Wound localization and housing conditions dictate repair dynamics and scar formation
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The decreasing housing utilization efficiency in China’s cities
‘Ghost cities’ are a well-known phenomenon of (almost) complete vacancy of urban living space in China. Underutilization of urban living space, however, is far more common than complete vacancy. Here we propose the concept of housing utilization efficiency (HUE) and present the following findings: (1) the overall HUE in China’s highly urbanized areas decreased from 84% in 2010 to 78% in 2020, (2) the HUE in central, old urban areas was generally lower than that in the outer layers of urban areas and declined more from 2010 to 2020 and (3) four development types are found to represent different patterns of urban population movement, urban housing growth and HUE change at the intraurban level. These findings provide comprehensive insight into the discrepancies between urban housing supply and demand in China and highlight their connections to the country’s particular urbanization characteristics and policies, which are crucial for future housing development and planning.
Urban inequality, the housing crisis and deteriorating water access in US cities
The housing unaffordability and cost-of-living crisis is affecting millions of people in US cities, yet the implications for urban dwellers’ well-being and social reproduction remain less clear. This Article presents a longitudinal analysis of household access to running water—a vital component of social infrastructure—in the 50 largest US cities since 1970. The results indicate that water access has worsened in an increasing number and typology of US cities since the 2008 global financial crash, disproportionately affecting households of color in 12 of the 15 largest cities. We provide evidence to suggest that a ‘reproductive squeeze’—systemic, compounding pressures on households’ capacity to reproduce themselves on a daily and societal basis—is forcing urban households into more precarious living arrangements, including housing without running water. We analyze the case study of Portland (Oregon) to illustrate the racialized nature of the reproductive squeeze under a housing crisis. Our insights reveal that plumbing poverty—a lack of household running water—is expanding in scope and severity to a broader array of US cities, raising doubts about equitable progress towards Sustainable Development Goals for clean water and sanitation for all (SDG 6) and sustainable cities (SDG 11) in an increasingly urbanized United States.
An axis-specific mitral annuloplasty ring eliminates mitral regurgitation allowing mitral annular motion in an ovine model
Current mitral annuloplasty rings fail to restrict the anteroposterior distance while allowing dynamic mitral annular changes. We designed and manufactured a mitral annuloplasty ring that demonstrated axis-specific, selective flexibility to meet this clinical need. The objectives were to evaluate ex vivo biomechanics of this ring and to validate the annular dynamics and safety after ring implantation in vivo.
FGFR antagonists restore defective mandibular bone repair in a mouse model of osteochondrodysplasia
Gain-of-function mutations in fibroblast growth factor receptor (FGFR) genes lead to chondrodysplasia and craniosynostoses. FGFR signaling has a key role in the formation and repair of the craniofacial skeleton. Here, we analyzed the impact of Fgfr2– and Fgfr3-activating mutations on mandibular bone formation and endochondral bone repair after non-stabilized mandibular fractures in mouse models of Crouzon syndrome (Crz) and hypochondroplasia (Hch). Bone mineralization of the calluses was abnormally high in Crz mice and abnormally low in Hch mice. The latter model presented pseudarthrosis and impaired chondrocyte differentiation. Spatial transcriptomic analyses of the Hch callus revealed abnormally low expression of Col11, Col1a, Dmp1 genes in mature chondrocytes. We found that the expression of genes involved in autophagy and apoptosis (Smad1, Comp, Birc2) was significantly perturbed and that the Dusp3, Dusp9, and Socs3 genes controlling the mitogen-activated protein kinase pathway were overexpressed. Lastly, we found that treatment with a tyrosine kinase inhibitor (BGJ398, infigratinib) or a C-type natriuretic peptide (BMN111, vosoritide) fully rescued the defective endochondral bone repair observed in Hch mice. Taken as a whole, our findings show that FGFR3 is a critical orchestrator of bone repair and provide a rationale for the development of potential treatments for patients with FGFR3-osteochondrodysplasia.
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.
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