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This paper summarized the nursing management for a patient with autoimmune myocarditis after 2 courses of Sintilimab. The patient received hormonotherapy, immunoregulation and other drug treatment. Comprehensive nursing interventions including illness condition observation, medication nursing for intravenous therapy, guidance on rest and exercise, nutritional support and psychological care were carried out during the treatment. The patient's condition improved and was discharged in good condition. (总结1例信迪利单抗治疗2个疗程后发生免疫性心肌炎患者的护理经验。患者住院期间, 给予激素、免疫调节等药物治疗, 密切观察病情变化, 加强静脉治疗与用药护理, 正确指导患者休息与活动, 增强饮食营养, 做好患者心理护理。经过系统的治疗和护理后, 患者病情好转, 顺利出院。)

Methyltransferase-like 3 (Mettl3) is a component of methyltransferase complex that mediates m6A modification of RNAs, and participates in multiple biological processes. However, the role of Mettl3 in cardiac electrophysiology remains unknown. This study aims to explore the ventricular arrhythmia susceptibility of Mettl3+/– mice and the underlying mechanisms. Mice were anesthetized with 2% avertin (0.1 mL/10 g body weight) for echocardiography and programmed electrical pacing. Whole-cell patch clamp technique was used to examine the electrophysiological property of cardiomyocytes. The expression of Cav1.2 was determined by qRT-PCR and western blot analysis. The m6A medication of mRNA was examined by MeRIP-Seq and MeRIP-qPCR. No differences are found in the morphology and function of the hearts between Mettl3+/– mice and wild-type (WT) controls. The QT and QTc intervals of Mettl3+/– mice are significantly longer. High-frequency electrical stimulation showed that heterozygous knockout of Mettl3 increases ventricular arrhythmia susceptibility. The whole-cell patch-clamp recordings showed that the APD is prolonged in Mettl3+/– ventricular myocytes and more EADs were observed. The density of ICa-L is substantially increased in ventricular myocytes of Mettl3+/– mice. The pore-forming subunit of L-type calcium channel Cav1.2 is upregulated in Mettl3+/– mice, while the mRNA of its coding gene CACNA1C does not change. MeRIP-Seq and MeRIP-qPCR showed that the m6A methylation of CACNA1C mRNA is decreased in cultured Mettl3-knockdown cardiomyocytes and Mettl3+/– hearts. Collectively, deficiency of Mettl3 increases ventricular arrhythmia susceptibility due to the upregulation of Cav1.2 by reducing m6A modification on CACNA1C mRNA in mice. This study highlights the role of m6A modification in the regulation of cardiac electrophysiology.

At present, frequent outages have become the major source of power customer complaints and, seriously affect improvement of customer service satisfaction. The current control of frequent outages, complaints has been in a passive state of compensation, which can only get half the result with twice the, effort and has caused adverse perception of customers. In response to this problem, this article takes the, initiative to prevent as a starting point, through studying rules of complaints business for the frequent power outage, constructs the early warning model of the frequent outages complaints, which takes statistics, of outages as the data mining object and uses Chinese word segmentation matching algorithm as data, mining technology and displays through network map technology, and eventually realizes a frequent power, outage scientific and accurate complaints warning. It provides an accurate reference for properly arrange of, troubleshooting and maintenance of the power supply enterprises and line reconstruction plans, offers, technical support for the forward service gateway and lays a solid foundation for effectively reducing the volume of complaints.

Abstract: Plenty of evidence suggests that increased blood levels of homocysteine (Hcy) are an independent risk factor for the development of vascular diseases, but the underlying mechanisms are not well understood. It is well known that the larger conductance Ca2+-activated K+ channels (BKCa) play an essential role in vascular function, so the present study was conducted to determine direct effects of Hcy on BKCa channel properties of smooth muscle cells. Whole-cell patch–clamp recordings were made in mesenteric artery smooth muscle cells isolated from normal rat and patients to investigate effects of 5, 50 and 500 μM Hcy on BKCa, the main current mediating vascular responses in these cells. In human artery smooth muscle cells, maximum BKCa density (measured at +60 mV) was inhibited by about 24% (n =6, P <0.05). In rat artery smooth muscle cells, maximum BKCa density was decreased by approximately 27% in the presence of 50 μM Hcy (n =8, P <0.05). In addition, when rat artery smooth muscle cells was treated with 50 μM Hcy for 24 h, maximum BKCa density decreased by 58% (n =5, P <0.05). These data suggest that Hcy significantly inhibited BKCa currents in isolated human and rat artery smooth muscle cells. BKCa reduced and impaired by elevated Hcy levels might contribute to abnormal vascular diseases. [Copyright &y& Elsevier]