkanen S
- Subjects
- Adult, Aged, Animals, Down-Regulation, Epithelium metabolism, Exons, Female, Fluorescent Antibody Technique, Indirect, Gene Expression Regulation, Neoplastic radiation effects, Humans, Hyaluronan Receptors immunology, Immunohistochemistry, Male, Mice, Mice, SCID, Middle Aged, Skin Diseases genetics, Skin Diseases metabolism, Tumor Cells, Cultured, Ultraviolet Rays, Up-Regulation, Carcinoma, Squamous Cell genetics, Carcinoma, Squamous Cell metabolism, Head and Neck Neoplasms genetics, Head and Neck Neoplasms metabolism, Hyaluronan Receptors genetics, Hyaluronan Receptors metabolism, Isomerism
- Abstract
CD44 is a family of molecules involved in cell-cell and cell-matrix interactions. Various isoforms of CD44 arise by insertion of one or more of the variant exons into the common backbone shared by all forms of CD44. In this work, we studied the expression of CD44 and exon v6-containing CD44 isoforms (CD44v6) in several nonmalignant and malignant conditions and the possibilities for regulating the expression of CD44v6. In primary squamocellular carcinomas of the head and neck, CD44 and CD44v6 were down-regulated in poorly differentiated tumors, whereas these molecules were uniformly expressed in the normal squamocellular epithelium, in proliferating skin diseases, and in nonmalignant tumors. When CD44v6 expression of original tumors and that of squamocellular carcinoma cell lines derived from them were compared, no CD44v6 up-regulation could be observed on in vitro growing cells. Moreover, several regulators were unable to up-regulate CD44v6 expression on cultured cell lines in vitro. When the same cell lines formed tumors after s.c. injection into severe combined immunodeficient mice, some of them up-regulated their CD44v6 expression. These data suggest that cell lines at certain differentiation stages can be induced to express CD44v6. Our results further indicate that CD44v6 positivity cannot be used as a universal indicator of tumor metastasis. Instead, the down-regulation of CD44v6 in squamocellular tumors is a sign of malignant transformation of the epithelium.
- Published
- 1997
46. Effect of psoriasis heliotherapy on epidermal urocanic acid isomer concentrations.
- Author
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Snellman E, Koulu L, Pasanen P, Lammintausta K, Neuvonen K, Ayräs P, and Jansén CT
- Subjects
- Adult, Follow-Up Studies, Humans, Middle Aged, Psoriasis metabolism, Skin metabolism, Urocanic Acid metabolism, Heliotherapy, Psoriasis therapy, Skin radiation effects, Urocanic Acid radiation effects
- Abstract
A noninvasive Finn Chamber sampling method and HPLC analysis were used to determine epidermal urocanic acid (UCA) concentrations of psoriasis patients during 4 weeks of heliotherapy on the Spanish Canary Islands and a follow-up period of 8 weeks. During heliotherapy the epidermal cis-UCA concentration increased from a mean initial value of 0.2 nmol/cm2 to a mean final value of 2.9 nmol/cm2. The total UCA concentration decreased during the first week of heliotherapy from an initial value of 5.5 nmol/cm2 to a nadir of 2.0 nmol/cm2. Thereafter, a steady increase was recorded in the total UCA level, with a maximum of 10.2 nmol/cm2 in week 2 of the post-treatment follow-up period. Suberythemal sun exposures caused near-maximal UCA isomerization, and during heliotherapy the cis isomer constituted 63.7-74.3% of the total UCA concentration. Clinical response of psoriasis to heliotherapy, however, seemed to be independent of UCA isomer levels.
- Published
- 1992
- Full Text
- View/download PDF
47. Effect of oral retinoid treatment on human natural killer cell activity.
- Author
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Jansén CT, Viander M, and Koulu L
- Subjects
- Administration, Oral, Adult, Aged, Etretinate administration & dosage, Female, Humans, Isotretinoin, Male, Middle Aged, Skin Diseases immunology, Stimulation, Chemical, Tretinoin administration & dosage, Etretinate therapeutic use, Killer Cells, Natural drug effects, Skin Diseases drug therapy, Tretinoin therapeutic use
- Abstract
Peripheral blood natural killer (NK) cell activity was screened in patients with non-malignant disorders of the skin who took oral etretinate or 13-cis-retinoic acid for up to 11 months. Compared to pretreatment values, the basic NK activity rose during the first 2 months of treatment, but thereafter returned to starting values. Interferon reactivity (IFN-alpha, IFN-gamma) was essentially unaltered by the treatment. It is concluded that moderate oral retinoid doses cause a mild, transient stimulation of this natural immune surveillance system in man.
- Published
- 1985
- Full Text
- View/download PDF
48. Antipsoriatic, erythematogenic, and Langerhans cell marker depleting effect of bath-psoralens plus ultraviolet A treatment. Comparison of 8-methoxypsoralen and trimethylpsoralen photosensitization.
- Author
-
Koulu LM and Jansén CT
- Subjects
- Adenosine Triphosphatases metabolism, Adolescent, Adult, Dose-Response Relationship, Drug, Erythema chemically induced, Female, HLA-DR Antigens analysis, Humans, Langerhans Cells immunology, Male, Methoxsalen therapeutic use, Middle Aged, Psoriasis pathology, Trioxsalen therapeutic use, Erythema pathology, Langerhans Cells enzymology, PUVA Therapy methods, Psoriasis drug therapy
- Abstract
Successful results have been reported for bath-psoralens plus ultraviolet A (PUVA) treatment of psoriasis with the use of either a low-sensitizing psoralen (methoxsalen) or a high-sensitizing psoralen (trioxsalen), but no evidence has been presented that phototoxicity would be a prerequisite for antipsoriatic activity of these treatments. To study therapeutic-to-phototoxic ratios, bath-PUVA was applied to psoriasis patients with the use of either a 0.2 mg/L solution of trioxsalen or a 0.4 mg/L solution of methoxsalen. The average minimal phototoxic ultraviolet A (UVA) dose (MPD) obtained after 15 minutes' bathing was 0.86 joule/cm2 for trioxsalen and 9.76 joules/cm2 for methoxsalen. In the first part of the study phototoxically equipotent treatment schedules were used, compensating the much lower phototoxic potential of methoxsalen by using about 10 times larger UVA doses compared to the doses used with trioxsalen. A healing rate of 71% +/- 25% was recorded for trioxsalen and 63% +/- 34% for methoxsalen treatment (mean +/- SD). Both PUVA treatments decreased epidermal Langerhans cell counts to 10% to 20% of the control value. In the second part of the study, the much lower phototoxic potential of methoxsalen was not compensated for. Instead, methoxsalen bath-PUVA was carried out with the use of UVA doses physically similar to those used in the trioxsalen therapy series. Surprisingly enough, even this very suberythemal methoxsalen therapy caused a significant healing effect (51% +/- 10%). Langerhans cell depletion in methoxsalen-bathed areas (reduction to 53% of the control value) was much less than that caused in trioxsalen-bathed areas (reduction to 11% of the control value).(ABSTRACT TRUNCATED AT 250 WORDS)
- Published
- 1988
- Full Text
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49. Effect of UVA and UVB irradiation on human epidermal Langerhans cell membrane markers defined by ATPase activity and monoclonal antibodies (OKT 6 and anti-Ia).
- Author
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Koulu L, Jansén CT, and Viander M
- Subjects
- Adult, Cell Count, Erythema etiology, Female, Humans, Langerhans Cells enzymology, Langerhans Cells immunology, Male, Adenosine Triphosphatases analysis, Antibodies, Monoclonal immunology, Histocompatibility Antigens Class II analysis, Langerhans Cells radiation effects, Ultraviolet Rays adverse effects
- Abstract
Healthy human volunteers were irradiated with graded doses of UVA and UVB radiation on the volar aspect of their forearms. The UVA doses ranged from 8 to 100 J/cm2, and the UVB doses from 37 to 416 mJ/cm2, corresponding to 5 to 52 mJ/cm2 of erythemally effective (300 nm) radiation (1/4-3 X MED). 7 days after irradiation, punch biopsy specimens were obtained from UVA and UVB irradiated spots. Epidermal sheets were stained for Langerhans cells (LC) using 3 different histochemical methods, viz: ATPase activity and immunoperoxidase staining with monoclonal antibodies against T6 and Ia antigens. A slightly higher control LC count was obtained with anti-T6 staining (848 cells/mm2) than with anti-Ia or ATPase staining (728 and 721 cells/mm2 respectively). No significant change in LC count was detected with any of the staining methods after UVA doses of up to 100 J/cm2. In contrast, UVB irradiation caused a dose-dependent decrease in the LC counts. The decrease was quite similar whether measured by anti-T6 or anti-Ia staining. With ATPase staining, the decrease in LC numbers was somewhat more pronounced at low to medium UVB doses, but at the dose of 416 mJ/cm2 (52 mJ of erythemally effective UVB, corresponding to approx. 3 X MED), the residual LC count as determined with any of the 3 histochemical methods was within the range of 23-30% of the control LC count. We conclude that the activity of the membrane-bound enzyme, ATPase, is more sensitive to abrogation by moderate UVB doses than the immunological reactivity of the 2 surface antigens, T6 and Ia.
- Published
- 1985
50. UV sensitivity of human keratinocyte and Langerhans cell-expressed HLA-DR antigens: a comparison.
- Author
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Koulu L and Jansén CT
- Subjects
- Adult, Epidermal Cells, Epidermis immunology, Female, Fluorescent Antibody Technique, Humans, Langerhans Cells immunology, Male, Pemphigus immunology, Epidermis radiation effects, HLA-D Antigens radiation effects, HLA-DR Antigens radiation effects, Keratins radiation effects, Langerhans Cells radiation effects, Ultraviolet Rays
- Abstract
HLA-DR expression on human keratinocytes (KC) was induced in vivo by intradermal injection of purified protein derivative of tuberculin (PPD). Neither preceding nor subsequent exposure of the PPD injection site to a dose of approximately 2 MED of UVB radiation abolished KC HLA-DR, though subsequent irradiation caused a slight diminution in the intensity of the antigen expression. By contrast, epidermal Langerhans cell (LC) HLA-DR and T6 expressions in normal epidermis were greatly reduced by an identical dose of UVB. Pemphigus antigen on the surface of KC was not affected by irradiation or PPD injection.
- Published
- 1987
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