A hysteresis model with dipole interaction: one more devil-staircase

Magnetic properties of 2D systems of magnetic nanoobjects (2D regular lattices of the magnetic nanoparticles or magnetic nanostripes) are considered. The analytical calculation of the hysteresis curve of the system with interaction between nanoobjects is provided. It is shown that during the magnetization reversal system passes through a number of metastable states. The kinetic problem of the magnetization reversal was solved for three models. The following results have been obtained. 1) For 1D system (T=0) with the long-range interaction with the energy proportional to $r^{-p}$, the staircase-like shape of the magnetization curve has self-similar character. The nature of the steps is determined by interplay of the interparticle interaction and coercivity of the single nanoparticle. 2) The influence of the thermal fluctuations on the kinetic process was examined in the framework of the nearest-neighbor interaction model. The thermal fluctuations lead to the additional splitting of the steps on the magnetization curve. 3) The magnetization curve for system with interaction and coercivity dispersion was calculated in mean field approximation. The simple method to experimentally distinguish the influence of interaction and coercivity dispersion on the magnetization curve is suggested.Comment: 22 pages, 8 figure

Transition from localized surface plasmon resonance to extended surface plasmon-polariton as metallic nanoparticles merge to form a periodic hole array

W. Andrew Murray, Simion Astilean, and William L. Barnes, Physical Review B, Vol. 69, article 165407 (2004). "Copyright © 2004 by the American Physical Society."We present results of experiments to determine the dispersion of the plasmon modes associated with periodic silver nanoparticle and nanohole arrays fabricated using an extension of the nanosphere lithography technique. Ordered monolayers of polystyrene nanospheres were used as a deposition mask through which silver was deposited by thermal evaporation, subsequent removal of the nanospheres thus leaving an array of metallic nanoparticles. By reactive-ion etching of the nanospheres in an oxygen plasma prior to silver deposition, arrays consisting of particles of increasing size were fabricated. The extremities of the particles eventually merge to create a continuous metallic network perforated by subwavelength holes, thus allowing a study of the particle-hole transition. Combining optical measurements of transmittance and reflectance with information gained using scanning electron microscopy, three separate regimes were observed. For low etch times the samples comprise mainly individual nanoparticles and the optical response is dominated by localized surface plasmon resonances that show no dispersion. As the etch time is increased almost all of the nanoparticles merge with adjacent particles, although many defects are present—notably where some particles fail to merge, a small gap being left between them. The presence of these defects prevents an abrupt structural transition from metallic nanoparticles to a continuous metallic film perforated by an array of nanoholes. The presence of such gaps also results in dispersion data that lack clearly defined features. A further increase in etch time leads to samples with no gaps: instead, a continuous metal film perforated by a nanohole array is produced. The optical response of these structures is dominated by extended surface plasmon-polariton modes

Features of Idebenone and Related Short-Chain Quinones that Rescue ATP Levels under Conditions of Impaired Mitochondrial Complex I

Short-chain quinones have been investigated as therapeutic molecules due to their ability to modulate cellular redox reactions, mitochondrial electron transfer and oxidative stress, which are pathologically altered in many mitochondrial and neuromuscular disorders. Recently, we and others described that certain short-chain quinones are able to bypass a deficiency in complex I by shuttling electrons directly from the cytoplasm to complex III of the mitochondrial respiratory chain to produce ATP. Although this energy rescue activity is highly interesting for the therapy of disorders associated with complex I dysfunction, no structure-activity-relationship has been reported for short-chain quinones so far. Using a panel of 70 quinones, we observed that the capacity for this cellular energy rescue as well as their effect on lipid peroxidation was influenced more by the physicochemical properties (in particular logD) of the whole molecule than the quinone moiety itself. Thus, the observed correlations allow us to explain the differential biological activities and therapeutic potential of short-chain quinones for the therapy of disorders associated with mitochondrial complex I dysfunction and/or oxidative stress

NQO1-Dependent Redox Cycling of Idebenone: Effects on Cellular Redox Potential and Energy Levels

Short-chain quinones are described as potent antioxidants and in the case of idebenone have already been under clinical investigation for the treatment of neuromuscular disorders. Due to their analogy to coenzyme Q10 (CoQ10), a long-chain quinone, they are widely regarded as a substitute for CoQ10. However, apart from their antioxidant function, this provides no clear rationale for their use in disorders with normal CoQ10 levels. Using recombinant NAD(P)H:quinone oxidoreductase (NQO) enzymes, we observed that contrary to CoQ10 short-chain quinones such as idebenone are good substrates for both NQO1 and NQO2. Furthermore, the reduction of short-chain quinones by NQOs enabled an antimycin A-sensitive transfer of electrons from cytosolic NAD(P)H to the mitochondrial respiratory chain in both human hepatoma cells (HepG2) and freshly isolated mouse hepatocytes. Consistent with the substrate selectivity of NQOs, both idebenone and CoQ1, but not CoQ10, partially restored cellular ATP levels under conditions of impaired complex I function. The observed cytosolic-mitochondrial shuttling of idebenone and CoQ1 was also associated with reduced lactate production by cybrid cells from mitochondrial encephalomyopathy, lactic acidosis and stroke-like episodes (MELAS) patients. Thus, the observed activities separate the effectiveness of short-chain quinones from the related long-chain CoQ10 and provide the rationale for the use of short-chain quinones such as idebenone for the treatment of mitochondrial disorders

Biallelic null variants in PNPLA8 cause microcephaly by reducing the number of basal radial glia.

Patatin-like phospholipase domain-containing lipase 8 (PNPLA8), one of the calcium-independent phospholipase A2 enzymes, is involved in various physiological processes through the maintenance of membrane phospholipids. Biallelic variants in PNPLA8 have been associated with a range of paediatric neurodegenerative disorders. However, the phenotypic spectrum, genotype-phenotype correlations and the underlying mechanisms are poorly understood. Here, we newly identified 14 individuals from 12 unrelated families with biallelic ultra-rare variants in PNPLA8 presenting with a wide phenotypic spectrum of clinical features. Analysis of the clinical features of current and previously reported individuals (25 affected individuals across 20 families) showed that PNPLA8-related neurological diseases manifest as a continuum ranging from variable developmental and/or degenerative epileptic-dyskinetic encephalopathy to childhood-onset neurodegeneration. We found that complete loss of PNPLA8 was associated with the more profound end of the spectrum, with congenital microcephaly. Using cerebral organoids generated from human induced pluripotent stem cells, we found that loss of PNPLA8 led to developmental defects by reducing the number of basal radial glial cells and upper-layer neurons. Spatial transcriptomics revealed that loss of PNPLA8 altered the fate specification of apical radial glial cells, as reflected by the enrichment of gene sets related to the cell cycle, basal radial glial cells and neural differentiation. Neural progenitor cells lacking PNPLA8 showed a reduced amount of lysophosphatidic acid, lysophosphatidylethanolamine and phosphatidic acid. The reduced number of basal radial glial cells in patient-derived cerebral organoids was rescued, in part, by the addition of lysophosphatidic acid. Our data suggest that PNPLA8 is crucial to meet phospholipid synthetic needs and to produce abundant basal radial glial cells in human brain development

Modulating mitophagy in mitochondrial disease

Mitochondrial diseases may result from mutations in the maternally-inherited mitochondrial DNA (mtDNA) or from mutations in nuclear genes encoding mitochondrial proteins. Their bi-genomic nature makes mitochondrial diseases a very heterogeneous group of disorders that can present at any age and can affect any type of tissue. The autophagic-lysosomal degradation pathway plays an important role in clearing dysfunctional and redundant mitochondria through a specific quality control mechanism termed mitophagy. Mitochondria could be targeted for autophagic degradation for a variety of reasons including basal turnover for recycling, starvation induced degradation, and degradation due to damage. While the core autophagic machinery is highly conserved and common to most pathways, the signaling pathways leading to the selective degradation of damaged mitochondria are still not completely understood. Type 1 mitophagy due to nutrient starvation is dependent on PI3K (phosphoinositide 3-kinase) for autophagosome formation but independent of mitophagy proteins, PINK1 (PTEN-induced putative kinase 1) and Parkin. Whereas type 2 mitophagy that occurs due to damage is dependent on PINK1 and Parkin but does not require PI3K. Autophagy and mitophagy play an important role in human disease and hence could serve as therapeutic targets for the treatment of mitochondrial as well as neurodegenerative disorders. Therefore, we reviewed drugs that are known modulators of autophagy (AICAR and metformin) and may effect this by activating the AMP-activated protein kinase signaling pathways. Furthermore, we reviewed data available on supplements, such as Coenzyme Q and the quinone idebenone, that we assert rescue increased mitophagy in mitochondrial disease by benefiting mitochondrial function

Estimation of surface long wave radiation and broadband emissivity using Moderate Resolution Imaging Spectroradiometer (MODIS) land surface temperature/emissivity products

The Moderate Resolution Imaging Spectroradiometer (MODIS) global land surface temperature (LST)/emissivity products supply daily, 8-day, and monthly global temperature and narrowband emissivity data. This article uses these products to calculate the surface long wave radiation of natural objects such as sand, soil, vegetation, etc., based on the Planck function and the Stefan-Boltzmann law. The results show that using the narrowband emissivity of a single band instead of the broadband emissivity results in large errors of up to 100 W m?2 of the calculated long wave radiation. A method to calculate broadband emissivity in the entire TIR spectral region from the narrowband emissivities of the MODIS bands (29, 31, and 32) in the thermal infrared region is proposed. Using the broadband emissivity, the surface long wave radiation could be calculated to an accuracy better than 6 W m?2 in the temperature region of 240–330 K, with a standard deviation of 1.22 W m?2, and a maximum error of 6.05 W m?2 (not considering the uncertainty associated with the MODIS LST/emissivity products themselves). The satellite estimated broadband emissivity was compared with 3-year (January 2001 to December 2003) ground-based measurements of emissivity at Gaize (32.30°N, 84.06°E, 4420 m) on the western Tibetan Plateau. The results show that the broadband emissivity calculated from MODIS narrowband emissivities by this method matches well the ground measurements, with a standard deviation of 0.0085 and a bias of 0.0015

The Mechanism Behind the Oxidation Protection of High Mg Al Alloys with Beryllium

The addition of beryllium to Al-Mg alloys is known to cause a dramatic decrease in oxidation; however, the mechanism behind this protective effect is not yet fully understood. To aid in finding an alternative to the toxic Be, a fundamental study of Be additions has been carried out. Industrial samples containing 2 ppm Be and a model alloy with 100 ppm Be were oxidized at temperatures between 550 °C and 750 °C in a horizontal tube furnace. The oxide layer and oxide–metal interface were investigated using SEM, FIB, and XPS. It was found that Be forms a uniform oxide layer at the oxide–metal interface which slows the diffusion of Mg and Al from the metal into the oxide layer resulting in a reduced oxidation rate and an increase in the time for breakaway oxidation to occur