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In the process of rational development and utilisation of nuclear energy, people often face nuclear accidents such as lost and stolen radioactive sources; so, the means of searching for these sources quickly in highly radioactive environments is an important security challenge. In the past, these jobs were limited to workers specialising in nuclear technology. They used gamma-ray detection equipment to search for radioactive sources, but the search efficiency was low. The main purpose of this article is to design a meta-heuristic algorithm based on imitating professional technicians to locate radioactive sources in a computer-aided manner. At the same time, due to the complexity that may characterise the actual search, the search strategy must be optimised. The article established an intelligent random search model with human thinking. Finally, it was proved based on the mathematical theory that the complexity of the model search algorithm is linear, and the simulation experiment results show that the optimisation algorithm has good efficiency and fault tolerance.

Peroxidasin (PXDN) is a secreted heme peroxidase that catalyzes the oxidative crosslinking of collagen IV within the extracellular matrix (ECM) via intermediate hypobromous acid (HOBr) synthesis from hydrogen peroxide and bromide, but recent findings have also suggested alternative ECM protein modifications by PXDN, including incorporation of bromide into tyrosine residues. In this work, we sought to identify the major target proteins for tyrosine bromination by HOBr or by PXDN-mediated oxidation in ECM from mouse teratocarcinoma PFHR9 cells. We detected 61 bromotyrosine (BrY)-containing peptides representing 23 proteins in HOBr-modified ECM from PFHR9 cells, among which laminins displayed the most prominent bromotyrosine incorporation. Moreover, we also found that laminin α1, laminin β1, and tubulointerstitial nephritis antigen-like (TINAGL1) contained BrY in untreated PFHR9 cells, which depended on PXDN. We extended these analyses to lung tissues from both healthy mice and mice with experimental lung fibrosis, and in lung tissues obtained from human subjects. Analysis of ECM-enriched mouse lung tissue extracts showed that 83 ECM proteins were elevated in bleomycin-induced fibrosis, which included various collagens and laminins, and PXDN. Similarly, mRNA and protein expression of PXDN and laminin α/β1 were enhanced in fibrotic mouse lung tissues, and also in mouse bone-marrow-derived macrophages or human fibroblasts stimulated with transforming growth factor β1, a profibrotic growth factor. We identified 11 BrY-containing ECM proteins, including collagen IV α2, collagen VI α1, TINAGL1, and various laminins, in both healthy and mouse fibrotic lung tissues, although the relative extent of tyrosine bromination of laminins was not significantly increased during fibrosis. Finally, we also identified 7 BrY-containing ECM proteins in human lung tissues, again including collagen IV α2, collagen VI α1, and TINAGL1. Altogether, this work demonstrates the presence of several bromotyrosine-modified ECM proteins, likely involving PXDN, even in normal lung tissues, suggesting a potential biological function for these modifications., Competing Interests: Declaration of competing interest None, (Copyright © 2024 The Authors. Published by Elsevier B.V. All rights reserved.)

Lung transplantation is often the only option for patients in the later stages of severe lung disease, but this is limited both due to the supply of suitable donor lungs and both acute and chronic rejection after transplantation. Ascertaining novel bioengineering approaches for the replacement of diseased lungs is imperative for improving patient survival and avoiding complications associated with current transplantation methodologies. An alternative approach involves the use of decellularized whole lungs lacking cellular constituents that are typically the cause of acute and chronic rejection. Since the lung is such a complex organ, it is of interest to examine the extracellular matrix components of specific regions, including the vasculature, airways, and alveolar tissue. The purpose of this approach is to establish simple and reproducible methods by which researchers may dissect and isolate region-specific tissue from fully decellularized lungs. The current protocol has been devised for pig and human lungs, but may be applied to other species as well. For this protocol, four regions of the tissue were specified: airway, vasculature, alveoli, and bulk lung tissue. This procedure allows for the procurement of samples of tissue that more accurately represent the contents of the decellularized lung tissue as opposed to traditional bulk analysis methods.

Alveolar type 2 epithelial cells (AT2s) derived from human induced pluripotent stem cells (iAT2s) have rapidly contributed to our understanding of AT2 function and disease. However, while iAT2s are primarily cultured in three-dimensional (3D) Matrigel, a matrix derived from cancerous mouse tissue, it is unclear how a physiologically relevant matrix will impact iAT2s phenotype. As extracellular matrix (ECM) is recognized as a vital component in directing cellular function and differentiation, we sought to derive hydrogels from decellularized human lung alveolar-enriched ECM (aECM) to provide an ex vivo model to characterize the role of physiologically relevant ECM on iAT2 phenotype. We demonstrate aECM hydrogels retain critical in situ ECM components, including structural and basement membrane proteins. While aECM hydrogels facilitate iAT2 proliferation and alveolosphere formation, a subset of iAT2s rapidly change morphology to thin and elongated ring-like cells. This morphological change correlates with upregulation of recently described iAT2-derived transitional cell state genetic markers. As such, we demonstrate a potentially underappreciated role of physiologically relevant aECM in iAT2 differentiation., (© 2023. The Author(s).)

Chronic lung diseases, such as chronic obstructive pulmonary disease (COPD) and idiopathic pulmonary fibrosis (IPF), are characterized by regional extracellular matrix (ECM) remodeling which contributes to disease progression. Previous proteomic studies on whole decellularized lungs have provided detailed characterization on the impact of COPD and IPF on total lung ECM composition. However, such studies are unable to determine the differences in ECM composition between individual anatomical regions of the lung. Here, we employ a post-decellularization dissection method to compare the ECM composition of whole decellularized lungs (wECM) and specific anatomical lung regions, including alveolar-enriched ECM (aECM), airway ECM (airECM), and vasculature ECM (vECM), between non-diseased (ND), COPD, and IPF human lungs. We demonstrate, using mass spectrometry, that individual regions possess a unique ECM signature characterized primarily by differences in collagen composition and basement-membrane associated proteins, including ECM glycoproteins. We further demonstrate that both COPD and IPF lead to alterations in lung ECM composition in a region-specific manner, including enrichment of type-III collagen and fibulin in IPF aECM. Taken together, this study provides methodology for future studies, including isolation of region-specific lung biomaterials, as well as a dataset that may be applied for the identification of novel ECM targets for therapeutics., Competing Interests: Declaration of competing interest The authors declare the following financial interests/personal relationships which may be considered as potential competing interests: Daniel J. Weiss reports financial support was provided by University of Vermont. Daniel J. Weiss reports a relationship with National Heart Lung and Blood Institute that includes: funding grants. None to declare., (Copyright © 2022. Published by Elsevier Ltd.)

The 9th biennial conference titled "Stem Cells, Cell Therapies, and Bioengineering in Lung Biology and Diseases" was hosted virtually, due to the ongoing COVID-19 pandemic, in collaboration with the University of Vermont Larner College of Medicine, the National Heart, Lung, and Blood Institute, the Alpha-1 Foundation, the Cystic Fibrosis Foundation, and the International Society for Cell & Gene Therapy. The event was held from July 12th through 15th, 2021 with a pre-conference workshop held on July 9th. As in previous years, the objectives remained to review and discuss the status of active research areas involving stem cells (SCs), cellular therapeutics, and bioengineering as they relate to the human lung. Topics included 1 ) technological advancements in the in situ analysis of lung tissues, 2 ) new insights into stem cell signaling and plasticity in lung remodeling and regeneration, 3 ) the impact of extracellular matrix in stem cell regulation and airway engineering in lung regeneration, 4 ) differentiating and delivering stem cell therapeutics to the lung, 5 ) regeneration in response to viral infection, and 6 ) ethical development of cell-based treatments for lung diseases. This selection of topics represents some of the most dynamic and current research areas in lung biology. The virtual workshop included active discussion on state-of-the-art methods relating to the core features of the 2021 conference, including in situ proteomics, lung-on-chip, induced pluripotent stem cell (iPSC)-airway differentiation, and light sheet microscopy. The conference concluded with an open discussion to suggest funding priorities and recommendations for future research directions in basic and translational lung biology.

A workshop entitled "Stem Cells, Cell Therapies and Bioengineering in Lung Biology and Diseases" was hosted by the University of Vermont Larner College of Medicine in collaboration with the National Heart, Lung and Blood Institute, the Alpha-1 Foundation, the Cystic Fibrosis Foundation, the International Society for Cell and Gene Therapy and the Pulmonary Fibrosis Foundation. The event was held from July 15 to 18, 2019 at the University of Vermont, Burlington, Vermont. The objectives of the conference were to review and discuss the current status of the following active areas of research: 1) technological advancements in the analysis and visualisation of lung stem and progenitor cells; 2) evaluation of lung stem and progenitor cells in the context of their interactions with the niche; 3) progress toward the application and delivery of stem and progenitor cells for the treatment of lung diseases such as cystic fibrosis; 4) progress in induced pluripotent stem cell models and application for disease modelling; and 5) the emerging roles of cell therapy and extracellular vesicles in immunomodulation of the lung. This selection of topics represents some of the most dynamic research areas in which incredible progress continues to be made. The workshop also included active discussion on the regulation and commercialisation of regenerative medicine products and concluded with an open discussion to set priorities and recommendations for future research directions in basic and translation lung biology., Competing Interests: Conflict of interest: D.E. Wagner reports a grant from the US NIH (R13 HL149436, conference grant), and grants for conference support from the Alpha-1 Foundation, the International Society for Cell and Gene Therapy, and the Pulmonary Fibrosis Foundation, during the conduct of the study; and honoraria from Boehringer Ingelheim outside the submitted work. In addition, D.E. Wagner has patent US20160067378A1 pending. Conflict of interest: L. Ikonomou has nothing to disclose. Conflict of interest: S.E. Gilpin has nothing to disclose. Conflict of interest: C.M. Magin reports consulting fees from Sharklet Technologies, Inc., outside the submitted work; and a patent, “3D in vitro models of lung tissue”, pending. Conflict of interest: F. Cruz has nothing to disclose. Conflict of interest: A. Greaney has nothing to disclose. Conflict of interest: M. Magnusson has nothing to disclose. Conflict of interest: Y-W. Chen has nothing to disclose. Conflict of interest: B. Davis has nothing to disclose. Conflict of interest: K. Vanuytsel has nothing to disclose. Conflict of interest: S. Rolandsson Enes has nothing to disclose. Conflict of interest: A. Krasnodembskaya reports grants from the Medical Research Council (MRC) UK during the writing of this article. She is funded by the MRC (national funder for medical and translational research) to conduct research in the area of stem cell-based therapies for lung diseases. Conflict of interest: M. Lehmann has nothing to disclose. Conflict of interest: G. Westergren-Thorsson has nothing to disclose. Conflict of interest: J. Stegmayr has nothing to disclose. Conflict of interest: H.N. Alsafadi has nothing to disclose. Conflict of interest: E.T. Hoffman has nothing to disclose. Conflict of interest: D.J. Weiss reports grants from the NIH during the conduct of the study. Conflict of interest: A.L. Ryan reports grants from the Cystic Fibrosis Foundation and the NIH, outside the submitted work., (Copyright ©ERS 2020.)