Histopathological alterations in gill,liver and kidney of common carp exposed to chlorpyrifos

Histopathological alterations in gill, liver and kidney of common carp, Cyprinus carpio, intoxicated with sub-lethal concentrations of chlorpyrifos (O,O,-diethyl-O-3,5,6-trichloro-2-pyridyl phosphorothioate) pesticide (1 and 100 μg/L) for a period of 14 days were analyzed under light microscope. Gill exhibited hyperplasia and hypertrophy of gill epithelium, blood congestion, dilation of marginal channel, epithelial lifting, lamellar fusion, lamellar disorganization, lamellar aneurysm, rupture of the lamellar epithelium, rupture of pillar cells and necrosis. Alterations in hepatocytes were more pronounced, including nuclear and cellular hypertrophy, cellular atrophy, irregular contour of cells and nucleus, cytoplasmic vacuolation, cytoplasmic and nuclear degeneration, cellular rupture, pyknotic nucleus, necrosis and melanomacrophages aggregations. Histopathological lesions in kidney were cellular and nuclear hypertrophy, narrowing of tubular lumen, cytoplasmic vacuolation, hyaline droplet degeneration, nuclear degeneration, occlusion of tubular lumen, tubular regeneration, dilation of glomerular capillaries, degeneration of glomerulus and hemorrhage in Bowman's space. The most significant conclusion drawn from this study was that with the increased concentration and duration the toxicosis of chlorpyrifos would be enhanced as shown through the analysis of mean assessment value (MAV) and degree of tissue changes (DTC) also.     

Development of injury criteria for pelvic fracture in frontal crashes

OBJECTIVE: This article assesses the position-dependent injury tolerance of the hip in the frontal direction based on testing of eight postmortem human subjects. METHODS: For each subject, the left and right hemipelvis complex was axially loaded using a previously developed test configuration. Six positions were defined from a seated femur neutral condition, combining flexed, neutral, and extended femur positions with abducted, neutral, and adducted positions. RESULTS: Axial injury tolerances based on peak force were found to be 6,850 +/- 840 N in the extended, neutral position and 4,080 +/- 830 N in the flexed, neutral position. From the flexed neutral orientation, the peak axial force increased 18% for 20 degrees abduction and decreased 6% for 20 degrees adduction. From the extended, neutral orientation, the peak axial force decreased 4% for 20 degrees abduction and decreased 3% for 20 degrees adduction. However, as there is evidence that increases in loading may occur after the initiation of fracture, the magnitude of the peak force is likely related to the extent of injury, not to the initial tolerance. Using the axial femur force at the initiation of fracture (assessed with acoustic crack sensors) as a potentially more relevant indicator of injury may lower the existing injury criteria. This fracture initiation force varied by position from 3,010 +/- 560 N in the flexed, neutral position to 5,470 N in the extended, abducted position. Further, there was a large position-dependent variation in the ratio of fracture initiation force to the peak axial force. The initiation of fracture was 83% of the peak axial force in the extended, abducted position, but the ratio was 34% in the extended, adducted position. CONCLUSIONS: This may have significant implications for the development of pelvic injury criteria by automobile designers attempting to mitigate pelvis injuries.