Publications by authors named "W Hubbard"
Intercellular mitochondrial transfer (IMT) is an intriguing biological phenomenon where mitochondria are transferred between different cells and notably, cell types. IMT is physiological, occurring in normal conditions, but also is utilized to deliver healthy mitochondria to cells in distress. Transferred mitochondria can be integrated to improve cellular metabolism, and mitochondrial function.
View Article and Find Full Text PDFBackground: Neurovascular deficits and blood-brain barrier (BBB) dysfunction are major hallmarks of brain trauma and neurodegenerative diseases. Oxidative stress is a prominent contributor to neurovascular unit (NVU) dysfunction and can propagate BBB disruption. Oxidative damage results in an imbalance of mitochondrial homeostasis, which can further drive functional impairment of brain capillaries.
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- Current research indicates that females generally recover better than males after severe traumatic brain injury (TBI), while the opposite occurs with mild TBI, raising questions about the underlying causes of these sex differences.
- The hormone estrogen may provide protective benefits to mitochondria, which are crucial for energy production and often suffer damage during TBI, and studies have shown that mitochondrial impairment is more pronounced in males.
- The study hypothesized that treating isolated mitochondria with estrogen would enhance their function post-TBI in mice, revealing sex-specific differences in mitochondrial injury 24 hours after severe injury, with males experiencing more extensive bioenergetic and functional deficits compared to females.
Better techniques for imaging ferroelectric polarization would aid the development of new ferroelectrics and the refinement of old ones. Here we show how scanning transmission electron microscope (STEM) electron beam-induced current (EBIC) imaging reveals ferroelectric polarization with obvious, simply interpretable contrast. Planar imaging of an entire ferroelectric hafnium zirconium oxide (HfZrO, HZO) capacitor shows an EBIC response that is linearly related to the polarization determined with the positive-up, negative-down (PUND) method.
View Article and Find Full Text PDFApolipoprotein ε4 (APOE4) carriers develop brain metabolic dysfunctions decades before the onset of Alzheimer's disease (AD). A goal of the study is to identify if rapamycin, an inhibitor for the mammalian target of rapamycin (mTOR) inhibitor, would enhance synaptic and mitochondrial function in asymptomatic mice with human APOE4 gene (E4FAD) before they showed metabolic deficits. A second goal is to determine whether there may be genetic-dependent responses to rapamycin when compared to mice with human APOE3 alleles (E3FAD), a neutral AD genetic risk factor.
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