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Search Results (308)

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Keywords = Prenatal stress

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16 pages, 990 KiB  
Review
Impact of E-Cigarettes on Fetal and Neonatal Lung Development: The Influence of Oxidative Stress and Inflammation
by Antonella Gambadauro, Francesca Galletta, Beatrice Andrenacci, Simone Foti Randazzese, Maria Francesca Patria and Sara Manti
Antioxidants 2025, 14(3), 262; https://doi.org/10.3390/antiox14030262 - 25 Feb 2025
Viewed by 390
Abstract
Electronic cigarettes (e-cigs) recently increased their popularity as “safer” alternatives to traditional tobacco smoking, including among pregnant women. However, the effect of e-cig exposure on fetal and neonatal developing lungs remains poorly investigated. In this review, we analysed the impact of e-cig aerosol [...] Read more.
Electronic cigarettes (e-cigs) recently increased their popularity as “safer” alternatives to traditional tobacco smoking, including among pregnant women. However, the effect of e-cig exposure on fetal and neonatal developing lungs remains poorly investigated. In this review, we analysed the impact of e-cig aerosol components (e.g., nicotine, solvents, and flavouring agents) on respiratory system development. We particularly emphasized the role of e-cig-related oxidative stress and inflammation on lung impairment. Nicotine contained in e-cigs can impair lung development at anatomical and molecular levels. Solvents and flavours induce inflammation and oxidative stress and contribute to compromising neonatal lung function. Studies suggest that prenatal e-cig aerosol exposure may increase the risk of future development of respiratory diseases in offspring, such as asthma and chronic obstructive pulmonary disease (COPD). Preventive strategies, such as smoking cessation programs and antioxidant supplementation, may be essential for safeguarding respiratory health. There is an urgent need to explore the safety profile and potential risks of e-cigs, especially considering the limited studies in humans. This review highlights the necessity of regulating e-cig use during pregnancy and promoting awareness of its potential consequences on fetal and neonatal development. Full article
(This article belongs to the Special Issue Oxidative Stress in the Newborn)
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<p>Stages of normal lung development and impact of adverse exposures.</p>
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<p>The role of e-cig-induced oxidative stress on the airways.</p>
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<p>Multiple integrated prevention strategies to influence e-cig use during pregnancy.</p>
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16 pages, 1900 KiB  
Article
Maternal Resveratrol Supplementation Attenuates Prenatal Stress Impacts on Anxiety- and Depressive-like Behaviors by Regulating Bdnf Transcripts Expression in the Brains of Adult Male Offspring Rats
by Gerardo Vera-Juárez, Edgar Ricardo Vázquez-Martínez, Raquel Gómez-Pliego, Margarita López-Martínez and Judith Espinosa-Raya
Brain Sci. 2025, 15(2), 210; https://doi.org/10.3390/brainsci15020210 - 19 Feb 2025
Viewed by 319
Abstract
Background: Prenatal stress has been reported to harm the physiological and biochemical functions of the brain of the offspring, potentially resulting in anxiety- and depression-like behaviors later in life. Trans-Resveratrol (RESV) is known for its anti-inflammatory, anxiolytic, and antidepressant properties. However, whether administering [...] Read more.
Background: Prenatal stress has been reported to harm the physiological and biochemical functions of the brain of the offspring, potentially resulting in anxiety- and depression-like behaviors later in life. Trans-Resveratrol (RESV) is known for its anti-inflammatory, anxiolytic, and antidepressant properties. However, whether administering RESV during pregnancy can counteract the anxiety- and depression-like behaviors induced by maternal stress is unknown. Objective: This study aimed to assess the protective potential of RESV against molecular and behavioral changes induced by prenatal stress. Methods: During pregnancy, the dams received 50 mg/kg BW/day of RESV orally. They underwent a movement restriction for forty-five minutes, three times a day, in addition to being exposed to artificial light 24 h before delivery. The male offspring were left undisturbed until early adulthood, at which point they underwent behavioral assessments, including the open field test, elevated plus maze, and forced swim test. Subsequently, they were euthanized, and the hippocampus and prefrontal cortex were extracted for RT-qPCR analysis to measure Bdnf mRNA expression. Results: By weaning, results showed that prenatal stress led to reduced weight gain and, in adulthood, increased anxiety- and depression-like behaviors and changes in Bdnf mRNA expression. However, these effects were attenuated by maternal RESV supplementation. Conclusions: The findings suggest that RESV can prevent anxiety- and depression-like behaviors induced by prenatal stress by modulating Bdnf mRNA expression. Full article
(This article belongs to the Section Neuropsychiatry)
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<p>Experimental protocol. This study used restraint of movement to establish a prenatal stress model. Twenty-four pregnant rats were divided into 4 groups of 6 as follows: (1) Control (CTL)-VEH group, (2) CTL-RSV group, (3) PS-VEH group, and (4) PS-RSV group. On PND 21, two male offspring were taken from each litter, were weaned, and grouped into four groups according to their respective treatments. The male offspring were left undisturbed until early adulthood. They underwent behavioral assessments: an open field test at PND 100, an elevated plus maze at PND 102, and a forced swim test at PND 105. The offspring’s cerebral tissue was collected PND 110, and the expression of <span class="html-italic">Bdnf</span> exons was measured using RT-qPCR. (Created in <a href="https://BioRender.com" target="_blank">https://BioRender.com</a>).</p>
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<p>Effects of maternal resveratrol supplementation in the open field test of prenatal stress adult male offspring. (<b>a</b>) Number of crossings; (<b>b</b>) Number of rearing. All data are mean ± SEM with 10 animals in CTL-VEH and -RESV groups, 9 animals in PS-VEH group, and 11 animals in PS-RESV group. * <span class="html-italic">p</span> &lt; 0.05; ** <span class="html-italic">p</span> &lt; 0.01 by two-way ANOVA followed by Bonferroni post hoc tests. CTL = control; PS = prenatal stress; VEH = vehicle; RESV = resveratrol.</p>
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<p>Effects of maternal resveratrol supplementation in the elevated plus maze of prenatal stress adult male offspring. (<b>a</b>) Total entries; (<b>b</b>) Rearings; (<b>c</b>) Head dips; (<b>d</b>) Open arm entries; (<b>e</b>) Open arm duration; (<b>f</b>) Closed arm entries; (<b>g</b>) Closed arm duration. All data are mean ± SEM with 10 animals in CTL-VEH and -RESV groups, 9 animals in PS-VEH group, and 11 animals in PS-RESV group. * <span class="html-italic">p</span> &lt; 0.05; ** <span class="html-italic">p</span> &lt; 0.01; *** <span class="html-italic">p</span> &lt; 0.001; **** <span class="html-italic">p</span> &lt; 0.0001 by two-way ANOVA followed by Bonferroni post hoc tests. CTL = control; PS = prenatal stress; VEH = vehicle; RESV = resveratrol.</p>
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<p>Effects of maternal resveratrol supplementation in the forced swim test of prenatal stress adult male offspring. (<b>a</b>) Swimming; (<b>b</b>) Immobility; (<b>c</b>) Climbing. All data are mean ± SEM with 10 animals in CTL-VEH and -RESV groups, 9 animals in PS-VEH group, and 11 animals in PS-RESV group. ** <span class="html-italic">p</span> &lt; 0.01; *** <span class="html-italic">p</span> &lt; 0.001; **** <span class="html-italic">p</span> &lt; 0.0001 by two-way ANOVA followed by Bonferroni post hoc tests. CTL = control; PS = prenatal stress; VEH = vehicle; RESV = resveratrol.</p>
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<p>Effects of maternal supplementation of resveratrol on the expression of exons IV, IV, and IX of the <span class="html-italic">Bdnf</span> in the prefrontal cortex (<b>a</b>–<b>c</b>) and hippocampus (<b>d</b>–<b>f</b>) of prenatal stress adult male offspring. All data are mean ± SEM with 4 animals in each group. ** <span class="html-italic">p</span> &lt; 0.01; *** <span class="html-italic">p</span> &lt; 0.001; **** <span class="html-italic">p</span> &lt; 0.0001 by two-way ANOVA followed by Bonferroni post hoc tests. CTL = control; PS = prenatal stress; VEH = vehicle; RESV = resveratrol.</p>
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19 pages, 1298 KiB  
Article
Long-Term Effects of Adverse Maternal Care on Hypothalamic–Pituitary–Adrenal (HPA) Axis Function of Juvenile and Adolescent Macaques
by Kai McCormack, Sara Bramlett, Elyse L. Morin, Erin R. Siebert, Dora Guzman, Brittany Howell and Mar M. Sanchez
Biology 2025, 14(2), 204; https://doi.org/10.3390/biology14020204 - 15 Feb 2025
Viewed by 328
Abstract
Early life adversity (ELA) is a known risk factor for psychopathology, including stress-related anxiety and depressive disorders. The underlying mechanisms and developmental changes remain poorly understood. A likely underpinning is the impact of ELA on the development of stress response systems, including the [...] Read more.
Early life adversity (ELA) is a known risk factor for psychopathology, including stress-related anxiety and depressive disorders. The underlying mechanisms and developmental changes remain poorly understood. A likely underpinning is the impact of ELA on the development of stress response systems, including the hypothalamic–pituitary–adrenal (HPA) axis. Our group studied a translational ELA model of spontaneous infant maltreatment by the mother in rhesus macaques, where we used a cross-fostering design to randomly assign infant macaques to either Control or Maltreating (MALT) foster mothers at birth to examine the impact of adverse caregiving on the development of the HPA axis, while controlling for the confounding effects of heritable and prenatal factors. We previously reported higher levels of plasma and hair cortisol (CORT) across the first 6 postnatal months (equivalent to the first 2 years of life in humans) in the MALT than in the Control infants. Here, we followed the same cohort of infants longitudinally to assess the long-term developmental impact of this adverse experience on HPA axis function during the juvenile (12, 18 months) and late adolescent (~5 years) periods. For this, we collected measurements of diurnal CORT rhythm and glucocorticoid negative feedback using the dexamethasone suppression test (DST). At 12 months, we found higher diurnal CORT secretion in MALT females compared to Control females, and impaired negative feedback in response to the DST in both sexes in the MALT group. However, ELA group differences in the HPA axis function disappeared by 18 months and late adolescence, while sex differences in diurnal CORT rhythm emerged or became stronger. These results suggest that infant maltreatment causes dysregulation of the HPA axis during the first year of life, with HPA axis function normalizing later, during the pre-pubertal juvenile period and adolescence. This suggests that the impact of maltreatment on HPA axis function may be transient, at least if the adverse experience stops. Our findings are consistent with human evidence of recalibration/normalization of HPA axis function during adolescence in children that switch from adverse/deprived environments to supportive adoptive families. This research has broad implications regarding the biological processes that translate ELA to psychopathology during development and the pathways to resiliency. Full article
(This article belongs to the Section Developmental and Reproductive Biology)
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<p>Diurnal CORT rhythms during the juvenile and adolescence periods. (Mean ± SEM). (<b>A</b>) Twelve months: Significant time effect (<span class="html-italic">F</span><sub>(2,50)</sub> = 3.03, <span class="html-italic">p</span> &lt; 0.05), with CORT levels decreasing across the day for all groups and maternal care x sex effect (<span class="html-italic">F</span><sub>(1,25)</sub> = 4.78, <span class="html-italic">p</span> = 0.04), with post hoc tests revealing maternal care effects on females (<span class="html-italic">F</span><sub>(1,18)</sub> = 6.37, <span class="html-italic">p</span> = 0.02) but not males (<span class="html-italic">F</span><sub>(1,18)</sub> = 0.08, <span class="html-italic">p</span> = 0.78). (<b>B</b>) Eighteen months: significant time effect (<span class="html-italic">F</span><sub>(2,56)</sub> = 14.19, <span class="html-italic">p</span> &lt; 0.001), with CORT levels decreasing across the day and time of day × sex interaction effect (<span class="html-italic">F</span><sub>(2,56)</sub> = 3.72, <span class="html-italic">p</span> = 0.03). (<b>C</b>) Adolescence: Significant time effect (<span class="html-italic">F</span><sub>(2,38)</sub> = 22.72, <span class="html-italic">p</span> &lt; 0.001), with CORT levels decreasing across the day, sex effect (<span class="html-italic">F</span><sub>(1,19)</sub> = 15.54, <span class="html-italic">p</span> &lt; 0.001), and time of day × sex interaction effect (<span class="html-italic">F</span><sub>(2,38)</sub> = 5.48, <span class="html-italic">p</span> = 0.008), with post hoc tests revealing higher CORT in females than males at the AM (<span class="html-italic">F</span><sub>(1,19)</sub> = 12.90, <span class="html-italic">p</span> = 0.002) and PM time points (<span class="html-italic">F</span><sub>(1,19)</sub> = 9.65, <span class="html-italic">p</span> = 0.006, η<sup>2</sup><span class="html-italic"><sub>p</sub></span> = 0.34).</p>
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<p>Diurnal CORT rhythms during the juvenile and adolescence periods. (Mean ± SEM). (<b>A</b>) Twelve months: Significant time effect (<span class="html-italic">F</span><sub>(2,50)</sub> = 3.03, <span class="html-italic">p</span> &lt; 0.05), with CORT levels decreasing across the day for all groups and maternal care x sex effect (<span class="html-italic">F</span><sub>(1,25)</sub> = 4.78, <span class="html-italic">p</span> = 0.04), with post hoc tests revealing maternal care effects on females (<span class="html-italic">F</span><sub>(1,18)</sub> = 6.37, <span class="html-italic">p</span> = 0.02) but not males (<span class="html-italic">F</span><sub>(1,18)</sub> = 0.08, <span class="html-italic">p</span> = 0.78). (<b>B</b>) Eighteen months: significant time effect (<span class="html-italic">F</span><sub>(2,56)</sub> = 14.19, <span class="html-italic">p</span> &lt; 0.001), with CORT levels decreasing across the day and time of day × sex interaction effect (<span class="html-italic">F</span><sub>(2,56)</sub> = 3.72, <span class="html-italic">p</span> = 0.03). (<b>C</b>) Adolescence: Significant time effect (<span class="html-italic">F</span><sub>(2,38)</sub> = 22.72, <span class="html-italic">p</span> &lt; 0.001), with CORT levels decreasing across the day, sex effect (<span class="html-italic">F</span><sub>(1,19)</sub> = 15.54, <span class="html-italic">p</span> &lt; 0.001), and time of day × sex interaction effect (<span class="html-italic">F</span><sub>(2,38)</sub> = 5.48, <span class="html-italic">p</span> = 0.008), with post hoc tests revealing higher CORT in females than males at the AM (<span class="html-italic">F</span><sub>(1,19)</sub> = 12.90, <span class="html-italic">p</span> = 0.002) and PM time points (<span class="html-italic">F</span><sub>(1,19)</sub> = 9.65, <span class="html-italic">p</span> = 0.006, η<sup>2</sup><span class="html-italic"><sub>p</sub></span> = 0.34).</p>
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<p>Dexamethasone suppression of diurnal CORT (−DEX) secretion at 12 and 18 months (juvenile period). (Mean ± SEM). (<b>A</b>) Twelve months: Significant DEX effect with lower CORT values in all groups under +DEX compared to −DEX <span class="html-italic">F</span><sub>(1,23)</sub> = 17.78, <span class="html-italic">p</span> &lt; 0.001), time of day × DEX interaction effect (<span class="html-italic">F</span><sub>(1,23)</sub> = 10.37, <span class="html-italic">p</span> = 0.004), with levels decreasing from the AM to PM time points under the −DEX condition; however, in the +DEX condition values increased from the AM (suppressed CORT) to PM (escape) time points. A maternal care × DEX interaction effect was also found (<span class="html-italic">F</span><sub>(1,23)</sub> = 8.50, <span class="html-italic">p</span> = 0.008) with post hoc analyses revealing that this effect was driven by lower CORT levels across the day in MALT than in Control animals in the +DEX condition (F<sub>(1,23)</sub> = 4.96, <span class="html-italic">p</span> = 0.04). (<b>B</b>) Eighteen months: Significant DEX effect with lower CORT values in all groups under +DEX compared to −DEX (<span class="html-italic">F</span><sub>(1,30)</sub> = 186.77, <span class="html-italic">p</span> &lt; 0.001) and a time of day × DEX interaction effect (<span class="html-italic">F</span><sub>(1,30)</sub> = 8.74, <span class="html-italic">p</span> = 0.01), with values decreasing from the AM to PM time points under the −DEX condition, but remaining the same (suppressed) at AM and PM time points in the +DEX condition. In contrast to 12 months, no maternal care × DEX interaction effects were detected at this age. Solid lines represent basal diurnal CORT levels (−DEX condition), dashed lines represent CORT levels after DEX treatment (+DEX condition).</p>
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14 pages, 280 KiB  
Review
The Influence of Heat on Pediatric and Perinatal Health: Risks, Evidence, and Future Directions
by Nicola Principi, Beatrice Rita Campana, Alberto Argentiero, Valentina Fainardi and Susanna Esposito
J. Clin. Med. 2025, 14(4), 1123; https://doi.org/10.3390/jcm14041123 - 10 Feb 2025
Viewed by 544
Abstract
Children, particularly infants and those with chronic conditions, are highly vulnerable to heat-induced health risks, similarly to the elderly. This narrative review synthesizes current evidence on the impact of heat exposure on pediatric and perinatal health. A systematic literature search was conducted using [...] Read more.
Children, particularly infants and those with chronic conditions, are highly vulnerable to heat-induced health risks, similarly to the elderly. This narrative review synthesizes current evidence on the impact of heat exposure on pediatric and perinatal health. A systematic literature search was conducted using PubMed/MEDLINE and manual reference checks, focusing on studies from 2000 to 2024. Findings indicate that maternal heat exposure is associated with adverse pregnancy outcomes, including pre-eclampsia, gestational diabetes, hypertension, and increased hospital admissions. Additionally, prenatal heat stress correlates with preterm birth, low birth weight, birth defects, and stillbirth. In childhood, heat-related health consequences range from heatstroke and dehydration to renal impairment, respiratory diseases, and gastrointestinal infections. Psychosocial effects, including cognitive impairment, sleep disturbances, and mental health issues, have also been reported in school-age children and adolescents. Despite strong epidemiological evidence, critical knowledge gaps remain, including the exact temperature thresholds that increase disease risk and how these thresholds vary by age and underlying health conditions. Urgent public health measures are required to mitigate these risks, while further research is needed to define exposure–response relationships and effective interventions. Addressing the rising burden of heat-related pediatric illness is essential in the context of climate change and increasing global temperatures. Full article
(This article belongs to the Section Intensive Care)
17 pages, 289 KiB  
Article
Fetal Growth Is Associated with Amniotic Fluid Antioxidant Capacity, Oxidative Stress, Minerals and Prenatal Supplementation: A Retrospective Study
by Mozhgan Kohzadi, Stan Kubow and Kristine G. Koski
Antioxidants 2025, 14(2), 184; https://doi.org/10.3390/antiox14020184 - 5 Feb 2025
Viewed by 637
Abstract
Background: Associations of antioxidants in prenatal over-the-counter multivitamin-mineral (OTC MVM) supplements with in-utero oxidative stress (OS), antioxidant capacity, and fetal growth are limited. Our objectives were to determine if five fetal ultrasound measurements [biparietal diameter (BPD), head circumference (HC), abdominal circumference (AC), femur [...] Read more.
Background: Associations of antioxidants in prenatal over-the-counter multivitamin-mineral (OTC MVM) supplements with in-utero oxidative stress (OS), antioxidant capacity, and fetal growth are limited. Our objectives were to determine if five fetal ultrasound measurements [biparietal diameter (BPD), head circumference (HC), abdominal circumference (AC), femur length (FL), and estimated fetal weight] were associated with OTC MVM supplements and with minerals, biomarkers of OS, and total antioxidant capacity in amniotic fluid (AF). Methods: For this retrospective study, 176 pregnant women who had undergone age-related amniocentesis for genetic testing were included. Questionnaires recorded prenatal OTC MVM supplementation (yes, no). Ultrasound measurements for early (16–20 weeks) and late (32–36 weeks) gestation were extracted from medical charts. AF concentrations for 15 minerals and trace elements and OS biomarkers in AF [nitric oxide (NO), thiobarbituric acid-reactive substances (TBARS), and ferric-reducing antioxidant power (FRAP)] were measured at 12–20 weeks of gestation. Associations of AF minerals, OS biomarkers, and ultrasound measures were analyzed using multiple linear regressions. Results: Positive associations were observed between AF TBARS and seven AF minerals/elements (calcium, copper, magnesium, nickel, strontium, zinc and iron). At 16–20 weeks, AF copper, nickel, strontium, and selenium were positively associated with BPD, HC, AC, and FL, respectively, NO was positively associated with FL, and FRAP was inversely associated with estimated weight. At 32–36 weeks, calcium was positively associated with BPD and chromium and arsenic were negatively with HC. At 16–20 weeks, higher AF FRAP was inversely associated with FL and this exposure continued to be inversely associated with estimated weight at 32–36 weeks. Conclusions: Concentrations of AF minerals, trace elements and biomarkers of OS and in-utero antioxidant capacity were linked to specific ultrasound measurements at different stages of gestation, suggesting a complex interplay among in utero OS, antioxidant capacity, OTC MVM supplements, and fetal growth. Full article
(This article belongs to the Special Issue Oxidative Stress in Reproduction of Mammals)
40 pages, 4205 KiB  
Article
Evaluation of Prenatal Transportation Stress on DNA Methylation (DNAm) and Gene Expression in the Hypothalamic–Pituitary–Adrenal (HPA) Axis Tissues of Mature Brahman Cows
by Audrey L. Earnhardt-San, Emilie C. Baker, Kubra Z. Cilkiz, Rodolfo C. Cardoso, Noushin Ghaffari, Charles R. Long, Penny K. Riggs, Ronald D. Randel, David G. Riley and Thomas H. Welsh
Genes 2025, 16(2), 191; https://doi.org/10.3390/genes16020191 - 4 Feb 2025
Viewed by 435
Abstract
Background/Objectives: The experience of prenatal stress results in various physiological disorders due to an alteration of an offspring’s methylome and transcriptome. The objective of this study was to determine whether PNS affects DNA methylation (DNAm) and gene expression in the stress axis tissues [...] Read more.
Background/Objectives: The experience of prenatal stress results in various physiological disorders due to an alteration of an offspring’s methylome and transcriptome. The objective of this study was to determine whether PNS affects DNA methylation (DNAm) and gene expression in the stress axis tissues of mature Brahman cows. Methods: Samples were collected from the paraventricular nucleus (PVN), anterior pituitary (PIT), and adrenal cortex (AC) of 5-year-old Brahman cows that were prenatally exposed to either transportation stress (PNS, n = 6) or were not transported (Control, n = 8). The isolated DNA and RNA samples were, respectively, used for methylation and RNA-Seq analyses. A gene ontology and KEGG pathway enrichment analysis of each data set within each sample tissue was conducted with the DAVID Functional Annotation Tool. Results: The DNAm analysis revealed 3, 64, and 99 hypomethylated and 2, 93, and 90 hypermethylated CpG sites (FDR < 0.15) within the PVN, PIT, and AC, respectively. The RNA-Seq analysis revealed 6, 25, and 5 differentially expressed genes (FDR < 0.15) in the PVN, PIT, and AC, respectively, that were up-regulated in the PNS group relative to the Control group, as well as 24 genes in the PIT that were down-regulated. Based on the enrichment analysis, several developmental and cellular processes, such as maintenance of the actin cytoskeleton, cell motility, signal transduction, neurodevelopment, and synaptic function, were potentially modulated. Conclusions: The methylome and transcriptome were altered in the stress axis tissues of mature cows that had been exposed to prenatal transportation stress. These findings are relevant to understanding how prenatal experiences may affect postnatal neurological functions. Full article
(This article belongs to the Section Animal Genetics and Genomics)
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<p>MA plots showing the relationship between the average concentration (logCPM) and fold-change (logFC) across the CpG sites in each tissue. Each site is represented by a dot with differentially methylated CpG sites (FDR &lt; 0.15) colored in (<b>A</b>) red for the PVN, (<b>B</b>) blue for the PIT, and (<b>C</b>) orange for the AC. The blue solid lines represent a logFC ± 1 threshold, and the gray dotted lines represent a logFC ± 2 threshold.</p>
Full article ">Figure 2
<p>MA plots showing the relationship between the average concentration (logCPM) and fold-change (logFC) across the genes in each tissue. Each gene is represented by a dot with the differentially expressed genes (FDR &lt; 0.15) colored in (<b>A</b>) red for the PVN, (<b>B</b>) blue for the PIT, and (<b>C</b>) orange for the AC. The blue solid lines represent a logFC ± 1 threshold, and the gray dotted lines represent a logFC ± 2 threshold.</p>
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<p>Gene ontology enrichment results of genes that are differentially expressed within the (<b>A</b>) PVN, (<b>B</b>) PIT, and (<b>C</b>) AC. <span class="html-italic">y</span>-axis contains GO terms and <span class="html-italic">x</span>-axis contains number of genes enriched within each GO term; <span class="html-italic">p</span>-value of each enriched term is within each individual bar.</p>
Full article ">Figure 3 Cont.
<p>Gene ontology enrichment results of genes that are differentially expressed within the (<b>A</b>) PVN, (<b>B</b>) PIT, and (<b>C</b>) AC. <span class="html-italic">y</span>-axis contains GO terms and <span class="html-italic">x</span>-axis contains number of genes enriched within each GO term; <span class="html-italic">p</span>-value of each enriched term is within each individual bar.</p>
Full article ">Figure 4
<p>Gene ontology enrichment results for genes that are differentially methylated within the (<b>A</b>) PIT and (<b>B</b>) AC. <span class="html-italic">y</span>-axis contains GO terms and <span class="html-italic">x</span>-axis contains number of genes enriched within each GO term; <span class="html-italic">p</span>-value of each enriched term is within each individual bar.</p>
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<p>KEGG pathway enrichment results for the genes that are differentially expressed within the PVN and AC. The <span class="html-italic">y</span>-axis contains the KEGG pathway terms and the <span class="html-italic">x</span>-axis contains the number of genes enriched within each term; the <span class="html-italic">p</span>-value of each enriched term is within each individual bar.</p>
Full article ">Figure 6
<p>KEGG pathway enrichment results for genes that are differentially methylated within the PIT and AC. The <span class="html-italic">y</span>-axis contains the KEGG pathway terms and the <span class="html-italic">x</span>-axis contains the number of genes enriched within each term; the <span class="html-italic">p</span>-value of each enriched term is within each individual bar.</p>
Full article ">
16 pages, 617 KiB  
Review
Impact of Stress and Anxiety on Cardiovascular Health in Pregnancy: A Scoping Review
by Brenda-Cristiana Bernad, Mirela-Cleopatra Tomescu, Dana Emilia Velimirovici, Minodora Andor, Diana Lungeanu, Virgil Enătescu, Adina-Ioana Bucur, Ana Lascu, Andreea-Luciana Raţă, Elena Silvia Bernad, Vlad Nicoraș, Diana-Aurora Arnăutu, Oana Neda-Stepan and Lavinia Hogea
J. Clin. Med. 2025, 14(3), 909; https://doi.org/10.3390/jcm14030909 - 30 Jan 2025
Viewed by 1031
Abstract
Complex biological processes that enable optimal foetal growth throughout pregnancy are linked to notable haemodynamic and metabolic changes in the mother’s body. An inability to adapt to these changes can affect cardiovascular health. During pregnancy, women may experience mood swings, anxiety, and emotional [...] Read more.
Complex biological processes that enable optimal foetal growth throughout pregnancy are linked to notable haemodynamic and metabolic changes in the mother’s body. An inability to adapt to these changes can affect cardiovascular health. During pregnancy, women may experience mood swings, anxiety, and emotional ambivalence. These symptoms can lead to stress and harm the mental well-being of expectant mothers. It is crucial to know the aspects that can influence the development of cardiovascular problems among pregnant women. Effective management requires identifying risk factors. Applying the PRISMA ScR guidelines, we conducted a scoping review to explore and summarise the evidence regarding the impact of stress and anxiety on cardiovascular health in pregnant women. The following enquiries were looked into as research topics: What effects do anxiety and stress have on a pregnant woman’s cardiovascular health? How is it quantifiable? It is essential to comprehend the physiological changes that the body undergoes throughout pregnancy in order to inform and assist both patients and medical professionals. This makes it possible for them to identify any pathological disorders or risk factors that could worsen the health of expectant mothers. Psychological and cardiovascular risk factor screening, either before or during pregnancy, may be able to uncover circumstances that require specific medical and psychological therapies in order to lower maternal morbidity and death from cardiovascular disease. Our findings underscore the need for systematic psychological and cardiovascular screening during prenatal care to mitigate adverse outcomes and improve maternal–foetal health. Full article
(This article belongs to the Section Mental Health)
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<p>Review process flow chart based on PRISMA ScR principles.</p>
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22 pages, 732 KiB  
Review
A Framework for Comprehensive Dairy Calf Health Investigations
by Kristen Y. Edwards and David L. Renaud
Animals 2025, 15(2), 181; https://doi.org/10.3390/ani15020181 - 11 Jan 2025
Viewed by 810
Abstract
The objective of this narrative review is to provide a systematic framework for veterinarians to investigate dairy calf health, focusing on critical control points and key performance indicators (KPIs) to address morbidity and mortality challenges in preweaned calves. Recommendations target prenatal maternal nutrition, [...] Read more.
The objective of this narrative review is to provide a systematic framework for veterinarians to investigate dairy calf health, focusing on critical control points and key performance indicators (KPIs) to address morbidity and mortality challenges in preweaned calves. Recommendations target prenatal maternal nutrition, heat stress abatement, and optimal calving management to minimize risks associated with perinatal mortality and preweaning morbidity. Further, comprehensive colostrum management is discussed to ensure excellent transfer of passive immunity, which includes prompt collection and feeding within two hours of birth at a volume of 8.5–10% of calf body weight. Nutritional guidance emphasizes the importance of transition milk and feeding higher planes of nutrition to support immunity, with recommendations that milk total solids exceed 10% to meet energy needs. Environmental management recommendations include a minimum of 3.3 m2 of space per calf, the use of low-dust bedding, and air quality controls to reduce respiratory disease. Lastly, regular health data collection and KPI monitoring, such as average daily gain and morbidity rates, are essential for data-driven improvements. By implementing these evidence-based recommendations, veterinarians can support dairy farmers in reducing calf morbidity and mortality, ultimately enhancing calf welfare and lifetime productivity. Full article
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<p>Proportion of calves with (<b>A</b>) diarrhea, (<b>B</b>) respiratory disease, (<b>C</b>) any preweaning disease, and (<b>D</b>) mortality dependent on the category of transfer of passive immunity (poor to excellent) using data from Lombard et al. [<a href="#B67-animals-15-00181" class="html-bibr">67</a>], Sutter et al. [<a href="#B68-animals-15-00181" class="html-bibr">68</a>], and Crannell and Abuelo [<a href="#B69-animals-15-00181" class="html-bibr">69</a>].</p>
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15 pages, 459 KiB  
Review
Oral Health, Anxiety, Depression, and Stress in Pregnancy: A Rapid Review of Associations and Implications for Perinatal Care
by Abiola A. Adeniyi, Swathi Ramachandran and Cecilia Marie Jevitt
Int. J. Environ. Res. Public Health 2025, 22(1), 32; https://doi.org/10.3390/ijerph22010032 - 29 Dec 2024
Viewed by 1336
Abstract
Research demonstrates associations between oral health and specific mental health conditions in the general population, yet these relationships remain understudied during pregnancy, despite pregnancy’s profound effects on both oral and psychological well-being. Our rapid review examines current evidence on associations between oral health [...] Read more.
Research demonstrates associations between oral health and specific mental health conditions in the general population, yet these relationships remain understudied during pregnancy, despite pregnancy’s profound effects on both oral and psychological well-being. Our rapid review examines current evidence on associations between oral health conditions and psychological states (anxiety, depression, and stress) during pregnancy, aiming to inform and strengthen integrated prenatal care strategies. Following PRISMA-RR guidelines, we conducted a systematic search on OVID Medline, CINAHL, and PsycINFO (January 2000–November 2024) for studies examining relationships between oral health conditions (periodontal disease, dental caries) and psychological status during pregnancy and up to one year postpartum. Systematic screening of 1201 records yielded 22 eligible studies (13 cross-sectional studies, 3 longitudinal cohort studies, 3 comparative studies, 2 prospective studies, and 1 case–control study). Analysis confirmed significant associations between oral health and psychological well-being during pregnancy through three pathways: psychological (dental anxiety directly limits oral healthcare utilization), behavioral (maternal depression reduces oral health self-efficacy), and physiological (elevated stress biomarkers correlate with periodontal disease, and periodontal therapy is associated with reduced salivary cortisol). These interactions extend intergenerationally, with maternal psychological distress showing significant associations with children’s caries risk. Evidence suggests interactions between oral health conditions and psychological states during pregnancy, warranting integrated care approaches. We recommend: (1) implementing combined oral–mental health screening in prenatal care, (2) developing interventions targeting both domains, and (3) establishing care pathways that address these interconnections. This integrated approach could improve both maternal and child health outcomes. Full article
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<p>PRISMA Flow Chart for the Scoping Review.</p>
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15 pages, 1364 KiB  
Article
Prenatal Stress Modulates Placental and Fetal Serotonin Levels and Determines Behavior Patterns in Offspring of Mice
by Victoria Melnikova, Nadezhda Lifantseva, Svetlana Voronova and Nadezhda Bondarenko
Int. J. Mol. Sci. 2024, 25(24), 13565; https://doi.org/10.3390/ijms252413565 - 18 Dec 2024
Viewed by 601
Abstract
Available evidence from animal studies suggests that placental serotonin plays an important role in proper fetal development and programming by altering brain circuit formation, which later translates into altered abnormal adult behaviors. Several environmental stimuli, including stress and maternal inflammation, affect placental and, [...] Read more.
Available evidence from animal studies suggests that placental serotonin plays an important role in proper fetal development and programming by altering brain circuit formation, which later translates into altered abnormal adult behaviors. Several environmental stimuli, including stress and maternal inflammation, affect placental and, hence, fetal serotonin levels and thus may disturb fetal brain development. We investigated the effect of prenatal stress of varying intensities on the formation of adaptive behaviors in mouse offspring and the role of placental serotonin in these processes. Mild prenatal stress increased placental serotonin synthesis, whereas exposure to moderate stress decreased it. Prenatal stress of varying intensities also resulted in multidirectional changes in animal behavior in progeny, consistent with changes in serotonin levels in the placenta and fetal tissues. Mice exposed to mild prenatal stress showed higher sociality and exploratory activity, whereas, after moderate stress, in contrast, they avoided contact with other individuals of their species and had reduced exploratory activity, with no effect on locomotor activity. Thus, in mice, stressors of varying intensities during the critical period of intrauterine development can affect the synthesis of serotonin by the placenta and lead to multidirectional changes in animal behavior in postnatal life. Full article
(This article belongs to the Special Issue Serotonin in Health and Diseases)
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<p>Changes in serotonin concentrations in the placenta and fetal tissues of mice at E15 (in pmol per mg tissue) under the influence of stress of varying intensities and after the administration of serotonin precursor 5-HTP. 5-HT was measured by the HPLC method in placentas, whole fetuses, and fetal trunks, heads, and brains. The data are presented as mean ± SEM, <span class="html-italic">n</span> = 9, for each group. * <span class="html-italic">p</span> &lt; 0.05 vs. control group. 5-HT—Serotonin, 5-HTP—5-hydroxytryptophan.</p>
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<p>Experimental design (<b>a</b>) and behavioral parameters of mice (P30) in the Open Field Test after exposure to stress of varying intensities during the period E11-E14 (<b>b</b>–<b>e</b>). <span class="html-italic">n</span> = 12 for each group, * <span class="html-italic">p</span> &lt; 0.05 vs. control group, # <span class="html-italic">p</span> &lt; 0.1 vs. control group.</p>
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<p>Experimental design (<b>a</b>) and behavioral parameters of mice (P30) in the Open Field Test after exposure to stress of varying intensities during the period E11-E14 (<b>b</b>–<b>e</b>). <span class="html-italic">n</span> = 12 for each group, * <span class="html-italic">p</span> &lt; 0.05 vs. control group, # <span class="html-italic">p</span> &lt; 0.1 vs. control group.</p>
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<p>Behavioral parameters of mice (P30) in the Elevated Plus Maze Test after exposure to stress of varying intensities during the period E11–E14. (<b>a</b>) Time spent by mice in the Elevated Plus Maze arms, (<b>b</b>) Head hanging. <span class="html-italic">n</span> = 12 for each group, * <span class="html-italic">p</span> &lt; 0.05 vs. control group.</p>
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<p>Effect of prenatal stress of varying intensities on the propensity to defend one’s territory in mouse offspring (P30), expressed as the number of intruder attacks, according to the Resident–Intruder Test. <span class="html-italic">n</span> = 21 for each group.</p>
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<p>Behavioral parameters of mice (P30) in the Three-Chambered Social Approach Task after exposure to stress of varying intensities during the period E11–E14. <span class="html-italic">n</span> = 8 for control group, <span class="html-italic">n</span> = 20 for both experimental groups. * <span class="html-italic">p</span> &lt; 0.05 vs. 1 h stress group, <b>#</b> <span class="html-italic">p</span> &lt; 0.1 vs. control group.</p>
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11 pages, 2678 KiB  
Article
The Placenta as the Main Source of Serotonin in Ontogenetic Dynamics: Inflammation-Induced Modulation of Placental Serotonin Can Be Prevented by Immunoglobulin Administration
by Nadezhda Bondarenko, Nadezhda Lifantseva, Svetlana Voronova and Victoria Melnikova
Int. J. Mol. Sci. 2024, 25(24), 13532; https://doi.org/10.3390/ijms252413532 - 18 Dec 2024
Viewed by 624
Abstract
Placental serotonin is recognized as a key component of feto-placental physiology and can be influenced by environmental factors such as maternal diet, drugs, stress, and immune activation. In this study, we compared the contribution of placental and fetal sources to the maintenance of [...] Read more.
Placental serotonin is recognized as a key component of feto-placental physiology and can be influenced by environmental factors such as maternal diet, drugs, stress, and immune activation. In this study, we compared the contribution of placental and fetal sources to the maintenance of serotonin levels required for normal fetal development during ontogenetic dynamics. Our results demonstrated the leading role of the placenta at almost all stages of development. We investigated the modulatory effect of inflammation on placental serotonin levels. The data obtained showed that the susceptibility to prenatal inflammation depends on its severity and varies considerably at different stages of development. According to our results, inflammation-induced modulation of placental serotonin levels can be prevented by immunoglobulin administration at both early and late stages of development. Disturbances in placental serotonin signaling during critical developmental periods may have long-lasting consequences for the health and behavior of the offspring. Therefore, the ability to prevent environmental modulation of placental serotonin, and hence negative effects on the developing fetus, is of great importance. Full article
(This article belongs to the Special Issue Serotonin in Health and Diseases)
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<p>The expression of tryptophan hydroxylase (TPH) in placenta at different developmental stages revealed by immunohistochemistry. Nuclei were stained with DAPI, “f”—fetal and “m”—maternal compartments of the placenta, bar—100 μm.</p>
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<p>Comparative analysis of different serotonin sources in feto-placental unit during ontogenetic dynamics, (<b>a</b>) serotonin contents in the placenta and in the head and trunk of the fetus during the ontogenetic dynamics (n = 9, * <span class="html-italic">p</span> &lt; 0.05 placenta vs. head, # <span class="html-italic">p</span> &lt; 0.05 placenta vs. trunk at each developmental stage), (<b>b</b>) the ontogenetic dynamics of the placental weight between stages E12 and E21 (n = 12, * <span class="html-italic">p</span> &lt; 0.05 vs. previous stage), (<b>c</b>), serotonin concentrations in the placenta and in the fetal head during the ontogenetic dynamics (n = 9, * <span class="html-italic">p</span> &lt; 0.05 placenta vs. head at each developmental stage).</p>
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<p>The effect of LPS administration on the placental serotonin content during ontogenetic dynamics. Pregnant rats received LPS at doses 25 or 250 μg/kg b.w., and the placental serotonin content was measured 24 h after injection. n = 8 for each experimental group, * <span class="html-italic">p</span> &lt; 0.05 vs. control.</p>
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<p>The preventive effect of immunoglobulin administration on the placental serotonin level in LPS-treated rats at E14 (<b>a</b>–<b>c</b>) and E20 (<b>d</b>–<b>f</b>). (<b>a</b>,<b>d</b>)—serotonin content per placenta, (<b>b</b>,<b>e</b>)—serotonin concentration per mg tissue, (<b>c</b>,<b>f</b>)—the weight of placenta. n = 8 for each experimental group, * <span class="html-italic">p</span> &lt; 0.05 vs. control, # <span class="html-italic">p</span> &lt; 0.05 between “LPS” and “LPS + Igs” groups.</p>
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21 pages, 4296 KiB  
Article
Comparative Analysis of the Effects of Maternal Hypoxia and Placental Ischemia on HIF1-Dependent Metabolism and the Glucocorticoid System in the Embryonic and Newborn Rat Brain
by Oleg Vetrovoy, Sofiya Potapova, Viktor Stratilov and Ekaterina Tyulkova
Int. J. Mol. Sci. 2024, 25(24), 13342; https://doi.org/10.3390/ijms252413342 - 12 Dec 2024
Viewed by 757
Abstract
Prenatal hypoxia, often accompanied by maternal glucocorticoid stress, can predispose offspring to neurological disorders in adulthood. If placental ischemia (PI) primarily reduces fetal oxygen supply, the maternal hypoxia (MH) model also elicits a pronounced fetal glucocorticoid exposure. Here, we compared MH and PI [...] Read more.
Prenatal hypoxia, often accompanied by maternal glucocorticoid stress, can predispose offspring to neurological disorders in adulthood. If placental ischemia (PI) primarily reduces fetal oxygen supply, the maternal hypoxia (MH) model also elicits a pronounced fetal glucocorticoid exposure. Here, we compared MH and PI in rats to distinguish their unique and overlapping effects on embryonic and newborn brain development. We analyzed glucocorticoid transport into the developing brain, glucocorticoid receptor (GR) expression, and GR-dependent transcription, along with key enzymes regulating glucocorticoid metabolism in maternal (MP) and fetal placentas (FP) and in the brain. Additionally, we examined hypoxia-inducible factor 1-alpha (HIF1α) and its downstream genes, as well as glycolysis and the pentose phosphate pathway, both associated with the transport of substrates essential for glucocorticoid synthesis and degradation. Both MH and PI induced HIF1-dependent metabolic alterations, enhancing glycolysis and transiently disrupting redox homeostasis. However, only MH caused a maternal glucocorticoid surge that altered early fetal brain glucocorticoid responsiveness. Over time, these differences may lead to distinct long-term outcomes in neuronal structure and function. This work clarifies the individual contributions of hypoxic and glucocorticoid stresses to fetal brain development, suggesting that combining the MH and PI models could provide valuable insights for future investigations into the mechanisms underlying developmental brain pathologies, including non-heritable psychoneurological and neurodegenerative disorders. Full article
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<p>The effect of MH and PI on HIF1α protein expression levels in the MP (<b>a</b>) and FP (<b>b</b>) at e15 and e20, detected by Western blotting. (<b>a</b>) HIF1α protein levels: e20: ** <span class="html-italic">p</span> &lt; 0.01 vs. control (Student’s test).</p>
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<p>The effect of MH and PI on mRNA levels of the glucocorticoid receptor (<span class="html-italic">nr3c1</span>) in the MP (<b>a</b>) and FP (<b>b</b>) at e15 and e20, detected by RT PCR. The effect of MH and PI on GR protein expression levels in the MP (<b>c</b>) and FP (<b>d</b>) at e15 and e20, detected by Western blotting. The effect of MH and PI on mRNA levels of the glucocorticoid-dependent genes <span class="html-italic">ztb16</span>, <span class="html-italic">dusp1</span>, and <span class="html-italic">fkbp5</span> in the MP (<b>e</b>) and FP (<b>f</b>) at e15 and e20, detected by RT PCR. (<b>e</b>) mRNA levels of <span class="html-italic">dusp1</span>: e15: * <span class="html-italic">p</span> &lt; 0.05 vs. control (Student’s test). mRNA levels of <span class="html-italic">fkbp5</span>: e15: ** <span class="html-italic">p</span> &lt; 0.01 vs. control (Kruskal-Wallis test, Dunn’s test). e20 ** <span class="html-italic">p</span> &lt; 0.01 vs. control (one-way ANOVA, Tukey’s test), &amp;&amp; <span class="html-italic">p</span> &lt; 0.01 between MH and PI (one-way ANOVA, Tukey’s test).</p>
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<p>The effect of MH and PI on mRNA levels of the <span class="html-italic">hsd11b1</span> and <span class="html-italic">hsd11b2</span> in the MP (<b>a</b>) and FP (<b>b</b>) at e15 and e20, detected by RT PCR. The effect of MH and PI on the protein expression levels of HSD11B1 and HSD11B2 in the MP (<b>c</b>) and HSD11B2 in the FP (<b>d</b>) at e15 and e20, detected by Western blotting. (<b>b</b>) mRNA levels of <span class="html-italic">hsd11b2</span>: e15: ** <span class="html-italic">p</span> &lt; 0.01 vs. control (Welch ANOVA, Dunnett’s test). (<b>c</b>) HSD11B2 protein levels: e20: ** <span class="html-italic">p</span> &lt; 0.01 vs. control (Student’s test).</p>
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<p>The effect of MH and PI on the corticosterone levels (<b>a</b>) in the brain at e15, e16, e17, e20 and p1, detected by ELISA. The effect of MH and PI on mRNA levels of the glucocorticoid receptor (<span class="html-italic">nr3c1</span>) (<b>b</b>) in the brain at e15, e16, e17, e20 and p1, detected by RT PCR. The effect of MH and PI on GR protein expression levels (<b>c</b>) in the brain at e15, e16, e17, e20 and p1, detected by Western blotting. The effect of MH and PI on mRNA levels of the glucocorticoid-dependent genes <span class="html-italic">ztb16</span>, <span class="html-italic">dusp1</span>, and <span class="html-italic">fkbp5</span> (<b>d</b>) in the brain at e15, e16, e17, e20 and p1, detected by RT PCR. (<b>a</b>) Corticosterone levels: e15, * <span class="html-italic">p</span> &lt; 0.05 vs. control (one-way ANOVA, Tukey’s test); &amp; <span class="html-italic">p</span> &lt; 0.05 between MH and PI (one-way ANOVA, Tukey’s test). e16, * <span class="html-italic">p</span> &lt; 0.05 vs. control (one-way ANOVA, Tukey’s test); ** <span class="html-italic">p</span> &lt; 0.01 vs. control (one-way ANOVA, Tukey’s test). (<b>d</b>) mRNA levels of <span class="html-italic">zbtb16</span>: e20, * <span class="html-italic">p</span> &lt; 0.05 vs. control (Kruskal-Wallis, Dunn’s test); ** <span class="html-italic">p</span> &lt; 0.01 vs. control (Kruskal-Wallis, Dunn’s test). mRNA levels of <span class="html-italic">dusp1</span>: e20, * <span class="html-italic">p</span> &lt; 0.05 vs. control (Kruskal-Wallis, Dunn’s test); ** <span class="html-italic">p</span> &lt; 0.01 vs. control (Kruskal-Wallis, Dunn’s test). mRNA levels of <span class="html-italic">fkbp5</span>: e16, * <span class="html-italic">p</span> &lt; 0.05 vs. control (Kruskal-Wallis, Dunn’s test); p1, * <span class="html-italic">p</span> &lt; 0.05 vs. control (Kruskal-Wallis, Dunn’s test); &amp;&amp; <span class="html-italic">p</span> &lt; 0.01 between MH and PI (Kruskal-Wallis, Dunn’s test).</p>
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<p>The effect of MH and PI on mRNA levels of <span class="html-italic">hsd11b1</span> and <span class="html-italic">hsd11b2</span> (<b>a</b>) in the brain at e15, e16, e17, e20 and p1, detected by RT PCR. The effect of MH and PI on the protein expression levels of the HSD11B2 (<b>b</b>) in the brain at e15, e16, e17, e20 and p1, detected by Western blotting. (<b>a</b>) mRNA levels of <span class="html-italic">hsd11b1</span>: e17, * <span class="html-italic">p</span> &lt; 0.05 vs. control (Kruskal-Wallis, Dunn’s test); p1, *** <span class="html-italic">p</span> &lt; 0.001 vs. control (Kruskal-Wallis, Dunn’s test). mRNA levels of <span class="html-italic">hsd11b2</span>: e16, ** <span class="html-italic">p</span> &lt; 0.01 vs. control (one-way ANOVA, Tukey’s test); e20, * <span class="html-italic">p</span> &lt; 0.05 vs. control (Kruskal-Wallis, Dunn’s test); &amp; <span class="html-italic">p</span> &lt; 0.05 between MH and PI (Kruskal-Wallis, Dunn’s test); p1, * <span class="html-italic">p</span> &lt; 0.05 vs. control (Welch ANOVA, Dunnett’s test); &amp; <span class="html-italic">p</span> &lt; 0.05 between MH and PI (Welch ANOVA, Dunnett’s test). (<b>b</b>) HSD11B2 protein levels: e17, * <span class="html-italic">p</span> &lt; 0.05 vs. control (Student’s test), ** <span class="html-italic">p</span> &lt; 0.01 vs. corresponding control (Student’s test); e20, ** <span class="html-italic">p</span> &lt; 0.01 vs. control (Mann-Whitney’s test).</p>
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<p>The effect of MH and PI on mRNA levels of <span class="html-italic">hif1α</span> (<b>a</b>) in the brain at e15, e16, e17, e20 and p1, detected by RT PCR. The effect of MH and PI on HIF1α protein expression levels (<b>b</b>) in the brain at e15, e16, e17, e20 and p1, detected by Western blotting. The effect of MH and PI on mRNA levels of the HIF1-dependent genes <span class="html-italic">glut1</span>, <span class="html-italic">hk1</span>, <span class="html-italic">pfkb3</span>, <span class="html-italic">ldha</span>, <span class="html-italic">pdk1</span>, and <span class="html-italic">mct4</span> (<b>c</b>) in the brain at e15, e16, e17, e20 and p1, detected by RT PCR. (<b>b</b>) HIF1α protein levels: e15: ** <span class="html-italic">p</span> &lt; 0.01 vs. control (Student’s test). (<b>c</b>) mRNA levels of <span class="html-italic">glut1</span>: e16, ** <span class="html-italic">p</span> &lt; 0.01 vs. control (one-way ANOVA, Tukey’s test), *** <span class="html-italic">p</span> &lt; 0.001 vs. control (one-way ANOVA, Tukey’s test); e20, * <span class="html-italic">p</span> &lt; 0.05 vs. control (Welch ANOVA, Dunnett’s test); p1, * <span class="html-italic">p</span> &lt; 0.05 PI vs. control (Welch ANOVA, Dunnett’s test). mRNA levels of <span class="html-italic">hk1</span>: e15, ** <span class="html-italic">p</span> &lt; 0.01 vs. control (one-way ANOVA, Tukey’s test); &amp;&amp;&amp; <span class="html-italic">p</span> &lt; 0.001 between MH and PI (one-way ANOVA, Tukey’s test); e16, * <span class="html-italic">p</span> &lt; 0.05 vs. control (Welch ANOVA, Dunnett’s test). mRNA levels of <span class="html-italic">pfkb3</span>: e16, * <span class="html-italic">p</span> &lt; 0.05 vs. control (Kruskal-Wallis, Dunn’s test), ** <span class="html-italic">p</span> &lt; 0.01 vs. control (Kruskal-Wallis, Dunn’s test); e20, ** <span class="html-italic">p</span> &lt; 0.01 vs. control (Kruskal-Wallis, Dunn’s test); p1, * <span class="html-italic">p</span> &lt; 0.05 vs. control (Kruskal-Wallis, Dunn’s test). mRNA levels of <span class="html-italic">ldha</span>: e20, * <span class="html-italic">p</span> &lt; 0.05 vs. control (one-way ANOVA, Tukey’s test); p1, * <span class="html-italic">p</span> &lt; 0.05 vs. control (Welch ANOVA, Dunnett’s test). mRNA levels of <span class="html-italic">pdk1</span>: p1, * <span class="html-italic">p</span> &lt; 0.05 vs. control (one-way ANOVA, Tukey’s test); &amp; <span class="html-italic">p</span> &lt; 0.05 between MH and PI (one-way ANOVA, Tukey’s test). mRNA levels of <span class="html-italic">mct4</span>: e15, * <span class="html-italic">p</span> &lt; 0.05 vs. control (one-way ANOVA, Tukey’s test); &amp; <span class="html-italic">p</span> &lt; 0.05 between MH and PI (one-way ANOVA, Tukey’s test).</p>
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<p>The effect of MH and PI on LDHA protein expression levels (<b>a</b>) in the brain at e15, e16, e17, e20 and p1, detected by Western blotting. The effect of MH and PI on LDH activity (<b>b</b>), lactate (<b>c</b>) and pyruvate (<b>d</b>) levels in the brain at e15, e16, e17, e20 and p1, detected by colorimetric tests. (<b>a</b>) LDHA protein levels: e15, ** <span class="html-italic">p</span> &lt; 0.01 MH vs. control (Student’s test), ** <span class="html-italic">p</span> &lt; 0.01 PI vs. control (Student’s test). (<b>b</b>) LDH activity: e15, ** <span class="html-italic">p</span> &lt; 0.01 vs. control (one-way ANOVA, Tukey’s test), *** <span class="html-italic">p</span> &lt; 0.001 vs. control (one-way ANOVA, Tukey’s test). (<b>c</b>) Lactate levels: e15, * <span class="html-italic">p</span> &lt; 0.05 vs. control (one-way ANOVA, Tukey’s test), ** <span class="html-italic">p</span> &lt; 0.01 vs. control (one-way ANOVA, Tukey’s test).</p>
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<p>The effect of MH and PI on mRNA levels of <span class="html-italic">g6pd</span> (<b>a</b>) in the brain at e15, e16, e17, e20 and p1, detected by RT PCR. The effect of MH and PI on G6PD activity (<b>b</b>), NADPH (<b>c</b>), GSHred (<b>d</b>) and MDA (<b>e</b>) levels in the brain at e15, e16, e17, e20 and p1, detected by colorimetric tests. (<b>a</b>) mRNA levels of <span class="html-italic">g6pd</span>: e15, * <span class="html-italic">p</span> &lt; 0.05 vs. control (Welch ANOVA, Dunnett’s test); e16, ** <span class="html-italic">p</span> &lt; 0.01 vs. control (one-way ANOVA, Tukey’s test); p1, * <span class="html-italic">p</span> &lt; 0.05 vs. control (Kruskal-Wallis, Dunn’s test); &amp; <span class="html-italic">p</span> &lt; 0.05 between MH and PI (Kruskal-Wallis, Dunn’s test). (<b>b</b>) G6PD activity: e15, * <span class="html-italic">p</span> &lt; 0.05 vs. control (one-way ANOVA, Tukey’s test); e16, * <span class="html-italic">p</span> &lt; 0.05 vs. control (Welch ANOVA, Dunnett’s test); e17, * <span class="html-italic">p</span> &lt; 0.05 vs. control (one-way ANOVA, Tukey’s test), *** <span class="html-italic">p</span> &lt; 0.001 vs. control (one-way ANOVA, Tukey’s test). (<b>c</b>) NADPH levels: e15, ** <span class="html-italic">p</span> &lt; 0.01 vs. control (one-way ANOVA, Tukey’s test). (<b>d</b>) GSHred levels: e15: * <span class="html-italic">p</span> &lt; 0.05 vs. control (one-way ANOVA, Tukey’s test); &amp; <span class="html-italic">p</span> &lt; 0.05 between MH and PI (one-way ANOVA, Tukey’s test). e17: * <span class="html-italic">p</span> &lt; 0.05 vs. control (one-way ANOVA, Tukey’s test).</p>
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<p>Schematic outline of the experimental study design. MH, maternal hypoxia; PI, placental ischemia; e0–e20, embryonic days; p0, day of birth; p1, first postnatal day.</p>
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32 pages, 738 KiB  
Review
Remote Sensing Technologies Quantify the Contribution of Ambient Air Pollution to Asthma Severity and Risk Factors in Greenness, Air Pollution, and Wildfire Ecological Settings: A Literature Review
by John T. Braggio
Atmosphere 2024, 15(12), 1470; https://doi.org/10.3390/atmos15121470 - 9 Dec 2024
Viewed by 686
Abstract
Numerous epidemiologic studies have used remote sensing to quantify the contribution of greenness, air pollution, and wildfire smoke to asthma and other respiration outcomes. This is the first review paper to evaluate the influence of remote sensing exposures on specific outcome severity and [...] Read more.
Numerous epidemiologic studies have used remote sensing to quantify the contribution of greenness, air pollution, and wildfire smoke to asthma and other respiration outcomes. This is the first review paper to evaluate the influence of remote sensing exposures on specific outcome severity and risk factors in different ecological settings. Literature searches utilizing PubMed and Google Scholar identified 61 unique studies published between 2009 and 2023, with 198 specific outcomes. Respiration-specific outcomes were lower in greenness and higher in air pollution and wildfire ecological settings. Aerosol optical depth (AOD)-PM2.5 readings and specific outcomes were higher in economically developing than in economically developed countries. Prospective studies found prenatal and infant exposure to higher ambient AOD-PM2.5 concentration level readings contributed to higher childhood asthma incidence. Lung function was higher in greenness and lower in the other two ecological settings. Age, environment, gender, other, and total risk factors showed significant differences between health outcomes and ecological settings. Published studies utilized physiologic mechanisms of immune, inflammation, and oxidative stress to describe obtained results. Individual and total physiologic mechanisms differed between ecological settings. Study results were used to develop a descriptive physiologic asthma model and propose updated population-based asthma intervention program guidelines. Full article
(This article belongs to the Special Issue Exposure Assessment of Air Pollution (2nd Edition))
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<p>Utilization of remote sensing to assess the contribution of live vegetation, ambient air pollution, wildfire smoke, and other attributes to asthma and other respiration-specific outcomes. Refer to these references for additional information: Greenness, Dadvand and associates [<a href="#B59-atmosphere-15-01470" class="html-bibr">59</a>]; AOD-Air Pollution, land use regression [<a href="#B23-atmosphere-15-01470" class="html-bibr">23</a>]; Hierarchical Bayesian models [<a href="#B19-atmosphere-15-01470" class="html-bibr">19</a>], and GEOS-Chem model [<a href="#B31-atmosphere-15-01470" class="html-bibr">31</a>,<a href="#B43-atmosphere-15-01470" class="html-bibr">43</a>]; Wildfire Attributes, AOD-PM<sub>2.5</sub> + smoke [<a href="#B45-atmosphere-15-01470" class="html-bibr">45</a>,<a href="#B60-atmosphere-15-01470" class="html-bibr">60</a>,<a href="#B61-atmosphere-15-01470" class="html-bibr">61</a>,<a href="#B62-atmosphere-15-01470" class="html-bibr">62</a>,<a href="#B63-atmosphere-15-01470" class="html-bibr">63</a>,<a href="#B64-atmosphere-15-01470" class="html-bibr">64</a>,<a href="#B65-atmosphere-15-01470" class="html-bibr">65</a>,<a href="#B66-atmosphere-15-01470" class="html-bibr">66</a>,<a href="#B67-atmosphere-15-01470" class="html-bibr">67</a>,<a href="#B68-atmosphere-15-01470" class="html-bibr">68</a>].</p>
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<p>The synergistic contribution of ecological setting exposures (top row, from left side to right side, wildfire, air pollution, and greenness, respectively) to lung and physiologic function (middle row), and respiration outcome onset (asthma, bronchitis, cough, and wheeze), as modified by epidemiologic and psychologic risk factors (bottom row, left side and right side, respectively). Abbreviation: remote sensing, RS. Arrow direction represents an aversive (↑) or protective (↓) contribution to the final outcome.</p>
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17 pages, 5954 KiB  
Article
Is There a Relationship Between Prenatal Dexamethasone and Postnatal Fructose Overexposure and Testicular Development, Function, and Oxidative Stress Parameters in Rats?
by Nataša Ristić, Slavica Borković-Mitić, Milica Manojlović-Stojanoski, Nataša Nestorović, Branko Filipović, Branka Šošić-Jurjević, Svetlana Trifunović, Bojan Mitić, Jovana Čukuranović-Kokoris and Slađan Pavlović
Int. J. Mol. Sci. 2024, 25(23), 13112; https://doi.org/10.3390/ijms252313112 - 6 Dec 2024
Viewed by 687
Abstract
Prenatal glucocorticoid overexposure alters the developmental program of fetal reproductive organs and results in numerous changes that can lead to various disorders later in life. Moderate fructose consumption during childhood and adolescence may impair the development and function of reproductive organs. The aim [...] Read more.
Prenatal glucocorticoid overexposure alters the developmental program of fetal reproductive organs and results in numerous changes that can lead to various disorders later in life. Moderate fructose consumption during childhood and adolescence may impair the development and function of reproductive organs. The aim of this study was to investigate the effects of prenatal dexamethasone (Dx) exposure in combination with postnatal fructose overconsumption on testicular development and function in fetal and adult male rat offspring. Pregnant female rats were treated with a subcutaneous injection of Dx at a dose of 0.5 mg/kg/day on gestation days 16, 17, and 18, and the effects on fetal growth and testicular development were analyzed. Spontaneously born male offspring were fed 10% fructose in drinking water until the age of 3 months. Prenatal exposure to Dx led to a reduction in fetal weight and testicular volume. However, testicular development normalized by adulthood, with testosterone levels decreasing. After moderate fructose consumption, impaired redox homeostasis and structural changes in the testicles and decreased testosterone levels were observed, indicating reduced testicular function. The results suggest that the synergistic effect of prenatal Dx exposure and moderate postnatal fructose consumption leads to more deleterious changes in testicular tissue. Full article
(This article belongs to the Special Issue Latest Advances in Reproduction Biology)
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<p>Representative micrographs of hematoxylin–eosin-stained sections of fetal testicles on day 21 of gestation in control (C) and Dx-exposed (Dx) fetuses. Testicular histology was not altered after fetal Dx exposure (<b>A</b>), but the testicular volume was significantly reduced (<b>B</b>). SNT—seminiferous tubules; I—interstitium; SC—Sertoli cells; GC—gonocytes. Scale bar (<b>A</b>) 50 µm and (<b>B</b>) 400 µm.</p>
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<p>Stereological parameters: (<b>A</b>) volume of fetal testicles; (<b>B</b>) volume density (%) of seminiferous tubules (SNT) and the interstitium (I) in fetal testicles in control (C) and Dx-exposed (Dx) fetuses. Results are presented as the mean ± SD (n = 6), **** <span class="html-italic">p</span> &lt; 0.0001.</p>
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<p>Representative micrographs of hematoxylin–eosin-stained testicular sections from adult 3-month-old offspring of C, Dx, F, and DxF groups. Testicular histology was not altered after prenatal exposure to Dx. Postnatal fructose overconsumption decreased the size of the seminiferous tubules only in offspring prenatally exposed to Dx (DxF). Scale bar 100 µm.</p>
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<p>(<b>A</b>) Volume density (%); (<b>B</b>) cross-section area of SNT (µm<sup>2</sup>); (<b>C</b>) diameter of SNT (µm); (<b>D</b>) height of the germinative epithelium (µm) in adult testicles of C, Dx, F, and DxF groups. SNT–seminiferous tubules. Results are presented as the mean ± SD (n = 6), **** <span class="html-italic">p</span> &lt; 0.0001, *** <span class="html-italic">p</span> &lt; 0.001.</p>
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<p>Serum concentrations of (<b>A</b>) FSH, (<b>B</b>) LH, and (<b>C</b>) testosterone in C, Dx, F, and DxF groups. Results are provided as the mean ± SD (n = 6), *** <span class="html-italic">p</span> &lt; 0.001.</p>
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<p>Discriminant function analysis (DA) for oxidative stress parameters in the testicles of groups C, Dx, F, and DxF. The groups were formed by root 1 (x-axis) and root 2 (y-axis). Statistical significance (the Wilks’ lambda distribution) was observed between groups.</p>
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<p>Experimental timeline.</p>
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<p>Morphometric parameters: diameter of a seminiferous tubules (SNT), height of the germinative epithelium (HE), and cross-section area (CSA); objective magnification 20×.</p>
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16 pages, 1494 KiB  
Article
Prenatal Maternal Psychological Stress (PMPS) and Its Effect on the Maternal and Neonatal Outcome: A Retrospective Cohort Study
by Joana Kathleen Aldinger, Harald Abele and Angela Kranz
Healthcare 2024, 12(23), 2431; https://doi.org/10.3390/healthcare12232431 - 3 Dec 2024
Viewed by 1051
Abstract
Background/Objectives: Prenatal psychology studies show that stress, depression, and psychological stress during pregnancy can have a significant impact on maternal and fetal health and are highly prevalent. The aim of the study was to compare maternal and neonatal short-term outcomes in pregnant women* [...] Read more.
Background/Objectives: Prenatal psychology studies show that stress, depression, and psychological stress during pregnancy can have a significant impact on maternal and fetal health and are highly prevalent. The aim of the study was to compare maternal and neonatal short-term outcomes in pregnant women* (the asterisk (*) is used at the appropriate places in this text to indicate that all genders are included) with a history of prenatal maternal psychological stress (PMPS) with those of pregnant women* not exposed to PMPS to determine differences and identify risk factors. Methods: Statistical tests for differences and relative risks between the groups were carried out with the perinatal data of University Hospital Tübingen from 2022 using IBM SPSS. Results: The study shows that PMPS has significant negative effects on various parameters, including the rate of premature births, preeclampsia, induction of birth, birth duration, and fetal asphyxia, as well as the birth weight of the children and their Apgar values (an assessment of newborn health scored shortly after birth). In addition, the risk of PMPS increases in women* with stillbirths and two or more previous miscarriages. However, the practical relevance must be critically scrutinized and confirmed by bigger studies. Conclusions: PMPS has a significant impact on the maternal and neonatal birth outcomes and must be identified as a risk factor in pregnancy. There is still a need for further research with larger samples, more balanced groups, and multivariate regression models to generate detailed, more transferable results and a deeper insight into the significant effects of PMPS and the role midwives can play in helping it. Full article
(This article belongs to the Special Issue Midwifery-Led Care and Practice: Promoting Maternal and Child Health)
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<p>Risk catalogue A of the maternity record (Mutterpass) [<a href="#B3-healthcare-12-02431" class="html-bibr">3</a>].</p>
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<p>Risk catalogue B of the maternity record (Mutterpass) [<a href="#B3-healthcare-12-02431" class="html-bibr">3</a>].</p>
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<p>Distribution of maternal age (IBM SPSS).</p>
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