Realistic Simulation on Reverse Characteristics of SiC/GaN p-n Junctions for High Power Semiconductor Devices

Guannan Wei,Yung C. Liang,Ganesh S. Samudra 전력전자학회 2011 ICPE(ISPE)논문집 Vol.2011 No.5

This paper presents a practical methodology for realistic simulation on reverse characteristics of Wide Bandgap (WBG) SiC/GaN p-n junctions. The adjustment on certain physic-based model parameters, such as the trap density and photo-generation for SiC junction, and impact ionization coefficients and critical field for GaN junction are described. The adjusted parameters were used in Synopsys Medici simulation to obtain a realistic p-n junction avalanche breakdown voltage. The simulation results were verified through benchmarking against independent data reported by others.

Realistic Simulations on Reverse Junction Characteristics of SiC and GaN Power Semiconductor Devices

Wei, Guannan,Liang, Yung C.,Samudra, Ganesh S. The Korean Institute of Power Electronics 2012 JOURNAL OF POWER ELECTRONICS Vol.12 No.1

This paper presents a practical methodology for realistic simulation on reverse characteristics of Wide Bandgap (WBG) SiC and GaN p-n junctions. The adjustment on certain physic-based model parameters, such as the trap density and photo-generation for SiC junction, and impact ionization coefficients and critical field for GaN junction are described. The adjusted parameters were used in Synopsys Medici simulation to obtain a realistic p-n junction avalanche breakdown voltage. The simulation results were verified through benchmarking against independent data reported by others.

Realistic Simulations on Reverse Junction Characteristics of SiC and GaN Power Semiconductor Devices

Guannan Wei,Yung C. Liang,Ganesh S. Samudra 전력전자학회 2012 JOURNAL OF POWER ELECTRONICS Vol.12 No.1

This paper presents a practical methodology for realistic simulation on reverse characteristics of Wide Bandgap (WBG) SiC and GaN p-n junctions. The adjustment on certain physic-based model parameters, such as the trap density and photo-generation for SiC junction, and impact ionization coefficients and critical field for GaN junction are described. The adjusted parameters were used in Synopsys Medici simulation to obtain a realistic p-n junction avalanche breakdown voltage. The simulation results were verified through benchmarking against independent data reported by others.

miR-135b Aggravates Fusobacterium nucleatum-Induced Cisplatin Resistance in Colorectal Cancer by Targeting KLF13

Zeng Wei,Pan Jia,Ye Guannan 한국미생물학회 2024 The journal of microbiology Vol.62 No.2

Cisplatin resistance is the main cause of colorectal cancer (CRC) treatment failure, and the cause has been reported to be related to Fusobacterium nucleatum (Fn) infection. In this study, we explored the role of Fn in regulating cisplatin resistance of CRC cells and its underlying mechanism involved. The mRNA and protein expressions were examined by qRT-PCR and western blot. Cell proliferation and cell apoptosis were assessed using CCK8 and flow cytometry assays, respectively. Dual-luciferase reporter gene assay was adopted to analyze the molecular interactions. Herein, our results revealed that Fn abundance and miR-135b expression were markedly elevated in CRC tissues, with a favorable association between the two. Moreover, Fn infection could increase miR-135b expression via a concentration-dependent manner, and it also enhanced cell proliferation but reduced apoptosis and cisplatin sensitivity by upregulating miR-135b. Moreover, KLF13 was proved as a downstream target of miR-135b, of which overexpression greatly diminished the promoting effect of miR-135b or Fn-mediated cisplatin resistance in CRC cells. In addition, it was observed that upstream 2.5 kb fragment of miR-135b promoter could be interacted by β-catenin/TCF4 complex, which was proved as an effector signaling of Fn. LF3, a blocker of β-catenin/TCF4 complex, was confirmed to diminish the promoting role of Fn on miR-135b expression. Thus, it could be concluded that Fn activated miR-135b expression through TCF4/β-catenin complex, thereby inhibiting KLF13 expression and promoting cisplatin resistance in CRC.

Transcriptomic view of survival during early seedling growth of the extremophyte <i>Haloxylon ammodendron</i>

Fan, Ligang,Wang, Guannan,Hu, Wei,Pantha, Pramod,Tran, Kieu-Nga,Zhang, Hua,An, Lizhe,Dassanayake, Maheshi,Qiu, Quan-Sheng Elsevier 2018 Vol. No.

<P><B>Abstract</B></P> <P>Seedling establishment in an extreme environment requires an integrated genomic and physiological response to survive multiple abiotic stresses. The extremophyte, <I>Haloxylon ammodendron</I> is a pioneer species capable of colonizing temperate desert sand dunes. We investigated the induced and basal transcriptomes in <I>H. ammodendron</I> under water-deficit stress during early seedling establishment. We find that not only drought-responsive genes, but multiple genes in pathways associated with salt, osmotic, cold, UV, and high-light stresses were induced, suggesting an altered regulatory stress response system. Additionally, <I>H. ammodendron</I> exhibited enhanced biotic stress tolerance by down-regulation of genes that were generally up-regulated during pathogen entry in susceptible plants. By comparing the <I>H. ammodendron</I> basal transcriptome to six closely related transcriptomes in Amaranthaceae, we detected enriched basal level transcripts in <I>H. ammodendron</I> that shows preadaptation to abiotic stress and pathogens. We found transcripts that were generally maintained at low levels and some induced only under abiotic stress in the stress-sensitive model, <I>Arabidopsis thaliana</I> to be highly expressed under basal conditions in the Amaranthaceae transcriptomes including <I>H. ammodendron</I>. <I>H. ammodendron</I> shows coordinated expression of genes that regulate stress tolerance and seedling development resource allocation to support survival against multiple stresses in a sand dune dominated temperate desert environment.</P> <P><B>Highlights</B></P> <P> <UL> <LI> We report the transcriptomic signals of <I>H. ammodendron</I> in response to drought that contribute to plant survival. </LI> <LI> We highlight the transcriptional and biological processes for the survival of <I>H. ammodendron</I> at early developmental stage. </LI> <LI> We find abundant orthologs in extremophytes that are rare in Arabidopsis. </LI> <LI> These orthologs provide novel candidates to discover networks naturally selected as adaptations to environmental stresses. </LI> </UL> </P>

MicroRNA-375 is a therapeutic target for castration-resistant prostate cancer through the PTPN4/STAT3 axis

Gan Junqing,Liu Shan,Zhang Yu,He Liangzi,Bai Lu,Liao Ran,Zhao Juan,Guo Madi,Jiang Wei,Li Jiade,Li Qi,Mu Guannan,Wu Yangjiazi,Wang Xinling,Zhang Xingli,Zhou Dan,Lv Huimin,Wang Zhengfeng,Zhang Yanqiao,Q 생화학분자생물학회 2022 Experimental and molecular medicine Vol.54 No.-

The functional role of microRNA-375 (miR-375) in the development of prostate cancer (PCa) remains controversial. Previously, we found that plasma exosomal miR-375 is significantly elevated in castration-resistant PCa (CRPC) patients compared with castration-sensitive PCa patients. Here, we aimed to determine how miR-375 modulates CRPC progression and thereafter to evaluate the therapeutic potential of human umbilical cord mesenchymal stem cell (hucMSC)-derived exosomes loaded with miR-375 antisense oligonucleotides (e-375i). We used miRNA in situ hybridization technique to evaluate miR-375 expression in PCa tissues, gain- and loss-of-function experiments to determine miR-375 function, and bioinformatic methods, dual-luciferase reporter assay, qPCR, IHC and western blotting to determine and validate the target as well as the effects of miR-375 at the molecular level. Then, e-375i complexes were assessed for their antagonizing effects against miR-375. We found that the expression of miR-375 was elevated in PCa tissues and cancer exosomes, correlating with the Gleason score. Forced expression of miR-375 enhanced the expression of EMT markers and AR but suppressed apoptosis markers, leading to enhanced proliferation, migration, invasion, and enzalutamide resistance and decreased apoptosis of PCa cells. These effects could be reversed by miR-375 silencing. Mechanistically, miR-375 directly interfered with the expression of phosphatase nonreceptor type 4 (PTPN4), which in turn stabilized phosphorylated STAT3. Application of e-375i could inhibit miR-375, upregulate PTPN4 and downregulate p-STAT3, eventually repressing the growth of PCa. Collectively, we identified a novel miR-375 target, PTPN4, that functions upstream of STAT3, and targeting miR-375 may be an alternative therapeutic for PCa, especially for CRPC with high AR levels.