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Background Bootleg innovation differs from traditional innovation in that it involves actions that either contravene established organizational rules and procedures or are conducted autonomously and covertly by individuals, with the aim of benefiting the organization. While prior research has highlighted a strong link between moral factors and bootleg innovation, there remains a paucity of studies exploring the moral foundations underlying such innovation. Drawing on moral licensing theory, this study examines the dual nature of bootleg innovation to elucidate the mechanism through which perceived organizational status influences employee engagement in bootleg innovation. Methods This study constructs and verifies a moderated mediating model of organizational status perception and bootleg innovation, using exploratory factor analysis and hierarchical regression analysis based on 394 survey responses. Results The findings indicate that: (1) Perceived organizational status has a significant positive effect on employee bootleg innovation behavior. (2) Both dimensions of moral licensing (moral credits and moral credentials) mediate the relationship between perceived organizational status and bootleg innovation behavior. (3) Intrinsic motivation positively moderates the impact of perceived organizational status on moral credits and moral credentials. Conclusion This study offers a unique perspective on the moral dilemmas employees face in bootleg innovation, thereby providing a novel lens for understanding their bootleg innovation behavior.

Background CD4 + T cells are critical effectors of anti-tumor immunity, but how tumor cells influence CD4 + T cell effector function is not fully understood. Tumor cell-released autophagosomes (TRAPs) are being recognized as critical modulators of host anti-tumor immunity during tumor progression. Here, we explored the mechanistic aspects of TRAPs in the modulation of CD4 + T cells in the tumor microenvironment. Methods TRAPs isolated from tumor cell lines and pleural effusions or ascites of cancer patients were incubated with CD4 + T cells to examine the function and mechanism of TRAPs in CD4 + T cell differentiation and function. TRAPs-elicited CD4 + T cells were tested for their suppression of effector T cell function, induction of regulatory B cells, and promotion of tumorigenesis and metastasis in a mouse model. Results Heat shock protein 90α (HSP90α) on the surface of TRAPs from malignant effusions of cancer patients and tumor cell lines stimulated CD4 + T cell production of IL-6 via a TLR2–MyD88–NF-κB signal cascade. TRAPs-induced autocrine IL-6 further promoted CD4 + T cells secretion of IL-10 and IL-21 via STAT3. Notably, TRAPs-elicited CD4 + T cells inhibited CD4 + and CD8 + effector T cell function in an IL-6- and IL-10-dependent manner and induced IL-10-producing regulatory B cells (Bregs) via IL-6, IL-10 and IL-21, thereby promoting tumor growth and metastasis. Consistently, inhibition of tumor autophagosome formation or IL-6 secretion by CD4 + T cells markedly retarded tumor growth. Furthermore, B cell or CD4 + T cell depletion impeded tumor growth by increasing effector T cell function. Conclusions HSP90α on the surface of TRAPs programs the immunosuppressive functions of CD4 + T cells to promote tumor growth and metastasis. TRAPs or their membrane-bound HSP90α represent important therapeutic targets to reverse cancer-associated immunosuppression and improve immunotherapy.

Linewidth narrowing and other quantum coherent effects based on three-photon coherent population trapping （CPT） in Ca＋ ions are investigated. If the propagation directions of the three lasers obey the phase matching condition, the dark linewidth resulting from the CPT can be very narrow, and it can be controlled by adjusting the parameters of the lasers.

Background Pancreatic cancer is currently one of the leading causes of cancer deaths without any effective therapies. Mir-145 has been found to be tumor-suppressive in various types of cancers. The aim of this study is to investigate the role of miR-145 in pancreatic cancer cells and explore its underlying mechanism. Methods Quantitative real time PCR was used to determine the expression level of miR-145 and angiopoietin-2 (Ang-2) mNRA, and the expression level of Ang-2 protein was measured by western blotting. The anti-cancer activities of miR-145 were tested both in in vitro by using cell invasion and colony formation assay and in vivo by using xenograft assay. The direct action of miR-145 on Ang-2 was predicted by TargetScan and confirmed by luciferase report assay. The vascularization of xenografts were performed by immunohistochemical analysis. Results The expression level of miR-145 was significantly lower and the expression levels of Ang-2 mRNA and protein was significantly higher in the more aggressive pancreatic cancer cells (MiaPaCa-2 and Panc-1) when compared to that in BxPC3 cells. Overexpression of miR-145 in the BxPC3, MiaPaCa-2 and Panc-1 cells suppressed the cell invasion and colony formation ability, and the expression level of Ang-2 protein in MiaPaCa-2 and Panc-1 cells was also suppressed after pre-miR-145 transfection. Intratumoral delivery of miR-145 inhibited the growth of pancreatic cancer xenografts and angiogenesis in vivo, and also suppressed the expression level of angiopoietin-2 protein. Luciferase report assay showed that Ang-2 is a direct target of miR-145, and down-regulation of angiopoietin-2 by treatment with Ang-2 siRNA in the BxPC3, MiaPaCa-2 and Panc-1 cells suppressed cell invasion and colony formation ability. The reverse transcription PCR results also showed that Tie1 and Tie2 were expressed in BxPC3, MiaPaCa-2 and Panc-1 cells. Conclusion MiR-145 functions as a tumor suppressor in pancreatic cancer cells by targeting Ang-2 for translation repression and thus suppresses pancreatic cancer cell invasion and growth, which suggests that restoring of miR-145 may be a potential therapeutic target for pancreatic cancer.

The eggplant was mutagenized with ethyl methane sulfonate (EMS) to enhance its genetic variability in our previous paper. In this article, we further analyzed the phenotype of M2 generation of mutant eggplants. A total of 325 independent M2 families were investigated for phenotypic variation. In addition to the visible phenotypic variation, chlorogenic acid (CGA) concentrations were analyzed in 26 fruits of mutants with High Performance Liquid Chromatography assay. Seventeen fruits exhibited significantly higher concentrations of CGAs than those in wild-type. The anthocyanin concentration of S9-1, the purple black mutant, was higher than WT, meanwhile, the anthocyanin concentration of L6-4 and U36-1 was lower than WT. Furthermore, our RT-PCR result demonstrated that the expression levels of anthocyanin biosynthetic genes, except for SmPAL, were increased in S9-1, and the regulator SmMYB1 was decreased in L6-4 and U36-1 mutants. Together, our data indicated that, M2 generation showed abundant phenotypic variations and the strong potential usage for next step of breeding and molecular genetic mechanisms in eggplant.

The eggplant was mutagenized with ethyl methane sulfonate (EMS) to enhance its genetic variability in our previous paper. In this article, we further analyzed the phenotype of M generation of mutant eggplants. A total of 325 independent M families were investigated for phenotypic variation. In addition to the visible phenotypic variation, chlorogenic acid (CGA) concentrations were analyzed in 26 fruits of mutants with High Performance Liquid Chromatography assay. Seventeen fruits exhibited significantly higher concentrations of CGAs than those in wild-type. The anthocyanin concentration of S9-1, the purple black mutant, was higher than WT, meanwhile, the anthocyanin concentration of L6-4 and U36-1 was lower than WT. Furthermore, our RT-PCR result demonstrated that the expression levels of anthocyanin biosynthetic genes, except for SmPAL, were increased in S9-1, and the regulator was decreased in L6-4 and U36-1 mutants. Together, our data indicated that, M generation showed abundant phenotypic variations and the strong potential usage for next step of breeding and molecular genetic mechanisms in eggplant.

Human ribonuclease inhibitor (RI) is a cytoplasmic acidic protein. RI is constructed almost entirely of leucine-rich repeats, which might be involved in some unknown biological functions like other structurally similar proteins besides inhibiting RNase A and angiogenin activities. Our previous experiments demonstrated that up-regulating RI might effectively inhibit some tumor growth and metastasis. However, the down-regulating RI influence on the tumor does not have any report until now, the mechanisms underlying antitumor of RI have not been fully understood. In this study, the efficient RNA interferences of RI were constructed using a plasmid vector and identified with RT-PCR, Western blot and Immunocytochemistry, then were transfected into non-invasive bladder cancer BIU-87 cells. We demonstrated that knockdown RI expression in BIU-87 cells could obviously change the cell morphology, rearrange the microfilaments and extend the lamellipodia, as well as enhance proliferation, increase migration, invasion and matrix metalloprotease level, and also reduce adhesion in vitro. BALB/C nude mice that were injected with the BIU-87 cells transfected RI siRNA showed a significant facilitation of the tumor with heavier tumor weight, higher density of microvessels, lower nm23-H1 and E-Cadherin expressions than those in the control group. Taken together, these experiments suggest that knockdown of RI could promote growth and metastasis potentials of BIU-87 cells. Our present findings reveal the novel mechanism that anti-tumor effect of RI is also involved in suppressing growth and metastasis, besides antiangiogenesis. The results show that RI may be a therapeutic target protein for bladder cancer and may be of biological importance.