Cercospora polygonatum, a new species causing gray leaf spot disease in Polygonatum cyrtonema.

This study identified a new species (Cercospora Polygonatum) that causes gray leaf spot (GLS) disease in cultivated Polygonatum cyrtonema. This fungal species was isolated from the affected region of GLS on P. cyrtonema leaves. Pathogenicity bioassays were conducted based on Koch's postulates. Morphology was examined based on the features of conidiomata, conidiogenous loci, conidia/conidiophores, and conidiogenous cells. The rDNA internal transcribed spacer region, calmodulin, translation elongation factor 1-alpha, and histone genes were subjected to phylogenetic analysis using MrBayes tool via in Phylosuite. Bootstrap support analysis for phylogenetic placement confirmed the new species, which was significantly different from the closely related species C. senecionis-walkeri and C. zeae-maydis. The morphological characteristics also supported this finding, with the conidiogenous of C. polygonatum being considerably shorter than those of C. senecionis-walkeri or C. zeae-maydis. In addition, C. polygonatum was distinguished by its cultural characteristics. As this fungus was isolated from P. cyrtonema, it was named C. polygonatum F.Q. Yin, M. Liu&W. L. Ma, sp. nov. The type specimen (H8-2) was preserved at the China General Microbiological Culture Collection Center. This is the first report of GLS caused by C. polygonatum on P. cyrtonema leaves in China. The current study enriches the knowledge regarding Cercospora sp., contributes to the identification of a species causing GLS in P. cyrtonema, and provides useful information for the effective management of this disease.

High-frequency repetitive transcranial magnetic stimulation ameliorates memory impairment by inhibiting neuroinflammation in the chronic cerebral hypoperfusion mice.

BACKGROUND: High-frequency repetitive transcranial magnetic stimulation (HF-rTMS) has been found to ameliorate cognitive impairment. However, the effects of HF-rTMS remain unknown in chronic cerebral hypoperfusion (CCH). AIM: To investigate the effects of HF-rTMS on cognitive improvement and its potential mechanisms in CCH mice. MATERIALS AND METHODS: Daily HF-rTMS therapy was delivered after bilateral carotid stenosis (BCAS) and continued for 14 days. The mice were randomly assigned to three groups: the sham group, the model group, and the HF-rTMS group. The Y maze and the new object recognition test were used to assess cognitive function. The expressions of MAP-2, synapsis, Myelin basic protein(MBP), and brain-derived growth factors (BDNF) were analyzed by immunofluorescence staining and western blot to evaluate neuronal plasticity and white matter myelin regeneration. Nissl staining and the expression of caspase-3, Bax, and Bcl-2 were used to observe neuronal apoptosis. In addition, the activation of microglia and astrocytes were evaluated by fluorescence staining. The inflammation levels of IL-1ß, IL-6, and Tumor Necrosis Factor(TNF)-α were detected by qPCR in the hippocampus of mice in each group. RESULTS: Via behavioral tests, the BCAS mice showed reduced a rate of new object preference and decreased a rate of spontaneous alternations, while HF-rTMS significantly improved hippocampal learning and memory deficits. In addition, the mice in the model group showed decreased levels of MAP-2, synapsis, MBP, and BDNF, while HF-rTMS treatment reversed these effects. As expected, activated microglia and astrocytes increased in the model group, but HF-rTMS treatment suppressed these changes. HF-rTMS decreased BCAS-induced neuronal apoptosis and the expression of pro-apoptotic protein (Caspase-3 and Bax) and increased the expression of anti-apoptotic protein (Bcl-2). In addition, HF-rTMS inhibited the expression of inflammatory cytokines (IL-1ß, IL-6, and TNF-α). CONCLUSIONS: HF-rTMS alleviates cognitive impairment in CCH mice by enhancing neuronal plasticity and inhibiting inflammation, thus serving as a potential method for vascular cognitive impairment.

Transcriptome Sequencing of CeRNA Network Constructing in Status Epilepticus Mice Treated by Low-Frequency Repetitive Transcranial Magnetic Stimulation.

It is shown that great progress was recently made in the treatment of repetitive transcranial magnetic stimulation (rTMS) for neurological and psychiatric diseases. This study aimed to address how rTMS exerted it therapeutic effects by regulating competitive endogenous RNAs (ceRNAs) of lncRNA-miRNA-mRNA. The distinction of lncRNA, miRNA and mRNA expression in male status epilepticus (SE) mice treated by two different ways, low-frequency rTMS (LF-rTMS) vs. sham rTMS, was analyzed by high-throughput sequencing. The Gene Ontology (GO) functional enrichment and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses were carried out. Gene-Gene Cross Linkage Network was established; pivotal genes were screened out. qRT-PCR was used to verify gene-gene interactions. Our results showed that there were 1615 lncRNAs, 510 mRNAs, and 17 miRNAs differentially which were expressed between the LF-rTMS group and the sham rTMS group. The expression difference of these lncRNAs, mRNAs, and miRNAs by microarray detection were consistent with the results by qPCR. GO functional enrichment showed that immune-associated molecular mechanisms, biological processes, and GABA-A receptor activity played a role in SE mice treated with LF-rTMS. KEGG pathway enrichment analysis revealed that differentially expressed genes were correlated to T cell receptor signaling pathway, primary immune deficiency and Th17 cell differentiation signaling pathway. Gene-gene cross linkage network was established on the basis of Pearson's correlation coefficient and miRNA. In conclusion, LF-rTMS alleviates SE through regulating the GABA-A receptor activity transmission, improving immune functions, and biological processes, suggesting the underlying ceRNA molecular mechanisms of LF-rTMS treatment for epilepsy.