Spermatogenesis starts with the onset of puberty within the seminiferous epithelium of the testes. It is a complex process under intricate control of the endocrine system. Physiological regulations by steroid hormones in general and by estrogens in particular are due to their chemical nature prone to be disrupted by exogenous factors acting as endocrine disruptors (EDs). 17α-Ethynylestradiol (EE2) is an environmental pollutant with a confirmed ED activity and a well-known effect on spermatogenesis and chromatin remodeling in haploid germ cells. The aim of our study was to assess possible effects of two doses (2.5ng/ml; 2.5 μg/ml) of EE2 on both histone-to-protamine exchange and epigenetic profiles during spermatogenesis performing a multi/transgenerational study in mice. Our results demonstrated an impaired histone-to-protamine exchange with a significantly higher histone retention in sperm nuclei of exposed animals, when this process was accompanied by the changes of histone post-translational modifications (PTMs) abundancies with a prominent effect on H3K9Ac and partial changes in protamine 1 promoter methylation status. Furthermore, individual changes in molecular phenotypes were partially transmitted to subsequent generations, when no direct trans-generational effect was observed. Finally, the uncovered specific localization of the histone retention in sperm nuclei and their specific PTMs profile after EE2 exposure may indicate an estrogenic effect on sperm motility and early embryonic development via epigenetic mechanisms.
- MeSH
- Endocrine Disruptors pharmacology toxicity MeSH
- Epigenesis, Genetic * drug effects MeSH
- Ethinyl Estradiol * pharmacology MeSH
- Histones * metabolism MeSH
- Mice MeSH
- Protein Processing, Post-Translational drug effects MeSH
- Protamines * metabolism genetics MeSH
- Spermatogenesis * drug effects genetics MeSH
- Spermatozoa drug effects metabolism MeSH
- Testis * drug effects metabolism MeSH
- Animals MeSH
- Check Tag
- Male MeSH
- Mice MeSH
- Female MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
Tento přehledový článek představuje koncepční rámce a preventivní intervence určené pro rodiny, ve kterých je rodič léčen s duševním onemocněním. Uvádí pojmy FAPMI (Families where a Parent has a Mental Illness – rodiny, v nichž má rodič duševní onemocnění) a COPMI (Children of Parents with a Mental Illness – děti rodičů s duševním onemocněním). Na osoby s duševní poruchou může rodičovství klást zvýšené nároky. Potomci pak čelí nejen vlivu duševních obtíží rodiče na běžné každodenní soužití a fungování rodiny, ale jsou vystaveni také riziku transgeneračního přenosu psychopatologie a vzniku duševního onemocnění u nich samotných. Preventivní intervence by měly vést ke snižování rizika vzniku, rozvoje a prohlubování psychopatologie u FAPMI a COPMI. Přestože některé studie dokládají jejich účinnost při cílení na FAPMI a COPMI, stále se jedná o oblast vyžadující další výzkum, který by prokázal efektivitu jednotlivých intervencí a vytvořil tak pro tyto rizikové skupiny platformu účinných protokolů založených na důkazech. Úspěšnost implementace preventivních intervencí pro FAPMI a COPMI do klinické praxe ale závisí také na systémové podpoře, legislativní i finanční, v rámci zdravotně sociální péče. Cílem článku je informovat o faktorech působících na FAPMI a COPMI v kontextu duševních poruch a o principech spolupráce a specifikách komunikace s FAPMI a COPMI. Dále představit dostupné teoretické a koncepční rámce problematiky FAPMI a COPMI, které se zabývají předcházením negativních dopadů duševního onemocnění, a prezentovat preventivní intervence, které z těchto rámců vycházejí. Jedná se o intervence založené na nejnovějších poznatcích výzkumu zaměřeného na zvýšení podpory dětí, rodičů a rodin. Vybrané intervence byly vytvořené a publikované ve studiích zejména v posledních 20 letech a poté různě implementované v rozličných zemích světa. Jen u některých z nich již efektivita byla také evaluována.
This review article presents conceptual frameworks and preventive interventions designed for families in which a parent is being treated for mental illness. It introduces the concepts of FAPMI (Families where a Parent has a Mental Illness), and COPMI (Children of Parents with a Mental Illness). Parenting increases demands on parents with mental illness. The offspring in such families must deal not only with the impact of the parent’s mental health difficulties and the functioning of the family but also face the risk of transgenerational transmission of psychopathology and the onset of mental illness in themselves. Preventive interventions should lead to a reduction in the occurrence, development, and severity of psychopathology in FAPMI and COPMI. Although some studies have shown the effectiveness of prevention interventions targeting FAPMI and COPMI, this is an area that requires further research to evaluate the effectiveness of interventions and an establishment of an Evidence-Based Platform of protocols for these groups. However, successful implementation of these preventive interventions in clinical practice depends also on legislative and financial support within the healthcare and social care system. The aim of the article is to report on the factors influencing FAPMI and COPMI in the context of mental disorders and to describe the principles of cooperation and the specifics of communication with FAPMI and COPMI. Furthermore, the article introduces the available theoretical and conceptual frameworks of work with FAPMI and COPMI and presents preventive interventions based on these frameworks. These interventions are based on the latest research findings aimed to improve support for children, their parents, and their families. The selected interventions in this study have been developed mainly in the last 20 years and implemented in different ways in different countries around the world, some have already been evaluated for effectiveness.
Confluence of environmental, genetic, and lifestyle variables is responsible for deterioration of human fecundity. Endocrine disruptors or endocrine disrupting chemicals (EDCs) may be found in a variety of foods, water, air, beverages, and tobacco smoke. It has been demonstrated in experimental investigations that a wide range of endocrine disrupting chemicals have negative effects on human reproductive function. However, evidence on the reproductive consequences of human exposure to endocrine disrupting chemicals is sparse and/or conflicting in the scientific literature. The combined toxicological assessment is a practical method for assessing the hazards of cocktails of chemicals, co-existing in the environment. The current review provides a comprehensive overview of studies emphasizing the combined toxicity of endocrine disrupting chemicals on human reproduction. Endocrine disrupting chemicals interact with each other to disrupt the different endocrine axes, resulting in severe gonadal dysfunctions. Transgenerational epigenetic effects have also been induced in germ cells, mostly through DNA methylation and epimutations. Similarly, after acute or chronic exposure to endocrine disrupting chemicals combinations, increased oxidative stress (OS), elevated antioxidant enzymatic activity, disrupted reproductive cycle, and reduced steroidogenesis are often reported consequences. The article also discusses the concentration addition (CA) and independent action (IA) prediction models, which reveal the importance of various synergistic actions of endocrine disrupting chemicals mixtures. More crucially, this evidence-based study addresses the research limitations and information gaps, as well as particularly presents the future research views on combined endocrine disrupting chemicals toxicity on human reproduction.
- Publication type
- Journal Article MeSH
- Review MeSH
BACKGROUND: Children of parents with a mental illness are at high risk of developing a mental disorder as a result of transgenerational transmission. Without effective intervention, they could form the next generation of psychiatric patients. ChildTalks+ is a preventive intervention involving four structured psychoeducational sessions designed for parents affected by a mental disorder and their children. Its aim is to reduce the risk of mental disorders in children of parents with mental illness. This study draws on our clinical practice and involves a group of patients with eating disorders. The aim of the project, which will run in the Czech Republic, is to evaluate the effectiveness of ChildTalks+ methodology. METHODS: ChildTalks+ therapists (professionals from health, social, and educational facilities) will recruit 66 families where a parent is treated for a mental disorder and the family includes children aged 6-18. Paired allocation into an intervention group (N = 33) and a control group (N = 33) will be based on the number of risk factors identified in the family. Both groups will complete questionnaires at the baseline, post-test, and follow-up assessments after six and 12 months. The intervention group will receive the ChildTalks+ intervention within 2 months of the baseline assessment; the control group after the last assessment. Questionnaires will be completed by parents and children aged 12+ and, in two cases, 15+ years. Quantitative data will be supplemented with qualitative data from ChildTalks+ therapists working with patients with eating disorders. DISCUSSION: The ChildTalks+ intervention is expected to strengthen parenting competencies and family protective factors, improve family communication, increase awareness of parental mental health issues, and improve the wellbeing of children of parents with mental illness with long-term sustainable outcomes. The study should contribute to the evidence base for the ChildTalks+ program and help identify key themes in the implementation of similar preventive interventions. TRIAL REGISTRATION: ClinicalTrials.gov Identifier: NCT05554458. Registered 26 September 2022. Retrospectively registered.
- MeSH
- Child MeSH
- Controlled Clinical Trials as Topic MeSH
- Humans MeSH
- Feeding and Eating Disorders * prevention & control MeSH
- Surveys and Questionnaires MeSH
- Parents * psychology MeSH
- Parenting psychology MeSH
- Research Design MeSH
- Check Tag
- Child MeSH
- Humans MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Clinical Trial Protocol MeSH
Sledování lidských rodů je složitou součástí psychologického zkoumání. Projekt Vyhnání, vykořenění a změna životní linie – mezigenerační studie se zabývá psychologickými dopady aktu zvůle komunistické tajné policie v Československu, tzv. akce Asanace. Projekt navazuje na kumulující se zkušenost s transgeneračním traumatem. Zaměřuje se na generaci přímých účastníků, disidentů, kteří byli nuceni opustit svoji zem v letech 1977–1984, dále na potomky – druhou a třetí generaci, kteří v některých případech žijí v zahraničí. Pomocí čtyř druhů metod (fokusové skupiny, hloubkové rozhovory, dotazníkové metody, modifikovaný Stroopův test) se snaží porozumět transgenerační transmisi traumatu, zkoumá vedle traumatické situace také resilienci a posttraumatický růst. Zajímáme se o to, jak se traumatická situace transformuje v průběhu let, co přináší do pokračující rodové linie. Vedle standardních výzkumných článků plánují autoři také shrnující monografii na toto téma.
Tracking the family lineage is a complicated part of psychological research. The project titled Expulsion, uprooting, and change of lifeline-intergenerational study investigates the psychological impact of the communist secret police terror in Czechoslovakia (so-called Action “Asanace”), following the cumulation of research and therapeutic experience with transgenerational trauma. It focuses on the generation of the primary victims, dissidents forced to leave their homeland between 1977–84, as well as the 2nd and 3rd generation of their offspring, some of whom live abroad. It aims to understand the transition of trauma, resilience, and posttraumatic growth using several methods (focus groups, in-depth interviews, surveys, Modified Stroop Test). We shall examine transformations of the traumatic situation in time and its aftermath in the family lineage. Besides standard research papers, the authors plan a monograph.
Male reproductive functions are an important area affecting men ́s overall health and well-being. However, during the last years, there has been observed increasing incidence of male reproductive issues. The radical growth has been recorded parallelly with a massive expanse of industrialization and agricultural chemigation. Many groups of experts have begun to identify several potential factors and substances that may have adverse effects on men ́s reproductive health. Since then, xenobiotics have become a major concern of many scientific studies. There is evidence that most of them have multigenerational and transgenerational effects on reproductive health, which is a serious problem for our population. Bisphenol A could be considered as one of the most studied endocrine disruptors. Until now, several negative effects of bisphenol A were associated with reduced weight testes, histological alterations, impairment spermatogenesis, and steroidogenesis as well as with testes or prostate cancer. Due to convincing evidence, bisphenol A has been started to replace by its analogues such as bisphenol B, S, F, in order to eliminate and suppress the risk of exposure to bisphenol A. However, it seems that a lack of toxicological analyses allows using of these hazardous substances in daily life. Their harmful effect was confirmed by the animal in vitro and in vivo models, while the epidemiological studies monitoring the impact of bisphenol analogues on men's reproductive health are markedly limited. This review provides information about the effects of bisphenol on reproductive health in men. At the same time, it is focused on physiological aspects of sperm viability, steroid hormone secretion, sperm motility, or testes histology in relation to bisphenols exposure.
Metabolic syndrome is a prevalent disease resulting from an interplay of genomic component and the exposome. Parental diet has been shown to affect offspring metabolic health via multiple epigenetic mechanisms. Excess carbohydrate intake is one of the driving forces of the obesity and metabolic syndrome pandemics. This review summarizes the evidence for the effects of maternal carbohydrate (fructose, sucrose, glucose) overnutrition on the modulation of metabolic syndrome components in the offspring. Despite substantial discrepancies in experimental design, common effects of maternal carbohydrate overnutrition include increased body weight and hepatic lipid content of the "programmed" offspring. However, the administration of sucrose to several rat models leads to apparently favorable metabolic outcomes. Moreover, there is evidence for the role of genomic background in modulating the metabolic programming effect in the form of nutri-epigenomic interaction. Comprehensive, robust studies are needed to resolve the temporal, sex-specific, genetic, epigenetic and nutritional aspects of parental overnutrition in the intergenerational and transgenerational pathogenesis of metabolic syndrome.
- MeSH
- Fructose MeSH
- Rats MeSH
- Humans MeSH
- Metabolic Syndrome * genetics MeSH
- Overnutrition * complications metabolism MeSH
- Parents MeSH
- Prenatal Exposure Delayed Effects * metabolism MeSH
- Animals MeSH
- Check Tag
- Rats MeSH
- Humans MeSH
- Male MeSH
- Female MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
- Review MeSH
Gestational diabetes mellitus (GDM), one of the major pregnancy-related complications, characterized as a transitory form of diabetes induced by insulin resistance accompanied by a low/absent pancreatic beta-cell compensatory adaptation to the increased insulin demand, causes the acute, long-term, and transgenerational health complications. The aim of the study was to assess if alterations in gene expression of microRNAs associated with diabetes/cardiovascular/cerebrovascular diseases are present in whole peripheral blood of children aged 3-11 years descending from GDM complicated pregnancies. A substantially altered microRNA expression profile was found in children descending from GDM complicated pregnancies. Almost all microRNAs with the exception of miR-92a-3p, miR-155-5p, and miR-210-3p were upregulated. The microRNA expression profile also differed between children after normal and GDM complicated pregnancies in relation to the presence of overweight/obesity, prehypertension/hypertension, and/or valve problems and heart defects. Always, screening based on the combination of microRNAs was superior over using individual microRNAs, since at 10.0% false positive rate it was able to identify a large proportion of children with an aberrant microRNA expression profile (88.14% regardless of clinical findings, 75.41% with normal clinical findings, and 96.49% with abnormal clinical findings). In addition, the higher incidence of valve problems and heart defects was found in children with a prior exposure to GDM. The extensive file of predicted targets of all microRNAs aberrantly expressed in children descending from GDM complicated pregnancies indicates that a large group of these genes is involved in ontologies of diabetes/cardiovascular/cerebrovascular diseases. In general, children with a prior exposure to GDM are at higher risk of later development of diabetes mellitus and cardiovascular/cerebrovascular diseases, and would benefit from dispensarisation as well as implementation of primary prevention strategies.
- MeSH
- Cerebrovascular Disorders etiology MeSH
- Child MeSH
- Diabetes, Gestational epidemiology MeSH
- Cardiovascular Diseases etiology MeSH
- Diabetes Complications complications MeSH
- Pregnancy Complications etiology MeSH
- Humans MeSH
- MicroRNAs genetics MeSH
- Child, Preschool MeSH
- Prospective Studies MeSH
- Pregnancy MeSH
- Check Tag
- Child MeSH
- Humans MeSH
- Male MeSH
- Child, Preschool MeSH
- Pregnancy MeSH
- Female MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
Obsedantně kompulsivní porucha (F42.1) bývá považována za terapeuticky těžko ovlivnitelnou diagnózu, jejíž léčba se neobejde bez dlouhodobé psychofarmakoterapie (WHO, 2017). Na našich pracovištích se s ní setkáváme především u dětí a rodinnou terapii pokládáme za metodu volby. Obtížné chování a myšlení dítěte vždy ovlivňuje celou rodinu. Z našeho hlediska jde o typický příznak, který vzniká i zaniká v závislosti na kvalitě a proměnách rodinných vztahů. Na zlomcích jedné kazuistiky ukážeme, jak lze tuto diagnózu úspěšně ovlivňovat v modu narativní rodinné terapie s externalizací za předpokladu dobré spolupráce s oběma rodiči, případně dalšími klíčovými postavami v rodině. Často je nezbytné pracovat paralelně s více rodinnými subsystémy: v dětském, dospělém, v subsystémech rodičovském a partnerském, případně transgeneračně. Zabývat se budeme významem symptomu v rodině, a jak právě proměna významů, které jednotliví členové rodiny poruše přisuzují, vede k nevratné změně druhého logického řádu tak, že symptom ztrácí svou náhradní regulační funkci v nevědomí rodiny.
Obsessive compulsive disorder (F 42.1) is considered rather challenging disease for treatment. A long-term pharmacotherapy is usually necessary (WHO, 2017). We work primarily with children at our clinic and we see family therapy as a therapeutic method of choice. The child´s troublesome behaviour and a way of thinking always affect the entire family. In our view, these could be the symptoms, which typically emerge and disappear depending on the quality and changes of family relationships. Through extracts of a case study, we will demonstrate how symptoms of the above mentioned disorder could be effectively relieved during narrative-informed family therapy including externalisation. A good therapeutic alliance with parents or other significant family members is a prerequisite for such therapeutic approach. Frequently we must work in parallel within various family subsystems such as the children´s and the adults´, the parents’ and the partners’. Sometimes we must even work in transgenerational modality. In the paper, we focus on the meanings of the symptom in the family. It is the transformation of meanings, which are ascribed to the disorder by each family member, that can result in irreversible second order change. In this process, the symptom loses its regulatory function in the unconscious of the family.
Despite essential progress towards understanding the evolution of cooperative behaviour, we still lack detailed knowledge about its underlying molecular mechanisms, genetic basis, evolutionary dynamics and ontogeny. An international workshop "Genetics and Development of Cooperation," organized by the University of Bern (Switzerland), aimed at discussing the current progress in this research field and suggesting avenues for future research. This review uses the major themes of the meeting as a springboard to synthesize the concepts of genetic and nongenetic inheritance of cooperation, and to review a quantitative genetic framework that allows for the inclusion of indirect genetic effects. Furthermore, we argue that including nongenetic inheritance, such as transgenerational epigenetic effects, parental effects, ecological and cultural inheritance, provides a more nuanced view of the evolution of cooperation. We summarize those genes and molecular pathways in a range of species that seem promising candidates for mechanisms underlying cooperative behaviours. Concerning the neurobiological substrate of cooperation, we suggest three cognitive skills necessary for the ability to cooperate: (i) event memory, (ii) synchrony with others and (iii) responsiveness to others. Taking a closer look at the developmental trajectories that lead to the expression of cooperative behaviours, we discuss the dichotomy between early morphological specialization in social insects and more flexible behavioural specialization in cooperatively breeding vertebrates. Finally, we provide recommendations for which biological systems and species may be particularly suitable, which specific traits and parameters should be measured, what type of approaches should be followed, and which methods should be employed in studies of cooperation to better understand how cooperation evolves and manifests in nature.
- MeSH
- Altruism MeSH
- Biological Evolution * MeSH
- Behavior, Animal MeSH
- Epigenesis, Genetic MeSH
- Phenotype MeSH
- Genetic Fitness MeSH
- Congresses as Topic MeSH
- Cooperative Behavior * MeSH
- Neurosecretory Systems physiology MeSH
- Memory MeSH
- Developmental Biology MeSH
- Animals MeSH
- Check Tag
- Animals MeSH
- Publication type
- Journal Article MeSH
- Review MeSH
- Geographicals
- Switzerland MeSH