Impacts of global change on Mediterranean forests and their services

The increase in aridity, mainly by decreases in precipitation but also by higher temperatures, is likely the main threat to the diversity and survival of Mediterranean forests. Changes in land use, including the abandonment of extensive crop activities, mainly in mountains and remote areas, and the increases in human settlements and demand for more resources with the resulting fragmentation of the landscape, hinder the establishment of appropriate management tools to protect Mediterranean forests and their provision of services and biodiversity. Experiments and observations indicate that if changes in climate, land use and other components of global change, such as pollution and overexploitation of resources, continue, the resilience of many forests will likely be exceeded, altering their structure and function and changing, mostly decreasing, their capacity to continue to provide their current services. A consistent assessment of the impacts of the changes, however, remains elusive due to the difficulty of obtaining simultaneous and complete data for all scales of the impacts in the same forests, areas and regions. We review the impacts of climate change and other components of global change and their interactions on the terrestrial forests of Mediterranean regions, with special attention to their impacts on ecosystem services. Management tools for counteracting the negative effects of global change on Mediterranean ecosystem- services are finally discussed

The V471A polymorphism in autophagy-related gene ATG7 modifies age at onset specifically in Italian Huntington disease patients

The cause of Huntington disease (HD) is a polyglutamine repeat expansion of more than 36 units in the huntingtin protein, which is inversely correlated with the age at onset of the disease. However, additional genetic factors are believed to modify the course and the age at onset of HD. Recently, we identified the V471A polymorphism in the autophagy-related gene ATG7, a key component of the autophagy pathway that plays an important role in HD pathogenesis, to be associated with the age at onset in a large group of European Huntington disease patients. To confirm this association in a second independent patient cohort, we analysed the ATG7 V471A polymorphism in additional 1,464 European HD patients of the “REGISTRY” cohort from the European Huntington Disease Network (EHDN). In the entire REGISTRY cohort we could not confirm a modifying effect of the ATG7 V471A polymorphism. However, analysing a modifying effect of ATG7 in these REGISTRY patients and in patients of our previous HD cohort according to their ethnic origin, we identified a significant effect of the ATG7 V471A polymorphism on the HD age at onset only in the Italian population (327 patients). In these Italian patients, the polymorphism is associated with a 6-years earlier disease onset and thus seems to have an aggravating effect. We could specify the role of ATG7 as a genetic modifier for HD particularly in the Italian population. This result affirms the modifying influence of the autophagic pathway on the course of HD, but also suggests population-specific modifying mechanisms in HD pathogenesis

Identification of genetic variants associated with Huntington's disease progression: a genome-wide association study

Background Huntington's disease is caused by a CAG repeat expansion in the huntingtin gene, HTT. Age at onset has been used as a quantitative phenotype in genetic analysis looking for Huntington's disease modifiers, but is hard to define and not always available. Therefore, we aimed to generate a novel measure of disease progression and to identify genetic markers associated with this progression measure. Methods We generated a progression score on the basis of principal component analysis of prospectively acquired longitudinal changes in motor, cognitive, and imaging measures in the 218 indivduals in the TRACK-HD cohort of Huntington's disease gene mutation carriers (data collected 2008–11). We generated a parallel progression score using data from 1773 previously genotyped participants from the European Huntington's Disease Network REGISTRY study of Huntington's disease mutation carriers (data collected 2003–13). We did a genome-wide association analyses in terms of progression for 216 TRACK-HD participants and 1773 REGISTRY participants, then a meta-analysis of these results was undertaken. Findings Longitudinal motor, cognitive, and imaging scores were correlated with each other in TRACK-HD participants, justifying use of a single, cross-domain measure of disease progression in both studies. The TRACK-HD and REGISTRY progression measures were correlated with each other (r=0·674), and with age at onset (TRACK-HD, r=0·315; REGISTRY, r=0·234). The meta-analysis of progression in TRACK-HD and REGISTRY gave a genome-wide significant signal (p=1·12 × 10−10) on chromosome 5 spanning three genes: MSH3, DHFR, and MTRNR2L2. The genes in this locus were associated with progression in TRACK-HD (MSH3 p=2·94 × 10−8 DHFR p=8·37 × 10−7 MTRNR2L2 p=2·15 × 10−9) and to a lesser extent in REGISTRY (MSH3 p=9·36 × 10−4 DHFR p=8·45 × 10−4 MTRNR2L2 p=1·20 × 10−3). The lead single nucleotide polymorphism (SNP) in TRACK-HD (rs557874766) was genome-wide significant in the meta-analysis (p=1·58 × 10−8), and encodes an aminoacid change (Pro67Ala) in MSH3. In TRACK-HD, each copy of the minor allele at this SNP was associated with a 0·4 units per year (95% CI 0·16–0·66) reduction in the rate of change of the Unified Huntington's Disease Rating Scale (UHDRS) Total Motor Score, and a reduction of 0·12 units per year (95% CI 0·06–0·18) in the rate of change of UHDRS Total Functional Capacity score. These associations remained significant after adjusting for age of onset. Interpretation The multidomain progression measure in TRACK-HD was associated with a functional variant that was genome-wide significant in our meta-analysis. The association in only 216 participants implies that the progression measure is a sensitive reflection of disease burden, that the effect size at this locus is large, or both. Knockout of Msh3 reduces somatic expansion in Huntington's disease mouse models, suggesting this mechanism as an area for future therapeutic investigation

Utility of the Parkinson’s disease-Cognitive Rating Scale for the screening of global cognitive status in Huntington’s disease

Background: Cognitive impairment is an essential feature of Huntington’s disease (HD) and dementia is a predictable outcome in all patients. However, validated instruments to assess global cognitive performance in the field of HD are lacking. Objectives: We aimed to explore the utility of the Parkinson’s disease-Cognitive Rating Scale (PD-CRS) for the screening of global cognition in HD. Methods: A multicenter cohort of 132 HD patients at different disease stages and 33 matched healthy controls were classified as having preserved cognition, mild cognitive impairment (HD-MCI) or dementia (HD-Dem) according to the Clinical Dementia Rating and Functional Independence Score. The PD-CRS and the Mini-Mental State Examination were administered. Receiver operating characteristic curve analysis was used to determine optimal cutoffs to differentiate patients according to their cognitive status. Results: A PD-CRS cutoff score ≤ 81/82 was optimal to detect HD-MCI (sensitivity = 93%; specificity = 80%; area under the curve (AUC) = 0.940), and ≤ 63/64 was optimal to detect HD-Dem (sensitivity = 90%; specificity = 87%; AUC = 0.933). MMSE scores failed to show robust psychometric properties in this context. Discussion: The PD-CRS is a valid and reliable instrument to assess global cognition in HD in routine clinical care and clinical trials

Correction to: Utility of the Parkinson’s disease-Cognitive Rating Scale for the screening of global cognitive status in Huntington’s disease (Journal of Neurology, (2020), 267, 5, (1527-1535), 10.1007/s00415-020-09730-6)

The original version of this article unfortunately contained a mistake. Affiliation 4 was incorrect. The corrected affiliation is given below. Department of Medicine, Autonomous University of Barcelona, Barcelona, Spain

Arithmetic Word-Problem Solving as Cognitive Marker of Progression in Pre-Manifest and Manifest Huntington's Disease

Background: Arithmetic word-problem solving depends on the interaction of several cognitive processes that may be affected early in the disease in gene-mutation carriers for Huntington's disease (HD). Objective: Our goal was to examine the pattern of performance of arithmetic tasks in premanifest and manifest HD, and to examine correlations between arithmetic task performance and other neuropsychological tasks. Methods: We collected data from a multicenter cohort of 165 HD gene-mutation carriers. The sample consisted of 31 premanifest participants: 16 far-from (>12 years estimated time to diagnosis; preHD-A) and 15 close-to (≤12 years estimated time to diagnosis; preHD-B), 134 symptomatic patients (early-mild HD), and 37 healthy controls (HC). We compared performance between groups and explored the associations between arithmetic word-problem solving and neuropsychological and clinical variables. Results: Total arithmetic word-problem solving scores were lower in preHD-B patients than in preHD-A (p < 0.05) patients and HC (p < 0.01). Early-mild HD patients had lower scores than preHD patients (p < 0.001) and HC (p < 0.001). Compared to HC, preHD and early-mild HD participants made more errors as trial complexity increased. Moreover, arithmetic word-problem solving scores were significantly associated with measures of global cognition (p < 0.001), frontal-executive functions (p < 0.001), attention (p < 0.001) visual working memory (p < 0.001), mental rotation (p < 0.001), and confrontation naming (p < 0.05). Conclusion: Arithmetic word-problem solving is affected early in the course of HD and is related to deficient processes in frontal-executive and mentalizing-related processes

Spanish HTT gene study reveals haplotype and allelic diversity with possible implications for germline expansion dynamics in Huntington disease

We aimed to determine the genetic diversity and molecular characteristics of the Huntington disease (HD) gene (HTT) in Spain. We performed an extended haplotype and exon one deep sequencing analysis of the HTT gene in a nationwide cohort of population-based controls (n = 520) and families with symptomatic individuals referred for HD genetic testing. This group included 331 HD cases and 140 carriers of intermediate alleles. Clinical and family history data were obtained when available. Spanish normal alleles are enriched in C haplotypes (40.1%), while A1 (39.8%) and A2 (31.6%) prevail among intermediate and expanded alleles, respectively. Alleles ≥50 CAG repeats are primarily associated with haplotypes A2 (38.9%) and C (32%), which are also present in 50% and 21.4%, respectively, of HD families with large intergenerational expansions. Non-canonical variants of exon one sequence are less frequent, but much more diverse, in alleles of ≥27 CAG repeats. The deletion of CAACAG, one of the six rare variants not observed among smaller normal alleles, is associated with haplotype C and appears to correlate with larger intergenerational expansions and early onset of symptoms. Spanish HD haplotypes are characterised by a high genetic diversity, potentially admixed with other non-Caucasian populations, with a higher representation of A2 and C haplotypes than most European populations. Differences in haplotype distributions across the CAG length range support differential germline expansion dynamics, with A2 and C showing the largest intergenerational expansions. This haplotype-dependent germline instability may be driven by specific cis-elements, such as the CAACAG deletion

β-Defensin genomic copy number does not influence the age of onset in Huntington's Disease

none498siHuntington's disease (HD) is an autosomal dominant neurodegenerative disorder caused by the abnormal expansion of a CAG triplet repeat tract in the huntingtin gene. While the length of this CAG expansion is the major determinant of the age of onset (AO), other genetic factors have also been shown to play a modulatory role. Recent evidence suggests that neuroinflammations is a pivotal factor in the pathogenesis of HD, and that targeting this process may have important therapeutic ramifications. The human β-defensin 2 (hBD2)- encoded by DEFB4- is an antimicrobial peptide that exhibits inducible expression in astrocytes during inflammation and is an important regulator of innate and adaptive immune response. Therefore, DEFB4 may contribute to the neuroinflammatory processes observed in HD.openVittori A, Orth M, Roos RA, Outeiro TF, Giorgini F, Hollox EJ, Bachoud-Levi AC, Bentivoglio AR, Biunno I, Bonelli RM, Burgunder JM, Dunnett SB, Ferreira JJ, Handley OJ, Heiberg A, Illmann T, Landwehrmeyer GB, Levey J, Martinez-Jaurrieta MD, Nielsen JE, Pro Koivisto S, Piiiviirinta M, Roos RA, Sebastian AR, Tabrizi SJ, Vandenberghe W, Verellen-Dumoulin C, Zaremba J, Uhrova T, Wahlstrom J, Barth K, Correia-Guedes L, Finisterra AM, Bascuiiana Garde M, Betz S, Bos R, Ecker D, Handley OJ, Held C, Koppers K, Laura M, Descals AM, Mestre T, Monza D, Townhill J, Padieu H, Paterski L, Peppa N, Rialland A, Røren N, Sasinkova P, Trigo Cubillo P, van Walsem M, Witjes-Ane MN, Yudina E, Zielonka D, Zielonka E, Zinzi P, Bonelli RM, Herranhof B, HOd A, Kapfhammer HP, Koppitz M, Magnet M, Otti D, Painold A, Reisinge K, Scheib M, Hecht K, Lilek S, Muller N, Schoggl H, Ullah J, Ribal P, Verellen-Dumoulin C, Klempff J, Majerova V, Roth J, Hjermind LE, Jakobsen O, Vinthev-Jensen T, Larsen IU, Nielsen JE, Stokholm J, Hiivola H, Martikainen K, Tuuha K, Santala M, Milkereit E, Kosinski CM, Probst D, Reetz K, Sass C, Schiefer J, Schlangen C, Werner CJ, Andrich J, Ellrichmann G, Hoffmann R, Kaminski B, Saft C, Stamm C, Lange H, Lohle M, Schmidt S, Storch A, Wolz A, Wolz M, Capetian P, Lambeck J, Zucker B, Boelmans K, Ganos C, Hidding U, Lewerenz J, Miinchau A, Orth M, Schmalfeld J, Stubbe L, Zittel S, Heinicke W, Ribbat M, Longinus B, Miihlau M, Peinemann A, Stiidtler M, Weindl A, Winkelmann J, Ziegler C, Bechtel N, Beckmann H, Bohlen S, Holzner E, Lange H, Reilmann R, Rohm S, Rumpf S, Schepers S, Dose M, Leythaeuser G, Marquard R, Raab T, Schrenk C, Schuierer M, Barth K, Buck A, Ecker D, Eschenbach C, Held C, Landwehrmeyer B, Lezius F, Nepper S, Niess A, Orth M, Schwenk D, Siissmuth S, Trautmann S, Weydt P, Cormio C, de Tommaso M, Sciruicchio V, Serpino C, Ghelli E, Ginestroni A, Bertini E, Massaro F, Mechi C, Paganini M, Piacentini S, Pradella S, Romoli AM, Sorbi S, Abbruzzese G, Ferrandes MB, Di Maria E, Ferrandes G, Mandich P, Marchese R, Di Donato S, Gellera C, Genitrini S, Mariotti C, Nanetti L, Monza D, Soliveri P, Tomasello C, De Michele G, DiMaio L, Massarelli M, Rinaldi C, Roca A, Rossi F, Russo CV, Salvatore E, Sorrentino P, Tucci T, De Nicola A, Elifani F, Petrollini M, Martino T, Lovo F, Squitieri F, Bentivoglio AR, Catalli C, Di Giacopo R, Fasano A, Frontali M, Guidubaldi A, Ialongo T, Jacopini G, Loria G, Piano C, Piccininni C, Quaranta D, Romano S, Soleti F, Spadaro M, Zinzi P, van Hout MS, van Vugt JP, de Weert A, Bolwijn JJ, Neurologie P, Dekker M, Neurologie P, Leenders KL, van Oostrom JC, Bos R, Dumas EM, Jurgens CK, van den Bogaard SJ, Roos RA, 't Hart EP, Kremer B, Verstappen CC, Heiberg A, van Walsem MR, Frich J, Aaserud O, Wehus R, Bjørgo K, Fannemel M, Gørvell P, Lorentzen E, Koivisto SP, Retterstøl L, Stokke B, Bjørnevoll I, Sando SB, Dziadkiewicz A, Nowak M, Robowski P, Sitek E, Slawek J, Soltan W, Szinwelski M, Blaszczyk M, Boczarska-Jedynak M, Ciach-Wysocka E, Gorzkowska A, Jasinska-Myga B, Opala G, Klodowska G, Stompel D, Ciach-Wysocka E, Banaszkiewicz K, Boewiriska D, Bojakowska-Jaremek K, Neurologii A, Dec M, Krawczyk M, Rudziriska M, Szczudlik A, Szczygiel E, Wasielewska A, Wojcik M, Wojcik M, Bryl A, Ciesielska A, Klimberg A, Marcinkowski J, Samara H, Sempolowicz J, Zielonka D, Janik P, Kalbarczyk A, Kwiecinski H, Jamrozik Z, Antczak J, Jachinska K, Krysa W, Rakowicz M, Richter P, Rola R, Ryglewicz D, Sienkiewicz-Jarosz H, Sulek A, Witkowski G, Zdzienicka E, Zaremba J, Zieora-Jakutowicz K, Coelho M, Correia-Guedes L, Ferreira JJ, Mestre T, Mendes T, Valadas A, Andrade C, Joao PS, Gago M, Garrett C, Joao PS, Guerra MR, Joao PS, Solis P, Herrera CD, Garcia PM, Cubo E, Mariscal N, Sanchez J, Barrero FJ, Alonso-Frech F, Perez MR, Fenollar M, Garda R, Rivera SV, Villanueva C, Alegre J, Bascuiiana M, Ventura MF, Ribas GG, Moreno JL, Cubillo PT, Rufz PJ, Frech FA, Dfaz J, Guerrero R, Dfaz J, Artiga MJ, Dfaz J, Sanchez V, Alcaraz LF, de Ia Arrixaca V, Manzanares S, de Ia Arrixaca V, Perea MF, Reinante G, Arrixaca Ia, Torres MM, Moreau LV, de Ia Arrixaca V, Barbera MA, Guia DB, Hernanz LC, Catena JL, Sebastian R, Ferrer PQ, Carruesco GT, Bas J, Busquets N, Calopa M, Buongiorno MT, Munoz E, Elorza MD, Lopez CD, Terol DS, Robert MF, Rufz BG, Casado AG, Martinez IH, Viladrich CM, Pons R, Roca E, Llesoy JR, Idiago JM, Vergara MR, Garcia SS, Riballo AV, Hoglund A, Palhagen SE, Paucar M, Sandstrom B, Svenningsson P, Reza-Soltani TW, Burgunder JM, Kaelin A, Romero I, Schupbach M, Stebler Y, Zaugg SW, Akhtar S, Crooks J, Curtis A, de Souza J, Rickards H, Wright J, Barker RA, Di Pietro A, Fisher K, Goodman AO, Hill S, Kershaw A, Mason S, O'Keefe D, Swain R, Guzman NV, Busse M, Butcher C, Clenaghan C, Dunnett S, Fullam R, Jones L, Jones U, Khalil H, Minster S, Owen M, Hunt S, Price K, Rosser A, Townhill J, Edwards M, Ho C, McGill M, Pearson P, Porteous M, Brockie P, Foster J, Johns N, McKenzie S, Rothery J, Thomas G, Yates S, Burrows L, Chu C, Fletcher A, Gallantrae D, Harding A, Hamer S, Kraus A, Laver F, Longthorpe M, Markova I, Raman A, Silva M, Thomson A, Wild S, Yardumian P, Hobson E, Jamieson S, Musgrave H, Rowett L, Toscano J, Wild S, Yardumian P, Clayton C, Dipple H, Middleton J, Patino D, Andrews T, Dougherty A, Kavalier F, Golding C, Laing H, Lashwood A, Robertson D, Ruddy D, Whaite A, Santhouse A, Andrews T, Bruno S, Doherty K, Lahiri N, Novak M, Patel A, Rosser E, Tabrizi S, Taylor R, Warner T, Wild E, Arran N, Bek J, Callaghan J, Craufurd D, Fullam R, Howard L, Hare M, Huson S, Johnson L, Jones M, Murphy H, Oughton E, Partington-Janes L, Rogers D, Snowden J, Sollom A, Stopford C, Thompson J, Trender-Gerhard I.Vittori, A; Orth, M; Roos, Ra; Outeiro, Tf; Giorgini, F; Hollox, Ej; Bachoud-Levi, Ac; Bentivoglio, Ar; Biunno, I; Bonelli, Rm; Burgunder, Jm; Dunnett, Sb; Ferreira, Jj; Handley, Oj; Heiberg, A; Illmann, T; Landwehrmeyer, Gb; Levey, J; Martinez-Jaurrieta, Md; Nielsen, Je; Pro Koivisto, S; Piiiviirinta, M; Roos, Ra; Sebastian, Ar; Tabrizi, Sj; Vandenberghe, W; Verellen-Dumoulin, C; Zaremba, J; Uhrova, T; Wahlstrom, J; Barth, K; Correia-Guedes, L; Finisterra, Am; Bascuiiana Garde, M; Betz, S; Bos, R; Ecker, D; Handley, Oj; Held, C; Koppers, K; Laura, M; Descals, Am; Mestre, T; Monza, D; Townhill, J; Padieu, H; Paterski, L; Peppa, N; Rialland, A; Røren, N; Sasinkova, P; Trigo Cubillo, P; van Walsem, M; Witjes-Ane, Mn; Yudina, E; Zielonka, D; Zielonka, E; Zinzi, P; Bonelli, Rm; Herranhof, B; Hod, A; Kapfhammer, Hp; Koppitz, M; Magnet, M; Otti, D; Painold, A; Reisinge, K; Scheib, M; Hecht, K; Lilek, S; Muller, N; Schoggl, H; Ullah, J; Ribal, P; Verellen-Dumoulin, C; Klempff, J; Majerova, V; Roth, J; Hjermind, Le; Jakobsen, O; Vinthev-Jensen, T; Larsen, Iu; Nielsen, Je; Stokholm, J; Hiivola, H; Martikainen, K; Tuuha, K; Santala, M; Milkereit, E; Kosinski, Cm; Probst, D; Reetz, K; Sass, C; Schiefer, J; Schlangen, C; Werner, Cj; Andrich, J; Ellrichmann, G; Hoffmann, R; Kaminski, B; Saft, C; Stamm, C; Lange, H; Lohle, M; Schmidt, S; Storch, A; Wolz, A; Wolz, M; Capetian, P; Lambeck, J; Zucker, B; Boelmans, K; Ganos, C; Hidding, U; Lewerenz, J; Miinchau, A; Orth, M; Schmalfeld, J; Stubbe, L; Zittel, S; Heinicke, W; Ribbat, M; Longinus, B; Miihlau, M; Peinemann, A; Stiidtler, M; Weindl, A; Winkelmann, J; Ziegler, C; Bechtel, N; Beckmann, H; Bohlen, S; Holzner, E; Lange, H; Reilmann, R; Rohm, S; Rumpf, S; Schepers, S; Dose, M; Leythaeuser, G; Marquard, R; Raab, T; Schrenk, C; Schuierer, M; Barth, K; Buck, A; Ecker, D; Eschenbach, C; Held, C; Landwehrmeyer, B; Lezius, F; Nepper, S; Niess, A; Orth, M; Schwenk, D; Siissmuth, S; Trautmann, S; Weydt, P; Cormio, C; de Tommaso, M; Sciruicchio, V; Serpino, C; Ghelli, E; Ginestroni, A; Bertini, E; Massaro, F; Mechi, C; Paganini, M; Piacentini, S; Pradella, S; Romoli, Am; Sorbi, S; Abbruzzese, G; Ferrandes, Mb; Di Maria, E; Ferrandes, G; Mandich, P; Marchese, R; Di Donato, S; Gellera, C; Genitrini, S; Mariotti, C; Nanetti, L; Monza, D; Soliveri, P; Tomasello, C; De Michele, G; Dimaio, L; Massarelli, M; Rinaldi, C; Roca, A; Rossi, F; Russo, Cv; Salvatore, E; Sorrentino, P; Tucci, T; De Nicola, A; Elifani, F; Petrollini, M; Martino, T; Lovo, F; Squitieri, F; Bentivoglio, Ar; Catalli, C; Di Giacopo, R; Fasano, A; Frontali, M; Guidubaldi, A; Ialongo, T; Jacopini, G; Loria, G; Piano, C; Piccininni, C; Quaranta, D; Romano, S; Soleti, F; Spadaro, M; Zinzi, P; van Hout, Ms; van Vugt, Jp; de Weert, A; Bolwijn, Jj; Neurologie, P; Dekker, M; Neurologie, P; Leenders, Kl; van Oostrom, Jc; Bos, R; Dumas, Em; Jurgens, Ck; van den Bogaard, Sj; Roos, Ra; 't Hart, Ep; Kremer, B; Verstappen, Cc; Heiberg, A; van Walsem, Mr; Frich, J; Aaserud, O; Wehus, R; Bjørgo, K; Fannemel, M; Gørvell, P; Lorentzen, E; Koivisto, Sp; Retterstøl, L; Stokke, B; Bjørnevoll, I; Sando, Sb; Dziadkiewicz, A; Nowak, M; Robowski, P; Sitek, E; Slawek, J; Soltan, W; Szinwelski, M; Blaszczyk, M; Boczarska-Jedynak, M; Ciach-Wysocka, E; Gorzkowska, A; Jasinska-Myga, B; Opala, G; Klodowska, G; Stompel, D; Ciach-Wysocka, E; Banaszkiewicz, K; Boewiriska, D; Bojakowska-Jaremek, K; Neurologii, A; Dec, M; Krawczyk, M; Rudziriska, M; Szczudlik, A; Szczygiel, E; Wasielewska, A; Wojcik, M; Wojcik, M; Bryl, A; Ciesielska, A; Klimberg, A; Marcinkowski, J; Samara, H; Sempolowicz, J; Zielonka, D; Janik, P; Kalbarczyk, A; Kwiecinski, H; Jamrozik, Z; Antczak, J; Jachinska, K; Krysa, W; Rakowicz, M; Richter, P; Rola, R; Ryglewicz, D; Sienkiewicz-Jarosz, H; Sulek, A; Witkowski, G; Zdzienicka, E; Zaremba, J; Zieora-Jakutowicz, K; Coelho, M; Correia-Guedes, L; Ferreira, Jj; Mestre, T; Mendes, T; Valadas, A; Andrade, C; Joao, Ps; Gago, M; Garrett, C; Joao, Ps; Guerra, Mr; Joao, Ps; Solis, P; Herrera, Cd; Garcia, Pm; Cubo, E; Mariscal, N; Sanchez, J; Barrero, Fj; Alonso-Frech, F; Perez, Mr; Fenollar, M; Garda, R; Rivera, Sv; Villanueva, C; Alegre, J; Bascuiiana, M; Ventura, Mf; Ribas, Gg; Moreno, Jl; Cubillo, Pt; Rufz, Pj; Frech, Fa; Dfaz, J; Guerrero, R; Dfaz, J; Artiga, Mj; Dfaz, J; Sanchez, V; Alcaraz, Lf; de Ia Arrixaca, V; Manzanares, S; de Ia Arrixaca, V; Perea, Mf; Reinante, G; Arrixaca, Ia; Torres, Mm; Moreau, Lv; de Ia Arrixaca, V; Barbera, Ma; Guia, Db; Hernanz, Lc; Catena, Jl; Sebastian, R; Ferrer, Pq; Carruesco, Gt; Bas, J; Busquets, N; Calopa, M; Buongiorno, Mt; Munoz, E; Elorza, Md; Lopez, Cd; Terol, Ds; Robert, Mf; Rufz, Bg; Casado, Ag; Martinez, Ih; Viladrich, Cm; Pons, R; Roca, E; Llesoy, Jr; Idiago, Jm; Vergara, Mr; Garcia, Ss; Riballo, Av; Hoglund, A; Palhagen, Se; Paucar, M; Sandstrom, B; Svenningsson, P; Reza-Soltani, Tw; Burgunder, Jm; Kaelin, A; Romero, I; Schupbach, M; Stebler, Y; Zaugg, Sw; Akhtar, S; Crooks, J; Curtis, A; de Souza, J; Rickards, H; Wright, J; Barker, Ra; Di Pietro, A; Fisher, K; Goodman, Ao; Hill, S; Kershaw, A; Mason, S; O'Keefe, D; Swain, R; Guzman, Nv; Busse, M; Butcher, C; Clenaghan, C; Dunnett, S; Fullam, R; Jones, L; Jones, U; Khalil, H; Minster, S; Owen, M; Hunt, S; Price, K; Rosser, A; Townhill, J; Edwards, M; Ho, C; Mcgill, M; Pearson, P; Porteous, M; Brockie, P; Foster, J; Johns, N; Mckenzie, S; Rothery, J; Thomas, G; Yates, S; Burrows, L; Chu, C; Fletcher, A; Gallantrae, D; Harding, A; Hamer, S; Kraus, A; Laver, F; Longthorpe, M; Markova, I; Raman, A; Silva, M; Thomson, A; Wild, S; Yardumian, P; Hobson, E; Jamieson, S; Musgrave, H; Rowett, L; Toscano, J; Wild, S; Yardumian, P; Clayton, C; Dipple, H; Middleton, J; Patino, D; Andrews, T; Dougherty, A; Kavalier, F; Golding, C; Laing, H; Lashwood, A; Robertson, D; Ruddy, D; Whaite, A; Santhouse, A; Andrews, T; Bruno, S; Doherty, K; Lahiri, N; Novak, M; Patel, A; Rosser, E; Tabrizi, S; Taylor, R; Warner, T; Wild, E; Arran, N; Bek, J; Callaghan, J; Craufurd, D; Fullam, R; Howard, L; Hare, M; Huson, S; Johnson, L; Jones, M; Murphy, H; Oughton, E; Partington-Janes, L; Rogers, D; Snowden, J; Sollom, A; Stopford, C; Thompson, J; Trender-Gerhard, I