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      • KCI등재

        Preparation and Characterization of Disorderly PCL Crystal Lamellae Electrostatic Direct Writing Scaffolds with Polydopamine Coating

        Jiaqi Zeng,Wenchao Li,Min Lei,Chunfa Dong,Kui Zhou 한국섬유공학회 2023 Fibers and polymers Vol.24 No.10

        Polycaprolactone (PCL) exhibits limited applicability in the application of biological tissue engineering scaffolds due to its lower surface hydrophilicity and surface energy. In this paper, PCL crystal lamellae scaffolds with different surface roughness were fabricated by immersing electrostatic direct-written PCL scaffolds in PCL/Amyl acetate (AC) solution for 15 , 30 , 60 and 120 min, respectively, using solution incubation for crystallization. The rough scaffolds were subsequently coated with polydopamine (PDA) for 4 h, 8 h, 12 h and 16 h. Surface morphology, chemical properties and water contact angle tests were performed on both types of scaffolds. To evaluate the feasibility of the modified scaffold as a bionic scaffold, L929 mouse fibroblasts were inoculated on the surface of the scaffold and cultured for 1, 3 and 7 days. When compared to the untreated scaffolds, the surface of the scaffolds treated for 15 , 30 , 60 , and 120 min, respectively exhibited a distinct PCL crystal lamellae structure, accompanied by a significant increase in surface roughness and corresponding water contact angle elevation. In the cell experiments, the 30 min treatment group demonstrated superior cellular activity compared to the other experimental groups. The water contact angle of the PDA-modified scaffolds decreased over time with extended treatment durations, ultimately reaching 0°. In the cell experiments, the 8 h treatment scaffolds exhibited a more pronounced improvement in activity compared to the other groups. Based on these results, it can be concluded that the PDA-modified PCL crystal lamellae electrostatic direct-write scaffold promotes cell proliferation and differentiation, thereby facilitating tissue regeneration.

      • Sensitization of Cervical Carcinoma Cells to Paclitaxel by an IPP5 Active Mutant

        Zeng, Qi-Yan,Huang, Yu,Zeng, Lin-Jie,Huang, Min,Huang, Yong-Qi,Zhu, Qi-Fang Asian Pacific Journal of Cancer Prevention 2014 Asian Pacific journal of cancer prevention Vol.15 No.19

        Paclitaxel is one of the best anticancer agents that has been isolated from plants, but its major disadvantage is its dose-limiting toxicity. In this study, we obtained evidence that the active mutant IPP5 ($8-60hIPP5^m$), the latest member of the inhibitory molecules for protein phosphatase 1, sensitizes human cervix carcinoma cells HeLa more efficiently to the therapeutic effects of paclitaxel. The combination of $8-60hIPP5^m$ with paclitaxel augmented anticancer effects as compared to paclitaxel alone as evidenced by reduced DNA synthesis and increased cytotoxicity in HeLa cells. Furthermore, our results revealed that $8-60hIPP5^m$ enhances paclitaxel-induced G2/M arrest and apoptosis, and augments paclitaxel-induced activation of caspases and release of cytochrome C. Evaluation of signaling pathways indicated that this synergism was in part related to downregulation of NF-${\kappa}B$ activation and serine/threonine kinase Akt pathways. We noted that $8-60hIPP5^m$ downregulated the paclitaxel-induced NF-${\kappa}B$ activation, $I{\kappa}B{\alpha}$ degradation, PI3-K activity and phosphorylation of the serine/threonine kinase Akt, a survival signal which in many instances is regulated by NF-${\kappa}B$. Together, our observations indicate that paclitaxel in combination with $8-60hIPP5^m$ may provide a therapeutic advantage for the treatment of human cervical carcinoma.

      • KCI등재
      • SCOPUSKCI등재
      • KCI등재

        Power Efficient Classification Method for Sensor Nodes in BSN Based ECG Monitoring System

        Min Zeng,Jeong-A Lee 한국통신학회 2010 韓國通信學會論文誌 Vol.35 No.9b

        As body sensor network (BSN) research becomes mature, the need for managing power consumption of sensor nodes has become evident since most of the applications are designed for continuous monitoring. Real time Electrocardiograph (ECG) analysis on sensor nodes is proposed as an optimal choice for saving power consumption by reducing data transmission overhead. Smart sensor nodes with the ability to categorize lately detected ECG cycles communicate with base station only when ECG cycles are classified as abnormal. In this paper, ECG classification algorithms are described, which categorize detected ECG cycles as normal or abnormal, or even more specific cardiac diseases. Our Euclidean distance (ED) based classification method is validated to be most power efficient and very accurate in determining normal or abnormal ECG cycles. A close comparison of power efficiency and classification accuracy between our ED classification algorithm and generalized linear model (GLM) based classification algorithm is provided. Through experiments we show that, CPU cycle power consumption of ED based classification algorithm can be reduced by 31.21% and overall power consumption can be reduced by 13.63% at most when compared with GLM based method. The accuracy of detecting NSR, APC, PVC, SVT, VT, and VF using GLM based method range from 55% to 99% meanwhile, we show that the accuracy of detecting normal and abnormal ECG cycles using our ED based method is higher than 86%.

      • SCIESCOPUSKCI등재

        LncRNA PART1 Attenuates Myocardial Ischemia-Reperfusion Injury by Regulating TFAP2C/DUSP5 Axis via miR-302a-3p

        Min Zeng,Xin Wei,Jinchao Zhou,Siqi Luo The Korean Society of Cardiology 2024 Korean Circulation Journal Vol.54 No.2

        Background and Objectives: Myocardial ischemia-reperfusion injury (MIRI) refers to the damage of cardiac function caused by restoration of blood flow perfusion in ischemic myocardium. However, long non-coding RNA prostate androgen regulated transcript 1 (PART1)'s role in MIRI remain unclear. Methods: Immunofluorescence detected LC3 expression. Intermolecular relationships were verified by dual luciferase reporter assay. 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide, flow cytometry and transferase-mediated dUTP nick-end labeling (TUNEL) assays analyzed cell viability and apoptosis. The release of lactate dehydrogenase was tested via enzyme-linked immunosorbent assay (ELISA). Left anterior descending coronary artery surgery induced a MIRI mouse model. Infarct area was detected by 2,3,5-triphenyltetrazolium chloride staining. Hematoxylin and eosin staining examined myocardial injury. ELISA evaluated myocardial marker (creatine kinase MB) level. Results: PART1 was decreased in hypoxia/reoxygenation (H/R) induced AC16 cells and MIRI mice. PART1 upregulation attenuated the increased levels of Bax, beclin-1 and the ratio of LC3II/I, and enhanced the decrease of Bcl-2 and p62 expression in H/R-treated cells. PART1 upregulation alleviated H/R-triggered autophagy and apoptosis via miR-302a-3p. Mechanically, PART1 targeted miR-302a-3p to upregulate transcription factor activating enhancer-binding protein 2C (TFAP2C). TFAP2C silencing reversed the protected effects of miR-302a-3p inhibitor on H/R treated AC16 cells. We further established TFAP2C combined to dual-specificity phosphatase 5 (DUSP5) promoter and activated DUSP5. TFAP2C upregulation suppressed H/R-stimulated autophagy and apoptosis through upregulating DUSP5. Overexpressed PART1 reduced myocardial infarction area and attenuated MIRI in mice. Conclusion: PART1 improved the autophagy and apoptosis in H/R-exposed AC16 cells through miR-302a-3p/TFAP2C/DUSP5 axis, which might provide novel targets for MIRI treatment.

      • KCI등재
      • SCIEKCI등재

        Differential Gene Expression Profiles in Human THP-1 Monocytes Treated with Lactobacillus plantarum or Staphylococcus aureus Lipoteichoic Acid

        Zeng, Ri-Zhong,Kim, Han-Geun,Kim, Na-Ra,Gim, Min-Geun,Ko, Mi-Yeon,Lee, Seung-Yeon,Kim, Chul-Min,Chung, Dae-Kyun The Korean Society for Applied Biological Chemistr 2011 Applied Biological Chemistry (Appl Biol Chem) Vol.54 No.5

        The lipoteichoic acid (LTA) of Staphylococcus aureus (aLTA) and Lactobacillus plantarum (pLTA) engage the same toll-like receptor 2 (TLR2) signaling pathway but exert different effects on innate immunity and inflammation. The mechanisms underlying these differential effects are not yet clear. Human oligonucleotide microarrays were used to investigate the transcriptome of human THP-1 monocytes upon exposure to aLTA or pLTA, and differential gene expression profiles were observed between the aLTA- and pLTA-treated cells. The expression level of 1,302 genes in aLTA-treated cells increased more than 2-fold; some of which have been implicated in immune or inflammatory responses, cell adhesion, cell signal transduction, transcription factors, anion transport, proteolysis, and oxidative processes. Particularly, a variety of genes that encode cytokines and chemokines, and TLR signaling-related molecules belonging to the tumor necrosis factor receptor-associated factor (TRAF), nuclear factor-kappa B, and signal transducer and activator of transcription families were remarkably up-regulated by aLTA stimulation. In contrast, pLTA treatment altered the expression of only 90 genes by more than 1.5-fold, and these genes were not correlated with innate immunity, inflammation or other related processes. The different effects mediated by aLTA and pLTA were further verified and compared by analysis of the expression of a selected group of genes, including TRAFs and some cytokines and chemokines, using real time-polymerase chain reaction and ELISA. These data suggest that aLTA and pLTA have different immunomodulatory potentials. Compared with pLTA, aLTA is a stronger stimulator and impacts the expression of many innate immunity- and/or inflammation-related genes.

      • SCISCIESCOPUS

        Native Store-operated Ca2+ Influx Requires the Channel Function of Orai1 and TRPC1.

        Kim, Min Seuk,Zeng, Weizhong,Yuan, Joseph P,Shin, Dong Min,Worley, Paul F,Muallem, Shmuel American Society for Biochemistry and Molecular Bi 2009 The Journal of biological chemistry Vol.284 No.15

        <P>With the discovery of STIM1 and Orai1 and gating of both TRPC and Orai1 channels by STIM1, a central question is the role of each of the channels in the native store-operated Ca(2+) influx (SOCs). Here, we used a strategy of knockdown of Orai1 and of TRPC1 alone and in combination and rescue by small interfering RNA-protected mutants (sm) of smOrai1 and smTRPC1 to demonstrate that in human embryonic kidney (HEK) cells, rescue of SOCs required co-transfection of low levels of both smOrai1 and smTRPC1. The pore mutant Orai1(E106Q) failed to rescue the SOCs in the presence or absence of TRPC1 and, surprisingly, the pore mutant TRPC1(F562A) failed to rescue the SOCs in the presence or absence of Orai1. TRPC1 is gated by electrostatic interaction between TRPC1(D639D,D640D) with STIM1(K684K, K685K). Strikingly, the channel-dead TRPC1(D639K,D640K) that can be rescued only by the STIM1(K684E,K685E) mutant could restore SOCs only when expressed with Orai1 and STIM1(K684E,K685E). Accordingly, we found a mutual requirement of Orai1 and TRPC1 for their interaction with the native STIM1 in HEK cells. By contrast, SOC and the CRAC current in Jurkat cells were inhibited by knockdown of Orai1 but were not influenced by knockdown on TRPC1 or TRPC3. These findings define the molecular makeup of the native SOCs in HEK cells and the role of a STIM1-Orai1-TRPC1 complex in SOC activity.</P>

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