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The spatial distributions of single‐frequency and dual‐frequency Electromagnetic ion cyclotron (EMIC) waves in the subauroral ionosphere are investigated under varying geomagnetic activities, using high‐resolution magnetic field data from dual Swarm satellites spanning from 2015 to 2017. Single‐frequency EMIC waves predominantly occur in the dawn sector, whereas dual‐frequency waves exhibit peaks around both dawn and dusk. The occurrence rate of dual‐frequency waves shows a more pronounced increase with increasing geomagnetic activity. As magnetic storms evolve, both types of EMIC waves shift from dusk to dawn. The South Atlantic Anomaly (SAA) emerges as a high‐incidence region for ionospheric EMIC waves. Dual‐frequency EMIC waves display lower frequencies compared to other regions. Additionally, the low‐frequency components of dual‐frequency waves observed at higher latitudes demonstrate greater power density and longer durations than their high‐frequency counterparts. This suggests that higher frequency waves experience more significant damping during propagation. Most dual‐frequency EMIC waves observed in the ionosphere belong to the O‐band and He‐band waves, indicating that magnetospheric bands below the cyclotron frequency of H+ are more likely to propagate into the ionosphere. Key Points: Single‐frequency ionospheric electromagnetic ion cyclotron (EMIC) waves mainly occur in the dawn sector while dual‐frequency EMIC waves peak around dawn and duskThe occurrence rate of dual‐frequency waves increases more significantly with enhanced geomagnetic activity than single‐frequency wavesLow‐frequency components of dual‐frequency waves observed at higher latitudes exhibit greater power density and extended duration [ABSTRACT FROM AUTHOR]

Lipopolysaccharide can induce myocardial cell injury, which has been widely used in the preparation of septic cardiomyopathy models. We herein aimed to evaluate the protective effects of sodium hydrosulfide against oxidative stress and endoplasmic reticulum stress on the cell model of septic cardiomyopathy and to explore whether the protein kinase RNA-like endoplasmic reticulum kinase-eukaryotic initiation factor 2 alpha signaling pathways was involved. The sepsis induced cardiomyopathy model which was established by inducing rat cardiomyoblast cell line H9c2 cells with lipopolysaccharide and sodium hydrosulfide and endogenous hydrogen sulfide inhibitor (DL-propargylglycine) were used for intervention treatment. Then, cell viability, endogenous hydrogen sulfide levels, lactate dehydrogenase, reactive oxygen species, superoxide dismutase, glutathione and malondialdehyde were determined using commercial assay kits; enzyme-linked immunosorbent assay was used to determine creatine kinase-myoglobin binding, interleukin-6, tumor necrosis factor alpha and interleukin-10; reverse transcription-polymerase chain reaction was used to determine cystathionine gamma-lyase messenger RNA expression; and Western blot was used to determine glucose-regulated protein 78, protein kinase RNA-like endoplasmic reticulum kinase, phosphorylated protein kinase RNA-like endoplasmic reticulum kinase, eukaryotic initiation factor alpha, phosphorylated eukaryotic initiation factor alpha, activating transcription factor 4 and C/EBP-homologous protein levels. Sodium hydrosulfide increased the hydrogen sulfide contents of cells, but did not affect the messenger RNA expression of cystathionine gamma-lyase. It attenuated the decrease in cell viability caused by lipopolysaccharide; reduced the release of the myocardial enzymes like lactate dehydrogenase and creatine kinase-myoglobin binding; reduced the level of inflammatory factors like interleukin-6 and tumor necrosis factor alpha; reduced the level of oxidative stress; inhibited the expression of protein kinase RNA-like endoplasmic reticulum kinase pathway proteins. Sodium hydrosulfide treatment improves septic cardiomyopathy by inhibiting oxidative stress and endoplasmic reticulum stress via the protein kinase RNA-like endoplasmic reticulum kinase-eukaryotic initiation factor alpha pathway, which may be a theory for the treatment of septic cardiomyopathy. [ABSTRACT FROM AUTHOR]

OBJECTIVE: We investigated the effect of electrical stimulation (ES) of varying pulse frequency on differentiation and proliferation of canine myloglossus satellite cells in vitro. MATERIALS AND METHODS: Cellular viability and proliferation were assayed using the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetra-zoliumbromide (MTT) assay and flow cytometry fluorescence-activated cell sorting analysis. Cellular differentiation and expression of mark molecule were assayed by Real Time-PCR and Western blot. RESULTS: With increasing frequency ES, we found a significant increase in Myod (r=0.988, p<0.0001), myogenin (r=0.988, p<0.0001), My-HC-slow (r=0.988, p<0.0001), MyHC-fast (r=0.875, p<0.0001) protein expression, and Pax7 mRNA expression (r=0.712, p=0.001). CONCLUSIONS: Pax7 mRNA expression and MyoD, myogenin, and MyHC protein expression were increased with increment of electrical stimulation frequency in myloglossus muscle satellite. Higher frequency ES enhanced myloglossus satellite cell differentiation, not proliferation and viability. [ABSTRACT FROM AUTHOR]

OBJECTIVE: Intervertebral disc (IVD) degeneration (IDD) is a well-known consequence of low back pain, as characterized by aberrant cell proliferation and apoptosis of nucleus pulposus (NP) cells. In the present study, we aimed to investigate the effect of lncRNA small nucleolar RNA host gene 6 (SN-HG6) on deregulated functions of degenerative NP cells. MATERIALS AND METHODS: After the establishment of rat IDD models, the mRNA and protein levels of collagen-I (Col-I) and collagen II (Col-II), and mRNA level of SNHG6 were detected by using reverse transcription quantitative Real Time-PCR (RT-qPCR) and Western blot. We further investigated the role and molecular mechanisms of SNHG6 by overexpressing or silencing it in degenerative NP cells. Cell proliferation was measured by MTT assay and EdU staning, and apoptosis was measured by flow cytometry. The target of SNHG6 was identified by starBase and Dual-Luciferase reporter assay. RESULTS: Upregulation of SNHG6 was found in IDD NP cells than in normal cells, associated with higher level of Col-I and lower level of Col-II. Overexpression of SNHG6 inhibited cell proliferation and enhanced apoptosis, accompanied by increased expression of Bax, caspase-3, and p21, as well as decreased expression of Bcl-2, which was in reverse to the treatment of SNHG6 silencing. Moreover, miR-101-3p was indicated as a target of SNHG6, and inhibition of miR-101-3p reversed the effects on proliferation and apoptosis induced by SNHG6. CONCLUSIONS: SNHG6 suppressed cell proliferation and induced apoptosis by increasing expression of Bax, caspase-3, p21 and decreasing Bcl-2 through targeting miR-101-3p, which suggested that SNHG6 could be a potential target in the treatment of IDD. [ABSTRACT FROM AUTHOR]