Intralesional Infiltrations of Arteriosclerotic Tissue Cells-Free Filtrate Reproduce Vascular Pathology in Healthy Recipient Rats

Lower-extremity arterial disease is a major health problem with increasing prevalence, often leading to non-traumatic amputation, disability and mortality. The molecular mechanisms underpinning abnormal vascular wall remodeling are not fully understood. We hypothesized on the existence of a vascular tissue memory that may be transmitted through soluble signaling messengers, transferred from humans to healthy recipient animals, and consequently drive the recapitulation of arterial wall thickening and other vascular pathologies. We examined the effects of the intralesional infiltration for 6 days of arteriosclerotic popliteal artery-derived homogenates (100 µg of protein) into rats’ full-thickness wounds granulation tissue. Animals infiltrated with normal saline solution or healthy brachial arterial tissue homogenate obtained from traumatic amputation served as controls. The significant thickening of arteriolar walls was the constant outcome in two independent experiments for animals receiving arteriosclerotic tissue homogenates. This material induced other vascular morphological changes including an endothelial cell phenotypic reprogramming that mirrored the donor’s vascular histopathology. The immunohistochemical expression pattern of relevant vascular markers appeared to match between the human tissue and the corresponding recipient rats. These changes occurred within days of administration, and with no cross-species limitation. The identification of these “vascular disease drivers” may pave novel research avenues for atherosclerosis pathobiology.     

Disassembly and Mislocalization of AQP4 in Incipient Scar Formation after Experimental Stroke

There is an urgent need to better understand the mechanisms involved in scar formation in the brain. It is well known that astrocytes are critically engaged in this process. Here, we analyze incipient scar formation one week after a discrete ischemic insult to the cerebral cortex. We show that the infarct border zone is characterized by pronounced changes in the organization and subcellular localization of the major astrocytic protein AQP4. Specifically, there is a loss of AQP4 from astrocytic endfoot membranes that anchor astrocytes to pericapillary basal laminae and a disassembly of the supramolecular AQP4 complexes that normally abound in these membranes. This disassembly may be mechanistically coupled to a downregulation of the newly discovered AQP4 isoform AQP4ex. AQP4 has adhesive properties and is assumed to facilitate astrocyte mobility by permitting rapid volume changes at the leading edges of migrating astrocytes. Thus, the present findings provide new insight in the molecular basis of incipient scar formation.     

Microwave-assisted synthesis of isosorbide-derived diols for the preparation of thermally stable thermoplastic polyurethane

In order to prepare thermally stable isosorbide-derived thermoplastic polyurethane, the synthesis of two new chiral exo–exo configured diols, prepared from isosorbide, and two types of diphenols (bisphenol A and thiodiphenol) was described. The synthesis conditions were optimized under conventional heating and microwave irradiations. To prove their suitability in polymerization, these monomers were successfully polymerized using 4,4′-diphenylmethane diisocyanate (MDI) and hexamethylene diisocyanate (HDI). Both monomers and polymers have been studied by NMR, FT-IR, TGA, DSC; intrinsic viscosity of polymers has also been determined. The results showed the effectiveness of the synthetic strategy proposed; moreover, a dramatic reduction of the reaction time and an important improvement of the monomers yield using microwave irradiation have been demonstrated. The monomers, as well as the polymers, showed excellent thermal stability both in air and nitrogen. It was also shown that the introduction of sulphur in the polyurethane backbone was effective in delaying the onset of degradation as well as the degradation rate.     

Inhibition of enterotoxicogenic strains Bacillus cereus GT1 and Staphylococcus aureus S1 isolated from double white cream cheese

In this study three different food preservatives (sodium nitrate, sodium benzoate and sodium sorbate) were used to evaluate their effect on two enterotoxicogenic strains (Bacillus cereus GT1 and Staphylococcus aureus S1). A significant decrease in the viability and production of virulence factors was observed. Yet, obvious tolerance to increasing concentrations (from 1 to 6?g/l) of the three preservatives was recorded reflecting possible resistance mechanisms within the tested strains. The two strains were subjected to increasing doses of gamma radiation (1, 2, 3, 4, 5, 6, 7, 8, 9 and 10?kGy). Obvious correlation was observed between the initial counts of bacterial spores contaminating the products and the required dose for their complete elimination. Whereas the eliminating dose of B. cereus GT1 strain was 10?kGy only 4?kGy was sufficient to suppress the growth and virulence of S. aureus S1, reflecting its sensitivity to low doses of gamma irradiation. Also, inhibition of the two strains by probiotic strain Bacillus pumilus G4 was studied both in situ (in cheese) and in vitro (in culture media). The viable cell population of B. cereus GT1 increased from 10⁶ to 2.9?×?10⁸?CFU/g within 60?h in controls but decreased from 2.1?×?10⁶ to 2.3?×?10³?CFU/g after treatment with the probiotic strain. No viable count was observed after 60?h of incubation. Whereas, the viable cell population of S. aureus S1 increased from 10⁶ to 2.5?×?10⁸?CFU/g within 60?h in controls but decreased from 1.5?×?10⁶ to 4.3?×?10²?CFU/g after treatment with the probiotic strain. No viable count was observed after 54?h of incubation.