Background: Autologous growth factors have proved to promote tissue regeneration in various medical fields. Recent findings suggest that platelet rich plasma may also play an important role in hair follicle restoration.
Objective: The objective of this study was to evaluate the safety and clinical efficacy of plasma rich in growth factors (PRGFs) for the treatment of androgenetic alopecia (AGA).
Materials And Methods: Five PRGF injections were administered over 19 patients with AGA. Phototrichograms regarding follicle density/diameter and terminal/vellus hair ratio were performed at baseline and after 1 year follow-up period. Consenting participants underwent histologic scalp examination. At the end of the study, overall patient satisfaction and clinical improvement were determined.
Results: After PRGF therapy, mean hair density/diameter increased and terminal/vellus hair ratio was also improved. Patients presented epidermal thickness, perifollicular neoangiogenesis, cell proliferation, and terminal/miniaturized hair ratio improvement. Plasma rich in growth factors seemed to reduce the perivascular inflammatory infiltrate, promote the remodeling of dermo-epidermal tissue, and increase bulge stem cell niches. Patients declared an overall positive satisfaction, and a high clinical improvement score was achieved when comparing premacrophotographs and postmacrophotographs.
Conclusion: Although randomized clinical trials are needed, this study provides preliminary data supporting the positive therapeutic effect of autologous growth factors on hair follicle regeneration.
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http://dx.doi.org/10.1097/DSS.0000000000001049 | DOI Listing |
Purpose: Radiotherapy (RT)/cetuximab (C) demonstrated superiority over RT alone for locally advanced squamous head and neck cancer. We tested this in completely resected, intermediate-risk cancer.
Methods: Patients had squamous cell carcinoma of the head and neck (SCCHN) of the oral cavity, oropharynx, or larynx, with one or more risk factors warranting postoperative RT.
Sci Adv
January 2025
Department of Medicine, Northwestern University Feinberg School of Medicine, Chicago, IL, USA.
Mitochondrial electron transport chain (ETC) function modulates macrophage biology; however, mechanisms underlying mitochondria ETC control of macrophage immune responses are not fully understood. Here, we report that mutant mice with mitochondria ETC complex III (CIII)-deficient macrophages exhibit increased susceptibility to influenza A virus (IAV) and LPS-induced endotoxic shock. Cultured bone marrow-derived macrophages (BMDMs) isolated from these mitochondria CIII-deficient mice released less IL-10 than controls following TLR3 or TLR4 stimulation.
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January 2025
School of Biochemistry and Immunology, Trinity Biomedical Sciences Institute, Trinity College Dublin, Dublin 2, Ireland.
The cytokine interleukin-10 (IL-10) limits the immune response and promotes resolution of acute inflammation. Because of its immunosuppressive effects, IL-10 up-regulation is a common feature of tumor progression and metastasis. Recently, IL-10 regulation has been shown to depend on mitochondria and redox-sensitive signals.
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January 2025
Laboratory of Mitochondrial Biology and Metabolism, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD, USA.
Although lipid-derived acetyl-coenzyme A (CoA) is a major carbon source for histone acetylation, the contribution of fatty acid β-oxidation (FAO) to this process remains poorly characterized. To investigate this, we generated mitochondrial acetyl-CoA acetyltransferase 1 (ACAT1, distal FAO enzyme) knockout macrophages. C-carbon tracing confirmed reduced FA-derived carbon incorporation into histone H3, and RNA sequencing identified diminished interferon-stimulated gene expression in the absence of ACAT1.
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January 2025
Department of Biochemistry, College of Life Science and Biotechnology, Brain Korea 21 Project, Yonsei University, Seoul 03722, Republic of Korea.
Until now, Hippo pathway-mediated nucleocytoplasmic translocation has been considered the primary mechanism by which yes-associated protein (YAP) and transcriptional co-activator with PDZ-binding motif (TAZ) transcriptional coactivators regulate cell proliferation and differentiation via transcriptional enhanced associate domain (TEAD)-mediated target gene expression. In this study, however, we found that TAZ, but not YAP, is associated with the Golgi apparatus in macrophages activated via Toll-like receptor ligands during the resolution phase of inflammation. Golgi-associated TAZ enhanced vesicle trafficking and secretion of proinflammatory cytokines in M1 macrophage independent of the Hippo pathway.
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