1. "Dermatology: New Treatments and Technology" This article discusses new treatments and technology that are being used in dermatology today. It covers advances such as new laser treatments, photodynamic therapy, and other treatments that are being used to treat skin conditions. It also discusses how these treatments are being used to improve the quality of life of patients suffering from skin conditions. 2. "Dermatology: The Impact of Skin Diseases on Quality of Life" This article discusses the impact that skin diseases have on the quality of life of patients. It looks at the psychological impact of skin conditions, as well as the physical impact that they can have on a person's daily life. It also looks at the available treatments and how they can help improve the quality of life of those suffering from skin diseases. 3. "The Latest in Dermatology: A Look at the Latest Treatments and Technologies" This article takes a look at the newest treatments and technologies being used in dermatology today. It looks at treatments such as laser resurfacing, microdermabrasion, and other treatments that are helping to improve the appearance and health of patients. It also looks at the advances in technology that are making these treatments
ERAP1, ERAP2 and LNPEP are aminopeptidases implicated in autoimmune pathophysiology. Here, we demonstrate that ERAP2 is upregulated and ERAP1 is downregulated in patients with psoriasis who are homozygous for autoimmune-linked variants of ERAP. We also demonstrate that aminopeptidase expression is not uniform in the skin. Specifically, the intracellular antigen-processing aminopeptidases ERAP1 and ERAP2 were strongly expressed in basal and early spinous layer keratinocytes, while granular layer keratinocytes expressed predominantly LNPEP, an aminopeptidase specialized in the processing of extracellular antigens for MHC class I cross-presentation.
Symmetrical acral keratoderma (SAK) is a rare skin disorder characterized by brownish-black hyperkeratotic patches symmetrically distributed on the acral regions (Fan et al., 2010, Vinay et al., 2016). Our previous study found that many patients have a family history, with an autosomal dominant inheritance pattern (Li et al., 2014a), and that congenital genetic factors are likely to play a pivotal role in the pathogenesis of SAK. Here, we clarify the underlying genes and genotype-phenotype correlations of SAK.
Normal skin contains numerous clones carrying cancer driver mutations. However, the mutational landscape of normal skin and its clonal relationship with skin cancer requires further elucidation. The aim of our study was to investigate the mutational landscape of normal human skin. We performed whole-exome sequencing using physiologically normal skin tissues and the matched peripheral blood (n = 39), and adjacent-matched skin cancers from a subset of patients (n = 10). Exposed skin harbored a median of 530 mutations (10.4/Mb, range 51–2947), whereas non-exposed skin majorly exhibited significantly fewer mutations (median 13, 0.25/Mb, range 1–166).
Rituximab (RTX), a chimeric monoclonal antibody targeting CD20 on B lymphocytes, is an effective disease-modifying agent in the treatment of pemphigus vulgaris (PV), a rare autoimmune blistering disease (AIBD) (Witte et al. 2018; Yuan et al. 2022). PV is caused by serum IgG autoantibodies targeting adhesion molecules of the cadherin family, particularly desmoglein (Dsg)3 and Dsg1, two major components of desmosomes (Spindler and Waschke 2018). PV usually arise with oral erosions first and then spreading to the skin with a chronic-relapsing course (Feliciani et al.
Despite remarkable advances in treating patients with metastatic melanoma, management of melanoma brain metastases remains challenging. Recent evidence suggests that epigenetic reprogramming is an important mechanism for the adaptation of melanoma cells to the brain environment. In this study, methylomes and transcriptomes of a cohort of matched melanoma metastases were evaluated by integrated omics data analysis. The identified 38 candidate genes displayed distinct promoter methylation and corresponding gene expression changes in intracranial compared to extracranial metastases.
Keloids represent a fibrotic disorder characterized by the excessive deposition of extracellular matrix (ECM). However, the mechanisms by which ECM deposition in keloids is regulated remain elusive. Here, we found that the expression of both TWEAK and its cognate receptor Fn14 was significantly downregulated in keloids and that TWEAK/Fn14 signaling repressed the expression of ECM-related genes in keloid fibroblasts. The IRF1 gene was essential for this repression, and the TWEAK/Fn14 downstream transcription factor P65 directly bound to the promoter of the IRF1 gene and induced its expression.
Start codon mutations in ubiquitin ligase Kelch-like protein 24 (KLHL24) lead to a gain-of-function mutant KLHL24-ΔN28, which mediates the excessive degradation of keratin 15, desmin, and keratin 14, resulting in alopecia, cardiopathy, and epidermolysis bullosa syndrome (ACES). ACES patients normally present atrophic scars after wounds heal, which is rare in KRT14-related epidermolysis bullosa (EB). The mechanisms underlying the formation of atrophic scars in EB of ACES patients remain unclear. This study demonstrated that KLHL24-ΔN28 impaired skin wound healing by excessively degrading vimentin.