Vigilance and feeding behaviour of Ruffs Philomachus pugnax during spring migration in Eastern Austria

Die vorliegende Studie testete Effekte von Truppgröße und anderen potentiell wichtigen Variablen (Standort, Vegetationsbedeckung, Windstärke, Bewölkung, Datum, Tageszeit und Nahrungshabitat) auf das Sicherungsverhalten und die Nahrungsaufnahme von Kampfläufern Philomachus pugnax während des Frühjahrszuges im Seewinkel, einem wichtigen Rastplatz für Limikolen in Ostösterreich. Hierfür wurden Kampfläufer während der Nahrungssuche an vier Salzlacken gefilmt. Insgesamt standen 681 Filmsequenzen für Analysen zur Verfügung. Die zwei Hauptkomponenten des Furagierverhaltens, Sichern und Nahrungsaufnahme, quantifiziert als Sicherungsrate (Häufigkeit von Sicherungsverhalten pro 30 s) bzw. Pickrate (Häufigkeit von Pickverhalten pro 30 s), waren nicht korreliert. Um Effekte der Prädiktorvariablen auf Sicherungs- und Pickrate furagierender Kampfläufer zu testen, wurden Generalisierte Lineare Modelle (GLMs) berechnet, wobei alle Variablen und alle möglichen Kombinationen von Teilmengen der berücksichtigten Variablen inkludiert wurden. Drei Variablen verblieben in den 12 besten GLMs (ausgewählt nach dem Akaike 3 Informationskriterium) zum Testen von Effekten auf die Sicherungsrate von Kampfläufern: Standort, Nahrungshabitat und Truppgröße. Diese Variablen hatten nach der Wald-Statistik auch einen signifikanten Effekt auf die Sicherungsrate. Neben Unterschieden der Sicherungsrate zwischen den Standorten, wiesen am Land furagierende Kampfläufer eine signifikant höhere Sicherungsrate auf als semiaquatisch furagierende Vögel. Zudem nahm die Sicherungsrate mit zunehmender Truppgröße ab. Um Effekte der vorher erwähnten Prädiktorvariablen auf die Pickrate zu testen, wurde die Mobilität der Kampfläufer während der Nahrungssuche – quantifiziert als Anzahl an Schritten pro 30 s – in die Modellselektion miteinbezogen. Vier der neun Prädiktorvariablen blieben im besten Modell: Standort, Windstärke, Bewölkung und Datum. Zwei von ihnen, Standort und Windstärke, waren in allen 23 besten Modellen inkludiert und hatten nach der Wald-Statistik einen starken Effekt auf die Pickrate. Die Pickrate stieg mit zunehmender Windstärke an. Um zusätzlich mögliche Effekte von Mauserstatus bzw. Gefiederfärbung der Männchen (als Indikator für ihren sozialen Status) auf Sicherungs- und Nahrungsaufnahmerate zu evaluieren, wurden nur jene Präditorvariablen herangezogen, die bereits einen signifikanten Effekt auf die Sicherungs- und/oder Pickrate zeigten (Standort, Nahrungshabitat, Truppgröße, Bewölkung und Windstärke). Außerdem wurde das Datum als Prädiktorvariable miteinbezogen und eine gegenseitige Interaktion zwischen Datum und Mauserstatus bzw. männlicher Gefiederfärbung zugelassen, da sich der Anteil an Vögeln in den verschiedenen Mauserstadien und Farbmorphen mit fortschreitendem Frühjahrszug änderte. Berechnete GLMs zeigten keine signifikanten Effekte des Mauserstatus oder des sozialen Status der Männchen auf die Sicherungs- und Pickrate. Unsere Arbeit hebt - bei gleichzeitiger Berücksichtigung anderer Variablen, die die Sicherungsrate beeinflussen - die Bedeutung der Truppgröße hervor, um die Varianz der Sicherungsrate von furagierenden Kampfläufern zu erklären. Im Gegensatz dazu hatte die Truppgröße keinen direkten Effekt auf die Nahrungsaufnahmerate. Jedoch nahm die Schrittzahl der Vögel mit zunehmender Truppgröße ab, was als Hinweis auf bessere Nahrungsverfügbarkeit an jenen Standorten, an denen sich größere Trupps bilden, gewertet werden kann. Das wird auch durch die Beobachtung verstärkt, dass die Nahrungsaufnahmerate mit abnehmender Schrittzahl anstieg. Außerdem ist unsere Beobachtung, dass sich das Sicherungs- und Nahrungsaufnahmeverhalten von 4 Kampfläufern zwischen den Salzlacken signifikant unterschied, von wichtiger Bedeutung für etwaige Schutzmaßnahmen.This study tested for effects of flock size and other potentially important variables (location, vegetation cover, wind force, cloud cover, date, time and feeding habitat) on vigilance level and food intake of foraging Ruffs Philomachus pugnax during spring migration at Seewinkel, an important stopover site for waders in Eastern Austria. Therefore, foraging Ruffs were filmed at four different salt ponds. Finally, a total of 681 film sequences were available for analysis. The two main components of foraging behaviour, vigilance and food intake, measured as scan rate (number of scans per 30 sec) and peck rate (number of pecks per 30 sec), respectively, were not correlated. To test for effects of predictor variables on scan and peck rate of foraging Ruffs Generalized Linear Models (GLMs) were calculated including all variables and all possible subsets. Three variables remained in the 12 best GLMs (selected according to Akaike´s Information Criterion) testing for effects on scan rate of foraging Ruffs: feeding location, feeding habitat and flock size. These variables also significantly affected Ruffs´ scan rates according to Wald statistics. Besides differences of scan rates between feeding locations, vigilance level was significantly higher in terrestrially foraging Ruffs than in birds feeding at semi-aquatic habitat patches. Furthermore, scan rate decreased with increasing flock size. To test for effects of the eight aforementioned predictor variables on peck rate, the mobility of Ruffs during foraging quantified as number of steps per 30 sec was included in all calculated GLMs. Four of the nine predictor variables remained in the best model: location, wind force, cloud cover and date. Two of them, feeding location and wind force, were included in all 23 best models and had a strong effect on peck rate according to Wald statistics. Peck rate increased with increasing wind force. GLMs to assess effects of moult stage and colour morph of males (indicating their social status) on vigilance and peck rate additionally only included predictor variables, 2 which already proved to have a significant effect on scan and/or peck rate (location, feeding habitat, flock size, cloud cover and wind force). Furthermore, we included the date as predictor variable and allowed for a two-way interaction between date and moult stage and male plumage colour, respectively, because both the proportion of birds with different moult stage and birds belonging to different colour morphs changed with progressing spring migration. Calculated GLMs did not indicate any significant effects of moult stage or social status of males on scan and peck rate. Our study emphasized that even when controlled for other variables affecting scan rates, flock size still remains important for explaining variance in vigilance levels of foraging Ruffs. In contradiction, flocking did not directly affect food intake rate. However, stepping rate of birds decreased with increasing flock size indicating a better access to prey at sites where larger flocks aggregate. This is confirmed by the observation that food intake indeed increased with declining stepping rate. Furthermore, our observation that Ruffs´ vigilance and food intake significantly differed between salt pans has important implications for conservation

CCDC26, CDKN2BAS, RTEL1 and TERT Polymorphisms in pediatric brain tumor susceptibility

The role of genetic polymorphisms in pediatric brain tumor (PBT) etiology is poorly understood. In this study, we tested the hypothesis that single nucleotide polymorphisms identified by genome-wide association studies on adult glioma are also associated with PBT ris

CCDC26, CDKN2BAS, RTEL1 and TERT Polymorphisms in pediatric brain tumor susceptibility

The role of genetic polymorphisms in pediatric brain tumor (PBT) etiology is poorly understood. In this study, we tested the hypothesis that single nucleotide polymorphisms identified by genome-wide association studies on adult glioma are also associated with PBT ris

A multinational case-control study on childhood brain tumours, anthropogenic factors, birth characteristics and prenatal exposures: A validation of interview data.

Little is known about the aetiology of childhood brain tumours. We investigated anthropometric factors (birth weight, length, maternal age), birth characteristics (e.g. vacuum extraction, preterm delivery, birth order) and exposures during pregnancy (e.g. maternal: smoking, working, dietary supplement intake) in relation to risk of brain tumour diagnosis among 7-19 year olds. The multinational case-control study in Denmark, Sweden, Norway and Switzerland (CEFALO) included interviews with 352 (participation rate=83.2%) eligible cases and 646 (71.1%) population-based controls. Interview data were complemented with data from birth registries and validated by assessing agreement (Cohen's Kappa). We used conditional logistic regression models matched on age, sex and geographical region (adjusted for maternal age and parental education) to explore associations between birth factors and childhood brain tumour risk. Agreement between interview and birth registry data ranged from moderate (Kappa=0.54; worked during pregnancy) to almost perfect (Kappa=0.98; birth weight). Neither anthropogenic factors nor birth characteristics were associated with childhood brain tumour risk. Maternal vitamin intake during pregnancy was indicative of a protective effect (OR 0.75, 95%-CI: 0.56-1.01). No association was seen for maternal smoking during pregnancy or working during pregnancy. We found little evidence that the considered birth factors were related to brain tumour risk among children and adolescents

Mobile Phone Use and Brain Tumors in Children and Adolescents: A Multicenter Case-Control Study

Background It has been hypothesized that children and adolescents might be more vulnerable to possible health effects from mobile phone exposure than adults. We investigated whether mobile phone use is associated with brain tumor risk among children and adolescents. Methods CEFALO is a multicenter case-control study conducted in Denmark, Sweden, Norway, and Switzerland that includes all children and adolescents aged 7-19 years who were diagnosed with a brain tumor between 2004 and 2008. We conducted interviews, in person, with 352 case patients (participation rate: 83%) and 646 control subjects (participation rate: 71%) and their parents. Control subjects were randomly selected from population registries and matched by age, sex, and geographical region. We asked about mobile phone use and included mobile phone operator records when available. Odds ratios (ORs) for brain tumor risk and 95% confidence intervals (CIs) were calculated using conditional logistic regression models. Results Regular users of mobile phones were not statistically significantly more likely to have been diagnosed with brain tumors compared with nonusers (OR = 1.36; 95% CI = 0.92 to 2.02). Children who started to use mobile phones at least 5 years ago were not at increased risk compared with those who had never regularly used mobile phones (OR = 1.26, 95% CI = 0.70 to 2.28). In a subset of study participants for whom operator recorded data were available, brain tumor risk was related to the time elapsed since the mobile phone subscription was started but not to amount of use. No increased risk of brain tumors was observed for brain areas receiving the highest amount of exposure. Conclusion The absence of an exposure-response relationship either in terms of the amount of mobile phone use or by localization of the brain tumor argues against a causal associatio

Common genetic variations in cell cycle and DNA repair pathways associated with pediatric brain tumor susceptibility.

Knowledge on the role of genetic polymorphisms in the etiology of pediatric brain tumors (PBTs) is limited. Therefore, we investigated the association between single nucleotide polymorphisms (SNPs), identified by candidate gene-association studies on adult brain tumors, and PBT risk.The study is based on the largest series of PBT cases to date. Saliva DNA from 245 cases and 489 controls, aged 7-19 years at diagnosis/reference date, was genotyped for 68 SNPs. Data were analyzed using unconditional logistic regression.The results showed EGFRrs730437 and EGFRrs11506105 may decrease susceptibility to PBTs, whereas ERCC1rs3212986 may increase risk of these tumors. Moreover, stratified analyses indicated CHAF1Ars243341, CHAF1Ars2992, and XRCC1rs25487 were associated with a decreased risk of astrocytoma subtype. Furthermore, an increased risk of non-astrocytoma subtype associated with EGFRrs9642393, EME1rs12450550, ATMrs170548, and GLTSCRrs1035938 as well as a decreased risk of this subtype associated with XRCC4rs7721416 and XRCC4rs2662242 were detected.This study indicates SNPs in EGFR, ERCC1, CHAF1A, XRCC1, EME1, ATM, GLTSCR1, and XRCC4 may be associated with the risk of PBTs. Therefore, cell cycle and DNA repair pathways variations associated with susceptibility to adult brain tumors also seem to be associated with PBT risk, suggesting pediatric and adult brain tumors might share similar etiological pathways

Spectrum and prevalence of genetic predisposition in medulloblastoma: a retrospective genetic study and prospective validation in a clinical trial cohort.

BACKGROUND: Medulloblastoma is associated with rare hereditary cancer predisposition syndromes; however, consensus medulloblastoma predisposition genes have not been defined and screening guidelines for genetic counselling and testing for paediatric patients are not available. We aimed to assess and define these genes to provide evidence for future screening guidelines. METHODS: In this international, multicentre study, we analysed patients with medulloblastoma from retrospective cohorts (International Cancer Genome Consortium [ICGC] PedBrain, Medulloblastoma Advanced Genomics International Consortium [MAGIC], and the CEFALO series) and from prospective cohorts from four clinical studies (SJMB03, SJMB12, SJYC07, and I-HIT-MED). Whole-genome sequences and exome sequences from blood and tumour samples were analysed for rare damaging germline mutations in cancer predisposition genes. DNA methylation profiling was done to determine consensus molecular subgroups: WNT (MBWNT), SHH (MBSHH), group 3 (MBGroup3), and group 4 (MBGroup4). Medulloblastoma predisposition genes were predicted on the basis of rare variant burden tests against controls without a cancer diagnosis from the Exome Aggregation Consortium (ExAC). Previously defined somatic mutational signatures were used to further classify medulloblastoma genomes into two groups, a clock-like group (signatures 1 and 5) and a homologous recombination repair deficiency-like group (signatures 3 and 8), and chromothripsis was investigated using previously established criteria. Progression-free survival and overall survival were modelled for patients with a genetic predisposition to medulloblastoma. FINDINGS: We included a total of 1022 patients with medulloblastoma from the retrospective cohorts (n=673) and the four prospective studies (n=349), from whom blood samples (n=1022) and tumour samples (n=800) were analysed for germline mutations in 110 cancer predisposition genes. In our rare variant burden analysis, we compared these against 53 105 sequenced controls from ExAC and identified APC, BRCA2, PALB2, PTCH1, SUFU, and TP53 as consensus medulloblastoma predisposition genes according to our rare variant burden analysis and estimated that germline mutations accounted for 6% of medulloblastoma diagnoses in the retrospective cohort. The prevalence of genetic predispositions differed between molecular subgroups in the retrospective cohort and was highest for patients in the MBSHH subgroup (20% in the retrospective cohort). These estimates were replicated in the prospective clinical cohort (germline mutations accounted for 5% of medulloblastoma diagnoses, with the highest prevalence [14%] in the MBSHH subgroup). Patients with germline APC mutations developed MBWNT and accounted for most (five [71%] of seven) cases of MBWNT that had no somatic CTNNB1 exon 3 mutations. Patients with germline mutations in SUFU and PTCH1 mostly developed infant MBSHH. Germline TP53 mutations presented only in childhood patients in the MBSHH subgroup and explained more than half (eight [57%] of 14) of all chromothripsis events in this subgroup. Germline mutations in PALB2 and BRCA2 were observed across the MBSHH, MBGroup3, and MBGroup4 molecular subgroups and were associated with mutational signatures typical of homologous recombination repair deficiency. In patients with a genetic predisposition to medulloblastoma, 5-year progression-free survival was 52% (95% CI 40-69) and 5-year overall survival was 65% (95% CI 52-81); these survival estimates differed significantly across patients with germline mutations in different medulloblastoma predisposition genes. INTERPRETATION: Genetic counselling and testing should be used as a standard-of-care procedure in patients with MBWNT and MBSHH because these patients have the highest prevalence of damaging germline mutations in known cancer predisposition genes. We propose criteria for routine genetic screening for patients with medulloblastoma based on clinical and molecular tumour characteristics. FUNDING: German Cancer Aid; German Federal Ministry of Education and Research; German Childhood Cancer Foundation (Deutsche Kinderkrebsstiftung); European Research Council; National Institutes of Health; Canadian Institutes for Health Research; German Cancer Research Center; St Jude Comprehensive Cancer Center; American Lebanese Syrian Associated Charities; Swiss National Science Foundation; European Molecular Biology Organization; Cancer Research UK; Hertie Foundation; Alexander and Margaret Stewart Trust; V Foundation for Cancer Research; Sontag Foundation; Musicians Against Childhood Cancer; BC Cancer Foundation; Swedish Council for Health, Working Life and Welfare; Swedish Research Council; Swedish Cancer Society; the Swedish Radiation Protection Authority; Danish Strategic Research Council; Swiss Federal Office of Public Health; Swiss Research Foundation on Mobile Communication; Masaryk University; Ministry of Health of the Czech Republic; Research Council of Norway; Genome Canada; Genome BC; Terry Fox Research Institute; Ontario Institute for Cancer Research; Pediatric Oncology Group of Ontario; The Family of Kathleen Lorette and the Clark H Smith Brain Tumour Centre; Montreal Children's Hospital Foundation; The Hospital for Sick Children: Sonia and Arthur Labatt Brain Tumour Research Centre, Chief of Research Fund, Cancer Genetics Program, Garron Family Cancer Centre, MDT's Garron Family Endowment; BC Childhood Cancer Parents Association; Cure Search Foundation; Pediatric Brain Tumor Foundation; Brainchild; and the Government of Ontario