Bioactive fatty acids of three commercial scallop species

The fat content and fatty acid profile of commercially important scallops Flexopecten glaber, Mimachlamys varia, and Pecten jacobaeus were investigated in samples of adductor muscle, gonad, mantle, and viscera. The viscera showed the highest lipid content in all species examined. Signi?cant differences were found in the fatty acid composition among tissues and among scallops. All pectinids exhibited high levels of eicosapentaenoic and docosahexaenoic acids in the adductor muscle, with a maximum value of 211 mg/100 g tissue and 252 mg/100 g tissue in the viscera of F. glaber. Highest n3/n6 ratios were recorded in F. glaber gonad and viscera, in P. jacobaeus muscle, and in the gonad of M. varia. M. varia adductor muscle had the lowest values of atherogenicity and thrombogenicity indices used as indicators of beneficial health effects. These data contribute to the overall evaluation of the nutritional quality of scallops and suggest that their consumption may provide health benefits.     

Molecular Mechanisms of Diabetic Kidney Disease

The inflammatory component of diabetic kidney disease has become of great interest in recent years, with genetic and epigenetic variants playing a fundamental role in the initiation and progression of the disease. Cells of the innate immune system play a major role in the pathogenesis of diabetic kidney disease, with a lesser contribution from the adaptive immune cells. Other components such as the complement system also play a role, as well as specific cytokines and chemokines. The inflammatory component of diabetic kidney disease is of great interest and is an active research field, with the hope to find potential innovative therapeutic targets.     

Adipose Tissue Secretion Pattern Influences β-Cell Wellness in the Transition from Obesity to Type 2 Diabetes

The dysregulation of the β-cell functional mass, which is a reduction in the number of β-cells and their ability to secure adequate insulin secretion, represents a key mechanistic factor leading to the onset of type 2 diabetes (T2D). Obesity is recognised as a leading cause of β-cell loss and dysfunction and a risk factor for T2D. The natural history of β-cell failure in obesity-induced T2D can be divided into three steps: (1) β-cell compensatory hyperplasia and insulin hypersecretion, (2) insulin secretory dysfunction, and (3) loss of β-cell mass. Adipose tissue (AT) secretes many hormones/cytokines (adipokines) and fatty acids that can directly influence β-cell function and viability. As this secretory pattern is altered in obese and diabetic patients, it is expected that the cross-talk between AT and pancreatic β-cells could drive the maintenance of the β-cell integrity under physiological conditions and contribute to the reduction in the β-cell functional mass in a dysmetabolic state. In the current review, we summarise the evidence of the ability of the AT secretome to influence each step of β-cell failure, and attempt to draw a timeline of the alterations in the adipokine secretion pattern in the transition from obesity to T2D that reflects the progressive deterioration of the β-cell functional mass.     

Novel Multifaceted Roles for RNF213 Protein

Ring Finger Protein 213 (RNF213), also known as Mysterin, is the major susceptibility factor for Moyamoya Arteriopathy (MA), a progressive cerebrovascular disorder that often leads to brain stroke in adults and children. Although several rare RNF213 polymorphisms have been reported, no major susceptibility variant has been identified to date in Caucasian patients, thus frustrating the attempts to identify putative therapeutic targets for MA treatment. For these reasons, the investigation of novel biochemical functions, substrates and unknown partners of RNF213 will help to unravel the pathogenic mechanisms of MA and will facilitate variant interpretations in a diagnostic context in the future. The aim of the present review is to discuss novel perspectives regarding emerging RNF213 roles in light of recent literature updates and dissect their relevance for understanding MA and for the design of future research studies. Since its identification, RNF213 involvement in angiogenesis and vasculogenesis has strengthened, together with its role in inflammatory signals and proliferation pathways. Most recent studies have been increasingly focused on its relevance in antimicrobial activity and lipid metabolism, highlighting new intriguing perspectives. The last area could suggest the main role of RNF213 in the proteasome pathway, thus reinforcing the hypotheses already previously formulated that depict the protein as an important regulator of the stability of client proteins involved in angiogenesis. We believe that the novel evidence reviewed here may contribute to untangling the complex and still obscure pathogenesis of MA that is reflected in the lack of therapies able to slow down or halt disease progression and severity.     

Maternal depression and the quality of early attachment: An examination of infants, preschoolers, and their mothers.

Relations between maternal depression and attachment security among 50 infant–mother and 54 preschool child–mother dyads were examined using the classification system of M. D. S. Ainsworth, M. C. Blehar, E. Waters, and S. Wall (1978) and M. Main and J. Solomon (1990) for infants and the Preschool Assessment of Attachment (P. M. Crittenden; see record 1993-01051-001) for preschoolers. Attachment insecurity was significantly associated with maternal depression among infants and preschoolers. Furthermore, children without unitary, coherent attachment strategies tended to have more chronically impaired mothers than did children with coherent, organized attachment strategies. Results stress the importance of severity-chronicity of parental illness in the study of depression and early attachment relations, and that differences between children with and without coherent organized attachment strategies are as clinically informative as are differences between secure and insecure children. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

11β-Hydroxysteroid Dehydrogenase Type 1 within Osteoclasts Mediates the Bone Protective Properties of Therapeutic Corticosteroids in Chronic Inflammation

Therapeutic glucocorticoids (GCs) are powerful anti-inflammatory tools in the management of chronic inflammatory diseases such as rheumatoid arthritis (RA). However, their actions on bone in this context are complex. The enzyme 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1) is a mediator of the anti-inflammatory actions of therapeutic glucocorticoids (GCs) in vivo. In this study we delineate the role of 11β-HSD1 in the effects of GC on bone during inflammatory polyarthritis. Its function was assessed in bone biopsies from patients with RA and osteoarthritis, and in primary osteoblasts and osteoclasts. Bone metabolism was assessed in the TNF-tg model of polyarthritis treated with oral GC (corticosterone), in animals with global (TNF-tg^11βKO), mesenchymal (including osteoblast) (TNF-tg^{11βflx/tw2cre}) and myeloid (including osteoclast) (TNF-tg^{11βflx/LysMcre}) deletion. Bone parameters were assessed by micro-CT, static histomorphometry and serum metabolism markers. We observed a marked increase in 11β-HSD1 activity in bone in RA relative to osteoarthritis bone, whilst the pro-inflammatory cytokine TNFα upregulated 11β-HSD1 within osteoblasts and osteoclasts. In osteoclasts, 11β-HSD1 mediated the suppression of bone resorption by GCs. Whilst corticosterone prevented the inflammatory loss of trabecular bone in TNF-tg animals, counterparts with global deletion of 11β-HSD1 were resistant to these protective actions, characterised by increased osteoclastic bone resorption. Targeted deletion of 11β-HSD1 within osteoclasts and myeloid derived cells partially reproduced the GC resistant phenotype. These data reveal the critical role of 11β-HSD1 within bone and osteoclasts in mediating the suppression of inflammatory bone loss in response to therapeutic GCs in chronic inflammatory disease.     

Temperature Tunable 4D Polymeric Photonic Crystals

Photonic crystals owe their multitude of optical properties to the way their structure creates interference effects. It is therefore possible to influence the photonic response by acting on their physical structure. In this article, tunable photonic crystals made by elastic polymers that respond to their environment are explored, in particular with a physical deformation under temperature variation. This creates a feedback process in which the photonic response depends on its physical structure, which itself is influenced by the environmental changes. By using a multi-photon polymerization process specifically optimized for soft responsive polymers such as Liquid Crystalline Networks, highly resolved, reproducible, and mechanically self-standing photonic crystals are fabricated. The physical structure of the 3D woodpile can be tuned by an external temperature variation creating a reversible spectral tuning of 50 nm in the telecom wavelength range. By comparing these results with finite element calculations and temperature induced shape-change, it is confirmed that the observed tuning is due to an elastic deformation of the structure. The achieved nanometric patterning of tunable anisotropic photonic materials will further foster the development of reconfigurable photonic crystals with point defects acting as tunable resonant cavities and, more in general, of 4D nanostructures.