Table_1_Enhancing organizational communication via intelligent voice assistant for knowledge workers: The role of perceived supervisor support, psychological capital, and employee wellbeing.DOCX

In the world of globalization, knowledge workers have grown in importance to organizational development. Currently, the intelligence voice assistant (IVA) has a high degree of participation in people's lives, displaying a trend of becoming an emotional partner for humans. Therefore, whether the application of IVA can help enhance organizational communication for knowledge workers is worthy to be explored. This study adopted an interactive situation-simulation survey experiment to explore the impact of the application of IVA on knowledge workers' perceived supervisor support, psychological capital, and employee wellbeing, using a 2 (voice gender: male/female) by 2 (voice characteristics: machine-like/anthropomorphic) between-subject experimental design with two additional control groups (text-only/no-interaction). Besides, voice interviews were designed to understand what knowledge workers need from the IVA. Results show that: (1) There were pair-wise correlations among perceived supervisor support, psychological capital, and employee wellbeing of knowledge workers, and psychological capital played a complete mediating role between perceived supervisor support and employee wellbeing; (2) There were significant differences among the scores of different groups (the experimental groups, the text-only control group and the no-interaction control group) on perceived supervisory support and employee wellbeing, with the experimental groups overall better than the control groups. (3) Knowledge workers hope that the services provided by the IVA mainly include three categories: work support, emotional support and life support. In conclusion, this study shows that the use of IVA can significantly improve perceived supervisor support, psychological capital, and employee wellbeing of knowledge workers, and provide some useful directions for the product design.</p

The CREB-miR-9 Negative Feedback Minicircuitry Coordinates the Migration and Proliferation of Glioma Cells

<div><p>Migration-proliferation dichotomy is a common mechanism in gliomagenesis; however, an understanding of the exact molecular mechanism of this “go or grow” phenomenon remains largely incomplete. In the present study, we first found that microRNA-9 (miR-9) is highly expressed in glioma cells. MiR-9 inhibited the proliferation and promoted the migration of glioma cells by directly targeting cyclic AMP response element-binding protein (CREB) and neurofibromin 1 (NF1), respectively. Our data also suggested a migration-inhibitory role for CREB through directly regulating the transcription of NF1. Furthermore, we found that the transcription of miR-9-1 is under CREB's control, forming a negative feedback minicircuitry. Taken together, miR-9 inhibits proliferation but promotes migration, whereas CREB plays a pro-proliferative and anti-migratory role, suggesting that the CREB-miR-9 negative feedback minicircuitry plays a critical role in the determination of “go or grow” in glioma cells.</p> </div

MiR-9 promotes migration through targeting NF1.

<p>(A) The NF1 3′UTR contains a putative miR-182 binding site which also has the potential to interact with miR-9. The mammalian alignment is shown on the top. A mutated NF1 3′UTR was generated by mutating the miR-182 binding site. (B) Luciferase reporter assays were performed to test the interactions between the miRNAs and the NF1 3′UTR. NF1 3′UTR luciferase reporter constructs were co-transfected with synthetic miRNA mimics (miR-9, miR-182 and miR-23a) or control mimics (miR-NC), and 24 h later the normalized luciferase activity was determined. Data are represented as the mean ± SD, n = 4. (C) MiR-9, miR-182 and miR-23a were knocked-down in T98G and U251 cells by transfection with miRNA antagomirs, and NF1 protein level was determined by western blotting and quantified by densitometric measurement (mean ± SD, n = 3). (D) T98G cells were transfected with miR-9 mimics (or control mimics, miR-NC) or siRNA targeting NF1 (or control non-specific siRNA), and whole cell protein was extracted for determination of NF1 protein levels by western blotting. (E) Over-expression of miR-9 or knockdown of NF1 enhances the migration of T98G cells in a transwell migration assay. Representative photographs are shown on the top. Crystal violet staining was removed and quantified by absorbance measurement (OD570-630) (mean ± SD, n = 4). (F) NF1 knockdown abolished the effect of decreased miR-9 on the migration of T98G cells. Crystal violet staining was removed and quantified by absorbance measurement (OD570-630) (mean ± SD, n = 4). **, <i>P</i><0.01, ***, <i>P</i><0.001, two-tailed unpaired Student's t test. On the bottom is a representative western blot result showing that knocking down miR-9 increased the NF1 protein level, whereas simultaneous transfection of siNF1 abolished the increased NF1 protein level.</p

CREB regulates NF1 and knocking down CREB inhibits migration.

<p>(A) The migratory capacity of AD-shcreb or AD-shNC-infected U87MG, T98G and U251 cells were analyzed in a transwell migration assay (top). The bound crystal violet staining was released and quantified by measuring the OD570-630 (mean ± SD, n = 3) (bottom). (B) The mRNA and protein levels of NF1 were detected in control T98G and U251 cells or in cells with CREB knocked down by quantitative RT-PCR and western blotting, respectively. *, <i>P</i><0.05; **, <i>P</i><0.01; ***, <i>P</i><0.001, two-tailed unpaired Student's t test. (C) T98G cells were transfected with miR-9 antagomirs or controls followed by infection of adenovirus-mediated shRNA for CREB (AD-shcreb) or AD-shNC, and the protein level of NF1 was detected by western blotting.</p

MiR-9 is highly expressed in glioma cell lines.

<p>(A) Schematic representation showing that miR-9 can be generated by the processing of any of the three primary transcripts encoded by three distinct genes (miR-9-1, miR-9-2 and miR-9-3). (B and C) The expression levels of mature miR-9 as well as pri-miR-9-1, pri-miR-9-2 and pri-miR-9-3 were determined in the human cervical carcinoma cell line (HeLa), normal human glial cell line (HEB) and four glioma cell lines (U87MG, T98G, A172 and U251) by quantitative RT-PCR (mean ± SD, n = 3). (D) Genomic DNA was extracted from the six cell lines (HeLa, HEB, U87MG, T98G, A172 and U251), and the gene copy numbers of miR-9-1, miR-9-2 and miR-9-3 were determined by quantitative real-time PCR (mean ± SD, n = 3). *, P<0.05, two-tailed unpaired Student's t test, relative to HEB and HeLa.</p

Introducing Solubility Control for Improved Organic P‑Type Dopants

To overcome the poor solubility of the widely used p-type dopant 2,3,5,6-tetrafluoro-7,7,8,8-tetracyanoquinodimethane (F4TCNQ), we have synthesized a series of structure-modified, organic p-type dopants to include alkyl ester groups designed to enable solubility and miscibility control. UV–vis–NIR and cyclic voltammetry measurements show increased solubility of mono- and diester substituted dopants with only modest changes to acceptor strength. Using absorption spectroscopy, photoluminescence, and in-plane conductivity measurements, we demonstrate that the new dopants can successfully p-type dope poly­(3-hexylthiophene-2,5-diyl) (P3HT). Monoester substituted dopants are characterized by only slightly reduced electron affinity relative to F4TCNQ, but greater doping effectiveness due to increased miscibility with P3HT. Diester substituted dopants undergo a dimerization reaction before assuming their doped states, which may help anchor dopants into position post deposition, thus decreasing the negative effect of dopant drift and diffusion. We conclude that increased dopant solubility/miscibility increases the overall effectiveness of doping in solution-cast polymer films and that ester modification is a practical approach to achieving solubility/miscibility control in TCNQ-type dopants

The effects of miR-9 knockdown on glioma cell growth, colony formation and migration.

<p>(A) MTT assays were performed to evaluate the effects of miR-9 knockdown on the growth and survival of glioma cells (U87MG, T98G and U251). Data are represented as the mean ± SD, n = 4. (B) Colony formation assays were utilized to test the effects of knocking down and over-expressing miR-9 on the colony formation ability of T98G and U251 cells. Data are represented as the mean ± SD, n = 4. (C) Transwell migration assays were employed to evaluate the effects of knocking down miR-9 and miR-23a (as a negative control) on the migration of glioma cells. On the top are representative photographs of transwell assays. The bound crystal violet staining was released with 33% glacial acetic acid and quantified by absorbance measurement (OD570-630) (mean ± SD, n = 4). *, <i>P</i><0.05, **, <i>P</i><0.01, two-tailed unpaired Student's t test.</p

MiR-9-1 is under CREB's control.

<p>(A) Location of putative CREs within the 5′ flanking regions of miR-9-1 and miR-9-2. MiR-9-1 is located in an intron of the gene c1orf61 (chromosome 1), whereas miR-9-2 is located in an exon of linc00461 (chromosome 5). Three pairs of primers (miR-9-1-a, miR-9-1-b and miR-9-2) were designed to detect the binding capacity of CREB to the predicted CREs of miR-9-1-a, miR-9-1-b and miR-9-2, respectively, by ChIP-qPCR assays. Both the 5′ flanking sequences (2 kb) and the pre-miRNA bodies of miR-9-1 and miR-9-2 were inserted upstream of the luciferase reporter (gray box shown by LUC). The arrows denote the positions of primers used for ChIP-qPCR. (B) ChIP-qPCR assays were performed in T98G and U251 cells to detect the binding capacity of CREB to the putative CREs of miR-9-1 and miR-9-2 (mean ± SD, n = 3). (C) In AD-shNC/AD-shcreb-infected T98G and U251 cells, ChIP-qPCR was performed to detect the binding capacity of CREB on CRE-miR-9-1-a (mean ± SD, n = 3). (D) CREB enhances the transcription of miR-9-1. The 5′ flanking sequences (−2 kb+miR-9-1; −2 kb, −570 bp; −560 bp+miR-9-1) without mutations or with a mutation of CRE-a (−569+miR-9-1, from TGACGGGC to TGGAGGGC) in miR-9-1 were inserted upstream of the luciferase cassette. The luciferase reporter constructs were co-transfected with CREB expression plasmids or control vectors and the normalized luciferase activity was determined (mean ± SD, n = 4). (E) The mRNA expression levels of CREB, pri-miR-9-1 and mature miR-9 were detected in T98G and U251 cells infected with AD-shcreb or AD-shNC by quantitative RT-PCR (mean ± SD, n = 3). *, <i>P</i><0.05, **, <i>P</i><0.01, two-tailed unpaired Student's t test.</p

Genes upregulated or downregulated in B117HS compared with B117P.

<p>Genes upregulated or downregulated in B117HS compared with B117P.</p

Establishment and characterization of an AML mouse model for evaluating treatment response by transplanting of BXH-2 derived myeloid leukemic cells into syngeneic mice (B6C3F1).

<p>Fig. 1A) Gross anatomic examination of spleen and lymph node collected from leukemic (left) or normal (right) mice. Fig. 1B) Morphological examination of peripheral blood smears from (a) recipient mice, (b) normal mice and (c) of B117 cells (Wright-Giemsa staining). Representative fields are shown here. Fig. 1C) Pathologic examination of organ sections, including liver (a & a’), lung (b & b’), lymph node (c & c’), kidney (d & d’), and spleen (e & e’), obtained from normal (a∼e) versus leukemic (a’∼e’) mice (H & E staining). Fig. 1D) Immunophenotypic analysis of bone marrow cells recovered from normal (a) or leukemic (b) mice.</p