Inorganic mercury was localized through autometallography (AMG) in kidney and liver of free-ranging, subsistence-harveste d beluga (Delphinapterus leucas; n 20) and bowhead (Balaena mysticetus; n 5) whales. AMG granules were not evident in bowhead tissues, conrming nominal mercury (Hg) concentrations (range 0.011 to 0.038 ug/g ww for total Hg). In belugas, total Hg ranged from 0.30 to 17.11 and from 0.33 to 82.47 ug/g ww in liver and kidney, respectivel y. AMG granules were restricted to cortical tubular epithelial cytoplasm in belugas with lower tissue burdens; whales with higher tissue burdens had granules throughout the uriniferous tubular epithelium. In liver, AMG granular densities differed between lobular zones, concentrating in stellate macrophage s and bile cannalicular domains of hepatocytes . AMG granules aggregated in periportal regions in belugas with lower hepatic Hg concentrations , yet among whales with higher Hg, AMG granule deposition extended to pericentral and midzonal regions of liver lobules. Mean areas occupied by AMG granules correlated well with hepatic Hg concentration s and age. In beluga livers, AMG staining density was not associated with lipofuscin quantity (an index of oxidative damage). Occasionally, AMG granules and lipofuscin were colocalized, but more often were not, implying that Hg was not a prominent factor in hepatic lipofuscin deposition in belugas.
Three types of model hydroxyapatite (HA) scaffolds were implanted in the metacarpal and metatarsal bones of goats. Scaffolds, consisting of a latticed pattern of rods, were fabricated with a solid freeform fabrication (SFF) technique. All scaffolds contained macropores; some were also fabricated with micropores (5.2 +/- 2.0 microm). Recombinant human bone morphogenetic protein-2 (rhBMP-2) was added to some microporous scaffolds. rhBMP-2 caused increased percent filled with bone tissue compared to microporous scaffolds without rhBMP-2. Lamellar bone in the scaffolds was aligned perpendicular to the long axis of the bone near the junctions of the rods that make up the scaffold but was more random away from the junctions of rods. Microporous scaffolds stained beneath areas of contact with new bone. This staining might indicate either extracellular matrix (ECM) in the rods, byproducts of ECM production, or reaction of cellular products with the scaffold.
The Salter-Harris classification system is widely used to describe the anatomical appearance of and predict the prognosis for physeal fractures in canine clinical patients. Salter and Harris classified experimentally induced physeal fractures on radiographic and histological appearance, however, the good prognosis afforded Salter-Harris type I and II fractures in experimental animals has been questioned for the canine patient. Twelve naturally occurring physeal fractures from five traumatized dogs, who were euthanatized at the request of their owners, and one resected femoral head were examined histologically. Ten of the 13 physeal fractures disrupted the cells in the proliferative zone. The histological appearance of growth plate disruption in the injured animal correlates more closely with the clinical observations of growth retardation than the experimental observation of continued growth after fracture through the hypertrophic zone. The results of this study indicated that considerable damage to the physeal cartilage occurred during the traumatic incident in most of these clinical animal patients.
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