Sequential Adaptive Detection for In-Situ Transmission Electron Microscopy (TEM)

We develop new efficient online algorithms for detecting transient sparse signals in TEM video sequences, by adopting the recently developed framework for sequential detection jointly with online convex optimization [1]. We cast the problem as detecting an unknown sparse mean shift of Gaussian observations, and develop adaptive CUSUM and adaptive SSRS procedures, which are based on likelihood ratio statistics with post-change mean vector being online maximum likelihood estimators with $\ell_1$. We demonstrate the meritorious performance of our algorithms for TEM imaging using real data

Neuronopathic Gaucher disease in the mouse: viable combined selective saposin C deficiency and mutant glucocerebrosidase (V394L) mice with glucosylsphingosine and glucosylceramide accumulation and progressive neurological deficits

Gaucher disease is caused by defective acid β-glucosidase (GCase) function. Saposin C is a lysosomal protein needed for optimal GCase activity. To test the in vivo effects of saposin C on GCase, saposin C deficient mice (C−/−) were backcrossed to point mutated GCase (V394L/V394L) mice. The resultant mice (4L;C*) began to exhibit CNS abnormalities ∼30 days: first as hindlimb paresis, then progressive tremor and ataxia. Death occurred ∼48 days due to neurological deficits. Axonal degeneration was evident in brain stem, spinal cord and white matter of cerebellum accompanied by increasing infiltration of the brain stem, cortex and thalamus by CD68 positive microglial cells and activation of astrocytes. Electron microscopy showed inclusion bodies in neuronal processes and degenerating cells. Accumulation of p62 and Lamp2 were prominent in the brain suggesting the impairment of autophagosome/lysosome function. This phenotype was different from either V394L/V394L or C−/− alone. Relative to V394L/V394L mice, 4L;C* mice had diminished GCase protein and activity. Marked increases (20- to 30-fold) of glucosylsphingosine (GS) and moderate elevation (1.5- to 3-fold) of glucosylceramide (GC) were in 4L;C* brains. Visceral tissues had increases of GS and GC, but no storage cells were found. Neuronal cells in thick hippocampal slices from 4L;C* mice had significantly attenuated long-term potentiation, presumably resulting from substrate accumulation. The 4L;C* mouse mimics the CNS phenotype and biochemistry of some type 3 (neuronopathic) variants of Gaucher disease and is a unique model suitable for testing pharmacological chaperone and substrate reduction therapies, and investigating the mechanisms of neuronopathic Gaucher disease

Multiple Twinning and Stacking Faults in Silver Dendrites

Detailed defect structure of dendrite formation was studied in order to connect the mesoscopic with the atomistic structure. It was demonstrated that twinning and stacking fault formation play a central role in the growth of electrodeposited Ag dendrites. The broad faces of Ag dendrites and the main trunk growth direction were found to be ((1) over bar 11) and [(1) over bar1 (2) over bar], respectively. Dendrite branches also formed and grew from the main trunk parallel to the [12 (1) over bar] and [(211) over bar] crystallographic directions. Twins and stacking faults were found to reside on the {111} crystallographic planes, as expected for a face centered cubic (FCC) Ag crystal. Using electron back scattered diffraction (EBSD) we found two variants of in-plane 60 degrees rotational twin domains in the ((1) over bar 11) broad dendrite surface plane. The intersections of twins and stacking faults with dendrite arm surfaces are perpendicular to the (112) arm growth directions. However, occasionally twins on the {111} planes parallel to the (112) arm growth directions were also observed. Although defect assisted dendrite growth is facilitated by twinning and stacking fault formation on {111} planes, the growth directions of the trunk and branches are not of the (111) type, but rather close to (112). The (112) growth directions are maintained by breaking dendrite facets into thermodynamically stable 111 and 200 steps and structural ledges of different length

Impact of in situ nanomechanics on physical metallurgy

The mechanical response of modern alloys results from a complex interplay between existing microstructure and its evolution with time under stress. To unravel these processes, in situ approaches intrinsically have a critical advantage to explore the basic mechanisms involving dislocations, grain boundaries (GBs), and their interactions in real time. In this article, we discuss recent findings using in situ nanomechanical testing techniques and refined crystallographic analysis tools. Advancements in in situ nanomechanics not only include multiaxial loading conditions, which bring us closer to real-world applications, but also high strain-rate testing, which is critical to compare experiments and simulations. In particular, unraveling the details of GB-based mechanisms and related microstructural changes will facilitate significant breakthroughs in our understanding of the behavior of materials on macroscopic length scales