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Deep learning is a branch of artificial intelligence that uses computational networks inspired by the human brain to extract patterns from raw data. Development and application of deep learning methods for image analysis, including classification, segmentation, and restoration, have accelerated in the last decade. These tools have been progressively incorporated into several research fields, opening new avenues in the analysis of biomedical imaging. Recently, the application of deep learning to dermatological images has shown great potential.
Many major breakthroughs in biomedical research and therapy development have been possible only because of close cooperation of academic researchers with the pharmaceutical industry. Outstanding historic examples include the discovery of penicillin and its further development, the invention of corticosteroids for therapeutic use, and the identification of streptomycin as a novel antibiotic. Thus, pharmaceutical companies have played crucial roles in the success stories of medicine. Today it is even more important to recognize that the continued development of modern medicine is dependent on technical innovations as well as large strategic investments, and that interactions between academia and industrial partners are increasingly important.
Editorial note: Welcome to the Journal of Investigative Dermatology (JID) SnapshotDx Quiz. In this monthly online-only quiz, the first question (“What is your diagnosis?”) relates to the clinical image shown, while additional questions concern the findings reported in the JID article by Halse et al. (https://doi.org/10.1016/j.jid.2019.07.725).
Scarring in mammals involves fibroblast migration and deposition of extracellular matrix in wounds. Previous models predicted that dermal fibroblasts migrate to wounds and deposit matrix de novo. Using matrix-tracing, live imaging, and genetic lineage–tracing techniques, Correa-Gallegos et al. provided evidence that fascial fibroblasts that express the engrailed 1 gene (EPFs) migrate to wounds, steering the locally prefabricated composite matrix to the wounds to facilitate quick sealing. Blockade of this migration resulted in chronic open wounds, whereas genetic ablation of fascial EPFs resulted in smaller scar formation in mice.
Although genetic factors contribute to hidradenitis suppurativa, the etiology of this chronic skin disease that responds to treatment with the tumor necrosis factor inhibitor adalimumab remains undefined. Liu et al. performed a genome-wide association study of 7 million genetic variants to identify those associated with adalimumab response. These investigations revealed that the single nucleotide variant rs5932114 in the intron of the BCL2 gene is associated with increased expression of BCL2 in hair outer root sheath cells and with adalimumab response.
Editorial note: Welcome to the Journal of Investigative Dermatology (JID) Cells to Surgery Quiz. In this monthly online-only quiz, the first question (“What is your diagnosis?”) relates to the clinical image shown, while additional questions concern the findings reported in a JID article by Sapkota et al. (2019) (https://dx.doi: 10.1016/j.jid.2019.02.029)
Treating rosacea begins with avoiding its triggers. Though they vary among patients, UVR is regarded as a universal rosacea trigger. Until now, the mechanism underlying this pathology has resisted characterization. The work of Kulkarni and colleagues sheds light on how UVR causes rosacea inflammation. Their findings appear to apply to all rosacea subtypes and suggest new therapeutic strategies.
Injuries of the largest anatomical organ, the skin, resulting from trauma, burns, or inflammatory disorders can lead to devastating health effects. Modern approaches to re-establishing critical barrier functions have evolved from simple biomaterial dressings to sophisticated skin grafts. A report by Magne et al. (2019) describes the exciting use of IL-1β–pretreated gingival mesenchymal stem cells to enhance skin graft functions.
Potassium iodide (KI), initially derived from seaweed in the early 19th century, is used for treating sporotrichosis in dermatological practice. KI has also been used to treat several noninfectious inflammatory skin diseases. However, the mechanisms underlying the improvement in such skin diseases remain unknown, and KI is not used widely. Thus, although KI is an old drug, physicians may not prescribe it frequently because they lack knowledge about it. While KI is very inexpensive and causes few side effects, it has been superseded by new powerful and expensive drugs, such as biological agents.
Epidermal barrier dysfunction is associated with a wide range of highly prevalent inflammatory skin diseases. However, the molecular processes that drive epidermal barrier maintenance are still largely unknown. Here, using quantitative proteomics, lipidomics and mouse genetics we characterize epidermal barrier maintenance versus a newly established barrier and functionally identify differential ceramide synthase 4 (CerS4) protein expression as one key difference. We show that epidermal loss of CerS4 first disturbs epidermal lipid metabolism and adult epidermal barrier function, ultimately resulting in chronic skin barrier disease, characterized by acanthosis, hyperkeratosis, and immune cell accumulations.
Langhans multinucleated giant cells (LGCs) are a specific type of multinucleated giant cell (MGC) containing a characteristic horseshoe-shaped ring of nuclei that are present within granulomas of infectious etiology. Although cytokines that trigger macrophage activation such as IFN-γ induce LGC formation, it is not clear whether cytokines that trigger macrophage differentiation contribute to LGC formation. Here, we found that IL-15, a cytokine that induces M1 macrophage differentiation, programs human peripheral blood adherent cells to form LGCs.
Today, we are witnessing a revolution in the treatment of cancer through the use of immunotherapy. In the last decade, work from many laboratories and clinicians have unequivocally demonstrated that the immune system can eradicate established cancers and enhance patient survival. However, immunotherapies have distinct tumor response-to-toxicity profiles due to distinct mechanisms of action. We have previously termed immunotherapies that activate a general, systemic immune response as “enhancement cancer immunotherapy” and those that target a specific dysfunctional immune response, especially within the tumor microenvironment, as “normalization cancer immunotherapy”.
Mutational heterogeneity can contribute to therapeutic resistance in solid cancers. In melanoma, the frequency of inter- and intra-tumoral heterogeneity is controversial. We examined mutational heterogeneity within individual melanoma patients using multi-platform analysis of commonly mutated driver and non-passenger genes.We analyzed paired primary and metastatic tumors from 60 patients, and multiple metastatic tumors from 39 patients whose primary tumors were unavailable (n=271 tumors). We used a combination of multiplex SNaPshot assays, Sanger Sequencing, Mutation-specific PCR, or droplet digital PCR to determine the presence of BRAFV600, NRASQ61, and TERT-124C>T and TERT-146C>T mutations.
Psoriasis, a chronic immune-mediated disease, is associated with an increased risk of cardiovascular events and mortality. Secukinumab selectively neutralizes IL-17A and has demonstrated high efficacy with a favorable safety profile in various psoriatic disease manifestations.
The metagenomics analysis performed in Schneider et al provided the first investigation into the functional role of microbial dysbiosis in Hidradenitis Suppurativa (HS). This study included a predictive analysis which utilized a publically-available dataset (Ring et al. 2017) and our dataset that was generated from a prospectively recruited cohort of HS subjects and normal controls (Schneider et al. 2019). These two datasets were generated using the same sequencing method (16S rRNA V3-V4), although the patient demographics, sampling procedures, and body sites sampled varied between them (Table 1a).
Due to the high rate of colonization, patients with atopic dermatitis are at risk of S. aureus bloodstream infection, the most severe manifestation of S. aureus infections. Intravascular devices and the skin are the major portals of entry for S. aureus in AD. With prompt and adequate diagnostic and therapeutic management, mortality is lower than in Non-AD patients with SAB and severe sequelae can be averted. Important preventive strategies include AD treatment to reduce S. aureus colonization and meticulous care of intravascular catheters, which should not be placed in/on lesional atopic skin.
Sweet's syndrome (SS) is a neutrophilic dermatoses (ND) that may occur in the context of malignancy, inflammatory disease or drug exposure (von den Driesch 1994). Approximately 20% of the reported SS patients have an associated cancer (Cohen et al. 1988), which is a myeloid neoplasm (MN) in half of the cases, predominantly an acute myeloid leukemia (AML) (Nelson et al. 2018). Although the association between MN and SS has been reported for a long time (Vignon-Pennamen and Wallach 1991), the pathophysiological link between these diseases remains unclear.