Melasma pathogenesis: a review of the latest research, pathological findings, and investigational therapies

Melasma is an acquired hyperpigmentation disorder most commonly affecting females with darker skin types. It is triggered by several factors including sun exposure, genetic influences, and female sex hormones. The pathology of melasma extends beyond melanocytes and recent literature points to interactions between keratinocytes, mast cells, gene regulation abnormalities, neovascularization, and disruption of basement membrane. This complex pathogenesis makes melasma difficult to target and likely to recur post treatment. A better understanding of the latest pathological findings is key to developing novel and successful treatment options. This review aims to provide a summary of the more novel pathological findings and latest investigational therapies

Sexual dimorphism and transgender medicine: appealing to a viewer's sense of beauty

Sexual dimorphism — the phenotypic structural differences between male and female faces — has been shown to be an important universal component of beauty. This concept plays a key role in facial feminization surgery (FFS), which consists of contouring and reshaping features of the skull itself to alter the foundation of the face. FFS has been shown to improve quality of life among transgender women and therefore an understanding of the procedure and the concept of sexual dimorphism is key for plastic surgeons, dermatologists, and other healthcare providers

Sexual dimorphism and transgender medicine: appealing to a viewer's sense of beauty

Sexual dimorphism — the phenotypic structural differences between male and female faces — has been shown to be an important universal component of beauty. This concept plays a key role in facial feminization surgery (FFS), which consists of contouring and reshaping features of the skull itself to alter the foundation of the face. FFS has been shown to improve quality of life among transgender women and therefore an understanding of the procedure and the concept of sexual dimorphism is key for plastic surgeons, dermatologists, and other healthcare providers

Melasma pathogenesis: a review of the latest research, pathological findings, and investigational therapies

Melasma is an acquired hyperpigmentation disorder most commonly affecting females with darker skin types. It is triggered by several factors including sun exposure, genetic influences, and female sex hormones. The pathology of melasma extends beyond melanocytes and recent literature points to interactions between keratinocytes, mast cells, gene regulation abnormalities, neovascularization, and disruption of basement membrane. This complex pathogenesis makes melasma difficult to target and likely to recur post treatment. A better understanding of the latest pathological findings is key to developing novel and successful treatment options. This review aims to provide a summary of the more novel pathological findings and latest investigational therapies

Contrasting Social Media Use Between Young Adults With Inflammatory Bowel Disease and Type 1 Diabetes: Cross-sectional Study

BackgroundSocial media is used by young adult patients for social connection and self-identification. ObjectiveThis study aims to compare the social media habits of young adults with inflammatory bowel disease (IBD) and type 1 diabetes (T1D). MethodsThis is a cross-sectional study of subjects from Boston Children’s Hospital outpatient IBD and diabetes clinics. Patients above 18 years of age were invited to complete a brief anonymous survey, which asked about the various ways they use several social media platforms. ResultsResponses were received from 108 patients (92.5% response rate), evenly split across disease type. We found that 83% of participants spent at least 30 minutes per day on social media, most commonly on Instagram and Facebook. Although the content varied based on the platform, patients with IBD posted or shared content related to their disease significantly less than those with T1D (23% vs 38%, P=.02). Among Instagram users, patients with IBD were less likely to engage with support groups (22% vs 56%, P=.04). Among Twitter users, patients with IBD were less likely to seek disease information (77% vs 29%, P=.005). Among Facebook users, patients with IBD were less likely to post about research and clinical trials (31% vs 65%, P=.04) or for information seeking (49% vs 87%, P=.003). Patients with IBD were also less likely to share their diagnosis with friends or family in person. ConclusionsYoung adults with IBD were less willing to share their diagnosis and post about or explore the disease on social media compared to those with T1D. This could lead to a sense of isolation and should be further explored

Retronychia: the importance of proper footwear

Retronychia is commonly underdiagnosed and exhibits classic features of proximal nail fold elevation and nail plate layering. Herein we summarize the literature and discuss cause, diagnosis, and treatment of this condition

Differential Expression of the Activator Protein 1 Transcription Factor Regulates Interleukin-1ß Induction of Interleukin 6 in the Developing Enterocyte.

The innate immune response is characterized by activation of transcription factors, nuclear factor kappa B and activator protein-1 and their downstream targets, the pro-inflammatory cytokines including interleukin 1β and interleukin 6. Normal development of this response in the intestine is critical to survival of the human neonate and delays can cause the onset of devastating inflammatory diseases such as necrotizing enterocolitis. Previous studies have addressed the role of nuclear factor kappa B in the development of the innate immune response in the enterocyte, however despite its central role in the control of multiple pro-inflammatory cytokine genes, little is known on the role of Activator Protein 1 in this response in the enterocyte. Here we show that the canonical Activator Protein 1 members, cJun and cFos and their upstream kinases JNK and p38 play an essential role in the regulation of interleukin 6 in the immature enterocyte. Our data supports a model whereby the cFos/cJun heterodimer and the more potent cJun homodimer downstream of JNK are replaced by less efficient JunD containing dimers, contributing to the decreased responsiveness to interleukin 1β and decreased interleukin 6 secretion observed in the mature enterocyte. The tissue specific expression of JunB in colonocytes and colon derived tissues together with its ability to repress Interleukin-1β induction of an Interleukin-6 gene reporter in the NCM-460 colonocyte suggests that induction of JunB containing dimers may offer an attractive therapeutic strategy for the control of IL-6 secretion during inflammatory episodes in this area of the intestine

Interleukin 1 induction of IL-6 in immature and mature enterocytes and in developing ileal xenografts.

<p><b>(A) IL-1</b>b <b>induction of IL-6 in immature H4 and in mature NCM460 enterocytes.</b> Cell lines were plated in 24 well plates overnight, incubated in low serum media for 3h and treated with IL-1β (0.5ng/ml). Tissue culture media was harvested after 6 h and assayed for IL-6 by ELISA Mean +/-S.E. (n = 3) from 3 experiments are presented ***p<0.001, *p<0.05 <b>(B). IL-1</b>β <b>induction of IL-6 in human ileal xenografts grown <i>ex vivo</i> in organ culture.</b> Human ileal explants derived from xenografts transplanted subcutaneously into the SCID mouse and harvested 16, 23 and 28 weeks post-transplantation were equilibrated for up to 6h in organ culture media and were either untreated or treated with IL-1b(0.5ng/ml). Tissue culture media was harvested for IL-6 measurement after 24h. Mean +/-S.E. (n = 3) from 2 experiments are presented ***p<0.001, *p<0.05.</p

Interleukin 1β induction of IL-6 is mediated by the Stress Activated Protein Kinases, JNK and p38 in immature H4 enterocytes.

<p>Immature H4 cells (A, B) and mature NCM-460 cells (C, D) were plated in 24 well plates overnight, incubated in low serum media for 3h and treated with IL-1β (0.5ng/ml) in the absence or presence of the JNK inhibitor SP600125 and the p38 inhibitor SB203580 (triplicate treatments) as indicated. Tissue culture media was harvested after 6 h and assayed for IL-6 by ELISA. Mean +/-S.E (n = 3) from 2 experiments are presented. Control un induced compared to IL-1 and IL-1 induced compared to IL-1 in the presence of inhibitors, ***p<0.001, **p<0.01 *p<0.05) analyzed by Student T-test.</p