Background: Discovery of the significant impact of filaggrin (FLG) mutations on the genetic predisposition to atopic dermatitis (AD) focused attention on the 1q21 locus, where not only FLG but also other epidermal genes are located. In the present study, we compared 1q21 gene expression in lesional versus nonlesional AD skin. Methods: A real-time quantitative PCR analysis of 10 1q21 genes, selected on the basis of a previous microarray study, was performed in skin biopsies from 33 individuals with AD. Three alternative pathway keratins were also evaluated. Results: In chronic AD skin lesions, we observed an increase in RNA encoding involucrin, S100 calcium-binding proteins A2 and A7–A9 and small proline-rich region (SPRR) proteins 1A and 2C, with fold changes ranging from 2.0 for S100A2 to 15.4 for S100A8 (p < 0.001, Bonferroni corrected), in parallel to the overexpression of the alternative pathway keratins 6A, 6B and 16. The loricrin (LOR) expression level was significantly decreased in lesional AD skin (fold change 0.5; p < 0.01). The expression of the majority of 1q21 genes and alternative keratins was closely correlated; however, for SPRR1A (and SPRR2C) in lesional skin, the correlation with other genes was lost. Conclusions: We hypothesize that the deregulated increase in SPRR1A expression in chronic atopic skin lesions reflects an insufficient rise in SPRR transcripts, unable to compensate for the lack of LOR and thus contributing to the persistence of chronic AD skin lesions. Turning off the stress response in the skin may be regarded as a goal in the treatment of AD skin lesions, and SPRR genes might be targets for such an approach.

Epidermal differentiation complex (EDC) comprises a number of genes associated with human skin diseases including psoriasis, atopic dermatitis and hyperkeratosis. These genes have also been linked to numerous cancers, among them skin, gastric, colorectal, lung, ovarian and renal carcinomas. The involvement of EDC components encoding S100 proteins, small proline-rich proteins (SPRRs) and other genes in the tumorigenesis of head and neck squamous cell cancer (HNSCC) has been previously suggested. The aim of the study was to systematically analyze the expression of EDC components on the transcript level in HNSCC. Tissue specimens from 93 patients with HNC of oral cavity and 87 samples from adjacent or distant grossly normal oral mucosa were analyzed. 48 samples (24 tumor and 24 corresponding surrounding tissue) were hybridized to Affymetrix GeneChip Human 1.0 ST Arrays. For validation by quantitative real-time PCR (QPCR) the total RNA from all www.fhc.viamedica.pl 180 samples collected in the study was analyzed with Real-Time PCR system and fluorescent amplicon specific--probes. Additional set of samples from 14 patients with laryngeal carcinoma previously obtained by HG-U133 Plus 2.0 microarray was also included in the analyses. The expression of analyzed EDC genes was heterogeneous. Two transcripts (S100A1 and S100A4) were significantly down-regulated in oral cancer when compared to normal mucosa (0.69 and 0.36-fold change, respectively), showing an opposite pattern of expression to the remaining S100 genes. Significant up-regulation in tumors was found for S100A11, S100A7, LCE3D, S100A3 and S100A2 genes. The increased expression of S100A7 was subsequently validated by QPCR, confirming significant differences. The remaining EDC genes, including all encoding SPRR molecules, did not show any differences between oral cancer and normal mucosa. The observed differences were also assessed in the independent set of laryngeal cancer samples, confirming the role of S100A3 and LCE3D transcripts in HNC. In HNC of oral cavity only one family of EDC genes (S100 proteins) showed significant cancer-related differences. A number of other transcripts which showed altered expression in HNC require further validation.

Elderly asthmatic patients presented a high rate of falls, which is comparable to that of patients with COPD.

Background and objectives: Biological treatment is an important and effective therapy for psoriasis. During the COVID-19 pandemic, it remains unclear whether this type of therapy affects the course of SARS-CoV-2 infection. The aim of the study was to observe patients with psoriasis undergoing biological or other systemic treatment in relation to the impact of SARS-CoV-2 infection on the course of psoriasis and the COVID-19 disease itself. Materials and methods: A one-year observational study included 57 patients with diagnosed psoriasis who qualified for biological treatment and a group of 68 similar patients who were administered a different systemic treatment. Patients were analyzed monthly for psoriasis (including Psoriasis Area Severity Index (PASI) assessment) and constantly for SARS-CoV-2 infection (telephone contact). Cases of COVID-19 were confirmed by Polymerase Chain Reaction (PCR) at the study center. Results: SARS-CoV-2 infection was confirmed by a positive Real Time Polymerase Chain Reaction (RT-PCR) test in eight patients (14.0%) with psoriasis on biological therapy. None of the cases in this group required hospitalization for COVID-19. Similar data were obtained in the control group. Specifically, 11 (16%) patients were confirmed to be infected with SARS-CoV-2. These results were statistically comparable (p > 0.05). In the group of patients undergoing biological treatment, six (75%) of eight patients developed an exacerbation of psoriasis during SARS-CoV-2 infection, and similar results were noted in the control group, with eight (72%) patients experiencing an exacerbation of psoriasis. Conclusions: Patients with psoriasis who were administered biological treatment or other systemic therapy may experience a mild course of SARS-CoV-2 infection but might also experience a temporary exacerbation of skin lesions.

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