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Seedlings sown in non-sterile conditions could be maintained on MSTT agar for up to a week without observable contamination. This medium was compatible with rapid screening methods for hygromycin B, phosphinothricin (BASTA) and nourseothricin resistance genes, meaning that positive transformants can be identified from non-sterile seeds in as little as 4 days after stratification, and transferred to soil before the onset of visible microbial contamination. By using MSTT agar we were able to select genetic transformants on solid media without seed surface sterilization, eliminating a tedious and time-consuming step. © 2020 The Authors. Physiologia Plantarum published by John Wiley & Sons Ltd on behalf of Scandinavian Plant Physiology Society.Dopaminergic (DAergic) neurons of the midbrain ventral tegmental area (VTA) are known to regulate the hypothalamic-pituitary-adrenal (HPA) axis but have no direct projections to the paraventricular nucleus (PVN) of the hypothalamus. This study investigated whether VTA DAergic afferents modulate glutamatergic transmission-dependent GABAergic neurons in dorsolateral bed nucleus of stria terminalis (dlBNST) to affect the activity of the HPA-axis. Herein, we demonstrate that systemic administration of the neurotoxicant 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) or the VTA-injection of 1-methyl-4-phenylpyridinium ion (MPP+) in male mice (MPTP-mice and MPP+mice) caused a decline of tyrosine hydroxylase positive (TH+) cells in VTA with a reduction in TH+fibers in the dlBNST. MPTP-mice and MPP+mice displayed a clear increase in serum levels of corticosterone (CORT) and adrenocorticotropic hormone, corticotropin-releasing hormone (CRH) expression, and CRH neuron activity in PVN. The presynaptic glutamate release, glutamatergic synaptic transmission and induction of long-term potentiation in dlBNST of MPTP-mice were suppressed, and these effects were rescued by a D1-like DAergic receptor (D1R) agonist and mimicked in control dlBNST by blockade of D1R. MPTP-mice exhibited low expression of glutamic acid decarboxylase and dysfunction of the excitatory-dependent GABAergic circuit in dlBNST, and these effects were recovered by the administration of D1R agonist. Furthermore, either dlBNST-injection of D1R agonist or PVN-injection of GABAA receptor (GABAA R) agonist could correct the increased secretion and expression of CRH in MPTP-mice. The results indicate that the DAergic afferents from VTA enhance excitatory-dependent activation of GABAergic neurons in dlBNST, which suppress the activity of the HPA-axis. © 2020 International Society for Neurochemistry.Women presenting with amenorrhea and elevated serum levels of FSH before the age of 40 may suffer from premature ovarian insufficiency (POI). POI can be caused by ovarian damage through surgery, irradiation and chemotherapy. Autoimmune disease and genetic causes are also possible causes for development of POI. Since today we have a wide diagnostic arsenal available for patients, all women should be offered extended investigation. It is also important that affected women receive sufficient estrogen supplementation to avoid complications of POI, such as cardiovascular disease, osteoporosis and cognitive impairment. Supplementation should be given at least until the normal age of menopause, about 51 years of age. Although the condition is often complicated by infertility, it is important to inform patients that some residual fertility potential may exist in the case of secondary amenorrhea and POI.Chronic obstructive pulmonary disease (COPD) and cardiovascular disease (CVD) are frequently associated and share common risk factors, pathophysiological processes, symptoms and clinical signs. Ischemic heart disease, heart failure, pulmonary hypertension and atrial fibrillation are common comorbidities of COPD. COPD has been described as an independent risk factor for CVD. Cardiac troponin elevation, indicating myocardial injury, is associated with both the stable state of COPD and acute exacerbation of COPD. The mechanisms of elevated troponin levels in these conditions are multiple and not fully understood. The aim of this article is to discuss the association between COPD, CVD and cardiac troponins.Systematic evidence mapping offers a robust and transparent methodology for facilitating evidence-based approaches to decision-making in chemicals policy and wider environmental health. Interest in the methodology is growing; however, its application in environmental health is still novel. To facilitate the production of effective systematic evidence maps for environmental health use cases, we survey the successful application of evidence mapping in other fields where the methodology is more established. Focusing on issues of "data storage technology", "data integrity", "data accessibility", and "transparency", we characterise current evidence-mapping practice and critically review its potential value for environmental health contexts. We note that rigid, flat data tables and schema-first approaches dominate current mapping methods and highlight how this practice is ill-suited to the highly connected, heterogeneous and complex nature of environmental health data. We propose this challenge is overcome by storing and structuring data as "knowledge graphs". Knowledge graphs offer a flexible, schemaless and scalable model for systematically mapping the environmental health literature. Associated technologies such as ontologies are well-suited to the long-term goals of systematic mapping methodology in promoting resource-efficient access to the wider environmental health evidence base. Apoptosis inhibitor Several graph storage implementations are readily available, with a variety of proven use cases in other fields. Thus, developing and adapting systematic evidence mapping for environmental health should utilise these graph-based resources to ensure the production of scalable, interoperable and robust maps to aid decision-making processes in chemicals policy and wider environmental health. © The Author(s) 2020. Published by Oxford University Press on behalf of the Society of Toxicology. All rights reserved. For permissions, please email journals.permissions@oup.com.