Habitat split as a driver of disease in amphibians

Anthropogenic habitat disturbance is fundamentally altering patterns of disease transmission and immunity across the vertebrate tree of life. Most studies linking anthropogenic habitat change and disease focus on habitat loss and fragmentation, but these processes often lead to a third process that is equally important: habitat split. Defined as spatial separation between the multiple classes of natural habitat that many vertebrate species require to complete their life cycles, habitat split has been linked to population declines in vertebrates, e.g. amphibians breeding in lowland aquatic habitats and overwintering in fragments of upland terrestrial vegetation. Here, we link habitat split to enhanced disease risk in amphibians (i) by reviewing the biotic and abiotic forces shaping elements of immunity and (ii) through a spatially oriented field study focused on tropical frogs. We propose a framework to investigate mechanisms by which habitat split influences disease risk in amphibians, focusing on three broad host factors linked to immunity: (i) composition of symbiotic microbial communities, (ii) immunogenetic variation, and (iii) stress hormone levels. Our review highlights the potential for habitat split to contribute to host-associated microbiome dysbiosis, reductions in immunogenetic repertoire, and chronic stress, that often facilitate pathogenic infections and disease in amphibians and other classes of vertebrates. We highlight that targeted habitat-restoration strategies aiming to connect multiple classes of natural habitats (e.g. terrestrial–freshwater, terrestrial–marine, marine–freshwater) could enhance priming of the vertebrate immune system through repeated low-load exposure to enzootic pathogens and reduced stress-induced immunosuppression.     

The length-weight relationship of four fish species captured in the Ibicuí River,southern Brazil

Length-Weight relationship (LWRs) were estimated for four fish species occurring in the Ibicuí River drainage basin, southern Brazil. Samples were captured monthly during the spring and summer seasons (October 2018 to March 2019). The fish were caught with gillnets of different meshes (15, 20, 25, 30, 40 mm between adjacent nodes) and a trawl net (5 mm mesh between adjacent nodes) Eighteen excursions were realized in three sites, with a length of approximately 100 km, in third-order flux, all distributed in sub-basin Ibicuí River. The captured tools were installed at the end of the day (6 p.m.) and removed around 6 a.m. the next day. The present study provides the length-weight relationship for four species (Astyanax dissensos, Galeocharax humeralis, Hypostomus roseopunctatus e Hypostomus uruguayensis).     

Length-weight relationship of 13 middle Uruguay River basin species,Southern Brazil

Length-weight relationship (LWRs) were determined for 13 fish species from the Uruguay River. The fish were caught in six locations and sampled at each location during each season, totaling 72 samplings, starting in May 2016 and ending in February 2018. Various materials were used such as gillnets (15; 20; 25 30; 40 and 80 mm, triple mesh 150.30.150 150.40.150 and 150.50.150 mm, 8 mm trawl). We also used two longlines, 100 m long, 30 hooks each (hooks 5/0 and 12/0), baited with small fish, corn and snail. Length-weight relationship were adjusted appropriately for all species (r² > .95). The b values of the LRW equations ranged from 2.38 in Steindachnerina brevipinna to 3.62 in Pimelodus atrobrunneus.     

Habitat size determine algae biomass in tank-bromeliads

The primary goal of this study was to evaluate the relative importance of habitat physical properties, bottom-up and top-down factors, and their interaction on algae biomass in tank-bromeliads. We sampled algae biomass (chlorophyll-a concentration), micro-metazoan density, mosquito abundance, and several environmental variables, including nutrient concentrations and characteristics of the habitat physical structure, in a survey of 64 tank-bromeliads of four different species (Aechmea nudicaulis, Aechmea lingulata, Neoregelia cruenta, and Vriesea neoglutinosa). We analyzed the complete and individual bromeliad species datasets using an information-theoretic model selection approach (Akaike’s information criterion). Bromeliad species, maximum water volume, and bromeliad diameter comprised the best model for determining chlorophyll-a concentrations for the complete dataset. The maximum water volume also comprised the best model to explain chlorophyll-a concentrations in three of four bromeliad species datasets. Interactions between consumers and nutrient concentration were included in the subsequent models, but they were not statistically significant. Taken together, these results demonstrate that the impact of habitat size on the associated autotrophic biomass occurs possibly via changes in community susceptibility to disturbances, particularly drought. We can conclude that habitat size is more important than resource availability or herbivory on phytotelm autotrophic biomass regulation in these natural microcosms.     

Molecular Dynamics,Flexible Docking,Virtual Screening,ADMET Predictions,and Molecular Interaction Field Studies to Design Novel Potential MAO-B Inhibitors

Abstract

Monoamine oxidase is a flavoenzyme bound to the mitochondrial outer membranes of the cells, which is responsible for the oxidative deamination of neurotransmitter and dietary amines. It has two distinct isozymic forms, designated MAO-A and MAO-B, each displaying different substrate and inhibitor specificities. They are the well-known targets for antidepressant, Parkinson's disease, and neuroprotective drugs. Elucidation of the x-ray crystallographic structure of MAO-B has opened the way for the molecular modeling studies. In this work we have used molecular modeling, density functional theory with correlation, virtual screening, flexible docking, molecular dynamics, ADMET predictions, and molecular interaction field studies in order to design new molecules with potential higher selectivity and enzymatic inhibitory activity over MAO-B.     

AAV-mediated inhibition of ULK1 promotes axonal regeneration in the central nervous system in vitro and in vivo

Axonal damage is an early step in traumatic and neurodegenerative disorders of the central nervous system (CNS). Damaged axons are not able to regenerate sufficiently in the adult mammalian CNS, leading to permanent neurological deficits. Recently, we showed that inhibition of the autophagic protein ULK1 promotes neuroprotection in different models of neurodegeneration. Moreover, we demonstrated previously that axonal protection improves regeneration of lesioned axons. However, whether axonal protection mediated by ULK1 inhibition could also improve axonal regeneration is unknown. Here, we used an adeno-associated viral (AAV) vector to express a dominant-negative form of ULK1 (AAV.ULK1.DN) and investigated its effects on axonal regeneration in the CNS. We show that AAV.ULK1.DN fosters axonal regeneration and enhances neurite outgrowth in vitro. In addition, AAV.ULK1.DN increases neuronal survival and enhances axonal regeneration after optic nerve lesion, and promotes long-term axonal protection after spinal cord injury (SCI) in vivo. Interestingly, AAV.ULK1.DN also increases serotonergic and dopaminergic axon sprouting after SCI. Mechanistically, AAV.ULK1.DN leads to increased ERK1 activation and reduced expression of RhoA and ROCK2. Our findings outline ULK1 as a key regulator of axonal degeneration and regeneration, and define ULK1 as a promising target to promote neuroprotection and regeneration in the CNS.Subject terms: Cell death in the nervous system, Neurodegeneration, Spinal cord injury