P2016050386-B1-4_results.zip

<p>In our study, melon transcriptome sequencing was used to identify key genes controlling the differentiation of callus into embryogenic callus. The overall gene expression levels were higher, photosynthesis-related gene expression was increased and the pathways related to metabolic processes and secondary metabolite biosynthesis were activated in the embryogenic callus compared with the non-embryogenic callus. Therefore, the genes associated with these pathways may be closely related to the control of melon callus differentiation into embryogenic callus.<b></b></p

Guanidine and Amidoxime Cofunctionalized Polypropylene Nonwoven Fabric for Potential Uranium Seawater Extraction with Antifouling Property

Uranium seawater extraction is strategically important to the sustainable development of nuclear energy. Nevertheless, a challenge remains in uranium enrichment to overcome the microorganisms’ adhesion. In this article, we propose guanidine and amidoxime cofunctionalized polypropylene nonwoven fabric for potential uranium seawater extraction with an antifouling property. Specifically, glycidyl methacrylate was first grafted onto polypropylene nonwoven fabric under γ-ray irradiation, and then reacted with dicyandiamide, and followed by amidoximation to give the functionalized sorbents. The effect of sorbent dose, contact time, and coexisting ions on uranium adsorption and antibacterial assay were investigated. The sorption equilibrium could be reached with a capacity of 112 mg/g within 5 h at pH 8.0 and 298.15 K. The uranium sorption was not affected by other coexisting ions. The antibacterial assay indicated guanidine and amidoxime cofunctionalized fabric could efficiently inhibit the adhesion of Gram-negative <i>E. coli</i> and have bactericidal functions. In addition, it could be regenerated with high efficiency of uranium adsorption after five cycles. This work indicates that guanidine and amidoxime cofunctionalized polypropylene nonwoven fabric may be a promising material for uranium seawater extraction

Presentation_1_A Surprising Source of Self-Motivation: Prior Competence Frustration Strengthens One’s Motivation to Win in Another Competence-Supportive Activity.pdf

<p>According to self-determination theory (SDT), competence is among the three basic psychological needs essential for one’s well-being and optimal functioning, and the frustration of these needs is theoretically predicted to induce a restorative response. While previous studies have explored the restoration process of autonomy and relatedness, empirical evidence for such a process is still lacking for competence. In order to explore this process and to examine the effect of prior competence frustration on one’s motivation to win in a subsequent competence-supportive task, we adopted a between-group experimental design and manipulated one’s competence frustration through task difficulty in an electrophysiological study. Participants in both groups were instructed to work on the time-estimation task and the stop-watch task in two successive sessions respectively. Participants in the experimental group were asked to complete a highly difficult task in the first session and a task of medium difficulty in the second session, while those in the control group were instructed to work on tasks of medium difficulty in both sessions. In the second session, an enlarged feedback-related negativity (FRN) loss-win difference wave (d-FRN) was observed in the experimental group compared to the control group, indicating that the competence-frustrated participants have an enhanced motivation to win in a subsequent competence-supportive task. Thus, results of the present study provided original neural evidence for the restoration process of frustrated competence, which provided important guidelines for the managerial practice.</p

miRNA-29c Suppresses Lung Cancer Cell Adhesion to Extracellular Matrix and Metastasis by Targeting Integrin β1 and Matrix Metalloproteinase2 (MMP2)

<div><p>Our pilot study using miRNA arrays found that miRNA-29c (miR-29c) is differentially expressed in the paired low-metastatic lung cancer cell line 95C compared to the high-metastatic lung cancer cell line 95D. Bioinformatics analysis shows that integrin β1 and matrix metalloproteinase 2 (MMP2) could be important target genes of miR-29c. Therefore, we hypothesized that miR-29c suppresses lung cancer cell adhesion to extracellular matrix (ECM) and metastasis by targeting integrin β1 and MMP2. The gain-of-function studies that raised miR-29c expression in 95D cells by using its mimics showed reductions in cell proliferation, adhesion to ECM, invasion and migration. In contrasts, loss-of-function studies that reduced miR-29c by using its inhibitor in 95C cells promoted proliferation, adhesion to ECM, invasion and migration. Furthermore, the dual-luciferase reporter assay demonstrated that miR-29c inhibited the expression of the luciferase gene containing the 3′-UTRs of integrin β1 and MMP2 mRNA. Western blotting indicated that miR-29c downregulated the expression of integrin β1 and MMP2 at the protein level. Gelatin zymography analysis further confirmed that miR-29c decreased MMP2 enzyme activity. Nude mice with xenograft models of lung cancer cells confirmed that miR-29c inhibited lung cancer metastasis in vivo, including bone and liver metastasis. Taken together, our results demonstrate that miR-29c serves as a tumor metastasis suppressor, which suppresses lung cancer cell adhesion to ECM and metastasis by directly inhibiting integrin β1 and MMP2 expression and by further reducing MMP2 enzyme activity. The results show that miR-29c may be a novel therapeutic candidate target to slow lung cancer metastasis.</p></div

Effect of miR-29c on lung cancer cell migration and invasion <i>in vitro</i>.

<p>(A) In a Matrigel invasion assay, miR-29c mimics transfected 95D cells vs MiNC transfected cells in a 200× light scope after crystal violet staining. (B) Matrigel invasion and transwell migration: 95D cells were counted in a light scope in four random views. **<i>p</i><0.01 (Student's <i>t</i>-test, n = 4 ). (C) In a Matrigel invasion assay, miR-29c inhibitor transfected 95C cells vs IhNC transfected cells in a 200× light scope after crystal violet staining. (D) Matrigel invasion and transwell migration: 95C cells were counted in a light scope in four random views. **<i>p</i><0.01 (Student's <i>t</i>-test, n = 4).</p

Effect of miR-29c on lung cancer cell adhesion to ECM <i>in vitro</i>.

<p>(A) 95D cells transfected with miR-29c mimics adhesion to Matrigel was measured by counting as described in Materials and Methods. Representative fields of 95D 29c and 95D MiNC (magnification ×100). (B) Average adhesion cell number per random field. **<i>P</i><0.01(Student's <i>t</i>-test, n = 3). (C) miR-29c inhibits 95D cell adhesion (MTT assay). **<i>p</i><0.01(Student's <i>t</i>-test, n = 3). (D) Representative fields from 95D 29ci and 95C IhNC lung cancer cells (magnification ×100). (E) Average adhesion cell number per random field. **<i>P</i><0.01(Student's <i>t</i>-test, n = 3). (F) Suppression of miR-29c enhanced cell adhesion in 95C cells (MTT assay). **<i>p</i><0.01 (Student's <i>t</i>-test, n = 3).</p

Differential expression of miR-29c in the paired high- and low-metastatic lung cancer cell lines, and the effects of miR-29c on lung cancer cell proliferation <i>in vitro</i>.

<p>(A) qRT-PCR of miR-29c in 95D and 95C cell lines. Change was calculated using 2^−ΔΔCt relative quantitative analysis; **<i>p</i><0.01 (Student's <i>t</i>-test). Experiments were repeated at least thrice (n = 3). (B) miR-29c inhibits cellular proliferation in 95D cells by MTT assay. **<i>p</i><0.01(Student's <i>t</i>-test, n = 3). (C) miR-29c inhibitor increased cellular proliferation in 95C cells by MTT assay. **<i>p</i><0.01 (Student's <i>t</i>-test, n = 3).</p

Frequency of metastasis in nude mice xenograft model from 95D and 95C lung cancer cells using bioluminescence imaging.

**<p>indicates P<0.01 compared to 95D MiNC; * indicates P<0.05 compared to 95C IhNC by X² test.</p

MiR-29c directly targets 3′-UTRs of the human integrin β1 (Intβ1) and MMP2 gene.

<p>(A) Conserved targeting of 3′-UTRs of the human int β1 by miR-29c (underlined). The wild-type and mutant sequences of int β1 3′-UTR are listed for comparison. (B) Dual-luciferase reporter assay for target gene int β1 in 95D cells transfected with miR-29c mimics. **<i>p</i><0.01 (Student's <i>t</i>-test, n = 3 ). (C) Dual-luciferase reporter assay for target gene int β1 in 95C cells with or without transfecting mir-29c inhibitors. **<i>p</i><0.01 (Student's <i>t</i>-test, n = 3). (D) miR-29c binding sites in the MMP2 3′UTR region (underlined); binding site is highly conserved in vertebrate animals, including humans. The wild-type and mutant sequences of MMP2 3′UTR are listed for comparison. (E) Dual-luciferase reporter assay of MMP2 mRNA in 95D cells transfected with miR-29c mimics. **<i>p</i><0.01 (Student's <i>t</i>-test, n = 3). (F) Dual-luciferase reporter assay of MMP2 mRNA in 95C cells with or without transfecting mir-29c inhibitors. **<i>p</i><0.01 (Student's <i>t</i>-test, n = 3).</p

MiR-29c inhibits tumor metastasis <i>in vivo</i>.

<p>(A) miR-29c mimics suppress 95D cells metastasis to bone <i>in vivo</i> as shown by bioluminescence imaging after injection of 95D cells transfected with MiNC for 3–4 weeks, (□bone metastasis sites). (B) miR-29c inhibitor promotes 95C cells metastasis <i>in vivo</i> as shown by bioluminescence imaging. (C) miR-29c mimics can suppress 95D cells metastasis to liver <i>in vivo</i> as shown by bioluminescence imaging (□liver metastasis sites). 95D MiNC cells can metastasize to bone. (D) miR-29c inhibitor promotes 95C cells metastasis to liver <i>in vivo</i> as shown by bioluminescence imaging. (E) miR-29c mimics suppress 95D cells metastasis to bone <i>in vivo.</i> Bone metastasis shown by X-ray radiography 6–8 weeks after injection. The bone was destroyed by osteolytic metastasis (red arrow) caused by 95D cells transfected with MiNC. (F) miR-29c mimics suppress 95D cells metastasis to liver <i>in vivo.</i> Representative anatomical photos of livers from mice injected with 95D 29c or 95D MiNC cells. Liver metastasis was not found 6–8 weeks after injection from 95D 29c (red arrow). (G) Representative liver tissue sections from each group were shown (hematoxylin and eosin stain; magnification, ×100). Red arrows indicate liver metastasis.</p