Bridging theory and experiment in defect-tolerant semiconductors for photovoltaics
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Differential bone and vessel type formation at superior and dura periosteum during cranial bone defect repair
The cranial mesenchyme, originating from both neural crest and mesoderm, imparts remarkable regional specificity and complexity to postnatal calvarial tissue. While the distinct embryonic origins of the superior and dura periosteum of the cranial parietal bone have been described, the extent of their respective contributions to bone and vessel formation during adult bone defect repair remains superficially explored. Utilizing transgenic mouse models in conjunction with high-resolution multiphoton laser scanning microscopy (MPLSM), we have separately evaluated bone and vessel formation in the superior and dura periosteum before and after injury, as well as following intermittent treatment of recombinant peptide of human parathyroid hormone (rhPTH), Teriparatide. Our results show that new bone formation along the dura surface is three times greater than that along the superior periosteal surface following injury, regardless of Teriparatide treatment. Targeted deletion of PTH receptor PTH1R via SMA-CreER and Col 1a (2.3)-CreER results in selective reduction of bone formation, suggesting different progenitor cell pools in the adult superior and dura periosteum. Consistently, analyses of microvasculature show higher vessel density and better organized arterial-venous vessel network associated with a 10-fold more osteoblast clusters at dura periosteum as compared to superior periosteum. Intermittent rhPTH treatment further enhances the arterial vessel ratio at dura periosteum and type H vessel formation in cortical bone marrow space. Taken together, our study demonstrates a site-dependent coordinated osteogenic and angiogenic response, which is determined by regional osteogenic progenitor pool as well as the coupling blood vessel network at the site of cranial defect repair.
Promises and challenges of indoor photovoltaics
Indoor photovoltaics (IPVs) harvest ambient light to produce electricity and can cleanly power the rapidly growing number of Internet-of-Things (IoT) sensors. The surge in IPV development, with new proposed materials, devices and products, creates the need to critically evaluate how IPV devices have advanced and to assess their prospects. In this Review, we analyse the status, challenges and opportunities of established and emerging IPV technologies, including metal-halide perovskite, organic photovoltaics, dye-sensitized solar cell and perovskite-inspired materials. Many emerging low-toxicity semiconductor materials could reach IPV efficiencies of up to 50%, but carrier localization and defect trapping hinder their performance. Wide adoption of standardized performance assessment methods is essential, and further harmonization is needed for stress tests, qualification standards and energy rating assessments. For seamless IPV integration in IoT devices, series-connected cell modules and appropriate power management hardware are crucial to maximize energy extraction. IPV device stability, technology upscaling and cost-effective integration in IoT sensors must be further developed but balanced with sustainability across the entire value chain.
Anthrone/XLPE: an adaptive charge capture intelligent insulation material for advanced electric power transmission
The degradation of electrical insulation is mainly attributed to local defects. Although incorporating organic small molecules into dielectric polymers promotes the insulation strength, accurate suppression of defect development is a long-term and formidable challenge. Here we utilize the adaptive charge capture methodology to achieve precise defect suppression, leading to a 123% increase in the initiation voltage of electrical trees in anthrone/cross-linked polyethylene, significantly outperforming existing dielectric polymers and polymer composites. A significant observation is the confinement of charge at the interface between the anode and cross-linked polyethylene in anthrone/cross-linked polyethylene, generating a reverse inherent electric field near the interface and reducing the internal electric field strength of cross-linked polyethylene by up to 18%. These findings not only open avenues for further exploration of materials for ultra-high voltage cables but also play a crucial role in the commercialization and practical application of organic semiconductors in insulation dielectrics.
Microbiota transplantation for cotton leaf curl disease suppression—core microbiome and transcriptome dynamics
Microbiota transplantation is a strong tool for managing plant disease. This study investigates the effects of microbiota transplantation on Cotton Leaf Curl Disease (CLCuD) resistance in Gossypium hirsutum, a species with good fiber length but high susceptibility to biotic stresses. Using metabarcoding for V3-V4 16S rRNA gene amplicon, microbial fractions from both rhizosphere and phyllosphere of CLCuD-resistant species Gossypium arboreum, and susceptible cotton varieties are analyzed. Unique bacterial taxa have been identified associated with disease resistance. Interspecies and intraspecies microbiota transplantation is conducted, followed by CLCuD incidence assays. It is seen that rhizospheric microbiota transplantation from G. arboreum FDH228 significantly suppresses CLCuD in G. hirsutum varieties, outperforming exogenous salicylic acid application. While phyllospheric transplants also reduce disease incidence, they are less effective than rhizospheric transplants. Differential expression analysis DESeq2 is utilized to identify key bacterial genera correlated with CLCuD suppression, including Pseudoxanthomonas and Stenotrophomonas in the rhizosphere of G. arboreum FDH228. Functional pathway analysis reveals upregulation of stress response and metabolism in tolerant species. Transcriptomics reveals upregulation of genes involved in protein phosphorylation and stress response in interspecies rhizospheric microbiota transplants. This study highlights microbiota transplantation as a sustainable method for controlling CLCuD along with specific microbial and genetic mechanisms contributing to CLCuD resistance.
Enhanced osteogenic potential of iPSC-derived mesenchymal progenitor cells following genome editing of GWAS variants in the RUNX1 gene
Recent genome-wide association studies (GWAS) identified 518 significant loci associated with bone mineral density (BMD), including variants at the RUNX1 locus (rs13046645, rs2834676, and rs2834694). However, their regulatory impact on RUNX1 expression and bone formation remained unclear. This study utilized human induced pluripotent stem cells (iPSCs) differentiated into osteoblasts to investigate these variants’ regulatory roles. CRISPR/Cas9 was employed to generate mutant (Δ) iPSC lines lacking these loci at the RUNX1 locus. Deletion lines (Δ1 and Δ2) were created in iPSCs to assess the effects of removing regions containing these loci. Deletion lines exhibited enhanced osteogenic potential, with increased expression of osteogenic marker genes and Alizarin Red staining. Circularized chromosome conformation capture (4C-Seq) was utilized to analyze interactions between BMD-associated loci and the RUNX1 promoter during osteogenesis. Analysis revealed altered chromatin interactions with multiple gene promoters including RUNX1 isoform, as well as SETD4, a histone methyltransferase, indicating their regulatory influence. Interestingly, both deletion lines notably stimulated the expression of the long isoform of RUNX1, with more modest effects on the shorter isoform. Consistent upregulation of SETD4 and other predicted targets within the Δ2 deletion suggested its removal removed a regulatory hub constraining expression of multiple genes at this locus. In vivo experiments using a bone defect model in mice demonstrated increased bone regeneration with homozygous deletion of the Δ2 region. These findings indicate that BMD-associated variants within the RUNX1 locus regulate multiple effector genes involved in osteoblast commitment, providing valuable insights into genetic regulation of bone density and potential therapeutic targets.
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