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Article Synopsis
  • * Detailed protocols are provided for preparing and expanding airway basal stem cells from mice and induced pluripotent stem cells, followed by methods for their transplantation into mice.
  • * Successful engraftment leads to the restoration of key airway functions and cell types, with timelines for generating and using these stem cells outlined for researchers.
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Oral gavage (OG) with the use of a cannula attached to a syringe is one of the most common methods used to deliver precise dosing of compounds to the stomach of research animals. Unfortunately, this method comes with difficulties for both the operator and the research animal. Studies have shown that OG may lead to complications, including esophagitis, perforation of the esophagus, and inadvertent tracheal drug administration.

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Changes in the Proportion of Each Cell Type After hiPSC-Derived Airway Epithelia Transplantation.

Cell Transplant

February 2024

Department of Otolaryngology-Head and Neck Surgery, Graduate School of Medicine, Kyoto University, Kyoto, Japan.

No radical treatment is available for the regeneration of dysfunction and defects in airway epithelia. Artificial tracheae made of polypropylene and collagen sponge were used in clinical studies to reconstitute tracheae after resection. For early epithelialization of the luminal surface of the artificial trachea, a model was established, that is, an artificial trachea covered with human-induced pluripotent stem cell-derived airway epithelial cells (hiPSC-AECs) was transplanted into a tracheal defect in an immunodeficient rat.

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Persistent tracheo-cutaneous fistulae necessitate a closure with pedicled or free flaps. The modality adopted is to reconstitute the anterior tracheal wall without compromising the tracheal lumen. We have developed the lateral U advancement Burrow's flap over the strap muscles and tracheal lateral fibrous flaps, to repair a large trachea-cutaneous fistula.

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COPD causes significant morbidity and mortality worldwide. Epithelial damage is fundamental to disease pathogenesis, although the mechanisms driving disease remain undefined. Published evidence from a COPD cohort (SPIROMICS) and confirmed in a second cohort (COPDgene) demonstrate a polymorphism in is a trans-pQTL for E-cadherin, which is critical in COPD pathogenesis.

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