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http://dx.doi.org/10.1177/0969733019845268 | DOI Listing |
Zhongguo Xiu Fu Chong Jian Wai Ke Za Zhi
June 2024
Department of Orthopedic Trauma, Yantaishan Hospital, Yantai Shandong, 264000, P. R. China.
J Invest Dermatol
May 2024
Graduate Institute of Clinical Research, College of Medicine, National Taiwan University, Taipei, Taiwan; Research Center for Developmental Biology and Regenerative Medicine, National Taiwan University, Taipei, Taiwan; Department of Biomedical Engineering, College of Medicine and College of Engineering, National Taiwan University, Taipei, Taiwan; Department of Medical Research, National Taiwan University Hospital, Taipei, Taiwan; Center for Frontier Medicine, National Taiwan University Hospital, Taipei, Taiwan. Electronic address:
In adult mammals, wound healing predominantly follows a fibrotic pathway, culminating in scar formation. However, cutaneous microwounds generated through fractional photothermolysis, a modality that produces a constellation of microthermal zones, exhibit a markedly different healing trajectory. Our study delineates the cellular attributes of these microthermal zones, underscoring a temporally limited, subclinical inflammatory milieu concomitant with rapid re-epithelialization within 24 hours.
View Article and Find Full Text PDFJ Invest Dermatol
September 2023
Department of Cell and Molecular Biology, Karolinska Institute, Stockholm, Sweden. Electronic address:
Single-cell technologies have become essential to driving discovery in both basic and translational investigative dermatology. Despite the multitude of available datasets, a central reference atlas of normal human skin, which can serve as a reference resource for skin cell types, cell states, and their molecular signatures, is still lacking. For any such atlas to receive broad acceptance, participation by many investigators during atlas construction is an essential prerequisite.
View Article and Find Full Text PDFProc Natl Acad Sci U S A
October 2019
Institute for Memory Impairments and Neurological Disorders, University of California, Irvine, CA 92697;
Defects in interleukin-1β (IL-1β)-mediated cellular responses contribute to Alzheimer's disease (AD). To decipher the mechanism associated with its pathogenesis, we investigated the molecular events associated with the termination of IL-1β inflammatory responses by focusing on the role played by the target of Myb1 (TOM1), a negative regulator of the interleukin-1β receptor-1 (IL-1R1). We first show that TOM1 steady-state levels are reduced in human AD hippocampi and in the brain of an AD mouse model versus respective controls.
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