No abstract available.
Paraplegia*

Obesity, which continues to increase worldwide, was shown to irreversibly impair the differentiation potential and angiogenic properties of adipose tissue mesenchymal stromal cells (ADSCs). Because these cells are intended for regenerative medicine, especially for the treatment of inflammatory conditions, and the effects of obesity on the immunomodulatory properties of ADSCs are not yet clear, here we investigated how ADSCs isolated from former obese subjects (Ex-Ob) would influence macrophage differentiation and polarization, since these cells are the main instructors of inflammatory responses. Analysis of the subcutaneous adipose tissue (SAT) of overweight (OW) and Ex-Ob subjects showed the maintenance of approximately twice as many macrophages in Ex-Ob SAT, contained within the CD68＋ /FXIII-A− inflammatory pool. Despite it, in vitro, coculture experiments revealed that Ex-Ob ADSCs instructed monocyte differentiation into a M2-like profile, and under inflammatory conditions induced by LPS treatment, inhibited HLA-DR upregulation by resting M0 macrophages, originated a similar percentage of TNF-α＋ cells, and inhibited IL-10 secretion, similar to OW-ADSCs and BMSCs, which were used for comparison, as these are the main alternative cell types available for therapeutic purposes. Our results showed that Ex-Ob ADSCs mirrored OW-ADSCs in macrophage education, favoring the M2 immunophenotype and a mixed (M1/M2) secretory response. These results have translational potential, since they provide evidence that ADSCs from both Ex-Ob and OW subjects can be used in regenerative medicine in eligible therapies. Further in vivo studies will be fundamental to validate these observations.

OBJECTIVE: In vitro cell and blood compatibility of three dietary supplements, comprised of multiple plant extracts, Pneumo Go (PG), Green active (GA) and Equistasi (Eq), and their main component, the phytocomplex Matrix U.B.® (Union Bio S.r.l.) (M), were evaluated. Moreover, preliminary in vivo tests were performed on GA in order to assess its ability to reduce pain in an animal model. METHODS: Cell compatibility was determined using fibroblasts (NIH3T3) and primary adult human microvascular endothelial cells (HMVECad) and the neutral red uptake test. Blood compatibility was evaluated by analyzing blood parameters after incubation of the products with sodium citrate anticoagulated whole blood. Thrombin time was determined by adding thrombin to aliquots of human plasma containing the samples. Clotting time was revealed by an automatic coagulometer. The in vivo analgesic effect of GA was evaluated in Wistar rats using the formalin test. RESULTS: M and PG reduced the percentage of viable NIH3T3 cells, indicating their interference in the cell cycle. GA and Eq stimulated fibroblast proliferation and neutralized the toxic effect of M. M and PG reduced HMVECad cell viability. GA and Eq did not affect cell viability as well as negative control. The hemocompatibility tests indicated that all the samples did not interfere with fibrinogen. The in vivo test carried out in male rats showed a significant analgesic effect of GA in all formalin-induced pain behaviors. CONCLUSION No hemotoxicity and good cell compatibility were found for all the tested samples. GA and Eq were the best candidates for further biocompatibility testing. Moreover, GA reduced pain in the animal model.