Experimental traumatic brain injury

Traumatic brain injury, a leading cause of death and disability, is a result of an outside force causing mechanical disruption of brain tissue and delayed pathogenic events which collectively exacerbate the injury. These pathogenic injury processes are poorly understood and accordingly no effective neuroprotective treatment is available so far. Experimental models are essential for further clarification of the highly complex pathology of traumatic brain injury towards the development of novel treatments. Among the rodent models of traumatic brain injury the most commonly used are the weight-drop, the fluid percussion, and the cortical contusion injury models. As the entire spectrum of events that might occur in traumatic brain injury cannot be covered by one single rodent model, the design and choice of a specific model represents a major challenge for neuroscientists. This review summarizes and evaluates the strengths and weaknesses of the currently available rodent models for traumatic brain injury

Nanoscale Variation of Bioadhesive Substrates as a Tool for Engineering of Cell Matrix Assembly

ABSTRACT Although molecular and physical mechanisms of fibroblast matrix assembly have been widely investigated, the role of adhesive ligand presentation on matrix assembly has only been recently probed (Pereira et al. Tissue Eng., 2007). In the present study, various-sized albumin-derived nanocarriers (ANCs) were fabricated as nanoscale organization units for functionalization with the cell adhesion domain of fibronectin. The adhesion, morphology, and matrix assembly of human dermal fibroblasts were compared on substrate-deposited, ligand-ANCs of varying size. At early time points, fibroblast attachment, stress fiber formation, and spreading were higher on functionalized, larger-sized carriers than on smaller carriers. Matrix assembly was greatest at the highest ligand density on larger nanocarriers but was undetectable at the same ligand density on smaller carriers. Tracking of fluorophore-encapsulated ANCs showed that larger carriers were displaced less than smaller carriers and that atomic force microscopy of ligand-ANCs binding to adherent cells demonstrated that the larger ligand-ANCs required larger dissociation forces. Taken together, these data suggest that the greater inertia of larger adhesive nanocarriers may generate more cellular tension, which in turn, promotes up-regulation of matrix assembly. Thus, the size of the nanocarrier and the density of ligand on that nanocarrier combine to dictate the early kinetics of fibroblast matrix assembly. These insights may be useful for understanding cell-matrix interactions, as well as for development of bioactive materials with defined cell-adhesive activities such as wound repair and matrix remodeling events