Miracle-dz/UniFAR-FTUs huggingface dataset:
Movement guidelines for young children: Engaging stakeholders to design dissemination strategies in the Hong Kong early childhood education context

Background Early childhood is a critical period during which patterns of movement behaviors are formed. The World Health Organization had endorsed guidelines for physical activity, sedentary behavior and sleep over a 24-h time period, which had been adopted by the Center for Health Protection of Hong Kong. This paper reports on stakeholder engagements that were conducted to inform the design of strategies to disseminate the guidelines in early childhood education (ECE) settings. Methods Using a mixed-methods study design, we sought to (a) assess the stakeholders' levels of awareness and knowledge of the Hong Kong movement guidelines for young children and (b) identify the factors that influence the uptake of the said guidelines. We conducted an online survey of early childhood education teachers (N =314), twelve focus groups involving teachers (N = 18) and parents (N = 18), and individual interviews of key informants (N = 7) and domestic workers who provide care for preschool-aged children (N = 7). Descriptive statistics were used for the quantitative data, and thematic analysis was performed on the qualitative data using an inductive and semantic approach following a realist framework. Findings Our findings show that teachers were aware of the movement guidelines for young children, but their knowledge of the specific guidelines was deficient; parents and domestic workers had limited awareness and knowledge of the guidelines. Uptake of the movement guidelines is enabled by parent engagement, activities in the ECE centers, home-school cooperation, and community activities for children. The challenges include the time poverty of parents, local curriculum requirements, limited physical spaces, social values, and pandemic-related restrictions. Conclusion We recommend that dissemination strategies in the ECE context should deliver knowledge content and support stakeholders in mitigating the challenges associated with time, space, and social conditions.
A Comparison of Representation Learning Methods for Medical Concepts in MIMIC-IV

Objective: To compare and release the diagnosis (ICD-10-CM), procedure (ICD-10-PCS), and medication (NDC) concept (code) embeddings trained by Latent Dirichlet Allocation (LDA), Word2Vec, GloVe, and BERT, for more efficient electronic health record (EHR) data analysis. Materials and Methods: The embeddings were pre-trained by the four aforementioned models separately using the diagnosis, procedure, and medication information in MIMIC-IV. We interpreted the embeddings by visualizing them in 2D space and used the silhouette coefficient to assess the clustering ability of these embeddings. Furthermore, we evaluated the embeddings in three downstream tasks without fine-tuning: next visit diagnoses prediction, ICU patients mortality prediction, and medication recommendation. Results: We found that embeddings pre-trained by GloVe have the best performance in the downstream tasks and the best interpretability for all diagnosis, procedure, and medication codes. In the next-visit diagnosis prediction, the accuracy of using GloVe embeddings was 12.2% higher than the baseline, which is the random generator. In the other two prediction tasks, GloVe improved the accuracy by 2%-3% over the baseline. LDA, Word2Vec, and BERT marginally improved the results over the baseline in most cases Discussion and Conclusion: GloVe shows superiority in mining diagnoses, procedures, and medications information of MIMIC-IV compared with LDA, Word2Vec, and BERT. Besides, we found that the granularity of training samples can affect the performance of models according to the downstream task and pre-train data.
Brain microstructural changes and fatigue after COVID-19

Background Fatigue and cognitive complaints are the most frequent persistent symptoms in patients after severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. This study aimed to assess fatigue and neuropsychological performance and investigate changes in the thickness and volume of gray matter (GM) and microstructural abnormalities in the white matter (WM) in a group of patients with mild-to-moderate coronavirus disease 2019 (COVID-19). Methods We studied 56 COVID-19 patients and 37 matched controls using magnetic resonance imaging (MRI). Cognition was assessed using Montreal Cognitive Assessment and Cambridge Neuropsychological Test Automated Battery, and fatigue was assessed using Chalder Fatigue Scale (CFQ-11). T1-weighted MRI was used to assess GM thickness and volume. Fiber-specific apparent fiber density (FD), free water index, and diffusion tensor imaging data were extracted using diffusion-weighted MRI (d-MRI). d-MRI data were correlated with clinical and cognitive measures using partial correlations and general linear modeling. Results COVID-19 patients had mild-to-moderate acute illness (95% non-hospitalized). The average period between real-time quantitative reverse transcription polymerase chain reaction-based diagnosis and clinical/MRI assessments was 93.3 (±26.4) days. The COVID-19 group had higher total CFQ-11 scores than the control group (p < 0.001). There were no differences in neuropsychological performance between groups. The COVID-19 group had lower FD in the association, projection, and commissural tracts, but no change in GM. The corona radiata, corticospinal tract, corpus callosum, arcuate fasciculus, cingulate, fornix, inferior fronto-occipital fasciculus, inferior longitudinal fasciculus, superior longitudinal fasciculus, and uncinate fasciculus were involved. CFQ-11 scores, performance in reaction time, and visual memory tests correlated with microstructural changes in patients with COVID-19. Conclusions Quantitative d-MRI detected changes in the WM microstructure of patients recovering from COVID-19. This study suggests a possible brain substrate underlying the symptoms caused by SARS-CoV-2 during medium- to long-term recovery.
Cumulative Social Disadvantage and Health-Related Quality of Life: National Health Interview Survey 2013-2017

Background: Evidence of the association between social determinants of health (SDoH) and health-related quality of life (HRQoL) is largely based on single SDoH measures, with limited evaluation of cumulative social disadvantage. We examined the association between cumulative social disadvantage and the Health and Activity Limitation Index (HALex). Methods: We used data of respondents from the 2013-2017 National Health Interview Survey. A cumulative SDoH index was created by aggregating 46 SDoH from 6 domains, and respondents were grouped by quartiles (SDoH-Q1 to Q4). A higher SDoH index or quartile indicates greater disadvantage. Two outcomes were assessed: HALex scores using two-part models, and a binary poor HALex (HALex score < 0.79 [20th percentile]) using logistic regression. Regression analyses adjusted for demographics and comorbidities and were performed in the overall sample, and by age, sex, and race/ethnicity categories. Results: Among 156,182 adults (mean age 46 years; 51.7% women), higher SDoH quartile groups averaged lower HALex scores and had higher proportions with poor HALex. A unit increase in SDoH index was associated with 0.01 decrease in HALex score ({beta} = -0.01; 95% CI [-0.01, -0.01]) and 14% higher odds of poor HALex (odds ratio, OR = 1.14; 95% CI [1.14, 1.15]). Relative to SDoH-Q1, SDoH-Q4 was associated with HALex score decrease of -0.13 (95% CI [-0.13, -0.13]) and OR 8.67 (95% CI [8.08, 9.30]) for poor HALex. Hispanic persons, despite a relatively higher burden of cumulative social disadvantage, had a weaker SDoH-HALex association than their counterparts. Conclusion: Higher cumulative social disadvantage was independently associated with lower HRQoL in an incremental fashion. The more favorable HRQoL profile observed in the Hispanic could be related to a resilient concept of health derived from cultural values and acceptance, and this highlights the need for population wellness interventions to be responsive to such phenomenon.
Near-infrared images of the Serpens cloud core : the stellar cluster.

JHKnbL and «ice» images of the Serpens molecular cloud core are presented. 163 stellar objects are detected which represents an increase of ∼ 140 objects with respect to the number of stars detected at wavelengths shorter than 1 μm. By using different criteria, 51 stars are identified as members of the Serpens young stellar cluster. The rest of the objects remain unidentified. They could be either background stars or additional embedded Serpens objects of very low luminosity. In a near-infrared colour-magnitude diagram most of the identified Serpens stars are bright and red and seem to be reddened T Tauri-like stars
Standardization of Human IL-29 (IFN- l 1): Establishment of a World Health Organization International Reference Reagent for IL-29 (IFN- l 1) Participants of the Collaborative Study

Human interleukin-29 (IL-29), a helical cytokine with interferon-like activities, is currently being developed as a clinical biotherapeutic to treat chronic hepatitis C infection and some cancers. As such, the World Health Organization (WHO) has recognized a need for biological standardization of IL-29 and the establishment of an internationally available reference reagent of IL-29. In order to accomplish this, an international collaborative study that evaluates WHO candidate reference reagents of IL-29 was instigated by the National Institute for Biological Standards and Control (NIBSC) in 2010 and was carried out in the succeeding year. Two preparations of human sequence recombinant IL-29, one expressed in murine NS0 cells and the other in Escherichia coli , were formulated and lyophilized at NIBSC before evaluation in the collaborative study for their suitability to serve as a reference reagent. The preparations were tested by 6 laboratories from 4 countries using in vitro bioassays and also evaluated for thermal stability within the NIBSC laboratory. On the basis of the results of the collaborative study, both preparations, 07/212 (NS0-derived) and 10/176 ( E. coli -derived) were judged sufﬁciently active and stable to serve as a reference reagent. However, since IL-29 produced in E. coli is in development for clinical applications, it was recommended that the preparation coded 10/176 be established as the WHO international reference reagent for human IL-29. This recom-mendation was accepted, and the IL-29 preparation coded 10/176 was formally established by the WHO ECBS at its meeting in October 2012 as the WHO international reference reagent for IL-29 with an assigned unitage of 5,000 reference units per ampoule.
Curcumin inhibits PKC α activity by binding to its C1 domain

Curcumin is a polyphenolic nutraceutical that acts on multiple biological targets, including protein kinase C (PKC). PKC is a family of serine-threonine kinases central to intracellular signal transduction. We have recently shown that curcumin selectively inhibits PKC α , but not PKC ε in CHO-K1 cells (Pany, S. (2016) Biochemistry 55, 2135–43). To understand which domain(s) of PKC α is/are responsible for curcumin binding and inhibitory activity, we made several domain-swapped mutants in which the C1 (combination of C1A and C1B) and C2 domains are swapped between PKC α and PKC ε . Phorbol ester-induced membrane translocation studies using confocal microscopy and immune-blotting revealed that curcumin inhibited phorbol ester induced membrane translocation of PKC ε mutants, in which ε C1 domain was replaced with α C1, but not the PKC α mutant in which α C1 was replaced with ε C1 domain, suggesting that α C1 is a determinant for curcumin’s inhibitory effect. Further, curcumin inhibited membrane translocation of PKC ε mutants, in which ε C1A and ε C1B domain were replaced with α C1A and α C1B domains, respectively, indicating the role of both α C1A and α C1B domains in curcumin’s inhibitory effects. Phorbol 13-acetate inhibited curcumin binding to α C1A and α C1B with IC 50 values of 6.27 μM and 4.47 μM, respectively. Molecular docking and molecular dynamics studies also supported higher affinity of curcumin for α C1B than α C1A. The C2 domain swapped mutants were inactive in phorbol ester induced membrane translocation. These results indicate that curcumin binds to the C1 domain of C1B, which bind DAG/phorbol ester These sub-domains differ in their binding affinities for phorbol ester and DAG. In contrast, the atypical PKCs are non-responsive to DAG/phorbol ester. There is high homology within domains among different members of the superfamily but the novel kinases differ in having the C2 domain at the N-terminal. PKCs are translocated from the cytosol to the plasma membrane, bind to DAG, become activated and subsequently phosphorylate different target proteins (13, 14). Each domain plays a distinct role in the activation and sub-cellular translocation of PKC. role of the PKC α domains responsible for the curcumin binding and modulation, we made several chimeric proteins swapping the C1 and C2 domains of PKC α and PKC ε and studied their modulation by curcumin in HEK293 cells. We find that curcumin modulates those proteins where the C1 domain of PKC α is conserved. This result indicates that modulation of PKC α by curcumin is C1 domain dependent. membrane translocation when co-treated with TPA and curcumin.
Solar-blind ultraviolet band-pass filter based on metal—dielectric multilayer structures

Solar-blind ultraviolet (UV) band-pass filter has significant value in many scientific, commercial, and military applications, in which the detection of weak UV signal against a strong background of solar radiation is required. In this work, a solar-blind filter is designed based on the concept of "transparent metal". The filter consisting of Al/SiO2 multilayers could exhibit a high transmission in the solar-blind wavelength region and a wide stopband extending from near-ultraviolet to infrared wavelength range. The central wavelength, bandwidth, Q factor, and rejection ratio of the passband are numerically studied as a function of individual layer thickness and multilayer period.
I (cid:2) B Kinase Subunits (cid:3) and (cid:4) Are Required for Activation of NF- (cid:2) B and Induction of Apoptosis by Mammalian Reovirus (cid:1)

Reoviruses induce apoptosis both in cultured cells and in vivo. Apoptosis plays a major role in the pathogenesis of reovirus encephalitis and myocarditis in infected mice. Reovirus-induced apoptosis is dependent on the activation of transcription factor NF- (cid:1) B and downstream cellular genes. To better understand the mechanism of NF- (cid:1) B activation by reovirus, NF- (cid:1) B signaling intermediates under reovirus control were investigated at the level of Rel, I (cid:1) B, and I (cid:1) B kinase (IKK) proteins. We found that reovirus infection leads initially to nuclear translocation of p50 and RelA, followed by delayed mobilization of c-Rel and p52. This biphasic pattern of Rel protein
Plasma-enhanced chemical-vapor deposition of silicon nitride film for high resistance to potential-induced degradation

The antireflection coating (ARC) on crystalline silicon solar cells plays an important role in preventing potential-induced degradation (PID). In a previous work, we reported that the module, which has an ARC prepared by plasma-enhanced chemical-vapor deposition (PE-CVD) using a hollow cathode, indicated high resistance to PID with a constant conventional refractive index (RI). In this work, we report further investigation of the high-PID-resistant ARC. The results indicate that the high-PID resistant ARC had high conductivity, high Si–H bond density, and low N–H bond density. Furthermore, both higher PID resistance and higher conversion efficiency are achieved using an ARC of double or triple layers comprising stacked silicon nitride layers of different RI than those of a conventional single-layer ARC.
Rapid Publication a1-Adrenergic Receptor Stimulation of Sarcomeric Actin Isogene

During pressure-load hypertrophy of the adult heart in vivo, there is up-regulation of the mRNA encoding skeletal a-actin, the sarcomeric actin iso-mRNA characteristic of mature skeletal muscle and the fetal/neonatal heart. We have shown previously that during al-adrenergic receptor-stimulated hypertrophy of cultured rat heart myocytes, the induction of skeletal a-actin mRNA is greater than that of the mRNA encoding cardiac a-actin, the sarcomeric actin iso-mRNA characteristic of the adult heart. To determine if this actin iso-mRNA switch during cardiac hypertrophy reflects changes in the transcriptional status of the myocyte nucleus, we quantified the rate of transcription of actin mRNAs and total RNA, using an in vitro run-on transcription assay with nuclei isolated from the cultured myocytes after stimulation with norepinephrine (NE). Transcription of skeletal a-actin was increased at 3 h after NE, reached a maximum 6.1-fold increase at 12 h, and returned to the control level at 24 h. The EC50 for NE was 200 nM, and pharmacologic studies indicated a,-receptor specificity. Transcription of cardiac a-actin was also increased rapidly by NE (maximum 4.6-fold vs. control at 3 h). However, cardiac aactin transcription had returned to the control level at 6 h, when NE-stimulated skeletal a-actin transcription was still increasing. Transcription of the cytoskeletal (f) actin gene was not changed significantly by NE treatment. Total RNA transcription was not increased until 6 h after NE (1.5-fold vs. control) and remained elevated through 24 h. Inhibition of protein synthesis did not attenuate NE-stimulated actin gene transcription. Thus the a1-adrenoceptor mediates a rapid, transient, and selective increase in transcription of the sarcomeric actin isogenes during cardiac myocyte hypertrophy. Skeletal a-actin, the fetal/neonatal isogene, is induced preferentially to cardiac a-actin, the adult isogene. The different kinetics of actin isogene and total RNA transcription and the independence of transcription from protein synthesis suggest that transcriptional induction via the a, receptor is complex and may involve preexisting regulatory factors. These results A preliminary report of this work has been published in abstract form (1988. Circulation. 78[Suppl. II]:11-562). Address reprint requests to Dr. Simpson, VA Medical Center (1 1-C), 4150 Clement Street, San Francisco, CA 94121. Receivedfor publication 30 September 1988 and in revisedform 12 December 1988. are the first to demonstrate that the a1-adrenergic receptor is a molecular mediator of transcriptional changes underlying an isogene switch that is known to be associated with cardiac myocyte hypertrophy.
Associations between sleep and cognitive performance in a racially/ethnically diverse cohort: the Study of Women’s Health Across the Nation

Study Objectives: To determine whether actigraphy-assessed indices of sleep are associated with cognitive performance in women, and explore whether these associations vary by race/ethnicity. Methods: Participants were 1,126 postmenopausal community-dwelling females (mean age 65 years) from the observational Study of Women’s Health Across the Nation (SWAN); 25% were black, 46% white, 13% Chinese, 11% Japanese, and 5% Hispanic. Actigraphy-assessed sleep measures included total sleep time, wake after sleep onset (WASO), and fragmentation. Cognitive measures included immediate and delayed verbal memory, working memory, and information processing speed. All measures were assessed in conjunction with SWAN annual visit 15. Results: Across the sample, after covariate adjustment, greater WASO and fragmentation were concurrently associated with slower information processing speed. Black participants had significantly worse sleep relative to other race/ethnic groups. Significant race/sleep interactions were observed; in black, but not white, participants, greater fragmentation was concurrently associated with worse verbal memory and slower information processing speed, and greater WASO was concurrently associated with slower information processing speed. Sleep-cognitive performance associations were not different in Chinese and Japanese participants relative to white participants. Conclusions: Greater wakefulness and fragmentation during sleep are concurrently associated with slower information processing. Sleep continuity impacted concurrent cognitive performance in black, but not white, women. This effect may not have been detected in white women because their sleep was largely within the normal range. Future longitudinal studies in diverse samples are critical to further understand whether race/ethnicity moderates the influence of sleep on cognitive performance. sample to disentangle determinants of racial in
Downregulation of Spry-1, an inhibitor of GDNF/Ret, as a mechanism for angiotensin II-induced ureteric bud branching

Mutations of the renin-angiotensin system (RAS) genes are associated with congenital abnormalities of the kidney and urinary tract. We have shown that angiotensin (Ang) II stimulates ureteric bud (UB) branching in vitro . The present study tested the hypothesis that Ang II stimulates the GDNF/ c-Ret/Wnt11 pathway. E12.5 mice metanephroi were grown for 24 hours in the presence or absence of Ang II or AT 1 R receptor antagonist candesartan and subjected to whole-mount ISH. c- Ret , a receptor tyrosine kinase for GDNF, and its downstream target Wnt11 were induced by Ang II in the UB tip cells. GDNF , a Wnt11 -regulated gene expressed in the mesenchyme, was also upregulated by Ang II. In contrast, Ang II treatment downregulated Spry1 , an endogenous inhibitor of Ret tyrosine kinase activity, in an AT 1 R-dependent manner. Quantitative RT-PCR analysis confirmed that Ang II decreases Spry1 mRNA levels in cultured UB cells. In vivo BrdU incorporation indicated that exogenous Ang II preferentially stimulates UB tip cell proliferation, while AT 1 R blockade increases TUNEL-positive apoptotic cells. These findings suggest a model in which AT 1 R-mediated inhibition of Spry1 gene expression releases c-Ret tyrosine kinase activity leading to upregulation of c- Ret and its downstream target gene, Wnt11 . Enhanced Wnt11 expression induces GDNF in the adjacent mesenchyme. This causes focal bursts of UB tip cell proliferation, a decrease in UB tip cell apoptosis and branching.
Lipocalin-2 resistance of Salmonella enterica serotype Typhimurium confers an advantage during life in the inflamed intestine

Salmonella enterica serotype Typhimurium thrives in the lumen of the acutely inflamed intestine, which suggests that this pathogen is resistant to antimicrobials encountered in this environment. However, the identity of these antimicrobials and the corresponding bacterial resistance genes remains elusive. Here we show that enteric infection with S . Typhimurium evoked marked interleukin (IL)–22/IL-17 mediated induction in intestinal epithelial cells of lipocalin-2, an antimicrobial protein that prevents bacterial iron acquisition. Lipocalin-2 accumulated in the intestinal lumen of rhesus macaques during S . Typhimurium infection. Resistance to lipocalin-2, mediated by the iroBCDE iroN locus, conferred a competitive advantage upon the S. Typhimurium wild-type in colonizing the inflamed intestine of wild-type, but not of lipocalin-2 deficient mice. These data support that resistance to lipocalin-2 defines a specific adaptation to growth in the inflamed intestine. To determine the complete molecular profile of of or and gene host to S. Typhimurium in the intestinal mucosa of rhesus macaques, a highly relevant for gastroenteritis. Our results suggest that acquisition of the iroBCDE iroN gene cluster by S. Typhimurium may represent a specific adaptation to life in the inflamed intestine. A potential role of lipocalin-2 resistance in promoting colonization of the inflamed nasal mucosa has recently been proposed for Streptococcus pneumoniae and Haemophilus influenzae