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This study followed up ADHD/autistic symptoms and attentional performance in children/adolescents with ASD and typically developing ones (TD) over 5-7 years. The participants were stratified by age at baseline into child (< 12 years) and adolescent (12-19 years) groups. ADHD symptoms, especially hyperactivity, and attentional functions significantly improved during follow-up, more in children than in adolescents, in both ASD and TD. Significantly more omission errors and perseverations were noted in ASD than TD through the follow-up. Children with ASD had more improvement in reaction time while adolescents with ASD had less improvement in commission errors and detectability than TD. No correlation of attentional functions and ADHD symptoms in ASD implied different neural mechanisms of ADHD symptoms between ASD and ADHD.

This study was conducted to explore the effects of an augmented-reality (AR) creative project on English L2 learners' perceptions of creativity, as well as to investigate how to stimulate students' learning motivation. The AR project was developed and integrated into the course syllabus of a university English class, and 39 Taiwanese freshmen completed the project step by step. Data for analysis primarily emerged from the Preference Scale, the Instructional Materials Motivation Survey (IMMS), and an AR student survey. Following a pretest-posttest design, this study showed that the participants demonstrated a higher level of favorable perceptions of creative thinking, such as "preference for ideation" and "valuing new ideas," and a lower "tendency for premature critical evaluation of ideas," although these differences were non-significant. However, working on the project also led to a significantly higher level of self-awareness of being "too busy for new ideas." According to the results of the IMMS, "attention" yields significantly positive relationships with "relevance," "confidence," and "satisfaction." This finding suggests that the students who were more engaged tended to see the project as relevant to their needs; they were also more confident and had a more satisfying AR experience. Based on the results, pedagogical implications are discussed.

BackgroundExistence of breast cancer stem cells (BCSCs) is implicated in disease relapse, metastasis, and resistance of treatment. β1,3-Galactosyltransferase 5 (B3GALT5) has been shown to be a pro-survival marker for BCSCs. However, little is known about the prognostic significance of B3GALT5 in breast cancer.MethodsPaired tissues (tumor part and adjacent non-tumor part) from a cohort of 202 women with breast cancer were used to determine the expression levels of B3GALT5 mRNA by qRT-PCR. Kaplan-Meier and multivariable Cox proportional hazard models were used to assess survival differences in terms of relapse-free survival (RFS) and overall survival (OS). Both breast cancer cells and cancer stem cells (BCSCs) were used to see the in vitro effects of knockdown or overexpression of B3GALT5 on cell migration, invasion, and epithelial-to-mesenchymal transition (EMT). A patient-derived xenograft (PDX) model was used to see the in vivo effects of knockdown of B3GALT5 in BCSCs on tumor growth and metastasis.ResultsHigher expression of B3GALT5 in 202 breast cancer tissues, especially in adjacent non-tumor tissue, correlated with poor clinical outcomes including shorter OS and RFS in all patients, especially those with early stage breast cancer. In vitro studies showed B3GALT5 could enhance cell migration, invasion, mammosphere formation, and EMT. Of note, B3GALT5 upregulated the expression of β-catenin and EMT activator zinc finger E-box binding homeobox 1 (ZEB1) pathway in BCSCs. In vivo studies showed B3GALT5 expression in BCSCs is critical for not only tumor growth but also lymph node and lung metastasis in PDX mice.ConclusionOur results demonstrated the value of B3GALT5 as a prognostic marker of breast cancer, especially among the early stage patients, and its crucial roles in regulating EMT, cell migration, and stemness thereby promoting breast cancer progression.

Cancer stem cells (CSC) play a pivotal role in cancer metastasis and resistance to therapy. Previously, we compared the phosphoproteomes of breast cancer stem cells (BCSCs) enriched subpopulation and non-BCSCs sorted from breast cancer patient-derived xenograft (PDX), and identified a function unknown protein, transmembrane and coiled-coil domain family 3 (TMCC3) to be a potential enrichment marker for BCSCs. We demonstrated greater expression of TMCC3 in BCSCs than non-BCSCs and higher expression of TMCC3 in metastatic lymph nodes and lungs than in primary tumor of breast cancer PDXs. TMCC3 silencing suppressed mammosphere formation, ALDH activity and cell migration in vitro, along with reduced tumorigenicity and metastasis in vivo. Mechanistically, we found that AKT activation was reduced by TMCC3 silencing, but enhanced by TMCC3 overexpression. We further demonstrated that TMCC3 interacted directly with AKT through its 1-153 a.a. domain by cell-free biochemical assay in vitro and co-immunoprecipitation and interaction domain mapping assays in vivo. Based on domain truncation studies, we showed that the AKT-interacting domain of TMCC3 was essential for TMCC3-induced AKT activation, self-renewal, and metastasis. Clinically, TMCC3 mRNA expression in 202 breast cancer specimens as determined by qRT-PCR assay showed that higher TMCC3 expression correlated with poorer clinical outcome of breast cancer, including early-stage breast cancer. Multivariable analysis identified TMCC3 expression as an independent risk factor for survival. These findings suggest that TMCC3 is crucial for maintenance of BCSCs features through AKT regulation, and TMCC3 expression has independent prognostic significance in breast cancer. Thus, TMCC3 may serve as a new target for therapy directed against CSCs.

Transmission of SARS-CoV-2 through direct, person-to-person contact has been recognized since the early stages of the COVID-19 pandemic (1). However, mounting evidence suggests that the virus can be transmitted through [...]

Teachers in K-12 settings increasingly demand instructional materials beyond textbooks to follow the upward momentum of personalized instruction. Especially during the outbreak of COVID-19, K-12 teachers are forced to quickly adapt to online teaching and thus have more difficulties of delivering personalized instruction in a relatively resource-restraint situation. Open educational resources (OER), allowing teachers to retain, reuse, revise, remix, and redistribute high-quality educational resources at no costs, can be a viable option for teachers. However, the acceptance of OER in K-12 education still remains low. Effective strategies are needed to reinforce teacher intention to adopt OER. This research showcased a two-phase sequential explanatory mixed method inquiry to investigate whether engaging K-12 teachers in open educational practices (OEP)--such as renewable assignments--increased their acceptance of OER. The quantitative phase, referring to the technology acceptance model (TAM), examined the change in factors influencing teachers' acceptance of OER. The qualitative phase was followed up to provide supplementary perspectives of the quantitative findings. By integrating complementary findings, this research found that OEP increased teachers' perceived ease of and self-efficacy towards using OER. Although teachers' intention of implementing OER is not significantly improved, qualitative findings offered additional insights into the benefits of OEP in promoting OER usage and the recommended directions for future effort. Practical implications on improving teachers' acceptance of OER in K-12 curriculum are discussed at the end.

G protein-coupled estrogen receptor-1 (GPER), a member of the G protein-coupled receptor (GPCR) superfamily, mediates estrogen-induced proliferation of normal and malignant breast epithelial cells. However, its role in breast cancer stem cells (BCSCs) remains unclear. Here we showed greater expression of GPER in BCSCs than non-BCSCs of three patient-derived xenografts of ER- /PR+ breast cancers. GPER silencing reduced stemness features of BCSCs as reflected by reduced mammosphere forming capacity in vitro, and tumor growth in vivo with decreased BCSC populations. Comparative phosphoproteomics revealed greater GPER-mediated PKA/BAD signaling in BCSCs. Activation of GPER by its ligands, including tamoxifen (TMX), induced phosphorylation of PKA and BAD-Ser118 to sustain BCSC characteristics. Transfection with a dominant-negative mutant BAD (Ser118Ala) led to reduced cell survival. Taken together, GPER and its downstream signaling play a key role in maintaining the stemness of BCSCs, suggesting that GPER is a potential therapeutic target for eradicating BCSCs.