this paper proposes an adaptive dc-link voltage control method for the two-stage photovoltaic (PV) inverter during the low voltage ride-through (LVRT) operation period. The dc-link voltage will be controlled to follow the change of grid voltage during the low voltage ride-through operation to maintain the high modulation ratio so that the high frequency harmonics injected into the grid can be attenuated significantly. Besides, when suffering the asymmetrical grid faults, the proposed control method could to some extent attenuate the double-line-frequency dc-link voltage ripple to keep the dc-link voltage in the safe operational range by shifting the double-line-frequency power ripple to the front-end dc input source, which can be achieved by intentionally fluctuating the dc input power or employing a bi-directional dc-dc converter depending on the voltage drop ratio and the input power level. The theoretical findings were verified by Matlab simulations and the constructed experimental prototype.Index Terms-Low voltage ride-through, photovoltaic inverter, dc-link voltage, two-stage inverter. 1 0885-8993 (c)

Immune thrombocytopenia (ITP) is an autoimmune disorder characterized by low platelet count which can cause fatal hemorrhage. ITP patients with antiplatelet glycoprotein (GP) Ib-IX autoantibodies appear refractory to conventional treatments, and the mechanism remains elusive. Here we show that the platelets undergo apoptosis in ITP patients with anti-GPIbα autoantibodies. Consistent with these findings, the anti-GPIbα monoclonal antibodies AN51 and SZ2 induce platelet apoptosis in vitro. We demonstrate that anti-GPIbα antibody binding activates Akt, which elicits platelet apoptosis through activation of phosphodiesterase (PDE3A) and PDE3A-mediated PKA inhibition. Genetic ablation or chemical inhibition of Akt or blocking of Akt signaling abolishes anti-GPIbα antibody-induced platelet apoptosis. We further demonstrate that the antibody-bound platelets are removed in vivo through an apoptosis-dependent manner. Phosphatidylserine (PS) exposure on apoptotic platelets results in phagocytosis of platelets by macrophages in the liver. Notably, inhibition or genetic ablation of Akt or Akt-regulated apoptotic signaling or blockage of PS exposure protects the platelets from clearance. Therefore, our findings reveal pathogenic mechanisms of ITP with anti-GPIbα autoantibodies and, more importantly, suggest therapeutic strategies for thrombocytopenia caused by autoantibodies or other pathogenic factors.

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This paper proposed a novel battery energy storage system based on modular multilevel converter (MMC), which has several merits compared with two-level and cascaded multilevel battery energy storage systems. The proposed system can manage the state-of-charges (SOCs) of all batteries to be equal to avoid the overcharge or over discharge of single battery stack as traditional. Besides, the inherent power exchange characteristics using circulating current could increase the control flexibility for SOC balancing, and improve output waveform quality, maximize storage capacity and reduce internal losses. The key issues regarding injected dc current control, SOC balancing control and circulating current control are discussed in this paper. Finally, the proposed system were verified through Matlab/Simulink simulation and a scaled down experiment prototype.

Previous studies have shown that receptor-interacting protein kinase 3 (RIP3) is involved in many important biological processes, including necroptosis, apoptosis, and inflammation. Here we show that RIP3 plays a critical role in regulating platelet functions and in vivo thrombosis and hemostasis. Tail bleeding times were significantly longer in -knockout (RIP3) mice compared with their wild-type (WT) littermates. In an in vivo model of arteriole thrombosis, mice lacking RIP3 exhibited prolonged occlusion times. WT mice repopulated with RIP3 bone marrow-derived cells had longer occlusion times than RIP3 mice repopulated with WT bone marrow-derived cells, suggesting a role for RIP3-deficient platelets in arterial thrombosis. Consistent with these findings, we observed that RIP3 was expressed in both human and mice platelets. Deletion of RIP3 in mouse platelets caused a marked defect in aggregation and attenuated dense granule secretion in response to low doses of thrombin or a thromboxane A analog, U46619. Phosphorylation of Akt induced by U46619 or thrombin was diminished in RIP3 platelets. Moreover, RIP3 interacted with Gα Platelet spreading on fibrinogen and clot retraction were impaired in the absence of RIP3. RIP3 inhibitor dose-dependently inhibited platelet aggregation in vitro and prevented arterial thrombus formation in vivo. These data demonstrate a role for RIP3 in promoting in vivo thrombosis and hemostasis by amplifying platelet activation. RIP3 may represent a novel promising therapeutic target for thrombotic diseases.