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A systematic review and meta-analytic synthesis of the relationship between compulsory citizenship behaviors and its theoretical correlates
Data availability statement:
The original contributions presented in the study are included in the article/Supplementary material, further inquiries can be directed to the corresponding author.Supplementary material:
The Supplementary Material for this article can be found online at: https://www.frontiersin.org/articles/10.3389/fpsyg.2023.1120209/full#supplementary-materialCopyright © 2023 Yildiz, Kaptan, Yildiz, Elibol, Yildiz and Ozbilgin. Background: Compulsory citizenship behaviors (CCBs) are increasingly endorsed and expected of workers in contexts where managerial worker protections are low and performance demands on workers are high. Although studies on compulsory citizenship behaviors have shown a significant increase in recent years, the literature still lacks a comprehensive meta-analysis. To fill this gap the purpose of this study is to synthesize the collective outcomes of prior quantitative research on CCBs with the objective of identifying the factors linked to the concept and offering a primary reference for future researchers. Methods: Forty-three different correlates with CCBs were synthesized. The dataset of this meta-analysis consists of 53 independent samples with a sample size of 17.491, contributing to 180 effect sizes. PRISMA flow diagram and PICOS framework were used for the study design. Result: Results showed only gender and age were significant among demographic characteristics related to CCBs. Correlates between CCBs and counterproductive workplace behaviors, felt obligation, work-family conflict, organizational-based self-esteem, organizational cynicism, burnout, anger toward the organization, and work alienation were found as large. We also found turnover intention, moral disengagement, careerism, abusive supervision, citizenship pressure, job stress, facades of conformity, and feeling trusted to be moderately related to CCBs. Next, there was a small relationship between CCBs and social loafing. On the other hand, LMX, psychological safety, organizational identification, organizational justice, organizational commitment, job satisfaction, and job autonomy were found as significant deterrents of CCBs. These results suggest that CCBs flourish in contexts with low levels of worker protection and low road practices to people management. Conclusion: In sum, we found solid cumulative evidence that CCBs are a harmful and undesirable phenomenon for employees and organizations. Also, positive correlations of felt obligation, feeling trusted, and organization-based self-esteem with CCBs, showed that, contrary to general acceptance, positive factors could also cause CCBs. Lastly, we found CCBs as a dominant phenomenon in eastern culture
Variantâspecific effects of GBA1 mutations on dopaminergic neuron proteostasis
Glucocerebrosidase 1 (GBA1) mutations are the most important genetic risk factors for Parkinson's disease (PD). Clinically, mild (e.g., p.N370S) and severe (e.g., p.L444P and p.D409H) GBA1 mutations have different PD phenotypes, with differences in age at disease onset, progression, and the severity of motor and nonâmotor symptoms. We hypothesize that GBA1 mutations cause the accumulation of αâsynuclein by affecting the crossâtalk between cellular protein degradation mechanisms, leading to neurodegeneration. Accordingly, we tested whether mild and severe GBA1 mutations differentially affect the degradation of αâsynuclein via the ubiquitinâproteasome system (UPS), chaperoneâmediated autophagy (CMA), and macroautophagy and differentially cause accumulation and/or release of αâsynuclein. Our results demonstrate that endoplasmic reticulum (ER) stress and total ubiquitination rates were significantly increased in cells with severe GBA1 mutations. CMA was found to be defective in induced pluripotent stem cell (iPSC)âderived dopaminergic neurons with mild GBA1 mutations, but not in those with severe GBA1 mutations. When examining macroautophagy, we observed reduced formation of autophagosomes in cells with the N370S and D409H GBA1 mutations and impairments in autophagosomeâlysosome fusion in cells with the L444P GBA1 mutation. Accordingly, severe GBA1 mutations were found to trigger the accumulation and release of oligomeric αâsynuclein in iPSCâderived dopaminergic neurons, primarily as a result of increased ER stress and defective macroautophagy, while mild GBA1 mutations affected CMA, which is mainly responsible for the degradation of the monomeric form of αâsynuclein. Overall, our findings provide new insight into the molecular basis of the clinical variability in PD associated with different GBA1 mutations
Natural history of SLC11 genes in vertebrates: tales from the fish world
<p>Abstract</p> <p>Background</p> <p>The <it>SLC11A1/Nramp1 </it>and <it>SLC11A2/Nramp2 </it>genes belong to the <it>SLC11/Nramp </it>family of transmembrane divalent metal transporters, with <it>SLC11A1 </it>being associated with resistance to pathogens and <it>SLC11A2 </it>involved in intestinal iron uptake and transferrin-bound iron transport. Both members of the <it>SLC11 </it>gene family have been clearly identified in tetrapods; however <it>SLC11A1 </it>has never been documented in teleost fish and is believed to have been lost in this lineage during early vertebrate evolution. In the present work we characterized the <it>SLC11 </it>genes in teleosts and evaluated if the roles attributed to mammalian <it>SLC11 </it>genes are assured by other fish specific <it>SLC11 </it>gene members.</p> <p>Results</p> <p>Two different <it>SLC11 </it>genes were isolated in the European sea bass (<it>Dicentrarchus. labrax</it>), and named <it>slc11a2-α </it>and <it>slc11a2-ÎČ</it>, since both were found to be evolutionary closer to tetrapods <it>SLC11A2</it>, through phylogenetic analysis and comparative genomics. Induction of <it>slc11a2-α </it>and <it>slc11a2-ÎČ </it>in sea bass, upon iron modulation or exposure to <it>Photobacterium damselae </it>spp. <it>piscicida</it>, was evaluated in <it>in vivo </it>or <it>in vitro </it>experimental models. Overall, <it>slc11a2-α </it>was found to respond only to iron deficiency in the intestine, whereas <it>slc11a2-ÎČ </it>was found to respond to iron overload and bacterial infection in several tissues and also in the leukocytes.</p> <p>Conclusions</p> <p>Our data suggests that despite the absence of <it>slc11a1</it>, its functions have been undertaken by one of the <it>slc11a2 </it>duplicated paralogs in teleost fish in a case of synfunctionalization, being involved in both iron metabolism and response to bacterial infection. This study provides, to our knowledge, the first example of this type of sub-functionalization in iron metabolism genes, illustrating how conserving the various functions of the SLC11 gene family is of crucial evolutionary importance.</p
Relevance of genetic testing in the gene-targeted trial era: the Rostock Parkinson\u27s disease study
\ua9 The Author(s) 2024. Estimates of the spectrum and frequency of pathogenic variants in Parkinsonâs disease (PD) in different populations are currently limited and biased. Furthermore, although therapeutic modification of several genetic targets has reached the clinical trial stage, a major obstacle in conducting these trials is that PD patients are largely unaware of their genetic status and, therefore, cannot be recruited. Expanding the number of investigated PD-related genes and including genes related to disorders with overlapping clinical features in large, well-phenotyped PD patient groups is a prerequisite for capturing the full variant spectrum underlying PD and for stratifying and prioritizing patients for gene-targeted clinical trials. The Rostock Parkinsonâs disease (ROPAD) study is an observational clinical study aiming to determine the frequency and spectrum of genetic variants contributing to PD in a large international cohort. We investigated variants in 50 genes with either an established relevance for PD or possible phenotypic overlap in a group of 12 580 PD patients from 16 countries [62.3% male; 92.0% White; 27.0% positive family history (FH+), median age at onset (AAO) 59 years] using a next-generation sequencing panel. Altogether, in 1864 (14.8%) ROPAD participants (58.1% male; 91.0% White, 35.5% FH+, median AAO 55 years), a PD-relevant genetic test (PDGT) was positive based on GBA1 risk variants (10.4%) or pathogenic/likely pathogenic variants in LRRK2 (2.9%), PRKN (0.9%), SNCA (0.2%) or PINK1 (0.1%) or a combination of two genetic findings in two genes (âŒ0.2%). Of note, the adjusted positive PDGT fraction, i.e. the fraction of positive PDGTs per country weighted by the fraction of the population of the world that they represent, was 14.5%. Positive PDGTs were identified in 19.9% of patients with an AAO †50 years, in 19.5% of patients with FH+ and in 26.9% with an AAO †50 years and FH+. In comparison to the idiopathic PD group (6846 patients with benign variants), the positive PDGT group had a significantly lower AAO (4 years, P = 9
7 10â34). The probability of a positive PDGT decreased by 3% with every additional AAO year (P = 1
7 10â35). Female patients were 22% more likely to have a positive PDGT (P = 3
7 10â4), and for individuals with FH+ this likelihood was 55% higher (P = 1
7 10â14). About 0.8% of the ROPAD participants had positive genetic testing findings in parkinsonism-, dystonia/dyskinesia- or dementia-related genes. In the emerging era of gene-targeted PD clinical trials, our finding that âŒ15% of patients harbour potentially actionable genetic variants offers an important prospect to affected individuals and their families and underlines the need for genetic testing in PD patients. Thus, the insights from the ROPAD study allow for data-driven, differential genetic counselling across the spectrum of different AAOs and family histories and promote a possible policy change in the application of genetic testing as a routine part of patient evaluation and care in PD
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