Objectives/Hypothesis This study aimed to evaluate the olfactory status in children with laboratory confirmed SARS‐CoV‐2 using subjective and psychophysical methods. Study Design Prospective clinical cross‐sectional study. Methods This is a prospective clinical cross‐sectional study of 79 children with COVID‐19. The 21st item of SNOT‐22 questionnaire and odor identification test were used for smell assessment. Children were examined twice during the hospitalization, and a telephone survey was conducted 60 days after hospital discharge. Results Immediately after confirmation of COVID‐19, smell impairment was detected in 86.1% of children by means of the Identification test and in 68.4% of children by means of the survey ( P = .010). After 5 days survey revealed a statistically significant decrease in the number of patients with hyposmia (41 out of 79, 51.9%). On the first visit, the mean Identification test score corresponded to “hyposmia” (9.5 ± 2.7), while on the second visit, the average value was 13.1 ± 1.9, which corresponded to “normosmia.” According to the telephone survey, recovery of the olfactory function occurred within 10 days in 37 of 52 patients (71.2%), 11 to 29 days ‐ in 12 children (23.1%), and later than 30 days ‐ in three cases (5.7%). Conclusions In the pediatric population, olfactory dysfunction is an early and common symptom of COVID‐19. There is a trend to quick recovery of olfactory function in children with COVID‐19. The overwhelming majority of patients (94.3%) had no subjective olfactory complaints by the end of the first month. Level of Evidence 4 Laryngoscope , 2021

The recessive form of dystrophic epidermolysis bullosa (RDEB) is a debilitating disease caused by impairments in the junctions of the dermis and the basement membrane of the epidermis. Mutations in the COL7A1 gene induce multiple abnormalities, including chronic inflammation and profibrotic changes in the skin. However, the correlations between the specific mutations in COL7A1 and their phenotypic output remain largely unexplored. The mutations in the COL7A1 gene, described here, were found in the DEB register. Among them, two homozygous mutations and two cases of compound heterozygous mutations were identified. We created the panel of primary patient-specific RDEB fibroblast lines (FEB) and compared it with control fibroblasts from healthy donors (FHC). The set of morphological features and the contraction capacity of the cells distinguished FEB from FHC. We also report the relationships between the mutations and several phenotypic traits of the FEB. Based on the analysis of the available RNA-seq data of RDEB fibroblasts, we performed an RT-qPCR gene expression analysis of our cell lines, confirming the differential status of multiple genes while uncovering the new ones. We anticipate that our panels of cell lines will be useful not only for studying RDEB signatures but also for investigating the overall mechanisms involved in disease progression.

Lipopolysaccharide (LPS), a fragment of the bacterial cell wall, specifically interacting with protein complexes on the cell surface, can induce the production of pro-inflammatory and apoptotic signaling molecules, leading to the damage and death of brain cells. Similar effects have been noted in stroke and traumatic brain injury, when the leading factor of death is glutamate (Glu) excitotoxicity too. But being an amphiphilic molecule with a significant hydrophobic moiety and a large hydrophilic region, LPS can also non-specifically bind to the plasma membrane, altering its properties. In the present work, we studied the effect of LPS from Escherichia coli alone and in combination with the hyperstimulation of Glu-receptors on the functional state of mitochondria and Ca2+ homeostasis, oxygen consumption and the cell survival in primary cultures from the rats brain cerebellum and cortex. In both types of cultures, LPS (0.1–10 μg/ml) did not change the intracellular free Ca2+ concentration ([Ca2+]i) in resting neurons but slowed down the median of the decrease in [Ca2+]i on 14% and recovery of the mitochondrial potential (ΔΨm) after Glu removal. LPS did not affect the basal oxygen consumption rate (OCR) of cortical neurons; however, it did decrease the acute OCR during Glu and LPS coapplication. Evaluation of the cell culture survival using vital dyes and the MTT assay showed that LPS (10 μg/ml) and Glu (33 μM) reduced jointly and separately the proportion of live cortical neurons, but there was no synergism or additive action. LPS-effects was dependent on the type of culture, that may be related to both the properties of neurons and the different ratio between neurons and glial cells in cultures. The rapid manifestation of these effects may be the consequence of the direct effect of LPS on the rheological properties of the cell membrane.