Cyber-resilient Automatic Generation Control for Systems of AC Microgrids

In this paper we propose a co-design of the secondary frequency regulation in systems of AC microgrids and its cyber securty solutions. We term the secondary frequency regulator a Micro-Automatic Generation Control (Micro-AGC) for highlighting its same functionality as the AGC in bulk power systems. We identify sensory challenges and cyber threats facing the Micro-AGC. To address the sensory challenges, we introduce a new microgrid model by exploiting the rank-one deficiency property of microgrid dynamics. This model is used to pose an optimal Micro-AGC control problem that is easily implemented, because it does not require fast frequency measurements. An end-to-end cyber security solution to the False Data Injection (FDI) attack detection and mitigation is developed for the proposed Micro-AGC. The front-end barrier of applying off-the-shelf algorithms for cyber attack detection is removed by introducing a data-driven modeling approach. Finally, we propose an observer-based corrective control for an islanded microgrid and a collaborative mitigation schemes in systems of AC microgrids. We demonstrate a collaborative role of systems of microgrids during cyber attacks. The performance of the proposed cyber-resilient Micro-AGC is tested in a system of two networked microgrids.Comment: The manuscript has been accepted by IEEE Transactions on Smart Gri

Sphingosine kinase 2 activates autophagy and protects neurons against ischemic injury through interaction with Bcl-2 via its putative BH3 domain

Our previous findings suggest that sphingosine kinase 2 (SPK2) mediates ischemic tolerance and autophagy in cerebral preconditioning. The aim of this study was to determine by which mechanism SPK2 activates autophagy in neural cells. In both primary murine cortical neurons and HT22 hippocampal neuronal cells, overexpression of SPK2 increased LC3II and enhanced the autophagy flux. SPK2 overexpression protected cortical neurons against oxygen glucose deprivation (OGD) injury, as evidenced by improvement of neuronal morphology, increased cell viability and reduced lactate dehydrogenase release. The inhibition of autophagy effectively suppressed the neuroprotective effect of SPK2. SPK2 overexpression reduced the co-immunoprecipitation of Beclin-1 and Bcl-2, while Beclin-1 knockdown inhibited SPK2-induced autophagy. Both co-immunoprecipitation and GST pull-down analysis suggest that SPK2 directly interacts with Bcl-2. SPK2 might interact to Bcl-2 in the cytoplasm. Notably, an SPK2 mutant with L219A substitution in its putative BH3 domain was not able to activate autophagy. A Tat peptide fused to an 18-amino acid peptide encompassing the native, but not the L219A mutated BH3 domain of SPK2 activated autophagy in neural cells. The Tat-SPK2 peptide also protected neurons against OGD injury through autophagy activation. These results suggest that SPK2 interacts with Bcl-2 via its BH3 domain, thereby dissociating it from Beclin-1 and activating autophagy. The observation that Tat-SPK2 peptide designed from the BH3 domain of SPK2 activates autophagy and protects neural cells against OGD injury suggest that this structure may provide the basis for a novel class of therapeutic agents against ischemic stroke

Committed emissions from existing energy infrastructure jeopardize 1.5 °C climate target.

Net anthropogenic emissions of carbon dioxide (CO2) must approach zero by mid-century (2050) in order to stabilize the global mean temperature at the level targeted by international efforts1-5. Yet continued expansion of fossil-fuel-burning energy infrastructure implies already 'committed' future CO2 emissions6-13. Here we use detailed datasets of existing fossil-fuel energy infrastructure in 2018 to estimate regional and sectoral patterns of committed CO2 emissions, the sensitivity of such emissions to assumed operating lifetimes and schedules, and the economic value of the associated infrastructure. We estimate that, if operated as historically, existing infrastructure will cumulatively emit about 658 gigatonnes of CO2 (with a range of 226 to 1,479 gigatonnes CO2, depending on the lifetimes and utilization rates assumed). More than half of these emissions are predicted to come from the electricity sector; infrastructure in China, the USA and the 28 member states of the European Union represents approximately 41 per cent, 9 per cent and 7 per cent of the total, respectively. If built, proposed power plants (planned, permitted or under construction) would emit roughly an extra 188 (range 37-427) gigatonnes CO2. Committed emissions from existing and proposed energy infrastructure (about 846 gigatonnes CO2) thus represent more than the entire carbon budget that remains if mean warming is to be limited to 1.5 degrees Celsius (°C) with a probability of 66 to 50 per cent (420-580 gigatonnes CO2)5, and perhaps two-thirds of the remaining carbon budget if mean warming is to be limited to less than 2 °C (1,170-1,500 gigatonnes CO2)5. The remaining carbon budget estimates are varied and nuanced14,15, and depend on the climate target and the availability of large-scale negative emissions16. Nevertheless, our estimates suggest that little or no new CO2-emitting infrastructure can be commissioned, and that existing infrastructure may need to be retired early (or be retrofitted with carbon capture and storage technology) in order to meet the Paris Agreement climate goals17. Given the asset value per tonne of committed emissions, we suggest that the most cost-effective premature infrastructure retirements will be in the electricity and industry sectors, if non-emitting alternatives are available and affordable4,18

Clinical Study of Endovascular Treatment of Severe Middle Cerebral Artery Stenosis or Occlusion and Vascular Cognitive Impairment

Objective: It is very important to study the factors affecting the incidence, progress and prognosis of patients with vascular dementia.  Methods: 50 cases of severe middle cerebral artery stenosis or occlusion underwent endovascular treatment (25 cases of mild cognitive dysfunction, 25 cases of moderate cognitive dysfunction) were divided into two groups, where a medical drug treatment group and a control group established with 25 cases in each group. The cognitive function of each group of patients was evaluated before operation, 7 days after operation, 30 days after operation, and 180 days after operation. CTP was used to compare the hemodynamic changes in patients before and after operation.  Results: The severe stenosis or occlusion of the middle cerebral artery in patients can be improved, and the intracranial blood supply of patients with poorly compensated medial cranial circulation and hypoperfusion can be restored to a certain extent. Meanwhile, improvement of cognitive function was definitive in some patients with cognitive dysfunction.  Conclusion: To guide the formulation of treatment plans for patients with severe middle cerebral artery stenosis or occlusion