invadans. Phylogenetic analysis based on the internal transcribed spacer region of the rRNA gene showed that the same clone of pathogen has spread across different continents regardless of fish species and ecotypes (fresh/estuarine environments). Altogether, the present study provides baseline data which can be applied in EUS management strategies within brackish-water ecosystems. We recommend strict surveillance and development of sound biosecurity measures against the disease.In this study, spontaneous swim bladder mycosis was documented in a farmed fingerling rainbow trout from a raceway culture system. At necropsy, the gross lesions included a thickened swim bladder wall, and the posterior portion of the swim bladder was enlarged due to massive hyperplasia of muscle. A microscopic wet mount examination of the swim bladder contents revealed abundant septate hyphae, and histopathological examination showed periodic acid-Schiff-positive mycelia in the lumen and wall of the swim bladder. Histopathological examination of the thickened posterior swim bladder revealed muscle hyperplasia with expansion by inflammatory cells. The causative agent was identified as Phoma herbarum through morphological analysis and DNA sequencing. The disease was reproduced in rainbow trout fingerlings using intraperitoneal injection of a spore suspension. Necropsy in dead and moribund fish revealed extensive congestion and haemorrhages in the serosa of visceral organs and in liver and abdominal serosanguinous fluid. Histopathological examination showed severe hepatic congestion, sinusoidal dilatation, Kupffer cell reactivity, leukostasis and degenerative changes. Fungi were disseminated to the liver, pyloric caeca, kidney, spleen and heart. Although infections caused by Phoma spp. have been repeatedly reported in fish, species identification has been hampered by extensive taxonomic changes. The results of this study confirmed the pathogenicity of P. herbarum in salmonids by using a reliably identified strain during experimental fish infection and provides new knowledge regarding the course of infection.Tachaea chinensis, a parasitic isopod, negatively affects the production of several commercially important shrimp species in China. The mechanism of parasite-host interaction cannot be accurately described by transcriptomic and proteomic approaches individually. Here, comparative metabolite profiling was used to achieve a broad coverage of primary metabolite changes in Chinese grass shrimp Palaemonetes sinensis following T. chinensis parasitization. In total, 66 metabolites were significantly differentially accumulated between the control and infected groups; of these, 19 were upregulated and 47 were downregulated after T. chinensis infection. Moreover, the Kyoto Encyclopedia of Genes and Genomes pathway enrichment analysis revealed that 10 pathways were significantly enriched. The protein digestion and absorption pathways were highly enriched, followed by the mineral absorption, aminoacyl-tRNA biosynthesis, biosynthesis of amino acids, and metabolic metabolism pathways. Parasitization by T. chinensis enhanced the glycolytic pathway and tricarboxylic acid (TCA) cycle in P. sinensis, thereby releasing more energy for swimming, foraging, and evading predation. Glucogenic amino acids such as alanine, histidine, glutamine, and proline were consumed to generate glutamate and enhance the TCA cycle.  https://www.selleckchem.com/products/AZD6244.html  Nucleotide-related metabolic pathways were downregulated, possibly because T. chinensis can secrete molecules to degrade nucleotides and inhibit hemostasis and inflammatory responses. These results suggest that the isopod parasite can increase the host's metabolic burden by enhancing the host's TCA cycle and secreting molecules to degrade host proteins, thereby enabling the parasite to feed on the host and inhibit an inflammatory response. The results will be a valuable contribution to understanding the metabolic responses of crustaceans to isopod parasitism.The melanoma-associated antigen family A (MAGEA) antigens are expressed in a wide variety of malignant tumors but not in adult somatic cells, rendering them attractive targets for cancer immunotherapy. Here we show that a number of cancer-associated MAGEA mutants that undergo proteasome-dependent degradation in vitro could negatively impact their utility as immunotherapeutic targets. Importantly, in pancreatic ductal adenocarcinoma cell models, MAGEA6 suppresses macroautophagy (autophagy). The inhibition of autophagy is released upon MAGEA6 degradation, which can be induced by nutrient deficiency or by acquisition of cancer-associated mutations. Using xenograft mouse models, we demonstrated that inhibition of autophagy is critical for tumor initiation whereas reinstitution of autophagy as a consequence of MAGEA6 degradation contributes to tumor progression. These findings could inform cancer immunotherapeutic strategies for targeting MAGEA antigens and provide mechanistic insight into the divergent roles of MAGEA6 during pancreatic cancer initiation and progression. © 2020, Tsang et al.Most mammals maintain their body temperature around 37°C, whereas in hibernators it can approach 0°C without triggering a thermogenic response. The remarkable plasticity of the thermoregulatory system allowed mammals to thrive in variable environmental conditions and occupy a wide range of geographical habitats, but the molecular basis of thermoregulation remains poorly understood. Here we leverage the thermoregulatory differences between mice and hibernating thirteen-lined ground squirrels (Ictidomys tridecemlineatus) to investigate the mechanism of cold sensitivity in the preoptic area (POA) of the hypothalamus, a critical thermoregulatory region. We report that, in comparison to squirrels, mice have a larger proportion of cold-sensitive neurons in the POA. We further show that mouse cold-sensitive neurons express the cyclic nucleotide-gated ion channel CNGA3, and that mouse, but not squirrel, CNGA3 is potentiated by cold. Our data reveal CNGA3 as a hypothalamic cold sensor and a molecular marker to interrogate the neuronal circuitry underlying thermoregulation. © 2020, Feketa et al.