Impact of diet and nutraceutical supplementation on inflammation in elderly people. Results from the RISTOMED study, an open-label randomized control trial.

BACKGROUND & AIMS: Eating habits may influence the life span and the quality of ageing process by modulating inflammation. The RISTOMED project was developed to provide a personalized and balanced diet, enriched with or without nutraceutical compounds, to decrease and prevent inflammageing, oxidative stress and gut microbiota alteration in healthy elderly people. This paper focused on the effect on inflammation and metabolism markers after 56 days of RISTOMED diet alone or supplementation with three nutraceutical compounds. METHODS: A cohort of 125 healthy elderly subjects was recruited and randomized into 4 arms (Arm A, RISTOMED diet; Arm B, RISTOMED diet plus VSL#3 probiotic blend; Arm C, RISTOMED diet plus AISA d-Limonene; Arm D, RISTOMED diet plus Argan oil). Inflammatory and metabolism parameters as well as the ratio between Clostridium cluster IV and Bifidobacteria (CL/B) were collected before and after 56 days of dietary intervention, and their evolution compared among the arms. Moreover, participants were subdivided according to their baseline inflammatory parameters (erythrocytes sedimentation rate (ESR), C-Reactive Protein, fibrinogen, Tumor Necrosis Factor-alfa (TNF-α), and Interleukin 6) in two clusters with low or medium-high level of inflammation. The evolution of the measured parameters was then examined separately in each cluster. RESULTS: Overall, RISTOMED diet alone or with each nutraceutical supplementation significantly decreased ESR. RISTOMED diet supplemented with d-Limonene resulted in a decrease in fibrinogen, glucose, insulin levels and HOMA-IR. The most beneficial effects were observed in subjects with a medium-high inflammatory status who received RISTOMED diet with AISA d-Limonene supplementation. Moreover, RISTOMED diet associated with VSL#3 probiotic blend induced a decrease in the CL/B ratio. CONCLUSIONS: Overall, this study emphasizes the beneficial anti-inflammageing effect of RISTOMED diet supplemented with nutraceuticals to control the inflammatory status of elderly individuals.

[Cellularity and extracellularity: the multi-fibrillar system: from cytoskeleton to connective tissue]. / Cellularité et extracellularité: le système multi-fibrillaire: du cytosquelette au tissu conjonctif.

This brief text aims at illustrating the interactions between connective tissue fibers and cell cytoskeleton fibers. These two networks are connected by molecular bridges at the level of the cell membrane of the cells of the connective and vascular tissues, allowing functional adjustments across the two domains, but also the transduction of forces and tensions into a biochemical alphabet. The signaling between the cell kern and its environment, but equally the other way round, from the environment to the core of the cell, depends on it.

In vivo experiments indicate that relatively high platelet deposition in von Willebrand's disease 'Vicenza' is caused by normal platelet-VWF levels rather than by high VWF-multimers in plasma.

Von Willebrand's disease (vWD) 'Vicenza' is characterized by low plasma von Willebrand Factor antigen (vWF:Ag) and very low levels of Ristocetin Cofactor activity (RiCof). The hemorrhagic tendency in vWD 'Vicenza' is, however, mild and bleeding times in this rare vWD-subtype are only slightly prolonged (1). Larger than normal multimers of plasma-vWF and normal levels of platelet-vWF have both been suggested to compensate the defects that are normally present in vWD. To elucidate the mechanisms involved, whole blood of four patients with vWD 'Vicenza' was circulated through a rectangular perfusion chamber (2) with fibrillar collagen as adhesive surface. Under these conditions, both plasma and platelet vWF participate to platelet adhesion. Compared to perfusion results with blood of normal donors, platelet adhesion of 'Vicenza' patients was decreased. However, the Vicenza defect was less than was observed in parallel experiments with blood of vWD type 1 subtype platelet-low patients and blood of a severe vWD patient. Adhesion was not increased in perfusions with only plasma of the 'Vicenza' vWD-patients. Equal vWF:Ag concentrations of normal multimeric composition were just as effective as the high multimeric 'Vicenza' vWF. Therefore, the abnormal plasma-vWF in 'Vicenza' patients does not cause the relatively high adhesion obtained with whole blood. In contrast, platelets of vWD 'Vicenza' patients resuspended in human albumine solution (HAS) showed far better adhesion than (vWF-poor) platelets of a patient with severe vWD. The values were at least comparable and tended to be higher than those obtained with normal platelets or with platelets of patients with vWD type I subtype platelet normal.(ABSTRACT TRUNCATED AT 250 WORDS)

Fibronectin in platelet adhesion to human collagen types I and III. Use of nonfibrillar and fibrillar collagen in flowing blood studies.

Platelet deposition at high wall shear rates on collagen type I and type III purified from human umbilical arteries is dependent on the presence of fibronectin and von Willebrand factor (VWF). The role of fibronectin at low wall shear rates (less than or equal to 500 s-1), where platelet deposition was independent of VWF, was studied with purified collagen I and III. Platelet deposition on nonfibrillar collagen I was fibronectin-dependent at all wall shear rates. Platelet deposition on nonfibrillar collagen type III was fibronectin-dependent at 300 s-1 and higher shear rates. By using a mixture of nonfibrillar type I and III, platelet deposition was found to be fibronectin-dependent at the tested wall shear rates (20, 100, and 300 s-1). This dependency was less than with nonfibrillar type I only, but more than with nonfibrillar type III. For platelet deposition on reconstituted type I or type III collagen fibrils, no fibronectin dependency was observed up to the highest wall shear rate tested (1800 s-1). The same results were obtained with a mixture of native type I and III fibrils. Thus, the dependence of platelet deposition on fibronectin is determined by the collagen type and the wall shear rate. The dependence on the fibronectin concentration was tested with nonfibrillar collagen type I at a wall shear rate of 300 s-1. Platelet deposition increased with increased fibronectin concentration up to a level of 700 micrograms/ml and leveled off above this concentration.