Sex-specific Responses Research Articles

The Influence of Fetal Sex on Antepartum Treatments in a Murine Model of Preterm Birth [ID: 2369702

INTRODUCTION: Preterm neonates exposed to magnesium sulfate (MgSO4) and corticosteroids such as betamethasone (BMTZ) in utero have a lower incidence of neurodevelopmental disability, specifically cerebral palsy. The efficacy of MgSO4/BMTZ remains poor, particularly in male offspring. The mechanisms by which MgSO4/BMTZ confer “neuroprotection” in only some patients and in relation to fetal sex, remain unknown. Our objective was to examine sex-specific responses to MgSO4/BMTZ in a murine model of fetal neuroinflammatory injury. METHODS: Utilizing an established murine model of preterm birth, dams were injected intrauterine with either phosphate-buffered saline or bacterial endotoxin (lipopolysaccharide [LPS]) on embryonic day 15.5 to induce fetal inflammation. Thereafter, dams received MgSO4/BMTZ or the vehicle. Fetal brains and placentas were collected 6 hours postinjection for gene expression analysis of key inflammatory cytokines: Il1b, Il6, and Tnf. RESULTS: Irrespective of sex, LPS exposure up-regulated all three cytokines. With MgSO4/BMTZ, Il1b expression was significantly lower in female, but not male brains. In contrast, MgSO4/BMTZ lowered Il6 expression in placentas from males, but not females. No sex differences were observed with Tnf expression. CONCLUSION: Within the context of LPS-mediated in utero inflammation, fetal sex influenced the efficacy of MgSO4/BMTZ. The anti-inflammatory effect of MgSO4/BMTZ also appeared tissue specific, with protection shown in female brains and male placentas. These results suggest that the neuroprotective effects of MgSO4/BMTZ are more robust in females, whereas placental inflammation is more affected in males. Further investigation is warranted to determine whether these sex-specific patterns govern fetal outcomes.

Sex-specific differences in kidney clock gene expression in mice in response to a low potassium, high salt diet

Clinical studies demonstrate that women have exacerbated salt-sensitive blood pressure (BP) responses compared to men. However, most studies examining the molecular mechanisms involved in salt-sensitive hypertension focus on males. Accumulating evidence suggests the molecular circadian clock is crucial for BP control and our lab has a particular interest in how kidney circadian clocks contribute to BP and salt-sensitivity in males and females. Core components of the circadian clock are the proteins BMAL1, CLOCK, CRY, and PER. BMAL1 and CLOCK are the positive arm and PER and CRY are the negative arm of this transcriptional/translational feedback loop. We have found sex-specific responses in BP/electrolyte handling in circadian gene knockout models, suggesting the clock mechanism may differ between males and females. Therefore, we hypothesize that kidney clock gene expression differs between males and females and that this is altered in response to the salt-sensitive environment created by a low potassium, high salt diet. To test this, we performed RNAseq analysis on kidney medulla from male and female mice on a C57BL/6 background on either a control diet or in response to a 0% potassium, high salt (0KHS; 4% NaCl) diet. Dissected kidney medulla RNA samples were collected at the onset of the rest phase and the active phase (6AM and 6PM; n=4-7). RNA sequencing was performed using pooled samples and analyses from raw counts were performed. Clock gene expression was assessed and initial comparisons were made using 3-way ANOVA to determine the effect of time, sex and diet with Sidak multiple comparisons post hoc analysis.As expected, we show significant time-of-day effects on all clock gene expression assessed in the kidney medulla, including Bmal1, Clock, Cry1, and Per1 (time effect p<0.0001). There were sex-specific differences as Bmal1, Clock, Cry1, and Per1 were higher both at 6AM and 6PM in females compared to males on a control diet (sex effect p<0.0001). Interestingly, these sex differences were lost in Clock and Per1 expression in animals on a 0KHS diet. This was caused by Clock significantly decreasing at 6AM in females ( p=0.0019) but increasing at 6AM in males ( p=0.0360). Furthermore, 0KHS diet caused Per1 expression to decrease at 6PM in females ( p=0.0026) with no change in males. Bmal1 expression decreased at both 6AM ( p<0.0001) and 6PM ( p=0.0076), with no change in Bmal1 expression in males in response to 0KHS. Unlike Bmal1, Cry1 expression increased at both 6AM ( p=0.0002) and 6PM ( p=0.0007) in males in response to 0KHS diet, with no change in females and expression remaining higher in females.Consistent with our hypothesis, clock gene expression in the kidney medulla differs between males and females with sex-specific alterations in clock gene expression in response to a 0KHS diet. Future work will focus on whether these sex-specific differences in the kidney clock contribute to regulation of BP and salt-sensitivity. NIDDK, ASN, AHA This is the full abstract presented at the American Physiology Summit 2023 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.

897 HERC6 is an Interferon induced E3 ubiquitin ligase that negatively regulates sex-specific STING-IRF3 responses through modulation of LATS2/VGLL3 Hippo signaling

897 HERC6 is an Interferon induced E3 ubiquitin ligase that negatively regulates sex-specific STING-IRF3 responses through modulation of LATS2/VGLL3 Hippo signaling

Sex-dependent PD-L1/sPD-L1 trafficking in human endothelial cells in response to inflammatory cytokines and VEGF

Programmed cell death 1 ligand 1 (PD-L1) expressed in non-immune cells is involved in immune-mediated tissue damage in the context of inflammatory conditions and tumor immune escape. Emerging evidence suggests soluble (s)PD-L1 as a marker of inflammation. Based on well-established sex-specific differences in immunity, we tested the novel hypotheses that (i) endothelial cell PD-L1 is modulated by inflammatory cytokines and vascular endothelial growth factor (VEGF) in a sex-specific fashion, and (ii) the endothelium is a source of sPD-L1. After exposure of human umbilical vein endothelial cells (HUVECs) to lipopolysaccharide, interleukin (IL)1β or VEGF for 24 h, total PD-L1 levels were upregulated solely in cells from female donors, while being unchanged in those from male donors. Accordingly, exposure to synovial fluids from patients with inflammatory arthritis upregulated PD-L1 levels in HUVECs from female donors only. Membrane PD-L1 expression as measured by flow cytometry was unchanged in response to inflammatory stimuli. However, exposure to 2 ng/mL IL-1β or 50 ng/mL VEGF time-dependently increased sPD-L1 release by HUVECs from female donors. Treatment with the metalloproteinase (MMP) inhibitor GM6001 (10 μM) prevented IL-1β-induced sPD-L1 release and enhanced membrane PD-L1 levels. The anti-VEGF agents bevacizumab and sunitinib reduced both VEGF-induced PD-L1 accumulation and sPD-L1 secretion. Thus, inflammatory agents and VEGF rapidly increased endothelial PD-L1 levels in a sex-specific fashion. Furthermore, the vascular endothelium may be a sPD-L1 source, whose production is MMP-dependent and modulated by anti-VEGF agents. These findings may have implications for sex-specific immunity, vascular inflammation and response to anti-angiogenic therapy.

Growth-Restricted Fetuses and Offspring Reveal Adverse Sex-Specific Metabolic Responses in Preeclamptic Mice Expressing Human sFLT1.

Fetal adaptations to harmful intrauterine environments due to pregnancy disorders such as preeclampsia (PE) can negatively program the offspring's metabolism, resulting in long-term metabolic changes. PE is characterized by increased circulating levels of sFLT1, placental dysfunction and fetal growth restriction (FGR). Here we examine the consequences of systemic human sFLT1 overexpression in transgenic PE/FGR mice on the offspring's metabolic phenotype. Histological and molecular analyses of fetal and offspring livers as well as examinations of offspring serum hormones were performed. At 18.5 dpc, sFLT1 overexpression resulted in growth-restricted fetuses with a reduced liver weight, combined with reduced hepatic glycogen storage and histological signs of hemorrhages and hepatocyte apoptosis. This was further associated with altered gene expression of the molecules involved in fatty acid and glucose/glycogen metabolism. In most analyzed features males were more affected than females. The postnatal follow-up revealed an increased weight gain of male PE offspring, and increased serum levels of Insulin and Leptin. This was associated with changes in hepatic gene expression regulating fatty acid and glucose metabolism in male PE offspring. To conclude, our results indicate that sFLT1-related PE/FGR in mice leads to altered fetal liver development, which might result in an adverse metabolic pre-programming of the offspring, specifically targeting males. This could be linked to the known sex differences seen in PE pregnancies in human.

Acute Ozone-Induced Transcriptional Changes in Markers of Oxidative Stress and Glucocorticoid Signaling in the Rat Hippocampus and Hypothalamus Are Sex-Specific.

Exposure to a prototypic air pollutant ozone (O3) has been associated with the activation of neuroendocrine stress response along with neural changes in oxidative stress (OS), inflammation, and Alzheimer's disease-like pathologies in susceptible animal models. We hypothesized that neural oxidative and transcriptional changes induced by O3 in stress responsive regions are sex-dependent. Male and female adult Long-Evans rats were exposed to filtered air or O3 for two consecutive days (0.8 ppm, 4 h/day) and brain regions were flash-frozen. Activities of cerebellar OS parameters and mitochondrial complex I, II, and IV enzymes were assessed to confirm prior findings. We assessed transcriptional changes in hypothalamus (HYP) and hippocampus (HIP) for markers of OS, microglial activity and glucocorticoid signaling using qPCR. Although there were no O3 or sex-related differences in the cerebellar activities of OS and mitochondrial enzymes, the levels of protein carbonyls and complex II activities were higher in females regardless of O3. There were no statistical differences in baseline expression of genes related to OS (Cat, Dhcr24, Foxm1, Gpx1, Gss, Nfe2l2, Sod1) except for lower HYP Sod1 expression in air-exposed females than males, and higher HIP Gss expression in O3-exposed females relative to matched males. Microglial marker Aif1 expression was higher in O3-exposed females relative to males; O3 inhibited Itgam only in males. The expression of Bdnf in HIP and HYP was inhibited by O3 in both sexes. Genes related to glucocorticoid signaling (Fkbp4, Fkbp5, Hsp90aa1, Hspa4, nr3c1, nr3c2) showed sex-specific effects due to O3 exposure. Baseline expression of HIP Fkbp4 was higher in females relative to males. O3 inhibited Nr3c1 in female HIP and male HYP, but Nr3c2 was inhibited in male HYP. Fkbp4 expression was higher in O3-exposed females when compared to matched males, whereas Fkbp5 was expressed at higher levels in both brain regions of males and females. These results indicate that sex-specific brain region responses to O3 might, in part, be caused by OS and regulation of glucocorticoid signaling.

A learning experience elicits sex-dependent neurogenomic responses in Bicyclus anynana butterflies.

Sexually dimorphic behaviour is pervasive across animals, with males and females exhibiting different mate selection, parental care, foraging, dispersal, and territorial strategies. However, the genetic underpinnings of sexually dimorphic behaviours are poorly understood. Here we investigate gene networks and expression patterns associated with sexually dimorphic imprinting-like learning in the butterfly Bicyclus anynana. In this species, both males and females learn visual preferences, but learn preferences for different traits and use different signals as salient, unconditioned cues. To identify genes and gene networks associated with this behaviour, we examined gene expression profiles of the brains and eyes of male and female butterflies immediately post training and compared them to the same tissues of naïve individuals. We found more differentially expressed genes and a greater number of associated gene networks in the eyes, indicating a role of the peripheral nervous system in visual imprinting-like learning. Females had higher chemoreceptor expression levels than males, supporting the hypothesized sexual dimorphic use of chemical cues during the learning process. In addition, genes that influence B. anynana wing patterns (sexual ornaments), such as invected, spalt, and apterous, were also differentially expressed in the brain and eye, suggesting that these genes may influence both sexual ornaments and the preferences for these ornaments. Our results indicate dynamic and sex-specific responses to social scenario in both the peripheral and central nervous systems and highlight the potential role of wing patterning genes in mate preference and learning across the Lepidoptera.

Endosymbiont-mediated resistance to entomotoxic nanoparticles and sex-specific responses in a seed beetle

Endosymbiont-mediated resistance to entomotoxic nanoparticles and sex-specific responses in a seed beetle

Sex-biased gene expression in nutrient-sensing pathways.

Differences in lifespan between males and females are found across many taxa and may be determined, at least in part, by differential responses to diet. Here we tested the hypothesis that the higher dietary sensitivity of female lifespan is mediated by higher and more dynamic expression in nutrient-sensing pathways in females. We first reanalysed existing RNA-seq data, focusing on 17 nutrient-sensing genes with reported lifespan effects. This revealed, consistent with the hypothesis, a dominant pattern of female-biased gene expression, and among sex-biased genes there tended to be a loss of female-bias after mating. We then tested directly the expression of these 17 nutrient-sensing genes in wild-type third instar larvae, once-mated 5- and 16-day-old adults. This confirmed sex-biased gene expression and showed that it was generally absent in larvae, but frequent and stable in adults. Overall, the findings suggest a proximate explanation for the sensitivity of female lifespan to dietary manipulations. We suggest that the contrasting selective pressures to which males and females are subject create differing nutritional demands and requirements, resulting in sex differences in lifespan. This underscores the potential importance of the health impacts of sex-specific dietary responses.

Predatory stink bug, Eocanthecona furcellata (Wolff) responses to oral exposure route of λ-cyhalothrin via sex-specific modulation manner

The toxic effects of insecticides on predatory arthropods have closely related to their exposure routes. However, little is known about the effects of insecticide on reproductive parameters when the route of exposure occurs at a trophic level via prey intake. We therefore conducted current studies assessing whether Eocanthecona furcellata adults would be affected by feeding with λ-cyhalothrin-contaminated prey. Reproductive parameters, i.e. prolonged premating and preoviposition durations, reduced number of egg batches and egg amount, disturbed ovarian development, and suppressed expression of reproductive related genes were observed in E. furcellata females by feeding with treated prey. Moreover, reduced survival rate and altered carbohydrate metabolism parameters were detected in male bugs. Biochemical parameters, including MDA content, the activities of three antioxidant enzymes and three detoxification enzymes exhibited sex-specific responses after oral-exposure to λ-cyhalothrin in E. furcellata. The results indicate that the insecticide affects the fitness and leads to impairing reproductive potential via sex-specific modulation manner in predator insects. Taken together, our results provide a comprehensive assessment about detrimental impacts of λ-cyhalothrin-exposure on predators via prey intake, as well as a solid basis for further research to protect the predators from hazardous impacts of insecticides.

Sex-specific physiological and growth responses to elevated temperature and CO2 concentration in Chinese seabuckthorn (Hippophae rhamnoides subsp. sinensis Rousi)

Sex-specific physiological and growth responses to elevated temperature and CO2 concentration in Chinese seabuckthorn (Hippophae rhamnoides subsp. sinensis Rousi)

Sex-Specific Response of the Brain Free Oxylipin Profile to Soluble Epoxide Hydrolase Inhibition.

Oxylipins are the oxidation products of polyunsaturated fatty acids and have been implicated in neurodegenerative disorders, including dementia. Soluble epoxide hydrolase (sEH) converts epoxy-fatty acids to their corresponding diols, is found in the brain, and its inhibition is a treatment target for dementia. In this study, male and female C57Bl/6J mice were treated with an sEH inhibitor (sEHI), trans-4-[4-(3-adamantan-1-yl-ureido)-cyclohexyloxy]-benzoic acid (t-AUCB), for 12 weeks to comprehensively study the effect of sEH inhibition on the brain oxylipin profile, and modulation by sex. Ultra-high-performance liquid chromatography-tandem mass spectrometry was used to measure the profile of 53 free oxylipins in the brain. More oxylipins were modified by the inhibitor in males than in females (19 versus 3, respectively) and favored a more neuroprotective profile. Most were downstream of lipoxygenase and cytochrome p450 in males, and cyclooxygenase and lipoxygenase in females. The inhibitor-associated oxylipin changes were unrelated to serum insulin, glucose, cholesterol, or female estrous cycle. The inhibitor affected behavior and cognitive function as measured by open field and Y-maze tests in males, but not females. These findings are novel and important to our understanding of sexual dimorphism in the brain's response to sEHI and may help inform sex-specific treatment targets.

Sex-Dependent Differences in Mouse Placental Gene Expression following a Maternal High-Fat Diet.

In utero fetal exposures may have sex-specific placental gene responses. Our objective was to measure sex-based differences in placental gene expression from dams fed high-fat diet (HFD) versus control diet (CD). We fed timed pregnant Friend virus B-strain dams either a CD (n = 5) or an HFD (n = 5). We euthanized dams on embryonic day 17.5 to collect placentas. We extracted placental RNA and hybridized it to a customized 96-gene Nanostring panel focusing on angiogenic, inflammatory, and growth genes. We compared normalized gene expression between CD and HFD, stratified by fetal sex, using analysis of variance. Pathway analysis was used to further interpret the genomic data. Pups from HFD-fed dams were heavier than those from CD-fed dams (0.97 ± 0.06 vs. 0.84 ± 0.08 g, p < 0.001). Male pups were heavier than females in the HFD (0.99 ± 0.05 vs. 0.94 ± 0.06 g, p = 0.004) but not CD (0.87 ± 0.08 vs. 0.83 ± 0.07 g, p = 0.10) group. No sex-based differences in placental gene expression in CD-fed dams were observed. Among HFD-fed dams, placentas from female pups exhibited upregulation of 15 genes (q = 0.01). Network analyses identified a cluster of genes involved in carbohydrate metabolism, cellular function and maintenance, and endocrine system development and function (p = 1 × 10-23). The observed female-specific increased gene expression following in utero HFD exposure was predicted to be regulated by insulin (p = 5.79 × 10-13). In female compared with male pups, in utero exposure to HFD upregulated placental gene expression in 15 genes predicted to be regulated by insulin. Sex-specific differences in placental expression of these genes should be further investigated. · Male pups were heavier than female pups at the time of sacrifice when dams were fed an HFD.. · HFD was associated with upregulated gene expression in female placentas.. · Female-specific increased gene was predicted to be regulated by insulin..

Sex-specific transcriptional signatures in the medial prefrontal cortex underlying sexually dimorphic behavioural responses to stress in rats.

Converging evidence suggests that stress alters behavioural responses in a sex-specific manner; however, the underlying molecular mechanisms of stress remain largely unknown. We adapted unpredictable maternal separation (UMS) and adult restraint stress (RS) paradigms to mimic stress in rats in early life or adulthood, respectively. The sexual dimorphism of the prefrontal cortex was noted, and we performed RNA sequencing (RNA-Seq) to identify specific genes or pathways responsible for sexually dimorphic responses to stress. We then performed quantitative reverse transcription polymerase chain reaction (qRT-PCR) to verify the results of RNA-Seq. Female rats exposed to either UMS or RS showed no negative effects on anxiety-like behaviours, whereas the emotional functions of the PFC were impaired markedly in stressed male rats. Leveraging differentially expressed genes (DEG) analyses, we identified sex-specific transcriptional profiles associated with stress. There were many overlapping DEGs between UMS and RS transcriptional data sets, where 1406 DEGs were associated with both biological sex and stress, while only 117 DEGs were related to stress. Notably, Uba52 and Rpl34-ps1 were the first-ranked hub gene in 1406 and 117 DEGs respectively, and Uba52 was higher than Rp134-ps1, suggesting that stress may have led to a more pronounced effect on the set of 1406 DEGs. Pathway analysis revealed that 1406 DEGs were primarily enriched in ribosomal pathway. These results were confirmed by qRT-PCR. Sex-specific transcriptional profiles associated with stress were identified in this study, but more in-depth experiments, such as single-cell sequencing and manipulation of male and female gene networks in vivo, are needed to verify our findings. Our findings show sex-specific behavioural responses to stress and highlight sexual dimorphism at the transcriptional level, shedding light on developing sex-specific therapeutic strategies for stress-related psychiatric disorders.

Sex-specific responses to juvenile stress on the dopaminergic system in an animal model of attention-deficit hyperactivity disorder

The etiology of attention-deficit hyperactivity disorder (ADHD) strongly suggests a genetic component as the main cause; however, environmental factors such as early adverse experiences in childhood may play an interactive role with the genetic susceptibility. Spontaneously hypertensive rats (SHRs), a genetic ADHD model, and control Wistar Kyoto rats (WKYs) were subjected to chronic unpredictable mild stress during the juvenile period. The behavioral characteristics were monitored, and dopamine-related factors in the core regions of dopaminergic pathways were measured. Higher ADHD symptom-related behaviors were observed in response to juvenile stress in male SHRs than control WKYs. For the SHRs subjected to juvenile stress, hyperactivity in males, recognition in females, and depressant potential in both sexes were markedly observed. In the expression of 17 dopamine-related genes and proteins, greater changes were detected in male SHRs subjected to juvenile stress, especially in dopamine metabolic factors. Dopamine clearance factors involved in dopamine degradation and transport, especially catechol-O-methyltransferase (COMT) and dopamine transporter (DAT), showed sex-specific differences induced by juvenile stress in dopamine metabolite assays. Moreover, stressed male SHRs treated with methylphenidate showed better improvement in behavior than the females, resulting in different levels of COMT and DAT amelioration. These results suggest that juvenile stress potentially increased the incidence of ADHD in a genetic rat model, which showed sex-specific differences based on the expression of COMT and DAT. Therefore, our results could help develop gender-specific diagnostics and healthcare options for juvenile stress in patients with ADHD.

Integrative assessment of immunity, health-state, growth and survival of Magellanic penguin chicks in a colony exposed to ecotourism

Accumulating reports of negative impacts of tourist activities on wildlife emphasize the importance of closely monitoring focal populations. Although some effects are readily noticed, more subtle ones such as changes in physiological functions of individuals might go overlooked. Based on evidence of altered physiology associated with ecotourism on Magellanic penguins Spheniscus magellanicus, here we performed an integrated assessment using a diverse physiological toolkit together with more traditional fitness-related measures to better understand mechanisms and potential consequences. Chicks exposed to tourism showed altered immune parameters and elevated flea prevalence, reinforcing previous findings. Tourism-exposed female, but not male, chicks also showed relatively lower hematocrit and plasma protein levels, providing evidence consistent with a sex-specific response to tourist visitation. Physiological alterations detected in tourism-exposed young chicks (week 1–2) were maintained and the effect on flea infestation increased during the study period (week 4–5 of post-hatch). Despite the effects on physiology, these did not seem to translate into immediate fitness costs. No detectable tourism effects were found on brood sex ratios, chick growth and body condition, and survival until week 5–6 post-hatch. We detected no effects on reproductive output and only a marginal effect on nest survival during incubation despite previous reports of tourism-associated alterations in stress indices of adults. This disconnection could result if the physiological changes are not strong enough to impact fitness, if effects balance each other out, or if changes are part of a copying strategy. Alternatively, the physiological alterations might only show impacts later in the brooding cycle or even after chick emancipation from their parents. Our results suggest that integrative monitoring of potential anthropogenic impacts on wildlife should include evaluation of physiological mechanisms and individual-level responses in populations exposed to human activities.

Sex-Specific Microglial Responses to Glucocerebrosidase Inhibition: Relevance to GBA1-Linked Parkinson's Disease.

Microglia are heterogenous cells characterized by distinct populations each contributing to specific biological processes in the nervous system, including neuroprotection. To elucidate the impact of sex-specific microglia heterogenicity to the susceptibility of neuronal stress, we video-recorded with time-lapse microscopy the changes in shape and motility occurring in primary cells derived from mice of both sexes in response to pro-inflammatory or neurotoxic stimulations. With this morpho-functional analysis, we documented distinct microglia subpopulations eliciting sex-specific responses to stimulation: male microglia tended to have a more pro-inflammatory phenotype, while female microglia showed increased sensitivity to conduritol-B-epoxide (CBE), a small molecule inhibitor of glucocerebrosidase, the enzyme encoded by the GBA1 gene, mutations of which are the major risk factor for Parkinson's Disease (PD). Interestingly, glucocerebrosidase inhibition particularly impaired the ability of female microglia to enhance the Nrf2-dependent detoxification pathway in neurons, attenuating the sex differences observed in this neuroprotective function. This finding is consistent with the clinical impact of GBA1 mutations, in which the 1.5-2-fold reduced risk of developing idiopathic PD observed in female individuals is lost in the GBA1 carrier population, thus suggesting a sex-specific role for microglia in the etiopathogenesis of PD-GBA1.

Garbage in may not equal garbage out: sex mediates effects of ‘junk food’ in a synanthropic species

AbstractHuman influence on ecosystems is rapidly expanding, and one consequence is the increased availability of human food subsidies to wildlife. Human food subsidies like refuse and food scraps are widely hypothesized to be ‘junk food’ that is nutritionally incomplete; however, the impacts of ‘junk foods’ on the health and fitness of individual organisms remain unclear. In this study, we aimed to understand how human food consumption affects the body condition and fecundity of a generalist predator, the Steller’s jay (Cyanocitta stelleri). We used stable isotope analysis to quantify individual human food consumption (using δ13C as a proxy), estimated individual body condition based on body mass and feather growth bar width and assessed jay fecundity. Adults consumed more human food than juveniles on average, and we observed sex-specific responses to human food use where male body condition tended to increase, whereas female body condition tended to decline with human food consumption. However, fecundity was not strongly related. Thus, we found some evidence for the ‘junk food’ hypothesis in this system, which suggests that human foods may not be an equal replacement for natural foods from a nutritional perspective, especially for females. Human foods tend to be carbohydrate rich, but protein poor, which may benefit males because they are larger and limited overall by calorie intake. Females, particularly reproducing females, are more nutritionally limited and thus may experience fewer benefits from ‘junk food’. Our study advances knowledge of human–wildlife interactions by increasing the resolution of our understanding of the fitness benefits, or detriments, experienced by individuals that consume human foods.

Sex-Related Ecophysiological Responses of Hippophae rhamnoide Saplings to Simulate Sand Burial Treatment in Desertification Areas

(1) Background: In recent years, Hippophae rhamnoides has been used extensively to prevent desertification in China due to its nitrogen (N) fixation and sand stabilization abilities. However, as a dioecious species, few studies have focused on the sexual dimorphism of H. rhamnoides in response to sand burial, which frequently presents in desertification areas. (2) Methods: In this paper, we explored the ecophysiological responses of female and male saplings of H. rhamnoides under unburied treatment (control) and different sand burial depths (denoted as T33, T67, T90 and T133, corresponding to sand burial depths of 33, 67, 90 and 133 percent of the mean initial height of the saplings, respectively). (3) Results: Compared with unburied controls, the T33 treatment significantly promoted biomass accumulation and photosynthetic capacity, whereas T67 and T90 treatments inhibited biomass and physiological parameters of the two sexes. Deeper sand burial treatments, i.e., T90 and T133, significantly decreased the survival rates of the two sexes. Furthermore, the sex-specific responses of the two sexes of H. rhamnoides were affected by different depths of sand burial. Males had higher levels of stem starch and root sucrose and exhibited a larger increase in root nodule biomass under the T33 treatment, indicating better carbohydrate utilization and N fixation, whereas females showed lower total biomass and fewer root nodules, as well as more inhibition of photosynthetic and chlorophyll fluorescence parameters, water potential and root carbohydrates, indicating more negative effects on females than males under the T67 treatment. (4) Conclusions: We conclude that sex-related response and adaptation to sand burial depths may potentially affect the colonization, sex ratio and ecological function of the two sexes of H. rhamnoides in desertification areas.

СТАТЕВІ ВІДМІННОСТІ РІВНІВ МАРКЕРІВ ЕНДОГЕННОЇ ІНТОКСИКАЦІЇ У ЩУРІВ З ЕКСПЕРИМЕНТАЛЬНИМ ОЖИРІННЯМ ЗА УМОВ ПРОФІЛАКТИЧНОГО ЗАСТОСУВАННЯ ОРЛІСТАТУ ТА БІОНАНОКОМПОЗИТУ НА ОСНОВІ ПАЖИТНИКА

Obesity is a complex disease involving an excessive amount of body fat. Obesity is generally caused by eating too much and physical activity too little. High-calorie diet-induced obesity occurs in both sexes, but more pronounced changes in blood parameters associated with this disease are more common in men. However, the gender-specific mechanisms of obesity development are little known. Therefore, the purpose of our study was to determine the sex-specific response to the content of the middle mass molecules and oligopeptides in the serum of rats under conditions of highcalorie diet consumption and after administration of a bionanocomposite based on fenugreek and orlistat. To do this, we used a modified Gabrielian method and mathematical processing and statistical analysis of the results.