The diploid rainbow trout Oncorhynchus mykiss reached sexual maturity 3 years after hatching and its oogenesis underwent four stages, which were oogonia, primary oocyte, secondary oocyte and egg. Reproductive development and hormone changes of 4 to 35 month-old female O. mykiss were investigated using histological and radioimmunoassay methods in order to provide a theoretical and practical basis for the use of triploid female O. mykiss. The oogonium of the triploid female could develop into the oocytes of the prophase with abortion occurring later; the oogonium was surrounded by stroma cells to form the oogonium cluster and the gonads showed a virilescent tendency when the oogonium clusters were gradually replaced by spermatogenic-like cytocysts. After 13 months, amounts of gonadotropic hormone (GtH-I, GtH-II) and oestradiol (17beta-E(2)) in triploid females were lower than in diploid fish at corresponding time periods, but the amounts of testosterone (T) increased consistently after 21 months and were more than in diploid fish in the corresponding time periods (P > 0.05). The infertility of triploid females resulted from meiosis failure, which caused developmental abortion of oocytes and oogonium formed cytocysts before the prophase oocytes. The cytocyst formation was due to the lack of the normal interaction of ovum and follicular cells, the development of follicular cells producing steroids were inhibited, the arylate path from T to 17beta-E(2) was interrupted, concentration of 17beta-E(2) decreased and concentration of T increased in the blood, the content of vitellogenin (Vg) decreased in the liver with a low 17beta-E(2) and high T caused to ovaries to show a tendency to be virilescent.

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Infectious hematopoietic necrosis virus (IHNV) is a highly contagious disease of juvenile salmonid fish. Six genome target fragments of the complete genome sequence of IHNV HLJ-09 were amplified by RT-PCR, and the 3'-terminal and 5'-terminal region of the genomic RNA were amplified using the RACE method. The complete genome sequence of HLJ-09 comprises 11,132 nucleotides (nt) (Accession number JX649101) and is different from that of other IHNV strains published in GenBank. Homology comparison and phylogenetic analysis of six ORF sequences were carried out using HLJ-09 and other IHNV strains published in GenBank. From phylogenetic tree analysis, the N gene, M gene, and P gene had the closest genetic relationship to IHNV-PRT from Korea. Phylogenetic analysis for the full length of the G gene showed that the HLJ-09 strain exhibited very close homology to the ChYa07, RtNag96, RtUi02, and RtGu01 strains from Korea and Japan, indicating that the HLJ-09 strain belonged to the genotype JRt. Ultimately, the Chinese IHNV HLJ-09 strain may have originated in Korea and Japan.

BackgroundTraumatic brain injury (TBI) is a leading cause of long‐term disability in young adults and induces complex neuropathological processes. Cellular autonomous and intercellular changes during the subacute phase contribute substantially to the neuropathology of TBI. However, the underlying mechanisms remain elusive. In this study, we explored the dysregulated cellular signaling during the subacute phase of TBI.MethodsSingle‐cell RNA‐sequencing data (GSE160763) of TBI were analyzed to explore the cell–cell communication in the subacute phase of TBI. Upregulated neurotrophic factor signaling was validated in a mouse model of TBI. Primary cell cultures and cell lines were used as in vitro models to examine the potential mechanisms affecting signaling.ResultsSingle‐cell RNA‐sequencing analysis revealed that microglia and astrocytes were the most affected cells during the subacute phase of TBI. Cell–cell communication analysis demonstrated that signaling mediated by the non‐canonical neurotrophic factors midkine (MDK), pleiotrophin (PTN), and prosaposin (PSAP) in the microglia/astrocytes was upregulated in the subacute phase of TBI. Time‐course profiling showed that MDK, PTN, and PSAP expression was primarily upregulated in the subacute phase of TBI, and astrocytes were the major source of MDK and PTN after TBI. In vitro studies revealed that the expression of MDK, PTN, and PSAP in astrocytes was enhanced by activated microglia. Moreover, MDK and PTN promoted the proliferation of neural progenitors derived from human‐induced pluripotent stem cells (iPSCs) and neurite growth in iPSC‐derived neurons, whereas PSAP exclusively stimulated neurite growth.ConclusionThe non‐canonical neurotrophic factors MDK, PTN, and PSAP were upregulated in the subacute phase of TBI and played a crucial role in neuroregeneration.

In this study, we successfully prepared two monoclonal antibodies (mAbs) against three subtypes of salmonid alphavirus (SAV), and established an indirect immunofluorescence assay that can be used to diagnose and prevent SAV from entering SAV unreported countries, such as China, through international trade. The application of this method will contribute to controlling SAV infection and reducing economic losses.