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Scientific communication is facilitated by a data-driven, scientifically sound taxonomy that considers the end-user's needs and established successful practice. In 2013, the Fusarium community voiced near unanimous support for a concept of Fusarium that represented a clade comprising all agriculturally and clinically important Fusarium species, including the F. solani species complex (FSSC). Subsequently, this concept was challenged in 2015 by one research group who proposed dividing the genus Fusarium into seven genera, including the FSSC described as members of the genus Neocosmospora, with subsequent justification in 2018 based on claims that the 2013 concept of Fusarium is polyphyletic. Here, we test this claim and provide a phylogeny based on exonic nucleotide sequences of 19 orthologous protein-coding genes that strongly support the monophyly of Fusarium including the FSSC. We reassert the practical and scientific argument in support of a genus Fusarium that includes the FSSC and several other basal lineages, consistent with the longstanding use of this name among plant pathologists, medical mycologists, quarantine officials, regulatory agencies, students, and researchers with a stake in its taxonomy. In recognition of this monophyly, 40 species described as genus Neocosmospora were recombined in genus Fusarium, and nine others were renamed Fusarium. Here the global Fusarium community voices strong support for the inclusion of the FSSC in Fusarium, as it remains the best scientific, nomenclatural, and practical taxonomic option available.

Recent studies have uncovered the vital roles played by microRNAs in regulating cardiac injury. Among them, the cardiac enriched microRNA-1 (miR-1) has been extensively studied and proven to be detrimental to cardiac myocytes. Hence, the current study aimed to explore whether miR-1 affects myocardial ischemia-reperfusion injury (MIRI) in rats undergoing sevoflurane preconditioning and the underlying mechanism. After successful model establishment, rats with MIRI were transfected with mimics or inhibitors of miR-1, or siRNA against MAPK3, and then were injected with sevoflurane. A luciferase reporter gene assay was conducted to evaluate the targeting relationship between miR-1 and MAPK3. Reverse transcription quantitative polymerase chain reaction and Western blot analysis were employed to evaluate the expressions of miR-1, MAPK3, phosphatidylinositol 3-kinase (PI3K), and Akt. Additionally, the concentration of lactate dehydrogenase (LDH) was determined. Cell apoptosis and viability were assessed using TUNEL and cell counting kit-8 assays, and the ischemic area at risk and infarct size were detected using Evans blue and triphenyltetrazolium chloride staining. MAPK3 was found to be the target gene of miR-1. miR-1 expressed at a high level whereas MAPK3 expressed at a low level in MIRI rats. Overexpressing miR-1 or silencing MAPK3 blocked the PI3K/Akt pathway to increase cell apoptosis, ischemic area at risk, and infarct area but decreased cell viability and increased LDH concentration. In contrast, miR-1 downregulation abrogated the effects induced by miR-1 mimics or siRNA against MAPK3. These findings indicate that inhibition of miR-1 promotes MAPK3 to protect against MIRI in rats undergoing sevoflurane preconditioning through activation of the PI3K/Akt pathway.

Myocardial ischemia and reperfusion injury (MIRI) includes major drawbacks, such as excessive formation of free radicals and also overload of calcium, which lead to cell death, tissue scarring, and remodeling. The current study aims to explore whether KRT1 silencing may ameliorate MIRI via the Notch signaling pathway in mouse models. Myocardial tissues were used for the determination of the positive rate of KRT1 protein expression, apoptosis of myocardial cells, creatine kinase (CK) and lactate dehydrogenase (LDH) expression, expression of related biomarkers as well as myocardial infarction area. The transfected myocardial cells were treated with KRT1-siRNA, Jagged1, and DAPT (inhibitor of Notch-1 signaling pathway). The expression of KRT1, NICD, Hes1, Bcl-2, and Bax protein was detected. The MTT assay was applied for cell proliferation and flow cytometry was used for cell apoptosis. Mice with MIRI had a higher positive rate of KRT1 protein expression, apoptosis of myocardial cells, CK and LDH expression, myocardial infarction area, increased expression of MDA, NO, SDH, IL-1, IL-6, TNF-α, CRP, KRT1, Bax protein, CK, and LDH, and decreased expression of SOD, NICD, Hes1, and Bcl-2. The downregulation of KRT1 led to decreased expression of KRT1 and Bax protein, increased expression of NICD, Hes1, and Bcl-2, decreased cell apoptosis, and improved cell proliferation. The inhibition of the Notch signaling pathway leads to reduced expression of Bax, increased expression of NICD, Hes1, and Bcl 2, and also decreased cell apoptosis and increased cell proliferation. Our data conclude that KRT1 silencing is able to make MIRI better by activating the Notch signaling pathway in mice.

To explore the effects of Rho-kinase inhibitor on cardiac hypertrophy of left ventricle in spontaneously hypertensive rats (SHR).SHRs (n = 30) were randomly divided into 5 groups (n = 6 each): SHR control group, 5 mg/kg fasudil group (SHRL), 10 mg/kg fasudil group (SHRM), 20 mg/kg fasudil group (SHRH) and nifedipine group (XBDP, 10 mg/kg). Six male Wistar-Kyoto rats were selected as normal control group (WKY group). Systolic blood pressure (SBP) was measured before and after treatment every 2 weeks. The hypertrophic parameters of left ventricular weight index (LVWI) and cardiomyocyte transverse diameter (TDM) were measured. In addition, the expression levels of Rho kinase mRNA and protein in cardiomyocytes were observed by reverse transcription-polymerase chain reaction (RT-PCR) and Western blot.The levels of LVWI and TDM in WKY group were significantly lower than those in SHR control group [(2.98 ± 0.05) vs (3.16 ± 0.08) mg/g, (18.18 ± 0.75) vs (21.32 ± 1.25) µm, P0.01]. After 8 weeks, the levels of LVWI and TDM in three fasudil groups were markedly lower than those in SHR control group [SHRL group: (3.12 ± 0.05) mg/g, SHRM group: (3.10 ± 0.07) mg/g, SHRH group: (3.08 ± 0.09) mg/g vs SHR control group: (3.16 ± 0.08) mg/g, SHRL group: (20.11 ± 1.15) µm, SHRM group: (19.63 ± 1.62) µm, SHRH group: (18.91 ± 1.05) µm vs SHR control group: (21.32 ± 1.25) µm, P0.05 or P0.01]. But the levels of LVWI and TDM were not different between SHR control and XBDP groups [(3.14 ± 0.08) mg/g,(21.42 ± 1.23) µm, P0.05]. Compared with SHR control group, the expression of Rho kinase mRNA and protein in cardiomyocytes significantly decreased in three fasudil groups [SHRL group mRNA: (0.45 ± 0.08), SHRM group mRNA: (0.37 ± 0.07), SHRH group mRNA: (0.32 ± 0.07) vs SHR control group mRNA: (0.63 ± 0.07), SHRL group protein: 0.78 ± 0.11), SHRM group protein: (0.73 ± 0.10), SHRH group protein: (0.68 ± 0.10) vs SHR control group protein: (0.90 ± 0.1), P0.05 or P0.01], but showed no obvious change in XBDP group [mRNA: (0.56 ± 0.07), protein: (0.85 ± 0.10), P0.05].Rho kinase inhibitor may significantly down-regulate the expression of Rho kinase in cardiomyocytes of SHR. The mechanism is probably due to the favorable effects of Rho kinase inhibitor in the prevention of cardiac hypertrophy of left ventricle.

To investigate the correlation between vascular remodeling index (RI) and serum adiponectin, plasma monocyte chemoattractant protein-1 (MCP-1), endothelial function and evaluate the mechanism of coronary in-stent restenosis.RI 6 months after percutaneous coronary intervention (PCI), serum adiponectin, plasma MCP-1 and flow-mediated dilation (FMD) before and 3 days,6 months after PCI were measured in 30 patients with and 30 without coronary in-stent restenosis.Compared with patients without restenosis and those with restenosis before PCI, the patients with coronary in-stent restenosis showed significantly increased plasma MCP-1 3 days and 6 months after PCI (P0.05) and reduced RI 6 months after PCI, serum adiponectin and FMD 3 days and 6 months after PCI (P0.05). RI was positively correlated to serum adiponectin and FMD and inversely to MCP-1.The occurrence of coronary in-stent restenosis is the result of the interrelations between multiple factors.