E-Knitted Textile with Polymer Optical Fibers for Friction and Pressure Monitoring in Socks.

The objective of this paper is to study the ability of polymer optical fiber (POF) to be inserted in a knitted fabric and to measure both pressure and friction when walking. Firstly, POF, marketed and in development, have been compared in terms of the required mechanical properties for the insertion of the fiber directly into a knitted fabric on an industrial scale, i.e. elongation, bending rigidity, and minimum bending radius before plastic deformation. Secondly, the chosen optical fiber was inserted inside several types of knitted fabric and was shown to be sensitive to friction and compression. The knitted structure with the highest sensitivity has been chosen for sock prototype manufacturing. Finally, a feasibility study with an instrumented sock showed that it is possible to detect the different phases of walking in terms of compression and friction.

IFN-α and CD46 stimulation are associated with active lupus and skew natural T regulatory cell differentiation to type 1 regulatory T (Tr1) cells.

Immune suppressive activities exerted by regulatory T-cell subsets have several specific functions, including self-tolerance and regulation of adaptive immune reactions, and their dysfunction can lead to autoimmune diseases and contribute to AIDS and cancer. Two functionally distinct regulatory T-cell subsets are currently identified in peripheral tissues: thymus-developed natural T regulatory cells (nTregs) controlling self-tolerance and antiinflammatory IL-10-secreting type 1 regulatory T cells (Tr1) derived from Ag-stimulated T cells, which regulate inflammation-dependent adaptive immunity and minimize immunopathology. We establish herein that cell contact-mediated nTreg regulatory function is inhibited by inflammation, especially in the presence of the complement C3b receptor (CD46). Instead, as with other T-cell subsets, the latter inflammatory conditions of stimulation skew nTreg differentiation to Tr1 cells secreting IL-10, an effect potentiated by IFN-α. The clinical relevance of these findings was verified in a study of 152 lupus patients, in which we showed that lupus nTreg dysfunction is not due to intrinsic defects but is rather induced by C3b stimulation of CD46 and IFN-α and that these immune components of inflammation are directly associated with active lupus. These results provide a rationale for using anti-IFN-α Ab immunotherapy in lupus patients.

An optical fibre-based sensor for respiratory monitoring.

In this paper, a textile-based respiratory sensing system is presented. Highly flexible polymeric optical fibres (POFs) that react to applied pressure were integrated into a carrier fabric to form a wearable sensing system. After the evaluation of different optical fibres, different setups were compared. To demonstrate the feasibility of such a wearable sensor, the setup featuring the best performance was placed on the human torso, and thus it was possible to measure the respiratory rate. Furthermore, we show that such a wearable system enables to keep track of the way of breathing (diaphragmatic, upper costal and mixed) when the sensor is placed at different positions of the torso. A comparison of the results with the output of some commercial respiratory measurements devices confirmed the utility of such a monitoring device.

Aldehyde dehydrogenase activity identifies a population of human skeletal muscle cells with high myogenic capacities.

Aldehyde dehydrogenase 1A1 (ALDH) activity is one hallmark of human bone marrow (BM), umbilical cord blood (UCB), and peripheral blood (PB) primitive progenitors presenting high reconstitution capacities in vivo. In this study, we have identified ALDH(+) cells within human skeletal muscles, and have analyzed their phenotypical and functional characteristics. Immunohistofluorescence analysis of human muscle tissue sections revealed rare endomysial cells. Flow cytometry analysis using the fluorescent substrate of ALDH, Aldefluor, identified brightly stained (ALDH(br)) cells with low side scatter (SSC(lo)), in enzymatically dissociated muscle biopsies, thereafter abbreviated as SMALD(+) (for skeletal muscle ALDH(+)) cells. Phenotypical analysis discriminated two sub-populations according to CD34 expression: SMALD(+)/CD34(-) and SMALD(+)/CD34(+) cells. These sub-populations did not initially express endothelial (CD31), hematopoietic (CD45), and myogenic (CD56) markers. Upon sorting, however, whereas SMALD(+)/CD34(+) cells developed in vitro as a heterogeneous population of CD56(-) cells able to differentiate in adipoblasts, the SMALD(+)/CD34(-) fraction developed in vitro as a highly enriched population of CD56(+) myoblasts able to form myotubes. Moreover, only the SMALD(+)/CD34(-) population maintained a strong myogenic potential in vivo upon intramuscular transplantation. Our results suggest that ALDH activity is a novel marker for a population of new human skeletal muscle progenitors presenting a potential for cell biology and cell therapy.

RhoA induces MMP-9 expression at CD44 lamellipodial focal complexes and promotes HMEC-1 cell invasion.

Much progress has been made in recent years in the understanding of angiogenesis, yet signalling pathways involved remain poorly defined. Here we report that small RhoA GTPase is implicated in the invasion of human microvascular endothelial cells (HMEC-1). Ectopic expression of active-RhoA GTPase induced the expression of MMP-9 metalloproteinase, a key proteinase of the basement membrane, and promoted migration of endothelial cells through a 3D-matrix protein gel. MMP-9 was either directed as vesicular-like patches to the apical side of cells, or addressed to specific membrane sites at the cell surface. Confocal microscopy analyses indeed revealed clustering of MMP-9 in advancing lamellipodia at the forefront of endothelial cells, where this proteinase colocalized with RhoA and CD44, a transmembrane receptor known to be proteolysed in tumor cell progression. In addition, TIMP-1, a natural MMP inhibitor, significantly reduced the invasion of RhoAV14 expressing cells, suggesting that MMP-9 was a critical metalloproteinase responsible, at least partly, for the RhoAV14-induced endothelial cell invasion. We propose that RhoA triggers signalling pathways that, upregulating expression of a proteinase at specific membrane localizations, may confer an highly invasive phenotype to endothelial cells.