A coordinated control method of voltage and reactive power for active distribution net-works based on soft open point. Abstract-The increasing penetration of distributed generators (DGs) exacerbates the risk of voltage violations in active distribution networks (ADNs). The conventional voltage regulation devices limited by the physical constraints are difficult to meet the requirement of real-time voltage and VAR control (VVC) with high precision when DGs fluctuate frequently. However, soft open point (SOP), a flexible power electronic device, can be used as the continuous reactive power source to realize the fast voltage regulation. Considering the cooperation of SOP and multiple regulation devices, this paper proposes a coordinated VVC method based on SOP for ADNs. First, a time-series model of coordinated VVC is developed to minimize operation costs and eliminate voltage violations of ADNs. Then, by applying the linearization and conic relaxation, the original nonconvex mixed-integer nonlinear optimization model is converted into a mixed-integer second-order cone programming model which can be efficiently solved to meet the requirement of voltage regulation rapidity. Case studies are carried out on the IEEE 33-node system and IEEE 123-node system to illustrate the effectiveness of the proposed method. Index Terms-Active distribution network (ADN), distributed generator (DG), mixed-integer second-order cone programming (MISOCP), soft open point (SOP), voltage and VAR control (VVC). NOMENCLATURE Sets Ω bSet of branches without OLTC Ω O Set of branches with OLTC Variables P t,ij , Q t,ij Active/reactive power flow of branch ij without OLTC at period t

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Mechanically activated (MA) ion channels convert physical forces into electrical signals. Despite the importance of this function, the involvement of mechanosensitive ion channels in human disease is poorly understood. Here we report heterozygous missense mutations in the gene encoding the MA ion channel TMEM63A that result in an infantile disorder resembling a hypomyelinating leukodystrophy. Four unrelated individuals presented with congenital nystagmus, motor delay, and deficient myelination on serial scans in infancy, prompting the diagnosis of Pelizaeus-Merzbacher (like) disease. Genomic sequencing revealed that all four individuals carry heterozygous missense variants in the pore-forming domain of TMEM63A. These variants were confirmed to have arisen de novo in three of the four individuals. While the physiological role of TMEM63A is incompletely understood, it is highly expressed in oligodendrocytes and it has recently been shown to be a MA ion channel. Using patch clamp electrophysiology, we demonstrated that each of the modeled variants result in strongly attenuated stretch-activated currents when expressed in naive cells. Unexpectedly, the clinical evolution of all four individuals has been surprisingly favorable, with substantial improvements in neurological signs and developmental progression. In the three individuals with follow-up scans after 4 years of age, the myelin deficit had almost completely resolved. Our results suggest a previously unappreciated role for mechanosensitive ion channels in myelin development.

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