scholarly journals The strengths and capacities of Authentic Followership

2016 ◽  
Vol 37 (3) ◽  
pp. 310-324 ◽  
Author(s):  
Deanna de Zilwa
Keyword(s):  
Positive Feedback ◽  
Feedback Loop ◽  
Organisational Culture ◽  
Positive Outcomes ◽  
Dyadic Relationships ◽  
Organisational Performance ◽  
Positive Feedback Loop ◽  
Content Type ◽  
Authentic Followership ◽  
Three Components

Purpose – Exploring a new conceptual framework for authentic followership (AF) comprised of three components: individual, dyadic and organisational. The purpose of this paper is to explain how the components of AF interact as a positive, non-linear feedback loop. It presents three propositions of positive outcomes arising from AF. First, AF builds follower’s strengths and capacities. Second, AF strengthens dyadic relationships between followers and leaders. Third, AF deepens and strengthens positive organisational culture thereby improving organisational performance. It discusses the practical significance of these propositions for followers, leaders and firms. Design/methodology/approach – The paper provides an overview of AF. Then three propositions of positive outcomes arising from AF are presented. It identifies how these propositions could benefit followers, leaders and firms. In conclusion, it offers suggestions for future research directions and notes some limitations of this work. Findings – The key finding of this paper is that AF could potentially strengthen the capacities and performance of followers, leaders and organisations if the propositions presented in this work are correct – if the three components of AF interact with each other as a positive feedback loop strengthening and reinforcing each component of AF. To establish the validity of the AF model and the three propositions the paper suggests that investigations in different empirical settings are undertaken: SME’s and multinational corporations, in different countries under different market conditions, with followers and leaders of different gender, age, education level, roles and tenure of employment. Originality/value – The paper’s core contention that the components of AF interact as a positive feedback loop has significant practical implications – beneficial outcomes for followers, leaders and firms. P1 explains how AF enables followers to gain confidence, maturity and create solid foundations from which to thrive and flourish. P2 explains how dyadic relationships between followers and leaders could be strengthened, deepening trust and respect between each party, thereby enhancing leadership effectiveness. P3 explains how the dynamic processes of AF can strengthen and deepen positive organisational culture and enhance organisational performance.

scholarly journals Flagellar Stators Activate a Diguanylate Cyclase To Inhibit Flagellar Stators

2019 ◽  
Vol 201 (18) ◽  
Author(s):  
Daniel B. Kearns
Keyword(s):  
Pseudomonas Aeruginosa ◽  
Secondary Metabolite ◽  
Positive Feedback ◽  
Biofilm Formation ◽  
Feedback Loop ◽  
Diguanylate Cyclase ◽  
Positive Feedback Loop ◽  
Content Type ◽  
Dependent Inhibition

ABSTRACT The bacterial secondary metabolite cyclic di-GMP is a widespread, cytoplasmic signal that promotes a physiological transition in which motility is inhibited and biofilm formation is activated. A paper published in this issue (A. E. Baker, S. S. Webster, A. Diepold, S. L. Kuchma, E. Bordeleau, et al., J Bacteriol 201:e00741-18, 2019, https://doi.org/10.1128/JB.00741-18) makes an important connection between cyclic di-GMP and flagellar components. They show that stator units, which normally interact with the flagellum to power rotation, can alternatively interact with and activate an enzyme that synthesizes cyclic di-GMP in Pseudomonas aeruginosa. Moreover, the same stator units are also the target of cyclic-di-GMP-dependent inhibition such that the more the stators are inhibited, the more cyclic di-GMP is made. The resulting positive-feedback loop not only inhibits motility but also may initiate and stabilize biofilm formation.

Positive feedback loop of interleukin-1β upregulating production of inflammatory mediators in human intervertebral disc cells in vitro

2005 ◽  
Vol 2 (5) ◽  
pp. 589-595 ◽  
Author(s):  
Kotaro Jimbo ◽  
Jin Soo Park ◽  
Kimiaki Yokosuka ◽  
Kimiaki Sato ◽  
Kensei Nagata
Keyword(s):  
Intervertebral Disc ◽  
Positive Feedback ◽  
Protein Concentration ◽  
Feedback Loop ◽  
Serum Free Medium ◽  
Free Medium ◽  
Positive Feedback Loop ◽  
Content Type ◽  
Cox 2 ◽  
Fine Print

Object. Interleukin-1β (IL-1β) induces neurological symptoms in intervertebral disc herniation (IDH). Recently, the existence of a positive feedback loop of IL-1β, which encourages an inflammatory reaction or degeneration in the cells of tendon, has been reported. The authors hypothesized that there is a positive feedback loop of IL-1β in the cells of IDH. Methods. Eight human intervertebral disc specimens were harvested during spinal surgery for lumbar disc herniation. The cells were stimulated in serum-free medium with or without exogenous IL-1β. The messenger RNA (mRNA) was extracted for reverse-transcription polymerase chain reaction (PCR) and real-time PCR to quantify the mRNA of endogenous IL-1β, IL-6, cyclooxygenase-2 (COX-2), and matrix metalloproteinases (MMPs). The cells were then stimulated in serum-free medium with or without exogenous IL-1β, and then exogenous IL-1β was removed. After 2, 4, and 6 days, the medium was collected, and enzyme-linked immunosorbent assay was used to measure the protein concentration of endogenous IL-1β. The mRNA expressions of endogenous IL-1β, IL-6, COX-2, and MMPs were increased significantly depending on the concentration of exogenous IL-1β. The protein concentration of endogenous IL-1β was increased over time. Conclusions. There was a positive feedback loop of IL-1β in the cells of IDH. Furthermore, the productions of IL-6, COX-2, MMP-1, and MMP-3 were upregulated as a result of the increasing concentration of IL-1β in a positive feedback loop of IL-1β. The authors concluded that this positive feedback loop of IL-1β upregulated the production of mediators and thus can cause cessation of symptoms in IDH.

scholarly journals A positive-feedback loop between HBx and ALKBH5 promotes hepatocellular carcinogenesis

BMC Cancer ◽  
2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Siming Qu ◽  
Li Jin ◽  
Hanfei Huang ◽  
Jie Lin ◽  
Weiwu Gao ◽  
...  
Keyword(s):  
Positive Feedback ◽  
Feedback Loop ◽  
Hbv Infection ◽  
Cell Counting ◽  
Regulation Mechanism ◽  
Dependent Manner ◽  
Liver Carcinogenesis ◽  
Nude Mouse Model ◽  
Positive Feedback Loop

Abstract Background Hepatitis B Virus (HBV) contributes to liver carcinogenesis via various epigenetic mechanisms. The newly defined epigenetics, epitranscriptomics regulation, has been reported to involve in multiple cancers including Hepatocellular Carcinoma (HCC). Our previous study found that HBx, HBV encodes X protein, mediated H3K4me3 modification in WDR5-dependent manner to involve in HBV infection and contribute to oncogene expression. AlkB Homolog 5 (ALKBH5), one of epitranscriptomics enzymes, has been identified to be associated with various cancers. However, whether and how ALKBH5 is dysregulated in HBV-related HCC remains unclear yet. This study aims to investigate ALKBH5 function, clinical significance and mechanism in HBV related HCC (HBV-HCC) patients derived from Chinese people. Methods The expression pattern of ALKBH5 was evaluated by RT-qPCR, Western blot, data mining and immunohistochemistry in total of 373 HBV-HCC tissues and four HCC cell lines. Cell Counting Kit 8 (CCK8) assay, Transwell and nude mouse model were performed to assess ALKBH5 function by both small interference RNAs and lentiviral particles. The regulation mechanism of ALKBH5 was determined in HBx and WDR5 knockdown cells by CHIP-qPCR. The role of ALKBH5 in HBx mRNA N6-methyladenosine (m6A) modification was further evaluated by MeRIP-qPCR and Actinomycin D inhibitor experiment in HBV-driven cells and HBx overexpression cells. Result ALKBH5 increased in tumor tissues and predicts a poor prognosis of HBV-HCC. Mechanically, the highly expressed ALKBH5 is induced by HBx-mediated H3K4me3 modification of ALKBH5 gene promoter in a WDR5-dependent manner after HBV infection. The increased ALKBH5 protein catalyzes the m6A demethylation of HBx mRNA, thus stabilizing and favoring a higher HBx expression level. Furthermore, there are positive correlations between HBx and ALKBH5 in HBV-HCC tissues, and depletion of ALKBH5 significantly inhibits HBV-driven tumor cells’ growth and migration in vitro and in vivo. Conclusions HBx-ALKBH5 may form a positive-feedback loop to involve in the HBV-induced liver carcinogenesis, and targeting the loop at ALKBH5 may provide a potential way for HBV-HCC treatment.

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