Detecting h-index manipulation through self-citation analysis

The h-index has received an enormous attention for being an indicator that measures the quality of researchers and organizations. We investigate to what degree authors can inflate their h-index through strategic self-citations with the help of a simulation. We extended Burrell’s publication model with a procedure for placing self-citations, following three different strategies: random self-citation, recent self-citations and h-manipulating self-citations. The results show that authors can considerably inflate their h-index through self-citations. We propose the q-index as an indicator for how strategically an author has placed self-citations, and which serves as a tool to detect possible manipulation of the h-index. The results also show that the best strategy for an high h-index is publishing papers that are highly cited by others. The productivity has also a positive effect on the h-index

An index to quantify an individual's scientific research output that takes into account the effect of multiple coauthorship

I propose the index $\hbar$ ("hbar"), defined as the number of papers of an individual that have citation count larger than or equal to the $\hbar$ of all coauthors of each paper, as a useful index to characterize the scientific output of a researcher that takes into account the effect of multiple coauthorship. The bar is higher for $\hbar$.Comment: A few minor changes from v1. To be published in Scientometric

Statistical regularities in the rank-citation profile of scientists

Recent science of science research shows that scientific impact measures for journals and individual articles have quantifiable regularities across both time and discipline. However, little is known about the scientific impact distribution at the scale of an individual scientist. We analyze the aggregate production and impact using the rank-citation profile ci(r) of 200 distinguished professors and 100 assistant professors. For the entire range of paper rank r, we fit each ci(r) to a common distribution function. Since two scientists with equivalent Hirsch h-index can have significantly different ci(r) profiles, our results demonstrate the utility of the βi scaling parameter in conjunction with hi for quantifying individual publication impact. We show that the total number of citations Ci tallied from a scientist's Ni papers scales as . Such statistical regularities in the input-output patterns of scientists can be used as benchmarks for theoretical models of career progress

No Plan B: the Achilles heel of high performance sport management

Research question: The severity and immediacy of funding cuts to UK National Governing Bodies of Sport (NGBs), driven by the ‘No Compromise’ policy framework for Olympic funding, triggers a cyclical need for turnaround management. Adept strategies during times of considerable challenge is stark, yet literature investigating turnaround management within NGBs remains limited. Consequently, this paper examines two questions: how do NGBs respond to UK Sport funding cuts and how are their responses enabled or restricted by their organisational context? Research methods: A case study methodology was used to develop in-depth insights into how three NGBs responded over a twelve-month period of turnaround management. This was informed by 21 semi-structured interviews with chief executives/presidents, performance managers/head coaches and elite athletes. The actions of the NGBs were analysed through a thematic analysis that made use of Boyne’s (2004) 3 Rs of turnaround strategy. Results and findings: The results highlight that NGBs’ turnaround strategies were constrained by extreme funding dependency and a prohibitive institutional environment that led to states of flux and a focus on short-term operational survival. As a result, the measures taken undermined future success. Implications: An embedded feature of the ‘No Compromise’ framework is severe funding cuts. This should be a significant theme in NGB strategy development. The evidence of this study is that NGBs do not prepare, nor react strategically, when faced with the prospect (or fact of) severe cuts. Consequently, the cases of turnaround management in this study signal the urgent need for further research into the impact of the ‘No Compromise’ framework on the management of NGBs

DOK3 Negatively Regulates LPS Responses and Endotoxin Tolerance

Innate immune activation via Toll-like receptors (TLRs), although critical for host defense against infection, must be regulated to prevent sustained cell activation that can lead to cell death. Cells repeatedly stimulated with lipopolysaccharide (LPS) develop endotoxin tolerance making the cells hypo-responsive to additional TLR stimulation. We show here that DOK3 is a negative regulator of TLR signaling by limiting LPS-induced ERK activation and cytokine responses in macrophages. LPS induces ubiquitin-mediated degradation of DOK3 leading to SOS1 degradation and inhibition of ERK activation. DOK3 mice are hypersensitive to sublethal doses of LPS and have altered cytokine responses in vivo. During endotoxin tolerance, DOK3 expression remains stable, and it negatively regulates the expression of SHIP1, IRAK-M, SOCS1, and SOS1. As such, DOK3-deficient macrophages are more sensitive to LPS-induced tolerance becoming tolerant at lower levels of LPS than wild type cells. Taken together, the absence of DOK3 increases LPS signaling, contributing to LPS-induced tolerance. Thus, DOK3 plays a role in TLR signaling during both naïve and endotoxin-induced tolerant conditions

The Microphenotron: a robotic miniaturized plant phenotyping platform with diverse applications in chemical biology

Background Chemical genetics provides a powerful alternative to conventional genetics for understanding gene function. However, its application to plants has been limited by the lack of a technology that allows detailed phenotyping of whole-seedling development in the context of a high-throughput chemical screen. We have therefore sought to develop an automated micro-phenotyping platform that would allow both root and shoot development to be monitored under conditions where the phenotypic effects of large numbers of small molecules can be assessed. Results The ‘Microphenotron’ platform uses 96-well microtitre plates to deliver chemical treatments to seedlings of Arabidopsis thaliana L. and is based around four components: (a) the ‘Phytostrip’, a novel seedling growth device that enables chemical treatments to be combined with the automated capture of images of developing roots and shoots; (b) an illuminated robotic platform that uses a commercially available robotic manipulator to capture images of developing shoots and roots; (c) software to control the sequence of robotic movements and integrate these with the image capture process; (d) purpose-made image analysis software for automated extraction of quantitative phenotypic data. Imaging of each plate (representing 80 separate assays) takes 4 min and can easily be performed daily for time-course studies. As currently configured, the Microphenotron has a capacity of 54 microtitre plates in a growth room footprint of 2.1 m², giving a potential throughput of up to 4320 chemical treatments in a typical 10 days experiment. The Microphenotron has been validated by using it to screen a collection of 800 natural compounds for qualitative effects on root development and to perform a quantitative analysis of the effects of a range of concentrations of nitrate and ammonium on seedling development. Conclusions The Microphenotron is an automated screening platform that for the first time is able to combine large numbers of individual chemical treatments with a detailed analysis of whole-seedling development, and particularly root system development. The Microphenotron should provide a powerful new tool for chemical genetics and for wider chemical biology applications, including the development of natural and synthetic chemical products for improved agricultural sustainability

Plant perception of β-aminobutyric acid is mediated by an aspartyl-tRNA synthetase

Specific chemicals can prime the plant immune system for augmented defense. β-aminobutyric acid (BABA) is a priming agent that provides broad-spectrum disease protection. However, BABA also suppresses plant growth when applied in high doses, which has hampered its application as a crop defense activator. Here we describe a mutant of Arabidopsis thaliana that is impaired in BABA-induced disease immunity (ibi1) but is hypersensitive to BABA-induced growth repression. IBI1 encodes an aspartyl-tRNA synthetase. Enantiomer-specific binding of the R enantiomer of BABA to IBI1 primed the protein for noncanonical defense signaling in the cytoplasm after pathogen attack. This priming was associated with aspartic acid accumulation and tRNA-induced phosphorylation of translation initiation factor eIF2α. However, mutation of eIF2α-phosphorylating GCN2 kinase did not affect BABA-induced immunity but relieved BABA-induced growth repression. Hence, BABA-activated IBI1 controls plant immunity and growth via separate pathways. Our results open new opportunities to separate broad-spectrum disease resistance from the associated costs on plant growth

Angiotensin Converting Enzyme (ACE) and ACE2 Bind Integrins and ACE2 Regulates Integrin Signalling

The angiotensin converting enzymes (ACEs) are the key catalytic components of the renin-angiotensin system, mediating precise regulation of blood pressure by counterbalancing the effects of each other. Inhibition of ACE has been shown to improve pathology in cardiovascular disease, whilst ACE2 is cardioprotective in the failing heart. However, the mechanisms by which ACE2 mediates its cardioprotective functions have yet to be fully elucidated. Here we demonstrate that both ACE and ACE2 bind integrin subunits, in an RGD-independent manner, and that they can act as cell adhesion substrates. We show that cellular expression of ACE2 enhanced cell adhesion. Furthermore, we present evidence that soluble ACE2 (sACE2) is capable of suppressing integrin signalling mediated by FAK. In addition, sACE2 increases the expression of Akt, thereby lowering the proportion of the signalling molecule phosphorylated Akt. These results suggest that ACE2 plays a role in cell-cell interactions, possibly acting to fine-tune integrin signalling. Hence the expression and cleavage of ACE2 at the plasma membrane may influence cell-extracellular matrix interactions and the signalling that mediates cell survival and proliferation. As such, ectodomain shedding of ACE2 may play a role in the process of pathological cardiac remodelling