Freshwater Dothideomycetes are a highly diverse group of fungi, which are mostly saprobic in freshwater habitats worldwide. They are important decomposers of submerged woody debris and leaves in water. In this paper, we outline the genera of freshwater Dothideomycetes with notes and keys to species. Based on multigene analyses and morphology, we introduce nine new genera, viz. Aquimassariosphaeria, Aquatospora, Aquihelicascus, Fusiformiseptata, Neohelicascus, Neojahnula, Pseudojahnula, Purpureofaciens, Submersispora; 33 new species, viz. Acrocalymma bipolare, Aquimassariosphaeria kunmingensis, Aquatospora cylindrica, Aquihelicascus songkhlaensis, A. yunnanensis, Ascagilis submersa, A. thailandensis, Bambusicola aquatica, Caryospora submersa, Dictyocheirospora thailandica, Fusiformiseptata crocea, Helicosporium thailandense, Hongkongmyces aquaticus, Lentistoma aquaticum, Lentithecium kunmingense, Lindgomyces aquaticus, Longipedicellata aquatica, Neohelicascus submersus, Neohelicomyces dehongensis, N. thailandicus, Neohelicosporium submersum, Nigrograna aquatica, Occultibambusa kunmingensis, Parabambusicola aquatica, Pseudoasteromassaria aquatica, Pseudoastrosphaeriella aquatica, Pseudoxylomyces aquaticus, Purpureofaciens aquatica, Roussoella aquatica, Shrungabeeja aquatica, Submersispora variabilis, Tetraploa puzheheiensis, T. yunnanensis; 16 new combinations, viz. Aquimassariosphaeria typhicola, Aquihelicascus thalassioideus, Ascagilis guttulaspora, A. queenslandica, A. seychellensis, A. sunyatsenii, Ernakulamia xishuangbannaensis, Neohelicascus aquaticus, N. chiangraiensis, N. egyptiacus, N. elaterascus, N. gallicus, N. unilocularis, N. uniseptatus, Neojahnula australiensis, Pseudojahnula potamophila; 17 new geographical and habitat records, viz. Aliquandostipite khaoyaiensis, Aquastroma magniostiolata, Caryospora aquatica, C. quercus, Dendryphiella vinosa, Ernakulamia cochinensis, Fissuroma neoaggregatum, Helicotruncatum palmigenum, Jahnula rostrata, Neoroussoella bambusae, N. leucaenae, Occultibambusa pustula, Paramonodictys solitarius, Pleopunctum pseudoellipsoideum, Pseudocapulatispora longiappendiculata, Seriascoma didymosporum, Shrungabeeja vadirajensis and ten new collections from China and Thailand, viz. Amniculicola guttulata, Aquaphila albicans, Berkleasmium latisporum, Clohesyomyces aquaticus, Dictyocheirospora rotunda, Flabellascoma fusiforme, Pseudoastrosphaeriella bambusae, Pseudoxylomyces elegans, Tubeufia aquatica and T. cylindrothecia. Dendryphiella phitsanulokensis and Tubeufia roseohelicospora are synonymized with D. vinosa and T. tectonae, respectively. Six orders, 43 families and 145 genera which belong to freshwater Dothideomycetes are reviewed. Of these, 46 genera occur exclusively in freshwater habitats. A world map illustrates the distribution of freshwater Dothideomycetes.

Cortico-basal ganglia circuits are critical for speech and language and are implicated in autism spectrum disorder (ASD), in which language function can be severely affected. We demonstrate that in the striatum, the gene, Foxp2, negatively interacts with the synapse suppressor, Mef2C. We present causal evidence that Mef2C inhibition by Foxp2 in neonatal mouse striatum controls synaptogenesis of corticostriatal inputs and vocalization in neonates. Mef2C suppresses corticostriatal synapse formation and striatal spinogenesis, but can, itself, be repressed by Foxp2 through direct DNA binding. Foxp2 deletion de-represses Mef2C, and both intrastriatal and global decrease of Mef2C rescue vocalization and striatal spinogenesis defects of Foxp2-deletion mutants. These findings suggest that Foxp2-Mef2C signaling is critical to corticostriatal circuit formation. If found in humans, such signaling defects could contribute to a range of neurologic and neuropsychiatric disorders.

Porcine deltacoronavirus (PDCoV) is an emerging swine coronavirus that causes diarrhea in piglets. Since the first outbreak of PDCoV in the United States in 2014, this novel porcine coronavirus has been detected in South Korea, Canada, Mexico, Thailand, and China. In this study, a Chinese PDCoV strain, designated CHN-HN-2014, was isolated from piglets with severe diarrhea on a pig farm in Henan Province, China, and examined with a specific immunofluorescence assay and electron microscopy. Genomic analysis showed that CHN-HN-2014 shares 91.6%-99.4% nucleotide identity with other known PDCoV strains. The pathogenicity of CHN-HN-2014 was further investigated in 5-day-old and 21-day-old piglets. Both kinds of piglets developed clear clinical symptoms, including vomiting, anorexia, lethargy, and severe diarrhea, by 2days postinoculation (DPI), and diarrhea persisted for about 5-6 days. Viral shedding was detected in rectal swabs until 14 DPI in challenged 5-day-old pigs and until 18 DPI in challenged 21-day-old pigs. At necropsy at 4 DPI, macroscopic and microscopic lesions were observed and viral antigen was detected in the small intestines with immunohistochemical staining. These data demonstrate that Chinese PDCoV strain CHN-HN-2014 shares high nucleotide identity with previously reported PDCoV strains and is pathogenic in 5-day-old and 21-day-old piglets.

Macrophages, whether M1 or M2 subtype, have been found to be implicated in the pathogenesis of osteoarthritis (OA). However, no study regarding the status of M1 and M2 macrophages has been reported in knee OA. To investigate the status of M1 and M2 macrophages in knee OA, synovial fluid as well as peripheral blood were collected from 80 patients with knee OA and 80 healthy controls. Reverse transcription-quantitative PCR was used to quantitatively detect the expression of CD11c as a marker for M1 macrophages and CD206 as a marker for M2 macrophages from synovial fluids. As confirmation, flow cytometry was employed to count the number of monocytes from whole blood using the CD86 (M1) and CD163 (M2) markers on monocytes. The ratio of M1 to M2 macrophages was shown to be markedly higher in knee OA than that of control and that the ratio was significantly positively correlated with level of Kellgren-Lawrence grade in knee OA, that is, the higher the ratio the more severe the knee OA seems to be. Thus, our study presented direct evidence for the involvement of macrophages in the pathogenesis of knee OA.

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Dysregulated transforming growth factor beta (TGF-b) signaling is associated with a spectrum of osseous defects as seen in Loeys-Dietz syndrome, Marfan syndrome, and Camurati-Engelmann disease. Intriguingly, neurofibromatosis type 1 (NF1) patients exhibit many of these characteristic skeletal features, including kyphoscoliosis, osteoporosis, tibial dysplasia, and pseudarthrosis; however, the molecular mechanisms mediating these phenotypes remain unclear. Here, we provide genetic and pharmacologic evidence that hyperactive TGFb1 signaling pivotally underpins osseous defects in Nf1 flox/À ;Col2.3Cre mice, a model which closely recapitulates the skeletal abnormalities found in the human disease. Compared to controls, we show that serum TGF-b1 levels are fivefold to sixfold increased both in Nf1 flox/À ;Col2.3Cre mice and in a cohort of NF1 patients. Nf1-deficient osteoblasts, the principal source of TGF-b1 in bone, overexpress TGF-b1 in a gene dosage-dependent fashion. Moreover, Nf1-deficient osteoblasts and osteoclasts are hyperresponsive to TGF-b1 stimulation, potentiating osteoclast bone resorptive activity while inhibiting osteoblast differentiation. These cellular phenotypes are further accompanied by p21-Ras-dependent hyperactivation of the canonical TGF-b1-Smad pathway. Reexpression of the human, fulllength neurofibromin guanosine triphosphatase (GTPase)-activating protein (GAP)-related domain (NF1 GRD) in primary Nf1-deficient osteoblast progenitors, attenuated TGF-b1 expression levels and reduced Smad phosphorylation in response to TGF-b1 stimulation. As an in vivo proof of principle, we demonstrate that administration of the TGF-b receptor 1 (TbRI) kinase inhibitor, SD-208, can rescue bone mass deficits and prevent tibial fracture nonunion in Nf1 flox/À ;Col2.3Cre mice. In sum, these data demonstrate a pivotal role for hyperactive TGF-b1 signaling in the pathogenesis of NF1-associated osteoporosis and pseudarthrosis, thus implicating the TGF-b signaling pathway as a potential therapeutic target in the treatment of NF1 osseous defects that are refractory to current therapies.