EDA Fibronectin in Keloids Create a Vicious Cycle of Fibrotic Tumor Formation.

During the early phase of wound healing, first plasma fibronectin (FN) and then in situ FN are deposited at the site of injury. In situ FN--FN made by tissue cells at the injury site--often contains an extra domain A (EDA) insert. Multiple wound-related signal transduction pathways control the deposition of EDA FN, and the EDA insert can in turn trigger pathways that induce inflammation, increased extracellular matrix molecule deposition including FN and collagen, and activation of fibroblasts.

Topographical changes in extracellular matrix: Activation of TLR4 signaling and solid tumor progression.

The relationship between cancer progression and chronic inflammation is well documented but poorly understood. The innate immune system has long been recognized as the first line of defense against invading pathogens. More recently, endogenous molecules released from tissue matrix (Damage Associated Molecular Patterns [DAMPs]) following tissue injury or periods of active matrix remodeling have also been identified as regulators of innate immunity.

Ultrafast time-resolved carotenoid to-bacteriochlorophyll energy transfer in LH2 complexes from photosynthetic bacteria.

Steady-state and ultrafast time-resolved optical spectroscopic investigations have been carried out at 293 and 10 K on LH2 pigment-protein complexes isolated from three different strains of photosynthetic bacteria: Rhodobacter (Rb.) sphaeroides G1C, Rb. sphaeroides 2.