The hydrogenation of metals upon interaction with water

Hydrogen evolution at 600 deg and 5 x 10 to the 7th power - 10 to the 6th power torr from AVOOO Al samples, which were pickled in 10 percent NaOH, is discussed. An H evolution kinetic equation is derived for samples of equal vol. and different surfaces (5 and 20 sq cm). The values of the H evolution coefficient K indicated an agreement with considered H diffusion mechanism through an oxide layer. The activation energy for the H evolution process, obtained from the K-temp. relation, was 13,000 2000 cal/g-atom

Spin-flip processes and ultrafast magnetization dynamics in Co - unifying the microscopic and macroscopic view of femtosecond magnetism

The femtosecond magnetization dynamics of a thin cobalt film excited with ultrashort laser pulses has been studied using two complementary pump-probe techniques, namely spin-, energy- and time-resolved photoemission and time-resolved magneto-optical Kerr effect. Combining the two methods it is possible to identify the microscopic electron spin-flip mechanisms responsible for the ultrafast macroscopic magnetization dynamics of the cobalt film. In particular, we show that electron-magnon excitation does not affect the overall magnetization even though it is an efficient spin-flip channel on the sub-200 fs timescale. Instead we find experimental evidence for the relevance of Elliott-Yafet type spin-flip processes for the ultrafast demagnetization taking place on a time scale of 300 fs.Comment: 12 pages, 3 figures; accepted by Physical Review Letter

Shape of primary proton spectrum in multi-TeV region from data on vertical muon flux

It is shown, that primary proton spectrum, reconstructed from sea-level and underground data on muon spectrum with the use of QGSJET 01, QGSJET II, NEXUS 3.97 and SIBYLL 2.1 interaction models, demonstrates not only model-dependent intensity, but also model-dependent form. For correct reproduction of muon spectrum shape primary proton flux should have non-constant power index for all considered models, except SIBYLL 2.1, with break at energies around 10-15 TeV and value of exponent before break close to that obtained in ATIC-2 experiment. To validate presence of this break understanding of inclusive spectra behavior in fragmentation region in p-air collisions should be improved, but we show, that it is impossible to do on the basis of the existing experimental data on primary nuclei, atmospheric muon and hadron fluxes.Comment: Submitted to Phys. Rev.

Inhibition of the mitochondrial pyruvate carrier protects from excitotoxic neuronal death.

Glutamate is the dominant excitatory neurotransmitter in the brain, but under conditions of metabolic stress it can accumulate to excitotoxic levels. Although pharmacologic modulation of excitatory amino acid receptors is well studied, minimal consideration has been given to targeting mitochondrial glutamate metabolism to control neurotransmitter levels. Here we demonstrate that chemical inhibition of the mitochondrial pyruvate carrier (MPC) protects primary cortical neurons from excitotoxic death. Reductions in mitochondrial pyruvate uptake do not compromise cellular energy metabolism, suggesting neuronal metabolic flexibility. Rather, MPC inhibition rewires mitochondrial substrate metabolism to preferentially increase reliance on glutamate to fuel energetics and anaplerosis. Mobilizing the neuronal glutamate pool for oxidation decreases the quantity of glutamate released upon depolarization and, in turn, limits the positive-feedback cascade of excitotoxic neuronal injury. The finding links mitochondrial pyruvate metabolism to glutamatergic neurotransmission and establishes the MPC as a therapeutic target to treat neurodegenerative diseases characterized by excitotoxicity

Wolfram Syndrome protein, Miner1, regulates sulphydryl redox status, the unfolded protein response, and Ca2+ homeostasis.

Miner1 is a redox-active 2Fe2S cluster protein. Mutations in Miner1 result in Wolfram Syndrome, a metabolic disease associated with diabetes, blindness, deafness, and a shortened lifespan. Embryonic fibroblasts from Miner1(-/-) mice displayed ER stress and showed hallmarks of the unfolded protein response. In addition, loss of Miner1 caused a depletion of ER Ca(2+) stores, a dramatic increase in mitochondrial Ca(2+) load, increased reactive oxygen and nitrogen species, an increase in the GSSG/GSH and NAD(+)/NADH ratios, and an increase in the ADP/ATP ratio consistent with enhanced ATP utilization. Furthermore, mitochondria in fibroblasts lacking Miner1 displayed ultrastructural alterations, such as increased cristae density and punctate morphology, and an increase in O2 consumption. Treatment with the sulphydryl anti-oxidant N-acetylcysteine reversed the abnormalities in the Miner1 deficient cells, suggesting that sulphydryl reducing agents should be explored as a treatment for this rare genetic disease

Mitochondrial dysfunction in an Opa1Q285STOP mouse model of dominant optic atrophy results from Opa1 haploinsufficiency

Mutations in the opa1 (optic atrophy 1) gene lead to autosomal dominant optic atrophy (ADOA), a hereditary eye disease. This gene encodes the Opa1 protein, a mitochondrial dynamin-related GTPase required for mitochondrial fusion and the maintenance of normal crista structure. The majority of opa1 mutations encode truncated forms of the protein, lacking a complete GTPase domain. It is unclear whether the phenotype results from haploinsufficiency or rather a deleterious effect of truncated Opa1 protein. We studied a heterozygous Opa1 mutant mouse carrying a defective allele with a stop codon in the beginning of the GTPase domain at residue 285, a mutation that mimics human pathological mutations. Using an antibody raised against an N-terminal portion of Opa1, we found that the level of wild-type protein was decreased in the mutant mice, as predicted. However, no truncated Opa1 protein was expressed. In embryonic fibroblasts isolated from the mutant mice, this partial loss of Opa1 caused mitochondrial respiratory deficiency and a selective loss of respiratory Complex IV subunits. Furthermore, partial Opa1 deficiency resulted in a substantial resistance to endoplasmic reticulum stress-induced death. On the other hand, the enforced expression of truncated Opa1 protein in cells containing normal levels of wild-type protein did not cause mitochondrial defects. Moreover, cells expressing the truncated Opa1 protein showed reduced Bax activation in response to apoptotic stimuli. Taken together, our results exclude deleterious dominant-negative or gain-of-function mechanisms for this type of Opa1 mutation and affirm haploinsufficiency as the mechanism underlying mitochondrial dysfunction in ADOA

Intruder bands and configuration mixing in the lead isotopes

A three-configuration mixing calculation is performed in the context of the interacting boson model with the aim to describe recently observed collective bands built on low-lying $0^+$ states in neutron-deficient lead isotopes. The configurations that are included correspond to the regular, spherical states as well as two-particle two-hole and four-particle four-hole excitations across the Z=82 shell gap.Comment: 20 pages, 4 figures, accepted by PRC, reference added for section 1 in this revised versio

Subungual melanoma – the rare clinical form

The article deals with a clinical case of a patient with subungual melanoma, like a private form of an acral-lentiginous melanoma. An epidemiological situation is described in terms of the incidence of melanoma in the Sverdlovsk Region. The necessity of development of medical and organizational technologies for the prevention of melanoma is substantiated.В статье рассмотрен клинический случай пациента с подногтевой меланомой, как частной формы акрально-лентигинозной меланомы. Описана эпидемиологическая ситуации по заболеваемости меланомой в Свердловской области. Обосновывается необходимость разработки медико-организационных технологий по профилактике меланомы

S-Nitrosylation-mediated dysfunction of TCA cycle enzymes in synucleinopathy studied in postmortem human brains and hiPSC-derived neurons

A causal relationship between mitochondrial metabolic dysfunction and neurodegeneration has been implicated in synucleinopathies, including Parkinson disease (PD) and Lewy body dementia (LBD), but underlying mechanisms are not fully understood. Here, using human induced pluripotent stem cell (hiPSC)-derived neurons with mutation in the gene encoding α-synuclein (αSyn), we report the presence of aberrantly S-nitrosylated proteins, including tricarboxylic acid (TCA) cycle enzymes, resulting in activity inhibition assessed by carbon-labeled metabolic flux experiments. This inhibition principally affects α-ketoglutarate dehydrogenase/succinyl coenzyme-A synthetase, metabolizing α-ketoglutarate to succinate. Notably, human LBD brain manifests a similar pattern of aberrantly S-nitrosylated TCA enzymes, indicating the pathophysiological relevance of these results. Inhibition of mitochondrial energy metabolism in neurons is known to compromise dendritic length and synaptic integrity, eventually leading to neuronal cell death. Our evidence indicates that aberrant S-nitrosylation of TCA cycle enzymes contributes to this bioenergetic failure

Subungual melanoma – the rare clinical form

The article deals with a clinical case of a patient with subungual melanoma, like a private form of an acral-lentiginous melanoma. An epidemiological situation is described in terms of the incidence of melanoma in the Sverdlovsk Region. The necessity of development of medical and organizational technologies for the prevention of melanoma is substantiated.В статье рассмотрен клинический случай пациента с подногтевой меланомой, как частной формы акрально-лентигинозной меланомы. Описана эпидемиологическая ситуации по заболеваемости меланомой в Свердловской области. Обосновывается необходимость разработки медико-организационных технологий по профилактике меланомы