Descriptive analysis of scalp vs skin transcriptomes.

<p>(a) Principal component analysis (PCA) was performed to reveal the internal structure of the individual transcriptomes and to best explain the variance among samples when comparing the studied areas. In our data, PCA showed a better discrimination for skin samples than for scalp biopsies. (b) Scatter plot of log2FCH of LS vs NL DEGs on skin vs scalp transcriptomes. (c) Venn diagram of LS vs NL DEGs on scalp vs skin or MAD5 transcriptomes. (d) Heat map of genomic expression differences in scalp or skin psoriasis comparing LS, NL and N samples and (e) heat map showing three clusters of genes involved in differentiation of LS/NL samples in scalp vs skin areas. (f) Clustering heatmap of GSVA estimate values for a group of immune-related gene-sets comparing LS vs NL on scalp vs skin psoriasis. Terms of the X-axis refer to several set of genes up-regulated in cell culture by addition of cytokines. Unique: when a gene set is unique for that cell-cytokines combination, and no gene appears in other gene set. Synergistic: effect due to adding two cytokines to the cell culture at the same time. Additive: effect due to adding two cytokines to the cell culture sequentially. KC: Keratinocytes; RHE: Reconstituted Epidermis; DC: Dendritic Cells; iDC: inflammatory Dendritic Cells.</p

Triangle plot of GSEA results.

<p>Each panel represents NES values and p-values of GSEA analysis for LS and NL comparisons considering scalp vs skin areas for ‘psoriasis genetic print’ (a), ‘immune response’ (b, e), ‘cells biology’ (c), ‘epidermis biology’ (d), and ‘genetic regulation’ (f) gene-sets. NGS, next generation sequencing; MAD5, meta-analysis derived transcriptome of psoriasis 5; MAD3, meta-analysis derived transcriptome of psoriasis 3; SF7, Suarez-Farinas transcriptome 7; PsO, psoriasis; EDC, epidermal differentiation complex; CE, cornified envelope; KC, keratinocyte; TNF<i>α</i>, tumor necrosis factor alpha; IFNα, interferon α; IFNγ, interferon γ; PMBCs: peripheral blood mononucleated cells; DCs, dendritic cells; iDCs, immature dendritic cells; BDCA, blood dendritic cell antigen; Treg, regulatory T-cells; MIFT, microphthalmia-associated transcription factor; Met, methylated; RDGP, residual disease genomic profile.</p

Distribution and number of CD3+, CD11c+, DC-Lamp+ and CD83+ cells in the various compartments of the study groups.

<p>Panels a, c, e and g show the histological pictures. Graphs b, d, f and h show the number of cells and statistical analysis. IFL, interfolicular; inFD, infundibular; LF, low follicule; Epid, epidermis; Epith, epithelium; Ors, outer root sheath; Periinf, periinfundibular area; Perifoll, perifollicular area. Cells were counted per mm2 epidermis and dermis in the IFL area. Median and ranges of log transformed values are given. Statistics: <0.05 = *; p<0.01 = **; p<0.001 = ***.</p

Enrichment of cytokine-related inflammatory pathways (gene sets) in human psoriasis transcriptomes as compared with murine models of psoriasis.

<p>Each panel represents NES values and p-values of GSEA analysis for LS and NL comparisons of STAT3, Tie2, and TGF<i>β</i> transgene models and the imiquimod-induced model; KC, keratinocyte; TNF<i>α</i>, tumor necrosis factor <i>α</i>; IFN<i>α</i>, interferon <i>α</i>; IFNγ, interferon γ; PMBCs: peripheral blood mononucleated cells; DCs, dendritic cells; iDCs, immature dendritic cells; BDCA, blood dendritic cell antigen; Treg, regulatory T cells; KC, keratinocytes; DCs, Myeloid dendritic cells; RHE, reconstituted human epidermis. (a-d) Expression of these cytokine pathways in human psoriasis vulgaris is shown for lesional (LS) versus non lesional (NL) and for NL versus normal (N) skin and scalp. (e–k) Cytokine enrichment in the six mouse models is illustrated as follows: K14-amphiregulin (AREG) ear skin (e) and tail skin (f), IL-23 (g), K5-Stat3C (Stat-3) (h), K5-Tie2 (Tie-2) (i), K5-TGF-<i>β</i>1 (TGF-<i>β</i>) (j), and Imiquimod (k).</p

Keratin and immune-set gene expression profile of scalp psoriasis vs skin psoriasis, atopic dermatitis, and alopecia areata.

<p>Average log2FCH for alopecia areata (AA), atopic dermatitis (AA), scalp psoriasis and skin psoriasis for a representative group of (a) keratin and keratin associated proteins (KRTAPs) and (b) immune-related pathways genes adjusted by region (normalized to normal scalp [AA and scalp psoriasis] or normal skin [AD and skin psoriasis].</p

Clinical and Biological Principles of Cold Atmospheric Plasma Application in Skin Cancer

<p><b>Article full text</b></p> <p><br></p> <p>The full text of this article can be found here<b>. </b><a href="https://link.springer.com/article/10.1007/s12325-016-0338-1?view=classic">https://link.springer.com/article/10.1007/s12325-016-0338-1?view=classic</a></p><p></p> <p><br></p> <p><b>Provide enhanced content for this article</b></p> <p><br></p> <p>If you are an author of this publication and would like to provide additional enhanced content for your article then please contact <a href="http://www.medengine.com/Redeem/”mailto:[email protected]”"><b>[email protected]</b></a>.</p> <p><br></p> <p>The journal offers a range of additional features designed to increase visibility and readership. All features will be thoroughly peer reviewed to ensure the content is of the highest scientific standard and all features are marked as ‘peer reviewed’ to ensure readers are aware that the content has been reviewed to the same level as the articles they are being presented alongside. Moreover, all sponsorship and disclosure information is included to provide complete transparency and adherence to good publication practices. This ensures that however the content is reached the reader has a full understanding of its origin. No fees are charged for hosting additional open access content.</p> <p><br></p> <p>Other enhanced features include, but are not limited to:</p> <p><br></p> <p>• Slide decks</p> <p>• Videos and animations</p> <p>• Audio abstracts</p> <p>• Audio slides</p

DataSheet_1_Efficacy and safety of anakinra and canakinumab in PSTPIP1-associated inflammatory diseases: a comprehensive scoping review.pdf

IntroductionThis scoping review explores the effectiveness of IL-1 pathway inhibitors in managing PSTPIP1-associated inflammatory diseases (PAID). These diseases are marked by abnormal IL-1 pathway activation due to genetic mutations.MethodsOur methodology adhered to a pre-published protocol and involved a thorough search of MEDLINE and EMBASE databases up to February 2022, following the Joanna Briggs Institute Reviewer’s Manual and the PRISMA Extension for Scoping Reviews. The review included studies reporting on IL-1 pathway inhibitor use in PAID patients.ResultsFrom an initial pool of 5,225 articles, 36 studies involving 43 patients were selected. The studies predominantly used observational designs and exhibited diversity in patient demographics, treatment approaches, and outcomes. Anakinra and canakinumab demonstrated promise in treating sterile pyogenic arthritis, pyoderma gangrenosum, and acne (PAPA) and PSTPIP1-associated myeloid-related-proteinemia inflammatory (PAMI) syndromes, with scant data on other syndromes. Notably, there was a paucity of information on the adverse effects of these treatments, necessitating cautious interpretation of their safety profile.ConclusionCurrent evidence on IL-1 pathway inhibitors for PAID is primarily from observational studies and remains limited. Rigorous research with larger patient cohorts is imperative for more definitive conclusions. Collaborative efforts among specialized research centers and international health initiatives are key to advancing this field.</p

Author-paper affiliation network architecture influences the methodological quality of systematic reviews and meta-analyses of psoriasis

<div><p>Moderate-to-severe psoriasis is associated with significant comorbidity, an impaired quality of life, and increased medical costs, including those associated with treatments. Systematic reviews (SRs) and meta-analyses (MAs) of randomized clinical trials are considered two of the best approaches to the summarization of high-quality evidence. However, methodological bias can reduce the validity of conclusions from these types of studies and subsequently impair the quality of decision making. As co-authorship is among the most well-documented forms of research collaboration, the present study aimed to explore whether authors’ collaboration methods might influence the methodological quality of SRs and MAs of psoriasis. Methodological quality was assessed by two raters who extracted information from full articles. After calculating total and per-item Assessment of Multiple Systematic Reviews (AMSTAR) scores, reviews were classified as low (0-4), medium (5-8), or high (9-11) quality. Article metadata and journal-related bibliometric indices were also obtained. A total of 741 authors from 520 different institutions and 32 countries published 220 reviews that were classified as high (17.2%), moderate (55%), or low (27.7%) methodological quality. The high methodological quality subnetwork was larger but had a lower connection density than the low and moderate methodological quality subnetworks; specifically, the former contained relatively fewer nodes (authors and reviews), reviews by authors, and collaborators per author. Furthermore, the high methodological quality subnetwork was highly compartmentalized, with several modules representing few poorly interconnected communities. In conclusion, structural differences in author-paper affiliation network may influence the methodological quality of SRs and MAs on psoriasis. As the author-paper affiliation network structure affects study quality in this research field, authors who maintain an appropriate balance between scientific quality and productivity are more likely to develop higher quality reviews.</p></div

Cumulative frequency of node degree distributions.

<p>The cumulative node degree distribution shows the cumulative number of nodes of each degree class. The distribution of degree values over all nodes characterizes the network as a whole.</p

Influence of authors’ scientific quality and productivity on methodological quality of SRs and MAs about psoriasis.

<p>Panel (a-c): Bubble plot that represents the number of publications by author. Bubble size is proportional to the author’s H-index. Authors are sorted by their institution’s country. Panel (d-f) represents a scatter plot of author’s H-index vs. number of authored publications. Smoothed fitted lines represent predictions using linear regression for every country. Points and lines are colored based on author institution country.</p