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Jinlong Hong,Liang Lu,Bingzhao Gao,Lin Zhang,Hong Chen 한국자동차공학회 2021 International journal of automotive technology Vol.22 No.2
For the torque decoupled hybrid electric vehicles (HEVs) equipped with automated manual transmission (AMT), the motor torque can be used to compensate for traction loss during gear shift. Thus, engine speed regulation can be used to achieve speed synchronization, and the clutch can be removed, which simplifies the overall structure of AMT. A triple-step nonlinear method is proposed in this paper to improve the engine speed tracking accuracy, which utilizes the steady-state, reference trajectory dynamics, and the tracking error information comprehensively. By the expense of the intake manifold pressure tracking performance, the developed controller can guarantee the asymptotic convergence of the engine speed tracking error. After the triple-step controller is deduced, it is verified through co-simulation between AMT HEV plant model in AMESim and controller model in Simulink. The simulation results demonstrate that the proposed controller can exert the advantages of the two control inputs: throttle opening α and spark advance deviation Δθ, and certificate the overall gear shift quality, including shift time and vehicle jerk.
Numerical investigation of the large over-reading of Venturi flow rate in ARE of nuclear power plant
Wang, Hong,Zhu, Zhimao,Zhang, Miao,Han, Jinlong Korean Nuclear Society 2021 Nuclear Engineering and Technology Vol.53 No.1
Venturi meter is frequently used in feed water flow control system in a nuclear power plant. Its accurate measurement plays a vital role in the safe operation of the plant. This paper firstly investigates the influence of the length of each section of pipeline, the throat inner diameter of Venturi and the flow characteristics in a single-phase flow on the accuracy of Venturi measurement by numerical calculation. Then the flow and the accuracy are discussed in a multi-phase flow. Numerical results show that the geometrical parameters and the characteristics of complex turbulent flow in the single-phase flow have little impact on the accuracy of Venturi flow rate measurement. In the multi-phase flow, the calculated flow rate of Venturi deviated from the actual flow rate and this deviation value is closely related to the amount of steam in the pipeline and increases sharply with the increase of the amount of steam. The over-reading of Venturi flow rate is present.
Yin, Jinlong,Oh, Young Taek,Kim, Jeong-Yub,Kim, Sung Soo,Choi, Eunji,Kim, Tae Hoon,Hong, Jun Hee,Chang, Nakho,Cho, Hee Jin,Sa, Jason K.,Kim, Jeong Cheol,Kwon, Hyung Joon,Park, Saewhan,Lin, Weiwei,Naka American Association for Cancer Research 2017 Cancer research Vol.77 No.18
<P>Inhibition of a cellular enzyme that blocks the conversion from nonmesenchymal to mesenchymal forms of glioblastoma may prevent recurrence and resistance to radiation therapy, the latter of which continues to pose a major clinical challenge.</P><P>Necrosis is a hallmark of glioblastoma (GBM) and is responsible for poor prognosis and resistance to conventional therapies. However, the molecular mechanisms underlying necrotic microenvironment-induced malignancy of GBM have not been elucidated. Here, we report that transglutaminase 2 (TGM2) is upregulated in the perinecrotic region of GBM and triggered mesenchymal (MES) transdifferentiation of glioma stem cells (GSC) by regulating master transcription factors (TF), such as C/EBPβ, TAZ, and STAT3. TGM2 expression was induced by macrophages/microglia-derived cytokines via NF-κB activation and further degraded DNA damage–inducible transcript 3 (GADD153) to induce C/EBPβ expression, resulting in expression of the MES transcriptome. Downregulation of TGM2 decreased sphere-forming ability, tumor size, and radioresistance and survival in a xenograft mouse model through a loss of the MES signature. A TGM2-specific inhibitor GK921 blocked MES transdifferentiation and showed significant therapeutic efficacy in mouse models of GSC. Moreover, TGM2 expression was significantly increased in recurrent MES patients and inversely correlated with patient prognosis. Collectively, our results indicate that TGM2 is a key molecular switch of necrosis-induced MES transdifferentiation and an important therapeutic target for MES GBM. <I>Cancer Res; 77(18); 4973–84. ©2017 AACR</I>.</P>
Yin, Jinlong,Park, Gunwoo,Kim, Tae Hoon,Hong, Jun Hee,Kim, Youn-Jae,Jin, Xiong,Kang, Sangjo,Jung, Ji-Eun,Kim, Jeong-Yub,Yun, Hyeongsun,Lee, Jeong Eun,Kim, Minkyung,Chung, Junho,Kim, Hyunggee,Nakano, I Public Library of Science 2015 PLoS biology Vol.13 No.5
<▼1><P>Epidermal growth factor receptor variant III (EGFRvIII) has been associated with glioma stemness, but the direct molecular mechanism linking the two is largely unknown. Here, we show that EGFRvIII induces the expression and secretion of pigment epithelium-derived factor (PEDF) via activation of signal transducer and activator of transcription 3 (STAT3), thereby promoting self-renewal and tumor progression of glioma stem cells (GSCs). Mechanistically, PEDF sustained GSC self-renewal by Notch1 cleavage, and the generated intracellular domain of Notch1 (NICD) induced the expression of Sox2 through interaction with its promoter region. Furthermore, a subpopulation with high levels of PEDF was capable of infiltration along corpus callosum. Inhibition of PEDF diminished GSC self-renewal and increased survival of orthotopic tumor-bearing mice. Together, these data indicate the novel role of PEDF as a key regulator of GSC and suggest clinical implications.</P></▼1><▼2><P>A permanently activated mutant form of the epidermal growth factor receptor found in glioblastoma promotes self-renewal and tumor progression by inducing autocrine signalling via pigment epithelium-derived factor (PEDF).</P></▼2><▼3><P><B>Author Summary</B></P><P>Malignant gliomas are among the most lethal types of cancer, due in part to the stem-cell-like characteristics and invasive properties of the brain tumor cells. However, little is known about the underlying molecular mechanisms that govern such processes. Here, we identify pigment epithelium-derived factor (PEDF) as a critical factor controlling stemness and tumor progression in glioma stem cells. We found that PEDF is secreted from glioblastoma expressing EGFRvIII, a frequently occurring mutation in primary glioblastoma that yields a permanently activated epidermal growth factor receptor. We delineate an EGFRvIII-STAT3-PEDF signaling axis as a signature profile of highly malignant gliomas, which promotes self-renewal of glioma stem cells. Our results demonstrate a previously unprecedented function of PEDF and implicate potential therapeutic approaches against malignant gliomas.</P></▼3>
DEAD-box RNA helicase DDX23 modulates glioma malignancy via elevating miR-21 biogenesis
Yin, Jinlong,Park, Gunwoo,Lee, Jeong Eun,Choi, Eun Young,Park, Ju Young,Kim, Tae-Hoon,Park, Nayun,Jin, Xiong,Jung, Ji-Eun,Shin, Daye,Hong, Jun Hee,Kim, Hyunggee,Yoo, Heon,Lee, Seung-Hoon,Kim, Youn-Jae Oxford University Press 2015 Brain Vol.138 No.9
<P>Upregulation of microRNA-21 (miR-21) is strongly associated with glioma malignancy, but the regulatory mechanism that governs miR-21 biogenesis is unclear. Yin <I>et al.</I> demonstrate that the DEAD-box RNA helicase DDX23 promotes miR-21 biogenesis at the post-transcriptional level in glioma cells, and that DDX23 inhibition reduces glioma growth in mouse xenografts.</P><P> [Figure] </P><P>Upregulation of microRNA-21 (miR-21) is known to be strongly associated with the proliferation, invasion, and radio-resistance of glioma cells. However, the regulatory mechanism that governs the biogenesis of miR-21 in glioma is still unclear. Here, we demonstrate that the DEAD-box RNA helicase, DDX23, promotes miR-21 biogenesis at the post-transcriptional level. The expression of DDX23 was enhanced in glioma tissues compared to normal brain, and expression level of DDX23 was highly associated with poor survival of glioma patients. Specific knockdown of DDX23 expression suppressed glioma cell proliferation and invasion <I>in vitro</I> and <I>in vivo</I>, which is similar to the function of miR-21. We found that DDX23 increased the level of miR-21 by promoting primary-to-precursor processing of miR-21 through an interaction with the Drosha microprocessor. Mutagenesis experiments critically demonstrated that the helicase activity of DDX23 was essential for the processing (cropping) of miR-21, and we further found that ivermectin, a RNA helicase inhibitor, decreased miR-21 levels by potentially inhibiting DDX23 activity and blocked invasion and cell proliferation. Moreover, treatment of ivermectin decreased glioma growth in mouse xenografts. Taken together, these results suggest that DDX23 plays an essential role in glioma progression, and might thus be a potential novel target for the therapeutic treatment of glioma.</P>
Ze Luo,Jinlong Li,Guozhe Sui,Yan Zhuang,Dongxuan Guo,Rongping Xu,Shuang Liang,Hong Yao,Chao Wang,Shijie Chen 한국화학공학회 2022 Korean Journal of Chemical Engineering Vol.39 No.8
Developing an efficient, environmentally friendly, and pollution-free catalyst with excellent visible light catalyticactivity is a promising strategy for dye wastewater treatment. Herein, the rod-like hollow BiOClxBr1x (x=1, 0.75, 0.5,0.25, 0), with an adjustable band gap, was successfully prepared using Bi-based metal-organic framework as template. The corresponding hollow assembly and introduction of Br imparted valuable structural advantages and intrinsic characteristicsfor improved photocatalytic activity. Significantly, the degradation efficiency of BiOCl0.5Br0.5 for the RhodamineB (RhB) solution reached 92% under visible light illumination for 90 min, which is considerably higher than that ofCAU-17-derived Bi2O3 and BiOCl. Overall, these findings shed fundamental insight on constructing novel photocatalystswith excellent visible light driven photocatalytic activity and offered a new method for treating dye wastewater.
SNPs in the coding region of bovine MGAT2 gene are associated with body weight and weight gain
Lian Qu,Mingjuan Yang,Jinlong Zhu,Junxia Liu,Mijie Li,Liangzhi Zhang,Xianyong Lan,Chuzhao Lei,Chunlei Zhang,Hong Chen 한국유전학회 2011 Genes & Genomics Vol.33 No.3
Monoacylglycerol acyltransferase 2 (MGAT2), as a candidate gene for quantitative traits, relates to dietary fat uptake, lipids synthesis and storage, which plays a major role in the absorption of dietary fat by catalyzing the resynthesis of triacylglycerol in enterocytes. In this study, based on DNA pool sequencing and PCR‐RFLP methods, polymorphisms of the MGAT2 gene were detected in 1145 Chinese indigenous cattle. The results revealed two novel mutations located on exon 1and exon 5 (NM_001099136.1:m.84G>T and 756A>G). Hence, we described the HaeIII forced PCR–RFLP method in exon1 and a MluI PCR–RFLP method in exon5 to detect them. In addition, the associations of these polymorphisms with growth traits were evaluated in Nanyang cattle. The results showed that only HaeIII locus was associated with body weight and average daily gain aged 6 months, and individuals with genotype TT showed significantly higher body weight and average daily gain than those with genotype GG.
Park, Hye-Kyung,Hong, Jun-Hee,Oh, Young Taek,Kim, Sung Soo,Yin, Jinlong,Lee, An-Jung,Chae, Young Chan,Kim, Jong Heon,Park, Sung-Hye,Park, Chul-Kee,Park, Myung-Jin,Park, Jong Bae,Kang, Byoung Heon American Association for Cancer Research 2019 Cancer Research Vol.79 No.7
<P>Discovery and functional analysis of a TRAP1-SIRT3 complex in glioma stem cells identify potential target proteins for glioblastoma treatment.</P><P><B></B></P><P>Glioblastoma (GBM) cancer stem cells (CSC) are primarily responsible for metastatic dissemination, resistance to therapy, and relapse of GBM, the most common and aggressive brain tumor. Development and maintenance of CSCs require orchestrated metabolic rewiring and metabolic adaptation to a changing microenvironment. Here, we show that cooperative interplay between the mitochondrial chaperone TRAP1 and the major mitochondria deacetylase sirtuin-3 (SIRT3) in glioma stem cells (GSC) increases mitochondrial respiratory capacity and reduces production of reactive oxygen species. This metabolic regulation endowed GSCs with metabolic plasticity, facilitated adaptation to stress (particularly reduced nutrient supply), and maintained “stemness.” Inactivation of TRAP1 or SIRT3 compromised their interdependent regulatory mechanisms, leading to metabolic alterations, loss of stemness, and suppression of tumor formation by GSC <I>in vivo</I>. Thus, targeting the metabolic mechanisms regulating interplay between TRAP1 and SIRT3 may provide a novel therapeutic option for intractable patients with GBM.</P><P><B>Significance:</B></P><P>Discovery and functional analysis of a TRAP1–SIRT3 complex in glioma stem cells identify potential target proteins for glioblastoma treatment.</P>