Neonatal vascular malformation of parietal bone.

Vascular malformations (VaMs) are congenital lesions and are present at birth. They grow commensurately with age. These lesions often affect the soft tissues with intraosseous involvement of the scalp being rare. Here, we discuss a case of intraosseous VaM in a 2-month-old infant which was involving the parietal bone.

Classification of the Residual Cranial Defects and Selection of Reconstruction Materials.

The cranial defects are complex in nature and are due to various causes. Therefore, there is a need for a common term of reference to these defects. This requirement stood as a prime reason for proposing a classification system for cranial defects. The classification is based on 2 decades of experience in cranioplasty. This efficient and simple way of representation would fill the existing lacunae for a systematic communication on cranial defects. Over the ages the evolution of reconstruction and grafting had undergone a massive progress. Therefore, it is essential to enumerate all available graft and bio-materials for restoring the cranial defects. The aetiology for these defects, age and sex of the patient, site and size of the defect, associated systemic conditions, cost factor, and operator's choice are the factors that play key role in the selection of the reconstructive material. This article discusses on these factors in cranioplasty. High success rate with excellent function and cosmetic outcome in using a variety of materials, as shared in this article. The advantages of autografts cannot be matched by any existing alloplast. However, in case of larger defects, for a better cosmetic outcome and to reduce the donor site morbidity, alloplasts are the most widely preferred material of choice.

Unexpected Role for Adaptive αßTh17 Cells in Acute Respiratory Distress Syndrome.

Acute respiratory distress syndrome (ARDS) is a devastating disorder characterized by increased alveolar permeability with no effective treatment beyond supportive care. Current mechanisms underlying ARDS focus on alveolar endothelial and epithelial injury caused by products of innate immune cells and platelets. However, the role of adaptive immune cells in ARDS remains largely unknown. In this study, we report that expansion of Ag-specific αßTh17 cells contributes to ARDS by local secretion of IL-17A, which in turn directly increases alveolar epithelial permeability. Mice with a highly restrictive defect in Ag-specific αßTh17 cells were protected from experimental ARDS induced by a single dose of endotracheal LPS. Loss of IL-17 receptor C or Ab blockade of IL-17A was similarly protective, further suggesting that IL-17A released by these cells was responsible for this effect. LPS induced a rapid and specific clonal expansion of αßTh17 cells in the lung, as determined by deep sequencing of the hypervariable CD3RßVJ region of the TCR. Our findings could be relevant to ARDS in humans, because we found significant elevation of IL-17A in bronchoalveolar lavage fluid from patients with ARDS, and rIL-17A directly increased permeability across cultured human alveolar epithelial monolayers. These results reveal a previously unexpected role for adaptive immune responses that increase alveolar permeability in ARDS and suggest that αßTh17 cells and IL-17A could be novel therapeutic targets for this currently untreatable disease.

An age-dependent reversal in the protective capacities of JNK signaling shortens Caenorhabditis elegans lifespan.

Stress-activated protein kinase (SAPK) pathways are evolutionarily conserved signaling modules that orchestrate protective responses to adverse environmental conditions. However, under certain conditions, their activation can be deleterious. Thus, activation of the c-Jun N-terminal kinase (JNK) SAPK pathway exacerbates a diverse set of pathologies, many of which are typical of old age. The contexts determining whether the outcome of JNK signaling is protective or detrimental are not fully understood. Here, we show that the age of an animal defines such a context. The Caenorhabditis elegans JNK homolog, KGB-1, provides protection from heavy metals and protein folding stress in developing animals. However, we found that with the onset of adulthood, KGB-1 activity becomes detrimental, reducing stress resistance and lifespan. Genetic analyses coupled with fluorescent imaging linked this phenotypic switch to age-dependent antagonistic modulation of DAF-16/FOXO: KGB-1 activation enhanced DAF-16 nuclear localization and transcriptional activity during development but decreased it in adults. Epistasis analyses showed that DAF-16 was necessary and sufficient to explain some of the kgb-1-dependent detrimental phenotypes, but not all. The identification of early adulthood as a point following which the contribution of KGB-1 activity reverses from beneficial to detrimental sheds new light on the involvement of JNK signaling in age-related pathologies. Furthermore, the age-dependent reversal has intriguing implications for our understanding of aging.