Microscopic defect dynamics during a brittle-to-ductile transition.

Deformation of all materials necessitates the collective propagation of various microscopic defects. On Earth, fracturing gives way to crystal-plastic deformation with increasing depth resulting in a "brittle-to-ductile" transition (BDT) region that is key for estimating the integrated strength of tectonic plates, constraining the earthquake cycle, and utilizing deep geothermal resources. Here, we show that the crossing of a BDT in marble during deformation experiments in the laboratory is accompanied by systematic increase in the frequency of acoustic emissions suggesting a profound change in the mean size and propagation velocity of the active defects. We further identify dominant classes of emitted waveforms using unsupervised learning methods and show that their relative activity systematically changes as the rocks cross the brittle-ductile transition. As pressure increases, long-period signals are suppressed and short-period signals become dominant. At higher pressures, signals frequently come in avalanche-like patterns. We propose that these classes of waveforms correlate with individual dominant defect types. Complex mixed-mode events indicate that interactions between the defects are common over the whole pressure range, in agreement with postmortem microstructural observations. Our measurements provide unique, real-time data of microscale dynamics over a broad range of pressures (10 to 200 MPa) and can inform micromechanical models for semi-brittle deformation.

Alterations to the middle cerebral artery of the hypertensive-arthritic rat model potentiates intracerebral hemorrhage.

AIMS: We have recently created an age-dependent hypertensive-mono-arthritic animal model from the stroke-resistant spontaneously hypertensive rat to model populations with autoimmune disease who are hypertensive and are prone to stroke. The model exhibits signs of hemorrhagic stroke (HS) subsequent to chronic inflammation and hypertension. HS is also associated with the inability of middle cerebral arteries to undergo pressure dependent constriction (PDC). We investigated alterations in the cerebrovasculature of our hypertensive mono-arthritic animals that develop stroke. MAIN METHODS: Animals were fed either a high salt diet (HSD) (4% NaCl) or Purina chow (0.58% NaCl) from weaning. Complete Freund's Adjuvant (CFA) was injected into the left hind paw at 21-28 weeks; controls received saline and histological and functional studies were performed. RESULTS: Brain damage was more prominent with the high salt, with inflammation exacerbating the damage. High salt alone significantly decreased middle cerebral artery's (MCA's) ability to undergo PDC. Inflammation significantly decreased the ability of cerebrovasculature to respond to pressure step in the regular salt diet. The responses to vasoactive peptides were also significantly attenuated in both inflamed groups regardless of diet. CONCLUSION: Induction of chronic systemic inflammation increases brain damage, and affect the MCA's vasogenic function, decreasing its ability to respond to intraluminal pressure. HSD further exacerbates organ damage associated with chronic inflammation, further compromising cerebrovascular function, and likely increasing the incidence of intracerebral hemorrhage and injury.