Background and aims: Immediate recurrence (Im-Recurr), a type of atrial fibrillation (AF) recurrence occurring during the blanking period after radiofrequency catheter ablation (RFCA), has received little attention. Therefore, this study was aimed at exploring the clinical significance of Im-Recurr in patients with AF after RFCA. Methods: This study retrospectively included patients with AF who underwent RFCA at our center. Regression, propensity score matching (PSM), and survival curve analyses were conducted to investigate the effects of Im-Recurr on costs, hospitalization durations, AF recurrence rates, and predictors of Im-Recurr. Results: A total of 898 patients were included, among whom 128 developed Im-Recurr after RFCA. Multiple linear regression analysis revealed that Im-Recurr correlated with greater cost, hospitalization duration, and hospitalization duration after ablation. Logistic regression and PSM analyses indicated that intraoperative electric cardioversion (IEC) was an independent predictor of Im-Recurr. The follow-up results suggested a significantly higher 1-year cumulative AF recurrence rate in the Im-Recurr group than the control group. Conclusions: Im-Recurr significantly increases the cost and length of hospitalization for patients with AF undergoing RFCA and is associated with an elevated 1-year cumulative AF recurrence rate. IEC serves as an independent predictor of Im-Recurr. Registration number: ChiCTR2200065235.
Although many long non-coding RNAs (lncRNAs) have been identified in muscle, some of their physiological functions and regulatory mechanisms remain elusive.Here we report the functional identification and characterization of a novel lncRNA 2310043L19Rik (lnc-231), which is highly expressed in muscle.The expression level of lnc-231 in skeletal muscle of young mice is higher than that in aged mice.Functional analysis showed that overexpression of lnc-231 restrained differentiation and promoted proliferation of myoblast, while inhibition of lnc-231 revealed completely opposite effects in vitro.RNA molecules of lnc-231 acted mechanistically as competing endogenous RNAs (ceRNA) to target miR-125a-5p, whereas miR-125a-5p binds to the 3'-UTR of E2F3 mRNA to inhibit its function.Collectively, lncRNA 2310043L19Rik promotes proliferation and inhibits differentiation of myoblast cells by attenuating the function of miR-125a-5p.
Neoruscogenin is a plant-origin sapogenin that has the potential to modulate muscle growth among the small-molecule compounds that we previously predicted by artificial intelligence to target myostatin (MSTN). This study aimed to elucidate the biological role of neoruscogenin on muscle growth and its relationship with MSTN. Using molecular biological techniques, we found that neoruscogenin inhibited MSTN maturation, thereby repressing its signal transduction; further facilitated protein synthesis metabolism and reduced protein degradation metabolism, ultimately promoting the differentiation of myoblasts and hypertrophy of muscle fibers; and had the effect of repairing muscle injury. This study enriched the biological functions of neoruscogenin and provided a theoretical basis for the treatment of human myopathy and its application in the livestock industry.
Testicular hypoplasia can affect the sexual and reproductive ability in adulthood, and even increase the risk of cancer. Abnormal development of the gubernaculum is one of the important factors of testicular hypoplasia. Therefore, a study of the structure and function of the gubernaculum is an important but neglected new breakthrough point for investigating the normal/abnormal development of the testis. Previous findings showed that Insulin like factor 3 (INSL3) is a key factor regulating the growth of gubernaculum, however, the mechanism by which INSL3 acts on the gubernaculum remains unknown. Therefore, we probed the mechanism associated with INSL3-induced the proliferation, migration, and apoptosis of gubernacular cells in mice.A culture cell model of neonatal mice gubernaculum is established by INSL3 intervention. We blocked PLC/PKC signaling pathway with U73122 pretreat to investigate the role of the PLC/PKC signaling pathway. The changes of cell proliferation, migration, and apoptosis were detected by molecular biological methods. In addition, the levels of PCNA and F-action were detected by immunofluorescence and western blotting.We found that INSL3 can promote the proliferation and migration of gubernacular cells and inhibit their apoptosis, meanwhile, INSL3 significantly up-regulated PLC/PKC protein phosphorylation. However, treatment with the PLC/PKC signaling pathway inhibitor U73122 significantly inhibited these effects of INSL3. Besides, we found that INSL3 could up-regulate the protein expression level of PCNA and F-actin, while the PCNA and F-actin expression was significantly weakened after U73122 pretreatment.This research revealed that INSL3 binding to RXFP2 may up-regulate the expression levels of PCNA and F-actin by activating the PLC/PKC signaling pathway to promote the proliferation and migration of gubernacular cells. It suggests that the RXFP2-PLC/PKC axis may serve as a novel molecular mechanism by which INSL3 regulates growth of the gubernaculum.
In mammals, a vast majority of ovarian follicles undergo atresia, which is caused by granulosa cell (GC) apoptosis. GCs in follicles are exposed to low oxygen. Hypoxia triggers reactive oxygen species (ROS) generation, which leads to cell oxidative stress and apoptosis. Sulforaphane (SFN), a phytochemical isothiocyanate enriched in cruciferous vegetables, has exhibited a crucial role in mitigating oxidative stress. To explore the effect of SFN on porcine GC apoptosis in a hypoxic environment, we handled the established hypoxia model (1% O2) of cultured porcine GCs with SFN. Results showed that SFN rescued hypoxia-induced apoptosis and viability of GCs. Meanwhile, SFN increased the expression of antioxidant enzymes and reduced the accumulation of ROS in GC cytoplasm and mitochondria under hypoxia. Mechanically, SFN activated the transcription factor of redox-sensitive nuclear factor-erythroid 2-related factor 2 (NFE2L2) entering the nucleus, further inducing mitophagy and increased antioxidant capacity, finally alleviating the adverse effect of hypoxia on porcine GCs. In conclusion, SFN inhibited hypoxia-evoked GC apoptosis by activating antioxidant defenses and mitophagy through NFE2L2. New targets may be provided for regulating follicular development and atresia by these findings.
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