Dicrocoeliosis, caused by Dicrocoelium dendriticum is a hepatic parasitic disease of clinical and financial significance in ruminant breeding, which causes direct losses due to condemnation of parasitized livers. The purpose of our study was to assess the effects of natural dicrocoeliosis on the antioxidant defence capability of the liver in sheep. For this purpose, livers of 40 infected sheep with D. dendriticum along with livers of 20 healthy (control) sheep were collected from animals slaughtered in Khuzestan province, Iran. An increase in malondialdehyde concentrations accompanied by decreased activities of SOD and GPX of infected liver was noticed when compared with control values. Our data indicate that through dicrocoeliosis insufficient scavenging of reactive oxygen species takes place and caused oxidative liver damage.
Football exposes its players to traumatic brain, neck, and spinal injury. It is unknown whether the adolescent football player develops imaging abnormalities of the brain and spine that are detectable on magnetic resonance imaging (MRI). The objective of this observational study was to identify potential MRI signatures of early brain and cervical spine (c-spine) injury in high school football players. Eighteen football players (mean age, 17.0 ± 1.5 years; mean career length, 6.3 ± 4.0 years) had a baseline brain MRI, and 7 had a follow-up scan 9–42 months later. C-spine MRIs were performed on 11 of the 18 subjects, and 5 had a follow-up scan. C-spine MRIs from 12 age-matched hospital controls were also retrospectively retrieved. Brain MRIs were reviewed by a neuroradiologist, and no cerebral microbleeds were detected. Three readers (a neuroradiologist, a neurosurgeon, and an orthopedic spine surgeon) studied the cervical intervertebral discs at six different cervical levels and graded degeneration using an established five-grade scoring system. We observed no statistically significant difference in disc degeneration or any trend toward increased disc degeneration in the c-spine of football players as compared with age-matched controls. Further research is needed to validate our findings and better understand the true impact of contact sports on young athletes.
Introduction: Cerebral microhemorrhages (CMH) are tiny deposits of blood degradation products in the brain and are the pathological substrate of cerebral microbleeds (MB). The existing animal models of MB are either β-amyloid-, anti-amyloid antibody-, or hypertension-induced; however, MB may develop independent of hypertension or amyloid deposition. In fact, MB are associated with normal aging, sepsis and neurodegenerative conditions. One common factor among the above pathologies is inflammation, and recent studies show a link between systemic inflammation and MB. Hence, we hypothesize that systemic inflammation (induced by lipopolysaccharide; LPS) will result in MB development, and an inflammation-induced animal model will be appropriate to study MB. In the current study we used two different dosing regimens for LPS and observed rapid and robust development of CMH and MB. Methods: Adult C57BL/6 mice were injected with LPS (1mg/kg or 3mg/kg, i.p.) or saline at 0, 6, and 24h. At 2 or 7 days after first LPS injection, brains were harvested. Hematoxylin and eosin (H&E) and Prussian blue (PB) were used to stain fresh (acute) hemorrhages and hemosiderin (subacute hemorrhages), respectively. Results: No surface and negligible H&E-positive CMH were observed in saline controls (n=4). LPS (3mg/kg; n=13) resulted in significantly higher number (p<0.01), size (p<0.05) and area (p<0.01) of H&E-positive CMH at 2 days. Negligible PB-positive CMH were observed at 2 days after LPS (3 or 1 mg/kg) injection. However, LPS (1mg/kg) resulted in robust development of PB-positive CMH at 7 days, with significantly higher number (p<0.05), size (p<0.05) and area (p<0.01) in LPS (n=9) versus saline (n=4) treated mice. MRI confirmed the presence of MB in this model. The number of CMH was significantly higher in the cerebellum (p<0.05) compared to cortical or subcortical regions. Conclusion: In summary, LPS produced rapid development of H&E-positive CMH (at 2 and 7 days) and PB-positive CMH (at 7 days) with low mortality. Thus, this appears to be an appropriate model to study the pathophysiology of CMH and MB.
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