Nuclear wastewater decontamination by 3D-Printed hierarchical zeolite monoliths

3D-printed monoliths of zeolites chabazite and 4A were made, characterized, and shown effective for removing strontium and caesium from water

Does Product Type Affect Electronic Word-of-Mouth Richness Effectiveness? Influences of Message Valence and Consumer Knowledge

Drawing on the information richness theory, this study attempts to address how valence of electronic word-of-mouth (eWOM), product type and consumer knowledge will yield different levels of eWOM richness. The results based on an experimental study suggest that negative eWOM has a stronger effect in producing eWOM information richness than does positive eWOM, and such effect is more pronounced for a leisure farm tour (experience goods) than for digital camera (search goods). The tendency that negative eWOM will provide richer information for the leisure farm tour is more evident for high-knowledge consumers than for low-knowledge consumers. The study’s results caution against the aggravated harm of negative eWOM incurred from the dissatisfactory experience of a leisure farm tour

Parents' views of self-management for children with moderate to severe persistent asthma

AbstractObjectivesChildren with moderate to severe persistent asthma, including those with asthma attacks more than once daily, asthma symptoms at night more than once a week, or asthma attacks that affect activities and sleep, may have irregular and recurrent symptoms until adolescence. Such symptoms may affect quality of life and even cause death. This study explored the self-management experiences of children with asthma in Hualien City, Taiwan, based on the views expressed by their parents.Materials and methodsThis study used a qualitative inquiry of 15 parents of children with asthma, in order to understand the children's self-management experiences.ResultsThe findings from this study, as derived from content analysis, showed the following six domains of self-management: (1) knowledge of asthma; (2) use of asthma medications; (3) issues related to physical exercise; (4) self-care in daily life; (5) prevention and handling of asthmatic episodes; and (6) other issues related to asthma.ConclusionThe results of the study can help health professionals understand the self-management experiences of families who have a child with persistent asthma, which in turn could provide appropriate guidelines and valuable information for development of self-management programs for children with asthma

Pik3r1 Is Required for Glucocorticoid-Induced Perilipin 1 Phosphorylation in Lipid Droplet for Adipocyte Lipolysis.

Glucocorticoids promote lipolysis in white adipose tissue (WAT) to adapt to energy demands under stress, whereas superfluous lipolysis causes metabolic disorders, including dyslipidemia and hepatic steatosis. Glucocorticoid-induced lipolysis requires the phosphorylation of cytosolic hormone-sensitive lipase (HSL) and perilipin 1 (Plin1) in the lipid droplet by protein kinase A (PKA). We previously identified Pik3r1 (also called p85α) as a glucocorticoid receptor target gene. Here, we found that glucocorticoids increased HSL phosphorylation, but not Plin1 phosphorylation, in adipose tissue-specific Pik3r1-null (AKO) mice. Furthermore, in lipid droplets, the phosphorylation of HSL and Plin1 and the levels of catalytic and regulatory subunits of PKA were increased by glucocorticoids in wild-type mice. However, these effects were attenuated in AKO mice. In agreement with reduced WAT lipolysis, glucocorticoid- initiated hepatic steatosis and hypertriglyceridemia were improved in AKO mice. Our data demonstrated a novel role of Pik3r1 that was independent of the regulatory function of phosphoinositide 3-kinase in mediating the metabolic action of glucocorticoids. Thus, the inhibition of Pik3r1 in adipocytes could alleviate lipid disorders caused by excess glucocorticoid exposure

Paxillin facilitates timely neurite initiation on soft-substrate environments by interacting with the endocytic machinery.

Neurite initiation is the first step in neuronal development and occurs spontaneously in soft tissue environments. Although the mechanisms regulating the morphology of migratory cells on rigid substrates in cell culture are widely known, how soft environments modulate neurite initiation remains elusive. Using hydrogel cultures, pharmacologic inhibition, and genetic approaches, we reveal that paxillin-linked endocytosis and adhesion are components of a bistable switch controlling neurite initiation in a substrate modulus-dependent manner. On soft substrates, most paxillin binds to endocytic factors and facilitates vesicle invagination, elevating neuritogenic Rac1 activity and expression of genes encoding the endocytic machinery. By contrast, on rigid substrates, cells develop extensive adhesions, increase RhoA activity and sequester paxillin from the endocytic machinery, thereby delaying neurite initiation. Our results highlight paxillin as a core molecule in substrate modulus-controlled morphogenesis and define a mechanism whereby neuronal cells respond to environments exhibiting varying mechanical properties

EXPLORING E-LEARNING BEHAVIOR THROUGH LEARNING DISCOURSES

As many studies predict e-learning behaviors through intention, few of them investigate user’s learning behaviors directly. In addition to intention, individual’s e-learning behaviors may be influenced by technology readiness and group influences, such as social identity and social bond. This research-in-progress study explores how e-learning behaviors vary with intention, technology readiness, social identity and social bond. Our investigation was based on analyzing the speech acts embedded in fourteen learners’ online discourses in an eighteen-week e-learning course. We then compared how speech acts varied among groups with different degree of intention, technology readiness, social identity, and social bond. Our findings contribute e-learning research by clarifying how intention, technology readiness, social identity, and social bond influence learning behaviors in e-learning context

By protecting against cutaneous inflammation, epidermal pigmentation provided an additional advantage for ancestral humans.

Pigmentation evolved in ancestral humans to protect against toxic, ultraviolet B irradiation, but the question remains: "what is being protected?" Because humans with dark pigmentation display a suite of superior epidermal functions in comparison with their more lightly pigmented counterparts, we hypothesized and provided evidence that dark pigmentation evolved in Africa to support cutaneous function. Because our prior clinical studies also showed that a restoration of a competent barrier dampens cutaneous inflammation, we hypothesized that resistance to inflammation could have provided pigmented hominins with yet another, important evolutionary benefit. We addressed this issue here in two closely related strains of hairless mice, endowed with either moderate (Skh2/J) or absent (Skh1) pigmentation. In these models, we showed that (a) pigmented mice display a markedly reduced propensity to develop inflammation after challenges with either a topical irritant or allergen in comparison with their nonpigmented counterparts; (b) visible and histologic evidence of inflammation was paralleled by reduced levels of pro-inflammatory cytokines (i.e., IL-1α and INFα); (c) because depigmentation of Skh2/J mouse skin enhanced both visible inflammation and pro-inflammatory cytokine levels after comparable pro-inflammatory challenges, the reduced propensity to develop inflammation was directly linked to the presence of pigmentation; and (d) furthermore, in accordance with our prior work showing that pigment production endows benefits by reducing the surface pH of skin, acidification of albino (Skh1) mouse skin also protected against inflammation, and equalized cytokine levels to those found in pigmented skin. In summary, pigmentation yields a reduced propensity to develop inflammation, consistent with our hypothesis that dark pigmentation evolved in ancestral humans to provide a suite of barrier-linked benefits that now include resistance to inflammation

THE STUDY OF SHOULDER INTERNAL AND EXTERNAL ROTATION STRENGTH IN COLLEGE BASEBALL PLAYERS

The purpose of this study was to investigate the different of dominant arm shoulder rotation torque between the baseball pitchers, infielders, and ouffielders. Participants were 27 first-level collegiate baseball players, including 9 pitchers, 10 infielders, 8 outfielders. A Biodex lsokinetic Dynamometer was used for estimation of shoulder muscle strength. This system's test velocity was set at 60 "Is and the range of motion of dominant arm shoulder in flexion, abduction, 90' of abduction with external rotation, and 90" abduction with internal rotation. The results indicated that there was no significant different in internal rotation peak torque and ERllR ratio between pitchers, infielders, and outfielders. There was significantly different in external rotation peak torque. The infielders and ouffielders possess greater external rotation peak torque than pitchers

Transcriptional regulation of FoxO3 gene by glucocorticoids in murine myotubes.

Glucocorticoids and FoxO3 exert similar metabolic effects in skeletal muscle. FoxO3 gene expression was increased by dexamethasone (Dex), a synthetic glucocorticoid, both in vitro and in vivo. In C2C12 myotubes the increased expression is due to, at least in part, the elevated rate of FoxO3 gene transcription. In the mouse FoxO3 gene, we identified three glucocorticoid receptor (GR) binding regions (GBRs): one being upstream of the transcription start site, -17kbGBR; and two in introns, +45kbGBR and +71kbGBR. Together, these three GBRs contain four 15-bp glucocorticoid response elements (GREs). Micrococcal nuclease (MNase) assay revealed that Dex treatment increased the sensitivity to MNase in the GRE of +45kbGBR and +71kbGBR upon 30- and 60-min Dex treatment, respectively. Conversely, Dex treatment did not affect the chromatin structure near the -17kbGBR, in which the GRE is located in the linker region. Dex treatment also increased histone H3 and/or H4 acetylation in genomic regions near all three GBRs. Moreover, using chromatin conformation capture (3C) assay, we showed that Dex treatment increased the interaction between the -17kbGBR and two genomic regions: one located around +500 bp and the other around +73 kb. Finally, the transcriptional coregulator p300 was recruited to all three GBRs upon Dex treatment. The reduction of p300 expression decreased FoxO3 gene expression and Dex-stimulated interaction between distinct genomic regions of FoxO3 gene identified by 3C. Overall, our results demonstrate that glucocorticoids activated FoxO3 gene transcription through multiple GREs by chromatin structural change and DNA looping