Biomarkers of brain injury in foals with hypoxic-ischemic encephalopathy.

Background: Neonatal hypoxic-ischemic encephalopathy (NHIE) is a disease affecting newborn foals for which there is no antemortem diagnostic test.

Hypothesis: Ubiquitin C-terminal hydrolase 1 (UCHL1) and the phosphorylated axonal forms of neurofilament H (pNF-H) are markers of brain injury in foals with NHIE.

Animals: Thirty-three foals with a clinical diagnosis consistent with NHIE and 17 healthy foals.

A novel marker for traumatic brain injury: CSF alphaII-spectrin breakdown product levels.

Currently, there is no definitive diagnostic test for traumatic brain injury (TBI) to help physicians determine the seriousness of injury or the extent of cellular pathology. Calpain cleaves alphaII-spectrin into breakdown products (SBDP) after TBI and ischemia. Mean levels of both ipsilateral cortex (IC) and cerebral spinal fluid (CSF) SBDP at 2, 6, and 24 h after two levels of controlled cortical impact (1.

Effects of injury severity on regional and temporal mRNA expression levels of calpains and caspases after traumatic brain injury in rats.

Despite a preponderance of studies demonstrating gene expression and/or enzymatic activation of calpain and caspase proteases after traumatic brain injury (TBI), no studies have examined the effects of injury magnitude on expression levels of these cell death effectors after TBI. Determination of the degree to which injury severity affects specific expression profiles is critical to understanding the relevant pathways contributing to post-trauma pathology and for developing targeted therapeutics. This investigation tested the hypothesis that different injury magnitudes (1.

TNF-alpha stimulates caspase-3 activation and apoptotic cell death in primary septo-hippocampal cultures.

Primary septo-hippocampal cell cultures were incubated in varying concentrations of tumor necrosis factor (TNF-alpha; 0.3-500 ng/ml) to examine proteolysis of the cytoskeletal protein alpha-spectrin (240 kDa) to a signature 145 kDa fragment by calpain and to the apoptotic-linked 120-kDa fragment by caspase-3. The effects of TNF-alpha incubation on morphology and cell viability were assayed by fluorescein diacetate-propidium iodide (FDA-PI) staining, assays of lactate dehydrogenase (LDH) release, nuclear chromatin alterations (Hoechst 33258), and internucleosomal DNA fragmentation.