Biology subjects

Gomes, G.

Publications and source records attributed to Gomes, G..

6 recordsLinked to original sources

bioRxiv2025

Regional heterothermy in Megasoma gyas is not related to active heat dissipation by the horns

Animals rely on physiological and behavioral processes to maintain thermal balance. Some animals, however, bear structures that help dissipate excess heat when body temperatures rise. Although widespread in animals, animal weapons--exaggerated morphological structures with multiple characteristics that can make them good at dissipating heat--have rarely been studied in the context of thermoregulation. Here, we investigated whether the horns of the Rhinoceros Beetle (Megasoma gyas) acted as a thermal window. We heated live and dead beetles to 30{o}C and allowed them to cool to 20{o}C while measuring surface temperature changes in four body regions: the cephalic and thoracic horns, the scutellum, and the abdomen. If horns actively dissipated heat, they would show the lowest cooling rate among body regions. Contrary to this expectation, we found that the cephalic horn had the highest cooling rate, followed by the abdomen, thoracic horn, and scutellum, respectively. This suggests that the horns are not used for active heat dissipation in M. gyas. The low cooling rate of the scutellum can be explained by the presence of large flight muscles in the thorax, which play a role in heat generation, but could also aid in heat dissipation by pumping hemolymph across tagmata or through the low-insulated cuticle to prevent thoracic overheating. We also demonstrate that beetles show regional heterothermy even in the absence of exercise or stress. As such, we propose that regional heterothermy may result from both active (control of hemolymph flow) and passive (heat dissipation through poorly insulated structures) processes within individuals.

animal behavior and cognition↗

bioRxiv2022

Targeting C5aR1 signaling reduced neutrophil extracellular traps and ameliorates COVID-19 pathology

Patients with severe COVID-19 develop acute respiratory distress syndrome (ARDS) that may progress to cytokine storm syndrome, organ dysfunction, and death. Considering that complement component 5a (C5a), through its cellular receptor C5aR1, has potent proinflammatory actions, and plays immunopathological roles in inflammatory diseases, we investigated whether C5a/C5aR1 pathway could be involved in COVID-19 pathophysiology. C5a/C5aR1 signaling increased locally in the lung, especially in neutrophils of critically ill COVID-19 patients compared to patients with influenza infection, as well as in the lung tissue of K18-hACE2 Tg mice (Tg mice) infected with SARS-CoV-2. Genetic and pharmacological inhibition of C5aR1 signaling ameliorated lung immunopathology in Tg-infected mice. Mechanistically, we found that C5aR1 signaling drives neutrophil extracellular trap (NET)s-dependent immunopathology. These data confirm the immunopathological role of C5a/C5aR1 signaling in COVID-19 and indicate that antagonist of C5aR1 could be useful for COVID-19 treatment.

immunology↗

bioRxiv2019

On the Mathematics of Populations

Selection acting on unobserved heterogeneity is a fundamental issue in the mathematics of populations. As recognised in disciplines as diverse as demography [11, 23, 24], ecology [10, 9], evolution [21] and epidemiology [1, 4, 5], in any population, individuals differ in many characteristics and it is essential that researchers understand which of these are under selection and how selection processes operate. Here I describe conceptual and methodological developments in demography and ecology, and discuss the importance of adopting similar approaches in evolution and epidemiology.

epidemiology↗

bioRxiv2019

Synaptic control of DNA-methylation involves activity-dependent degradation of DNMT3a1 in the nucleus

DNA-methylation is a crucial epigenetic mark for activity-dependent gene expression in neurons. Very little is known how synaptic signals impact promoter methylation in neuronal nuclei. In this study we show that protein levels of the principal de novo DNA-methyltransferase in neurons, DNMT3a1, are tightly controlled by activation of N-methyl-D-aspartate receptors (NMDAR) containing the GluN2A subunit. Interestingly, synaptic NMDAR drive degradation of the methyltransferase in a neddylation-dependent manner. Inhibition of neddylation, the conjugation of the small ubiquitin-like protein NEDD8 to lysine residues, interrupts degradation of DNMT3a1 and results in deficits of promoter methylation of activity-dependent genes, synaptic plasticity as well as memory formation. In turn, the underlying molecular pathway is triggered by the induction of synaptic plasticity and in response to object location learning. Collectively the data show that GluN2A containing NMDAR control synapse-to-nucleus signaling that links plasticity-relevant signals to activity-dependent DNA-methylation involved in memory formation.

neuroscience↗

bioRxiv2018

Introducing risk inequality metrics in tuberculosis policy development

Global stakeholders including the World Health Organization rely on predictive models for developing strategies and setting targets for tuberculosis care and control programs. Failure to account for variation in individual risk leads to substantial biases that impair data interpretation and policy decisions1,2. Anticipated impediments to estimating heterogeneity for each parameter are discouraging despite considerable technical progress in recent years. Here we identify acquisition of infection as the single process where heterogeneity most fundamentally impacts model outputs, due to cohort selection imposed by dynamic forces of infection. Individuals with higher risk of acquiring infection are predominantly affected by the pathogen, leaving the unaffected pool with those whose intrinsic risk is lower. This causes susceptibility pools to attain average risks which are lower under higher forces of infection. Interventions that modify the force of infection change the strength of selection, and therefore alter average risks in the pools which feed further incidence. Inability to account for these dynamics is what makes homogenous models unsuitable. We introduce concrete metrics to approximate risk inequality in tuberculosis, demonstrate their utility in mathematical models, and pack the information into a risk inequality coefficient which can be calculated and reported by national tuberculosis programs for use in policy development and modeling.

epidemiology↗

bioRxiv2018

Non-heritable variation in individual fitness adds stability to neutral theories in ecology and evolution

Neutral theories in ecology1 and evolution2 contend that high diversity of natural communities and high rates of molecular evolution conform to models where individuals have equal fitness and mutations have no effects. Demographic stochasticity makes community and population compositions inherently unstable under these models, with overall levels of diversity being maintained by random processes. This is in contrast with niche and adaptive theories which emphasize differences between species or genotypes as the key to their coexistence3. Here we show that non-heritable variation in individual fitness within species or genotypes can stabilize coexistence without evoking niche differentiation. We construct two classes of mathematical models based on experimental evidence: (1) bacterial growth with variation in cell longevity4,5; and (2) microbial transmission in a host population with variation in host susceptibility6-11. We find stable coexistence of 2 bacterial species in the first model under a single oscillating resource, and 3 or more in the second with independent distributions of host susceptibility to the various microbial species. We discuss the implications of these findings for the interpretation of common measures of relative fitness and for the maintenance of biodiversity.

ecology↗