Inflammatory linear verrucous epidermal nevus associated with erosive monoarthritis

Inflammatory linear verrucous epidermal nevus and linear psoriasis are different entities with clinical and histopathologic similarities. Isolated reports of inflammatory linear verrucous epidermal nevus with concomitant psoriasis or a positive family history of psoriasis have been described, and the possibility that inflammatory linear verrucous epidermal nevus may be a mosaic form of cutaneous psoriasis has been postulated. We report a 17‐year‐old boy with a congenital, linear, erythematous, keratotic plaque on the dorsum of the fifth finger of the left hand with ipsilateral nail dystrophy. Histopathologic examination showed epidermal hyperplasia with alternating orthokeratosis and parakeratosis. During follow‐up, he developed erosive monoarthritis of the distal interphalangeal joint. This case seems to confirm the association between inflammatory linear verrucous epidermal nevus and arthritis and supports a possible relationship between inflammatory linear verrucous epidermal nevus and psoriasis.     

Tissue-Specific Inactivation of Type 2 Deiodinase Reveals Multilevel Control of Fatty Acid Oxidation by Thyroid Hormone in the Mouse

Type 2 deiodinase (D2) converts the prohormone thyroxine (T4) to the metabolically active molecule 3,5,3′-triiodothyronine (T3), but its global inactivation unexpectedly lowers the respiratory exchange rate (respiratory quotient [RQ]) and decreases food intake. Here we used FloxD2 mice to generate systemically euthyroid fat-specific (FAT), astrocyte-specific (ASTRO), or skeletal-muscle-specific (SKM) D2 knockout (D2KO) mice that were monitored continuously. The ASTRO-D2KO mice also exhibited lower diurnal RQ and greater contribution of fatty acid oxidation to energy expenditure, but no differences in food intake were observed. In contrast, the FAT-D2KO mouse exhibited sustained (24 h) increase in RQ values, increased food intake, tolerance to glucose, and sensitivity to insulin, all supporting greater contribution of carbohydrate oxidation to energy expenditure. Furthermore, FAT-D2KO animals that were kept on a high-fat diet for 8 weeks gained more body weight and fat, indicating impaired brown adipose tissue (BAT) thermogenesis and/or inability to oxidize the fat excess. Acclimatization of FAT-D2KO mice at thermoneutrality dissipated both features of this phenotype. Muscle D2 does not seem to play a significant metabolic role given that SKM-D2KO animals exhibited no phenotype. The present findings are unique in that they were obtained in systemically euthyroid animals, revealing that brain D2 plays a dominant albeit indirect role in fatty acid oxidation via its sympathetic control of BAT activity. D2-generated T3 in BAT accelerates fatty acid oxidation and protects against diet-induced obesity.     

Heart remodeling produced by aortic stenosis promotes cardiomyocyte apoptosis mediated by collagen V imbalance

Cardiac remodeling (CR) is a structural change of the heart due to chronic hemodynamic overload related to changes in both myocyte and extracellular matrix (ECM). We investigated that the imbalance of collagen V promotes cardiomyocyte apoptosis that contributes to heart failure and cell death. Aortic stenosis was induced surgically and male Wistar rats were randomized to 18 weeks (Sham 18?w, n?=?12; AoS 18?w, n?=?12) and severe of heart failure (Sham HF, n?=?12; AoS HF, n?=?12) groups. Functional and structural echocardiogram, immunohistochemistry for Ki-67, TUNEL assay and Immunofluorescence for collagen were performed. Our main results were: (1) Progressive reduction of cardiac functional capacity due to cardiac remodeling with decreased eject fraction in heart failure; (2) Imbalance of collagen deposition with increased, crowded and irregular collagen I in situ expression; (3) Dysregulation of dynamic control of collagen fibers with exposed epitopes of collagen V; (4) Additional apoptosis that are dependent to cardiac injury. The collagen V expression in cardiac remodeling is for the first time described and may be related to additional apoptosis and autoimmune response. Our findings suggest a critical role of collagen V in cardiac remodeling to modulate and promote heart failure and death.     

Updates in biological therapies for knee injuries: menisci

The preservation of meniscal tissue is paramount for long-term joint function, especially in younger patients who are athletically active. Many studies have reported encouraging results following the repair of meniscus tears, including both simple longitudinal tears located in the periphery and complex multiplanar tears that extend into the central third avascular region. However, most types of meniscal lesions are managed with a partial meniscectomy. Options to restore the meniscus range from an allograft transplantation to the use of synthetic and biological technologies. Recent studies have demonstrated good long-term outcomes with meniscal allograft transplantation, although the indications and techniques continue to evolve, and the long-term chondroprotective potential of this approach has yet to be determined. Several synthetic implants, most of which are approved in the European market, have shown some promise for replacing part of or the entire meniscus, including collagen meniscal implants, hydrogels, and polymer scaffolds. Currently, there is no ideal implant generated by means of tissue engineering. However, meniscus tissue engineering is a fast developing field that promises to develop an implant that mimics the histologic and biomechanical properties of a native meniscus.     

Myofibroblasts and their relationship with oral squamous cell carcinoma

Myofibroblasts are hybrid-phenotype differentiated cells in between fibroblasts and smooth muscle cells. Due to their contractile features and ability to synthesize extracellular matrix components, cytokines, proteases, and proangiogenic factors, myofibroblasts have been implicated in the pathogenesis of fibrocontractive diseases and in the progression of many tumors, including oral squamous cell carcinoma (SCC).ObjectiveTo perform a literature review on the origin of myofibroblasts, their main morpho-physiological and immunohistochemical aspects, and to discuss the correlations with oral SCC.MethodA search was made on the PUBMED database to select the main papers in the literature in English related to the subject, published between January 1991 and December 2011.ConclusionMyofibroblasts are an important component of the stroma of oral SCCs, although they are not present in all tumors. Abundant presence of myofibroblasts may be associated with local disease recurrence and decreased patient survival. However, given the relatively limited number of studies on the subject, further research is needed to clarify the molecular mechanisms by which myofibroblasts influence the biological behavior of oral SCC.