Journal Of Investigative Dermatology

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Table of Contents

Thu, 2017-06-01 00:00

Subscription Information

Thu, 2017-06-01 00:00

Editorial Board

Thu, 2017-06-01 00:00

Following in the Footsteps…

Thu, 2017-06-01 00:00
In 1938, Marion Sulzberger wrote the following announcement and editorial excerpt, heralding the creation of the Society of Investigative Dermatology (SID) and the Journal for Investigative Dermatology (JID; now the Journal of Investigative Dermatology).ANNOUNCEMENTFor several years, the question of forming a new Dermatologic Society and publishing a new Dermatologic Journal has been under discussion. The objectives of the new Society and Journal include the effort eventually to assemble under one cover all of the numerous types of investigative work dealing with the skin, its functions and reactions, both physiologic and pathologic.

Cells to Surgery Quiz: June 2017

Thu, 2017-06-01 00:00
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 above, while additional questions concern the findings reported in a JID article that provides new information about that disease entity.

BJD Editor's Choice

Thu, 2017-06-01 00:00
GP2015 is a proposed etanercept biosimilar. The objective of this study was to demonstrate equivalent efficacy, and comparable safety and immunogenicity of GP2015 and the etanercept originator (ETN) in patients with moderate-to-severe chronic plaque-type psoriasis. In total 531 eligible patients were randomized 1 : 1 to self-administer GP2015 or ETN twice weekly subcutaneously. The difference in ≥ 75% improvement in Psoriasis Area and Severity Index response rates at week 12 between GP2015 and ETN (primary end point) was –2.3%.

Clinical Snippets

Thu, 2017-06-01 00:00
The estimated surface area of the skin is 2 m2, and for the purposes of heat and water loss and topical drug delivery, this estimate is reasonable. Richard Gallo, however, reminds us that in terms of interaction with the microbiome, which is becoming increasingly relevant to human health, the surface area of the skin is actually at least 100 m2. This updated value takes into account the hair follicle epithelial surface, because although this surface is protected below the follicular opening, it is known to interact with the microbiome.

SnapshotDx Quiz: June 2017

Thu, 2017-06-01 00:00
Editorial note: Welcome to the Journal of Investigative Dermatology (JID) Snapshot Dx Quiz— In this monthly online-only quiz, the first question (“What is your diagnosis?”) relates to the clinical image above, while additional questions concern the findings reported in a JID article that provides new information about that disease entity.

Editors' Picks

Thu, 2017-06-01 00:00
Single-cell genomic approaches reveal genetic and transcriptional features present in thousands of individual cells in tumors, allowing researchers to examine the heterogeneities in malignant and non-malignant cell types. Tirosh and colleagues utilized single-cell RNA sequencing (RNA-seq) to charactrize 4645 malignant, immune, and stromal cells from 19 human melanoma tumors. This analysis unearthed heterogeneity at the individual, functional, and genetic levels in both melanoma and associated tumor cells.

Research Techniques Made Simple: High-Throughput Sequencing of the T-Cell Receptor

Thu, 2017-06-01 00:00
High-throughput sequencing (HTS) of the T-cell receptor (TCR) is a rapidly advancing technique that allows sensitive and accurate identification and quantification of every distinct T-cell clone present within any biological sample. The relative frequency of each individual clone within the full T-cell repertoire can also be studied. HTS is essential to expand our knowledge on the diversity of the TCR repertoire in homeostasis or under pathologic conditions, as well as to understand the kinetics of antigen-specific T-cell responses that lead to protective immunity (i.e., vaccination) or immune-related disorders (i.e., autoimmunity and cancer).

The “Kelch” Surprise: KLHL24, a New Player in the Pathogenesis of Skin Fragility

Thu, 2017-06-01 00:00
A new protein, kelch-like 24, has recently been associated with a distinct subtype of epidermolysis bullosa simplex, a heterogeneous group of disorders associated with mechanical fragility of epidermal keratinocytes. All mutations involve the translation initiation codon and lead to a degradation-resistant N-terminally truncated kelch-like 24. Kelch-like 24 appears to be involved in the turnover of intermediated filaments, in particular of keratin 14, in keratinocytes.

Redox-Redux and NADPH Oxidase (NOX): Even More Complicated than We Thought it Might Be

Thu, 2017-06-01 00:00
The NOX (nicotinamide adenine dinucleotide phosphate oxidase) family includes seven unique members that are involved in a multitude of physiological functions, including extensive interaction with UVR and the skin. NOX1 is uniquely present and activated by UVB radiation with biphasic expression of the enzyme immediately and then after a several-hour delay. Specific inhibition of both early and late NOX1 activation leads to evidence of decreased photocarcinogenesis in in vitro keratinocytes and in well-characterized mouse models in which antitumor efficacy has been shown; inhibiting only late NOX activation does not exhibit such effects.

5-Fluorouracil for Actinic Keratosis Treatment and Chemoprevention: A Randomized Controlled Trial

Thu, 2017-06-01 00:00
Actinic keratosis (AK), a UVR-induced keratinocyte dysplasia (Rossi et al., 2007), is a marker for increased risk of keratinocyte carcinoma (KC), that is, cutaneous basal and squamous cell carcinoma (SCC) (Chen et al., 2005; Karimkhani et al., 2015), and costs the United States over one billion dollars annually (Bickers et al., 2006). AKs transform into SCC at a rate of up to 0.6% per year, and SCC arises from an AK in 60% of cases (Criscione et al., 2009).

Amlexanox enhances premature termination codon read-through in COL7A1 and expression of full length type VII collagen: potential therapy for recessive dystrophic epidermolysis bullosa

Tue, 2017-05-23 00:00
Recessive dystrophic epidermolysis bullosa (RDEB) is a rare monogenic blistering disorder caused by lack of functional type VII collagen, leading to skin fragility and subsequent trauma-induced separation of the epidermis from the underlying dermis. 46% of RDEB patients harbor at least one premature termination codon (PTC) mutation in COL7A1 and previous studies have shown that aminoglycosides are able to overcome RDEB PTC mutations by inducing “read-through” and incorporation of an amino acid at the PTC site.

Requirement of Zinc Transporter SLC39A7/ZIP7 for Dermal Development to Fine-Tune Endoplasmic Reticulum Function by Regulating Protein Disulfide Isomerase

Mon, 2017-05-22 00:00
Skin is the first area that manifests zinc deficiency. However, the molecular mechanisms by which zinc homeostasis affects skin development remain largely unknown. Here, we show that zinc-regulation transporter-/iron-regulation transporter-like protein 7 (ZIP7) localized to the endoplasmic reticulum plays critical roles in connective tissue development. Mice lacking the Slc39a7/Zip7 gene in collagen 1-expressing tissue exhibited dermal dysplasia. Ablation of ZIP7 in mesenchymal stem cells inhibited cell proliferation thereby preventing proper dermis formation, indicating that ZIP7 is required for dermal development.

Systemic sclerosis dermal fibroblasts suppress Th1 cytokine production via galectin-9 overproduction due to Fli1 deficiency

Thu, 2017-05-18 00:00
Dermal fibroblasts promote skin-localized transdifferentiation of Tregs to Th2-like cells in systemic sclerosis (SSc). However, the entire effect of SSc dermal fibroblasts on immune cells still remains unknown. Since galectin-9 induces Th2 cytokine-predominant immune imbalance by negatively regulating Th1/Th17 cells in inflammatory diseases, we investigated the contribution of galectin-9 to Th immune balance in SSc lesional skin. We utilized human clinical samples and Fli1+/- mice because Fli1 deficiency induces SSc-like phenotypes in various cell types.

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