Proc Natl Acad Sci U S A
August 2024
The fundamental question of "what is the transport path of electrons through proteins?" initially introduced while studying long-range electron transfer between localized redox centers in proteins in vivo is also highly relevant to the transport properties of solid-state, dry metal-protein-metal junctions. Here, we report conductance measurements of such junctions, Au-( monolayer ensemble)-Bismuth (Bi) ones, with well-defined nanopore geometry and ~10 proteins/pore. Our results can be understood as follows.
View Article and Find Full Text PDFJunctions based on electronic ballistic waveguides, such as semiconductor nanowires or nanoribbons with transverse structural variations in the order of a large fraction of their Fermi wavelength, are suggested as highly efficient thermoelectric (TE) devices. Full harnessing of their potential requires a capability to either deterministically induce structural variations that tailor their transmission properties at the Fermi level or alternatively to form waveguides that are disordered (chaotic) but can be structurally modified continuously until favorable TE properties are achieved. Well-established methods to realize either of these routes do not exist.
View Article and Find Full Text PDFWe report of a high yield method to form nanopore molecular ensembles junctions containing ~40,000 molecules, in which the semimetal bismuth (Bi) is a top contact. Conductance histograms of these junctions are double-peaked (bi-modal), a behavior that is typical for single molecule junctions but not expected for junctions with thousands of molecules. This unique observation is shown to result from a new form of quantum interference that is inter-molecular in nature, which occurs in these junctions since the very long coherence length of the electrons in Bi enables them to probe large ensembles of molecules while tunneling through the junctions.
View Article and Find Full Text PDFHyperglycemia aggravates brain damage caused by cerebral ischemia/reperfusion (I/R) and increases the permeability of the blood‑brain barrier (BBB). However, there are relatively few studies on morphological changes of the BBB. The present study aimed to investigate the effect of hyperglycemia on BBB morphological changes following cerebral I/R injury.
View Article and Find Full Text PDFAs a special subgroup of multiple intracranial aneurysms, mirror aneurysms are located bilaterally on the corresponding intracranial arteries. The current study sought to compare the clinical and demographic features of patients harboring mirror aneurysm, and to elucidate the corresponding risk factors. We performed a retrospective cohort study of 2641 intracranial aneurysms patients, who were admitted to our hospitals between January 2005 and June 2014.
View Article and Find Full Text PDFThe objectives of the study were to explore the mechanism of rotenone-induced cell damage and to examine the protective effects of water-soluble Coenzyme Q10 (CoQ10) on the toxic effects of rotenone. Murine hippocampal HT22 cells were cultured with mitochondrial complex I inhibitor rotenone. Water-soluble CoQ10 was added to the culture media 3 h prior to the rotenone incubation.
View Article and Find Full Text PDFSelenoprotein P (Sel P) is a selenium-rich glycoprotein believed to play a key role in selenium (Se) transport throughout the body. Development of a Sel P knockout mouse model has supported this notion and initial studies have indicated that selenium supply to various tissues is differentially affected by genetic deletion of Sel P. Se in the form of the amino acid, selenocysteine, is incorporated into selenoproteins at UGA codons.
View Article and Find Full Text PDFSelenoproteins have been shown to exhibit a variety of biological functions, including antioxidant functions, maintaining cellular redox balance, and heavy metal detoxification. UV irradiation-induced damage is partially mediated by increased oxygen radical production. The present study is designed to examine the antioxidative effects of human selenoprotein H (hSelH) after brief period of UVB irradiation on the murine hippocampal neuronal cell line Ht22.
View Article and Find Full Text PDFDiabetes exacerbates neuronal cell death induced by cerebral ischemia. One contributing factor is enhanced acidosis during ischemia. Astrocytes are vulnerable to hypoxia under acidic conditions in vitro and may be targets of ischemia under diabetic conditions.
View Article and Find Full Text PDFTransient global cerebral ischemia results in selective neuronal death in the vulnerable hippocampal CA1 pyramidal neurons in a delayed manner. Hyperglycemia accelerates and exacerbates neuronal damage in this region. The object of this study was to determine whether hyperglycemia-enhanced damage is associated with increased production of superoxide anion after ischemia.
View Article and Find Full Text PDFLysyl oxidase-like protein (LOXL), part of the lysyl oxidase copper-dependent amine oxidase family, is expressed in the extracellular matrix and in the nucleus. It likely plays a role in cross-linking collagen and elastin, possibly modulating cellular functions. Immunohistochemical studies show the presence of LOXL in the pyramidal cell layer of the hippocampus; and in this study, we report that cells in the granule cell layer have significantly smaller somas in LOXL -/- compared to LOXL +/+ mice.
View Article and Find Full Text PDFBrain Res Mol Brain Res
September 2005
Hyperglycemia worsens the neuronal death induced by cerebral ischemia. A previous study demonstrated that diabetic hyperglycemia suppressed the expression of heat shock protein 70 (HSP70) in the liver. The objective of this study is to determine whether hyperglycemia exacerbates ischemic brain damage by suppressing the expression of heat shock proteins (HSPs) in the brain.
View Article and Find Full Text PDFMitochondrial release of cytochrome c (cyt-c) plays a critical role in initiating cell death after cerebral ischemia. The objective of this study was to determine whether bongkrekic acid (BKA) ameliorates ischemic neuronal damage by inhibiting the release of cyt-c. These results showed that a 10min period of global ischemia caused neuronal death, increased the release of cyt-c and activated astrocytes in the cortex and CA1.
View Article and Find Full Text PDFThe objective of present study was to determine whether leukocyte-endothelial cell adhesive molecule, intercellular cell adhesion molecule-1 (ICAM-1) was increased after ischemia in diabetic rats. The immunohistochemistry of ICAM showed that numbers of ICAM-1 positively stained microvessels in the cortex were markedly increased at 3 days of reperfusion in diabetic, but not in non-diabetic rats. These were further confirmed by Western analysis.
View Article and Find Full Text PDFMitochondria play a critical role in the pathogenesis of cerebral ischemia. Acute hyperglycemia has been shown to activate the mitochondria-initiated cell death pathway after an intermediate period of ischemia. The objective of the present study was to determine if diabetic hyperglycemia induced by streptozotocin activates the cell death pathway after a brief period of global ischemia.
View Article and Find Full Text PDFMutations of the copper-zinc superoxide dismutase (SOD1) gene can result in the development of amyotrophic lateral sclerosis (ALS). The exact cellular mechanisms causing ALS are not known, but oxidative stress is thought to play a prominent role. Lysyl oxidase (LOX) is one of the genes that are known to be up-regulated in ALS patients.
View Article and Find Full Text PDFHyperglycemia enhances brain damage due to transient cerebral ischemic stroke. The hyperglycemia-mediated detrimental effect is probably due to mitochondrial dysfunction and the resulting promotion of cell death pathways. In this study, we determined whether hyperglycemia suppresses cell survival signals that involve the cAMP-responsive element-binding protein (CREB) and activating transcription factor (ATF-2).
View Article and Find Full Text PDFIt is well known that diabetes aggravates brain damage in experimental and clinical stroke subjects. Diabetes accelerates maturation of neuronal damage, increases infarct volume, and induces postischemic seizures. The mechanism by which diabetes increases ischemic brain damage is still elusive.
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