Cardiac screening in school children: Combining auscultation and electrocardiography with a crowdsourcing model.

BACKGROUND/PURPOSE: School-based cardiac screening is useful for identifying children and adolescents with a high risk of sudden cardiac death. However, because of challenges associated with cost, distance, and human resources, cardiac screening is not widely implemented, especially in rural areas with limited medical resources. This study aims to establish a cloud-based system suitable for mass cardiac screening of schoolchildren in rural areas with limited medical resources. METHODS: Students from three schools were included. They or their guardians completed a simple questionnaire, administered in paper or electronic form. Heart sounds were recorded using an electronic stethoscope. Twelve-lead electrocardiograms (ECGs) were recorded and digitalized. The signals were transmitted through Bluetooth to a tablet computer and then uploaded to a cloud server over Wi-Fi. Crowdsourced pediatric cardiologists reviewed those data from a web-based platform and provided remote consultation. In cases in which abnormal heart sounds or ECGs were noted, the students were referred to the hospital for further evaluation. RESULTS: A total of 1004 students were enrolled in this study. Of the 138 students referred, 62 were diagnosed as having an abnormal heart condition and most had previously been undiagnosed. The interrater agreeability was high. CONCLUSION: An innovative strategy combining a cloud-based cardiac screening system with remote consultation by crowdsourced experts was established. This system allows pediatric cardiologists to provide consultation and make reliable diagnoses. Combined with crowdsourcing, the system constitutes a viable approach for mass cardiac screening in children and adolescents living in rural areas with insufficient medical resources.

The Treatment of Aquaculture Wastewater with Biological Aerated Filters: From the Treatment Process to the Microbial Mechanism.

Algal cell proliferation has posed significant problems for traditional water treatment facilities; these problems are attributed to surface hydrophilicity and electrostatic repulsion. Biological aerated filters (BAFs) have been extensively used in wastewater treatment to remove pollutants such as algal cells by utilizing the adsorption and separation capabilities of the filter media. In this study, a BAF was supplemented with biological filter medium (Marchantia polymorpha) to assess its effectiveness of pretreating aquaculture wastewater. In terms of process performance, steady and consistent treatment was achieved by the BAF with M. polymorpha (BAF2) under an algal cell density as high as 1.65 × 108 cell/L, with average removal rates for NH4+-N and algae cells of 74.4% and 81.9%, respectively. The photosynthetic activity parameters (rETRmax, α, Fv/Fm, and Ik) of the influent and effluent were quantitatively assessed, and M. polymorpha was found to remove algae by disrupting the photosynthetic system of the algal cells. Furthermore, the addition of the M. polymorpha filter medium enhanced the community structure of the functional microbes in the BAF system. The highest microbial community richness and diversity were observed in the BAF2. Meanwhile, M. polymorpha promoted an increase in the abundance of denitrifying bacteria, including Bdellovibrio and Pseudomonas. Overall, this work offers a unique perspective on the aquaculture wastewater pretreatment process and BAF design.

Transformation of bisphenol A by manganese oxide-coated sand.

Oxidative transformation of organic contaminants by manganese oxides was commonly investigated with pure MnO(2) suspension, which deviates from the fact that natural manganese oxides are seldom present as a pure form in the natural environment. In this study, we prepared manganese oxide-coated sand (MOCS) and evaluated its oxidative capacity using bisphenol A (BPA) as the model compound. BPA was transformed by MOCS and the reaction followed an exponential decay model. The reaction was pH dependent and followed the order of pH 4.5>pH 5.5>pH 6.5>pH 7.5>pH 8.6>pH 9.6, indicating that acidic conditions facilitated BPA transformation while basic conditions disfavored the reaction. Coexisting metal ions exhibited inhibitory effects and followed the order of Fe(3+) > Zn(2+) > Cu(2+) > Ca(2+) > Mg(2+) > Na(+). Transformation of BPA by MOCS was much slower than that by pure MnO(2) suspension. However, similar transformation products were identified in both studies, suggesting the same reaction pathways. This work suggests that the reactivity of MnO(2) in the environment might be overestimated if extrapolating the result from the pure MnO(2) suspension because natural MnO(2) is mainly present as coating on the surface of soils and sediments.

(E)-Ethyl 2-cyano-3-[4-(4,5-diphenyl-1H-imidazol-2-yl)phen-yl]acrylate dihydrate.

In the title compound, C(27)H(21)N(3)O(2)·2H(2)O, the three benzene rings attached to the heterocyclic imidazole ring are not coplanar with the latter, making dihedral angles of 14.8 (2), 31.4 (2), and 37.5 (2)°, respectively, for the benzene ring planes in the 2-, 4- and 5-positions. In the crystal, there are two water mol-ecules which serve as connectors between the acrylate mol-ecules and stabilize the structure via N-H⋯O, O-H⋯N, C-H⋯O and O-H⋯O hydrogen bonding.

Recent range-wide demographic expansion in a Taiwan endemic montane bird, Steere's Liocichla (Liocichla steerii).

BACKGROUND: The subtropical island of Taiwan is an area of high endemism and a complex topographic environment. Phylogeographic studies indicate that vicariance caused by Taiwan's mountains has subdivided many taxa into genetic phylogroups. We used mitochondrial DNA sequences and nuclear microsatellites to test whether the evolutionary history of an endemic montane bird, Steere's Liocichla (Liocichla steerii), fit the general vicariant paradigm for a montane organism. RESULTS: We found that while mountains appear to channel gene flow they are not a significant barrier for Steere's Liocichla. Recent demographic expansion was evident, and genetic diversity was relatively high across the island, suggesting expansion from multiple areas rather than a few isolated refugia. Ecological niche modeling corroborated the molecular results and suggested that populations of Steere's Liocichla are connected by climatically suitable habitat and that there was less suitable habitat during the Last Glacial Maximum. CONCLUSIONS: Genetic and ecological niche modeling data corroborate a single history--Steere's Liocichla was at lower density during the Last Glacial Maximum and has subsequently expanded in population density. We suggest that such a range-wide density expansion might be an overlooked cause for the genetic patterns of demographic expansion that are regularly reported. We find significant differences among some populations in FST indices and an admixture analysis. Though both of these results are often used to suggest conservation action, we affirm that statistically significant results are not necessarily biologically meaningful and we urge caution when interpreting highly polymorphic data such as microsatellites.

Histone H1-like protein participates in endothelial cell-specific activation of the von Willebrand factor promoter.

A region of the von Willebrand factor (VWF) promoter has been identified that is necessary to confer endothelial cell-specific activation to the VWF promoter. This region spans sequences +155 to +247 and contains binding sites for GATA6 and NFY transcription factors. To identify potential DNA binding transcription factors that directly interact with these sequences in an endothelial-specific manner, we have performed extensive gel mobility assays with use of 7 overlapping DNA probes that collectively span this entire region. An endothelial-specific protein DNA complex was formed with an oligonucleotide that corresponded to sequences +155 to +184 of the VWF gene. Mutation analysis identified a 6-nucleotide element corresponding to sequences +164 to +169 as the core-binding region for the formation of this complex. Transfection analysis demonstrated that the mutation, which abolished DNA-protein interaction, resulted in significant inhibition of the VWF promoter activity. DNA pull-down analysis, mass spectrometry, and Western blot analysis demonstrated that a 32-kDa polypeptide with homology to histone H1 constituted the endothelial-specific DNA binding protein, or a DNA binding subunit of this protein complex. On the basis of these results, we hypothesize that an H1-like protein functions as an endothelial cell-specific transcriptional activator of the VWF promoter.

A complex heterozygous mutation of His373Leu and Asp487-Ser488-Phe489 deletion in human cytochrome P450c17 causes 17alpha-hydroxylase/17,20-lyase deficiency in three Chinese sisters.

Cytochrome P450c17 deficiency is one of the rare forms of enzyme disorders in steroid biosynthesis, resulting from defects in 17alpha-hydroxylase and 17,20-lyase activities. The disease is caused by the mutations in CYP17 gene, inherited in an autosomal recessive pattern. We reported a Chinese family with three sisters suffering from P450c17 deficiency based on their clinical features and molecular genetics. The patients were found to be compound heterozygotes with two different mutations. Screened by polymerase chain reaction-single strand conformation polymorphism (PCR-SSCP), a heterozygous point mutation His373Leu was detected in the exon 6 of CYP17 gene which was proved to be derived from paternal allele. The other allele contained nine-base pair deletion, located in exon 8, eliminating codons 487-489 (Asp-Ser-Phe) near the carboxy-terminus of P450c17. The mother and the brother have been demonstrated to be carriers of deletion mutation through restriction enzyme analysis. Both mutations have been reported previously in Asia. This is the first report of the molecular genetic study of 17alpha-hydroxylase/17,20-lyase deficiency in mainland China with a novel compound heterozygous mutation.

The NFY transcription factor inhibits von Willebrand factor promoter activation in non-endothelial cells through recruitment of histone deacetylases.

Human von Willebrand factor (VWF) gene sequences +155 to +247 contain cis-acting elements that contribute toward endothelial specific activation of the VWF promoter. Analyses of this region demonstrated the presence of a GATA-binding site that is necessary for the promoter activation in endothelial cells. We have reported recently the presence of a novel NFY-binding sequence in this region that does not conform to the consensus NFY-binding sequence CCAAT. NFY was shown to function as a repressor of the VWF promoter through interaction with this novel binding site. Here we report that the NFY interacts with histone deacetylases (HDACs) in a cell type-specific manner and recruits them to the VWF promoter to inhibit the promoter activity in non-endothelial cells. Analyses of the acetylation status of histones in the chromatin region containing the VWF promoter sequences demonstrated that these sequences are associated with acetylated histone H4 specifically in endothelial cells. It was also demonstrated that HDACs are specifically recruited to the same chromatin region in non-endothelial cells. We also demonstrated that GATA6 is the GATA family member that interacts with the VWF promoter and that GATA6 is associated with NFY specifically in non-endothelial cells. We propose that NFY recruits HDACs to the VWF promoter, which may result in deacetylation of GATA6 as well as of histones in non-endothelial cells, thus leading to promoter inactivation. In endothelial cells, however, association of HDACs, NFY, and GATA6 is interrupted potentially through endothelial cell-specific signaling/mechanism, thus favoring the balance toward acetylation and activation of the VWF promoter.

The NFY transcription factor functions as a repressor and activator of the von Willebrand factor promoter.

Human von Willebrand factor (VWF) gene sequences -487 to +247 function as an endothelial-specific promoter in vitro. Analysis of the activation mechanism of the VWF promoter has resulted in the identification of a number of cis-acting elements and trans-acting factors that regulate its activity. The GATA and Ets transcription factors were shown to function as activators of transcription, whereas NF1 and Oct1 were shown to repress transcription. We have reported the presence of another repressor element in exon 1 that interacted with a protein complex designated "R." In the absence of NF1 binding, inhibition of this interaction resulted in promoter activation in nonendothelial cells. We have now identified the "R" protein complex as the NFY transcription factor. Using DNA methylation interference assay and base substitution mutation analysis, we show that NFY interacts with a novel DNA sequence corresponding to nucleotides +226 to +234 in the VWF promoter that does not conform to the consensus NFY binding sequence CCAAT. The VWF gene does contain a CCAAT element that is located downstream of the TATA box and we show that the NFY factor also interacts with this CCAAT element. Using antibodies specific against the A, B, and C subunits of NFY, we demonstrate that the NFY complexes interacting with the CCAAT sequence have a composition similar to that of the repressor binding to the first exon sequences. The results of mutation analysis and transfection studies demonstrated that the interaction of NFY with the upstream CCAAT element is required for VWF promoter activation. Based on these results, we hypothesize that NFY can function both as a repressor and activator of transcription and its function may be modulated through its DNA binding sequences.