scholarly journals Mild Muscle Mitochondrial Fusion Distress Extends Drosophila Lifespan through an Early and Systemic Metabolome Reorganization

2021 ◽  
Vol 22 (22) ◽  
pp. 12133
Author(s):  
Andrea Tapia ◽  
Martina Palomino-Schätzlein ◽  
Marta Roca ◽  
Agustín Lahoz ◽  
Antonio Pineda-Lucena ◽  
...  
Keyword(s):  
Healthy Aging ◽  
Mitochondrial Dynamics ◽  
Nuclear Genome ◽  
Mitochondrial Fusion ◽  
Factors Affecting ◽  
Muscle Aging ◽  
Global Aging ◽  
Muscular Integrity

In a global aging population, it is important to understand the factors affecting systemic aging and lifespan. Mitohormesis, an adaptive response caused by different insults affecting the mitochondrial network, triggers a response from the nuclear genome inducing several pathways that promote longevity and metabolic health. Understanding the role of mitochondrial function during the aging process could help biomarker identification and the development of novel strategies for healthy aging. Herein, we interfered the muscle expression of the Drosophila genes Marf and Opa1, two genes that encode for proteins promoting mitochondrial fusion, orthologues of human MFN2 and OPA1. Silencing of Marf and Opa1 in muscle increases lifespan, improves locomotor capacities in the long term, and maintains muscular integrity. A metabolomic analysis revealed that muscle down-regulation of Marf and Opa1 promotes a non-autonomous systemic metabolome reorganization, mainly affecting metabolites involved in the energetic homeostasis: carbohydrates, lipids and aminoacids. Interestingly, the differences are consistently more evident in younger flies, implying that there may exist an anticipative adaptation mediating the protective changes at the older age. We demonstrate that mild mitochondrial muscle disturbance plays an important role in Drosophila fitness and reveals metabolic connections between tissues. This study opens new avenues to explore the link of mitochondrial dynamics and inter-organ communication, as well as their relationship with muscle-related pathologies, or in which muscle aging is a risk factor for their appearance. Our results suggest that early intervention in muscle may prevent sarcopenia and promote healthy aging.

The modified mitochondrial outer membrane carrier MTCH2 links mitochondrial fusion to lipogenesis

2021 ◽  
Vol 220 (11) ◽  
Author(s):  
Katherine Labbé ◽  
Shona Mookerjee ◽  
Maxence Le Vasseur ◽  
Eddy Gibbs ◽  
Chad Lerner ◽  
...  
Keyword(s):  
Lipid Metabolism ◽  
Mitochondrial Dynamics ◽  
Mitochondrial Fusion ◽  
Mitochondrial Outer Membrane ◽  
Mitochondrial Carrier ◽  
Cellular Survival ◽  
Mitochondrial Elongation ◽  
Specific Lipid

Mitochondrial function is integrated with cellular status through the regulation of opposing mitochondrial fusion and division events. Here we uncover a link between mitochondrial dynamics and lipid metabolism by examining the cellular role of mitochondrial carrier homologue 2 (MTCH2). MTCH2 is a modified outer mitochondrial membrane carrier protein implicated in intrinsic cell death and in the in vivo regulation of fatty acid metabolism. Our data indicate that MTCH2 is a selective effector of starvation-induced mitochondrial hyperfusion, a cytoprotective response to nutrient deprivation. We find that MTCH2 stimulates mitochondrial fusion in a manner dependent on the bioactive lipogenesis intermediate lysophosphatidic acid. We propose that MTCH2 monitors flux through the lipogenesis pathway and transmits this information to the mitochondrial fusion machinery to promote mitochondrial elongation, enhanced energy production, and cellular survival under homeostatic and starvation conditions. These findings will help resolve the roles of MTCH2 and mitochondria in tissue-specific lipid metabolism in animals.

scholarly journals FOXO Transcriptional Factors and Long-Term Living

2017 ◽  
Vol 2017 ◽  
pp. 1-8 ◽  
Author(s):  
Ghulam Murtaza ◽  
Abida Kalsoom Khan ◽  
Rehana Rashid ◽  
Saiqa Muneer ◽  
Syed Muhammad Farid Hasan ◽  
...  
Keyword(s):  
Transcription Factors ◽  
Healthy Aging ◽  
Growth Stress ◽  
Human Longevity ◽  
Growth Factor Signaling ◽  
Forkhead Box ◽  
Foxo Transcription Factors ◽  
Genetic And Environmental Factors

Several pathologies such as neurodegeneration and cancer are associated with aging, which is affected by many genetic and environmental factors. Healthy aging conceives human longevity, possibly due to carrying the defensive genes. For instance, FOXO (forkhead box O) genes determine human longevity. FOXO transcription factors are involved in the regulation of longevity phenomenon via insulin and insulin-like growth factor signaling. Only one FOXO gene (FOXO DAF-16) exists in invertebrates, while four FOXO genes, that is, FOXO1, FOXO3, FOXO4, and FOXO6 are found in mammals. These four transcription factors are involved in the multiple cellular pathways, which regulate growth, stress resistance, metabolism, cellular differentiation, and apoptosis in mammals. However, the accurate mode of longevity by FOXO factors is unclear until now. This article describes briefly the existing knowledge that is related to the role of FOXO factors in human longevity.

scholarly journals Rural Households’ Poverty and Relocation and Settlement: Evidence from Western China

2019 ◽  
Vol 16 (14) ◽  
pp. 2609 ◽  
Author(s):  
Wei Liu ◽  
Jie Xu ◽  
Jie Li ◽  
Shuzhuo Li
Keyword(s):  
Logistic Model ◽  
Rural Households ◽  
Western China ◽  
Multinomial Logistic Model ◽  
Factors Affecting ◽  
Chronic Poverty ◽  
Southern Shaanxi ◽  
Transient Poverty

Based on survey data collected from five counties across southern Shaanxi, China, the present study employs a multinomial logistic model to explore the main factors related to the type of poverty of rural households, particularly focusing on the role of relocation time, reason for relocation, and type of relocation. The results showed that three types of poverty, “voluntary poverty”, “transient poverty”, and “chronic poverty”, are distinguished by combining income and consumption criteria. Moreover, relocation and settlement programs contribute to a certain degree to these three kinds of poverty, and the effects vary according to the relocation characteristics. Specifically, those relocated long-term were more likely to be trapped in “voluntary poverty” and “chronic poverty”, whereas those relocated short-term were less likely to fall into “voluntary poverty” and “transient poverty”. The poverty alleviation and disaster-related resettlers were less likely to be trapped in “chronic poverty”, whereas centralized resettlers were less likely to be trapped in “voluntary poverty” and “chronic poverty”. Additionally, demographic characteristics, capital endowment variables, and geographical features are all important factors affecting rural households’ type of poverty. This study can serve as a reference for further resettlement practice in China and other developing countries.

scholarly journals T-2 Toxin-Induced Oxidative Stress Leads to Imbalance of Mitochondrial Fission and Fusion to Activate Cellular Apoptosis in the Human Liver 7702 Cell Line

Toxins ◽  
2020 ◽  
Vol 12 (1) ◽  
pp. 43 ◽  
Author(s):  
Junhua Yang ◽  
Wenbo Guo ◽  
Jianhua Wang ◽  
Xianli Yang ◽  
Zhiqi Zhang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cell Apoptosis ◽  
Human Liver ◽  
Mitochondrial Dynamics ◽  
Mitochondrial Fission ◽  
Mitochondrial Fusion ◽  
Mitochondrial Dynamic ◽  
Normal Human Liver ◽  
Induced Apoptosis

T-2 toxin, as a highly toxic mycotoxin to humans and animals, induces oxidative stress and apoptosis in various cells and tissues. Apoptosis and mitochondrial fusion/fission are two tightly interconnected processes that are crucial for maintaining physiological homeostasis. However, the role of mitochondrial fusion/fission in apoptosis of T-2 toxin remains unknown. Hence, we aimed to explore the putative role of mitochondrial fusion/fission on T-2 toxin induced apoptosis in normal human liver (HL-7702) cells. T-2 toxin treatment (0, 0.1, 1.0, or 10 μg/L) for 24 h caused decreased cell viability and ATP concentration and increased production of (ROS), as seen by a loss of mitochondrial membrane potential (∆Ψm) and increase in mitochondrial fragmentation. Subsequently, the mitochondrial dynamic imbalance was activated, evidenced by a dose-dependent decrease and increase in the protein expression of mitochondrial fusion (OPA1, Mfn1, and Mfn2) and fission (Drp1 and Fis1), respectively. Furthermore, the T-2 toxin promoted the release of cytochrome c from mitochondria to cytoplasm and induced cell apoptosis triggered by upregulation of Bax and Bax/Bcl-2 ratios, and further activated the caspase pathways. Taken together, these results indicate that altered mitochondrial dynamics induced by oxidative stress with T-2 toxin exposure likely contribute to mitochondrial injury and HL-7702 cell apoptosis.

scholarly journals Return to Work Among Stroke Survivors

2019 ◽  
Vol 67 (2) ◽  
pp. 87-94 ◽  
Author(s):  
Kristin D. Ashley ◽  
Loretta T. Lee ◽  
Karen Heaton
Keyword(s):  
Occupational Health ◽  
Return To Work ◽  
Quantitative Research ◽  
Stroke Severity ◽  
Stroke Survivors ◽  
Factors Affecting ◽  
Work And Employment ◽  
Subsequent Failure

Despite improvements in the treatment of stroke, many individuals still face cognitive, emotional, and physical impairments. Stroke is a leading cause of serious long-term disability and subsequent failure to return to work (RTW). The purpose of this literature review was to synthesize and discuss the literature relevant to factors affecting RTW for stroke survivors, summarize the identified gaps, and discuss steps occupational health nurses can take to facilitate RTW among stroke survivors. A literature search was conducted using the keywords: “stroke,” “cerebrovascular disease,” “return to work,” and “employment.” After excluding articles based on inclusion/exclusion criteria, 19 quantitative research articles were reviewed. Consistent themes found in the literature affecting RTW following stroke included physical, social, and cognitive factors. One of the most consistent predictors of RTW found was stroke severity. Individuals who experienced a mild to moderate stroke, those of Caucasian ethnicity, and higher socioeconomic levels were more likely to RTW. Findings suggest the importance of future studies to examine factors among African American stroke survivors that predict RTW and the role of occupational health nurses.

Knowledge Utilisation in AgriFood SMEs: Effects of Organisational and Informational Factors

2020 ◽  
Vol 8 (7) ◽  
pp. 235-248
Author(s):  
David Eshun Yawson
Keyword(s):  
Critical Role ◽  
User Interaction ◽  
Consumer Information ◽  
Partial Least Squares Analysis ◽  
Factors Affecting ◽  
Knowledge Utilisation ◽  
The Uk ◽  
Role Of Information

Given the critical role of information and marketing in SME management it is surprising that little attention has been paid to the salient factors that motivate or inhibits consumer information used by agrifood SMEs. A model of organisational and informational factors affecting knowledge utilisation in Agri-food SMEs is presented and empirically tested through partial least squares analysis via SmartPLS. The results of the empirical testing of the conceptual model provide evidence to indicate that functional and technical qualities, provider-user interaction and usefulness in the market environment are determinants of knowledge utilisation. The findings of this study have implications for agri-food SME management in the UK regarding their growth and competitiveness in the medium and long term.

scholarly journals Determinanty generowania kredytów gospodarczych w okresie pokryzysowym na przykładzie polskiego sektora banków spółdzielczych

2015 ◽  
Vol 2 (3) ◽  
pp. 143-160
Author(s):  
Krzysztof Kil ◽  
Ewa Miklaszewska
Keyword(s):  
Balance Sheet ◽  
Local Market ◽  
Corporate Sector ◽  
Factors Affecting ◽  
Loan Portfolios ◽  
Area Growth ◽  
Cooperative Banks

The post-crisis period stressed the role of small, local banks in corporatelending, particularly for SME, due to such their advantages as being based onrelationship banking and extensive knowledge of local market. However, it isstill unclear whether it is a short or long-term advantage. The aim of this paper isto analyze the factors affecting the size and quality of the loan portfolios of thePolish cooperative banks. In the empirical part, the study is based on statisticaldata and panel research, based on individual balance sheet data for the banksaffiliated to the BPS SA. The results confirm that the role of cooperative banksin lending to businesses increases, but also pointed to internal diversity of thesector in this area: growth in loans to the corporate sector was particularly strongfor large banks with strong capital, but also resulted in their declining safety andincreasing bad loans portfolio.

scholarly journals Role of GTPase-Dependent Mitochondrial Dynamins in Heart Diseases

2021 ◽  
Vol 8 ◽  
Author(s):  
Jiangen Liu ◽  
Xianjing Song ◽  
Youyou Yan ◽  
Bin Liu
Keyword(s):  
Cell Function ◽  
Morphological Changes ◽  
Heart Function ◽  
Mitochondrial Dynamics ◽  
Heart Diseases ◽  
Ischemia Reperfusion ◽  
Mitochondrial Fission ◽  
Mitochondrial Fusion ◽  
Dependent Manner

Heart function maintenance requires a large amount of energy, which is supplied by the mitochondria. In addition to providing energy to cardiomyocytes, mitochondria also play an important role in maintaining cell function and homeostasis. Although adult cardiomyocyte mitochondria appear as independent, low-static organelles, morphological changes have been observed in cardiomyocyte mitochondria under stress or pathological conditions. Indeed, cardiac mitochondrial fission and fusion are involved in the occurrence and development of heart diseases. As mitochondrial fission and fusion are primarily regulated by mitochondrial dynamins in a GTPase-dependent manner, GTPase-dependent mitochondrial fusion (MFN1, MFN2, and OPA1) and fission (DRP1) proteins, which are abundant in the adult heart, can also be regulated in heart diseases. In fact, these dynamic proteins have been shown to play important roles in specific diseases, including ischemia-reperfusion injury, heart failure, and metabolic cardiomyopathy. This article reviews the role of GTPase-dependent mitochondrial fusion and fission protein-mediated mitochondrial dynamics in the occurrence and development of heart diseases.

The Role of the Business Analyst in Green ICT

2011 ◽  
pp. 1495-1503
Author(s):  
Adriana Beal
Keyword(s):  
Energy Use ◽  
Acceptance Testing ◽  
Environmentally Conscious ◽  
Factors Affecting ◽  
Online Purchase ◽  
Risk Management Process ◽  
Business Analyst ◽  
Environmentally Sound

This chapter presents the role of business analysts in the green initiative of an organization. As corporations become more environmentally conscious, business objectives such as decreasing energy use and producing fewer emissions require adjustments in processes and rules governing how ICT solutions are designed and implemented. For example, optimizing the process of buying an airline ticket from a green perspective might require changing the rules for online purchase and designing an ICT solution to switch the process to a paperless, secure electronic ticketing system. The entire optimization of a process such as passenger ticketing requires analysis of the solution, its alternatives and its associated risks. This is what a business analyst does. In the past decade, the role of business analysts has rapidly evolved in multiple directions to encompass activities such as business evaluation, risk management, process modeling, dealing with metrics and measurement and undertaking acceptance testing of solutions. This chapter discusses how business analysts can provide an invaluable contribution to the process of developing environmentally sound ICT practices within and around the organization. Organizations need to get their green credentials in order (Information Age, 2007). They also need to take a strategic, long term view of the environmental factors affecting their business. A business analyst, as discussed here, helps bring together myriad variables into a cohesive and comprehensive plan to address the various long-term and strategic aspects of greening ICT processes in the broad context of the corporation, the industry and the overall business ecosystem.

Mitochondrial Fusion Suppresses Tau Pathology-Induced Neurodegeneration and Cognitive Decline

2021 ◽  
pp. 1-13
Author(s):  
Luwen Wang ◽  
Mengyu Liu ◽  
Ju Gao ◽  
Amber M. Smith ◽  
Hisashi Fujioka ◽  
...  
Keyword(s):  
Mitochondrial Dynamics ◽  
Mitochondrial Fission ◽  
Neuronal Loss ◽  
Mitochondrial Fusion ◽  
Barnes Maze ◽  
Mitochondrial Fragmentation ◽  
Tau Pathology ◽  
Marked Suppression

Background: Abnormalities of mitochondrial fission and fusion, dynamic processes known to be essential for various aspects of mitochondrial function, have repeatedly been reported to be altered in Alzheimer’s disease (AD). Neurofibrillary tangles are known as a hallmark feature of AD and are commonly considered a likely cause of neurodegeneration in this devastating disease. Objective: To understand the pathological role of mitochondrial dynamics in the context of tauopathy. Methods: The widely used P301S transgenic mice of tauopathy (P301S mice) were crossed with transgenic TMFN mice with the forced expression of Mfn2 specifically in neurons to obtain double transgenic P301S/TMFN mice. Brain tissues from 11-month-old non-transgenic (NTG), TMFN, P301S, and P301S/TMFN mice were analyzed by electron microscopy, confocal microscopy, immunoblot, histological staining, and immunostaining for mitochondria, tau pathology, and tau pathology-induced neurodegeneration and gliosis. The cognitive function was assessed by the Barnes maze. Results: P301S mice exhibited mitochondrial fragmentation and a consistent decrease in Mfn2 compared to age-matched NTG mice. When P301S mice were crossed with TMFN mice (P301S/TMFN mice), neuronal loss, as well as mitochondria fragmentation were significantly attenuated. Greatly alleviated tau hyperphosphorylation, filamentous aggregates, and thioflavin-S positive tangles were also noted in P301S/TMFN mice. Furthermore, P301S/TMFN mice showed marked suppression of neuroinflammation and improved cognitive performance in contrast to P301S mice. Conclusion: These in vivo findings suggest that promoted mitochondrial fusion suppresses toxic tau accumulation and associated neurodegeneration, which may protect against the progression of AD and related tauopathies.

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