In ultraviolet (UV) radiation–exposed skin, mutations fuel clonal cell growth. The relationship between UV exposure and the accumulation of clonal mutations (CMs) and the correlation between CMs and skin cancer risk are largely unexplored. We characterized 450 individual-matched sun-exposed (SE) and non-SE (NE) normal human skin samples. The number and relative contribution of CMs were significantly different between SE and NE areas. Furthermore, we identified hotspots in TP53, NOTCH1, and GRM3 where mutations were significantly associated with UV exposure. In the normal skin from patients with cutaneous squamous cell carcinoma, we found that the cancer burden was associated with the UV-induced mutations, with the difference mostly conferred by the low-frequency CMs. These findings provide previously unknown information on UV’s carcinogenic effect and pave the road for future development of quantitative assessment of subclinical UV damage and skin cancer risk.
Herpes simplex virus (HSV)-1 and -2 infections are highly prevalent worldwide. HSV infection during pregnancy can result in neonatal herpes infection, which is characterized by lifelong infection with periods of latency and reactivation. HSV can be acquired by an infant during one of three periods: in utero (5 %), peripartum (85 %), or postnatal (10 %). Neonatal HSV is a rare but significant infection that may be associated with severe morbidity and mortality, especially if there is dissemination or central nervous system involvement. Diagnostic and therapeutic advances have led to a reduction in mortality and, to a lesser extent, improvement of neurodevelopmental outcomes, but further developments are still needed. It is essential to improve the clinician's ability to identify infants who are at increased risk of HSV infection and to prevent mother-to-child transmission. The development of novel antiviral agents with higher efficacy is a worthwhile aim for the future.
Onychomycosis is one of the most common diseases in the field of dermatology. It refers to the fungal infection of the nail plate or nail bed with high incidence in the general population. The available treatment options for onychomycosis have limited use due to side effects, drug interactions, and contraindications, which necessitates the application of an alternative treatment for onychomycosis. In the recent years, lasers and photodynamic therapy (PDT) have been recognized as alternative treatment options. Most of the previous studies have found them to be safe and effective treatment modalities in this indication; however, the results varied greatly and the in vitro and in vivo outcomes are contradictory. In the present review, studies related to the mechanism of action of lasers and PDT for the treatment of onychomycosis will be discussed, with a focus on to find explanation to the contradictory results.
The use of photodynamic therapy is extensive, due to its antitumoral, antibacterial and photorejuvenation effects. It destroys tumor via direct cell destruction and indirectly via vascular shutdown, induction of acute local inflammatory response and activation of the immune system. Both innate and adaptive immune cells are involved in the immunological effects of photodynamic therapy. In addition to UV-induced DNA damage, inflammation and immunosuppression are also essential elements in the pathogenesis of actinic keratosis. Both immunosuppression induced by UV and defective immune response to dysplastic keratinocytes may be the target of photodynamic therapy to eliminate actinic keratosis. These elements are discussed in the present review, highlighting the possible mechanism of photodynamic therapy to effectively treat actinic keratosis.
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