Assessing the quality of acne and rosacea treatment information on YouTube.

Cutaneous lupus erythematosus has different manifestation depending on the type. In this study, discoid lupus, extensive skin lesions, fairer skin types and scalp involvement were found to be positive predictive factors for more severe disease.

Evaluating social media as a source of patient information regarding psoriasis treatments using the DISCERN instrument.

With almost 1 billion monthly active users, social media platforms, such as Instagram, are now commonly used for patient support, education, and outreach. With potential misinformation targeted towards patients on Instagram, we sought to evaluate the accuracy, sources, and types of information regarding psoriasis treatments posted on Instagram using the DISCERN instrument. An Instagram search was performed using the search 'psoriasis treatment' and the first 100 posts in search result were scored. 34.7% of the videos analyzed were produced by hospitals/healthcare professionals. Four of the remaining posts, 18% were patient testimonials, 42% promoted products, 11% were educational, and 5% were news. 94% of the posts scored as 'poor' or 'very poor.' The average DISCERN score was 28.8 out of 75 for the posts analyzed. The areas of strength among the posts were strong aims. Significant weaknesses were seen in the sources used and whether a variety of options were discussed. Overall, the quality of information regarding psoriasis treatments posted on Instagram is poor, as evaluated by the DISCERN tool, and notably is poorer than other social media platforms such as YouTube.

Contrasting readability and availability of Spanish language with English language patient education materials.

Spanish is the leading non-English language in the United States, with more than 41 million speakers. The Hispanic population has one of the lowest health literacy rates. Amongst Spanish speakers, limited English proficiency can contribute to poorer health outcomes and greater health disparities, such as lower quality of care received. We sought to assess the availability and readability scores of Spanish-language dermatologic patient education materials (PEMs) compared with those materials in English.

Coincidental loss of DOCK8 function in NLRP10-deficient and C3H/HeJ mice results in defective dendritic cell migration.

Dendritic cells (DCs) are the primary leukocytes responsible for priming T cells. To find and activate naïve T cells, DCs must migrate to lymph nodes, yet the cellular programs responsible for this key step remain unclear. DC migration to lymph nodes and the subsequent T-cell response are disrupted in a mouse we recently described lacking the NOD-like receptor NLRP10 (NLR family, pyrin domain containing 10); however, the mechanism by which this pattern recognition receptor governs DC migration remained unknown. Using a proteomic approach, we discovered that DCs from Nlrp10 knockout mice lack the guanine nucleotide exchange factor DOCK8 (dedicator of cytokinesis 8), which regulates cytoskeleton dynamics in multiple leukocyte populations; in humans, loss-of-function mutations in Dock8 result in severe immunodeficiency. Surprisingly, Nlrp10 knockout mice crossed to other backgrounds had normal DOCK8 expression. This suggested that the original Nlrp10 knockout strain harbored an unexpected mutation in Dock8, which was confirmed using whole-exome sequencing. Consistent with our original report, NLRP3 inflammasome activation remained unaltered in NLRP10-deficient DCs even after restoring DOCK8 function; however, these DCs recovered the ability to migrate. Isolated loss of DOCK8 via targeted deletion confirmed its absolute requirement for DC migration. Because mutations in Dock genes have been discovered in other mouse lines, we analyzed the diversity of Dock8 across different murine strains and found that C3H/HeJ mice also harbor a Dock8 mutation that partially impairs DC migration. We conclude that DOCK8 is an important regulator of DC migration during an immune response and is prone to mutations that disrupt its crucial function.