Purpose
Ostracism within organizations may pose communication challenges and reduce opportunities for interactions, potentially affecting coworker knowledge sharing and subsequent performance outcomes. Drawing on conservation of resources theory, the purpose of this paper is to examine whether knowledge sharing mediates the association between workplace ostracism and employees’ task performance, and whether the mediating effect is moderated by task interdependence.
Design/methodology/approach
Matched data were collected from a two-wave survey among 210 employees and their direct supervisors who work in two Chinese enterprises.
Findings
Results indicate that workplace ostracism is negatively associated with task performance and that knowledge sharing mediates this relation. Further, task interdependence exacerbated the main effect of workplace ostracism and the indirect effect of knowledge sharing.
Originality/value
This paper offers an alternative perspective (i.e. pragmatic impacts of workplace ostracism) to understand how workplace ostracism undermines employees’ task performance. Moreover, the findings emphasize that contextual factors may strengthen the detrimental effects of workplace ostracism in the practical domain.
Background
Gut microbiota has been found involved in neuronal functions and neurological disorders. Whether and how gut microbiota impacts chronic somatic pain disorders remain elusive.
Methods
Neuropathic pain was produced by different forms of injury or diseases, the chronic constriction injury (CCI) of the sciatic nerves, oxaliplatin (OXA) chemotherapy, and streptozocin (STZ)-induced diabetes in mice. Continuous feeding of antibiotics (ABX) cocktail was used to cause major depletion of the gut microbiota. Fecal microbiota, biochemical changes in the spinal cord and dorsal root ganglion (DRG), and the behaviorally expressed painful syndromes were assessed.
Results
Under condition of gut microbiota depletion, CCI, OXA, or STZ treatment-induced thermal hyperalgesia or mechanical allodynia were prevented or completely suppressed. Gut microbiota depletion also prevented CCI or STZ treatment-induced glial cell activation in the spinal cord and inhibited cytokine production in DRG in OXA model. Interestingly, STZ treatment failed to induce the diabetic high blood glucose and painful hypersensitivity in animals with the gut microbiota depletion. ABX feeding starting simultaneously with CCI, OXA, or STZ treatment resulted in instant analgesia in all the animals. ABX feeding starting after establishment of the neuropathic pain in CCI- and STZ-, but not OXA-treated animals produced significant alleviation of the thermal hyeralgesia or mechanical allodynia. Transplantation of fecal bacteria from SPF mice to ABX-treated mice partially restored the gut microbiota and fully rescued the behaviorally expressed neuropathic pain, of which, Akkermansia, Bacteroides, and Desulfovibrionaceae phylus may play a key role.
Conclusion
This study demonstrates distinct roles of gut microbiota in the pathogenesis of chronic painful conditions with nerve injury, chemotherapy and diabetic neuropathy and supports the clinical significance of fecal bacteria transplantation.
Previous studies have suggested that polysaccharide from Enteromorpha clathrata (ECP) could be used as a potential prebiotic to treat dysbiosis-associated diseases. However, whether it has any therapeutic effects on obesity has not been investigated. In the present study, we explored the anti-obesity effect of ECP and illustrated that it can significantly reduce the body weight and decrease the serum levels of triacylglycerol and cholesterol in high-fat diet (HFD)-fed mice. As revealed by 16S rRNA high-throughput sequencing and bioinformatic analysis, HFD remarkably changed the composition of the gut microbiota and promoted the growth of opportunistic pathogens such as Mucispirillum, Desulfobacterota and Alphaproteobacteria in obese mice. Interestingly, ECP improved intestinal dysbiosis caused by HFD and reshaped the structure of the gut microbiota in diseased mice by increasing the abundance of butyrate-producing bacterium, Eubacterium xylanophilum, in the gut. Altogether, we demonstrate for the first time an anti-obesity effect of ECP and shed new light into its therapeutic mechanisms from the perspective of gut microbiota. Our study will pave the way for the development of ECP as new prebiotic for the treatment of obesity and its associated disorders.
The analysis of noncovalent interactions in several complexes constructed from 2,3,5,6-tetramethylpyrazine with different acid ligands, 1,4-cyclohexanedicarboxylic acid, 2,6-dihydroxybenzoic acid, 2,6-pyridinedicarboxylic acid, 6-hydroxy-2-naphthoic acid, 3-nitrophthalic acid, o-phthalic acid and 3-hydroxybenzoic acid, supported by single crystal X-ray diffraction analysis is presented. It reveals that all of these forms except 2 are organic supramolecular cocrystals without charge-transfer between the multicomponent acids and the base. The noncovalent interactions directing the assemblies of the eight structures are managed by classical O-H⋯O, O-H⋯N, weak C-H⋯O and π-π stacking interactions to generate 2D or 3D supermolecular architectures. For 5, 6, 7 and 8, carboxyl/pyrazine supramolecular heterosynthons R 2 2 (6) and R 2 2 (8) containing classical O-H⋯N and weak C-H⋯O interactions, usually observed in organic cocrystals of carboxylic acid and heterocyclic base, are again confirmed to participate in constructing these hydrogen-bonding supermolecular networks. In addition, weak C-H⋯O interactions were involved in building and consolidating their structures in all organic complexes. The thermal stability of crystals 1-8 has been investigated by thermogravimetric analysis (TGA) of mass loss.
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