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The coronavirus (COVID-19) pandemic led to a widespread use of vaccines that were approved based on their effectiveness against the virus. We performed a systematic review of the published literature to collect data regarding chronic dermatoses exacerbation after COVID-19 vaccination. Chronic dermatoses exacerbation after COVID-19 vaccination - A systematic review. [Extracted from the article]

Habitat development may affect wildlife behaviour, favouring individuals or behaviours that cope better with perceived threats (predators). Bolder behaviours in human‐dominated habitats (HDH; e.g. urban and rural settlements) may represent habituation specifically to humans, or a general reduction in predator‐avoidance response. However, such carry‐over effects across threat types (i.e. beyond humans) and phases of the escape sequence have not been well studied to date.Here we investigated escape behaviours of a locally common wader species, the spur‐winged lapwing Vanellus spinosus. We assayed their flight initiation distance (FID) and subsequent escape behaviours in agricultural areas and in HDH. We found that lapwings in HDH were bolder, and that the difference was manifested in several phases of the predator‐avoidance sequence (shorter FIDs, shorter distances fled, and a higher probability of escape by running vs. flying). When re‐approached (by an observer) after landing, lapwings in HDH were also more repetitive in their FID than those in other habitats.To determine whether this apparent bolder behaviour in HDH areas is merely a consequence of habituation to humans or represents a broader behavioural change, we introduced an additional threat type—a remotely‐operated taxidermic jackal ('Jack‐Truck'). Finding bolder responses in the HDH to the human threat alone (and not to the Jack‐Truck) could have supported the habituation hypothesis. In contrast, however, we found a bolder response in the HDH to both threat types, as well as a correlation between their FIDs across different sites. These bolder behaviours suggest that HDH impose a broader behavioural change on lapwings, rather than just simple habituation.Overall, our findings demonstrate how FID trials can reveal strong behavioural carry‐over effects of HDH following human and non‐human threats, including effects on the subsequent phases of escaping the predator. Further, FID assays may reveal consistent behavioural types when assessed under field conditions, and offer a direct way to differentiate among the various poorly understood and non‐mutually exclusive mechanisms that lead to behavioural differences among organisms in HDH. The mechanistic perspective is essential for understanding how rapid urbanization impacts wildlife behaviour, populations, and the range of behaviours within them, even in species apparently resilient to such environmental changes. [ABSTRACT FROM AUTHOR]

Neurofibromatosis 1 (NF1) is caused by germline mutations in the NF1 gene and manifests as proliferation of various tissues, including plexiform neurofibromas. The plexiform neurofibroma phenotype varies from indolent to locally aggressive, suggesting contributions of other modifiers in addition to somatic loss of NF1. In this study, we investigated a life‐threatening plexiform neurofibroma in a 9‐month‐old female infant with NF1. Germline mutations in two RASopathy‐associated genes were identified using whole‐exome sequencing—a de novo pathogenic variant in the NF1 gene, and a known pathogenic variant in the LZTR1 gene. Somatic analysis of the plexiform neurofibroma revealed NF1 loss of heterozygosity and a variant in GNAZ, a gene encoding a G protein‐coupled receptor. Cells expressing mutant GNAZ exhibited increased ERK 1/2 activation compared to those expressing wild‐type GNAZ. Taken together, we suggest the variants in NF1, LZRT1 and GNAZ act synergistically in our patient, leading to MAPK pathway activation and contributing to the severity of the patient's plexiform neurofibromatosis. After treatment with the MEK inhibitor, trametinib, a prominent clinical improvement was observed in this patient. This case study contributes to the knowledge of germline and somatic non‐NF1 variants affecting the NF1 clinical phenotype and supports use of personalized, targeted therapy. [ABSTRACT FROM AUTHOR]

Ichthyosis and deafness syndrome is a group of devastating genodermatoses caused by heterozygous mutations in GJB2, encoding the gap junction protein connexin 26. These syndromes are characterized by severe skin disease, hearing loss, recurrent infections, and cutaneous neoplasms. Cutaneous somatic mutations in the same gene are associated with porokeratotic eccrine ostial dermal duct nevus. Here we report a family in which a parent presented with localized epidermal nevus and his child suffered with hystrix‐like ichthyosis with deafness. Histologic examination of the parent's cutaneous lesion revealed verrucous epidermal nevus without features of porokeratotic eccrine ostial dermal duct nevus. Genetic analysis identified the same pathogenic variant, GJB2 c.148G>A (p.D50N), in DNA extracted from the parent's cutaneous lesion and the child's leukocytes, but not in the parent's leukocytes. This study expands the phenotypic heterogeneity of GJB2 mosaic variants in addition to porokeratotic eccrine ostial dermal duct nevus, and emphasizes the importance of molecular diagnosis of mosaic skin diseases considering the risk of severe inherited diseases in the offspring. [ABSTRACT FROM AUTHOR]

Acral peeling skin syndrome (APSS) is a heterogenous group of genodermatoses, manifested by peeling of palmo‐plantar skin and occasionally associated with erythema and epidermal thickening. A subset of APSS is caused by mutations in protease inhibitor encoding genes, resulting in unopposed protease activity and desmosomal degradation and/or mis‐localization, leading to enhanced epidermal desquamation. We investigated two Arab‐Muslim siblings with mild keratoderma and prominent APSS since infancy. Genetic analysis disclosed a homozygous mutation in SERPINB7, c.796C > T, which is the founder mutation in Nagashima type palmo‐plantar keratosis (NPPK). Although not previously formally reported, APSS was found in other patients with NPPK. We hypothesized that loss of SERPINB7 function might contribute to the peeling phenotype through impairment of keratinocyte adhesion, similar to other protease inhibitor mutations that cause APSS. Mis‐localization of desmosomal components was observed in a patient plantar biopsy compared with a biopsy from an age‐ and gender‐matched healthy control. Silencing of SERPINB7 in normal human epidermal keratinocytes led to increased cell sheet fragmentation upon mechanical stress. Immunostaining showed reduced expression of desmoglein 1 and desmocollin 1. This study shows that in addition to stratum corneum perturbation, loss of SERPINB7 disrupts desmosomal components, which could lead to desquamation, manifested by skin peeling. [ABSTRACT FROM AUTHOR]