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Keloid - Crossref

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Last Updated: 24 January 2023

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Ulcerated Keloid Secondary to a Coexisting Complicated Epidermal Inclusion Cyst: A Sonographic Diagnosis

Keloid is a benign fibroblastic tumor that is most common due to tissue damage. On the chest wall, a 29-year-old man with multiple large keloids on the chest wall was diagnosed with two-day pain history, increased frequency, and ulceration on one side. Physical examination revealed a keloid with edema, peripheral erythema, and a 1-cm central ulcer with purulent discharge. A complicated epidermal inclusion cyst was discovered with inflammatory changes within the ulcerated mass. Sonography can aid in obtaining a more effective presurgical approach in the differential diagnosis of ulcerated keloid.

Source link: https://doi.org/10.1177/8756479320914517


EFFICACY OF SURGICAL EXCISION COMBINED WITH INTRALESIONAL TRIAMCINOLONE ACETONIDE THERAPY IN EAR KELOID: CASE SERIES

Keloids develop as a result of abnormal wound healing, resulting in the growth of scar tissue beyond its original boundaries, and rarely regress spontaneously. Corticosteroids can also be used as adjuncts to surgical excision to prevent a recurrence. Six patients with ear keloid disease were treated for intralesional three doses of Triamcinolone acetonide injection, surgical excision, and post-operative two doses of Triamcinolone acetonide injection at the scar site, according to this prospective, interventional, and case series.

Source link: https://doi.org/10.22159/ajpcr.2023.v16i1.46230


Characterization of CD45RO+ memory T lymphocytes in keloid disease

Introduction to Memory T cells, a highly effective subset of T lymphocytes, has been shown to be involved in several inflammatory skin disorders, according to a research. However, the potential role of memory T cells in keloid disease remains uncertain. Memory T cells in KD were isolated from a similar blood sample, and flow cytometry was used to determine the phenotypic and functional abnormalities of memory T cells. Results We found that the majority of T lymphocytes in keloid scars had the memory phenotype, and that a greater number of the CD8+ memory T cells in keloid scars had lower amounts of tumour necrosis factor -u03b1. In addition, we discovered that there had been a significant rise in CD103+ memory T cells in keloid scars. Key Results Our results preliminarily clarify the abnormalities of CD45RO+ memory T cells in keloid scars and provide the first evidence that a disrupted T-cell response is a contributing to KD formation.

Source link: https://doi.org/10.1111/bjd.16173


Characterization of CD45RO+ memory T lymphocytes in keloid disease

Memory T lymphocytes are cells that can cause a rapid and highly effective immune response against pathogens while still recognizing a large variety of antigens. The majority of T lymphocytes in keloid scars are CD3+CD45RO+ memory T cells, according to the authors, who also describe how this type differs from another form of memory T cells called FOXP3-MT. In patients with multiple keloid scars, the authors also found a significant rise in CD4+CD25+ regulatory T cells in keloid scars, as well as a dramatic decrease in the number of cells in CD4+CD25+ regulatory T cells. The authors found that there are distinct differences in CD45RO+ memory T-cell subsets in keloid scarring, and that dysregulation of T cell responses may have a role in kieloid scarring.

Source link: https://doi.org/10.1111/bjd.16517


Bioinformatics analysis and verification of m6A related genes based on the construction of keloid diagnostic model

Background information: Keloid is caused by abnormal hyperplasia of skin connective tissue. Methods: From the Gene Expression Omnibus database, transcriptomic databases of keloid and normal skin tissue were obtained. Eventually, an immune infiltration study was carried out to explore the connection between keloid therapeutic potential and immune microenvironment. Results: Genes with differing expression trends in the three m6A genes, especially IGF2BP3 in the reader category, which is significantly elevated in keloid patients, have been found. We examined the immune cell permeability of immune cells in keloid mice with single sample. FIBERSORT and GSEA are two different acronyms. Conclusions: We analyzed the association between m6A-related genes and keloid by bioinformatics techniques in order to find corresponding sources for determining the molecular mechanism of keloid.

Source link: https://doi.org/10.21203/rs.3.rs-2452066/v1


MiR-21-5p Links Epithelial-Mesenchymal Transition Phenotype with Stem-Like Cell Signatures via AKT Signaling in Keloid Keratinocytes

To investigate miR-21-5p's role in keloid pathogenesis, we transplanted miR-21-5p mimic or inhibitor in keloid keratinocytes and investigated cell proliferation, apoptosis, migration, and invasion, the expressions of EMT-related genes, including vimentin and E-cadherin, EMT-related genes, cell proliferation, apoptosis, migration, and invasion, the presence of cell proliferation, kerloid kin kerloid keratin ker kerloid keratin kero kerloid keratin kerloid keratin kerloid keratin kerlock, keratin, kero, migration, migration and invasion, keloid and adhetadhet, EMT-like cells-related genes, kerloid, adhetadhetadhetaetapoptos, adhel, op, cytos, s, graft This molecular pathway of miR-21-5p on keloid keratinocytes related EMT with cell stemness and identified novel therapeutic keloids.

Source link: https://doi.org/10.1038/srep28281


TGF-β1 Induces Polypyrimidine Tract-Binding Protein to Alter Fibroblasts Proliferation and Fibronectin Deposition in Keloid

Human dermal fibrotic disease keloid has been a clinical challenge due to its tumor-like growth and a lack of effective therapy. In addition, we suppressed PTB using siRNA in keloid fibroblasts and in a keloid xenograft nude mouse model. The proliferation of keloid fibroblasts and accelerated the breakdown of transplanted keloid tissues, which was followed by a change in alternative splicing of USP5 and RTN4, which was accompanied by a change in alternative splicing of PTB and RTN4. In addition, when PTB was cut, there was a decrease in excessive deposition of FN1 and COL3A1 in transplanted keloid tissues. In keloid fibroblasts cultured in media supplemented with TGF-u03b21, only FN1 was downregulated, however, only FN1 was downregulated. PTB's involvement in keloid pathophysiology is explored in this study, which also gives a new therapeutic target for keloids. TGF-u03b21 regulation of PTB, most notable, could give new insight into the mechanisms that underwent inflammatory cytokine-induced fibrosis.

Source link: https://doi.org/10.1038/srep38033


Comorbidities of Keloid and Hypertrophic Scars Among Participants in UK Biobank

Keloids and hypertrophic scars are relatively understudied in terms of debating persistent skin diseases with high treatment resistance. Analysis of 521 UKB respondents were restricted to 230078 individuals with linked primary care records. The mean age of the total cohort was 64 years, with a higher proportion of female participants among the 972 people with excessive scarring and a smaller number of Whites. Results from ethnic groups revealed links with hypertension in Black participants and Asian participants' vitamin D deficiency. In Black women, the association of uterine leiomyoma was borderline significant, although white participants' atopic eczema was more prominent, and showed a similar trend in Asian and Black participants.

Source link: https://doi.org/10.1001/jamadermatol.2022.5607


Current Advances in Hypertrophic Scar and Keloid Management

Hypertrophic scars and keloids are a result of chronic tissue response to dermal injury, which can be attributed to local fibroblast proliferation and collagen overproduction. This reaction occurs due to pathologic wound repair in the inflammatory, proliferative, and/or remodeling phases. Patients with hypertrophic scars or keloids have reported reduced quality of life, physical appearance, and mental stability. Of the medications currently available for hypertrophic scars and keloids, only a few have been properly aided by studies with appropriate experimental design.

Source link: https://doi.org/10.1055/s-0041-1731461


Knockdown of lncRNA-ATB suppresses autocrine secretion of TGF-β2 by targeting ZNF217 via miR-200c in keloid fibroblasts

We investigated the role of lncRNA-ATB in the autocrine secretion of TGF-u03b2 in keloid fibroblasts and figured out the underlying molecular mechanism. However, we found that knockdown of lncRNA-ATB decreased autocrine secretion of TGF-U3b22 and ZNF217 expression in KFs, but that reduced expression of miR-200c was upregulated in KFs through gain-and-loss experiments. MiR-200c was endogenously linked to lncRNA-ATB and inhibition of miR-200c, which reversed the decline in ZNF217 expression in KFs.

Source link: https://doi.org/10.1038/srep24728

* Please keep in mind that all text is summarized by machine, we do not bear any responsibility, and you should always check original source before taking any actions

* Please keep in mind that all text is summarized by machine, we do not bear any responsibility, and you should always check original source before taking any actions