Radiation damage in tungsten from cascade overlap with voids and vacancy clusters.

We have performed a systematic molecular dynamics investigation of the effects of overlap of collision cascades in tungsten with pre-existing vacancy-type defects. In particular, we focus on the implications for fusion neutron irradiated tungsten in relation to comparisons with damage production under ion irradiation conditions. We find that overlap of a cascade with a vacancy-type defect decreases the number of new defects with roughly the same functional dependence as previously shown for interstitial clusters. We further find that different mechanisms govern the formation of dislocation loops, resulting in different Burgers vectors, depending on the degree of overlap between the cascade and the defect. Furthermore, we show that overlapping cascades consistently decrease the size of the pre-existing defect. We also observe void-induced cascade splitting at energies far below the subcascade splitting threshold in tungsten. The impact of these mechanisms on radiation damage accumulation and dose rate effects are discussed.

Collision cascades overlapping with self-interstitial defect clusters in Fe and W.

Overlap of collision cascades with previously formed defect clusters become increasingly likely at radiation doses typical for materials in nuclear reactors. Using molecular dynamics, we systematically investigate the effects of different pre-existing self-interstitial clusters on the damage produced by an overlapping cascade in bcc iron and tungsten. We find that the number of new Frenkel pairs created in direct overlap with an interstitial cluster is reduced to essentially zero, when the size of the defect cluster is comparable to that of the disordered cascade volume. We develop an analytical model for this reduced defect production as a function of the spatial overlap between a cascade and a defect cluster of a given size. Furthermore, we discuss cascade-induced changes in the morphology of self-interstitial clusters, including transformations between [Formula: see text] and [Formula: see text] dislocation loops in iron and tungsten, and between C15 clusters and dislocation loops in iron. Our results provide crucial new cascade-overlap effects to be taken into account in multi-scale modelling of radiation damage in bcc metals.

A model of defect cluster creation in fragmented cascades in metals based on morphological analysis.

The impacts of ions and neutrons in metals cause cascades of atomic collisions that expand and shrink, leaving microstructure defect debris, i.e. interstitial or vacancy clusters or loops of different sizes. In De Backer et al (2016 Europhys. Lett. 115 26001), we described a method to detect the first morphological transition, i.e. the cascade fragmentation in subcascades, and a model of primary damage combining the binary collision approximation and molecular dynamics (MD). In this paper including W, Fe, Be, Zr and 20 other metals, we demonstrate that the fragmentation energy increases with the atomic number and decreases with the atomic density following a unique power law. Above the fragmentation energy, the cascade morphology can be characterized by the cross pair correlation functions of the multitype point pattern formed by the subcascades. We derive the numbers of pairs of subcascades and observed that they follow broken power laws. The energy where the power law breaks indicates the second morphological transition when cascades are formed by branches decorated by chaplets of small subcascades. The subcascade interaction is introduced in our model of primary damage by adding pairwise terms. Using statistics obtained on hundreds of MD cascades in Fe, we demonstrate that the interaction of subcascades increases the proportion of large clusters in the damage created by high energy cascades. Finally, we predict the primary damage of 500 keV Fe ion in Fe and obtain cluster size distributions when large statistics of MD cascades are not feasible.

Endothelin-induced contractions in placental arteries is mediated by both ETA- and ETB-receptors.

We have examined the contractile response to the vasoconstrictor endothelin-1 (ET-1) in uteroplacental arteries from normal pregnant women in the presence and absence of specific ET-receptor antagonists and agonists, and the vasodilator nitric oxide. Segments of placental arteries (n = 97) obtained from 37 placentas immediately after delivery were mounted in organ baths superfused with Krebs-Ringer solution at 37 degrees C. The tension was recorded isometrically and registered on a polygraph. We found that the placental artery segments responded to ET with a dose-dependent vasoconstriction. Half-maximal response was obtained at 2.6 x 10(-8) M. At 10(-7) M, the contractile response was 52% of the maximum KCl-response. The ET-1 induced contraction at 10(-7) M was inhibited by 74% after addition of the ETA-antagonist BQ-123 (10(-6) M), and by 58% by the ETB-antagonist BQ-788 (10(-6) M). Both BQ-123 and BQ-788 almost completely abolished the response to ET (10(-7) M). The selective ETB-agonist IRL-1620 also elicited vasoconstriction in the placental artery with a half maximal response at 8 x 10(-7) M. On a molar basis at 10(-7) M, the contraction by IRL-1620 as compared to ET was 30-fold lower. The contractile response of IRL-1620 (10(-6) M) was inhibited by 99% by BQ-788 (10(-6) M). After pre-contraction of the placental arteries with ET-1 (10(-7) M), the vessels relaxed in response to the nitric oxide donor, nitroglycerin (10(-6) M). The present results show that ET-1 contracts placental arteries through both ETA- and ETB-receptor activation. Nitric oxide (10(-6) M) was able to relax more than half of the initial ET-1 contraction, indicating that nitric oxide may be an important vasodilator in the placenta.

Effects of nitric oxide donors and inhibitors of nitric oxide signalling on endothelin- and serotonin-induced contractions in human placental arteries.

In order to explore the role of nitric oxide (NO) in the control of fetoplacental vascular tone in normal pregnancy we have examined the effects of NO donors on uteroplacental arteries pre-contracted with the vasoconstrictor endothelin-1 (ET-1) or serotonin (5-HT). We have furthermore examined the effects of guanylate cyclase inhibitors on the NO-induced relaxation. Segments of placental arteries (n=102) obtained from 39 placentas immediately after delivery were mounted in organ baths and superfused with Krebs-Ringer solution at 37 degrees C. The vessel segments were exposed to drugs for various intervals and the tension was recorded isometrically and registered on a polygraph. Cyclic guanosine monophosphate (cGMP) analysis was performed after extraction of vessel segments using a specific radioimmunoassay. The placental artery segments responded to ET-1 and 5-HT with a dose-dependent vasoconstriction. After pre-contraction with ET-1 (10(-7) M) or 5-HT (10(-6) M), the vessels relaxed in response to the NO donors glyceryltrinitrate (GTN) (10(-6) M) and S-nitroso-N-acetyl-penicillamine (SNAP) (10(-5) M). In the presence of the non-specific guanylate cyclase inhibitor LY 83583 (10(-6) M), the vessels responded with a small contraction. In the presence of the soluble guanylate cyclase (sGC) inhibitor 1H[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one (ODQ) the non-treated vessels responded with a relaxation. 1H[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one gave no obvious relaxation in pre-contracted vessels. Addition of 8-Br-cGMP, the cell-permeant analogue of cGMP, with or without pre-contraction had no effect on the vessels. Cyclic guanosine monophosphate analysis showed that GTN treatment caused an increase in cGMP after 12 min. Our results indicate that NO acts as a vasodilator in placental vessels. The cGMP-dependent mechanisms may be involved in NO-induced relaxation but cGMP-independent mechanisms appear also to be involved.