The influence of carbon on the resistivity recovery of proton irradiated Fe–11at.% Cr alloys

AbstractThe effect of carbon on the point defect migration properties in Fe–Cr alloys with a concentration of 11 at.% Cr is studied by means of resistivity recovery measurements after low temperature proton irradiation. The presence of carbon mainly affects features of the resistivity recovery spectra in the temperature ranges of (a) 150–200K, which are linked to self-interstitial defects, and (b) 400–500K, which are probably due to vacancy and vacancy-carbon complexes. The experimental results are discussed in terms of the possible interactions of carbon with radiation defects and its influence on solute atom re-ordering

Infrared Thermal Images of Solar PV Panels for Fault Identification Using Image Processing Technique

Among the renewable forms of energy, solar energy is a convincing, clean energy and acceptable worldwide. Solar PV plants, both ground mounting and the rooftop, are mushrooming thought the world. One of the significant challenges is the fault identification of the solar PV module, since a vast power plant condition monitoring of individual panels is cumbersome. This paper attempts to identify the panel using a thermal imaging system and processes the thermal images using the image processing technique. An ordinary and thermal image has been processed in the image processing tool and proved that thermal images record the hot spots. Similarly, the new and aged solar photovoltaic panels were compared in the image processing technique since any fault in the panel has been recorded as hot spots. The image recorded in the aged panels records hot spots, and performance has been analyzed using conventional metrics. The experimental results have also been verified

Phase stability of Fe-5at%Cr and Fe-10at%Cr films under Fe+ ion irradiation

This work is within the objective of understanding the effects caused to Fe–Cr alloys by fast Fe ion irradiation. As the penetration length of Fe ion is of the order of hundreds of nanometers, 70 nm Fe-5at%C and Fe-10at%Cr films were irradiated at room temperature with 490 keV Fe+ ions at increasing fluence corresponding to a maximum damage of 50 displacements per atom (dpa). In Fe-5at%Cr alloy the Cr solute concentration remains unaltered even after a damage of 50 dpa. In the 10at%Cr the Cr solute concentration is reduced, with the increase of damage, asymptotically to a value of 7.2 at%

Nitrite protects against morbidity and mortality associated with TNF- or LPS-induced shock in a soluble guanylate cyclase–dependent manner

Nitrite (NO2−), previously viewed as a physiologically inert metabolite and biomarker of the endogenous vasodilator NO, was recently identified as an important biological NO reservoir in vasculature and tissues, where it contributes to hypoxic signaling, vasodilation, and cytoprotection after ischemia–reperfusion injury. Reduction of nitrite to NO may occur enzymatically at low pH and oxygen tension by deoxyhemoglobin, deoxymyoglobin, xanthine oxidase, mitochondrial complexes, or NO synthase (NOS). We show that nitrite treatment, in sharp contrast with the worsening effect of NOS inhibition, significantly attenuates hypothermia, mitochondrial damage, oxidative stress and dysfunction, tissue infarction, and mortality in a mouse shock model induced by a lethal tumor necrosis factor challenge. Mechanistically, nitrite-dependent protection was not associated with inhibition of mitochondrial complex I activity, as previously demonstrated for ischemia–reperfusion, but was largely abolished in mice deficient for the soluble guanylate cyclase (sGC) α1 subunit, one of the principal intracellular NO receptors and signal transducers in the cardiovasculature. Nitrite could also provide protection against toxicity induced by Gram-negative lipopolysaccharide, although higher doses were required. In conclusion, we show that nitrite can protect against toxicity in shock via sGC-dependent signaling, which may include hypoxic vasodilation necessary to maintain microcirculation and organ function, and cardioprotection

Gender-Specific Modulation of the Response to Arterial Injury by Soluble Guanylate Cyclase α1

Objective: Soluble guanylate cyclase (sGC), a heterodimer composed of α and β subunits, synthesizes cGMP in response to nitric oxide (NO). NO modulates vascular tone and structure but the relative contributions of cGMP-dependent versus cGMP-independent mechanisms remain uncertain. We studied the response to vascular injury in male (M) and female (F) mice with targeted deletion of exon 6 of the sGCα1 subunit (sGCα1-/-), resulting in a non-functional heterodimer. Methods: We measured aortic cGMP levels and mRNA transcripts encoding sGC α1, α2, and β1 subunits in wild type (WT) and sGCa1-/- mice. To study the response to vascular injury, BrdU-incorporation and neointima formation (maximum intima to media (I/M) ratio) were determined 5 and 28 days after carotid artery ligation, respectively. Results: Aortic cGMP levels were 4-fold higher in F than in M mice in both genotypes, and, within each gender, 4-fold higher in WT than in sGCa1-/-. In contrast, sGCα1, sGCα2, and sGCβ1 mRNA expression did not differ between groups. 3H-thymidine incorporation in cultured sGCa1-/- smooth muscle cells (SMC) was 27%±12% lower than in WT SMC and BrdU-incorporation in carotid arteries 5 days after ligation was significantly less in sGCa1-/- M than in WT M. Neointima area and I/M 28 days after ligation were 65% and 62% lower in sGCa1-/- M than in WT M mice (p<0,05 for both) but were not different in F mice. Conclusion: Functional deletion of sGCa1 resulted in reduced cGMP levels in male sGCa1-/- mice and a gender-specific effect on the adaptive response to vascular injury

Proteome Profiling in Murine Models of Multiple Sclerosis: Identification of Stage Specific Markers and Culprits for Tissue Damage

The identification of new biomarkers is of high interest for the prediction of the disease course and also for the identification of pathomechanisms in multiple sclerosis (MS). To specify markers of the chronic disease phase, we performed proteome profiling during the later phase of myelin oligodendrocyte glycoprotein induced experimental autoimmune encephalomyelitis (MOG-EAE, day 35 after immunization) as a model disease mimicking many aspects of secondary progressive MS. In comparison to healthy controls, high resolution 2 dimensional gel electrophoresis revealed a number of regulated proteins, among them glial fibrilary acidic protein (GFAP). Phase specific up-regulation of GFAP in chronic EAE was confirmed by western blotting and immunohistochemistry. Protein levels of GFAP were also increased in the cerebrospinal fluid of MS patients with specificity for the secondary progressive disease phase. In a next step, proteome profiling of an EAE model with enhanced degenerative mechanisms revealed regulation of alpha-internexin, syntaxin binding protein 1, annexin V and glutamate decarboxylase in the ciliary neurotrophic factor (CNTF) knockout mouse. The identification of these proteins implicate an increased apoptosis and enhanced axonal disintegration and correlate well the described pattern of tissue injury in CNTF −/− mice which involve oligodendrocyte (OL) apoptosis and axonal injury