Influence of Longitudinal Scratch Defects on the Bendability of Titanium Alloy

Post-manufacturing induced defects in the form of scratches are sometimes inadvertently introduced onto sheet metal surfaces during either transportation, storage or handling. However, limited research has been previously carried out to establish the impact of such surface defects on sheet formability. Test trial results after press brake forming of Ti-3Al-2.5V showed that for longitudinal scratches oriented along the sheet rolling direction, scratch profiles with depth in the ranges of -1μm to -18μm and pile up height between 1μm to 16μm can be successfully formed; hence could be deemed acceptable during the sheet selection process. Failure of the coupons during the press brake forming trials was due to the impact of the scratch defects in their role as stress raisers and occurred primarily at the longitudinal scratch defect zones

Temperature dependence of Raman shift in defective single-walled carbon nanotubes

Raman scatterings of both pristine and defective single-walled carbon nanotubes were measured. Defects on carbon nanotubes (CNTs) were induced by UV/O3 treatment, and the correlation between the temperature dependence of the Raman shift of the G-band and the crystallinity of CNTs was investigated. In the temperature range of 250–600 K, a gradual negative change in the slope was observed; the linear shift of the Raman G-band frequency with respect to temperature increased as the crystallinity deteriorated. This phenomenon is attributed to the increase in the fourth-order phonon-phonon scattering interaction resulting from the induced defects.

Signaling Proteins That Regulate Spermatogenesis Are the Emerging Target of Toxicant-Induced Male Reproductive Dysfunction

There is emerging evidence that environmental toxicants, in particular endocrine disrupting chemicals (EDCs) such as cadmium and perfluorooctanesulfonate (PFOS), induce Sertoli cell and testis injury, thereby perturbing spermatogenesis in humans, rodents and also widelife. Recent studies have shown that cadmium (e.g., cadmium chloride, CdCl2) and PFOS exert their disruptive effects through putative signaling proteins and signaling cascade similar to other pharmaceuticals, such as the non-hormonal male contraceptive drug adjudin. More important, these signaling proteins were also shown to be involved in modulating testis function based on studies in rodents. Collectively, these findings suggest that toxicants are using similar mechanisms that used to support spermatogenesis under physiological conditions to perturb Sertoli and testis function. These observations are physiologically significant, since a manipulation on the expression of these signaling proteins can possibly be used to manage the toxicant-induced male reproductive dysfunction. In this review, we highlight some of these findings and critically evaluate the possibility of using this approach to manage toxicant-induced defects in spermatrogenesis based on recent studies in animal models.

Lattice defects induced by microtubule-stabilizing agents exert a long-range effect on microtubule growth by promoting catastrophes

Microtubules are dynamic cytoskeletal polymers that spontaneously switch between phases of growth and shrinkage. The probability of transitioning from growth to shrinkage, termed catastrophe, increases with microtubule age, but the underlying mechanisms are poorly understood. Here, we set out to test whether microtubule lattice defects formed during polymerization can affect growth at the plus end. To generate microtubules with lattice defects, we used microtubule-stabilizing agents that promote formation of polymers with different protofilament numbers. By employing different agents during nucleation of stable microtubule seeds and the subsequent polymerization phase, we could reproducibly induce switches in protofilament number and induce stable lattice defects. Such drug-induced defects led to frequent catastrophes, which were not observed when microtubules were grown in the same conditions but without a protofilament number mismatch. Microtubule severing at the site of the defect was sufficient to suppress catastrophes. We conclude that structural defects within the microtubule lattice can exert effects that can propagate over long distances and affect the dynamic state of the microtubule end.

miR-124 regulates Notch and NeuroD1 to mediate transition states of neuronal development

MicroRNAs (miRNAs) regulate gene expression by destabilizing target mRNA and/or inhibiting translation in animal cells. The ability to mechanistically dissect the function of miR-124 during specification, differentiation, and maturation of neurons during development within a single system has not been accomplished. Using the sea urchin (Strongylocentrotus purpuratus) embryo, we take advantage of the manipulability of the embryo and its well-documented gene regulatory networks (GRNs). We incorporated NeuroD1 as part of the sea urchin neuronal GRN and determined that miR-124 inhibition resulted in decreased gut contractions, swimming velocity, and neuronal development. We further integrated post-transcriptional regulation of miR-124 into the neuronal GRN. Inhibition of miR-124 resulted in increased number of cells expressing transcription factors associated with progenitor neurons and a concurrent decrease of mature and functional neurons. Results revealed that miR-124 regulates undefined factors early in neurogenesis during neuronal specification and differentiation in the early blastula and gastrula stages. In the late gastrula and larval stages, miR-124 regulates Notch and NeuroD1. Specifically, miR-124 regulates the transition between neuronal differentiation and maturation, by directly suppressing NeuroD1. Removal of miR-124 ″s suppression of NeuroD1 results in increased mature neurons with decreased Synaptagmin B-positive mature, functional neurons. By removing both miR-124 suppression of NeuroD1 and Notch, we were able to phenocopy miR-124 inhibitor induced defects. Overall, we have improved the neuronal GRN and identified miR-124 to play a prolific role in regulating various transitions of neuronal development.