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It is our pleasure to introduce a special issue of the International Journal of Eating Disorders on eating disorders (EDs) in Asia.

We received such a robust response to the special edition that we were able to fill two issues. Contributions focused on seven main themes (1) prevalence, (2) time trends, (3) healthcare systems, (4) treatment, (5) risk factors, (6) assessment, and (7) orthorexia.

New prevalence and time trend data from China, Iran, Singapore, Japan, and Taiwan suggest that EDs are increasingly common in Asia but are not always detected in healthcare settings. Only a minority of individuals with EDs in Singapore receive treatment, and psychosocial treatment and prevention interventions that are evidence-based in the West may require cultural adaptation before they can be fully implemented in Japan, Singapore, China, and South Korea. Psychological risk factors for EDs are more similar than different in Iran, India, Japan, and China, but biological risk factors are understudied across the continent. Psychometrically sound assessment tools are available in many Asian languages.

We hope this special issue provides a catalyst and blueprint for global collaboration to relieve the burden of suffering of EDs in Asia and beyond.

We hope this special issue provides a catalyst and blueprint for global collaboration to relieve the burden of suffering of EDs in Asia and beyond.Piwi-interacting RNAs (piRNAs) play key roles in germline development and genome defence in metazoans. In C. elegans, piRNAs are transcribed from > 15,000 discrete genomic loci by RNA polymerase II (Pol II), resulting in 28 nt short-capped piRNA precursors. Here, we investigate transcription termination at piRNA loci. We show that the Integrator complex, which terminates snRNA transcription, is recruited to piRNA loci. Moreover, we demonstrate that the catalytic activity of Integrator cleaves nascent capped piRNA precursors associated with promoter-proximal Pol II, resulting in termination of transcription. Loss of Integrator activity, however, does not result in transcriptional readthrough at the majority of piRNA loci. Taken together, our results draw new parallels between snRNA and piRNA biogenesis in nematodes and provide evidence of a role for the Integrator complex as a terminator of promoter-proximal RNA polymerase II during piRNA biogenesis.β-defensin (BD) is a cysteine-rich cationic antibacterial peptide that is active against a wide range of bacteria. Here, a β-defensin homolog (LcBD2) was identified in large yellow croaker (Larimichthys crocea). The open reading frame of LcBD2 contains 195 nucleotides, encoding a protein of 64 amino acids that possesses a typical arrangement of six conserved cysteine residues (C31 , C37 , C41 , C53 , C59 and C60 ). LcBD2 transcripts were constitutively expressed in all examined tissues and significantly increased in head kidney, spleen and gills by Vibrio alginolyticus. The synthetic LcBD2 peptide imparted antimicrobial effects on both Gram-negative bacteria (V. campbellii, V. parahaemolyticus, V. alginolyticus, V. harveyi and Pseudomonas plecoglossicida) and Gram-positive bacteria (Bacillus subtilis). We also observed that after treatment with synthetic LcBD2 peptide, numerous blisters appeared on the membrane of P. plecoglossicida, which in turn may result in cell membrane breakage and bacterial death. Moreover, the synthetic LcBD2 peptide significantly upregulated the expression levels of TNF-α2, IL-1β and CXCL8_L1 in monocytes/macrophages, while downregulated expression level of IL-10. The LcBD2 peptide also remarkedly enhanced the phagocytosis of monocytes/macrophages. These results indicate that LcBD2 not only protects large yellow croaker against multiple bacterial pathogens but also plays a role in activation of monocytes/macrophages.The impairment of inhibitory control is often assumed to be the core deficit of several neurodevelopmental disorders characterized by poor impulse control. However, could the same deficit explain different clinical phenotypes? Evidence from behavioural studies is very mixed. This is partly because inhibition is a highly complex executive function. Thus, the different types of tasks that generically tap into inhibitory control are likely to provide different outcomes. Additionally, sample inhomogeneity in terms of age, comorbidity, and medical treatment are confounding factors. Therefore, to make a reliable assessment of the deficit of inhibitory control in a given disorder, the same task and samples with similar characteristics must be employed. This article reviews and discusses studies on five neurodevelopmental disorders with impaired impulse control where these criteria have been used Tourette syndrome; obsessive-compulsive disorder; attention-deficit/hyperactivity disorder; primary motor stereotypies; and autism spectrum disorder. Overall, they suggest that the mechanisms underlying the inability to control urges are extremely heterogeneous and cannot be ascribed to a general impairment of inhibition. selleck chemical These findings do not support the hypothesis that inhibitory deficits represent a transdiagnostic feature of neurodevelopmental disorders with poor impulse control. WHAT THIS PAPER ADDS The mechanisms underlying the inability to control urges in neurodevelopmental disorders are heterogeneous. Inhibition impairments cannot generally explain all neurodevelopmental disorders characterized by poor urge control.

Nucleic acid integrity can be compromised under many abiotic stresses. To date, however, few studies have considered whether nucleic acid damage and damage repair play a role in cold-stress adaptation. A further insufficiently explored question concerns how age affects cold stress adaptation among mature perennials. As a plant ages, the optimal trade-off between growth and stress tolerance may shift.

Oxidative damage to RNA and expression of genes involved in DNA repair were compared in multiple mature cohorts of Thinopyrum intermedium (an emerging perennial cereal) and in wheat and barley under intermittent freezing stress and under nonfreezing conditions. Activity of glutathione peroxidase (GPX) and four other antioxidative enzymes was also measured under these conditions. DNA repair genes included photolyases involved in repairing ultraviolet-induced damage and two genes involved in repairing oxidatively induced damage (ERCC1, RAD23).

Freezing stress was accompanied by large increases in photolyase expression and ERCC1 expression (in wheat and Thinopyrum) and in GPX and GR activity (particularly in Thinopyrum). This is the first report of DNA photolyases being overexpressed under freezing stress. Older Thinopyrum had lower photolyase expression and less freezing-induced overexpression of ERCC1. Younger Thinopyrum plants sustained more oxidative damage to RNA.

Overexpression of DNA repair genes is an important aspect of cold acclimation. When comparing adult cohorts, aging was associated with changes in the freezing stress response, but not with overall increases or decreases in stress tolerance.

Overexpression of DNA repair genes is an important aspect of cold acclimation. When comparing adult cohorts, aging was associated with changes in the freezing stress response, but not with overall increases or decreases in stress tolerance.The in vitro production of platelets could provide a life-saving intervention for patients that would otherwise require donor-derived platelets. Producing large numbers of platelets in vitro from their progenitor cells, megakaryocytes, remains remarkably difficult and inefficient. Here, a human megakaryoblast leukemia cell line (MEG-01) was used to assess the maturation of megakaryocytes and to develop a new methodology for producing high numbers of platelet-like particles from mature MEG-01 cells in vitro.As the field of organoid development matures, the need to transplant organoids to evaluate and characterize their functionality grows. Decades of research developing islet organoid transplantation for the treatment of type 1 diabetes can contribute substantially to accelerating diverse tissue organoid transplantation. Biomaterials-based organoid delivery methods offer the potential to maximize organoid survival and engraftment. In this protocol, we describe a vasculogenic degradable hydrogel vehicle and a method to deliver organoids to intraperitoneal tissue. Further, we describe a method to fluorescently label and image functional vasculature within the graft as a tool to investigate organoid engraftment.Cancer has now been established as one of the most common chronic diseases due to high mortality rate. The early stage of non-invasive tumors can now be successfully treated leading to have high survival rates; however, the late stage invasive and metastatic tumors still suffer from poor treatment outcomes. Among multiple contributing factors, the role of tumor microenvironment and its complexities has been well recognized in cancer progression. Stromal cells including cancer-associated fibroblasts (CAFs), endothelial cells, adipocytes, immune cells as well as extracellular matrix (ECM) continuously interact with malignant cells and regulate various hallmarks of cancer including tumor growth, invasion, and intravasation. To better understand the role of the interaction between tumor cells and their surrounding microenvironment, numerous model systems ranging from two-dimensional (2D) assays to 3D hydrogels and in vivo murine xenografts have been utilized. While each one of these model systems exhibit certain rganization of tumor and stromal entities with designated initial architecture and cellular positioning, therefore enabling to study the specific role of cell-cell and cell-ECM interaction on tumor proliferation/expansion, cancer cell migration as well as stromal activation. The developed platform is compatible with standard biological assays enabling gene and protein expression analyses across different types of cancer and co-culture of tumor and stromal cells.Cancer mortality predominantly results from distant metastases that are undetectable at diagnosis and escape initial therapies to lie as dormant micrometastases for years. To study the behavior of micrometastases-how they resist initial treatments and then awaken from a dormant state-we utilize the Legacy LiverChip®, an all-human ex vivo hepatic microphysiological system. The functional liver bioreactor, comprising hepatocytes and non-parenchymal cells in a 3D microperfused culture format, mimics the dormant-emergent metastatic progression observed in human patients (a) a subpopulation of cancer cells spontaneously enter dormancy, (b) cycling cells are eliminated by standard chemotherapies, while quiescent dormant cells remain, and (c) chemoresistant dormant cells can be stimulated to emerge. The system effluent and tissue can be queried for proteomic and genomic data, immunofluorescent imaging as well as drug efficacy and metabolism. This microphysiological system continues to provide critical insights into the biology of dormant and re-emergent micrometastases and serves as an accessible tool to identify new therapeutic strategies targeting the various stages of metastasis, while concurrently evaluating antineoplastic agent efficacy for metastasis, metabolism, and dose-limiting toxicity.