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These findings suggest that cooking shrimp at boiling temperature for at least 1 min might prevent any potential spread of WSSV from endemic countries to other geographical areas where WSSV has not yet been reported. © 2020 John Wiley & Sons Ltd.BACKGROUND There is scarce information detailing clinical and physiological effects of reversible injectable protocols of chemical restraint on Neotropical primates. METHODS Nineteen captive Spix´s Owl monkeys (Aotus vociferans) were assessed in a double-blind randomized crossover study using the following ketamine/xylazine [KX], ketamine/midazolam [KM] and ketamine/xylazine/midazolam [KXM]. During immobilization, respiratory and pulse rates, rectal temperature, haemoglobin oxygen saturation and arterial blood pressure were recorded at 5-minute intervals during a 20-minute period; afterwards, antagonist drugs (yohimbine for xylazine and flumazenil for midazolam) were, respectively, administered. Quality and duration of induction, immobilization and recovery periods were recorded. RESULTS Ketamine/xylazine increased manipulation sensitivity and produced poor muscle relaxation. KM maintained all assessed parameters within physiological ranges. KXM produced depressant cardiorespiratory effects and hypotension. All protocols produced hypothermia. CONCLUSIONS Based on its adequate anaesthetic depth and minimum effects on physiological parameters, KM is suitable for immobilizing A vociferans and performing short-term procedures lasting around 20 minutes. © 2020 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.Imbalance of T helper 17 (Th17)/regulatory T (Treg) cells is involved in the pathogenesis of myasthenia gravis with thymoma (MG-T). Long non-coding RNAs (lncRNAs) are implicated in the regulation of Th17/Treg balance. This study was designed to explore the role of XLOC_003810, a novel lncRNA, in regulating the Th17/Treg balance in MG-T. The thymic CD4+ T cells were isolated from control subjects and MG-T patients. The Th17/Treg balance was evaluated by determining proportions of Th17 and Treg cells and expression of Th17- and Treg- associated molecules. Lentivirus-mediated silencing and overexpression of XLOC_003810 in CD4+ T cells were performed. The results showed that XLOC_003810 expression was higher in MG-T thymic CD4+ T cells than that in the control group. Furthermore, the ratio of Th17/Treg cells, proportion of Th17 cells and levels of Th17-associated molecules were significantly increased, whereas the proportion of Treg cells and levels of Treg-associated molecules were decreased in MG-T thymic CD4+ T cells. Importantly, the Th17/Treg imbalance in MG-T thymic CD4+ T cells was aggravated by XLOC_003810 overexpression, whereas it was attenuated by XLOC_003810 silencing. Collectively, XLOC_003810 modulates thymic Th17/Treg balance in MG-T patients, providing the scientific basis for the clinical targeted therapy of MG-T. © 2020 John Wiley & Sons Australia, Ltd.γδ T cells play important roles in the development of rheumatoid arthritis (RA) through their antigen-presenting capacity, release of pro-inflammatory cytokines, immunomodulatory properties, interaction with CD4+ CD25+ Tregs and promotion of antibody production by helping B cells. Although prostaglandin E2 (PGE2) was proved to have the ability to enhance the antigen-presenting function of dendritic cells and IL-17 production of CD4+ αβ T cells in RA, the role of PGE2 in γδ T cells from RA disease has not yet been clarified. The goal of this study was to determine the role of PGE2 in γδ T cells in RA. We first demonstrated that the population of γδT17 cells increased in patients with RA compared to healthy controls. Then, IL-17A level in patients with RA was shown to increase compared to healthy controls. After adding PGE2 to γδ T cells from patients with RA, the IL-17A level increased accordingly, and the expression of the costimulatory molecules, CD80 and CD86, on these cells also increased. These results suggest that PEG2 can increase the production of IL-17A and the expression of CD80 and CD86 on γδ T cells in patients with RA. These findings will benefit to explore new therapeutic targets for RA disease. © 2020 The Scandinavian Foundation for Immunology.Small nucleolar RNA host gene 3 (SNHG3) is a long noncoding RNA (lncRNA), which is known to promote oncogenesis in many cancers but its role in human papillary thyroid carcinoma (PTC) remains poorly understood. We therefore assessed SNHG3 expression in PTC tissues via quantitative reverse transcription polymerase chain reaction. We additionally knocked down SNHG3 in PTC cells using short-hairpin RNAs (shRNAs) to explore its functional roles in PTC. The ability of SNHG3 to bind to specific microRNAs (miRNAs) was predicted using a bioinformatics tool, and this binding was confirmed via dual-luciferase reporter and RNA immunoprecipitation (RIP) assays. We then used a tumor xenograft model to assess the relevance of SNHG3 in vivo. We determined SNHG3 expression to be elevated in PTC tissues relative to controls, with advanced tumor-node-metastasis stage and lymph node metastasis being associated with this expression. Knocking down SNHG3 significantly reduced in vitro PTC cell migration, invasion, proliferation, and colony formation, and it further slowed the growth of tumors in vivo. We found that SNHG3 could bind to miR-214-3p as a competing endogenous RNA (ceRNA) for this miRNA, thereby regulating proteasome 26S subunit non-ATPase 10 (PSMD10) expression, a miR-214-3p target. These results thus indicate that SNHG3 is an oncogenic lncRNA in PTC, acting at least in part via the miR-214-3p/PSMD10 axis. © 2020 Wiley Periodicals, Inc.Polycystic ovarian syndrome (PCOS) is a disorder characterized by oligomenorrhea, anovulation, and hyperandrogenism. Altered mitochondrial biogenesis can result in hyperandrogenism. The goal of this study was to examine the effect of vitamin D3 on mitochondrial biogenesis of the granulosa cells in the PCOS-induced mouse model. Vitamin D3 applies its effect via the mitogen-activated pathway kinase-extracellular signal-regulated kinases (MAPK-ERK1/2) pathway. The PCOS mouse model was induced by the injection of dehydroepiandrosterone (DHEA). Isolated granulosa cells were subsequently treated with vitamin D3, MAPK activator, and MAPK inhibitor. Gene expression levels were measured using real-time polymerase chain reaction. MAPK proteins were investigated by western blot analysis. We also determined reactive oxygen species (ROS) levels with 2', 7'-dichlorofluorescein diacetate. Mitochondrial membrane potential (mtMP) was also measured by TMJC1. Mitochondrial biogenesis (peroxisome proliferator-activated receptor gamma coactivator 1-α and nuclear respiratory factor), antioxidant (superoxide dismutase, glutathione peroxidase, and catalase), and antiapoptotic (B-cell lymphoma-2) genes were upregulated in the PCOS mice that treated with vitamin D3 compared with the PCOS mice without any treatment. Vitamin D3 and MAPK activator-treated groups also reduced ROS levels compared with the nontreated PCOS group. In summary, vitamin D3 and MAPK activator increased the levels of mitochondrial biogenesis, MAPK pathway, and mtMP markers, while concomitantly decreased ROS levels in granulosa cells of the PCOS-induced mice. This study suggests that vitamin D3 may improve mitochondrial biogenesis through stimulation of the MAPK pathway in cultured granulosa cells of DHEA-induced PCOS mice which yet to be investigated. © 2020 Wiley Periodicals, Inc.Liver fibrosis is a central pathological process that occurs in most types of chronic liver diseases. Advanced liver fibrosis causes cirrhosis, hepatocellular carcinoma, and liver failure. However, the exact molecular mechanisms underlying the initiation and progression of liver fibrosis remain largely unknown. This study was designed to investigate the role of protein kinase D3 (PKD3, gene name Prkd3) in the regulation of liver homeostasis. We generated global Prkd3 knockout (Prkd3-/- ) mice and myeloid cell-specific Prkd3 knockout (Prkd3∆LysM ) mice, and we found that both Prkd3-/- mice and Prkd3∆LysM mice displayed spontaneous liver fibrosis. PKD3 deficiency also aggravated carbon tetrachloride (CCL4)-induced liver fibrosis. PKD3 is highly expressed in hepatic macrophages, and PKD3 deficiency skewed macrophage polarization toward a profibrotic phenotype. The activated profibrotic macrophages produced TGF-β that in turn activates hepatic stellate cells (HSCs) to become matrix-producing myofibroblasts. Moreover, PKD3 deficiency decreased the phosphatase activity of SHP1 (a bona fide PKD3 substrate) resulting in sustained STAT6 activation in macrophages. In addition, we observed that PKD3 expression in hepatic macrophages was downregulated in cirrhotic human liver tissues. Conclusion PKD3 deletion in mice drives liver fibrosis through the profibrotic macrophage activation. Vitamin chemical This article is protected by copyright. All rights reserved.PURPOSE Several studies have demonstrated potential improvements in treatment time through the use of dynamic arcs for delivery of stereotactic body radiation therapy (SBRT) on Cyberknife. However, the delivery system has a finite accuracy, so that potential exists for dosimetric uncertainties. This study estimates the expected dosimetric accuracy of dynamic delivery of SBRT, based on realistic estimates of the uncertainties in delivery parameters. METHODS Five SBRT patient cases (prostate A - conventional, prostate B - brachytherapy-type, lung, liver, partial left breast) were retrospectively studied. Treatment plans were produced for a fixed arc trajectory using fluence optimization, segmentation, and direct aperture optimization. Dose rate uncertainty was modeled as a smoothly varying random fluctuation of ± 1.0%, ±2.0% or ± 5.0% over a time period of 10, 30 or 60 s. Multileaf collimator uncertainty was modeled as a lag in position of each leaf up to 0.25 or 0.5 mm. Robot pointing error was modeled as a shncrease in mean dose by around 1%. CONCLUSIONS Based upon the limited data available on the dose rate stability and geometric accuracy of the Cyberknife system, this study estimates that dynamic arc delivery can be accomplished with sufficient accuracy for clinical application. Dose rate variation produces a change in dose to the planning target volume according to the perturbation of total monitor units delivered, while multileaf collimator lag and robot pointing error typically increase the mean dose to the planning target volume by up to 1%. © 2020 The Authors. Medical Physics published by Wiley Periodicals, Inc. on behalf of American Association of Physicists in Medicine.Neuroinflammation accompanied by microglial activation triggers multiple cell death after traumatic brain injury (TBI). The secondary injury caused by inflammation may persist for a long time. Recently, platelet C-type lectin-like 2 receptor (CLEC-2) has been shown to regulate inflammation in certain diseases. However, its possible effects on TBI remain poorly understood. Here, we aimed to investigate the role of platelet CLEC-2 in the pathological process of neuroinflammation after TBI. link2 In this study, mice were subjected to sham or controlled cortical impact injury, and arbitrarily received recombinant platelet CLEC-2. In parallel, BV2 cells were treated with lipopolysaccharide (LPS) to mimic microglial activation after TBI. Primary endothelial cells were also subjected to LPS in order to replicate the inflammatory damage caused by TBI. We used western blot analysis, reverse transcription polymerase chain reaction (RT-PCR), and immunostaining to evaluate the role of platelet CLEC-2 in TBI. link3 In conditional knock out platelet CLEC-2 mice, trauma worsened the integrity of the blood-brain barrier and amplified the release of inflammatory cytokines.