Risk assessment of low-dose ethanol in food.

A high variety of food contains low doses of ethanol which are sometimes difficult to identify by consumers (adults or children). However, even low doses of ethanol intake raises several toxicological concerns. In the present study, an enzymatic assay and an HS-GC/MS procedure were applied to determine the ethanol levels of 1260 samples from different food categories covering "nonalcoholic" beer, fruit juices/drinks, baked goods, bananas and baby foods.

Rheumatoid synovial fibroblasts differentiate into distinct subsets in the presence of cytokines and cartilage.

Background: We investigated two distinct synovial fibroblast populations that were located preferentially in the lining or sub-lining layers and defined by their expression of either podoplanin (PDPN) or CD248, and explored their ability to undergo self-assembly and transmigration in vivo.

Methods: Synovial fibroblasts (SF) were cultured in vitro and phenotypic changes following stimulation with interleukin (IL)-1β, tumor necrosis factor (TNF)-α, and transforming growth factor (TGF)-β1 were examined. To examine the phenotype of SF in vivo, a severe combined immunodeficiency (SCID) human-mouse model of cartilage destruction was utilised.

Activated human B cells induce inflammatory fibroblasts with cartilage-destructive properties and become functionally suppressed in return.

Background: Cross-talk between synovial fibroblasts (SF) and immune cells is suggested to play a crucial role in inflammation and chronification of rheumatoid arthritis (RA). The contribution of B cells in this process is poorly defined.

Methods: Here, primary B cells from healthy donors were polyclonally activated and cocultured with SF of non-synovitic origin from patients with osteoarthritis.

Rheumatoid arthritis progression mediated by activated synovial fibroblasts.

Rheumatoid arthritis (RA) is a chronic inflammatory disease characterized by synovial hyperplasia and progressive joint destruction. Rheumatoid arthritis synovial fibroblasts (RASFs) are leading cells in joint erosion and contribute actively to inflammation. RASFs show an activated phenotype that is independent of the inflammatory environment and requires the combination of several factors.

Adiponectin-mediated changes in effector cells involved in the pathophysiology of rheumatoid arthritis.

Objective: Rheumatoid arthritis (RA) is associated with increased production of adipokines, which are cytokine-like mediators that are produced mainly in adipose tissue but also in synovial cells. Since RA synovial fibroblasts (RASFs), lymphocytes, endothelial cells, and chondrocytes are key players in the pathophysiology of RA, this study was undertaken to analyze the effects of the key adipokine adiponectin on proinflammatory and prodestructive synovial effector cells.

Methods: Lymphocytes were activated in part prior to stimulation.

Migratory potential of rheumatoid arthritis synovial fibroblasts: additional perspectives.

Cell migration is a central part of physiological and pathophysiological processes including wound healing, immune defense, matrix remodeling and organ homeostasis. Different cell types have migratory potential including cells of the immune system and cells required in wound healing and tissue repair. These cells migrate locally through the tissue to the site of damage.