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Medical abortion has rapidly become the dominant abortion method in western countries. Pain is a known adverse effect; however, few studies have explored women's subjective experience of medical abortion pain. To explore Norwegian women's experiences of pain when performing a medical abortion at home. We recruited 24 women through an advertisement on Facebook and conducted semi-structured, face-to-face interviews. The interviews were transcribed verbatim and the data were analyzed using a phenomenological hermeneutical method. Our findings consisted of two main themes: 1) Being in pain or becoming pain, and 2) Being caught off guard and struggling to cope. Participants described undergoing severe pain, comparable to giving birth, during the medical abortion. Unprepared for the type and intensity of the pain, they felt anxious and insecure. Pain is physical, but it also has important psychological, social, and existential dimensions. Our culture (in)forms our thoughts and feelings about our pain, affecting our ability to endure suffering. The participants' experiences of abortion pain prompt timely questions concerning gendered socio-cultural and existential meanings connected to pain, specifically in relation to female reproductive functions. Women need realistic information about the type and intensity of abortion pain, as well as evidence-based pain medication. Psychological factors may affect the experience of abortion pain and should therefore be taken into account in abortion care.

Introduction Meeting daily energy demands is essential for maintaining health and reproductive function in women. When energy intake fails to meet energy expenditure, the reproductive system is among the first to be affected, often leading to subtle or overt disruptions in hormone production. While energy deficiency is known to impair reproductive function, less is known about whether subclinical energy deficits influence the degree of estrogen variability in regularly menstruating women. This study aims to evaluate the relationship between energetic status (ES; caloric intake relative to daily energy need) and estrogen (E) variability in recreationally active women using mixed-effects location scale modeling.Methods Healthy, recreationally active, women (EUM: n = 10; IUD: n = 6; OC: n = 8) (Mean ± SD; Age: 24 ± 4 yrs; FFM: 46.24 ± 5.17 kg) completed 22 ± 3 days of at-home urine hormone testing each morning to measure urinary E levels (ng/mL). Resting metabolic rate (RMR) via indirect calorimetry was measured in the low (LHP; 1–7 days post menstruation/placebo) and high hormone phase (HHP; 5–9 days post ovulation/active pill). Dietary intake (kcal) was averaged from a 3-day food log preceding the study visit. ES was calculated as the ratio of reported caloric intake to estimated daily energy needs (RMR adjusted with a moderate-exercise activity factor of 1.55), with values >1.0 indicating energy needs were met. Associations between ES and E were evaluated in the LHP and HHP using mixed-effect location scale modeling. E levels were modeled to estimate within-person means and variability within approximately ±7 days of the study visit.Results Daily energy needs were not met by 79% (LHP) and 75% (HHP) of participants. Significant between-person variability in E was observed (p < 0.05). However, ES was not significantly associated with mean E levels (LHP: Estimate = −0.006, p = 0.908; HHP: Estimate = −0.057, p = 0.366) or within-person variability of E (LHP: Estimate = −0.005, p = 0.930; HHP: Estimate = 0.019, p = 0.769) in either hormone phase.Conclusion While significant inter-individual variability in E levels was observed, ES was not significantly associated with intra-individual E variability during the LHP or HHP. Although energy balance is important for reproductive health, short-term estimates of caloric intake relative to predicted needs were not significantly associated with E variability. This may reflect the limited sensitivity of these measures or insufficient duration of energy deficit to affect hormonal regulation. Future research should incorporate more precise and direct measures of energy availability, such as exercise energy expenditure, and examine how long-term or cumulative energy imbalance might influence hormonal variability.

In the light of current data concerning the growing exposure to ionizing radiation (IR) originating from atrificial sources, especially from medical ones, and also related to occupational exposure, it is justifiable to systematize the state of knowledge concerning the effect of IR on the male reproductive system. There is no basis for the application of the hypothesis of hormesis in the area of male reproductive health. Regarding the impact of IR on spermatogenesis, spermatogonia are less susceptible to the occurrence of DNA damage after exposition to IR, but are characterized by slower DNA repair compared to somatic cells. Damage to the genes after exposure to IR is possible at each stage of spermatogenesis; however, haploidal spermatids show the highest radiosensitivity in this respect. The genetic risk of the cells differentiating during spermatogenesis is limited to one cycle of spermatogenesis, whereas the genetic instability may persist for the whole period of life, and DNA damage induced by IR may be transmitted to future generations. The minimum dose causing detectable DNA damage was 30 Gy. While exceeding this dose, the number of single-strand DNA breaks increases. Among males exposed to IR, a decrease was observed in sperm motility and in the percentage of morphologically normal spermatozoa as well as in an intensification of vacuolization. The genetic material in the sperm of these males showed higher fragmentation and methylation of genomic DNA. In the context of the epidemiological situation concerning the prevalence of infertility, while assessing the health effects of exposure to IR from artificial, including medical sources, the reproductive risk should be considered.

Ambient temperatures are predicted to rise in the future owing to several reasons associated with global climate changes. These temperature increases can result in heat stress- a severe threat to crop production in most countries. Legumes are wellknown for their impact on agricultural sustainability as well as their nutritional and health benefits. Heat stress imposes challenges for legume crops and has deleterious effects on the morphology, physiology, and reproductive growth of plants. High-temperature stress at the time of the reproductive stage is becoming a severe limitation for production of grain legumes as their cultivation expands to warmer environments and temperature variability increases due to climate change. The reproductive period is vital in the life cycle of all plants and is susceptible to high-temperature stress as various metabolic processes are adversely impacted during this phase, which reduces crop yield. Food legumes exposed to high-temperature stress during reproduction show flower abortion, pollen and ovule infertility, impaired fertilization, and reduced seed filling, leading to smaller seeds and poor yields. Through various breeding techniques, heat tolerance in major legumes can be enhanced to improve performance in the field. Omics approaches unravel different mechanisms underlying thermotolerance, which is imperative to understand the processes of molecular responses toward high-temperature stress.

Assisted reproductive techniques (ART) and parental nutritional status have profound effects on embryonic/fetal and placental development, which are probably mediated via “programming” of gene expression, as reflected by changes in their epigenetic landscape. Such epigenetic changes may underlie programming of growth, development, and function of fetal organs later in pregnancy and the offspring postnatally, and potentially lead to long-term changes in organ structure and function in the offspring as adults. This latter concept has been termed developmental origins of health and disease (DOHaD), or simply developmental programming, which has emerged as a major health issue in animals and humans because it is associated with an increased risk of non-communicable diseases in the offspring, including metabolic, behavioral, and reproductive dysfunction. In this review, we will briefly introduce the concept of developmental programming and its relationship to epigenetics. We will then discuss evidence that ART and periconceptual maternal and paternal nutrition may lead to epigenetic alterations very early in pregnancy, and how each pregnancy experiences developmental programming based on signals received by and from the dam. Lastly, we will discuss current research on strategies designed to overcome or minimize the negative consequences or, conversely, to maximize the positive aspects of developmental programming.

Lifestyle factors such as sedentary behavior and consumption of certain medications can disturb the function of the male reproductive system. In the present study, we investigated the potential co-treatment effects of low-volume high-intensity interval training (HIIT) on markers of reproductive function in adult male Wistar rats under aspirin (ASA) treatment. Eighteen adult male Wistar rats were randomized into three groups: control (C), aspirin treatment (AT), and aspirin treatment + exercise (ATE). Animals in the AT and ATE groups received an oral subchronic dose of aspirin (12.5 mg/kg body mass). The exercise was performed three times per week for 6 weeks (4–6 reps of 10-s sprints). Serum testosterone level, sperm parameters (sperm count, viability, maturity, and DNA fragmentation), histomorphometric (Leydig cell, tubule diameter, thickness of tubular epithelium, and indices of spermatogenesis and spermiogenesis), and histochemical parameter (testicular fat density) were assessed. Results revealed that compared to the C group, ASA consumption led to a negative alteration in serum testosterone levels, sperm parameters, and histomorphometric and histochemical parameters ( P  < 0.05). However, there were no significant differences between the C and ATE groups in terms of serum testosterone level, number of Leydig cells, epididymal fat density, tubule diameter, epithelium height, immature-to-mature sperm ratio, and DNA breakage ( P  > 0.05). These findings suggest that ASA treatment is associated with deleterious changes in male reproductive parameters. However, low-volume HIIT may prevent ASA-induced male reproductive impairments and could be considered a potential prophylactic measure in subjects under ASA treatment.

Abstract Context Androgen abuse impairs male reproductive and cardiac function, but the rate, extent, and determinants of recovery are not understood. Objective To investigate recovery of male reproductive and cardiac function after ceasing androgen intake in current and past androgen abusers compared with healthy non-users. Methods Cross-sectional, observational study recruited via social media 41 current and 31 past users (≥3 months since last use, median 300 days since last use) with 21 healthy, eugonadal non-users. Each provided a history, examination, and serum and semen sample and underwent testicular ultrasound, body composition analysis, and cardiac function evaluation. Results Current abusers had suppressed reproductive function and impaired cardiac systolic function and lipoprotein parameters compared with non- or past users. Past users did not differ from non-users, suggesting full recovery of suppressed reproductive and cardiac functions after ceasing androgen abuse, other than residual reduced testicular volume. Mean time to recovery was faster for reproductive hormones (anti-Mullerian hormone [AMH], 7.3 months; luteinizing hormone [LH], 10.7 months) than for sperm variables (output, 14.1 months) whereas spermatogenesis (serum follicle-stimulating hormone [FSH], inhibin B, inhibin) took longer. The duration of androgen abuse was the only other variable associated with slower recovery of sperm output (but not hormones). Conclusion Suppressed testicular and cardiac function due to androgen abuse is effectively fully reversible (apart from testis volume and serum sex hormone binding globulin) with recovery taking between 6 to 18 months after ceasing androgen intake with possible cumulative effects on spermatogenesis. Suppressed serum AMH, LH, and FSH represent convenient, useful, and underutilized markers of recovery from androgen abuse.

Iron is an important metal element involved in the regulation of male reproductive functions and has dual effects on testicular tissue. A moderate iron content is necessary to maintain testosterone synthesis and spermatogenesis. Iron overload can lead to male reproductive dysfunction by triggering testicular oxidative stress, lipid peroxidation, and even testicular ferroptosis. Ferroptosis is an iron-dependent form of cell death that is characterized by iron overload, lipid peroxidation, mitochondrial damage, and glutathione peroxidase depletion. This review summarizes the regulatory mechanism of ferroptosis and the research progress on testicular ferroptosis caused by endogenous and exogenous toxicants. The purpose of the present review is to provide a theoretical basis for the relationship between ferroptosis and male reproductive function. Some toxic substances or danger signals can cause male reproductive dysfunction by inducing testicular ferroptosis. It is crucial to deeply explore the testicular ferroptosis mechanism, which will help further elucidate the molecular mechanism of male reproductive dysfunction. It is worth noting that ferroptosis does not exist alone but rather coexists with other forms of cell death (such as apoptosis, necrosis, and autophagic death). Alleviating ferroptosis alone may not completely reverse male reproductive dysfunction caused by various risk factors.

Recent studies have indicated that epigenetic alterations are critical for normal function and development of spermatozoa during the fertilization process. This review will focus on the latest advances in epigenome profiling of the chromatin modifications during sperm development, as well as the potential roles of epigenetic mechanisms in the context of male infertility. In this review, all data were collected from published studies that considered the effect of epigenetic abnormalities on human spermatogenesis, sperm parameters quality, fertilization process, embryo development and live births. The database PubMed was searched for all experimental and clinical studies using the Keywords \"epigenetic modifications\", \"male infertility\", \"spermatogenesis\", \"embryo development\" and \"reproductive function\". Post-translational modifications of histone, DNA methylations and chromatin remodeling are among the most common forms of epigenetic modifications that regulate all stages of spermatogenesis and fertilization process. Incorrect epigenetic modifications of certain genes involved in the spermatogenesis and sperm maturation may be a main reason of male reproductive disorder and infertility. Most importantly, abnormal patterns of epigenetic modifications or transgenerational phenotypes and miRNAs expression may be transmitted from one generation to the next through assisted reproductive techniques (ART) and cause an increased risk of birth defects, infertility and congenital anomalies in children. Epigenetic modifications must be considered as a one of the main factors of unexplained male infertility etiology. Due to high risk of transmitting incorrect primary imprints to offspring, there is a need for more research into epigenetic alterations in couples who benefit of ART support.

Background/Objectives: Vortioxetine is a multimodal antidepressant that modulates serotonergic, noradrenergic, and dopaminergic systems, yet its effects on female reproductive physiology remain incompletely defined. This study investigated how short- and long-term vortioxetine exposure influences reproductive function in female rats, integrating measurements of oxidative-stress biomarkers, catecholamines, and endocrine endpoints (prolactin and corticosterone). Methods: Forty-two female Wistar albino rats were randomized into seven groups (n = 6): healthy control; short-term vortioxetine; long-term vortioxetine; and the same two regimens each combined with metyrosine or metyrapone. Metyrosine and metyrapone (50 mg/kg, oral gavage) were given 1 h before vortioxetine (10 mg/kg). Treatments lasted one week (short-term) or four weeks (long-term). Serum MDA, tGSH, SOD, CAT, adrenaline, noradrenaline, dopamine, serotonin, prolactin, and corticosterone were measured. Fertility outcomes were assessed by co-housing females with males for one month. Results: Vortioxetine increased MDA, catecholamines, and serotonin and decreased antioxidant markers and prolactin versus controls (p < 0.001). Long-term vortioxetine produced a marked rise in corticosterone that coincided with infertility and delayed parturition. Metyrosine lowered oxidative stress and catecholamines but did not reverse infertility. In contrast, metyrapone blunted corticosterone elevation and preserved reproductive capacity. Conclusions: Long-term vortioxetine induced infertility in female rats, likely mediated by corticosterone elevation consistent with hypothalamic–pituitary–adrenal axis dysregulation. These findings suggest the need to monitor reproductive risk when considering vortioxetine in women of reproductive age and warrant further mechanistic and translational studies.