ABSTRACT
Sports-related concussions are particularly common during adolescence, and there is insufficient knowledge about how recurrent concussions in this phase of life alter the metabolism of essential structures for memory in adulthood. In this sense, our experimental data revealed that seven recurrent concussions (RC) in 35-day-old rats decreased short-term and long-term memory in the object recognition test (ORT) 30 days after injury. The RC protocol did not alter motor and anxious behavior and the immunoreactivity of brain-derived neurotrophic factor (BDNF) in the cerebral cortex. Recurrent concussions induced the inflammatory/oxidative stress characterized here by increased glial fibrillary acidic protein (GFAP), interleukin 1ß (IL 1ß), 4-hydroxynonenal (4 HNE), protein carbonyl immunoreactivity, and 2',7'-dichlorofluorescein diacetate oxidation (DCFH) levels and lower total antioxidant capacity (TAC). Inhibited Na+,K+-ATPase activity (specifically isoform α2/3) followed by Km (Michaelis-Menten constant) for increased ATP levels and decreased immunodetection of alpha subunit of this enzyme, suggesting that cognitive impairment after RC is caused by the inability of surviving neurons to maintain ionic gradients in selected targets to inflammatory/oxidative damage, such as Na,K-ATPase activity.
Subject(s)
Brain Concussion , Cognitive Dysfunction , Hippocampus , Memory Disorders , Neuroinflammatory Diseases , Oxidative Stress/physiology , Sodium-Potassium-Exchanging ATPase/metabolism , Spatial Memory/physiology , Age Factors , Animals , Brain Concussion/complications , Brain Concussion/immunology , Brain Concussion/metabolism , Brain Concussion/physiopathology , Cognitive Dysfunction/etiology , Cognitive Dysfunction/immunology , Cognitive Dysfunction/metabolism , Cognitive Dysfunction/physiopathology , Disease Models, Animal , Hippocampus/immunology , Hippocampus/metabolism , Hippocampus/physiopathology , Male , Memory Disorders/etiology , Memory Disorders/immunology , Memory Disorders/metabolism , Memory Disorders/physiopathology , Neuroinflammatory Diseases/etiology , Neuroinflammatory Diseases/immunology , Neuroinflammatory Diseases/metabolism , Neuroinflammatory Diseases/physiopathology , Rats , Rats, WistarABSTRACT
PURPOSE: To evaluate the clinical usefulness of phosphorus-32 chromic phosphate synoviorthesis in patients with hemophilia, recurrent hemarthrosis, and synovitis. MATERIALS AND METHODS: Forty-four P-32 colloid synoviorthesis procedures were performed in 38 patients with these abnormalities. P-32 colloid was injected intramuscularly in a dose of 1.0 mCi (37.0 MBq) in adult knees and 0.5 mCi (18.5 MBq) in adult elbows. A thin-window Geiger-Müller counter was used to survey treated joints, lymph nodes, and liver in order to detect leakage from the joint. Follow-up extended to a maximum of 4 years after treatment. RESULTS: No evidence of clinically significant leakage was seen. Twenty-two of 28 treatments (78%) with longer than 6 months follow-up were associated with improvement in range of motion and frequency of hemorrhage. Of 15 treatments with longer than 2 years follow-up, 10 (67%) were associated with improvement in range of motion; 12 (80%), with improvement in frequency of hemorrhage; and 12 (80%) with improvement in quality-of-life activities. CONCLUSION: P-32 colloid synoviorthesis is a clinically useful out-patient procedure in patients with hemophilia, recurrent hemarthrosis, and synovitis in whom hemostatic therapy has failed.
