The Derby City Chapter of the National Spinal Cord Injury Association Network- Serving Kentuckiana.
Message From the President
Dear Members & Friends-
Our annual Christmas party will take place in lieu of December’s meeting. See below for details.
There will NOT be a meeting in January.
February’s meeting will be held at Frazier Rehab Institute; 220 Abraham Flexner Way; Louisville; 10th floor dining room.
- David Allgood
DERBY CITY CHAPTER
ANNUAL CHRISTMAS PARY
DATE: DECEMBER 15, 2008
TIME: 6:00 P.M.
PLACE / ADDRESS: HIGHLAND COURT APT.
1720 RICHMOND DR, #108; LOUISVILLE, KY 40205 Map & Directions
From KY Spinal Cord Injury Research Center newsletter
FOCUS ON SCIENCE: MICROVASCULAR Plasticity AS A THERAPEUTIC TARGET
IN SPINAL CORD I NJURY
By Richard L. Benton, Ph.D.
Spinal cord tissue, especially the Neuron-rich gray matter, is abundantly vascularized due to high metabolic demand. Spinal cord injury (SCI) results in immediate damage to this delicate vascular network, instantly giving rise to bleeding and loss of vascular support. Interestingly, in the days and weeks following SCI, spared blood vessels continue to be pathologically transformed in and around the injury site, exhibiting altered structure and function after SCI. As a first step toward these ultimate therapeutic goals, a better understanding of the precise time course response of vascular response to injury as well as the molecular effectors responsible for their initiation is critical. Both of these are the focus of ongoing collaborative research being conducted in my laboratory and those of Dr. Hagg and Dr. Whittemore.
In the brain and spinal cord, the precise regulation of the microcirculation are provided for by a Functional and anatomical network of cells and molecules referred to collectively as the neurovascular unit (NVU). In health, the NVU is primarily composed of endothelial cells (ECs), the principal cell type of blood vessels, which are in turn intimately invested and functionally supported by pericytes and astrocytes. In the normal spinal cord, these cells form a network between the spinal cord and both the immune and circulatory systems, which is referred to as the blood-spinal cord barrier (BSCB). Within hours after traumatic SCI, the BSCB is compromised, contributing to the loss of functional nervous tissue.
Until recently, several impediments existed preventing a better understanding of the genes and proteins responsible for this vascular dysfunction. First of all, it has been
