Microstructural Evolution of Cr-Rich ODS Steels as a Function of Heat Treatment at 475°C

In the current research, the effect of heat treatment on the morphology of the dispersoids and their phase composition were investigated in three Cr-rich ferritic oxide dispersion strengthened (ODS) steels: PM2000, MA956, and ODM751. The steels were aged at 475°C for times ranging from 100 to 1,000 h. The microstructure was characterized using transmission electron microscopy. Study of the as-recrystallized samples revealed nano-scale Y–Al–O complex-oxide particles dispersed in the ferritic matrix. These dispersoids, which differ in size (10–160 nm) and geometry (polygonal and spherical), were identified as Y4Al2O9, YAlO3, and Y3Al5O12. After heat treatment, a significant change in the morphology, size, and distribution of the dispersoids was observed. Changes in the phase composition of the oxide dispersoids were also observed: YAlO3 (with perovskite structure) was identified as the most dominant phase, indicating that it is probably the most stable phase in the Cr-rich ferritic ODS steels.JRC.F.4-Nuclear Reactor Integrity Assessment and Knowledge Managemen

Sensitivity of thermo-electric power measurements to alpha- alpha' phase separation in Cr-rich oxide dispersion strengthened steels

The sensitivity of thermo-electric power (TEP) measurement to detect the undesired α–α′ phase separation occurring in Cr-rich oxide dispersion strengthened steels was investigated. TEP values were found to increase with time of exposure to 475 °C—the maximum temperature of the miscibility gap in Fe–Cr alloys. Exposure to 650 °C did not induce any changes in the TEP value. By examining the bend contours in dark-field TEM images, α′ precipitates were evidenced in aged PM2000. Using the Fe–XCr–YAl model alloys and X-ray photoelectron spectroscopy, the changes in TEP were traced back to the depletion of Cr from the matrix, caused by the formation of the Cr-rich α′ phase. By quantifying the effect of Cr content on the TEP value of model alloys, it was estimated that following 1000 h of aging, the Cr concentration in the α matrix of PM2000 alloy was reduced from 20 to ~13.5 at.%.JRC.F.4-Innovative Technologies for Nuclear Reactor Safet

A dormant microbial component in the development of pre-eclampsia

Preeclampsia (PE) is a complex, multisystem disorder that remains a leading cause of morbidity and mortality in pregnancy. Four main classes of dysregulation accompany PE and are widely considered to contribute to its severity. These are abnormal trophoblast invasion of the placenta, anti-angiogenic responses, oxidative stress, and inflammation. What is lacking, however, is an explanation of how these themselves are caused. We here develop the unifying idea, and the considerable evidence for it, that the originating cause of PE (and of the four classes of dysregulation) is, in fact, microbial infection, that most such microbes are dormant and hence resist detection by conventional (replication-dependent) microbiology, and that by occasional resuscitation and growth it is they that are responsible for all the observable sequelae, including the continuing, chronic inflammation. In particular, bacterial products such as lipopolysaccharide (LPS), also known as endotoxin, are well known as highly inflammagenic and stimulate an innate (and possibly trained) immune response that exacerbates the inflammation further. The known need of microbes for free iron can explain the iron dysregulation that accompanies PE. We describe the main routes of infection (gut, oral, and urinary tract infection) and the regularly observed presence of microbes in placental and other tissues in PE. Every known proteomic biomarker of “preeclampsia” that we assessed has, in fact, also been shown to be raised in response to infection. An infectious component to PE fulfills the Bradford Hill criteria for ascribing a disease to an environmental cause and suggests a number of treatments, some of which have, in fact, been shown to be successful. PE was classically referred to as endotoxemia or toxemia of pregnancy, and it is ironic that it seems that LPS and other microbial endotoxins really are involved. Overall, the recognition of an infectious component in the etiology of PE mirrors that for ulcers and other diseases that were previously considered to lack one