University of Quindío

Urbanization alters habitat structure and resource availability, reshaping the diversity and functioning of biological communities. We evaluated how urbanization influences dung beetle (Scarabaeinae) assemblages in a Neotropical Andean city (Armenia, Colombia) across three urban contexts: ex-urban, peri-urban, and intra-urban zones. Community responses were assessed using complementary measures of abundance, expressed as the number of individuals and biomass, to examine how different facets of diversity respond to urban pressure. Dung beetle assemblages exhibited contrasting responses depending on the abundance measure considered. The number of individuals differed among urbanization zones, with peri-urban areas showing higher values than exurban sites, while biomass did not vary significantly across zones, suggesting a decoupling between numerical dominance and biomass patterns. Species-level patterns revealed marked functional contrasts, with a few large-bodied species contributing disproportionately to total biomass despite low number of individuals. Diversity analyses showed higher individual-based diversity in exurban zones, whereas biomass-based diversity was higher in exurban and peri-urban areas than in intra-urban zones. Compositional dissimilarity among zones was driven primarily by species turnover, indicating that changes in community composition are mainly associated with species replacement rather than differences in richness. Our findings highlight the importance of integrating biomass with traditional abundance measures to more accurately characterize community responses to urbanization. They also emphasize the relevance of urban and periurban green spaces for sustaining functionally diverse dung beetle assemblages in Andean urban landscapes.

Under the current global biodiversity crisis, there is a need for automated and noninvasive monitoring techniques that can gather large amounts of data cost-effectively at various ecological scales, from local to large spatial scales. These data can then be analyzed to inform stakeholders and decision-makers. One such technique is passive acoustic monitoring, which is commonly coupled with automatic identification of animal species based on their sound. Automated sound analyses usually require the training of sound detection and identification algorithms. These algorithms are based on annotated acoustic datasets which mark the occurrence of sounds of species inside sound recordings. However, compiling large annotated acoustic datasets is time-consuming and requires experts, and therefore, they normally cover reduced spatial, temporal, and taxonomic scales. This data paper presents WABAD, the World Annotated Bird Acoustic Dataset for passive acoustic monitoring. WABAD is designed to provide the public, the research community, and conservation managers with a novel and globally representative annotated acoustic dataset. This database includes 5047 min of audio files annotated to species-level by local experts with the start and end time and the upper and lower frequencies of each identified bird vocalization in the recordings. The database has a wide taxonomic and spatial coverage, including information on 91,931 vocalizations from 1192 bird species recorded at 72 recording sites in 29 recording locations (mainly countries) and distributed across 13 biomes. WABAD can be used, for example, for developing and/or validating automatic species detection algorithms, answering ecological questions, such as assessing geographical variations on bird vocalizations, or comparing acoustic diversity indices with species-based diversity indices. The dataset is published under a Creative Commons Attribution 4.0 International license that permits redistribution and reuse on the condition that the original work is properly credited.

Los episodios de alta frecuencia auricular se definen como eventos auriculares que superan el límite programado de frecuencia de detección establecido por los dispositivos electrónicos cardiacos implantables. La periodicidad y la duración de estos episodios son variables, considerándose clínicamente relevantes los que duran más de 5 minutos. En numerosos estudios, su presencia se ha asociado a la progresión a largo plazo a fibrilación auricular clínica y un mayor riesgo de ictus embólico. Los estudios han establecido que estas asociaciones están directamente relacionadas con la duración de los episodios de alta frecuencia auricular, junto con factores de riesgo como la edad, la hipertensión y los antecedentes de insuficiencia cardiaca. A pesar de existir un riesgo elevado de eventos embólicos, sigue existiendo incertidumbre respecto al inicio de la anticoagulación a largo plazo y los beneficios clínicos de dicho tratamiento. Por ello, esta revisión narrativa busca ofrecer una aproximación clínica actual y proponer un algoritmo de tratamiento para los episodios de alta frecuencia auricular según la evidencia actual.

BACKGROUND:To have maximal benefit, Alzheimer's disease-modifying treatments might need to be started before the onset of clinical symptoms. Mutations of the PSEN1 gene are inherited as fully penetrant, autosomal-dominant traits, which almost always result in the clinical onset of Alzheimer's disease before the age of 65 years. We aimed to evaluate the efficacy, including possible delayed emergence of cognitive impairment, and safety of crenezumab, an anti-amyloid monoclonal antibody, in cognitively unimpaired carriers of the PSEN1Glu280Ala mutation at high imminent risk of developing symptoms due to Alzheimer's disease. METHODS:This 5-8-year common-close, double-blind, placebo-controlled, single-centre trial screened kindred members aged 30-60 years from the main health-care site in Medellín, Colombia. Participants who were cognitively unimpaired and carried the PSEN1Glu280Ala autosomal-dominant mutation were randomly assigned 1:1 to receive placebo or subcutaneous crenezumab (investigators and participants were masked to treatment allocation), with an initial 300 mg dose every 2 weeks that increased to 720 mg every 2 weeks, and a later optional increase to 60 mg/kg intravenously every 4 weeks. Randomisation was stratified by age, education, APOE ɛ4 carrier status, and baseline Clinical Dementia Rating. Mutation non-carriers received placebo and were included in a 1:2 ratio of non-carriers to carriers to maintain genotype masking and include a genetic kindred control. Dual primary outcomes were the annualised rates of change in the Alzheimer's Prevention Initiative (API) preclinical autosomal-dominant Alzheimer's disease (ADAD) composite test total score and Free and Cued Selective Reminding Test-Cueing Index (FCSRT-CI) assessed in randomised participants who received at least one dose of the study drug, according to treatment assignment. Primary endpoints were assessed with a random coefficient regression model with a missing-at-random assumption adjusting for randomisation factors. Safety endpoints for mutation carriers were assessed in randomised participants who received at least one dose of the study drug. This trial is registered with ClinicalTrials.gov (NCT01998841) and is completed. FINDINGS:619 Colombian API registrants were prescreened, 315 were assessed for eligibility, and 252 were enrolled (crenezumab-carrier, n=85; placebo-carrier, n=84; placebo-non-carrier, n=83; 160 [63%] women and 92 [37%] men) between Dec 20, 2013, and Feb 27, 2017. 237 (94%) completed the trial, with final data collection on March 22, 2022. The annualised rate of change in the API ADAD composite was -1·10 (SE 0·29) in the crenezumab group and -1·43 (0·29) in the placebo group (between-group difference 0·33 [95% CI -0·48 to 1·13]; p=0·43). The annualised rate of change in FCSRT-CI was -0·03 (0·00) in the crenezumab group and -0·04 (0·00) in the placebo group (between-group difference 0·01 [0·00 to 0·02]; p=0·16). All participants had at least one adverse event; serious adverse events occurred in 23 (27%) of 84 in the crenezumab group and 21 (25%) of 84 in the placebo group. No fatalities occurred. INTERPRETATION:Crenezumab therapy administered for 5-8 years did not result in significant benefits on our primary clinical outcomes in cognitively unimpaired participants predisposed to developing ADAD dementia; secondary and exploratory outcomes also showed no significant effect on removal of amyloid plaques or other clinical or biomarker outcomes. Together with the results of other anti-amyloid β trials, robust fibrillar amyloid removal appears necessary for clinical efficacy in people with elevated brain amyloid. This study will further inform the biomarker, cognitive, and clinical trajectory of preclinical ADAD, the risk of clinical progression in amyloid-positive and amyloid-negative mutation carriers, and the size and design of future secondary and primary prevention trials. FUNDING:US National Institute on Aging (NIA), Banner Alzheimer's Institute, Genentech, F Hoffmann-La Roche.