ENERGETIC COSTS AND STRATEGIES OF POST‐JUVENAL MOLT IN AN EQUATORIAL BIRD, THE RUFOUS‐COLLARED SPARROW (ZONOTRICHIA CAPENSIS)

Abstract  ∙ Many tropical birds have slow‐paced life history strategies, exhibiting lower metabolic rates, reduced annual investment in reproduction, and longer lifespans relative to birds at higher latitudes. Life history strategies have been relatively well documented in adult individuals in the tropics, but we know comparatively little about the immature life history stage. Here we examine strategies of feather replacement (molt) and fattening in immature Rufous‐collared Sparrows (Zonotrichia capensis) in a high elevation equatorial population, following a parallel, previous study on an arctic congener, the White‐crowned Sparrow (Zonotrichia leucophrys gambelii). In captivity, Rufous‐ collared Sparrows incurred energetic costs of experimentally induced feather growth, similar to those previously described for Zonotrichia at higher latitudes. In contrast, free‐ranging immature Rufous‐collared Sparrows in natural molt had fat stores that declined over time, opposite to patterns evident in arctic Zonotrichia that fatten before migration. Equatorial birds in good condition molted more heavily (controlling for fat stores), suggesting that body condition limits the intensity of molt. Heavily molting equatorial sparrows also had lower amounts of fat (controlling for body condition), suggesting a trade‐off between allocation of resources to fat stores versus feather growth. Molt progressed slowly in Rufous‐collared Sparrows relative to previously described patterns in their arctic congener, which is concordant with a slower pace‐of‐life syndrome in tropical, as compared with high latitude, birds. Resumen ∙ Costos energéticos y estrategias de muda post‐juvenil en un ave ecuatorial, el Chingolo (Zonotrichia capensis) Muchas especies de aves tropicales presentan historias de vida lenta, exhibiendo bajas tasas metabólicas, esfuerzo reproductivo anual reducido, y mayor longevidad que las especies que habitan en latitudes más altas. La variación en historia de vida en especies tropicales ha sido bien documentada para individuos adultos, pero sabemos comparativa‐ mente poco de los individuos inmaduros. Aquí estudiamos las estrategias de muda y deposición de grasa en individuos inmaduros de Chingolo (Zonotrichia capensis) en una población ecuatorial de altura y comparamos los resultados con un estudio similar realizado en una población ártica del congénere Chingolo Coroniblanco (Zonotrichia leucophrys gambelii). En cautiverio, individuos juveniles de Z. capensis incurrieron costos energéticos debidos a la muda inducida, similar lo encontrado en Z. leucophrys gambelii. En contraste, Z. capensis inmaduros mudando en libertad presentaron depósitos de grasa que disminuyeron a lo largo del tiempo, lo opuesto a Z. l. gambelii, que deposita más grasa antes de migrar. Z. capensis inmaduros en buen estado nutricional (controlando por diferencias en deposición de grasa) mudaron de manera más intensa, lo que sugiere que el estado nutricional limita la muda. Individuos inmaduros de Z. capensis mudando de manera intensa presentaron menor cantidad de grasa depositada (controlando por diferencias en estado nutricional), lo que sugiere un balance entre la deposición de grasa y la muda. La muda fue más lenta en la población ecuatorial de Z. capensis comparado con la de Z. l. gambelii, lo que concuerda con lo esperado debido a la historia de vida más lenta en aves tropicales

Activity analysis of thermal imaging videos using a difference imaging approach

Infrared thermal imaging is a passive imaging technique that captures the emitted radiation from an object to estimate surface temperature, often for inference of heat transfer. Infrared thermal imaging offers the potential to detect movement without the challenges of glare, shadows, or changes in lighting associated with visual digital imaging or active infrared imaging. In this paper, we employ a frame subtraction algorithm for extracting the pixel-by-pixel relative change in signal from a fixed focus video file, tailored for use with thermal imaging videos. By summing the absolute differences across an entire video, we are able to assign quantitative activity assessments to thermal imaging data for comparison with simultaneous recordings of metabolic rates. We tested the accuracy and limits of this approach by analyzing movement of a metronome and provide an example application of the approach to a study of Darwin's finches. In principle, this “Difference Imaging Thermography” (DIT) would allow for activity data to be standardized to energetic measurements and could be applied to any radiometric imaging system

Shared genetic risk between eating disorder- and substance-use-related phenotypes:Evidence from genome-wide association studies

First published: 16 February 202

Genomic Relationships, Novel Loci, and Pleiotropic Mechanisms across Eight Psychiatric Disorders

Genetic influences on psychiatric disorders transcend diagnostic boundaries, suggesting substantial pleiotropy of contributing loci. However, the nature and mechanisms of these pleiotropic effects remain unclear. We performed analyses of 232,964 cases and 494,162 controls from genome-wide studies of anorexia nervosa, attention-deficit/hyper-activity disorder, autism spectrum disorder, bipolar disorder, major depression, obsessive-compulsive disorder, schizophrenia, and Tourette syndrome. Genetic correlation analyses revealed a meaningful structure within the eight disorders, identifying three groups of inter-related disorders. Meta-analysis across these eight disorders detected 109 loci associated with at least two psychiatric disorders, including 23 loci with pleiotropic effects on four or more disorders and 11 loci with antagonistic effects on multiple disorders. The pleiotropic loci are located within genes that show heightened expression in the brain throughout the lifespan, beginning prenatally in the second trimester, and play prominent roles in neurodevelopmental processes. These findings have important implications for psychiatric nosology, drug development, and risk prediction.Peer reviewe

Dissecting the Shared Genetic Architecture of Suicide Attempt, Psychiatric Disorders, and Known Risk Factors

Background Suicide is a leading cause of death worldwide, and nonfatal suicide attempts, which occur far more frequently, are a major source of disability and social and economic burden. Both have substantial genetic etiology, which is partially shared and partially distinct from that of related psychiatric disorders. Methods We conducted a genome-wide association study (GWAS) of 29,782 suicide attempt (SA) cases and 519,961 controls in the International Suicide Genetics Consortium (ISGC). The GWAS of SA was conditioned on psychiatric disorders using GWAS summary statistics via multitrait-based conditional and joint analysis, to remove genetic effects on SA mediated by psychiatric disorders. We investigated the shared and divergent genetic architectures of SA, psychiatric disorders, and other known risk factors. Results Two loci reached genome-wide significance for SA: the major histocompatibility complex and an intergenic locus on chromosome 7, the latter of which remained associated with SA after conditioning on psychiatric disorders and replicated in an independent cohort from the Million Veteran Program. This locus has been implicated in risk-taking behavior, smoking, and insomnia. SA showed strong genetic correlation with psychiatric disorders, particularly major depression, and also with smoking, pain, risk-taking behavior, sleep disturbances, lower educational attainment, reproductive traits, lower socioeconomic status, and poorer general health. After conditioning on psychiatric disorders, the genetic correlations between SA and psychiatric disorders decreased, whereas those with nonpsychiatric traits remained largely unchanged. Conclusions Our results identify a risk locus that contributes more strongly to SA than other phenotypes and suggest a shared underlying biology between SA and known risk factors that is not mediated by psychiatric disorders.Peer reviewe

Analysis of shared heritability in common disorders of the brain

ience, this issue p. eaap8757 Structured Abstract INTRODUCTION Brain disorders may exhibit shared symptoms and substantial epidemiological comorbidity, inciting debate about their etiologic overlap. However, detailed study of phenotypes with different ages of onset, severity, and presentation poses a considerable challenge. Recently developed heritability methods allow us to accurately measure correlation of genome-wide common variant risk between two phenotypes from pools of different individuals and assess how connected they, or at least their genetic risks, are on the genomic level. We used genome-wide association data for 265,218 patients and 784,643 control participants, as well as 17 phenotypes from a total of 1,191,588 individuals, to quantify the degree of overlap for genetic risk factors of 25 common brain disorders. RATIONALE Over the past century, the classification of brain disorders has evolved to reflect the medical and scientific communities' assessments of the presumed root causes of clinical phenomena such as behavioral change, loss of motor function, or alterations of consciousness. Directly observable phenomena (such as the presence of emboli, protein tangles, or unusual electrical activity patterns) generally define and separate neurological disorders from psychiatric disorders. Understanding the genetic underpinnings and categorical distinctions for brain disorders and related phenotypes may inform the search for their biological mechanisms. RESULTS Common variant risk for psychiatric disorders was shown to correlate significantly, especially among attention deficit hyperactivity disorder (ADHD), bipolar disorder, major depressive disorder (MDD), and schizophrenia. By contrast, neurological disorders appear more distinct from one another and from the psychiatric disorders, except for migraine, which was significantly correlated to ADHD, MDD, and Tourette syndrome. We demonstrate that, in the general population, the personality trait neuroticism is significantly correlated with almost every psychiatric disorder and migraine. We also identify significant genetic sharing between disorders and early life cognitive measures (e.g., years of education and college attainment) in the general population, demonstrating positive correlation with several psychiatric disorders (e.g., anorexia nervosa and bipolar disorder) and negative correlation with several neurological phenotypes (e.g., Alzheimer's disease and ischemic stroke), even though the latter are considered to result from specific processes that occur later in life. Extensive simulations were also performed to inform how statistical power, diagnostic misclassification, and phenotypic heterogeneity influence genetic correlations. CONCLUSION The high degree of genetic correlation among many of the psychiatric disorders adds further evidence that their current clinical boundaries do not reflect distinct underlying pathogenic processes, at least on the genetic level. This suggests a deeply interconnected nature for psychiatric disorders, in contrast to neurological disorders, and underscores the need to refine psychiatric diagnostics. Genetically informed analyses may provide important "scaffolding" to support such restructuring of psychiatric nosology, which likely requires incorporating many levels of information. By contrast, we find limited evidence for widespread common genetic risk sharing among neurological disorders or across neurological and psychiatric disorders. We show that both psychiatric and neurological disorders have robust correlations with cognitive and personality measures. Further study is needed to evaluate whether overlapping genetic contributions to psychiatric pathology may influence treatment choices. Ultimately, such developments may pave the way toward reduced heterogeneity and improved diagnosis and treatment of psychiatric disorders

Evidence of Feline Immunodeficiency Virus, Feline Leukemia Virus, and \u3ci\u3eToxoplasma gondii\u3c/i\u3e in Feral Cats on Mauna Kea, Hawaii

We determined prevalence to feline immunodeficiency virus (FIV) antibodies, feline leukemia virus (FeLV) antigen, and Toxoplasma gondii antibodies in feral cats (Felis catus) on Mauna Kea Hawaii from April 2002 to May 2004. Six of 68 (8.8%) and 11 of 68 (16.2%) cats were antibody positive to FIV and antigen positive for FeLV, respectively; 25 of 67 (37.3%) cats were seropositive to T. gondii. Antibodies to FeLV and T. gondii occurred in all age and sex classes, but FIV occurred only in adult males. Evidence of current or previous infections with two of these infectious agents was detected in eight of 64 cats (12.5%). Despite exposure to these infectious agents, feral cats remain abundant throughout the Hawaiian Islands

The Effects of Feral Cats on Insular Wildlife: The Club-Med Syndrome

Domestic cats have been introduced to many of the world’s islands where they have been particularly devastating to insular wildlife which, in most cases, evolved in the absence of terrestrial predatory mammals and feline diseases. We review the effects of predation, feline diseases, and the life history characteristics of feral cats and their prey that have contributed to the extirpation and extinction of many insular vertebrate species. The protozoan Toxoplasma gondii is a persistent landbased zoonotic pathogen hosted by cats that is known to cause mortality in several insular bird species. It also enters marine environments in cat feces, where it can cause the mortality of marine mammals. Feral cats remain widespread on islands throughout the world, and are frequently subsidized in colonies which caretakers often assert have little negative effect on native wildlife. However, population genetics, home range, and movement studies all suggest that there are no locations on smaller islands where these cats cannot penetrate within two generations. While the details of past vertebrate extinctions were rarely documented during contemporary time, a strong line of evidence is emerging that the removal of feral cats from islands can rapidly facilitate the recolonization of extirpated species, particularly seabirds. Islands offer unique, mostly self-contained ecosystems in which to conduct controlled studies of the effects of feral cats on wildlife, having implications for continental systems. The response of terrestrial wildlife such as passerine birds, small mammals, and herptiles still needs more thorough long-term monitoring and documentation after the removal of feral cats