Fructose consumption, which promotes insulin resistance, hypertension, and dyslipidemia, has increased by over 25% since the 1970s. In addition to metabolic dysregulation, fructose ingestion stimulates the hypothalamic-pituitary-adrenal (HPA) axis leading to elevations in glucocorticoids. Adolescents are the greatest consumers of fructose, and adolescence is a critical period for maturation of the HPA axis. Repeated consumption of high levels of fructose during adolescence has the potential to promote long-term dysregulation of the stress response. Therefore, we determined the extent to which consumption of a diet high in fructose affected behavior, serum corticosterone, and hypothalamic gene expression using a whole-transcriptomics approach. In addition, we examined the potential of a high-fructose diet to interact with exposure to chronic adolescent stress. Male Wistar rats fed the periadolescent high-fructose diet showed increased anxiety-like behavior in the elevated plus maze and depressive-like behavior in the forced swim test in adulthood, irrespective of stress history. Periadolescent fructose-fed rats also exhibited elevated basal corticosterone concentrations relative to their chow-fed peers. These behavioral and hormonal responses to the high-fructose diet did not occur in rats fed fructose during adulthood only. Finally, rats fed the high-fructose diet throughout development underwent marked hypothalamic transcript expression remodeling, with 966 genes (5.6%) significantly altered and a pronounced enrichment of significantly altered transcripts in several pathways relating to regulation of the HPA axis. Collectively, the data presented herein indicate that diet, specifically one high in fructose, has the potential to alter behavior, HPA axis function, and the hypothalamic transcriptome in male rats.

Both basic and clinical research indicates that females are more susceptible to stress-related affective disorders than males. One of the mechanisms by which stress induces depression is via inflammatory signaling in the brain. Stress during adolescence, in particular, can also disrupt the activation and continued development of both the hypothalamic–pituitary–adrenal (HPA) and –gonadal (HPG) axes, both of which modulate inflammatory pathways and brain regions involved in affective behavior. Therefore, we tested the hypothesis that adolescent stress differentially alters brain inflammatory mechanisms associated with affective-like behavior into adulthood based on sex. Male and female Wistar rats underwent mixed-modality stress during adolescence (PND 37–48) and were challenged with lipopolysaccharide (LPS; 250 μg/kg, i.p.) or saline 4.5 weeks later (in adulthood). Hippocampal inflammatory marker gene expression and circulating HPA and HPG axes hormone concentrations were then determined. Despite previous studies indicating that adolescent stress induces affective-like behaviors in female rats only, this study demonstrated that adolescent stress increased hippocampal inflammatory responses to LPS in males only, suggesting that differences in neuroinflammatory signaling do not drive the divergent affective-like behaviors. The sex differences in inflammatory markers were not associated with differences in corticosterone. In females that experienced adolescent stress, LPS increased circulating estradiol. Estradiol positively correlated with hippocampal microglial gene expression in control female rats, whereas adolescent stress negated this relationship. Thus, estradiol in females may potentially protect against stress-induced increases in neuroinflammation.

Heat fluxes at the lake surface play an integral part in determining the energy budget and thermal structure in lakes, including regulating how lakes respond to climate change. We explore patterns in turbulent heat fluxes, which vary across temporal and spatial scales, using in situ high‐frequency monitoring data from 45 globally distributed lakes. Our analysis demonstrates that some of the lakes studied follow a marked seasonal cycle in their turbulent surface fluxes and that turbulent heat loss is highest in larger lakes and those situated at low latitude. The Bowen ratio, which is the ratio of mean sensible to mean latent heat fluxes, is smaller at low latitudes and, in turn, the relative contribution of evaporative to total turbulent heat loss increases toward the tropics. Latent heat transfer ranged from ~ 60% to > 90% of total turbulent heat loss in the examined lakes. The Bowen ratio ranged from 0.04 to 0.69 and correlated significantly with latitude. The relative contributions to total turbulent heat loss therefore differ among lakes, and these contributions are influenced greatly by lake location. Our findings have implications for understanding the role of lakes in the climate system, effects on the lake water balance, and temperature‐dependent processes in lakes.

Turbulent fluxes across the air‐water interface are integral to determining lake heat budgets, evaporation, and carbon emissions from lakes. The stability of the atmospheric boundary layer (ABL) influences the exchange of turbulent energy. We explore the differences in over‐lake ABL stability using data from 39 globally distributed lakes. The frequency of unstable ABL conditions varied between lakes from 71 to 100% of the time, with average air temperatures typically several degrees below the average lake surface temperature. This difference increased with decreasing latitude, resulting in a more frequently unstable ABL and a more efficient energy transfer to and from the atmosphere, toward the tropics. In addition, during summer the frequency of unstable ABL conditions decreased with increasing lake surface area. The dependency of ABL stability on latitude and lake size has implications for heat loss and carbon fluxes from lakes, the hydrologic cycle, and climate change effects.

Chronic adolescent stress alters behavior in a sex-specific manner at the end of adolescence and in adulthood. Although prolonged behavioral repercussions of chronic adolescent stress have been documented, the potential underlying mechanisms are incompletely understood. In this study we demonstrate that a history of chronic adolescent stress modified the adult stress response, as measured by corticosterone concentration, such that a history of chronic adolescent stress resulted in a blunted response to a novel acute stressor. In order to begin to address potential mechanistic underpinnings, we assessed the extent to which chronic adolescent stress impacted global DNA methylation. Reduced global hippocampal methylation was evident in females with a history of chronic adolescent stress; thus, it was possible that chronic adolescent stress altered global transcription in the whole hippocampi of adult male and female rats. In addition, because acute stress can stimulate a genomic response, we assessed the transcriptome following exposure to an acute novel stressor to determine the extent to which a history of chronic adolescent stress modifies the adult transcriptional response to an acute stressor in males and females. In addition to the reduction in global methylation, chronic adolescent stress resulted in distinct patterns of gene expression in the adult hippocampus that differentiated by sex. Furthermore, both sex and a history of chronic adolescent stress influenced the transcriptional response to an acute novel stressor in adulthood, suggesting both latent and functional effects of chronic adolescent stress at the level of gene transcription. Pathway analysis indicated that ESR1 and IFN-α may be particularly influential transcription factors mediating these transcriptional differences and suggest candidate mechanisms for future studies. Collectively, these studies demonstrate sexspecific and enduring effects of adolescent stress exposure that are more pronounced in females than in males.

Adversity during development is a reliable predictor of psychiatric disorders such as depression and anxiety which are increasingly recognized to have an immune component. We have previously demonstrated that chronic adolescent stress (CAS) in rats leads to depressive-like behavior in adulthood along with long-lasting changes to the hypothalamic-pituitary-adrenal axis and pro-inflammatory cytokine induction in the hippocampus. However, the mechanisms by which CAS promotes hippocampal inflammation are not yet defined. Here we tested the hypothesis that a history of CAS exaggerates induction of the pro-inflammatory NFκB pathway in adult rat hippocampus without compromising the peripheral immune response. We also assessed potential sex differences because it is unclear whether females, who are twice as likely to suffer from mood disorders as males, are disproportionally affected by stress-primed inflammation. Male and female adolescent rats underwent a CAS paradigm or received no stress. Six weeks following the last stressor, all rats received a single systemic injection of either lipopolysaccharide or vehicle to unmask possible immune-priming effects of CAS. An NFκB signaling PCR array demonstrated that CAS exaggerated the expression of NFκB-related genes in the hippocampus of both males and females. Interestingly, targeted qPCR demonstrated that CAS potentiated the induction of hippocampal IL1B and REL mRNA in female rats only, suggesting that some immune effects of CAS are indeed sex-specific. In contrast to the hippocampal findings, indices of peripheral inflammation such as NFκB activity in the spleen, plasma IL-1β, IL-6, TNF-α, and corticosterone were not impacted by CAS in female rats. Despite showing no pro-inflammatory changes to hippocampal mRNA, male CAS rats displayed lower plasma corticosterone response to LPS at 2 hours after injection followed by an exaggerated plasma IL-1β response at 4 hours. This potentially blunted corticosterone response coupled with excessive innate immune signaling in the periphery is consistent with possible glucocorticoid resistance in males. In contrast, the effects of CAS manifested as excessive hippocampal immune reactivity in females. We conclude that while a history of exposure to chronic adolescent stress enhances adult immune reactivity in both males and females, the mechanism and manifestation of such alterations are sex-specific.

Euthanasia by anesthetic agents is commonly performed prior to tissue collection in order to minimize pain and distress to the animal. However, depending on their mechanism of action as well as administration regimen, different methods of anesthesia may trigger an acute stress response through engaging the hypothalamic-pituitary-adrenal (HPA) axis, which can impact numerous other physiological processes that the researcher may wish to examine as endpoints. We investigated the effects of the commonly used anesthetic agent isoflurane on two different endpoints related to the stress response: plasma corticosterone levels and gene expression of the glucocorticoid receptor (GR) as well as several of its regulators including FK506-binding protein 51 (Fkbp5) in the hippocampus of male and female rats. Our results indicate that brief exposure to anesthesia by isoflurane prior to decapitation can alter plasma corticosterone levels differentially in male and female rats within minutes without impacting gene expression in the hippocampus. We conclude that collection methods can influence stress-related physiological endpoints in female rats and the potential influence of even brief anesthesia as well as sex differences in response to anesthesia should be evaluated during the experimental design process and data interpretation. This finding is particularly important in light of new NIH standards regarding sex and reproducibility, and care should be taken to be certain that sex differences in endpoints of interest are not an artifact of sex differences in response to collection paradigms.

The European eel (Anguilla anguilla) population has been in decline at least since the 1960s and reliable regional information, particularly on the spawner production and escapement (i.e. the silver eel life stage), is a requirement of the EU stock recovery regulation. Two comparable time series exist in Burrishoole (Ireland) and Imsa (Norway), with monitoring of total silver eel production since the early 1970s. Numbers of emigrating silver eels fell significantly (p < 0.0001) in the 1980s (breakpoints: Burrishoole 1982; Imsa 1988), in both catchments from >4000 eels per annum to ∼2000 eels per annum. The proportion of male eels dropped and the average size of female eels increased. Biomass of silver eels escaping has remained similar in Burrishoole (1.1/1.2 kg/ha), but not in Imsa (2.1/0.9 kg/ha) between the early period and the 2000s. Factors that govern the onset of eel maturation (silvering) and the annual production of silver eels are little understood. In this paper, the influence of time-lagged environmental variables on silver eel production is examined. Annual variation in the time series was partly (r2 Burrishoole = 0.43, Imsa = 0.46) explained by variation in water temperature and water level. Annual number of migrating eels in both catchments was positively related to summer temperature and summer water flow, negatively related to summer temperatures in the previous year, and in the Burrishoole, also negatively related to high water levels in September/October. The models did not transfer well between catchments, indicating likely catchment specific environmental factors impacting on eel production. The reduction in eel numbers observed in both catchments, accompanied by the change in sex ratio and mean weight of females that contribute to maintain biomass production, calls into question the advisability of basing a spawner escapement recovery target on biomass alone, while numbers and proportions of males decline.