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Current societies are heavily reliant on employment as a cornerstone of prosperity, both in terms of individuals’ access to income and social security and to finance welfare states through tax revenues. At the same time, work is often linked to environmentally harmful activities and not necessarily oriented toward meeting human needs. Against this background, work emerges as a key lever for a social-ecological transformation, and public employment services (PES) as key actors in labor-market policy – an area that has largely ignored environmental objectives until now. This article contributes to the small but growing field of research on eco-social labor-market policies by developing a novel set of 15 measures for eco-social labor. These indicators are grouped into six key thematic clusters of action for PES: (1) information and consultancy; (2) eco-social retraining and qualification; (3) sustainable mobility; (4) working time distribution; (5) livelihood provisioning; and (6) ecological eligibility criteria for unemployment benefits. The proposed policy measures are PES-oriented and offer concrete options toward transformation. While the policy toolbox has been developed in the context of Austria, it can also be used as a framework for other countries.

Introduction: The developing epigenome changes rapidly, potentially making it more sensitive to toxicant exposures. DNA modifications, including methylation and hydroxymethylation, are important parts of the epigenome that may be affected by environmental exposures. However, most studies do not differentiate between these two DNA modifications, possibly masking significant effects.Methods: To investigate the relationship between DNA hydroxymethylation and developmental exposure to common contaminants, a collaborative, NIEHS-sponsored consortium, TaRGET II, initiated longitudinal mouse studies of developmental exposure to human-relevant levels of the phthalate plasticizer di(2-ethylhexyl) phthalate (DEHP), and the metal lead (Pb). Exposures to 25 mg DEHP/kg of food (approximately 5 mg DEHP/kg body weight) or 32 ppm Pb-acetate in drinking water were administered to nulliparous adult female mice. Exposure began 2 weeks before breeding and continued throughout pregnancy and lactation, until offspring were 21 days old. At 5 months, perinatally exposed offspring blood and cortex tissue were collected, for a total of 25 male mice and 17 female mice (n = 5–7 per tissue and exposure). DNA was extracted and hydroxymethylation was measured using hydroxymethylated DNA immunoprecipitation sequencing (hMeDIP-seq). Differential peak and pathway analysis was conducted comparing across exposure groups, tissue types, and animal sex, using an FDR cutoff of 0.15.Results: DEHP-exposed females had two genomic regions with lower hydroxymethylation in blood and no differences in cortex hydroxymethylation. For DEHP-exposed males, ten regions in blood (six higher and four lower) and 246 regions (242 higher and four lower) and four pathways in cortex were identified. Pb-exposed females had no statistically significant differences in blood or cortex hydroxymethylation compared to controls. Pb-exposed males, however, had 385 regions (all higher) and six pathways altered in cortex, but no differential hydroxymethylation was identified in blood.Discussion: Overall, perinatal exposure to human-relevant levels of two common toxicants showed differences in adult DNA hydroxymethylation that was specific to sex, exposure type, and tissue, but male cortex was most susceptible to hydroxymethylation differences by exposure. Future assessments should focus on understanding if these findings indicate potential biomarkers of exposure or are related to functional long-term health effects.

Liechtenstein is still far away from a comprehensive decriminalisation of abortion. The termination of pregnancy is still regulated by the Criminal Code and the person who performs the abortion is convicted under criminal law. Only the pregnant person acts legally when terminating an unplanned or unwanted pregnancy. But it took until 2015 for pregnant persons to be granted a (limited) right to self-determination, and there is still a lack of sufficient legal, medical and social support. In a difficult and psychologically stressful situation, pregnant persons must seek treatment abroad – not because they want to, but because they have to.

This article examines the factors affecting Americans’ trust in their federal government and its health agencies during the COVID-19 public health crisis. More specifically, we examine the evolution of Americans’ trust in their government and health system and how, in the context of the COVID-19 pandemic response, it has been affected by multiple factors. Several academic journals, government policy recommendations and public health polls were evaluated to understand the public’s trust in the federal government and its health institutions. Public trust in institutions during a global pandemic is essential in influencing adherence to a pandemic response (both non-pharmaceutical and medical interventions). Americans’ trust in institutions is built and maintained by a variety of factors. We focus on: political polarization and involvement, media influence and health communications, history of systemic racism and socioeconomic inequalities, and pandemic fatigue. Based on the interplay of these factors, we conclude with recommendations for future pandemic response strategies.

Using a mouse model for Rett syndrome (RTT), Neier et al analyze gut microbiome and metabolome profiles during disease progression. They show that pathophysiology and progression of RTT is different in females than in males and suggest that changes in the microbiome and metabolism of the gastrointestinal tract influence disease progression.

PURPOSECancer is becoming increasingly prevalent among the group of treatable diseases in African countries. There is a shortage of clinicians and pathologists available for cancer diagnosis and treatment. These limited resources must be efficiently used to maximize the number of patients treated. One of the critical factors in treatment efficiency is the correct and timely diagnosis of specimens by pathologists. However, there is currently a significant shortage of cancer care clinicians in Africa and an even more considerable shortage of pathologists. This article presents an example in which telepathology was used to mitigate the lack of pathologists in Cameroon.METHODSThe telepathology workaround was implemented in a district hospital based in Cameroon's Adamawa region, where a European surgeon provides cancer treatment. A small histology laboratory there is run by one histotechnologist who processes surgical biopsies into histology slides. As there are no pathologists on site, these slides are digitally scanned using a mobile phone and a whole slide imaging (WSI) scanner. The slides are then shared electronically with a volunteering pathologist in Europe who provides a diagnostic report.RESULTSFrom 2018 to July 2019, specimens for 101 patients were photographed through an iPhone connected to a microscope eyepiece producing several individual images per specimen. From July 2019 to December 2020, slides from 282 patients were scanned using WSI and digitally transmitted.CONCLUSIONWSI on hematoxylin and eosin histology slides for remote diagnosis can increase cancer treatment efficacy and reduce overtreatment of tumors clinically suspicious for malignancy in under-resourced countries with a lack of pathologists.

Early developmental environment can influence long-term health through reprogramming of the epigenome. Human environmental epigenetics studies rely on surrogate tissues, such as blood, to assess the effects of environment on disease-relevant but inaccessible target tissues. However, the extent to which environment-induced epigenetic changes are conserved between these tissues is unclear. A better understanding of this conservation is imperative for effective design and interpretation of human environmental epigenetics studies. The Toxicant Exposures and Responses by Genomic and Epigenomic Regulators of Transcription (TaRGET II) consortium was established by the National Institute of Environmental Health Sciences to address the utility of surrogate tissues as proxies for toxicant-induced epigenetic changes in target tissues. We and others have recently reported that perinatal exposure to lead (Pb) is associated with adverse metabolic outcomes. Here, we investigated the sex-specific effects of perinatal exposure to a human environmentally relevant level of Pb on DNA methylation in paired liver and blood samples from adult mice using enhanced reduced-representation bisulphite sequencing. Although Pb exposure ceased at 3 weeks of age, we observed thousands of sex-specific differentially methylated cytosines in the blood and liver of Pb-exposed animals at 5 months of age, including 44 genomically imprinted loci. We observed significant tissue overlap in the genes mapping to differentially methylated cytosines. A small but significant subset of Pb-altered genes exhibit basal sex differences in gene expression in the mouse liver. Collectively, these data identify potential molecular targets for Pb-induced metabolic diseases, and inform the design of more robust human environmental epigenomics studies.

(Series Information) European Papers - A Journal on Law and Integration, 2021 6(2), 941-954 | European Forum Insight of 9 October 2021 | (Table of Contents) I. Introduction. - II. Case c-718/19. - II.1. Legal and factual background. - II.2. Judgment of the Grand Chamber. - III. Case C-719/19. - III.1. Factual background. - III.2. Judgment of the Grand Chamber. - IV. New clarifications on ending the Union citizen's right of residence. - V. Conclusion. | (Abstract) In two Grand Chamber decisions of 22 June 2021 (case C-718/19 Ordre des barreaux francophones and germanophone and Others ECLI:EU:C:2021:505; and case C-719/19 Staatssecretaris van Justitie en Veiligheid ECLI:EU:C:2021:506), the European Court of Justice (ECJ) delivered new clarifications on ending the Union citizen's right of residence. The ECJ clarified, on the one hand, what measures EU Member States can take to effectively enforce an expulsion order against Union citizens and, on the other hand, in which cases they must grant a returning Union citizen a new right of residence. In addition, the Court confirmed its view expressed in the Petrea case, according to which national law implementing EU migration rules for third-country nationals may also apply to Union citizens, provided that their situation is comparable.

BACKGROUND: Maternal exposure to environmental chemicals can cause adverse health effects in offspring. Mounting evidence supports that these effects are influenced, at least in part, by epigenetic modifications. It is unknown whether epigenetic changes in surrogate tissues such as the blood are reflective of similar changes in target tissues such as cortex or liver. OBJECTIVE: We examined tissue- and sex-specific changes in DNA methylation (DNAm) associated with human-relevant lead (Pb) and di(2- ethylhexyl) phthalate (DEHP) exposure during perinatal development in cerebral cortex, blood, and liver. METHODS: Female mice were exposed to human relevant doses of either Pb (32 ppm) via drinking water or DEHP (5 mg/kg-day) via chow for 2 weeks prior to mating through offspring weaning. Whole genome bisulfite sequencing (WGBS) was utilized to examine DNAm changes in offspring cortex, blood, and liver at 5 months of age. Metilene and methylSig were used to identify differentially methylated regions (DMRs). Annotatr and ChIP-enrich were used for genomic annotations and gene set enrichment tests of DMRs, respectively. RESULTS: The cortex contained the majority of DMRs associated with Pb (66%) and DEHP (57%) exposure. The cortex also contained the greatest degree of overlap in DMR signatures between sexes (푛=13 and 8 DMRs with Pb and DEHP exposure, respectively) and exposure types (푛=55 and 39 DMRs in males and females, respectively). In all tissues, detected DMRs were preferentially found at genomic regions associated with gene expression regulation (e.g., CpG islands and shores, 5′ UTRs, promoters, and exons). An analysis of GO terms associated with DMR-containing genes identified imprinted genes to be impacted by both Pb and DEHP exposure. Of these, Gnas and Grb10 contained DMRs across tissues, sexes, and exposures, with some signatures replicated between target and surrogate tissues. DMRs were enriched in the imprinting control regions (ICRs) of Gnas and Grb10, and we again observed a replication of DMR signatures between blood and target tissues. Specifically, we observed hypermethylation of the Grb10 ICR in both blood and liver of Pb-exposed male animals. CONCLUSIONS: These data provide preliminary evidence that imprinted genes may be viable candidates in the search for epigenetic biomarkers of toxicant exposure in target tissues. Additional research is needed on allele- and developmental stage-specific effects, as well as whether other imprinted genes provide additional examples of this relationship. [ABSTRACT FROM AUTHOR]

Background & Aims: The pathogenesis of Wilson disease (WD) involves hepatic and brain copper accumulation resulting from pathogenic variants affecting the ATP7B gene and downstream epigenetic and metabolic mechanisms. Prior methylome investigations in human WD liver and blood and in the Jackson Laboratory (Bar Harbor, ME) C3He-Atp7btx-j/J (tx-j) WD mouse model revealed an epigenetic signature of WD, including changes in histone deacetylase (HDAC) 5. We tested the hypothesis that histone acetylation is altered with respect to copper overload and aberrant DNA methylation in WD. Methods: We investigated class IIa HDAC4 and HDAC5 and H3K9/H3K27 histone acetylation in tx-j mouse livers compared with C3HeB/FeJ (C3H) control in response to 3 treatments: 60% kcal fat diet, D-penicillamine (copper chelator), and choline (methyl group donor). Experiments with copper-loaded hepatoma G2 cells were conducted to validate in vivo studies. Results: In 9-week tx-j mice, HDAC5 levels increased significantly after 8 days of a 60% kcal fat diet compared with chow. In 24-week tx-j mice, HDAC4/5 levels were reduced 5- to 10-fold compared with C3H, likely through mechanisms involving HDAC phosphorylation. HDAC4/5 levels were affected by disease progression and accompanied by increased acetylation. D-penicillamine and choline partially restored HDAC4/5 and H3K9ac/H3K27ac to C3H levels. Integrated RNA and chromatin immunoprecipitation sequencing analyses revealed genes regulating energy metabolism and cellular stress/development, which, in turn, were regulated by histone acetylation in tx-j mice compared with C3H mice, with Pparα and Pparγ among the most relevant targets. Conclusions: These results suggest dietary modulation of class IIa HDAC4/5, and subsequent H3K9/H3K27 acetylation/deacetylation can regulate gene expression in key metabolic pathways in the pathogenesis of WD.