scholarly journals How is auxin linked with cellular energy pathways to promote growth?

2022 ◽  
Author(s):  
Nathan D Tivendale ◽  
A. Harvey Millar
Keyword(s):  
Cellular Energy ◽  
Energy Pathways

scholarly journals Development of Scenarios for a Multi-Model System Analysis Based on the Example of a Cellular Energy System

Energies ◽  
2020 ◽  
Vol 13 (4) ◽  
pp. 773 ◽  
Author(s):  
Matthias Kühnbach ◽  
Felix Guthoff ◽  
Anke Bekk ◽  
Ludger Eltrop
Keyword(s):  
System Analysis ◽  
Energy System ◽  
Model System ◽  
Added Value ◽  
Cellular Energy ◽  
Quantitative Parameters ◽  
Points Of View ◽  
Consistent Basis ◽  
Model Environment ◽  
Energy Pathways

Scenario analysis combined with system and market modelling is a well-established method to evaluate technological and societal developments and their impacts on future energy pathways. This paper presents a process-oriented method for developing consistent energy scenarios using multiple energy system models. Its added value is that the developed energy scenarios are consistent in a multi-model environment and practicable for a broader target group from scientists to practitioners. The scenarios consist of comprehensive storylines and systematically defined quantitative parameters. Following a step-by-step process, a condensed set of overlapping descriptors is generated and used to define the scenarios in a consistent parameter matrix. The set of descriptors allow consistent and comparable outputs independent of model-specific characteristics. The corresponding quantitative parameters can be used by diverse energy system tools. Using multiple models, a team of researchers can explore questions from differing points of view. In an example study, we apply the method to develop scenarios in the context of a cellular energy system. This approach enables the development of scenarios that provide a consistent basis for both stakeholder discourse and multi-model system analysis.

scholarly journals Chytridiomycosis causes catastrophic organism-wide metabolic dysregulation including profound failure of cellular energy pathways

2018 ◽  
Vol 8 (1) ◽  
Author(s):  
Laura F. Grogan ◽  
Lee F. Skerratt ◽  
Lee Berger ◽  
Scott D. Cashins ◽  
Robert D. Trengove ◽  
...  
Keyword(s):  
Cellular Energy ◽  
Metabolic Dysregulation ◽  
Energy Pathways

scholarly journals Transcriptomic, proteomic, and metabolomic analyses identify candidate pathways linking maternal cadmium exposure to altered neurodevelopment and behavior

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Kathleen M. Hudson ◽  
Emily Shiver ◽  
Jianshi Yu ◽  
Sanya Mehta ◽  
Dereje D. Jima ◽  
...  
Keyword(s):  
Molecular Mechanisms ◽  
Placental Transfer ◽  
Developing Brain ◽  
Rna Seq ◽  
Toxic Heavy Metal ◽  
Cellular Energy ◽  
Body Weights ◽  
And Behavior ◽  
Cd Exposure ◽  
Energy Pathways

AbstractCadmium (Cd) is a ubiquitous toxic heavy metal of major public concern. Despite inefficient placental transfer, maternal Cd exposure impairs fetal growth and development. Increasing evidence from animal models and humans suggests maternal Cd exposure negatively impacts neurodevelopment; however, the underlying molecular mechanisms are unclear. To address this, we utilized multiple -omics approaches in a mouse model of maternal Cd exposure to identify pathways altered in the developing brain. Offspring maternally exposed to Cd presented with enlarged brains proportional to body weights at birth and altered behavior at adulthood. RNA-seq in newborn brains identified exposure-associated increases in Hox gene and myelin marker expression and suggested perturbed retinoic acid (RA) signaling. Proteomic analysis showed altered levels of proteins involved in cellular energy pathways, hypoxic response, and RA signaling. Consistent with transcriptomic and proteomic analyses, we identified increased levels of retinoids in maternally-exposed newborn brains. Metabolomic analyses identified metabolites with significantly altered abundance, supportive of changes to cellular energy pathways and hypoxia. Finally, maternal Cd exposure reduced mitochondrial DNA levels in newborn brains. The identification of multiple pathways perturbed in the developing brain provides a basis for future studies determining the mechanistic links between maternal Cd exposure and altered neurodevelopment and behavior.

Potentiation of bromotrichloromethane hepatotoxicity in male rats exposed to 10 ppm dietary chlordecone: Electron Microscopic and biochemical study

1990 ◽  
Vol 48 (3) ◽  
pp. 284-285
Author(s):  
O. M. Faroon ◽  
R. W. Henry ◽  
M. G. Soni ◽  
H. M. Mehendale
Keyword(s):  
Free Radical ◽  
Biochemical Study ◽  
Prior Exposure ◽  
Male Rats ◽  
Cellular Injury ◽  
Low Doses ◽  
Mixed Function Oxidase ◽  
Electron Microscopic ◽  
Potent Inducer ◽  
Cellular Energy

Previous work has shown that mirex undergoes photolytic dechlorination to chlordecone (CD) (KeponeR) in the environment. Much work has shown that prior exposure to nontoxic levels of CD causes potentiation of hepatotoxicity and lethality of CCl4, BrCCl3 and other halomethane compounds. Potentiation of bromotrichloromethane hepatotoxicity has been associated with compounds that stimulate the activity of hepatic mixed-function oxidase (MFO). An increase in the metabolism of halomethane by the MFO to a free radical initiates peroxidative decomposition of membranal lipids ending in massive cellular injury. However, not all MFO inducers potentiate BrCCl3 hepatotoxicity. Potentiation by much larger doses of phenobarbital is minimal and th at by a more potent inducer of MFO, mirex, is negligible at low doses. We suggest that the CD and bromotrichloromethane interaction results in a depletion of cellular energy and thereby reducing the cellular ability to undergo mitosis.

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