Journal articles: 'Mimic-effect'

1

Gottlieb, S. "Smoking may mimic effect of antidepressants." BMJ 323, no. 7315 (September 29, 2001): 713. http://dx.doi.org/10.1136/bmj.323.7315.713.

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Tsai, Jessica Chia-Chin, Natalie Sebanz, and Günther Knoblich. "The GROOP effect: Groups mimic group actions." Cognition 118, no. 1 (January 2011): 135–40. http://dx.doi.org/10.1016/j.cognition.2010.10.007.

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Cao, Chunhua, Eun Sook Kim, Yi-Hsin Chen, John Ferron, and Stephen Stark. "Exploring the Test of Covariate Moderation Effects in Multilevel MIMIC Models." Educational and Psychological Measurement 79, no. 3 (August 17, 2018): 512–44. http://dx.doi.org/10.1177/0013164418793490.

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In multilevel multiple-indicator multiple-cause (MIMIC) models, covariates can interact at the within level, at the between level, or across levels. This study examines the performance of multilevel MIMIC models in estimating and detecting the interaction effect of two covariates through a simulation and provides an empirical demonstration of modeling the interaction in multilevel MIMIC models. The design factors include the location of the interaction effect (i.e., between, within, or across levels), cluster number, cluster size, intraclass correlation (ICC) level, magnitude of the interaction effect, and cross-level measurement invariance status. Type I error, power, relative bias, and root mean square of error of the interaction effects are examined. The results showed that multilevel MIMIC models performed well in detecting the interaction effect at the within or across levels. However, when the interaction effect was at the between level, the performance of multilevel MIMIC models depended on the magnitude of the interaction effect, ICC, and sample size, especially cluster number. Overall, cross-level measurement noninvariance did not make a notable impact on the estimation of interaction in the structural part of multilevel MIMIC models when factor loadings were allowed to be different across levels.

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Tran, Kim Ngan, and Jong-il Choi. "Mimic microgravity effect on muscle transcriptome under ionizing radiation." Life Sciences in Space Research 32 (February 2022): 96–104. http://dx.doi.org/10.1016/j.lssr.2021.12.002.

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Toker, Lilach, Yuly Bersudsky, Inbar Plaschkes, Vered Chalifa-Caspi, Gerard T. Berry, Roberto Buccafusca, Dieder Moechars, R. H. Belmaker, and Galila Agam. "Inositol-Related Gene Knockouts Mimic Lithium’s Effect on Mitochondrial Function." Neuropsychopharmacology 39, no. 2 (August 8, 2013): 319–28. http://dx.doi.org/10.1038/npp.2013.194.

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Muszyńska-Pytel, M., P. Mikołajczyk, M. A. Pszczółkowski, and B. Cymborowski. "Juvenilizing effect of ecdysone mimic RH 5849 inGalleria mellonella larvae." Experientia 48, no. 10 (October 1992): 1013–17. http://dx.doi.org/10.1007/bf01919156.

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Azanza, Maria J. "Steady magnetic fields mimic the effect of caffeine on neurons." Brain Research 489, no. 1 (June 1989): 195–98. http://dx.doi.org/10.1016/0006-8993(89)90025-5.

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Huang, Suning, Rongquan He, Minhua Rong, Yiwu Dang, and Gang Chen. "Synergistic Effect of MiR-146a Mimic and Cetuximab on Hepatocellular Carcinoma Cells." BioMed Research International 2014 (2014): 1–15. http://dx.doi.org/10.1155/2014/384121.

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Previously, we found that the expression of microRNA-146a (miR-146a) was downregulated in hepatocellular carcinoma (HCC) formalin-fixed paraffin-embedded (FFPE) tissues compared to the adjacent noncancerous hepatic tissues. In the current study, we have explored thein vitroeffect of miR-146a on the malignant phenotypes of HCC cells. MiR-146a mimic could suppress cell growth and increase cellular apoptosis in HCC cell lines HepG2, HepB3, and SNU449, as assessed by spectrophotometry, fluorimetry, and fluorescence microscopy, respectively. Furthermore, western blot showed that miR-146a mimic downregulated EGFR, ERK1/2, and stat5 signalings. These effects were less potent compared to that of a siRNA targeting EGFR, a known target gene of miR-146a. Moreover, miR-146a mimic could enhance the cell growth inhibition and apoptosis induction impact of various EGFR targeting agents. The most potent combination was miR-146a mimic with cetuximab, presenting a synergistic effect. In conclusion, miR-146a plays a vital role in the cell growth and apoptosis of HCC cells and inducing miR-146a level might be a critical targeted molecular therapy strategy for HCC.

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Jamali, Jamshid, Seyyed Mohammad Taghi Ayatollahi, and Peyman Jafari. "The Effect of Small Sample Size on Measurement Equivalence of Psychometric Questionnaires in MIMIC Model: A Simulation Study." BioMed Research International 2017 (2017): 1–12. http://dx.doi.org/10.1155/2017/7596101.

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Evaluating measurement equivalence (also known as differential item functioning (DIF)) is an important part of the process of validating psychometric questionnaires. This study aimed at evaluating the multiple indicators multiple causes (MIMIC) model for DIF detection when latent construct distribution is nonnormal and the focal group sample size is small. In this simulation-based study, Type I error rates and power of MIMIC model for detecting uniform-DIF were investigated under different combinations of reference to focal group sample size ratio, magnitude of the uniform-DIF effect, scale length, the number of response categories, and latent trait distribution. Moderate and high skewness in the latent trait distribution led to a decrease of 0.33% and 0.47% power of MIMIC model for detecting uniform-DIF, respectively. The findings indicated that, by increasing the scale length, the number of response categories and magnitude DIF improved the power of MIMIC model, by 3.47%, 4.83%, and 20.35%, respectively; it also decreased Type I error of MIMIC approach by 2.81%, 5.66%, and 0.04%, respectively. This study revealed that power of MIMIC model was at an acceptable level when latent trait distributions were skewed. However, empirical Type I error rate was slightly greater than nominal significance level. Consequently, the MIMIC was recommended for detection of uniform-DIF when latent construct distribution is nonnormal and the focal group sample size is small.

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MATSUBARA, Teruhiko, Ai ONISHI, Tomomi SAITO, Daisuke YAMAGUCHI, and Toshinori SATO. "Multivalent Effect in Influenza Hemagglutinin-Binding Activity of Sugar-Mimic Peptide." KOBUNSHI RONBUNSHU 73, no. 1 (2016): 62–68. http://dx.doi.org/10.1295/koron.2015-0052.

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Lin, Lin, and Yong Wang. "miR-548b-3p Regulates Proliferation, Apoptosis, and Mitochondrial Function by Targeting CIP2A in Hepatocellular Carcinoma." BioMed Research International 2018 (December 23, 2018): 1–9. http://dx.doi.org/10.1155/2018/7385426.

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The roles of miR-548b-3p in the progression of hepatocellular carcinoma (HCC) remain undiscovered. This study aims to explore the roles and mechanisms of miR-548b-3p in HCC. Using TCGA database, we found that miR-548b-3p expression was lower in HCC compared to the normal tissues, which was further confirmed by RT-qPCR of 20 cases of surgically resected HCC and corresponding normal tissues. miR-548b-3p mimic and inhibitor were transfected into Huh7 and SK-Hep-1 cells, respectively. MTT, colony formation, and cell cycle assays showed that miR-548b-3p mimic suppressed cell growth and G1/S cell cycle transition. In contrast, miR-548b-3p inhibitor facilitated cell growth and cell cycle transition. miR-548b-3p mimic also increased cisplatin sensitivity by upregulating apoptosis rate. JC-1 staining showed that miR-548b-3p mimic downregulated mitochondrial membrane potential, while miR-548b-3p inhibitor showed the opposite effects in SK-Hep-1 cells. Using prediction software, we found that CIP2A was on the target list of miR-548b-3p. miR-548b-3p mimic downregulated CIP2A and its downstream target protein c-Myc. Luciferase reporter assay demonstrated that CIP2A was as a direct target of miR-548b-3p. CIP2A depletion partly reduced the effect of miR-548b-3p mimic/inhibitor on c-Myc. CIP2A depletion also reduced the effect of miR-548b-3p mimic/inhibitor on proliferation. In conclusion, our data demonstrated that miR-548b-3p was downregulated in HCC. miR-548b-3p regulates proliferation, apoptosis and mitochondrial function by targeting CIP2A in HCC.

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Lapkina, E. Z., N. V. Palkinа, A. S. Averchuk, A. R. Esimbekova, and T. G. Ruksha. "Antitumor, toxicity and target gene expression evaluation of MiR-204-5p mimic application on melanoma b16-bearing mice." Siberian journal of oncology 21, no. 3 (June 29, 2022): 61–69. http://dx.doi.org/10.21294/1814-4861-2022-21-3-61-69.

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Objective. To evaluate anti-tumor, toxic effect of miR-204-5p mimic applicaton on melanoma B-16-bearing mice followed by miR-204-5p target gene expression estimation in melanoma tumor and distant organs. Material and Methods. C57Bl/6 melanoma B-16-bearing mice were used. The animals of the experimental group were intraperitoneally injected with a 5 nM miR-204-5p miRNA simulator (mimic) on the 8th, 10th, and 12th days after melanoma B-16 cell transplantation. Based on the results of bioinformatic analysis, miR-204-5p target genes BCL2 and SIRT1 expression levels were determined by quantitative real-time PCR. The toxic effect of miR-204-5p mimic was estimated by the evaluation of body weight, mass of the internal organs, and motor activity. Results. On the 13-14th days of the experiment, the motor activity of animals in the control groups decreased signifcantly compared to the group of animals treated by miR-204-5p. Target gene BCL2 showed increased expression in the lungs and kidneys and SIRT1 levels were increased in the lungs of miR-204-5p mimic treated animals (p˂0.05). Tumor mass tended to decrease in the animals treated by miR-204-5p mimic. Conclusion. Modulation of the level of miR-204-5p microRNA led to changes in the expression of SIRT1 and BCL2 in the lungs of animals, and changes in the expression of BCL2in the kidneys. MiR-204-5p mimic application did not have toxic effect on animals treated. Further studies are necessary to clarify miR-204-5p implication in melanoma cell proliferation regulation as well as it’s biodistibution in the tumor tissue.

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Xie, H., L. Cao, L. Ye, G. Shan, and W. Song. "The miR-1906 mimic attenuates bone loss in osteoporosis by down-regulating the TLR4/MyD88/NF‐κB pathway." Physiology International 107, no. 4 (January 12, 2021): 469–78. http://dx.doi.org/10.1556/2060.2020.00042.

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AbstractIn this study, the ability of microRNA-1906 (miR-1906) to attenuate bone loss in osteoporosis was evaluated by measuring the effects of a miR-1906 mimic and inhibitor on the cellular toxicity and cell viability of MC3T3‐E1 cells. Bone marrow-derived macrophage (BMM) cells were isolated from female mice, and tartrate-resistant acid phosphatase signalling was performed in miR-1906 mimic-treated, receptor-activated nuclear factor kappa-B (NF-κB) ligand (RANKL)-induced osteoclasts. In-vivo, osteoporosis was induced by ovariectomy (OVX). Rats were treated with 500 nmol/kg of the miR-1906 mimic via intrathecal administration for 10 consecutive days following surgery. The effect of the miR-1906 mimic on bone mineral density (BMD) in OVX rats was observed in the whole body, lumbar vertebrae and femur. Levels of biochemical parameters and cytokines in the serum of miR-1906 mimic-treated OVX rats were analysed. The mRNA expression of toll-like receptor 4 (TLR4), myeloid differentiation primary response 88 (MyD88), p-38 and NF-κB in tibias of osteoporotic rats (induced by ovariectomy) was observed using quantitative reverse-transcription polymerase chain reaction. Treatment with the miR-1906 mimic reduced cellular toxicity and enhanced the cell viability of MC3T3‐E1 cells. Furthermore, osteoclastogenesis in miR-1906 mimic-treated, RANKL-induced osteoclast cells was reduced, whereas the BMD in the miR-1906 mimic-treated group was higher than in the OVX group of rats. Treatment with the miR-1906 mimic also increased levels of biochemical parameters and cytokines in the serum of ovariectomised rats. Finally, mRNA expression levels of TLR4, MyD88, p-38 and NF-κB were lower in the tibias of miR-1906 mimic-treated rats than in those of OVX rats. In conclusion, the miR-1906 mimic reduces bone loss in rats with ovariectomy-induced osteoporosis by regulating the TLR4/MyD88/NF‐κB pathway.

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Wang, Xiaochuan, Yifei Wu, Peng Du, Liangheng Xu, Yuan Chen, Jingzi Li, Xuying Pan, and Zhiqiong Wang. "Study on the Mechanism of miR-125b-5p Affecting Melanocyte Biological Behavior and Melanogenesis in Vitiligo through Regulation of MITF." Disease Markers 2022 (November 16, 2022): 1–17. http://dx.doi.org/10.1155/2022/6832680.

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Objective. The goal was to confirm the mechanism by which miR-125b-5p influences melanocyte biological behavior and melanogenesis in vitiligo by regulating MITF. Methods. oe-MITF, sh-MITF, miR-125b-5p mimic, NC-mimic, NC-inhibitor, and miR-125b-5p inhibitor were transfected into cells by cell transfection. Western blotting was used to detect the related protein expression, qRT–PCR was used to detect miR-125b-5p and MITF expression, immunohistochemistry was used to detect the MITF-positive cells in vitiligo patients tissues, and a dual-luciferase reporter system was used to detect the target of miR-125b-5p and MITF. PIG1 and PIG3V cell proliferation by the CCK-8 method, cell cycle progression and apoptosis by flow cytometry, apoptosis was detected by TUNEL, Tyr activity and melanin content were measured using Tyr and melanin content assay kits. Results. Compared with the healthy control group, the expression of miR-125b-5p in the tissues and serum of vitiligo patients was upregulated, and the expression of MITF was downregulated; compared with PIG1 cells, the expression of miR-125b-5p and MITF in the PIG3V group was consistent with the above. Compared with the NC-minic group, the cell proliferation activity of the miR-125b-5p mimic group decreased, apoptosis increased, and the expression levels of melanogenesis-related proteins Tyr, Tyrp1, Tyrp2, and DCT were downregulated. Compared with the NC-inhibitor group, the above indices in the miR-125b-5p inhibitor group were all opposite to those in the miR-125b-5p mimic group. Transfection of oe-MITF into the miR-125b-5p mimic group reversed the effect of the miR-125b-5p mimic, while transfection of sh-MITF enhanced the effect of the miR-125b-5p mimic. Conclusion. miR-125b-5p affects vitiligo melanocyte biological behavior and melanogenesis by downregulating MITF expression.

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Scheiber, H., K. Lubke, D. Grutzmacher, C. G. Diskus, and H. W. Thim. "MIMIC-compatible GaAs and InP field effect controlled transferred electron (FECTED) oscillators." IEEE Transactions on Microwave Theory and Techniques 37, no. 12 (1989): 2093–98. http://dx.doi.org/10.1109/22.44127.

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Royall, Donald R., Ram J. Bishnoi, and Raymond F. Palmer. "Serum IGF-BP2 strongly moderates age's effect on cognition: a MIMIC analysis." Neurobiology of Aging 36, no. 7 (July 2015): 2232–40. http://dx.doi.org/10.1016/j.neurobiolaging.2015.04.003.

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Sui, H., W. Wang, and L. S. Liu. "THE PROTECTIVE EFFECT OF SELENO-GLUTATHIONE PEROXIDASE MIMIC AND PZS1 AGAINST DAMAGE." Journal of Hypertension 22, Suppl. 1 (February 2004): S79. http://dx.doi.org/10.1097/00004872-200402001-00334.

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Karaman, Mustafa, Nihat Çabuk, Demet Özyurt, and Özcan Köysüren. "Self-supporting superhydrophobic thin polymer sheets that mimic the nature's petal effect." Applied Surface Science 259 (October 2012): 542–46. http://dx.doi.org/10.1016/j.apsusc.2012.07.079.

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Altieri, Nicholas, and Cheng-Ta Yang. "Parallel linear dynamic models can mimic the McGurk effect in clinical populations." Journal of Computational Neuroscience 41, no. 2 (June 7, 2016): 143–55. http://dx.doi.org/10.1007/s10827-016-0610-z.

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Zabłocka, Agnieszka, Anna Urbaniak, Marianna Kuropatwa, Joanna Zyzak, Joanna Rossowska, and Maria Janusz. "Can proline-rich polypeptide complex mimic the effect of nerve growth factor?" BioFactors 40, no. 5 (July 7, 2014): 501–12. http://dx.doi.org/10.1002/biof.1174.

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Hiraka, Kazue, Mayuko Kanehisa, Miho Tamai, Shoichiro Asayama, Shoji Nagaoka, Kenichi Oyaizu, Makoto Yuasa, and Hiroyoshi Kawakami. "Preparation of pH-sensitive liposomes retaining SOD mimic and their anticancer effect." Colloids and Surfaces B: Biointerfaces 67, no. 1 (November 2008): 54–58. http://dx.doi.org/10.1016/j.colsurfb.2008.07.014.

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BALA, Ioana Alexandra, Bogdan TRICA, Florentina GEORGESCU, Emilian GEORGESCU, Diana CONSTANTINESCU-ARUXANDEI, Sergey SHAPOSNIKOV, and Florin OANCEA. "THE EFFECT OF A STRIGOLACTONE MIMIC ON GROWTH AND COLONY MORPHOLOGY IN PHYTOPATHOGENIC FUNGI." AgroLife Scientific Journal 10, no. 1 (June 30, 2021): 36–47. http://dx.doi.org/10.17930/agl202113.

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The paper investigates the effect of a strigolactone mimic, 3-Methyl-5-(benzo[de]isoquinoline-1,3-dione-2-yloxy)-5Hfuran-2-one, bearing a naphthylamide core linked by an ether group to the furan-2-one ring, on hyphal branching and radial fungal growth of two plant pathogenic fungi, Colletotrichum acutatum CBS 112980 and Sclerotinia minor DSM 63016. Our results demonstrated that the tested mimic compound, which is easier to synthetize comparing tostrigolactone analogues, have the same effect as the synthetic analogue GR24, inducing hyphal branching stress response and inhibiting phytopathogen growth. The results are discussed considering their importance for both fundamental studies (role and receptor of SLs D-ring in plant pathogenic fungi) and practical applications - shaping plant rhizomicrobiome.

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Tang, Hao-Cheng, Yin-Yan Lai, Jing Zheng, Hong-Yan Jiang, and Geng Xu. "miR-223-3p Inhibits Antigen Endocytosis and Presentation and Promotes the Tolerogenic Potential of Dendritic Cells through Targeting Mannose Receptor Signaling and Rhob." Journal of Immunology Research 2020 (June 18, 2020): 1–17. http://dx.doi.org/10.1155/2020/1379458.

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Background. The role of miR-223-3p in dendritic cells (DCs) is unknown. This study is aimed at investigating the effect of miR-223-3p on the antigen uptake and presentation capacities of DCs and the underlying molecular mechanism. Methods. FITC-OVA antigen uptake and cell surface markers in bone marrow-derived DCs (BMDCs) were analyzed by flow cytometry. BMDCs were transfected with the miR-223-3p mimic or inhibitor. Cytokine levels were determined by ELISA. CD4+ T cell differentiation was determined by mixed lymphocyte culture assay. Results. OVA treatment significantly downregulated miR-223-3p in BMDCs. The miR-223-3p mimic significantly inhibited OVA-induced antigen uptake and surface expression of MHC-II on BMDCs (P<0.01). The miR-223-3p mimic increased TGF-β1 production in OVA-treated DCs (P<0.01). Mixed lymphocyte reaction showed that the miR-223-3p mimic significantly promoted Treg cell differentiation. In addition, the miR-223-3p mimic significantly upregulated CD103 in DCs, indicating the promotion of tolerogenic DCs. The miR-223-3p mimic downregulated Rhob protein in OVA-induced DCs. Rhob knockdown significantly suppressed the ability of FITC-OVA endocytosis (P<0.01) and surface MHC-II molecule expression (P<0.01) in BMDCs, promoting promoted Treg cell differentiation. Mannose receptor (MR) knockdown significantly upregulated miR-223-3p, downregulated Rhob protein in OVA-treated DCs, inhibited the FITC-OVA endocytosis and surface MHC-II expression in BMDCs, and promoted Treg cell differentiation (all P<0.01). Conclusion. These data suggest that miR-223-3p has an inhibitory effect on the antigen uptake and presentation capacities of BMDCs and promotes Treg cell differentiation, which is, at least partially, through targeting MR signaling and Rhob.

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Wu, Hong-Lian, Zhen-Na Chen, Hui Zhang, Xiao-Min Zhang, and Xiao-Rong Li. "miRNA-451 regulates rhesus choroid-retinal endothelial cell function and proteome profile." International Journal of Ophthalmology 15, no. 6 (June 18, 2022): 894–904. http://dx.doi.org/10.18240/ijo.2022.06.06.

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AIM: To evaluate the effect of miRNA-451 on rhesus macaque choroid-retinal endothelial (RF/6A) cell function and proteome profile. METHODS: The RF/6A cells were transfected with miRNA-451 mimic and inhibitor. The role of miRNA-451 on proliferation ability was evaluated by CCK-8 assay. Furthermore, iTRAQ quantitative proteomic analysis was applied to comprehensively illuminate the change of cellular proteins and biological function between different groups. RESULTS: In miRNA-451 overexpression group, cell proliferation of RF/6A decreased both at 24h and 48h; while in miRNA-451 inhibition group, on the contrary, RF/6A cell proliferation was increased at 48h. Based on iTRAQ quantitative proteomic analysis, 23 differentially expressed proteins (DEPs) were detected in the comparison of miRNA-451 mimic and mimic control-transfected RF/6A cells, and 30 DEPs were identified in the comparison of RF/6A cells transfected with miRNA-451 inhibitor and inhibitor control. DEPs such as GORASP2, KRT1, SLC7A2, RIC8A, DDX42, CAP1, PCBP2 might be closely related to the inhibitory effect of miRNA-451 on RF/6A cell proliferation, while PCYT1A, MGAT1, TUBB, MCU, SIL1, BID, MSH6 might account for the positive effect of miRNA-451 inhibitor on RF/6A cell growth. PTPN1, as the only protein exhibiting an opposite trend between miRNA-451 mimic and inhibitor-transfected cells, was most likely accountable for the inhibition of miRNA-451 mimic on RF/6A cell growth, and the promotion of miRNA-451 inhibitor on RF/6A cell proliferation. CONCLUSION: miRNA-451 overexpression can suppress the growth of RF/6A cells while knockdown of miRNA-451 can promote RF/6A cell viability. Among all DEPs, increased PTPN1 is most likely to account for the negative regulation of miRNA-451 on RF/6A proliferation. miRNA-451 can be a protective factor for neovascular disease of fundus via regulating choroid retinal endothelial cell function.

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Yan, Shufang, Qinyu Shang, Haipeng Zhu, Ken Chen, Xinxia Li, Hongliang Gao, Bo Liu, Mei Feng, and Lixia Gao. "Effects of hsa-miR-28-5p on Adriamycin Sensitivity in Diffuse Large B-Cell Lymphoma." Evidence-Based Complementary and Alternative Medicine 2022 (July 13, 2022): 1–14. http://dx.doi.org/10.1155/2022/4290994.

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Background. Adriamycin (doxorubicin) is an important traditional drug that exhibits cytotoxicity in Diffuse Large B-cell Lymphoma (DLBCL). Doxorubicin affects the DLBCL cells at all stages of their cell cycle. Combined with our previous results, this study discovered that the overexpression of hsa-miR-28-5p inhibited the proliferation, promoted apoptosis, and triggered cell cycle arrest at the S-phase in DLBCL cells. However, the effect of (Homo sapiens, hsa)-microRNA (miR)-28-5p on doxorubicin sensitivity in DLBCL has not been investigated. This study aims to reveal the effects of hsa-miR-28-5p on doxorubicin sensitivity at the level of DLBCL cells. Methods. To determine the optimal concentration of doxorubicin, different concentrations of doxorubicin were used to treat DLBCL cells. CCK-8 assay was used to detect the proliferation of DLBCL cells. The hsa-miR-28-5p-mimic NC and hsa-miR-28-5p mimic were transfected to doxorubicin-mediated DLBCL cells. Simultaneously, blank control groups were set up. The cells were cultured and transfected for 24 h. Next, each group was administered with different concentrations of doxorubicin and cultured again for 24 h to observe the effects of hsa-miR-28-5p on doxorubicin sensitivity at different times. The proliferation, early apoptosis, and late apoptosis in DLBCL cells were determined using soft agar colony-forming assay, mitochondrial membrane potential assay, and caspase-3 activity assay, respectively. The apoptosis and cell cycle were explored using Annexin V-PE/7-AAD and PI/RNase staining buffer, respectively. We speculated that PD-L1 might be involved in the effect of hsa-miR-28-5p on the sensitivity of adriamycin (doxorubicin) in the DLBCL cells. Hence, we performed immunohistochemistry (IHC) to determine PD-L1 expression within formalin-fixed paraffin-embedded (FFPE) samples from 52 DLBCL cases. Results. The optimal concentration of doxorubicin targeting DLBCL cells was found to be 3.028 μmol/l. The effect of doxorubicin on DLBCL cells was time- and concentration-dependent. hsa-miR-28-5p mimic + doxorubicin remarkably decreased proliferation of DLBCL. DLBCL cell apoptosis rate was the highest in hsa-miR-28-5p mimic + doxorubicin group. Apart from that, hsa-miR-28-5p mimic plus doxorubicin had the best effect in promoting DLBCL cell apoptosis. After the intervention of hsa-miR-28-5p mimic + doxorubicin on DLBCL cells, the cell cycle was arrested in the S-phase and DNA synthesis was blocked. hsa-miR-28-5p mimic + doxorubicin could regulate the cycle of DLBCL cells. As a result, overexpression of hsa-miR-28-5p combined with doxorubicin is possibly involved in the development of DLBCL by affecting the proliferation, apoptosis, and cycle of DLBCL cells. PD-L1 showed an association with the prognosis of DLBCL patients. Combining with the literature, this suggested hsa-miR-28-5p may influence DLBCL occurrence and therapeutic effect by regulating the PD-L1 level. Conclusion. The combination of hsa-miR-28-5p mimic and doxorubicin may be considered more effective in inhibiting growth, arresting the cell cycle, and promoting cell apoptosis of DLBCL cells compared to using doxorubicin alone. The effects of doxorubicin on DLBCL cells were found to be time- and concentration-dependent. The overexpression of hsa-miR-28-5p enhanced the effect of doxorubicin on DLBCL cells, which may be attributed to the regulation of PD-L1 levels.

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Blut, C., J. Wilbrandt, D. Fels, E. I. Girgel, and K. Lunau. "The ‘sparkle’ in fake eyes - the protective effect of mimic eyespots in lepidoptera." Entomologia Experimentalis et Applicata 143, no. 3 (April 17, 2012): 231–44. http://dx.doi.org/10.1111/j.1570-7458.2012.01260.x.

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Hoogerheide, David P., Philip A. Gurnev, Tatiana K. Rostovtseva, and Sergey M. Bezrukov. "Effect of a post-translational modification mimic on protein translocation through a nanopore." Nanoscale 12, no. 20 (2020): 11070–78. http://dx.doi.org/10.1039/d0nr01577f.

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Kennaway, D. J., and R. W. Moyer. "Serotonin 5-HT2c agonists mimic the effect of light pulses on circadian rhythms." Brain Research 806, no. 2 (September 1998): 257–70. http://dx.doi.org/10.1016/s0006-8993(98)00746-x.

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Tan, Chao, Bensheng Huang, Da Liu, Jing Qiu, Hui Chen, Yulong Li, and Zhan Hu. "Effect of Mimic Vegetation with Different Stiffness on Regular Wave Propagation and Turbulence." Water 11, no. 1 (January 10, 2019): 109. http://dx.doi.org/10.3390/w11010109.

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Flume experiments were performed to test four plant mimics with different stiffness to reveal the effect of plant stiffness on the wave dissipation and turbulence process. The mimics were built of silica gel rod groups, and their bending elastic modulus was measured as a proxy for stiffness. The regular wave velocity distribution, turbulence characteristics, and wave dissipation effect of different groups were studied in a flume experiment. Results show that, when a wave ran through the flexible rod groups, the velocity period changed gradually from unimodal to bimodal, and the secondary wave peak was more apparent in the more flexible mimics. The change in the turbulence intensity in the different rod groups showed that the higher the rod stiffness, the greater the turbulence intensity. With an increase in the bending elastic modulus of a rod group, the wave dissipation coefficient increased. The increase in the wave dissipation coefficient was not linearly correlated with the bending elastic modulus, but it was sensitive within a certain range of the elastic modulus.

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Shen, Yuhua, Qingfeng Zhang, Long Chen, Anjian Xie, Xiangyun Kong, and Liangbao Yang. "Effect of Escherichia coliform on the biomineralization of calcium bilirubinate in mimic systems." Colloids and Surfaces B: Biointerfaces 65, no. 1 (August 2008): 11–17. http://dx.doi.org/10.1016/j.colsurfb.2008.02.008.

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Zhang, Jingru, Bo Lian, Yan Shang, Chun Li, and Qingkai Meng. "miR-135a Protects Dextran Sodium Sulfate-Induced Inflammation in Human Colorectal Cell Lines by Activating STAT3 Signal." Cellular Physiology and Biochemistry 51, no. 3 (2018): 1001–12. http://dx.doi.org/10.1159/000495481.

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Background/Aims: miR-135a is reduced in several cancers and has been suggested to mediate immune and inflammatory responses. However, the effect of miR-135a on inflammatory bowel diseases was obscure. This study firstly attempted to investigate the hypothesis that miR-135a alleviates dextran sodium sulfate (DSS)-induced inflammation in colonic cells and potential mechanisms are also studied. Methods: Caco-2 and HT-29 cells in this study were treated with DSS, miR-135a mimic, and S3I-201, and then CKK-8 assay was used to test cell viability. Expressions of miR-135a, cytokines, and signal transducers and activators of transcription factors (STATs) were determined by RT-PCR. Also, cytokine productions were further tested by using ELISA kits. Activation or inactivation of STAT3 signal was validated by western blotting analysis. Results: The results showed that DSS markedly downregulated miR-135a expression (P< 0.05) and induced inflammatory response in Caco-2 and HT-29 cells evidenced by the up regulations and productions of interleukin-1β (IL-1β) and tumor necrosis factor-ɑ (TNF-ɑ) (P< 0.05). Transfection with miR-135a mimic significantly alleviated DSS-induced upregulation and productions of IL-1β and TNF-ɑ in Caco-2 and HT-29 cells (P< 0.05). STATs were analyzed and miR-135a mimic treatment reversed STAT3 downregulation in DSS-challenged Caco-2 and HT-29 cells compared with the mimic control (P< 0.05). Also, STAT3 phosphorylation was inhibited in DSS-challenged Caco-2 cells and miR-135a mimic activated STAT3 signal (P< 0.05). S3I-201, an inhibitor of STAT3 signal, further used to inactivate STAT3 signal and the results showed that S3I-201 blocked the anti-inflammatory effect of miR-135a mimic on Caco-2 and HT-29 cells evidenced by the lowered expressions and productions of proinflammatory cytokines ((IL-1β and TNF-ɑ) (P< 0.05). Conclusion: Our results indicated that miR-135a alleviated DSS-induced inflammation and activated STAT3 signal in colonic cells. Inhibition of STAT3 reversed the anti-inflammatory function of miR-135a by regulating proinflammatory cytokines. Thus, STAT3 signal might serve, at least in part, as the potential mechanism of miR-135a-mediated anti-inflammatory effect in colonic cells.

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Li, Leilei, Kaixuan Liang, Zhentao Hua, Min Zou, Kezheng Chen, and Wei Wang. "A green route to water-soluble polyaniline for photothermal therapy catalyzed by iron phosphates peroxidase mimic." Polymer Chemistry 6, no. 12 (2015): 2290–96. http://dx.doi.org/10.1039/c4py01716a.

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Bansal, Ruby, and R. Thomas Zoeller. "Polychlorinated Biphenyls (Aroclor 1254) Do Not Uniformly Produce Agonist Actions on Thyroid Hormone Responses in the Developing Rat Brain." Endocrinology 149, no. 8 (April 17, 2008): 4001–8. http://dx.doi.org/10.1210/en.2007-1774.

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Thyroid hormone (TH) is essential for normal brain development, and polychlorinated biphenyls (PCBs) are known to interfere with TH action in the developing brain. Thus, it is possible that the observed neurotoxic effects of PCB exposure in experimental animals and humans are mediated in part by their ability to interfere with TH signaling. PCBs may interfere with TH signaling by reducing circulating levels of TH, acting as TH receptor analogs, or both. If PCBs act primarily by reducing serum TH levels, then their effects should mimic those of low TH. In contrast, if PCBs act primarily as TH agonists in the developing brain, then they should mimic the effect of T4 in hypothyroid animals. We used a two-factor design to test these predictions. Both hypothyroidism (Htx) and/or PCB treatment reduced serum free and total T4 on postnatal d 15. However, only Htx increased pituitary TSHβ expression. RC3/neurogranin expression was decreased by Htx and increased by PCB treatment. In contrast, Purkinje cell protein-2 expression was reduced in hypothyroid animals and restored by PCB treatment. Finally, PCB treatment partially ameliorated the effect of Htx on the thickness of the external granule layer of the cerebellum. These studies demonstrate clearly that PCB exposure does not mimic the effect of low TH on several important TH-sensitive measures in the developing brain. However, neither did PCBs mimic T4 in hypothyroid animals on all end points measured. Thus, PCBs exert a complex action on TH signaling in the developing brain.

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Uysal, Nermin Kibrislioglu, and Kubra Atalay Kabasakal. "The Effect of Background Variables on Gender DIF." European Journal of Multidisciplinary Studies 5, no. 1 (May 19, 2017): 490. http://dx.doi.org/10.26417/ejms.v5i1.p490-490.

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The purpose of this study is to investigate the presence of differential item functioning (DIF) between gender groups in PISA 2015 science items in nine selected countries. Moreover, the effect of socioeconomic status, reading ability, science self-efficacy and science motivation on the presence of gender-related DIF are examined, respectively. One cluster from computer-based assessment (CBA) is taken into consideration. The countries are selected among the ones that implemented CBA, on the basis of their rank in science achievement. Multiple Indicator Multiple Causes method (MIMIC) is used in our analysis. DIF analysis in the MIMIC involves fit comparisons of both full and reduced models to determine if the items can measure the latent trait equally among the specified groups. The MIMIC analysis is conducted in two steps. First, the items is being tested for showing DIF among gender groups. Then the socioeconomic status, the reading ability, the science self-efficacy and the motivation are added to the model to test gender-related DIF items and their effects, respectively. According to results of the study, gender-related DIF appeared in all of the selected countries vary between two and six items. In four of the countries none of the selected variables significantly affect the presence of gender-related DIF. Instead, in the remaining countries the number of gender-related DIF items is reduced by adding different combinations of the selected variables to the model. The effect of variables which reduce the number of gender-related DIF items will discussed within each country.

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He, Lijie, Jing Wang, Dandan Chang, Dandan Lv, Haina Li, and Heqiang Feng. "Effect of miRNA-200b on the proliferation and apoptosis of cervical cancer cells by targeting RhoA." Open Medicine 15, no. 1 (October 8, 2020): 1019–27. http://dx.doi.org/10.1515/med-2020-0147.

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AbstractObjectiveThis article aims to investigate the effect of miRNA-200b on the proliferation and apoptosis of cervical cancer cells by targeting RhoA.MethodsHeLa cells of cervical cancer were divided into five groups: blank control group, negative control group (miRNA-200b mimic NC), miRNA-200b mimic group, RhoA-negative control group, and RhoA overexpression group. Cells were collected 48 h after transfection. The expression levels of miRNA-200b were detected by RT-PCR. Target relationship between miRNA-200b and RhoA was verified by the dual-luciferase reporter assay. RhoA mRNA and protein expression were detected by western blot and RT-PCR methods. Flow cytometry was used to detect the apoptosis of cells in each group, and the CCK8 method was used to detect the proliferation of cells in each group. The mRNA and protein expression of Bax and cyclin D1 were detected by RT-PCR and western blot.ResultsThe results of the dual luciferase reporter assay showed that RhoA was the target gene of microRNA 200b. Compared with the blank control group and the miRNA-200b mimic-NC group, the proportion of apoptotic cells increased significantly in the miRNA-200b mimic group, and the proliferation of cells was inhibited (P < 0.05). After overexpression of RhoA, the percentage of apoptotic cells decreased and the ability of cell proliferation increased significantly (P < 0.05).ConclusionmiRNA-200b can inhibit the proliferation and promote the apoptosis of cervical cancer cells by targeting the RhoA gene.

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Iserbyt, Arne, Jessica Bots, Stefan Van Dongen, Janice J. Ting, Hans Van Gossum, and Thomas N. Sherratt. "Frequency-dependent variation in mimetic fidelity in an intraspecific mimicry system." Proceedings of the Royal Society B: Biological Sciences 278, no. 1721 (March 2, 2011): 3116–22. http://dx.doi.org/10.1098/rspb.2011.0126.

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Contemporary theory predicts that the degree of mimetic similarity of mimics towards their model should increase as the mimic/model ratio increases. Thus, when the mimic/model ratio is high, then the mimic has to resemble the model very closely to still gain protection from the signal receiver. To date, empirical evidence of this effect is limited to a single example where mimicry occurs between species. Here, for the first time, we test whether mimetic fidelity varies with mimic/model ratios in an intraspecific mimicry system, in which signal receivers are the same species as the mimics and models. To this end, we studied a polymorphic damselfly with a single male phenotype and two female morphs, in which one morph resembles the male phenotype while the other does not. Phenotypic similarity of males to both female morphs was quantified using morphometric data for multiple populations with varying mimic/model ratios repeated over a 3 year period. Our results demonstrate that male-like females were overall closer in size to males than the other female morph. Furthermore, the extent of morphological similarity between male-like females and males, measured as Mahalanobis distances, was frequency-dependent in the direction predicted. Hence, this study provides direct quantitative support for the prediction that the mimetic similarity of mimics to their models increases as the mimic/model ratio increases. We suggest that the phenomenon may be widespread in a range of mimicry systems.

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Sonnay, Marjorie, and Felix Zelder. "Stabilizing intramolecular cobalt–imidazole coordination with a remote methyl group in the backbone of a cofactor B12–protein model." Dalton Transactions 47, no. 31 (2018): 10443–46. http://dx.doi.org/10.1039/c8dt01298a.

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Zheng, Wen, Xia Jin, and Bo Zhang. "The Simulation Study Based on Multi-Agents of Mobile Market." Advanced Materials Research 143-144 (October 2010): 433–38. http://dx.doi.org/10.4028/www.scientific.net/amr.143-144.433.

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The holistic simulation study is based on multi-agents to stimulate the behavior of mobile communication. The paper intents to understand the effect of the regulation on the market of mobile communication on the methodology of complex adaptive system simulation in swarm platform. The simulation was on the condition of mimic surrounding. The simulation program includes four classes of Swarm objectives. Results reveal that reasonable, ordered and co-coordinated communication market is on the state of the regulatory of duopoly. Based on the multiple agents modeling on the platform of swarm software, we engendered an artificial mimic mobile market to imitate the mobile telecommunication market. The effect of regulatory rules can be adjusted as the time going by. The best effect appeared at the middle stage of the policy in practice.

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Zhang, Feifei, Feng Tang, Xiaolun Xu, Pierre-Michel Adam, Jérôme Martin, and Jérôme Plain. "Influence of order-to-disorder transitions on the optical properties of the aluminum plasmonic metasurface." Nanoscale 12, no. 45 (2020): 23173–82. http://dx.doi.org/10.1039/d0nr06334g.

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Jin, Ying, Nicholas D. Myers, Soyeon Ahn, and Randall D. Penfield. "A Comparison of Uniform DIF Effect Size Estimators Under the MIMIC and Rasch Models." Educational and Psychological Measurement 73, no. 2 (October 22, 2012): 339–58. http://dx.doi.org/10.1177/0013164412462705.

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Kimura, Tatsuya, Hiroshi Kaburaki, Tomomi Tsujino, Yoshitaka Ikeda, Hideo Kato, and Yoshinari Watanabe. "A non-peptide compound which can mimic the effect of thrombopoietin via c-Mpl." FEBS Letters 428, no. 3 (May 29, 1998): 250–54. http://dx.doi.org/10.1016/s0014-5793(98)00536-5.

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Huang, Suning, Rongquan He, Minhua Rong, Yiwu Dang, and Gang Chen. "Corrigendum to “Synergistic Effect of MiR-146a Mimic and Cetuximab on Hepatocellular Carcinoma Cells”." BioMed Research International 2020 (December 13, 2020): 1–2. http://dx.doi.org/10.1155/2020/9375214.

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Ishitsuka, Yuji, Lachelle Arnt, Jaroslaw Majewski, Shelli Frey, Maria Ratajczek, Kristian Kjaer, Gregory N. Tew, and Ka Yee C. Lee. "Amphiphilic Poly(phenyleneethynylene)s Can Mimic Antimicrobial Peptide Membrane Disordering Effect by Membrane Insertion." Journal of the American Chemical Society 128, no. 40 (October 2006): 13123–29. http://dx.doi.org/10.1021/ja061186q.

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Rehfeld, A., D. L. Egeberg, K. Almstrup, J. H. Petersen, S. Dissing, and N. E. Skakkebæk. "EDC IMPACT: Chemical UV filters can affect human sperm function in a progesterone-like manner." Endocrine Connections 7, no. 1 (January 2018): 16–25. http://dx.doi.org/10.1530/ec-17-0156.

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Human sperm cell function must be precisely regulated to achieve natural fertilization. Progesterone released by the cumulus cells surrounding the egg induces a Ca2+ influx into human sperm cells via the CatSper Ca2+-channel and thereby controls sperm function. Multiple chemical UV filters have been shown to induce a Ca2+ influx through CatSper, thus mimicking the effect of progesterone on Ca2+ signaling. We hypothesized that these UV filters could also mimic the effect of progesterone on sperm function. We examined 29 UV filters allowed in sunscreens in the US and/or EU for their ability to affect acrosome reaction, penetration, hyperactivation and viability in human sperm cells. We found that, similar to progesterone, the UV filters 4-MBC, 3-BC, Meradimate, Octisalate, BCSA, HMS and OD-PABA induced acrosome reaction and 3-BC increased sperm penetration into a viscous medium. The capacity of the UV filters to induce acrosome reaction and increase sperm penetration was positively associated with the ability of the UV filters to induce a Ca2+ influx. None of the UV filters induced significant changes in the proportion of hyperactivated cells. In conclusion, chemical UV filters that mimic the effect of progesterone on Ca2+ signaling in human sperm cells can similarly mimic the effect of progesterone on acrosome reaction and sperm penetration. Human exposure to these chemical UV filters may impair fertility by interfering with sperm function, e.g. through induction of premature acrosome reaction. Further studies are needed to confirm the results in vivo.

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Zhang, Yu, Kun Zhuang, Shanshan Yuan, Wangli Si, Yijun Li, Jun Zhang, and Jiaming Liu. "Effects of mir-195 Targeted Regulation of JAK2 on Proliferation, Invasion, and Apoptosis of Gastric Cancer Cells." Computational and Mathematical Methods in Medicine 2022 (July 26, 2022): 1–8. http://dx.doi.org/10.1155/2022/5873479.

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Background. Overexpression of miR-195 can make gastric cancer cells stay in G1/G2 phase. miR-195 has been shown to inhibit gastric cancer cell replication and accelerate cell death by targeting JAK2. However, the relationship between miR-195, JAK2, and gastric cancer is not clear. Objective. To observe the effect of mir-195 regulated by JAK2 on the growth, invasion, and death of gastric cancer cells. Methods. MGC803 and NCI gastric N87 cells were introduced into the negative control sequences of miR-195 and RNA, respectively. To detect the expression of miR-195 in cells, to detect the effect of miR-195 on mitosis and proliferation of tumor cells, to analyze the effect of miR-195 on cell invasion and metastasis, and to detect the regulation of miR-195 on JAK2 expression. Results. The level of miR-195 in miR-195-MIMICS group was significantly higher than that in miR-NC group. The cell survival rate of miR-195 mimic group was lower than that of miR-NC group ( P < 0.05 ). Compared with miR-NC group, the number of cells in G1 phase increased, the cells in G2 phase and S phase decreased, and the proportion of cells in G2 and S phase decreased in miR-195 mimic group. The scratch distance of miR-195 simulator group was larger than that of control group. The number of invasive cells in the miR-195 mimic group was significantly lower than that in the control group. The expression of JAK2 protein in miR-195 mimic group was lower than that in miR-NC group. There was a significant negative correlation between the expression level of miR-195 and JAK2 (rhabdomile 0.326 and record 0.00). There are continuous interaction fragments between JAK2 and miR-195. The luciferase activity of miR-195 mimic and wild type JAK2 sequence expression vector was significantly lower than that of wild type JAK2 sequence expression vector. Conclusion. miR-195 may inhibit the occurrence, metastasis, and invasion of gastric tumor by downregulating the expression of JAK2. miR-195/JAK2 may be a new molecular target for the treatment of gastrointestinal tumors.

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Maxian, Theresa, Lisa Gerlitz, Sabrina Riedl, Beate Rinner, and Dagmar Zweytick. "Effect of L- to D-Amino Acid Substitution on Stability and Activity of Antitumor Peptide RDP215 against Human Melanoma and Glioblastoma." International Journal of Molecular Sciences 22, no. 16 (August 6, 2021): 8469. http://dx.doi.org/10.3390/ijms22168469.

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The study investigates the antitumor effect of two cationic peptides, R-DIM-P-LF11-215 (RDP215) and the D-amino acid variant 9D-R-DIM-P-LF11-215 (9D-RDP215), targeting the negatively charged lipid phosphatidylserine (PS) exposed by cancer cells, such as of melanoma and glioblastoma. Model studies mimicking cancer and non-cancer membranes revealed the specificity for the cancer-mimic PS by both peptides with a slightly stronger impact by the D-peptide. Accordingly, membrane effects studied by DSC, leakage and quenching experiments were solely induced by the peptides when the cancer mimic PS was present. Circular dichroism revealed a sole increase in β-sheet conformation in the presence of the cancer mimic for both peptides; only 9D-RDP215 showed increased structure already in the buffer. Ex vitro stability studies by SDS-PAGE as well as in vitro with melanoma A375 revealed a stabilizing effect of D-amino acids in the presence of serum, which was also confirmed in 2D and 3D in vitro experiments on glioblastoma LN-229. 9D-RDP215 was additionally able to pass a BBB model, whereupon it induced significant levels of cell death in LN-229 spheroids. Summarized, the study encourages the introduction of D-amino acids in the design of antitumor peptides for the improvement of their stable antitumor activity.

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Zhao, Ruoxi, Rui Zhang, Lili Feng, Yushan Dong, Jialing Zhou, Songnan Qu, Shili Gai, Dan Yang, He Ding, and Piaoping Yang. "Constructing virus-like SiO_x/CeO₂/VO_x nanozymes for 1064 nm light-triggered mild-temperature photothermal therapy and nanozyme catalytic therapy." Nanoscale 14, no. 2 (2022): 361–72. http://dx.doi.org/10.1039/d1nr06128c.

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Xu, Ying, Yihua Bei, Shutong Shen, Jialiang Zhang, Yichao Lu, Junjie Xiao, and Xinli Li. "MicroRNA-222 Promotes the Proliferation of Pulmonary Arterial Smooth Muscle Cells by Targeting P27 and TIMP3." Cellular Physiology and Biochemistry 43, no. 1 (2017): 282–92. http://dx.doi.org/10.1159/000480371.

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Background/Aims: Aberrant vascular smooth muscle cell (VSMC) proliferation plays an important role in the development of pulmonary artery hypertension (PAH). Dysregulated microRNAs (miRNAs, miRs) have been implicated in the progression of PAH. miR-222 has a pro-proliferation effect on VSMCs while it has an anti-proliferation effect on vascular endothelial cells (ECs). As the biological function of a single miRNA could be cell-type specific, the role of miR-222 in pulmonary artery smooth muscle cell (PASMC) proliferation is not clear and deserves to be explored. Methods: PASMCs were transfected with miR-222 mimic or inhibitor and PASMC proliferation was determined by Western blot for PCNA, Ki-67 and EdU staining, and cell number counting. The target genes of miR-222 including P27 and TIMP3 were determined by luciferase assay and Western blot. In addition, the functional rescue experiments were performed based on miR-222 inhibitor and siRNAs to target genes. Results: miR-222 mimic promoted PASMC proliferation while miR-222 inhibitor decreased that. TIMP3 was identified to be a direct target gene of miR-222 based on luciferase assay. Meanwhile, P27 and TIMP3 were up-regulated by miR-222 inhibitor and down-regulated by miR-222 mimic. Moreover, P27 siRNA and TIMP3 siRNA could both attenuate the anti-proliferation effect of miR-222 inhibitor in PASMCs, supporting that P27 and TIMP3 are at least partially responsible for the regulatory effect of miR-222 in PASMCs. Conclusion: miR-222 promotes PASMC proliferation at least partially through targeting P27 and TIMP3.

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Chen, Feng, Huihui Chai, Zhaoxi Song, Ling Yu, and Can Fang. "Hydrophilic Porous Polydimethysiloxane Sponge as a Novel 3D Matrix Mimicking Heterogeneous Pores in Soil for Plant Cultivation." Polymers 12, no. 1 (January 6, 2020): 140. http://dx.doi.org/10.3390/polym12010140.

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In this work, a citric acid monohydrate (CAM)-templated polydimethylsiloxane (PDMS) sponge was proposed to mimic heterogeneous pore structures in the soil for plant cultivation. The porosity of the PDMS sponges was tuned by adjusting the CAM template. The water intake capability of the sponge was improved by (3-Aminopropyl) triethoxysilane (APTES) functionalization. The pore size and pore distribution were characterized by SEM and micro-computed tomography (micro-CT). The effect of pore structures on Oryzasativa (O. sativa) growth was investigated. Also, a 3D multi-layer PDMS sponge assembling was proposed to mimic the heterogeneous pore distribution at the different soil depth. The different growth rates of O. sativa and Nicotiana tabacum L. (N. tabacum) seeds on porous PDMS sponge indicated the impact of physical obstacles (pores) and chemical (water content) conditions on plant development. It is anticipated that this PDMS sponge could serve as a 3D matrix to mimic soil and provide a new idea for plant cultivation.

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Guo, Xiaoli, and Xiaodong Cheng. "miR-140-Modified Bone Marrow Mesenchymal Stem Cells Enhance Chemotherapy Sensitization in Cervical Squamous Cell Carcinoma Cells via Targeting Microtubule Depolymerization Protein 1 (STMN1)." Journal of Biomaterials and Tissue Engineering 12, no. 1 (January 1, 2022): 232–38. http://dx.doi.org/10.1166/jbt.2022.2883.

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Effect of bone marrow mesenchymal stem cells (BMSCs) on the sensitivity of chemotherapy drugs and microRNAs (miRNAs) is still unclear. This study explored the role of miR-140 modified BMSCs in enhancing paclitaxel sensitivity of cervical squamous cell carcinoma (CSCC). Hela cells, BMSCs cells, and miR-140 modified BMSCs were transfected with miR-140 mimic, miR-140 inhibitor, and miR-140 NC, respectively. After transfection, they were co-cultured with Hela cells and paclitaxel to set up miR-140 mimic group, miR-140 inhibitor group, and miR-140 NC group (without paclitaxel treatment) followed by analysis of cell proliferation, apoptosis, ROS generation, expression of miR-140, STMN1, STAT3, p-STAT3, and survivin mRNA and protein. miR-140 inhibitor group showed lowest cell proliferation number and expressions of miR-140, STMN1, STAT3, p-STAT3, and survivin mRNA and protein with highest number of apoptotic cells, which were all reversed in miR-140 mimic group. There was a positive correlation between STMN1 level and miR-140 expression (r = 0.449, P = 0.108). BMSCs modified with miR-140 inhibitor can target STMN1, enhance the sensitivity of chemotherapy drugs, and exert an inhibitory effect on CSCC cell proliferation, suggesting that STMN1 might be a therapy target for treating CSCC.

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Journal articles on the topic 'Mimic-effect'

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