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19 results on '"Oyarzabal M."'

3. Calibrating APSIM for forage sorghum using remote sensing and field data under sub-optimal growth conditions

Author

Della Nave, F., Ojeda, J. J., Irisarri, G. J. N., Pembleton, K., Oyarzabal, M., and Oesterheld, M.

Subjects
Crop modelling, Inter-annual biomass variability, Animal Science and Zoology, Remote sensing, Sentinel-2, Agronomy and Crop Science, Sorghum bicolor (L.) Moench, APSIM next generation
Abstract

CONTEXT Mechanistic sorghum models have been mostly used to estimate sorghum yield for grain sorghum for a range of genotype, management, and environmental conditions. There is a lack of model testing for crop growth and development responses for forage genotypes and information for phenological parameterization under sub-optimal water and nitrogen stress conditions in forage systems. OBJECTIVE The aims of this study were to (i) use NDVI to parametrize APSIM model to estimate forage sorghum phenology, (ii) calibrate APSIM to simulate green cover, intercepted solar radiation and aboveground biomass, and (iii) quantify the variance of inter-annual aboveground biomass and the effect of water availability on forage sorghum biomass under sub-optimal environment × management combinations. METHODS We used climate, soil, management records and sorghum crop observations collected from farm and field experiments in Argentina and Australia. NDVI values were gathered from Sentinel-2 and a handheld optical sensor and then related to fAPAR measurements. Phenological stages were derived from fAPAR seasonal dynamics and implemented as input in the APSIM calibration. Finally, we assessed the temporal AGB variability through long-term simulations analysis. RESULTS AND CONCLUSIONS NDVI seasonal dynamics accurately represented the fraction of the absorbed photosynthetically active radiation (R2=0.92) and then, the remote-sensing parametrized APSIM model satisfactorily simulated crop phenology (CCC=0.75-0.92, NRMSE=9-22%). The model was also able to satisfactorily simulate crop growth (CCC=0.89 and NRMSE=24.8% for green cover; CCC=0.81 and NRMSE=34.6% for intercepted solar radiation; CCC=0.91 and NRMSE=37% for aboveground biomass). APSIM simulations during 22 years across 5 contrasting locations showed high inter-annual variability of aboveground biomass (CV=47%), mainly driven by inter-annual variation of soil water availability (CV=20%). Our study demonstrated that (i) remote sensing data was a reliable source for APSIM phenology parametrization, (ii) the model was able to satisfactorily simulate crop growth and development of forage sorghum under sub-optimal conditions across several genotype × environment × management combinations and (iii) water availability was the main driver of aboveground biomass inter-annual variance. SIGNIFICANCE Given the pressure of the global human population to satisfy an increasing demand for food, our results provide a new path for the combined use of remote sensing and mechanistic modelling to improve forage sorghum biomass estimations in marginal environments.

Published
2022
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4. The comparative responsiveness of Hospital Universitario Princesa Index and other composite indices for assessing rheumatoid arthritis activity

Author

Gonzalez-Alvaro, Isidoro, Castrejon, Isabel, Carmona, Loreto, Dougados, M., Huizinga, T., Abu Shakra, M., Alberts, A., Alperi Lopez, M., Amital, H., Aringer, M., Aslanidis, S., Berenbaum, F., Bijlsma, H., Blanco Garcia, F. J., Bliddal, H., Borofsky, M., Brocq, O., Buldakov, S., Cantini, F., Carreno Perez, L., Chahade, W., Ciconelli, R., Codreanu, C., Dahlqvist, S. R., Damjanov, N., Diamantopoulos, A., Dimdina, L., Dimic, A., Dorokhov, A., Dubikov, A., Fadienko, G., Fano, N., Ferreira, G., Gabrielli, A., Gaffney, K., Gaudin, P., Gerlag, D. M., Gerli, R., Goncalves, C. R., Hansen, M. S., Hanvivadhanakul, P., Hoili, C., Hou, A., Hunter, J., Ilic, T., Ionescu, R., Kaine, J., Kakurina, N., Kamalova, R., Kelly, T., Knyazeva, L., Krumina, L., Kurthen, R., Lagrone, R. P., Lapadula, G., Lavrentjevs, V, Lawson, J. G., Lazic, Z., Lejnieks, A., Levy, Y., Lexberg, A., Mader, R., Mariette, X., Markovits, D., Mola, Martin E., Maugars, Y., Guarch, Maymo J., Mazurov, V., I, Mikkelsen, K., Vergles, Morovic J., Nabizadeh, S., Nanagara, R., Nasonov, E. L., Sarabia, Navarro F., Neumann, T., Novak, S., Olech, E., Oza, M., Paran, D., Parsik, E., Pegram, S., Suarez, Pombo M., Popova, T., Puechal, X., Raja, N., Ridley, D., Rosner, I, Rubbert-Roth, A., Rudin, A., Saraux, A., Saulite-Kandevica, D., Settas, L., Sfikakis, P., Sheeran, T., Sizikov, A., Stamenkovic, D., Stefanovic, D., Stolow, J. B., Tan, A. L., Tebib, J., Tishler, M., Tony, H. P., Troum, O. M., Uaratanawong, S., Ucar Angulo, E., Valenzuela, G., van der Laken, K., Van Laar, J., van Riel, P. L. C. M., Vasilopoulos, D., Veldi, T., Vinogradova, I, Vosse, D., Wassenberg, S., Weidmann, C., Weitz, M., Wollenhaupt, J., Xavier, R., Yakupova, S., Zagar, I, Zavgorodnaja, T., Zemerova, E., Zisman, D., Zonova, E., Camona, Loreto, Abasolo Alcazar, L., Alegre de Miguel, C., Andreu Sanchez, J. L., Aragon Diez, A., Balsa Criado, A., Batlle Gualda, E., Belmonte Serrano, M. A., Beltran Audera, J., Beltran Fabregat, J., Bonilla Hernan, G., Caro Fernandez, N., Casado, E., Cebrian Mendez, L., Corteguera Coro, M., Cuadra Diaz, J. L., Cuesta, E., Fiter Areste, J., Freire Gonzalez, M., Galindo Izquierdo, M., Garcia Meijide, J. A., Garcia Gomez, M. C., Gimenez Ubeda, E., Gomez Centeno, E., Gomez Vaquero, C., Gonzalez Fernandez, M. J., Gonzalez Gomez, M. L., Gonzalez Hernandez, T., Gonzalez-Alvaro, I, Gonzalez-Montagut Gomez, C., Grandal Delgado, Y., Gratacos Masmitja, J., Hernandez del Rio, A., Instxaurbe, A. R., Irigoyen Oyarzabal, M., V, Jimenez Palop, M., Juan Mas, A., Judez Navarro, E., Larrosa Padro, M., Lopez Longo, F. J., Loza Santamaria, E., Maese Manzano, J., Manero Ruiz, F. J., Mateo Bernardo, I, Mayordomo Gonzalez, L., Mazzucheli, R., Medrano San Idelfonso, M., Naranjo Hernandez, A., Pecondon Espanol, A., Peiro Callizo, E., Quiros Donate, J., Ramos Lopez, P., Rivera Redondo, J., Rodriguez Gomez, M., Rodriguez Lopez, M., Rosello Pardo, R., Sampedro Alvarez, J., Sanmarti Sala, R., Rey Rey, Santos J., Tena Marsa, X., Tenorio Martin, M., Torres Martin, M. C., Urena Garnica, I, Valdazo de Diego, J. P., Valls, M., Villaverde Garcia, V., Zarco Montejo, P., Zubieta Tabernero, J., Balsa, Alejandro, Sanmarti, Raimon, Cabezas, J. A., Cantalejo, M., Chamizo, E., Ciruelo, E., Corrales, A., Cruz, A., Diaz, C., Fiter, J., Freire, M. M., Galindo, M., Garcia de Vicuna, M. R., Gelman, S. M., Gonzalez Crespo, R., Gonzalez Fernandez, C., Gracia, A., Granados, J., Guzman, M. A., Irigoyen, M., V, Juan, A., Juanola, X., Laiz, A., Manero, F. J., Martinez, A., Martinez, F., Mata, C., Maymo, J., Navarro, F. J., Peiro, E., Perez, F., Perez, G., Perez, M., Pujol, M., Quiros, J., Ribas, B., Riera, M., Rivera, J., Rodriguez, J. M., Rosello, R., Tenorio, M., Toyos, F. J., ACT-RAY Study Grp, PROAR Study Grp, EMECAR Study Grp, Interne Geneeskunde, MUMC+: MA Reumatologie (9), and RS: CAPHRI - R3 - Functioning, Participating and Rehabilitation

Subjects
Male, medicine.medical_specialty, Science, humanos, Severity of Illness Index, RECOMMENDATIONS, VALIDATION, VARIABLES, ensayos clínicos como asunto, Arthritis, Rheumatoid, Cohort Studies, Internal medicine, Linear regression, Severity of illness, medicine, Humans, índice de gravedad de la enfermedad, estudios de cohortes, mediana edad, Clinical Trials as Topic, DISEASE-ACTIVITY MEASURES, Multidisciplinary, SCORES, business.industry, Arthritis, resultado del tratamiento, modelos lineales, Secondary data, Gold standard (test), Middle Aged, medicine.disease, Clinical trial, Treatment Outcome, Rheumatoid arthritis, Antirheumatic Agents, Cohort, Linear Models, Medicine, Female, GENDER, business, antirreumáticos, artritis, Cohort study
Abstract

Objective To evaluate the responsiveness in terms of correlation of the Hospital Universitario La Princesa Index (HUPI) comparatively to the traditional composite indices used to assess disease activity in rheumatoid arthritis (RA), and to compare the performance of HUPI-based response criteria with that of the EULAR response criteria. Methods Secondary data analysis from the following studies: ACT-RAY (clinical trial), PROAR (early RA cohort) and EMECAR (pre-biologic era long term RA cohort). Responsiveness was evaluated by: 1) comparing change from baseline (Delta) of HUPI with Delta in other scores by calculating correlation coefficients; 2) calculating standardised effect sizes. The accuracy of response by HUPI and by EULAR criteria was analyzed using linear regressions in which the dependent variable was change in global assessment by physician (Delta GDA-Phy). Results Delta HUPI correlation with change in all other indices ranged from 0.387 to 0.791); HUPI's standardized effect size was larger than those from the other indices in each database used. In ACT-RAY, depending on visit, between 65 and 80% of patients were equally classified by HUPI and EULAR response criteria. However, HUPI criteria were slightly more stringent, with higher percentage of patients classified as non-responder, especially at early visits. HUPI response criteria showed a slightly higher accuracy than EULAR response criteria when using Delta GDA-Phy as gold standard. Conclusion HUPI shows good responsiveness in terms of correlation in each studied scenario (clinical trial, early RA cohort, and established RA cohort). Response criteria by HUPI seem more stringent than EULAR's., Our study was supported by grants RD16/0012/0011 and PI14/00442 from the Ministerio de Economia y Competitividad (Instituto de Salud Carlos III; Spain) and cofunded by the Fondo Europeo de Desarrollo Regional (FEDER). Data from ACT-RAY clinical trial were kindly provided by Hoffmann-La Roche Ltd. No financial support was received from Hoffmann-La Roche Ltd Data from EMECAR and PROAR cohorts were provided by the Spanish Society of Rheumatology. No financial support was received from the Spanish Society of Rheumatology. None of these institutions played any role in the analysis or interpretation of data, nor were they involved in the writing of the manuscript. Roche and Sociedad Espanola de Reumatologia were involved in the collection of data from ACT-RAY, and EMECAR and PROAR, respectively. However, these funders had no role in study design, analysis, decision to publish, or preparation of the manuscript.

Published
2019

5. Effect of hydrolyzed infant formula vs conventional formula on risk of type 1 diabetes the TRIGR randomized clinical trial

Author

Knip M., Akerblom H. K., Altaji E., Becker D., Bruining J., Castano L., Danne T., De Beaufort C., Dosch H. -M., Dupre J., Fraser W. D., Howard N., Ilonen J., Konrad D., Kordonouri O., Krischer J. P., Lawson M. L., Ludvigsson J., Madacsy L., Mahon J. L., Ormisson A., Palmer J. P., Pozzilli P., Savilahti E., Serrano-Rios M., Songini M., Taback S., Vaarala O., White N. H., Virtanen S. M., Wasikowa R., Mandrup-Poulsen T., Arjas E., Lernmark A., Laara E., Schmidt B., Hyytinen M., Koski K., Koski M., Merentie K., Pajakkala E., Reunanen A., Salonen M., Terhonen T., Virkkunen S., Cuthbertson D., Gainer B., Hadley D., Malloy J., Nallamshetty L., Shanker L., Bradley B., Lough G., Fraser W., Sermer M., Taback S. P., Franciscus M., Nucci A., Palmer J., Alahuhta K., Barlund S., Korhonen T., Kovanen L., Lehtonen E., Niinisto S., Pekkala M., Sorkio S., Toivanen L., Vahatalo L., Uusitalo U., Ohman T., Bongiorno R., Catteau J., Fraser G., Lloyd M., Crock P., Giles M., Siech K., See D. W., Brown C., Craig M., Johnston A., Bere L. J., Clarson C. L., Jenner M., McManus R., Renato N., Lovell M., Higo D., Kent N., Kwan J., Marshall C., Metzger D., Chanoine J. -P., Stewart L., Thompson D., Edwards A., Lange I., Mercer J., Pacaud D., Josephine H., Schwarz W., Stephure D. K., Boer J., Chatur T., Chick C., Couch B., Demianczuk N., Girgis R., Marks S., Ryan E., Thompson M., Dean H. J., Grant L., Hamelin K., LaForte J., Murphy L., Catte D., Schneider C., Sellers E. A. C., Woo V., Boland A., Clark H. D., Cooper T., Gruslin A., Karovitch A., Keely E., Malcolm J. C., Sauro V., Tawagi G. F., Andrighetti S., Arnold G., Barrett J., Blumer I., Daneman D., Donat D., Ehrlich R., Feig D., Gottesman I., Gysler M., Karkanis S., Kenshole A., Knight B., Lackie E., Lewis V., Martin M. J., Maxwell C., Oliver G., Panchum P., Shilletto N., Simone A., Skidmore M., Turrini T., Wong S., Allen C., Belanger L., Bouchard I., Ferland S., Frenette L., Garrido-Russo M., Leblanc M., Imbeault J., Morin V., Olivier G., Weisnagell J., Costain G., Dornan J., Heath K., MacSween M. -C., McGibbon A., Ramsay C., Sanderson F., Sanderson S., Benabdesselam L., Gonthier M., Huot C., Thibeault M., Laforte D., Legault L., Perron P., Armson A., Canning P., Cummings E. A., Ivanko V., McLeod L., Mokashi A., Scott K., Bridger T., Crane J., Crummell C., Curtis J. C., Dawson C., Joyce C., Newhook L. A., Newman S., Druken E., Begum-Hasan J., Breen A., Houlden R., Woods M., Carrson G., Kelly S., Martel M. J., Penner M., Sankaran K., Hardy-Brown K., King N., White R. A., Park M., Popkin J., Robson L., Coles K., Al Taji E., Cerna M., Cerny M., Francova H., Hainerova I., Kothankova H., Koukalova R., Krakorova V., Mendlova P., Sitova R., Stechova K., Vavrinec J., Vosahlo J., Zlatohlavkova B., Brazdova L., Faksova P., Gregorova D., Kantor L., Malkova K., Venhacova J., Venhacova P., Cipra A., Skvor J., Budejovice C., Tomsikova Z., Botkova-Krauseova H., Mockova A., Paterova P., Gogelova P., Kandrnalova J., Einberg U., Jakovlev U., Posiadlo S., Rannaste E., Raukas R., Riikjarv M. -A., Valla K., Astover V., Kirss A., Retpap J., Taht E., Tillmann V., Vahtra S., Heikkila M., Hirvasniemi M., Luopajarvi K., Johansson S., Kleemola P., Laukkanen E., Parkkola A., Pigg H. -M., Puttonen H., Renlund M., Salonen K., Suomalainen H., Tenkula T., Teramo K., Jarvenpaa A. -L., Hamalainen A. -M., Jussila R., Kiiveri S., Haavisto H., Holopainen S., Kupiainen H., Leeve T., Lumme K., Nironen T., Tenhola S., Tiilikainen T., Keinonen H., Lautala P., Salonen P., Vesanto M., Aspholm A. S., Asunta P., Ikavalko H., Jason E., Jaminki S., Kekki P., Koskinen M., Lehtimaki S., Lahde J., Makela M., Peltoniemi S., Poutiainen L., Ranta K., Salonsaari T., Sarviharju-Tujula S. -L., Selvenius J., Siljander H., Haanpaa P. -L., Holm C., Juutilainen A., Jarvelainen V., Kangaskolkka-Keskilohko A. -M., Laino E., Marjamaki L., Suominen E., Ylitalo S., Hokkanen M., Lounamaa R., Matikainen M., Nuuja A., Paalanen I., Puupponen A. R., Salo-Edwards H., Alanne S., Kultti T., Linjama H., Muhonen K., Vaaraniemi M., Talvitie T., Backman M., Hanhijarvi R., Koivula P., Lindstrom K., Martikainen A., Nurmi P., Bjork A., Huopio H., Komulainen J., Lehtomaki S., Muikku E., Pesola J., Sankilampi U., Arkkola T., Hekkala A., Jurvakainen S., Koivikko M. -L., Kahonen M., Leinonen E., Mykkanen T., Pohjola H., Riikonen K., Niittyvuopio A., Stenius A., Tapanainen P., Veijola R., Alar A., Jovio S., Korpela P., Makinen E., Hietanen L., Kivisto J., Kaar M. -L., Lehtimaki P., Mustila T., Popov E., Saatela S., Taittonen L., Ahtiainen K., Laaksonen N., Luoto M., Viitala J., Virransalo R., Nykanen P., Paajanen S., Parkkinen S., Pyrhonen H., Sarkka T., Aschemeier B., Bektas S., Biester T., Datz N., Deiss D., Fath M., Lupke K., Muller B., Nestoris C., Rothes S., Sadeghian E., Semler K., Arato A., Krikovszky D., Nobilis A., Szenasi J., Benevento D., Anguissola G. B., Biagioni M., Bizzarri C., Cherubini V., Ferrito L., Giordano C., Giorgetti C., Khazrai Y. M., Kyanvash S., Maddaloni E., Napoli A., Piergiovanni F., Pitocco D., Suraci T., Tabacco G., Valente L., Visalli N., Carboni M. B., Cavallo R., Cau V., Isola C., Ledda A., Loddo M., Mannu C., Pettinau M., Pisano S., Porceddu M., Putzu C., Rita A., Peters D., Schierloh U., Bisschoff M., Blonk L., Lappenschaar T., Manai B., Seesink M., Sperling-Conrad M., Verhagen M., Zoethout J. A., Basiak A., Chalas M., Chesiak M., Gramza A., Iwankiewicz J., Sieradzan E., Wikiera B., Ciechanowska M., Dziatkowiak H., Futona B., Gorska A., Glowacka-Wony M., Kaim I., Klich B., Starzyk J., Wolanin M., Tokarska L., Chucherco D., Deja G., Firek-Pedras M., Jarosz-Chobot P., Kalina M., Kutrowska-Adamusiak K., Minkina-Pedras M., Muchaka-Bianga M., Bodalski J., Mlynarski W., Szadkowska A., Cieslak A., Cypryk K., Dziatosz K., Jastzebowska J., Krysiak A., Szymanska U., Wilcznski J., Zawodniak-Szalapska M., Aguay A., Bilbao J. R., Chueca M., Cortazar A., Echarte G., Frutos T. G., Jimenez P., Martul P., Moreno A., Oyarzabal M., Rica I., Salgado Y., Martinez-Larrad M. T., Hawkins F. G., Hernandez R., Herranz L., Pallardo L. F., Deibarra L. S., Fernandez B. H., Luis J. L., Ortiz-Quintana L., Recarte P. P., Arnau D. R., Aronsson L., Boden S., Fredriksson J., Isacsson E., Johansson I., Karlsson E., Lock C., Sandstrom A. -M., Konefal M. S., Andreasson C., Dahlstrom U., Hanas R., Lundqvist K., Windell L., Jansson I., Karlsson A. -K., Lindbladh B., Odenman I., Pettersson C., Sundberg F., Sundqvist M., Aronsson S., Bellman I., Bengtsson A. -B., Lyden G. -B., Nilsson N. -O., Soderblom M., Unt C., Augustsson M., Bengtsson M., Fors H., Helmrich A., Johansson T. O., Andersson A. -C., Boiard-Stomlid A., Hellgren G., Kallsholm H., Lindqvist J., Nilsson M., Nordwall M., Stromstedt C., Ahsberg C., Lindh A., Lindhe C., Samuelsson C., Wiik A., Edenwall H., Ljumgcrantz M., Persson I. -B., Strigard E., Svensson B. -L., Aman J., Breivik G. -E., Detlofsson I. -L., Kroon M., Sarnblad S., Johansson C., Ilvered R., Lundberg A., Akesson K., Beccarelli A., Gadient M., Rappold-Amrein C., Schoenle E., Daftary A., Damagro-Elias M. E., Gilmour C., Klein M. B., Lain C., Salerno D., Smith M. E., Vats K., Pfaff D. J., Malone P., Mansfield P., Munns M., Nickel K., Pompilio K., Siemion W., Taculad R., Van Horn K., Zdanadewic M., Chambliss C., Jones J., Sadler M., Tanner-Blasiar M., Bell C., Camper N., Devaskar S., Devaskar U., Horowitz H., Rogers L., Shannahan R., Silk K., Bermudez Z., Colon R., Frazer T., Martinez-Nieves B., Torres J., Vega J., Chan M., Cook S., Goland R., Greenberg E., Jules N., Montes J., Nelson M., Parra-Valencia Z., Schachner H., Softness B., Kiviniemi M., Suomenin R., Alexander A., Hyrckowian E., Nichol L., Trucco M., Karjalainen E., Louhio T., Sarnesto A., Valtonen E., Davydova B., Helander S., Hamalainen J., Harkonen T., Joutsjoki L., Kararic M., Latva-Koivisto M., Lonn E., Nurmi T., Ollila I., Rinkinen J., Ronkainen M., Tukiainen H., Cederlof A., Kiikeri M., Tsupari S., Cheng R., Bryant K., Chan Y., Maezawa Y., Paltser G., Rasavi R., Tsui H., Winer S., Wu P., Yantha J., Pediatrics, Knip M., Akerblom H.K., Altaji E., Becker D., Bruining J., Castano L., Danne T., De Beaufort C., Dosch H.-M., Dupre J., Fraser W.D., Howard N., Ilonen J., Konrad D., Kordonouri O., Krischer J.P., Lawson M.L., Ludvigsson J., Madacsy L., Mahon J.L., Ormisson A., Palmer J.P., Pozzilli P., Savilahti E., Serrano-Rios M., Songini M., Taback S., Vaarala O., White N.H., Virtanen S.M., Wasikowa R., Mandrup-Poulsen T., Arjas E., Lernmark A., Laara E., Schmidt B., Hyytinen M., Koski K., Koski M., Merentie K., Pajakkala E., Reunanen A., Salonen M., Terhonen T., Virkkunen S., Cuthbertson D., Gainer B., Hadley D., Malloy J., Nallamshetty L., Shanker L., Bradley B., Lough G., Fraser W., Sermer M., Taback S.P., Franciscus M., Nucci A., Palmer J., Alahuhta K., Barlund S., Korhonen T., Kovanen L., Lehtonen E., Niinisto S., Pekkala M., Sorkio S., Toivanen L., Vahatalo L., Uusitalo U., Ohman T., Bongiorno R., Catteau J., Fraser G., Lloyd M., Crock P., Giles M., Siech K., See D.W., Brown C., Craig M., Johnston A., Bere L.J., Clarson C.L., Jenner M., McManus R., Renato N., Lovell M., Higo D., Kent N., Kwan J., Marshall C., Metzger D., Chanoine J.-P., Stewart L., Thompson D., Edwards A., Lange I., Mercer J., Pacaud D., Josephine H., Schwarz W., Stephure D.K., Boer J., Chatur T., Chick C., Couch B., Demianczuk N., Girgis R., Marks S., Ryan E., Thompson M., Dean H.J., Grant L., Hamelin K., LaForte J., Murphy L., Catte D., Schneider C., Sellers E.A.C., Woo V., Boland A., Clark H.D., Cooper T., Gruslin A., Karovitch A., Keely E., Malcolm J.C., Sauro V., Tawagi G.F., Andrighetti S., Arnold G., Barrett J., Blumer I., Daneman D., Donat D., Ehrlich R., Feig D., Gottesman I., Gysler M., Karkanis S., Kenshole A., Knight B., Lackie E., Lewis V., Martin M.J., Maxwell C., Oliver G., Panchum P., Shilletto N., Simone A., Skidmore M., Turrini T., Wong S., Allen C., Belanger L., Bouchard I., Ferland S., Frenette L., Garrido-Russo M., Leblanc M., Imbeault J., Morin V., Olivier G., Weisnagell J., Costain G., Dornan J., Heath K., MacSween M.-C., McGibbon A., Ramsay C., Sanderson F., Sanderson S., Benabdesselam L., Gonthier M., Huot C., Thibeault M., Laforte D., Legault L., Perron P., Armson A., Canning P., Cummings E.A., Ivanko V., McLeod L., Mokashi A., Scott K., Bridger T., Crane J., Crummell C., Curtis J.C., Dawson C., Joyce C., Newhook L.A., Newman S., Druken E., Begum-Hasan J., Breen A., Houlden R., Woods M., Carrson G., Kelly S., Martel M.J., Penner M., Sankaran K., Hardy-Brown K., King N., White R.A., Park M., Popkin J., Robson L., Coles K., Al Taji E., Cerna M., Cerny M., Francova H., Hainerova I., Kothankova H., Koukalova R., Krakorova V., Mendlova P., Sitova R., Stechova K., Vavrinec J., Vosahlo J., Zlatohlavkova B., Brazdova L., Faksova P., Gregorova D., Kantor L., Malkova K., Venhacova J., Venhacova P., Cipra A., Skvor J., Budejovice C., Tomsikova Z., Botkova-Krauseova H., Mockova A., Paterova P., Gogelova P., Kandrnalova J., Einberg U., Jakovlev U., Posiadlo S., Rannaste E., Raukas R., Riikjarv M.-A., Valla K., Astover V., Kirss A., Retpap J., Taht E., Tillmann V., Vahtra S., Heikkila M., Hirvasniemi M., Luopajarvi K., Johansson S., Kleemola P., Laukkanen E., Parkkola A., Pigg H.-M., Puttonen H., Renlund M., Salonen K., Suomalainen H., Tenkula T., Teramo K., Jarvenpaa A.-L., Hamalainen A.-M., Jussila R., Kiiveri S., Haavisto H., Holopainen S., Kupiainen H., Leeve T., Lumme K., Nironen T., Tenhola S., Tiilikainen T., Keinonen H., Lautala P., Salonen P., Vesanto M., Aspholm A.S., Asunta P., Ikavalko H., Jason E., Jaminki S., Kekki P., Koskinen M., Lehtimaki S., Lahde J., Makela M., Peltoniemi S., Poutiainen L., Ranta K., Salonsaari T., Sarviharju-Tujula S.-L., Selvenius J., Siljander H., Haanpaa P.-L., Holm C., Juutilainen A., Jarvelainen V., Kangaskolkka-Keskilohko A.-M., Laino E., Marjamaki L., Suominen E., Ylitalo S., Hokkanen M., Lounamaa R., Matikainen M., Nuuja A., Paalanen I., Puupponen A.R., Salo-Edwards H., Alanne S., Kultti T., Linjama H., Muhonen K., Vaaraniemi M., Talvitie T., Backman M., Hanhijarvi R., Koivula P., Lindstrom K., Martikainen A., Nurmi P., Bjork A., Huopio H., Komulainen J., Lehtomaki S., Muikku E., Pesola J., Sankilampi U., Arkkola T., Hekkala A., Jurvakainen S., Koivikko M.-L., Kahonen M., Leinonen E., Mykkanen T., Pohjola H., Riikonen K., Niittyvuopio A., Stenius A., Tapanainen P., Veijola R., Alar A., Jovio S., Korpela P., Makinen E., Hietanen L., Kivisto J., Kaar M.-L., Lehtimaki P., Mustila T., Popov E., Saatela S., Taittonen L., Ahtiainen K., Laaksonen N., Luoto M., Viitala J., Virransalo R., Nykanen P., Paajanen S., Parkkinen S., Pyrhonen H., Sarkka T., Aschemeier B., Bektas S., Biester T., Datz N., Deiss D., Fath M., Lupke K., Muller B., Nestoris C., Rothes S., Sadeghian E., Semler K., Arato A., Krikovszky D., Nobilis A., Szenasi J., Benevento D., Anguissola G.B., Biagioni M., Bizzarri C., Cherubini V., Ferrito L., Giordano C., Giorgetti C., Khazrai Y.M., Kyanvash S., Maddaloni E., Napoli A., Piergiovanni F., Pitocco D., Suraci T., Tabacco G., Valente L., Visalli N., Carboni M.B., Cavallo R., Cau V., Isola C., Ledda A., Loddo M., Mannu C., Pettinau M., Pisano S., Porceddu M., Putzu C., Rita A., Peters D., Schierloh U., Bisschoff M., Blonk L., Lappenschaar T., Manai B., Seesink M., Sperling-Conrad M., Verhagen M., Zoethout J.A., Basiak A., Chalas M., Chesiak M., Gramza A., Iwankiewicz J., Sieradzan E., Wikiera B., Ciechanowska M., Dziatkowiak H., Futona B., Gorska A., Glowacka-Wony M., Kaim I., Klich B., Starzyk J., Wolanin M., Tokarska L., Chucherco D., Deja G., Firek-Pedras M., Jarosz-Chobot P., Kalina M., Kutrowska-Adamusiak K., Minkina-Pedras M., Muchaka-Bianga M., Bodalski J., Mlynarski W., Szadkowska A., Cieslak A., Cypryk K., Dziatosz K., Jastzebowska J., Krysiak A., Szymanska U., Wilcznski J., Zawodniak-Szalapska M., Aguay A., Bilbao J.R., Chueca M., Cortazar A., Echarte G., Frutos T.G., Jimenez P., Martul P., Moreno A., Oyarzabal M., Rica I., Salgado Y., Martinez-Larrad M.T., Hawkins F.G., Hernandez R., Herranz L., Pallardo L.F., Deibarra L.S., Fernandez B.H., Luis J.L., Ortiz-Quintana L., Recarte P.P., Arnau D.R., Aronsson L., Boden S., Fredriksson J., Isacsson E., Johansson I., Karlsson E., Lock C., Sandstrom A.-M., Konefal M.S., Andreasson C., Dahlstrom U., Hanas R., Lundqvist K., Windell L., Jansson I., Karlsson A.-K., Lindbladh B., Odenman I., Pettersson C., Sundberg F., Sundqvist M., Aronsson S., Bellman I., Bengtsson A.-B., Lyden G.-B., Nilsson N.-O., Soderblom M., Unt C., Augustsson M., Bengtsson M., Fors H., Helmrich A., Johansson T.O., Andersson A.-C., Boiard-Stomlid A., Hellgren G., Kallsholm H., Lindqvist J., Nilsson M., Nordwall M., Stromstedt C., Ahsberg C., Lindh A., Lindhe C., Samuelsson C., Wiik A., Edenwall H., Ljumgcrantz M., Persson I.-B., Strigard E., Svensson B.-L., Aman J., Breivik G.-E., Detlofsson I.-L., Kroon M., Sarnblad S., Johansson C., Ilvered R., Lundberg A., Akesson K., Beccarelli A., Gadient M., Rappold-Amrein C., Schoenle E., Daftary A., Damagro-Elias M.E., Gilmour C., Klein M.B., Lain C., Salerno D., Smith M.E., Vats K., Pfaff D.J., Malone P., Mansfield P., Munns M., Nickel K., Pompilio K., Siemion W., Taculad R., Van Horn K., Zdanadewic M., Chambliss C., Jones J., Sadler M., Tanner-Blasiar M., Bell C., Camper N., Devaskar S., Devaskar U., Horowitz H., Rogers L., Shannahan R., Silk K., Bermudez Z., Colon R., Frazer T., Martinez-Nieves B., Torres J., Vega J., Chan M., Cook S., Goland R., Greenberg E., Jules N., Montes J., Nelson M., Parra-Valencia Z., Schachner H., Softness B., Kiviniemi M., Suomenin R., Alexander A., Hyrckowian E., Nichol L., Trucco M., Karjalainen E., Louhio T., Sarnesto A., Valtonen E., Davydova B., Helander S., Hamalainen J., Harkonen T., Joutsjoki L., Kararic M., Latva-Koivisto M., Lonn E., Nurmi T., Ollila I., Rinkinen J., Ronkainen M., Tukiainen H., Cederlof A., Kiikeri M., Tsupari S., Cheng R., Bryant K., Chan Y., Maezawa Y., Paltser G., Rasavi R., Tsui H., Winer S., Wu P., Yantha J., University of Zurich, and Knip, Mikael

Subjects
Male, Risk, medicine.medical_specialty, Casein, Breastfeeding, 030209 endocrinology & metabolism, 610 Medicine & health, 2700 General Medicine, Endocrinology and Diabetes, Disease-Free Survival, law.invention, Follow-Up Studie, Nutrition Policy, 03 medical and health sciences, 0302 clinical medicine, Randomized controlled trial, Double-Blind Method, SDG 3 - Good Health and Well-being, law, Internal medicine, Diabetes mellitus, medicine, Humans, Cumulative incidence, 030212 general & internal medicine, Child, Infant Nutritional Physiological Phenomena, Original Investigation, 2. Zero hunger, Type 1 diabetes, business.industry, Hazard ratio, Absolute risk reduction, Infant, Newborn, Caseins, General Medicine, ta3121, medicine.disease, Infant Formula, 3. Good health, Diabetes Mellitus, Type 1, Infant formula, 10036 Medical Clinic, Endokrinologi och diabetes, Female, business, Human, Follow-Up Studies
Abstract

IMPORTANCE Early exposure to complex dietary proteins may increase the risk of type 1 diabetes in children with genetic disease susceptibility. There are no intact proteins in extensively hydrolyzed formulas. OBJECTIVE To test the hypothesis that weaning to an extensively hydrolyzed formula decreases the cumulative incidence of type 1 diabetes in young children. DESIGN, SETTING, AND PARTICIPANTS An international double-blind randomized clinical trial of 2159 infants with human leukocyte antigen-conferred disease susceptibility and a first-degree relative with type 1 diabetes recruited from May 2002 to January 2007 in 78 study centers in 15 countries; 1081 were randomized to be weaned to the extensively hydrolyzed casein formula and 1078 to a conventional formula. The follow-up of the participants ended on February 28, 2017. INTERVENTIONS The participants received either a casein hydrolysate or a conventional adapted cows milk formula supplemented with 20% of the casein hydrolysate. The minimum duration of study formula exposure was 60 days by 6 to 8 months of age. MAIN OUTCOMES AND MEASURES Primary outcome was type 1 diabetes diagnosed according to World Health Organization criteria. Secondary outcomes included age at diabetes diagnosis and safety (adverse events). RESULTS Among 2159 newborn infants (1021 female [47.3%]) who were randomized, 1744 (80.8%) completed the trial. The participants were observed for a median of 11.5 years (quartile [Q] 1-Q3, 10.2-12.8). The absolute risk of type 1 diabetes was 8.4% among those randomized to the casein hydrolysate (n = 91) vs 7.6% among those randomized to the conventional formula (n = 82) (difference, 0.8%[95% CI, -1.6% to 3.2%]). The hazard ratio for type 1 diabetes adjusted for human leukocyte antigen risk group, duration of breastfeeding, duration of study formula consumption, sex, and region while treating study center as a random effect was 1.1 (95% CI, 0.8 to 1.5; P = .46). The median age at diagnosis of type 1 diabetes was similar in the 2 groups (6.0 years [Q1-Q3, 3.1-8.9] vs 5.8 years [Q1-Q3, 2.6-9.1]; difference, 0.2 years [95% CI, -0.9 to 1.2]). Upper respiratory infections were the most common adverse event reported (frequency, 0.48 events/year in the hydrolysate group and 0.50 events/year in the control group). CONCLUSIONS AND RELEVANCE Among infants at risk for type 1 diabetes, weaning to a hydrolyzed formula compared with a conventional formula did not reduce the cumulative incidence of type 1 diabetes after median follow-up for 11.5 years. These findings do not support a need to revise the dietary recommendations for infants at risk for type 1 diabetes. Funding Agencies|Eunice Kennedy Shriver National Institute of Child Health and Development (NICHD); National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health [HD040364, HD042444, HD051997]; Canadian Institutes of Health Research; Commission of the European Communities [QLK1-2002-00372]; European Foundation for the Study of Diabates/JDRF/Novo Nordisk; Academy of Finland (Centre of Excellence in Molecular Systems Immunology and Physiology Research) [250114]; Dutch Diabetes Research Foundation; Finnish Diabetes Research Foundation; JDRF

Published
2018

8. Regional differences in milk and complementary feeding patterns in infants participating in an international nutritional type 1 diabetes prevention trial

Author

Nucci, A. M., Virtanen, S. M., Sorkio, S., Barlund, S., Cuthbertson, D., Uusitalo, U., Lawson, M. L., Salonen, M., Berseth, C. L., Ormisson, A., Lehtonen, E., Savilahti, E., Becker, D. J., Dupre, J., Krischer, J. P., Knip, M., Akerblom, H. K., Mandrup-Poulsen, T., Arjas, E., Laara, E., Lernmark, A., Schmidt, B., Hyytinen, M., Koski, K., Koski, M., Pajakkala, E., Shanker, L., Bradley, B., Dosch, H. -M., Fraser, W., Lawson, M., Mahon, J. L., Sermer, M., Taback, S. P., Becker, D., Franciscus, M., Nucci, A., Palmer, J., Pekkala, M., Catteau, J., Howard, N., Crock, P., Craig, M., Clarson, C. L., Bere, L., Thompson, D., Metzger, D., Kwan, J., Stephure, D. K., Pacaud, D., Ho, J., Schwarz, W., Girgis, R., Thompson, M., Catte, D., Daneman, D., Martin, M. -J., Morin, V., Frenette, L., Ferland, S., Sanderson, S., Heath, K., Huot, C., Gonthier, M., Thibeault, M., Legault, L., Laforte, D., Cummings, E. A., Scott, K., Bridger, T., Crummell, C., Newman, S., Houlden, R., Breen, A., Carson, G., Kelly, S., Sankaran, K., Penner, M., White, R. A., Hardy Brown, K., King, N., Popkin, J., Robson, L., Coles, K., Al Taji, E., Aldhoon, I., Mendlova, P., Vavrinec, J., Vosahlo, J., Brazdova, L., Venhacova, J., Venhacova, P., Cipra, A., Tomsikova, Z., Paterova, P., Gogelova, P., Einberg, U., Riikjarv, M. -A., Tillmann, V., Hirvasniemi, M., Kleemola, P., Parkkola, A., Suomalainen, H., Jarvenpaa, A. -L., Hamalainen, A. -M., Haavisto, H., Tenhola, S., Lautala, P., Salonen, P., Aspholm, S., Siljander, H., Holm, C., Ylitalo, S., Lounamaa, R., Nuuja, A., Talvitie, T., Lindstrom, K., Huopio, H., Pesola, J., Veijola, R., Tapanainen, P., Alar, A., Korpela, P., Kaar, M. -L., Mustila, T., Virransalo, R., Nykanen, P., Aschemeier, B., Danne, T., Kordonouri, O., Krikovszky, D., Madacsy, L., Khazrai, Y. M., Maddaloni, E., Pozzilli, P., Mannu, C., Songini, M., de Beaufort, C., Schierloh, U., Bruining, J., Basiak, A., Wasikowa, R., Ciechanowska, M., Deja, G., Jarosz-Chobot, P., Szadkowska, A., Cypryk, K., Zawodniak-Szalapska, M., Castano, L., Gonzalez Frutos, T., Oyarzabal, M., Serrano-Rios, M., Martinez-Larrad, M. T., Hawkins, F. G., Rodriguez Arnau, D., Ludvigsson, J., Smolinska Konefal, M., Hanas, R., Lindblad, B., Nilsson, N. -O., Fors, H., Nordwall, M., Lindh, A., Edenwall, H., Aman, J., Johansson, C., Gadient, M., Schoenle, E., Daftary, A., Klein, M. B., Gilmour, C., Malone, P., Tanner-Blasiar, M., White, N., Devaskar, U., Horowitz, H., Rogers, L., Colon, R., Frazer, T., Torres, J., Goland, R., Greenberg, E., Nelson, M., Schachner, H., Softness, B., Ilonen, J., Trucco, M., Nichol, L., Harkonen, T., Vaarala, O., and Luopajarvi, K.

Subjects
Canada, endocrine system diseases, infant feeding, breastfeeding, type 1 diabetes, breastfeeding duration, complementary feeding, infant formula, Infant, Article, United States, Diet, Nutrition Policy, Europe, Diabetes Mellitus, Type 1, Milk, Nutrition Assessment, Double-Blind Method, Surveys and Questionnaires, Animals, Humans, Infant Food, Prospective Studies, Infant Nutritional Physiological Phenomena
Abstract

Differences in breastfeeding, other milk feeding and complementary feeding patterns were evaluated in infants at increased genetic risk with and without maternal type 1 diabetes (T1D). The Trial to Reduce IDDM in the Genetically at Risk is an international nutritional primary prevention double-blinded randomized trial to test whether weaning to extensively hydrolyzed vs. intact cow's milk protein formula will decrease the development of T1D-associated autoantibodies and T1D. Infant diet was prospectively assessed at two visits and seven telephone interviews between birth and 8 months. Countries were grouped into seven regions: Australia, Canada, Northern Europe, Southern Europe, Central Europe I, Central Europe II and the United States. Newborn infants with a first-degree relative with T1D and increased human leukocyte antigen-conferred susceptibility to T1D were recruited. A lower proportion of infants born to mothers with than without T1D were breastfed until 6 months of age in all regions (range, 51% to 60% vs. 70% to 80%). Complementary feeding patterns differed more by region than by maternal T1D. In Northern Europe, a higher proportion of infants consumed vegetables and fruits daily compared with other regions. Consumption of meat was more frequent in all European regions, whereas cereal consumption was most frequent in Southern Europe, Canada and the United States. Maternal T1D status was associated with breastfeeding and other milk feeding patterns similarly across regions but was unrelated to the introduction of complementary foods. Infant feeding patterns differed significantly among regions and were largely inconsistent with current recommended guidelines.

Published
2017

9. Phenotypic characterization of the goat population of Santa Elena province (Ecuador).

Author

Solís-Lucas, L. A., Lanari, M. R., and Oyarzabal, M. I.

Subjects
ANIMAL coloration, GOATS, HUMAN skin color, MUCOUS membranes, BEARDS, PROVINCES, HOOFS
Abstract

Copyright of Archivos de Zootecnia is the property of Archivos de Zootecnia and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Published
2020
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10. Transcriptomic signatures of cold acclimated adipocytes reveal CXCL12 as a Brown autocrine and paracrine chemokine.

Author

Agueda-Oyarzabal M, Isidor MS, Plucińska K, Ingerslev LR, Dmytriyeva O, Petersen PSS, Laftih S, Pontoppidan AB, Henningsen JB, Rupar K, Brown EL, Schwartz TW, Barrès R, Gerhart-Hines Z, Schéele CC, and Emanuelli B

Abstract

Besides its thermogenic capacity, brown adipose tissue (BAT) performs important secretory functions that regulate metabolism. However, the BAT microenvironment and factors involved in BAT homeostasis and adaptation to cold remain poorly characterized. We therefore aimed to study brown adipocyte-derived secreted factors that may be involved in adipocyte function and/or may orchestrate intercellular communications. For this, mRNA levels in mature adipocytes from mouse adipose depots were assessed using RNA sequencing upon chronic cold acclimation, and bioinformatic analysis was used to identify secreted factors. Among 858 cold-sensitive transcripts in BAT adipocytes were 210 secreted factor-encoding genes, and Cxcl12 was the top brown adipocyte-enriched cytokine. Cxcl12 mRNA expression analysis by RT-qPCR and fluorescence in situ hybridization specified Cxcl12 distribution in various cell types, and indicated its enrichment in cold-acclimated brown adipocytes. We found that CXCL12 secretion from BAT was increased after chronic cold, yet its level in plasma remained unchanged, suggesting a local/paracrine function. Cxcl12 knockdown in mature brown adipocytes impaired thermogenesis, as assessed by norepinephrine (NE)-induced glycerol release and mitochondrial respiration. However, knockdown of Cxcl12 did not impact β-adrenergic signaling, suggesting that CXCL12 regulates adipocyte function downstream of the β-adrenergic pathway. Moreover, we provide evidence for CXCL12 to exert intercellular cross-talk via its capacity to promote macrophage chemotaxis and neurite outgrowth. Collectively, our results indicate that CXCL12 is a brown adipocyte-enriched, cold-induced secreted factor involved in adipocyte function and the BAT microenvironment communication network., Competing Interests: Declaration of competing interest The authors declare the following financial interests/personal relationships which may be considered as potential competing interests: Thue W. Schwartz, Zacchary Gerhart-Hines reports a relationship with Embark Biotech ApS that includes: employment. If there are other authors, they declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2025 The Authors. Published by Elsevier GmbH.. All rights reserved.)

Published
2025
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11. Knowledge about Chagas Disease among Family and Community Medicine Residents in a Non-Endemic Region: A Cross-Sectional Study.

Author

Ramos-Rincón JM, Mira-Solves JJ, Crespo-Mateos P, Oyarzabal M, Pérez-Ortiz CI, Ramos-Sesma V, and Navarro M

Subjects
Humans, Female, Cross-Sectional Studies, Infectious Disease Transmission, Vertical, Spain epidemiology, Community Medicine, Chagas Disease
Abstract

Chagas disease (CD) is a parasitic disease endemic to continental Latin America that has globalized in recent years. The most relevant mechanisms of transmission of CD in non-endemic countries are transfusion with infected blood and mother-to-child transmission. There is limited information regarding practicing physicians' knowledge of CD transmission, clinical presentation, and treatment in non-endemic countries, including Spain. Our objective was to analyze the level of knowledge about CD in family and community medicine residents and how it has evolved over the last 5 years. A cross-sectional study was performed in the framework of the training program for family and community medicine specialists in Alicante, Spain. Convenience sampling was used to enroll 214 fourth-year family and community medicine residents from 2016 to 2020. Participants completed the validated Chagas Level of Knowledge Scale questionnaire prior to attending the seminar "Health Care for the Immigrant Population." The mean score on the scale was 7.1/10 points. Only 12 participants (5.6%) answered all questions correctly. Resident physicians who reported having received prior information on CD scored better than those who were not informed (mean, 7.2 versus 6.1 points). Participants from Latin America had scores similar to those of the rest of the participants. Over the 5-year study period, questionnaire scores tended to increase. Knowledge about CD among family and community medicine residents has improved in recent years, although it is still not optimal. Specific training on CD during specialized health care training is warranted.

Published
2023
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12. Full activation of thermogenesis in brown adipocytes requires Basigin action.

Author

Rupar K, Isidor MS, Argemi-Muntadas L, Agueda-Oyarzabal M, Plucińska K, Brown EL, Mattanovich M, Bossi S, Tozzi M, Tandio D, Petersen PSS, Henriksen TI, Trošt K, Hansen JB, Gerhart-Hines Z, Nielsen S, Moritz T, and Emanuelli B

Subjects
Mice, Animals, Basigin metabolism, Lipolysis, Obesity metabolism, Thermogenesis genetics, Uncoupling Protein 1 genetics, Uncoupling Protein 1 metabolism, Adipocytes, Brown metabolism, Adipose Tissue, Brown metabolism
Abstract

Exploring mechanisms responsible for brown adipose tissue's (BAT) high metabolic activity is crucial to exploit its energy-dissipating ability for therapeutic purposes. Basigin (Bsg), a multifunctional highly glycosylated transmembrane protein, was recently proposed as one of the 98 critical markers allowing to distinguish 'white' and 'brown' adipocytes, yet its function in thermogenic brown adipocytes is unknown. Here, we report that Bsg is negatively associated with obesity in mice. By contrast, Bsg expression increased in the mature adipocyte fraction of BAT upon cold acclimation. Additionally, Bsg levels were highly induced during brown adipocyte maturation in vitro and were further increased upon β-adrenergic stimulation in a HIF-1α-dependent manner. siRNA-mediated Bsg gene silencing in cultured brown adipocytes did not impact adipogenesis nor mitochondrial function. However, a significant decrease in mitochondrial respiration, lipolysis and Ucp1 transcription was observed in adipocytes lacking Bsg, when activated by norepinephrine. Furthermore, using gas chromatography/mass spectrometry-time-of-flight analysis to assess the composition of cellular metabolites, we demonstrate that brown adipocytes lacking Bsg have lower levels of intracellular lactate and acetoacetate. Bsg was additionally required to regulate intracellular AcAc and tricarboxylic acid cycle intermediate levels in NE-stimulated adipocytes. Our study highlights the critical role of Bsg in active brown adipocytes, possibly by controlling cellular metabolism., (© 2023 The Authors. The FEBS Journal published by John Wiley & Sons Ltd on behalf of Federation of European Biochemical Societies.)

Published
2023
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13. Assessing multiple limiting factors of seasonal biomass production and N content in a grassland with a year-round production.

Author

Oyarzabal M and Oesterheld M

Subjects
Biomass, Seasons, Water, Nitrogen, Poaceae, Ecosystem, Grassland
Abstract

There is little evidence on the extent that multiple factors simultaneously limit ecosystem function of grasslands with year-round production. Here we test if multiple factors simultaneously limit (i.e., more than one factor at a time) grassland functioning in different seasons and how they interacted with N availability. In a Flooding Pampa grassland, we ran a separate factorial experiment in spring, summer, and winter with several treatments: control, mowing, shading, P addition, watering (only in summer), and warming (only in winter), each of them crossed with two nitrogen treatments: control and N addition. Grassland functioning was assessed by aboveground net primary productivity (ANPP), green and standing dead biomass, and N content at the species group level. Out of 24 potential cases (three seasons by eight response variables), 13 corresponded to just one limiting factor, 4 to multiple limiting factors, and the other 7 to no evidence of limitation. In conclusion, grassland functioning in each season was most often limited by just one factor, while multiple limiting factors were rarer. Nitrogen was the prevailing limiting factor. Our study expands our knowledge of limitations imposed by factors associated with disturbance and stress, such as mowing, shading, water availability, and warming in grasslands with year-round production., (© 2023. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature.)

Published
2023
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14. Immune Cells in Thermogenic Adipose Depots: The Essential but Complex Relationship.

Author

Agueda-Oyarzabal M and Emanuelli B

Subjects
Adipose Tissue, White metabolism, Animals, Mammals, Obesity metabolism, Adipose Tissue, Brown metabolism, Thermogenesis physiology
Abstract

Brown adipose tissue (BAT) is a unique organ in mammals capable of dissipating energy in form of heat. Additionally, white adipose tissue (WAT) can undergo browning and perform thermogenesis. In recent years, the research community has aimed to harness thermogenic depot functions for new therapeutic strategies against obesity and the metabolic syndrome; hence a comprehensive understanding of the thermogenic fat microenvironment is essential. Akin to WAT, immune cells also infiltrate and reside within the thermogenic adipose tissues and perform vital functions. As highly plastic organs, adipose depots rely on crucial interplay with these tissue resident cells to conserve their healthy state. Evidence has accumulated to show that different immune cell populations contribute to thermogenic adipose tissue homeostasis and activation through complex communicative networks. Furthermore, new studies have identified -but still not fully characterized further- numerous immune cell populations present in these depots. Here, we review the current knowledge of this emerging field by describing the immune cells that sway the thermogenic adipose depots, and the complex array of communications that influence tissue performance., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2022 Agueda-Oyarzabal and Emanuelli.)

Published
2022
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15. Dynamic interplay between Afadin S1795 phosphorylation and diet regulates glucose homeostasis in obese mice.

Author

Tozzi M, Brown EL, Petersen PSS, Lundh M, Isidor MS, Plucińska K, Nielsen TS, Agueda-Oyarzabal M, Small L, Treebak JT, and Emanuelli B

Subjects
Animals, Diet, High-Fat, Glucose metabolism, Homeostasis, Insulin metabolism, Mice, Mice, Inbred C57BL, Mice, Obese, Microfilament Proteins, Phosphorylation, Insulin Resistance physiology
Abstract

Key Points: Afadin is a ubiquitously expressed scaffold protein with a recently discovered role in insulin signalling and glucose metabolism. Insulin-stimulated phosphorylation of Afadin at S1795 occurs in insulin-responsive tissues such as adipose tissue, muscle, liver, pancreas and heart. Afadin abundance and Afadin S1795 phosphorylation are dynamically regulated in metabolic tissues during diet-induced obesity progression. Genetic silencing of Afadin S1795 phosphorylation improves glucose homeostasis in the early stages of diet-induced metabolic dysregulation. Afadin S1795 phosphorylation contributes to the early development of obesity-related complications in mice., Abstract: Obesity is associated with systemic insulin resistance and numerous metabolic disorders. Yet, the mechanisms underlying impaired insulin action during obesity remain to be fully elucidated. Afadin is a multifunctional scaffold protein with the ability to modulate insulin action through its phosphorylation at S1795 in adipocytes. In the present study, we report that insulin-stimulated Afadin S1795 phosphorylation is not restricted to adipose tissues, but is a common signalling event in insulin-responsive tissues including muscle, liver, pancreas and heart. Furthermore, a dynamic regulation of Afadin abundance occurred during diet-induced obesity progression, while its phosphorylation was progressively attenuated. To investigate the role of Afadin S1795 phosphorylation in the regulation of whole-body metabolic homeostasis, we generated a phospho-defective mouse model (Afadin SA) in which the Afadin phosphorylation site was silenced (S1795A) at the whole-body level using CRISPR-Cas9-mediated gene editing. Metabolic characterization of these mice under basal physiological conditions or during a high-fat diet (HFD) challenge revealed that preventing Afadin S1795 phosphorylation improved insulin sensitivity and glucose tolerance and increased liver glycogen storage in the early stage of diet-induced metabolic dysregulation, without affecting body weight. Together, our findings reveal that Afadin S1795 phosphorylation in metabolic tissues is critical during obesity progression and contributes to promote systemic insulin resistance and glucose intolerance in the early phase of diet-induced obesity., (© 2021 The Authors. The Journal of Physiology © 2021 The Physiological Society.)

Published
2022
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16. White adipose remodeling during browning in mice involves YBX1 to drive thermogenic commitment.

Author

Rabiee A, Plucińska K, Isidor MS, Brown EL, Tozzi M, Sidoli S, Petersen PSS, Agueda-Oyarzabal M, Torsetnes SB, Chehabi GN, Lundh M, Altıntaş A, Barrès R, Jensen ON, Gerhart-Hines Z, and Emanuelli B

Subjects
Adipocytes, Brown metabolism, Adipogenesis, Adipose Tissue, Brown metabolism, Animals, Cell Differentiation, Cell Line, Cell Proliferation, Gene Expression Regulation, Jumonji Domain-Containing Histone Demethylases genetics, Jumonji Domain-Containing Histone Demethylases metabolism, Male, Mesenchymal Stem Cells, Mice, Mice, Inbred C57BL, Obesity metabolism, Proteomics, Subcutaneous Fat metabolism, Transcriptome, Up-Regulation, Adipose Tissue, White metabolism, Thermogenesis genetics, Thermogenesis physiology, Transcription Factors genetics, Transcription Factors metabolism
Abstract

Objective: Increasing adaptive thermogenesis by stimulating browning in white adipose tissue is a promising method of improving metabolic health. However, the molecular mechanisms underlying this transition remain elusive. Our study examined the molecular determinants driving the differentiation of precursor cells into thermogenic adipocytes., Methods: In this study, we conducted temporal high-resolution proteomic analysis of subcutaneous white adipose tissue (scWAT) after cold exposure in mice. This was followed by loss- and gain-of-function experiments using siRNA-mediated knockdown and CRISPRa-mediated induction of gene expression, respectively, to evaluate the function of the transcriptional regulator Y box-binding protein 1 (YBX1) during adipogenesis of brown pre-adipocytes and mesenchymal stem cells. Transcriptomic analysis of mesenchymal stem cells following induction of endogenous Ybx1 expression was conducted to elucidate transcriptomic events controlled by YBX1 during adipogenesis., Results: Our proteomics analysis uncovered 509 proteins differentially regulated by cold in a time-dependent manner. Overall, 44 transcriptional regulators were acutely upregulated following cold exposure, among which included the cold-shock domain containing protein YBX1, peaking after 24 h. Cold-induced upregulation of YBX1 also occurred in brown adipose tissue, but not in visceral white adipose tissue, suggesting a role of YBX1 in thermogenesis. This role was confirmed by Ybx1 knockdown in brown and brite preadipocytes, which significantly impaired their thermogenic potential. Conversely, inducing Ybx1 expression in mesenchymal stem cells during adipogenesis promoted browning concurrent with an increased expression of thermogenic markers and enhanced mitochondrial respiration. At a molecular level, our transcriptomic analysis showed that YBX1 regulates a subset of genes, including the histone H3K9 demethylase Jmjd1c, to promote thermogenic adipocyte differentiation., Conclusion: Our study mapped the dynamic proteomic changes of murine scWAT during browning and identified YBX1 as a novel factor coordinating the genomic mechanisms by which preadipocytes commit to brite/beige lineage., (Copyright © 2020 The Author(s). Published by Elsevier GmbH.. All rights reserved.)

Published
2021
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17. Neutrophils do not impact viral load or the peak of disease severity during RSV infection.

Author

Kirsebom F, Michalaki C, Agueda-Oyarzabal M, and Johansson C

Subjects
Animals, Cells, Cultured, Chemokine CXCL1, Cytokines metabolism, Disease Models, Animal, Humans, Inflammation Mediators metabolism, Lung pathology, Mice, Inbred C57BL, Severity of Illness Index, Lung immunology, Negative Results, Neutrophils immunology, Respiratory Syncytial Virus Infections immunology, Respiratory Syncytial Virus Infections virology, Respiratory Syncytial Virus, Human, Viral Load
Abstract

Lung and airway neutrophils are a hallmark of severe disease in infants with respiratory syncytial virus (RSV)-induced lower respiratory tract infections. Despite their abundance in the lungs during RSV infection of both mice and man, the role of neutrophils in viral control and in immune pathology is not clear. Here, antibody mediated neutrophil depletion was used to investigate the degree to which neutrophils impact the lung immune environment, the control of viral replication and the peak severity of disease after RSV infection of mice. Neutrophil depletion did not substantially affect the levels of inflammatory mediators such as type I interferons, IL-6, TNF-α or IL-1β in response to RSV. In addition, the lack of neutrophils did not change the viral load during RSV infection. Neither neutrophil depletion nor the enhancement of lung neutrophils by administration of the chemoattractant CXCL1 during RSV infection affected disease severity as measured by weight loss. Therefore, in this model of RSV infection, lung neutrophils do not offer obvious benefits to the host in terms of increasing anti-viral inflammatory responses or restricting viral replication and neutrophils do not contribute to disease severity.

Published
2020
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18. Cyclical variation in the incidence of childhood-onset type 1 diabetes during 40 years in Navarra (Spain).

Author

Forga L, Chueca MJ, Tamayo I, Oyarzabal M, Toni M, and Goñi MJ

Subjects
Adolescent, Age of Onset, Child, Child, Preschool, Female, Humans, Incidence, Male, Periodicity, Poisson Distribution, Prospective Studies, Retrospective Studies, Spain epidemiology, Diabetes Mellitus, Type 1 epidemiology
Abstract

Objective: To trace the evolution of type 1 diabetes (T1D) in Navarre in children under 15, between 1977 and 2016, and their characteristics at onset regarding age and sex., Subjects and Methods: We performed a descriptive analysis, using prospective-retrospective information. The study included all cases of T1D diagnosed in Navarre in children aged 0 to 14 years old from 1 January 1977 until 31 December 2016. The capture-recapture method was used, retrieving information from three independent sources: the five hospitals in Navarre as a primary source, and the Navarre Association of Diabetics (ANADI) and the primary healthcare system as the secondary source. Estimates and confidence intervals were calculated assuming a subjacent Poisson distribution. Chi square test was used to compare incidence between groups. The analysis of changes in incidence since 1977, adjusted for age group, sex and year of diagnosis, were evaluated with a multivariate Poisson regression model and joinpoint regression., Results: A total of 577 cases were registered resulting in a crude incidence rate of 14.99/100 000 inhabitants-year (95% confidence interval [CI]: 13.79-16.26). From 1977, the incidence has increased in cycles, reaching an incidence rate of 22.98 (95% CI: 18.52-28.21) in 2016. The relative annual increase is 3% (95% CI: 2.3-3.8). The highest incidence is in the 10 to 14 age group (P < 0.001). No differences in sex were found. The mean age at onset in children under 15 years has not changed significantly (P = 0.572)., Conclusions: The incidence of T1D in Navarre has increased 4-fold in the last four decades but is stable since 2001., (© 2018 The Authors. Pediatric Diabetes published by John Wiley & Sons Ltd.)

Published
2018
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