Microstructural Investigations of VO2 Thermochromic Thin Films Grown by Pulsed Laser Deposition for Smart Windows Applications

Abstract The structural properties of VO2 thin films, grown on either LSAT or Si substrates by pulsed laser deposition (PLD), are elucidated by means of transmission electron microscopy (TEM) methods. The TEM observations confirmed the successful growth of VO2 by PLD in variable thicknesses, by optimizing the O2 partial pressure and growth temperature. The films adopt a columnar polycrystalline morphology with narrow columns, up to the film thickness height. Four VO2 polymorphs have been detected by electron diffraction and high-resolution TEM (HRTEM) analysis, with M1 being by far the most abundant phase. Post-experimental strain measurements in HRTEM images have revealed that the actual residual strain is minimized due to the columnar morphology of the VO2 grains, as well as intrinsic oxide layers in the VO2/Si epitaxy. The TEM outcomes confirmed the complementary electrical and magnetic measurements in the films, where a transition from a monoclinic M1 to a rutile VO2 R phase has been identified, influenced by the initial percentage of phases in thick VO2 films.publishedVersio

How Job Crafting is Shaping the Future of Hospitality Industry: through the Lens of Industry 4.0

The burgeoning of the global travel and tourism industry is the most significant contributor to the growth of the worldwide hospitality industry. The Asia Pacific comprises the largest percentage of global hospitality market share at 43%, followed by North America with 25%, and about 2% by Africa, and Eastern Europe. Although the compound annual growth rate of the global hospitality market is projected at 8% to $5,891 billion by 2022, the evolution of Industry 4.0 has a spillover effect on the workforce of manufacturing as well as the service industry. This paper explores the workforce challenges of Industry 4.0 in the hospitality sector, providing bottom-up job design, i.e., job crafting as a way out to accommodate technological advancements

Serotonergic axon development in the medulla oblongata in post-natal mice

Sudden Infant Death Syndrome (SIDS) is the sudden death of an infant younger than one year of age that remains unexplained after a complete investigation. For these infants, many different reasons have been hypothesized as to the cause of these deaths including: inherent vulnerability and improper hypoxic arousal. Studies done in other laboratories have shown that there seems to be a reduction in the levels of the neurotransmitter serotonin (5-HT) in the neurons of the raphe, extra-raphe, and ventral populations along with projection sites of these neurons. The huge implications of 5-HT in the control of respiration, prompted animal model studies to further investigate a potential connection between 5-HT and SIDS. 5-HT deficient mice were engineered by knocking out the Pet-1 transcription factor so that knockout mice only retained 30-40% of their brainstem 5-HT neurons. By comparing these 5-HT deficient Pet-1 knockout mice to wild-type mice, it was demonstrated that 5-HT deficient mice failed to autoresuscitate themselves after repeated bouts of hypoxia. Intriguingly, these mice only experienced an autoresuscitation deficit during a specific time period during development. To further evaluate the pathological development behind this behavior issue, in the current study we utilized mice that have modified Pet-1-Flpe driver, Egr2-Cre driver, along with a knock-in RC::FPSit allele to observe 5-HT development in the brainstem in a mature adult and across the critical period (postnatal days 8 and 13- P8 and P13). The transgenic mouse model Pet1-Krox20 gives us a way of exploring a specific subset of 5-HT neurons that rise from the developmental rhombomeres r3 and r5. The use of the knock-in RC::FPSit allele allows us to view the axonal projections of these specific 5-HT neurons by utilizing the presynaptic marker synaptophysin-GFP. This model (PKSit) will allow us to target 5-HT neurons that are implicated in respiration. We chose to compare two projection targets of the PKSit 5-HT neuron subtype through the vulnerable period of development and mature adult mouse: the Locus Coeruleus (LC) and the Nucleus Tractus Solitarius (NTS). In this study we tested the amount of colabeling between 5-HT and GFP in the LC and NTS at P8, P13, as well as the mature adult. We hypothesize that the LC undergoes significant serotonergic axon development and increases colocalization with GFP labeled axon projections between the ages of P8 and P13. We sliced mouse brains and ran immunofluorescence before taking confocal images. By utilizing ImageJ software to run colocalization analysis on the images obtained, we were able to quantify the amount of 5-HT labeled axon projections that are colocalized with GFP labeled axon projections. The parameters we used to quantify the amount of colocalization include the Pearson's Coefficient (PC), Mander's Coefficient (M1/M2), Cytofluorograms, Costes' Method, and van Steensel's Cross-Correlation Coefficient (CCF). We found that the LC shows significant changes with age in the colocalization of 5-HT with GFP while the NTS does not exhibit significant changes with age. The significant changes found in the LC 5-HT/GFP expression between the ages of P8 and P13 suggest one possible cause of failure of arousal. At P8, this lack of 5-HT colabeling with GFP projections suggests that there is some development occurring, which prevents the proper function of 5-HT. At P13, there is a significant increase in the colabeling of 5-HT with GFP, which indicates that the Pet1-Krox20 lineage is actively using 5-HT. The colocalization studies demonstrate that as the mouse ages, the amount of 5-HT labeling with GFP-synaptophysin in the NTS stays the same. The lack of overlap even in mature adult mice suggests that the expression of 5-HT in GFP labeled projections is not necessary. This colocalization study shows that there is an effect of age on the development of the serotonergic system in the LC, but no effect of age in the NTS. While this demonstrates that there is a critical period of development in relation to the LC, it is only one aspect of why mice pups failed to respond to repeated bouts of hypoxia