Academic publishing requires linguistically inclusive policies.

Scientific knowledge is produced in multiple languages but is predominantly published in English. This practice creates a language barrier to generate and transfer scientific knowledge between communities with diverse linguistic backgrounds, hindering the ability of scholars and communities to address global challenges and achieve diversity and equity in science, technology, engineering and mathematics (STEM). To overcome those barriers, publishers and journals should provide a fair system that supports non-native English speakers and disseminates knowledge across the globe. We surveyed policies of 736 journals in biological sciences to assess their linguistic inclusivity, identify predictors of inclusivity, and propose actions to overcome language barriers in academic publishing. Our assessment revealed a grim landscape where most journals were making minimal efforts to overcome language barriers. The impact factor of journals was negatively associated with adopting a number of inclusive policies whereas ownership by a scientific society tended to have a positive association. Contrary to our expectations, the proportion of both open access articles and editors based in non-English speaking countries did not have a major positive association with the adoption of linguistically inclusive policies. We proposed a set of actions to overcome language barriers in academic publishing, including the renegotiation of power dynamics between publishers and editorial boards.

Genetic and social contributions to sex differences in lifespan in Drosophila serrata.

Sex differences in lifespan remain an intriguing puzzle in evolutionary biology. While explanations range from sex differences in selection to sex differences in the expression of recessive lifespan-altering mutations (via X-linkage), little consensus has been reached. One unresolved issue is the extent to which genetic influences on lifespan dimorphism are modulated by the environment. For example, studies have shown that sex differences in lifespan can either increase or decrease depending upon the social environment. Here, we took an experimental approach, manipulating multiple axes of the social environment across inbred long- and short-lived genotypes and their reciprocal F1s in the fly Drosophila serrata. Our results reveal strong genetic effects and subtle yet significant genotype-by-environment interactions for male and female lifespan, specifically due to both population density and mating status. Further, our data do not support the idea that unconditional expression of deleterious X-linked recessive alleles in heterogametic males accounts for lower male lifespan.

Artemisia Iwayomogi Extract Attenuates High-Fat Diet-Induced Hypertriglyceridemia in Mice: Potential Involvement of the Adiponectin-AMPK Pathway and Very Low Density Lipoprotein Assembly in the Liver.

This study aimed to examine the protective effect of Artemisia iwayomogi extract (AI) against hypertriglyceridemia induced by a high-fat diet (HFD) in mice and to uncover the underlying molecular mechanisms. C57BL/6N mice were fed chow, HFD, HFD + 0.1% AI, HFD + 0.25% AI, or HFD + 0.5% AI for 10 weeks. The addition of 0.25% and 0.5% AI resulted in dose-dependent improvements in the major parameters of hypertriglyceridemia, including plasma triglyceride, free fatty acids, apolipoprotein B, and lipoprotein lipase, with parallel reductions in body weight gain, hepatic lipid accumulation, and insulin resistance. These beneficial effects were accompanied by the activation of adiponectin-adenosine monophosphate-activated protein kinase (AMPK) mediated signaling cascades in the liver, which downregulated molecules involved in lipogenesis and concurrently upregulated molecules related to fatty acid oxidation. The downregulation of molecules involved in very low density lipoprotein assembly, which was associated with improved hepatic insulin signaling, also appeared to contribute to the AI-induced attenuation of hypertriglyceridemia.

Misalignment of plastic and evolutionary responses of lifespan to novel carbohydrate diets.

Diet elicits varied effects on longevity across a wide range of animal species where dietary discordance between an organisms' evolutionary and developmental dietary history is increasingly recognized to play a critical role in shaping lifespan. However, whether such changes, predominantly assessed in a single generation, lead to evolutionary shifts in lifespan remains unclear. In this study, we used an experimental evolution approach to test whether changes in an organisms' evolutionary and developmental dietary history, specifically carbohydrate content, causes lifespan evolution in Drosophila serrata. After 30 generations, we investigated the evolutionary potential of lifespan in response to four novel diets that varied systematically in their ratio of carbohydrate-protein content. We also examined developmental plasticity effects using a set of control populations that were raised on the four novel environments allowing us to assess the extent to which plastic responses of lifespan mirrored adaptive responses observed following experimental evolution. Both high- and low-carbohydrate diets elicited plastic effects on lifespan; however, the plastic responses for lifespan to developmental diets bore little resemblance to the evolved responses on evolutionary diets. Understanding the dietary conditions regulating the match/mismatch of plastic and evolved responses will be important in determining whether a particular match/mismatch combination is adaptive for lifespan. While the differences in evolutionary diet by developmental diet interactions are only beginning to be elucidated, this study lays the foundation for future investigations of carbohydrate contributions to evolved and plastic effects on health and lifespan.

Systems biology approaches identify metabolic signatures of dietary lifespan and healthspan across species.

Dietary restriction (DR) is a potent method to enhance lifespan and healthspan, but individual responses are influenced by genetic variations. Understanding how metabolism-related genetic differences impact longevity and healthspan are unclear. To investigate this, we used metabolites as markers to reveal how different genotypes respond to diet to influence longevity and healthspan traits. We analyzed data from Drosophila Genetic Reference Panel (DGRP) strains raised under AL and DR conditions, combining metabolomic, phenotypic, and genome-wide information. We employed two computational and complementary methods across species-random forest modeling within the DGRP as our primary analysis and Mendelian randomization in human cohorts as a secondary analysis. We pinpointed key traits with cross-species relevance as well as underlying heterogeneity and pleiotropy that influence lifespan and healthspan. Notably, orotate was linked to parental age at death in humans and blocked the DR lifespan extension in flies, while threonine supplementation extended lifespan, in a strain- and sex-specific manner. Thus, utilizing natural genetic variation data from flies and humans, we employed a systems biology approach to elucidate potential therapeutic pathways and metabolomic targets for diet-dependent changes in lifespan and healthspan.

Systems biology and machine learning approaches identify metabolites that influence dietary lifespan and healthspan responses across flies and humans.

Dietary restriction (DR) is a potent method to enhance lifespan and healthspan, but individual responses are influenced by genetic variations. Understanding how metabolism-related genetic differences impact longevity and healthspan are unclear. To investigate this, we used metabolites as markers to reveal how different genotypes respond to diet to influence longevity and healthspan traits. We analyzed data from Drosophila Genetic Reference Panel strains raised under AL and DR conditions, combining metabolomic, phenotypic, and genome-wide information. Employing two computational methods across species-random forest modeling within the DGRP and Mendelian randomization in the UK Biobank-we pinpointed key traits with cross-species relevance that influence lifespan and healthspan. Notably, orotate was linked to parental age at death in humans and counteracted DR effects in flies, while threonine extended lifespan, in a strain- and sex-specific manner. Thus, utilizing natural genetic variation data from flies and humans, we employed a systems biology approach to elucidate potential therapeutic pathways and metabolomic targets for diet-dependent changes in lifespan and healthspan.

Digest: More than just a pretty fin: The evolution of sexual ornaments in killifish.

What conditions favor the evolution of elaborate sexual ornaments? In freshwater killifishes, Sowersby et al. found that larger sexual ornaments were negatively associated with locomotive performance. Although selection clearly favored large ornamental fins in environments with fewer predators, there was no clear association between large ornamental fins and differences in life-history strategy. This finding illustrates that habitat differences in predation risk have the potential to influence the evolution of secondary sexual traits such as ornaments through natural selection.

Genetically predicted glucosamine and longevity: A Mendelian randomization study.

BACKGROUND & AIMS: Glucosamine is known to affect different health outcomes, however its effect on male and female lifespan is still unclear. We conducted a two-sample Mendelian randomization (MR) study to investigate the association of genetically proxied glucosamine with longevity. METHODS: Using genetic data from the Medical Research Council Integrative Epidemiology Unit (MRC-IEU) consortium for 461,384 individuals, we identified five genetic variants as instrumental variables for genetically predicted glucosamine. We obtained genetic associations of these variants with parental longevity as combined parental age at death (n = 208,118), mother's age at death (n = 246,941) and father's age at death (n = 317,652). We used the inverse-variance weighted method to estimate the effect of a 1-standard deviation (SD) increase in genetically predicted glucosamine on parental longevity. RESULTS: We found a positive effect of genetically predicted higher glucosamine status on life expectancy using combined parental age at death. A 1-SD increase in genetically predicted glucosamine was associated with higher odds of combined parental age at death (odds ratio, 2.64; 95% CI 1.26, 5.54; P = 0.01), and maternal age at death (odds ratio, 1.73; 95 CI 1.04, 2.89; P = 0.03), but not paternal age at death (odds ratio, 1.32; 95% CI 0.81, 2.15; P = 0.27). Based on follow-up sensitivity analyses, we did not find evidence of pleiotropic effects of the genetic variants. CONCLUSIONS: Lifelong higher levels of glucosamine may increase life expectancy. Positive effects of glucosamine were associated with maternal age at death only. The clinical implications of this sex-specific finding warrant further investigation.

Digest: Deprivation of parental care reveals the value of sibling cooperation in burying beetles.

What conditions favor cooperation in sibling interactions? In burying beetles of the genus Nicrophorus, Prang et al. found that dependence on parental care cannot solely explain the degree of offspring cooperation. While only larvae of independent species cooperated when receiving pre-hatching care, both independent and dependent species cooperated in the absence of pre-hatching care. This finding suggests that offspring cooperation has persisted from an early ancestor of the genus Nicrophorus to the present species, highlighting the evolution from facultative to obligatory social behavior.

Digest: Nature and nurture: Influences of parental care and rearing environment on phenotypic plasticity in Nicrophorus vespilloides.

What conditions favor niche expansion in nature? In the burying beetle Nicrophorus vespilloides, Schrader et al. found that larvae reared with parental care on larger carcasses were better equipped for resource use than individuals reared without parental care on smaller carcasses. This finding illustrates that developmental plasticity induced by parental care and carcass size has the potential to influence adaptive diversification.

Digest: On the contribution of phenotypic plasticity to adaptation in desert environments.

How do organisms adapt to new environments, and what role does phenotypic plasticity play? Bittner et al. compared water consumption in laboratory-reared house mice derived from xeric and mesic populations and found evidence for adaptive phenotypic plasticity as well as genetic differences between populations.

Digest: Sexually selected weapons: Winning the fight, but losing the war for reproduction on a changing battlefield.

What conditions favor the evolution of large animal weapons? In the Japanese rhinoceros beetle, Trypoxylus dichotomus, del Sol et al. found that selection favors large horns in populations where males compete over guardianship of scarce female feeding territories. However, in other populations, an abundance of female feeding territories reduces the chance of mating success for these guarding males, leading to the evolution of relatively shorter horn sizes. This finding illustrates that female habitat and resource use have the potential to influence evolution of male weapon size through sexual selection.

Digest: Does size matter? Condition-dependent sexual selection in Drosophila melanogaster.

What conditions favor competitive outcomes at different stages of the reproductive process? De Nardo et al. found that in Drosophila melanogaster, the evolution of male secondary sexual traits was influenced by sexual selection through mating success and competitive fertilization.

Piperonal attenuates visceral adiposity in mice fed a high-fat diet: potential involvement of the adenylate cyclase-protein kinase A dependent pathway.

SCOPE: Piperonal is an aromatic compound found in vanilla and has a floral odor resembling vanillin. This study was aimed to test whether piperonal attenuates visceral adiposity induced by a high-fat diet (HFD) in mice and to explore the underlying molecular mechanisms. METHODS AND RESULTS: Male C57BL/6N mice were fed a normal diet, HFD, or 0.05% piperonal-supplemented HFD (PSD) for 10 weeks. PSD-fed mice showed attenuation of body weight gain, total visceral fat pad weights, and plasma lipid levels compared to HFD-fed mice. Piperonal supplementation of the HFD increased the mRNA expression of certain isotypes of adenylate cyclase (Adcy) and protein kinase A (PKA) in the white adipose tissue (WAT) of mice. The adipogenesis-related genes were downregulated, whereas fatty acid oxidation- and thermogenesis-related genes were upregulated in the WAT of PSD-fed mice compared to those in HFD-fed mice. Piperonal directly activated Adcy by decreasing the Km for its substrate (ATP) in plasma membranes prepared from the WAT of mice. Furthermore, piperonal-induced inhibition of adipocyte differentiation and elevation of Adcy and PKA activities in 3T3-L1 cells were abrogated by an Adcy inhibitor. CONCLUSION: The anti-adipogenic effect of piperonal in mice fed the high-fat diet appears to be associated with increased Adcy-PKA signaling in WAT.

Scopolin ameliorates high-fat diet induced hepatic steatosis in mice: potential involvement of SIRT1-mediated signaling cascades in the liver.

The present study aimed to investigate whether scopolin exhibits beneficial effects on high-fat diet (HFD)-induced hepatic steatosis in mice. The involvement of sirtuin 1 (SIRT1) as a molecular target for scopolin was also explored. Scopolin decreased the Km of SIRT1 for p53 and nicotinamide adenine dinucleotide without altering Vmax in a cell-free system. Scopolin alleviated oleic acid-induced lipid accumulation and downregulation of SIRT1 activity in HepG2 cells, and these beneficial effects of scopolin were abolished in the presence of SIRT1 inhibitor. Mice administered 0.02% scopolin for 8 weeks exhibited improved phenotypes of HFD-induced hepatic steatosis along with increased hepatic SIRT1 activity and protein expression. Scopolin resulted in increased deacetylation of sterol regulatory element-binding protein 1c with subsequent downregulation of lipogenic genes, and enhanced deacetylation of protein peroxisome proliferator-activated receptor-γ coactivator 1α with upregulation of fatty acid oxidation genes in livers. Scopolin also enhanced deacetylation of nuclear factor-kappa enhancer binding protein and liver kinase B1 (LKB1), facilitating LKB1/AMP-activated protein kinase signaling cascades. Scopolin attenuated hepatic steatosis through activation of SIRT1-mediated signaling cascades, a potent regulator of lipid homeostasis. Increased hepatic SIRT1 activity and protein expression appeared to be associated with these beneficial effects of scopolin.