An Integrated Single-phase On-board Charger

With the growing demand for transportation electrification, plug-in electric vehicles (PEVs), and plug-in hybrid electric vehicles (PHEVs), cumulatively called electric vehicles (EVs) are drawing more and more attention. The on-board charger (OBC), which is the power electronics interface between the power grid and the high voltage traction battery, is an important part for charging EVs. Besides the OBC, every EV is equipped with another separate power unit called the auxiliary power module (APM) to charge the low voltage (LV) auxiliary battery, which supplies all the electronics on car including audio, air conditioner, lights and controllers. The main target of this work is a novel way to integrate both units together to achieve a charger design that is not only capable of bi-directional operation with high efficiency, but also higher gravimetric and volumetric power density, as compared with those of the existing OBCs and APMs combined. To achieve this target, following contributions are made: (i) a three-port integrated DC/DC converter, which combines OBC and APM together through an innovative integration method; (ii) an innovative zero-crossing current spike compensation for interleaved totem pole power factor correction (PFC) and (iii) a new phase-shift based control strategy to achieve a regulated power flow management with minimum circulating losses

Downregulation of LncRNA GCLC-1 Promotes Microcystin-LR-Induced Malignant Transformation of Human Liver Cells by Regulating GCLC Expression

Microcystin-LR (MCLR) is an aquatic toxin, which could lead to the development of hepatocellular carcinoma (HCC). Long non-coding RNAs (lncRNAs) are considered important regulatory elements in the occurrence and development of cancer. However, the roles and mechanisms of lncRNAs during the process of HCC, induced by MCLR, remain elusive. Here, we identified a novel lncRNA, namely lnc-GCLC-1 (lncGCLC), which is in close proximity to the chromosome location of glutamate–cysteine ligase catalytic subunit (GCLC). We then investigated the role of lncGCLC in MCLR-induced malignant transformation of WRL68, a human hepatic cell line. During MCLR-induced cell transformation, the expression of lncGCLC and GCLC decreased continuously, accompanied with a consistently high expression of miR-122-5p. Knockdown of lncGCLC promoted cell proliferation, migration and invasion, but reduced cell apoptosis. A xenograft nude mouse model demonstrated that knockdown of lncGCLC promoted tumor growth. Furthermore, knockdown of lncGCLC significantly upregulated miR-122-5p expression, suppressed GCLC expression and GSH levels, and enhanced oxidative DNA damages. More importantly, the expression of lncGCLC in human HCC tissues was significantly downregulated in the high-microcystin exposure group, and positively associated with GCLC level in HCC tissues. Together, these findings suggest that lncGCLC plays an anti-oncogenic role in MCLR-induced malignant transformation, by regulating GCLC expression