Strain Energy During Mechanical Milling: Part II. Experimental

The strain energy stored in mechanically milled 5083 Al powders was investigated using two experimental approaches: thermal and microstructural analysis. The experimental results show that mechanically milled 5083 Al powders store strain energy on the order of a few tens of joules per gram. These experimental results are consistent with the calculated strain energy stored in mechanically milled powders. The experimentally measured strain energy stored in powders increases with an increase in attritor diameter, impeller\u27s rotational frequency, and ball-to-powder mass ratio; however, it decreases with an increase in ball diameter. These trends were in good agreement with the calculated strain energy stored in powders as a function of the corresponding processing parameters

The Neuronal Kinesin UNC-104/KIF1A Is a Key Regulator of Synaptic Aging and Insulin Signaling-Regulated Memory

Aging is the greatest risk factor for a number of neurodegenerative diseases, such as Alzheimer’s and Parkinson’s disease. Furthermore, normal aging is associated with a decline in sensory, motor, and cognitive functions. Emerging evidence suggests that synapse alterations, rather than neuronal cell death, are the causes of neuronal dysfunctions in normal aging, and in early stages of neurodegenerative diseases. However, little is known about the mechanisms underlying age-related synaptic decline. Here we uncover a surprising role of the anterograde molecular motor UNC-104/KIF1A as a key regulator of neural circuit deterioration in aging C. elegans. Through analyses of synapse protein localization, synaptic transmission, and animal behaviors, we find that reduced function of UNC-104 accelerates motor circuit dysfunction with age, while upregulation of UNC-104 significantly improves motor function at advanced ages and also mildly extends lifespan. In addition, UNC-104-overexpressing animals outperform wild-type controls in associative learning and memory tests. Further genetic analyses suggest that UNC-104 functions downstream of the DAF-2 signaling pathway, and is regulated by the FOXO transcription factor DAF-16, which contributes to the effects of DAF-2 in neuronal aging. Together, our cellular, electrophysiological, and behavioral analyses highlight the importance of axonal transport in the maintenance of synaptic structural integrity and function during aging, and raise the possibility of targeting kinesins to slow age-related neural circuit dysfunction