Probiotic-feeding continues to be a promising strategy to control the bacterial pathogens in aquaculture. A new Pediococcus pentosaceus strain (SL001) was isolated from 1000s of soil samples, which exhibited wide antimicrobial spectrum of against fish pathogens, involving Aeromonas hydrophila , Aeromonas veronii , Aeromonas sobria , Edwardsiella tarda , Lactococcus garvieae , and Plesiomonas shigelloide . The challenge test against A. hydrophila showed that the survival rate of SL001-supplemented group was significantly higher than that of control group ( P < 0.05). Moreover, SL001 could stably colonize in gut of grass carp and increased mucus-secreting goblet cells and extended intestinal villi could be observed in SL001-supplemented group ( P < 0.05). Feeding with SL001 supplemented diet could significantly enhance the growth rate ( P < 0.05) and markedly affect gut microbiota structure of grass carps, resulting in reduced potential pathogens and increased potential probiotics. Furthermore, feeding grass carps with SL001 caused the up-regulated expression of insulin-like growth factor (IGF-1 and IGF-2) and down-regulated expression of myostatin (MSTN-1 and MSTN-2) ( P < 0.05), which probably also account for the increased growth rate of SL001-fed group. Meanwhile, relative mRNA expression levels of immune-related genes in liver, spleen, and head kidney were analyzed in grass carps after feeding for 30 days with SL001 supplemented diets. In all three immune organs, the expression levels of immunoglobulin M (IgM) and complement 3 (C3) were significantly increased ( P < 0.05), whereas the interleukin-8 (IL-8) was down-regulated ( P < 0.05). Besides, whole genome sequencing revealed several probiotics properties of SL001, including organic acid synthesis, bacteriocin synthesis (coagulin), superoxide dismutase, and digestive enzymes. In conclusion, P. pentosaceus SL001 which could enhance immunity and promoter growth rate of grass carps, is prospective to be used as a dietary probiotic in freshwater fish aquaculture.
PurposeThe purpose of this study is to explore how inclusive leadership promotes organizational performance through ambidextrous innovation (i.e. exploratory and exploitative innovation). Moreover, the authors examine the moderating role of environmental uncertainty in the relationship between inclusive leadership and ambidextrous innovation.Design/methodology/approachThis study conducted a questionnaire survey of high-tech enterprises in China and obtained 325 useable samples. The hypotheses were tested using latent path analysis and ordinary least squares regression.FindingsThe results indicate that exploratory and exploitative innovations mediate the relationship between inclusive leadership and organizational performance. Moreover, environmental uncertainty positively moderated the relationship between inclusive leadership and exploitative innovation.Practical implicationsManagers should value the critical role of inclusive leadership in promoting exploratory and exploitative innovation, which in turn improves organizational performance. Meanwhile, managers need to pay attention to the risk caused by environmental uncertainty.Originality/valueThis paper extends the influence of inclusive leadership on innovation from the individual level to the organizational level and reveals the influence mechanism of inclusive leadership on organizational performance. In addition, this study supplements the knowledge regarding the boundary conditions under which the influence of inclusive leadership is strengthened or weakened.
Background Small nucleolar RNA host gene (SNHG) long noncoding RNAs (lncRNAs) are frequently dysregulated in human cancers and involved in tumorigenesis and progression. SNHG17 has been reported as a candidate oncogene in several cancer types, however, its regulatory role in colorectal cancer (CRC) is unclear. Methods SNHG17 expression in multiple CRC cohorts was assessed by RT-qPCR or bioinformatic analyses. Cell viability was evaluated using Cell Counting Kit-8 (CCK-8) and colony formation assays. Cell mobility and invasiveness were assessed by Transwell assays. Tumor xenograft and metastasis models were applied to confirm the effects of SNHG17 on CRC tumorigenesis and metastasis in vivo. Immunohistochemistry staining was used to measure protein expression in cancer tissues. RNA pull-down, RNA immunoprecipitation, chromatin immunoprecipitation, and dual luciferase assays were used to investigate the molecular mechanism of SNHG17 in CRC. Results Using multiple cohorts, we confirmed that SNHG17 is aberrantly upregulated in CRC and correlated with poor survival. In vitro and in vivo functional assays indicated that SNHG17 facilitates CRC proliferation and metastasis. SNHG17 impedes PES1 degradation by inhibiting Trim23-mediated ubiquitination of PES1. SNHG17 upregulates FOSL2 by sponging miR-339-5p, and FOSL2 transcription activates SNHG17 expression, uncovering a SNHG17-miR-339-5p-FOSL2-SNHG17 positive feedback loop. Conclusions We identified SNHG17 as an oncogenic lncRNA in CRC and identified abnormal upregulation of SNHG17 as a prognostic risk factor for CRC. Our mechanistic investigations demonstrated, for the first time, that SNHG17 promotes tumor growth and metastasis through two different regulatory mechanisms, SNHG17-Trim23-PES1 axis and SNHG17-miR-339-5p-FOSL2-SNHG17 positive feedback loop, which may be exploited for CRC therapy.
Cancer immunotherapy based on natural killer (NK) cells is demonstrated to be a promising strategy. However, NK cells are deficient in ligands that target specific tumors, resulting in limited antitumor efficacy. Here, a glycoengineering approach to imitate the chimeric antigen receptor strategy and decorate NK cells with nanobodies to promote NK‐based immunotherapy in solid tumors is proposed. Nanobody 7D12, which specifically recognizes the human epidermal growth factor receptor (EGFR) that is overexpressed on many solid tumors, is coupled to the chemically synthesized DBCO‐PEG4‐GGG‐NH2 by sortase A‐mediated ligation to generate DBCO‐7D12. The NK92MI cells bearing azide groups are then equipped with DBCO‐7D12 via bioorthogonal click chemistry. The resultant 7D12‐NK92MI cells exhibit high specificity and affinity for EGFR‐overexpressing tumor cells in vitro and in vivo by the 7D12‐EGFR interaction, causing increased cytokine secretion to more effectively kill EGFR‐positive tumor cells, but not EGFR‐negative cancer cells. Importantly, the 7D12‐NK92MI cells also show a wide anticancer spectrum and extensive tumor penetration. Furthermore, mouse experiments reveal that 7D12‐NK92MI treatment achieves excellent therapeutic efficacy and outstanding safety. The authors’ works provide a cell modification strategy using specific protein ligands without genetic manipulation and present a potential novel method for cancer‐targeted immunotherapy by NK cells.
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