Notes

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Hybrid seed inviability (HSI) is an important mechanism of reproductive isolation and speciation. HSI varies in strength among populations of diploid species but it remains to be tested whether similar processes affect natural variation in HSI within ploidy-variable species (triploid block). Here we used extensive endosperm, seed and F1 -hybrid phenotyping to explore HSI variation within a diploid-autotetraploid species. By leveraging 12 population pairs from three ploidy contact zones, we tested for the effect of interploidy crossing direction (parent of origin), ploidy divergence and spatial arrangement in shaping reproductive barriers in a naturally relevant context. We detected strong parent-of-origin effects on endosperm development, F1 germination and survival, which was also reflected in the rates of triploid formation in the field. Endosperm cellularization failure was least severe and F1 -hybrid performance was slightly better in the primary contact zone, with genetically closest diploid and tetraploid lineages. We demonstrated overall strong parent-of-origin effects on HSI in a ploidy variable species, which translate to fitness effects and contribute to interploidy reproductive isolation in a natural context. Subtle intraspecific variation in these traits suggests the fitness consequences of HSI are predominantly a constitutive property of the species regardless of the evolutionary background of its populations.
Life history theory, a branch of evolutionary theory, predicts the existence of trade-offs in energetic allocation between competing physiological functions. The core metabolic cost of self-maintenance, measured by resting metabolic rate (RMR), represents a large component of human daily energy expenditure. Despite strong selective pressures for energetic frugality and high observed interindividual variation in RMR, the link between RMR and energetic allocation to life-history traits remains understudied in humans.

In a sample of 105 (m = 57, f = 48), we investigated the relationship between adult RMR and investment in growth quality, as measured by fluctuating asymmetry (FA).

Measurement of RMR and FA in university rowers revealed a significant positive correlation amongst males (n = 57, r = 0.344, p = 0.005, 1-tailed; standardized 95% CI, 0.090 to 0.598). Convincing evidence for a correlation among females was not found (n = 48, r = 0.142, p = 0.169, 1-tailed, standardized 95% CI, -0.152 to 0.435).

size and increased male muscularity, which may amplify the inefficiencies arising from low-quality growth.Neonatal encephalopathy (NE) is characterized by altered neurological function in term infants and inflammation plays an important pathophysiological role. Inflammatory cytokines interleukin (IL)-1β, IL-1ra and IL-18 are activated by the nucleotide-binding and oligomerization domain (NOD)-, leucine-rich repeat domain (LRR)- and NOD-like receptor protein 3 (NLRP3) inflammasome; furthermore, we aimed to examine the role of the inflammasome multiprotein complex involved in proinflammatory responses from the newborn period to childhood in NE. Cytokine concentrations were measured by multiplex enzyme-linked immunosorbent assay (ELISA) in neonates and children with NE in the absence or presence of lipopolysaccharide (LPS) endotoxin. We then investigated expression of the NLRP3 inflammasome genes, NLRP3, IL-1β and ASC by polymerase chain reaction (PCR). Serum samples from 40 NE patients at days 1 and 3 of the first week of life and in 37 patients at age 4-7 years were analysed. An increase in serum IL-1ra and IL-18 in neonates with NE on days 1 and 3 was observed compared to neonatal controls. IL-1ra in NE was decreased to normal levels at school age, whereas serum IL-18 in NE was even higher at school age compared to school age controls and NE in the first week of life. Percentage of LPS response was higher in newborns compared to school-age NE. NLRP3 and IL-1β gene expression were up-regulated in the presence of LPS in NE neonates and NLRP3 gene expression remained up-regulated at school age in NE patients compared to controls. learn more Increased inflammasome activation in the first day of life in NE persists in childhood, and may increase the window for therapeutic intervention.It is often challenging to share detailed individual-level data among studies due to various informatics and privacy constraints. However, it is relatively easy to pool together aggregated summary level data, such as the ones required for standard meta-analyses. Focusing on data generated from case-control studies, we present a flexible inference procedure that integrates individual-level data collected from an "internal" study with summary data borrowed from "external" studies. This procedure is built on a retrospective empirical likelihood framework to account for the sampling bias in case-control studies. It can incorporate summary statistics extracted from various working models adopted by multiple independent or overlapping external studies. It also allows for external studies to be conducted in a population that is different from the internal study population. We show both theoretically and numerically its efficiency advantage over several competing alternatives.
Functional brain imaging using genetically encoded Ca
sensors in larval zebrafish is being developed for studying seizures and epilepsy as a more ethical alternative to rodent models. Despite this, few data have been generated on pharmacological mechanisms of action other than GABA
antagonism. Assessing larval responsiveness across multiple mechanisms is vital to test the translational power of this approach, as well as assessing its validity for detecting unwanted drug-induced seizures and testing antiepileptic drug efficacy.

Using light-sheet imaging, we systematically analysed the responsiveness of 4days post fertilisation (dpf; which are not considered protected under European animal experiment legislation) transgenic larval zebrafish to treatment with 57 compounds spanning more than 12 drug classes with a link to seizure generation in mammals, alongside eight compounds with no such link.

We show 4dpf zebrafish are responsive to a wide range of mechanisms implicated in seizure generation, with cerebellar circuitry activated regardless of the initiating pharmacology.
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