Electronic Asymmetric Distribution of RhCu Bimetallic Nanocrystals for Enhancing Trifunctional Electrocatalysis

2020 ◽  
Vol 12 (9) ◽  
pp. 10299-10306 ◽  
Author(s):  
Wenqing Zhang ◽  
Jun Zhao ◽  
Jian Zhang ◽  
Xijie Chen ◽  
Xin Zhang ◽  
...  
Keyword(s):  
Asymmetric Distribution ◽  
Bimetallic Nanocrystals

Redox Reactions in Lipid Membranes as a Model for Primordial Energy-Conserving Systems

1997 ◽  
Vol 161 ◽  
pp. 437-442
Author(s):  
Salvatore Di Bernardo ◽  
Romana Fato ◽  
Giorgio Lenaz
Keyword(s):  
Experimental Evidence ◽  
Lipid Membranes ◽  
Energy Supply ◽  
Redox Reactions ◽  
Living Systems ◽  
Asymmetric Distribution ◽  
Conservation Of Energy ◽  
Asymmetrical Distribution ◽  
Energy Conserving ◽  
Living Organisms

AbstractOne of the peculiar aspects of living systems is the production and conservation of energy. This aspect is provided by specialized organelles, such as the mitochondria and chloroplasts, in developed living organisms. In primordial systems lacking specialized enzymatic complexes the energy supply was probably bound to the generation and maintenance of an asymmetric distribution of charged molecules in compartmentalized systems. On the basis of experimental evidence, we suggest that lipophilic quinones were involved in the generation of this asymmetrical distribution of charges through vectorial redox reactions across lipid membranes.

scholarly journals The α-Synuclein Origin and Connectome Model (SOC Model) of Parkinson’s Disease: Explaining Motor Asymmetry, Non-Motor Phenotypes, and Cognitive Decline

2021 ◽  
Vol 11 (2) ◽  
pp. 455-474
Author(s):  
Per Borghammer
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Cognitive Decline ◽  
Explanatory Power ◽  
Anatomical Location ◽  
Asymmetric Distribution ◽  
Motor Asymmetry ◽  
Parasympathetic Innervation ◽  
Considerable Body ◽  
Dopaminergic Degeneration

A new model of Parkinson’s disease (PD) pathogenesis is proposed, the α-Synuclein Origin site and Connectome (SOC) model, incorporating two aspects of α-synuclein pathobiology that impact the disease course for each patient: the anatomical location of the initial α-synuclein inclusion, and α-synuclein propagation dependent on the ipsilateral connections that dominate connectivity of the human brain. In some patients, initial α-synuclein pathology occurs within the CNS, leading to a brain-first subtype of PD. In others, pathology begins in the peripheral autonomic nervous system, leading to a body-first subtype. In brain-first cases, it is proposed that the first pathology appears unilaterally, often in the amygdala. If α-synuclein propagation depends on connection strength, a unilateral focus of pathology will disseminate more to the ipsilateral hemisphere. Thus, α-synuclein spreads mainly to ipsilateral structures including the substantia nigra. The asymmetric distribution of pathology leads to asymmetric dopaminergic degeneration and motor asymmetry. In body-first cases, the α-synuclein pathology ascends via the vagus to both the left and right dorsal motor nuclei of the vagus owing to the overlapping parasympathetic innervation of the gut. Consequently, the initial α-synuclein pathology inside the CNS is more symmetric, which promotes more symmetric propagation in the brainstem, leading to more symmetric dopaminergic degeneration and less motor asymmetry. At diagnosis, body-first patients already have a larger, more symmetric burden of α-synuclein pathology, which in turn promotes faster disease progression and accelerated cognitive decline. The SOC model is supported by a considerable body of existing evidence and may have improved explanatory power.

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