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[Display omitted] • Use of a green and sustainable synthetic strategy to CHA-based polyesters. • Low temperature (35–55 °C) polycondensation in scCO 2 achieved. • The valuable epoxy groups of the monomers were preserved. • Our process led to reasonably high molecular weight polyesters. There is significant potential for industrial use of renewables for a wide range of materials demanded by society. Plants, trees and algae are increasingly attracting attention as sustainable sources for functionalised and polymerizable building blocks. In particular, the outer bark of the birch tree (Betula pendula) is a side stream of the forestry industry with so far very little utilisation besides energy recovery. It is composed of a macromolecular network, suberin, that could provide a renewable, low cost and competitive resource. Within raw suberin is the potentially very useful multifunctional extract cis -9,10-epoxy-18-hydroxyoctadecanoic acid (CHA). Our drive has been to develop a green and sustainable synthetic strategy to CHA-based polyesters, by exploiting supercritical carbon dioxide (scCO 2) as a reaction medium and leveraging the regio- and chemo-selective properties of the biocatalyst Novozym 435 (Lipase B). Low temperature (35–55 °C) polycondensation in scCO 2 shows significant advantages compared to traditional polymerisation methods leading to reasonably high molecular weight polyesters. The mild synthetic conditions also preserve the valuable epoxy groups of the CHA which we show can be exploited by post-polymerisation functionalisation to create sustainable resins for bio-renewable coatings. [ABSTRACT FROM AUTHOR]

Sphingolipids are both structural and bioactive compounds. In particular, ceramide and sphingosine 1-phosphate regulate cell fate, inflammation and excitability. 1-α,25-dihydroxyvitamin D3 (1,25(OH)2 D3 ) is known to play an important physiological role in growth and differentiation in a variety of cell types, including neural cells, through genomic actions mediated by its specific receptor, and non-genomic effects that result in the activation of specific signalling pathways. 1,25(OH)2 D3 and sphingolipids, in particular sphingosine 1-phosphate, share many common effectors, including calcium regulation, growth factors and inflammatory cytokines, but it is still not known whether they can act synergistically. Alterations in the signalling and concentrations of sphingolipids and 1,25(OH)2 D3 have been found in neurodegenerative diseases and fingolimod, a structural analogue of sphingosine, has been approved for the treatment of multiple sclerosis. This review, after a brief description of the role of sphingolipids and 1,25(OH)2 D3 , will focus on the potential crosstalk between sphingolipids and 1,25(OH)2 D3 in neural cells. [ABSTRACT FROM AUTHOR]

Background: Molecularly imprinted polymer (MIP) technique is a powerful mean to produce tailor made synthetic recognition sites. Here precipitation polymerization was exploited to produce a library of MIP nanoparticles (NPs) targeting the N terminus of the hormone Hepcidin-25, whose serum levels correlate with iron dis-metabolisms and doping. Biotinylated MIP NPs were immobilized to NeutrAvidin™ SPR sensor chip. The response of the MIP NP sensor to Hepcidin-25 was studied. Findings: Morphological analysis showed MIP NPs of 20-50 nm; MIP NP exhibited high affinity and selectivity for the target analyte: low nanomolar Kds for the interaction NP/Hepcidin-25, but none for the NP/non regulative Hepci-din-20. The MIP NP were integrated as recognition element in SPR allowing the detection of Hepcidin-25 in 3 min. Linearity was observed with the logarithm of Hepcidin-25 concentration in the range 7.2-720 pM. LOD was 5 pM. The response for Hepcidin-20 was limited. Hepcidin-25 determination in real serum samples spiked with known analyte concentrations was also attempted. Conclusion: The integration of MIP NP to SPR allowed the determination of Hepcidin-25 at picomolar concentrations in short times outperforming the actual state of art. Optimization is still needed for real sample measurements in view of future clinical applications. [ABSTRACT FROM AUTHOR]

Abstract Skeletal muscle (SkM) atrophy is caused by several and heterogeneous conditions, such as cancer, neuromuscular disorders and aging. In most types of SkM atrophy overall rates of protein synthesis are suppressed, protein degradation is consistently elevated and atrogenes, such as the ubiquitin ligase Atrogin-1/MAFbx, are up-regulated. The molecular regulators of SkM waste are multiple and only in part known. Sphingolipids represent a class of bioactive molecules capable of modulating the destiny of many cell types, including SkM cells. In particular, we and others have shown that sphingosine 1phosphate (S1P), formed by sphingosine kinase (SphK), is able to act as trophic and morphogenic factor in myoblasts. Here, we report the first evidence that the atrophic phenotype observed in both muscle obtained from mice bearing the C26 adenocarcinoma and C2C12 myotubes treated with dexamethasone was characterized by reduced levels of active phospho-SphK1. The importance of SphK1 activity is also confirmed by the specific pharmacological inhibition of SphK1 able to increase Atrogin-1/MAFbx expression and reduce myotube size and myonuclei number. Furthermore, we found that SkM atrophy was accomplished by significant increase of S1P transporter Spns2 and in changes in the pattern of S1P receptor (S1PRs) subtype expression paralleled by increased Atrogin-1/MAFbx expression, suggesting a role for the released S1P and of specific S1PR-mediated signaling pathways in the control of the ubiquitin ligase. Altogether, these findings provide the first evidence that SphK1/released S1P/S1PR axis acts as a molecular regulator of SkM atrophy, thereby representing a new possible target for therapy in many patho-physiological conditions. Highlights • The expression of S1P transporter Spns2 and S1P receptor 2 are upregulated in skeletal muscle from cachetic mice and in Dexa-treated myotubes • Functional Sphingosine kinase 1 activity and intracellular S1P are reduced in skeletal muscle from cachetic mice and in Dexa-treated myotubes • Muscular atrophy induced by dexamethasone is prevented by S1P2 antagonist. [ABSTRACT FROM AUTHOR]

Bone marrow-derived mesenchymal stromal cell- (BM-MSC-) based therapy is a promising option for regenerative medicine. An important role in the control of the processes influencing the BM-MSC therapeutic efficacy, namely, extracellular matrix remodelling and proliferation and secretion ability, is played by matrix metalloproteinase- (MMP-) 2. Therefore, the identification of paracrine/autocrine regulators of MMP-2 function may be of great relevance for improving BM-MSC therapeutic potential. We recently reported that BM-MSCs release the bioactive lipid sphingosine 1-phosphate (S1P) and, here, we demonstrated an impairment of MMP-2 expression/release when the S1P receptor subtype S1PR1 is blocked. Notably, active S1PR1/MMP-2 signalling is required for F-actin structure assembly (lamellipodia, microspikes, and stress fibers) and, in turn, cell proliferation. Moreover, in experimental conditions resembling the damaged/regenerating tissue microenvironment (hypoxia), S1P/S1PR1 system is also required for HIF-1α expression and vinculin reduction. Our findings demonstrate for the first time the trophic role of S1P/S1PR1 signalling in maintaining BM-MSCs’ ability to modulate MMP-2 function, necessary for cytoskeleton reorganization and cell proliferation in both normoxia and hypoxia. Altogether, these data provide new perspectives for considering S1P/S1PR1 signalling a pharmacological target to preserve BM-MSC properties and to potentiate their beneficial potential in tissue repair. [ABSTRACT FROM AUTHOR]

The efficiency of photomobile polymers (PMP) in the conversion of light into mechanical work plays a fundamental role in achieving cutting-edge innovation in the development of novel applications ranging from energy harvesting to sensor approaches. Because of their photochromic properties, azobenzene monomers have been shown to be an efficient material for the preparation of PMPs with appropriate photoresponsivity. Upon integration of the azobenzene molecules as moieties into a polymer, they act as an engine, allowing fast movements of up to 50 Hz. In this work we show a promising approach for integrating ZnO nanoparticles into a liquid crystalline polymer network. The addition of such nanoparticles allows the trapping of incoming light, which acts as diffusive points in the polymer matrix. We characterized the achieved nanocomposite material in terms of thermomechanical and optical properties and finally demonstrated that the doped PMP was better performing that the undoped PMP film. [ABSTRACT FROM AUTHOR]

Brucella is a foodborne pathogen globally affecting both the economy and healthcare. Surface Enhanced Raman Spectroscopy (SERS) nano-biosensing can be a promising strategy for its detection. We combined high-performance quasi-crystal patterned nanocavities for Raman enhancement with the use of covalently immobilized Tbilisi bacteriophages as high-performing bio-receptors. We coupled our efficient SERS nano-biosensor to a Raman system to develop an on-field phage-based bio-sensing platform capable of monitoring the target bacteria. The developed biosensor allowed us to identify Brucella abortus in milk by our portable SERS device. Upon bacterial capture from samples (104 cells), a signal related to the pathogen recognition was observed, proving the concrete applicability of our system for on-site and in-food detection. [ABSTRACT FROM AUTHOR]

Bone-marrow-derived mesenchymal stromal cells (BM-MSCs)–based therapy represents a promising option in the field of regenerative medicine. Their therapeutic potential is mainly dependent on paracrine secretion, proliferation and ECM remodeling abilities whose modulation involves Matrix Metalloproteinase (MMP)-2 functionality. Thus, the identification of paracrine/autocrine factors regulating MMP-2 expression/ activity may be of great biological relevance for potentiating BM-MSC theraputic efficacy. Our research group has demonstrated that BM-MSCs release the bioactive lipid sphingosine-1-phosphate (S1P). Here we demonstrated : i) the requirement for BMMSC of S1P production to synthesize functional gelatinases; ii) an impairment of gelatinolytic activity and MMP-2 expression/release when the S1P receptor subtype 1 (S1PR1) is blocked. Notably, in these experimental conditions BM-MSCs did not exhibit the formation of plasmamembrane-associated F-actin structures (lamellipodia, filopodia, microspikes) and, in turn, showed a reduction of the proliferation rate. Moreover, S1P1-mediated signaling is required for HIF-1alpha expression and MMP-2 expression/activity, reduction of vinculin expression and stress fiber formation and proliferation in hypoxia, an experimental condition mimicking the injured/regenerating tissue microenvironment. In conclusion, our findings, demonstrating the trophic role exerted by the autocrine S1P/S1PR1 signaling in maintaining BM-MSC ability to modulate MMP-2 function, required for ECM remodeling, cytoskeleton assembly and cell proliferation may provide perspectives for considering S1P/S1PR1 as a pharmacological target to preserve BM-MSCs properties and improve their efficacy in tissue repair. [ABSTRACT FROM AUTHOR]