scholarly journals Systems and classical biology approaches unraveled role of olfactory receptors in progression of kidney fibrosis

2020 ◽  
Author(s):  
Ali Motahharynia ◽  
Shiva Moein ◽  
Farnoush Kiyanpour ◽  
Kobra Moradzadeh ◽  
Yousof Gheisari

AbstractThe olfactory receptors (ORs) which are mainly known as odor-sensors in the olfactory epithelium are distributed in several non-sensory tissues. Despite the specified role of some of these receptors in normal physiology of the kidney, little is known about their potential effect in renal disorders. In this study, using the holistic view of systems biology, it was determined that ORs are significantly changed during the progression of kidney fibrosis. For further validation, common differentially expressed ORs resulted from reanalysis of two time-course microarray datasets were selected for experimental evaluation in a validated murine model of unilateral ureteral obstruction. Transcriptional analysis demonstrated considerable changes in the expression pattern of Olfr433, Olfr129, Olfr1393, and Olfr161 during the progression of kidney fibrosis. In conclusion, our results highlight the impact of systems biology in determination of the underlying mechanisms of chronic diseases and indicate the importance of time-course approaches to unravel the patterns of gene expression. The novel ORs proposed in this study could be the subject of further functional investigations in the kidney.

Antioxidants ◽  
2021 ◽  
Vol 10 (6) ◽  
pp. 933
Author(s):  
Andrea Gila-Diaz ◽  
Gloria Herranz Carrillo ◽  
Pratibha Singh ◽  
David Ramiro-Cortijo

Cardiovascular disease remains a leading cause of mortality worldwide. Unresolved inflammation plays a critical role in cardiovascular diseases development. Specialized Pro-Resolving Mediators (SPMs), derived from long chain polyunsaturated fatty acids (LCPUFAs), enhances the host defense, by resolving the inflammation and tissue repair. In addition, SPMs also have anti-inflammatory properties. These physiological effects depend on the availability of LCPUFAs precursors and cellular metabolic balance. Most of the studies have focused on the impact of SPMs in adult cardiovascular health and diseases. In this review, we discuss LCPUFAs metabolism, SPMs, and their potential effect on cardiovascular health and diseases primarily focusing in neonates. A better understanding of the role of these SPMs in cardiovascular health and diseases in neonates could lead to the development of novel therapeutic approaches in cardiovascular dysfunction.


Author(s):  
Shuyang Wang ◽  
Yun Liu ◽  
Yingying Du ◽  
Xingyuan Wang

Based on event systems theory, this study examined the impact of the COVID-19 pandemic on consumers’ impulse buying, as well as the underlying mechanisms and boundary conditions from the perspective of individual consumers. Results of three experiments (N = 437) show that, first, the COVID-19 pandemic enhanced consumers’ impulse buying behavior. Second, two key elements, loss of control and anxiety, mediated the relationship between the COVID-19 pandemic and impulse buying; and third, moderate thinking (also known as Zhong-Yong thinking) moderated the relationship between the COVID-19 pandemic and impulse buying. The findings indicate that in consumers with low moderate thinking, the COVID-19 pandemic has had a stronger effect on impulse buying and has mediated more between the loss of control and anxiety. Conversely, in consumers with high moderate thinking, COVID-19 has had a weaker effect on impulse buying and has mediated less between loss of control and anxiety. This study extends the application of event systems theory and enriches the literature on how the COVID-19 pandemic affects consumer behavior. Furthermore, it provides strategic recommendations for government and consumer responses to COVID-19 pandemic shocks.


2018 ◽  
Vol 21 (4) ◽  
pp. 672-694 ◽  
Author(s):  
Irem Demirkan

PurposeThe purpose of this paper is to propose that the resources that a firm owns and has full control (firm-level resources) and resources that a firm access through direct connection with other firms (network-level resources) will impact firm innovation when effectively deployed by the firm. While previous research examined these factors separately, the author takes a holistic view and looks into their effects on innovation simultaneously. The author also introduces the moderating effects, i.e. the variables that can enhance firm innovation through their interaction with internal and external resources.Design/methodology/approachThe author tested the role of financial resources and slack resources in the form of cash slack and human slack at the firm level, and network size, network tie strength, and network diversity at the network level on the firm innovation. Using generalized negative binomial model with Huber-White procedure, the author analyzed 306 firms from the biotechnology industry over a span of 17 years.FindingsThe analysis suggests that cash slack impact innovation negatively. However, this link is moderated by firm size such that for large firms cash slack affects innovation positively. Network-level resources all positively impact innovation and have more economic impact on firm innovation than firm-level resources. Furthermore, although human slack negatively affects innovation, its interaction with network size enhances innovation.Originality/valueThe research makes important contributions to both strategic management and innovation literatures especially when, the author considers the role of firm-level slack in driving firm innovation. Previous research reported conflicting findings about the availability of slack resources and firm performance. The results showed that the relationship between slack resources and firm innovation is negative and significant, both for available slack and human slack. This finding parallels with previous research which reported that constraints such as lack of slack resources can actually facilitate innovation. The author also contributes to the literature by introducing boundary conditions which can enhance firm innovation through their interaction with firm-level internal and network-level external resources. In this respect, to the author’s knowledge, this is among the first studies to combine the slack literature focusing on firm-level resources with the literature on network-level resources.


2007 ◽  
Vol 293 (5) ◽  
pp. F1489-F1500 ◽  
Author(s):  
Armin Just ◽  
William J. Arendshorst

Autoregulation of renal blood flow (RBF) is mediated by a fast myogenic response (MR; ∼5 s), a slower tubuloglomerular feedback (TGF; ∼25 s), and potentially additional mechanisms. A1 adenosine receptors (A1AR) mediate TGF in superficial nephrons and contribute to overall autoregulation, but the impact on the other autoregulatory mechanisms is unknown. We studied dynamic autoregulatory responses of RBF to rapid step increases of renal artery pressure in mice. MR was estimated from autoregulation within the first 5 s, TGF from that at 5–25 s, and a third mechanism from 25–100 s. Genetic deficiency of A1AR (A1AR−/−) reduced autoregulation at 5–25 s by 50%, indicating a residual fourth mechanism resembling TGF kinetics but independent of A1AR. MR and third mechanism were unaltered in A1AR−/−. Autoregulation in A1AR−/− was faster at 5–25 than at 25–100 s suggesting two separate mechanisms. Furosemide in wild-type mice (WT) eliminated the third mechanism and enhanced MR, indicating TGF-MR interaction. In A1AR−/−, furosemide did not further impair autoregulation at 5–25 s, but eliminated the third mechanism and enhanced MR. The resulting time course was the same as during furosemide in WT, indicating that A1AR do not affect autoregulation during furosemide inhibition of TGF. We conclude that at least one novel mechanism complements MR and TGF in RBF autoregulation, that is slower than MR and TGF and sensitive to furosemide, but not mediated by A1AR. A fourth mechanism with kinetics similar to TGF but independent of A1AR and furosemide might also contribute. A1AR mediate classical TGF but not TGF-MR interaction.


2021 ◽  
Vol 12 ◽  
Author(s):  
Chioma Enweasor ◽  
Cameron H. Flayer ◽  
Angela Haczku

Despite recent advances in using biologicals that target Th2 pathways, glucocorticoids form the mainstay of asthma treatment. Asthma morbidity and mortality remain high due to the wide variability of treatment responsiveness and complex clinical phenotypes driven by distinct underlying mechanisms. Emerging evidence suggests that inhalation of the toxic air pollutant, ozone, worsens asthma by impairing glucocorticoid responsiveness. This review discusses the role of oxidative stress in glucocorticoid resistance in asthma. The underlying mechanisms point to a central role of oxidative stress pathways. The primary data source for this review consisted of peer-reviewed publications on the impact of ozone on airway inflammation and glucocorticoid responsiveness indexed in PubMed. Our main search strategy focused on cross-referencing “asthma and glucocorticoid resistance” against “ozone, oxidative stress, alarmins, innate lymphoid, NK and γδ T cells, dendritic cells and alveolar type II epithelial cells, glucocorticoid receptor and transcription factors”. Recent work was placed in the context from articles in the last 10 years and older seminal research papers and comprehensive reviews. We excluded papers that did not focus on respiratory injury in the setting of oxidative stress. The pathways discussed here have however wide clinical implications to pathologies associated with inflammation and oxidative stress and in which glucocorticoid treatment is essential.


2019 ◽  
Vol 9 (7) ◽  
pp. 158 ◽  
Author(s):  
Claudia Jorgensen ◽  
James Taylor ◽  
Tyler Barton

Adult neurogenesis—the formation and functional integration of adult-generated neurons—remains a hot neuroscience topic. Decades of research have identified numerous endogenous (such as neurotransmitters and hormones) and exogenous (such as environmental enrichment and exercise) factors that regulate the various neurogenic stages. Stress, an exogenous factor, has received a lot of attention. Despite the large number of reviews discussing the impact of stress on adult neurogenesis, no systematic review on ethologically relevant stressors exists to date. The current review details the effects of conspecifically-induced psychosocial stress (specifically looking at the lack or disruption of social interactions and confrontation) as well as non-conspecifically-induced stress on mammalian adult neurogenesis. The underlying mechanisms, as well as the possible functional role of the altered neurogenesis level, are also discussed. The reviewed data suggest that ethologically relevant stressors reduce adult neurogenesis.


2021 ◽  
Vol ahead-of-print (ahead-of-print) ◽  
Author(s):  
Muhammd Usman ◽  
Yuxin Liu ◽  
Jianwei Zhang ◽  
Usman Ghani ◽  
Habib Gul

PurposeBased on the conservation of resources view, the objective of this paper is to examine the relationship between abusive supervision and workplace thriving. Further, this study investigates the underlying mechanisms role of agentic work behaviors (i.e. task focus, heedful relating) and moderating role of employee's core self-evaluations.Design/methodology/approachUsing a time-lag approach, data are collected from 360 full-time employees enrolled in an executive development program in a large university of China. To test the proposed model, data analysis is carried out through Statistical Product and Service Solutions (SPSS) and Analysis of Moment Structures (AMOS).FindingsThe results show that abusive supervision negatively influences workplace thriving. Further, the findings also confirm the mediating role of agentic work behaviors and the moderating role of core self-evaluations between the relationship of abusive supervision and thriving.Practical implicationsBased on study findings, this study draws the attention of managers toward the new deleterious outcomes of abusive supervision. Hence, to nurture a thriving workforce, organizations should keep abusive behaviors under keen observations to minimize their frequent occurrences. Further, it is proposed that hiring employees with higher core self-evaluations can mitigate the injurious effect of abusive supervision.Originality/valueThis is the first attempt to our knowledge to untapped the abusive supervision-thriving relationship via the underlying mechanisms of two agentic work behavior's and core self-evaluations as a moderator enriches the extant body of knowledge and provide valuable insight into the abusive supervision and workplace thriving literature.


Author(s):  
Byung-Jik Kim ◽  
Mohammad Nurunnabi ◽  
Tae-Hyun Kim ◽  
Se-Youn Jung

Although some previous studies have examined the impact of corporate social responsibility (CSR) on employees in an organization, they have mainly focused on employees’ perceptions or attitudes rather than behaviors. However, in that employees’ behaviors are the direct outcome of the perceptions or attitudes and critically affect organizational outcomes, we need to investigate the impact of CSR on employees’ behaviors. Based on the context-attitude-behavior framework, we investigate the underlying process of the association between CSR and employees’ behavior with a moderated mediation model. Specifically, we hypothesize (1) the intermediating effect of organizational commitment (OC) in the association between CSR and organizational citizenship behavior (OCB) and (2) the contingent role of employees’ perspective taking ability (PT) in the CSR-OC link. Using three-wave survey data from 301 currently working employees in Korea, we found that OC mediates the association between CSR and OCB and that PT can positively moderate the CSR-OC link. Our findings suggest that OC (as an intermediating process) and PT (as a contingent factor) function as important underlying mechanisms to elaborately describe the CSR-OCB link.


F1000Research ◽  
2017 ◽  
Vol 6 ◽  
pp. 405
Author(s):  
Adina Howe ◽  
Michael Howe ◽  
Amy L. Kaleita ◽  
D. Raj Raman

As part of a recent workshop entitled "Imagining Tomorrow's University”, we were asked to visualize the future of universities as research becomes increasingly data- and computation-driven, and identify a set of principles characterizing pertinent opportunities and obstacles presented by this shift. In order to establish a holistic view, we take a multilevel approach and examine the impact of open science on individual scholars as well as on the university as a whole. At the university level, open science presents a double-edged sword: when well executed, open science can accelerate the rate of scientific inquiry across the institution and beyond; however, haphazard or half-hearted efforts are likely to squander valuable resources, diminish university productivity and prestige, and potentially do more harm than good. We present our perspective on the role of open science at the university.


2019 ◽  
Author(s):  
Xiong Zhang ◽  
Lan-Bing Zhu ◽  
Jia-Hui He ◽  
Hong-Qiu Zhang ◽  
Shu-Ya Ji ◽  
...  

Abstract Background Astrocytes are the most abundant glial cells in a brain that mediate inflammatory responses and provide trophic support for neurons. We have previously disclosed that paroxetine, a common selective serotonin reuptake inhibitor, ameliorates LPS-induced microglia activation. However, it remains elusive of the role of paroxetine in astrocytic responses. Methods Isolated primary astrocytes were pretreated with paroxetine and stimulated with different stimuli, lipopolysaccharide (LPS) or microglia conditioned medium pre-activated with LPS (M/Lps). Inflammatory and neurotrophic responses, underlying mechanisms and the impact on neuronal survival were assessed. Results Paroxetine had no impact on LPS-stimulated iNOS, TNF-α and IL-1β expression, but inhibited M/Lps-induced TNF-α and IL-1β expression in primary astrocytes. Paroxetine suppressed M/Lps- but not LPS-induced activation of NF-κB and had no impact on activation of MAPKs and STAT3. Incubation with the resulted astrocyte conditioned media caused no change in viability of SH-SY5Y cells. BDNF and MANF mRNA expressions were upregulated by M/Lps and paroxetine, respectively. However, M/Lps- or LPS-induced extracellular releases of NO, TNF-α and/or BDNF in astrocytes were in minor amount compared to those by microglia. Conclusions Paroxetine ameliorates the reactive microglia-mediated inflammatory responses in astrocytes partially via inhibition of NF-κB pathway, but has no impact on LPS-stimulated astrocyte activation. While the secondary astrocytic responses are not robust compared to the innate immune responses of microglia, our results support a therapeutic potential of paroxetine against neuroinflammation-associated neurological disorders such as Parkinson’s disease.


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