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1. Quantitative analysis of facial shape in children to support respirator design

   Nemeth, Christopher; Hoskens, Hanne; Wilson, Graham; Jones, Mike; DiPietrantonio, Josef; Salami, Bukola; Harnish, Del; Claes, Peter; Weinberg, Seth M.; Shriver, Mark D.; Hallgrímsson, Benedikt. Applied Ergonomics. vol. 122, 104375. 2025.

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   The COVID-19 pandemic demonstrated the need for respiratory protection against airborne pathogens. Respirator options for children are limited, and existing designs do not consider differences in facial shape or size. We created a dataset of children’s facial images from three cohorts, then used geometric morphometric analyses of dense and sparse facial landmark representations to quantify age, sex and ancestry-related variation in shape. We found facial shape and size in children vary significantly with age from ages 2 to 18, particularly in dimensions relevant to respirator design. Sex differences are small throughout most of the age range of our sample. Ancestry is associated with significant facial shape variation in dimensions that may affect respirator fit. We offer guidance on how to our results can be used for the appropriate design of devices such as respirators for pediatric populations. We also highlight the need to consider ancestry-related variation in facial morphology to promote equitable, inclusive products.

2. Vascular architecture regulates mesenchymal stromal cell heterogeneity via P53-PDGF signaling in the mouse incisor

   Guo, Tingwei; Pei, Fei; Zhang, Mingyi; Yamada, Takahiko; Feng, Jifan; Jing, Junjun; Ho, Thach-Vu; Chai, Yang. Cell Stem Cell. vol. 31(6), 904–920.e6. June 2024.

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3. ARID1B maintains mesenchymal stem cell quiescence via inhibition of BCL11B-mediated non-canonical Activin signaling

   Zhang, Mingyi; Guo, Tingwei; Pei, Fei; Feng, Jifan; Jing, Junjun; Xu, Jian; Yamada, Takahiko; Ho, Thach-Vu; Du, Jiahui; Sehgal, Prerna; Chai, Yang. Nature Communications. vol. 15(1), 4614. May 2024.

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   Abstract ARID1B haploinsufficiency in humans causes Coffin-Siris syndrome, associated with developmental delay, facial dysmorphism, and intellectual disability. The role of ARID1B has been widely studied in neuronal development, but whether it also regulates stem cells remains unknown. Here, we employ scRNA-seq and scATAC-seq to dissect the regulatory functions and mechanisms of ARID1B within mesenchymal stem cells (MSCs) using the mouse incisor model. We reveal that loss of Arid1b in the GLI1+ MSC lineage disturbs MSCs’ quiescence and leads to their proliferation due to the ectopic activation of non-canonical Activin signaling via p-ERK. Furthermore, loss of Arid1b upregulates Bcl11b , which encodes a BAF complex subunit that modulates non-canonical Activin signaling by directly regulating the expression of activin A subunit, Inhba . Reduction of Bcl11b or non-canonical Activin signaling restores the MSC population in Arid1b mutant mice. Notably, we have identified that ARID1B suppresses Bcl11b expression via specific binding to its third intron, unveiling the direct inter-regulatory interactions among BAF subunits in MSCs. Our results demonstrate the vital role of ARID1B as an epigenetic modifier in maintaining MSC homeostasis and reveal its intricate mechanistic regulatory network in vivo, providing novel insights into the linkage between chromatin remodeling and stem cell fate determination.

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