ABSTRACT
Mast cell products, such as histamine, may contribute to the initiation and progression of the atherosclerotic plaque. To determine the relationship that may exist between early atherosclerotic plaques and mast cells we studied the aortas and coronary arteries of 115 young subjects aged 15 to 34 years who had traumatic deaths. Lesions were classified as normal intima, fatty streaks, fibro-fatty plaques, and fibrous plaques. Aortic and coronary artery segments with raised lesions had significantly greater numbers of mast cells in the adventitia (and occasionally intima and outer media) compared with those with a normal intima. In the aortic segments greater numbers of mast cells were located in the dorsal portion (lesion "prone") compared with the ventral half (lesion "resistant") (P < .05). These data support the concept that increased numbers of mast cells are associated with atherosclerosis and suggest a role for mast cell products in the evolution of the atherosclerotic plaque.
Subject(s)
Arteriosclerosis/pathology , Mast Cells/pathology , Adolescent , Adult , Age Factors , Aorta/pathology , Cell Count , Coronary Vessels/pathology , Female , Humans , MaleABSTRACT
Two cases of fatal attacks by large cats are presented. In the first case, a 30-year-old female zoo worker was attacked by a jaguar that had escaped its cage. In the second case, a 2-year-old girl was fatally injured by her father's pet leopard. The pattern of injuries in these cases is nearly identical to those of these cats' prey in the wild.
Subject(s)
Bites and Stings/pathology , Carnivora , Craniocerebral Trauma/pathology , Adult , Animals , Child, Preschool , Facial Injuries/pathology , Female , Humans , Neck Injuries , Scalp/injuries , Skull/injuriesSubject(s)
Carbon Monoxide Poisoning/diagnosis , Housing , Cyanides/poisoning , Diagnosis, Differential , Humans , Time FactorsABSTRACT
A systematic procedure provides one method of assessing xenobiotic-induced abnormalities in fish following environmental exposures. Behavioral, external (or gross), histopathological, and internal organ changes allow determination of the severity of toxicant impact on an endemic population provided a sufficient number of specimens is analyzed. Over the past 15 years, these methods have led to the establishment of causal factors in metal- and metalloid-induced toxicity.
Subject(s)
Environmental Pollutants/toxicity , Fishes/metabolism , AnimalsABSTRACT
Redear sunfish (Lepomis microlophus) were collected from Martin Lake in east Texas. For at least 8 months, 1 year earlier, aqueous selenium-laden effluent from man-made sources was released into this 5,000-acre reservoir (unpublished data). Redear sunfish from a reference lake, 8 km upstream, were collected for comparison to Martin Lake fish. The hepatopancreas (i.e., liver and associated, disseminated exocrine pancrease), mesonephros (i.e., kidney), gonads, heart, spleen, stomach, and gill arches were preserved for histopathological examination using optical and/or transmission electron microscopy. Livers from Martin Lake redear sunfish (which had accumulated approximately 20 ppm selenium in the liver) showed central necrosis, reduced quantities of rough endoplasmic reticulum and glycogen particles, and increased numbers of lysosome-like structures. Kidneys showed proliferative glomerulonephritis, and exocrine pancreas showed marked hypertrophy at the optical level. Ultrastructurally, architectural disorganization, reduced rough endoplasmic reticulum, increased cisternal space, and proliferation of smooth endoplasmic reticulum were evident. The stomach, spleen, gill, heart, and gonads showed no abnormalities.
Subject(s)
Fishes , Kidney/pathology , Liver/pathology , Pancreas/pathology , Selenium/adverse effects , Water Pollutants, Chemical/adverse effects , Water Pollutants/adverse effects , Animals , Glomerulonephritis/chemically induced , Kidney/ultrastructure , Liver/ultrastructure , Microscopy, Electron , Necrosis , Pancreas/ultrastructure , Selenium/analysis , TexasABSTRACT
This report provides morphological and analytical data for a group of green sunfish collected from an area relatively free of metals and a second group of the same species collected from a lake into which selenium had been discharged. Neutron activation data of livers (and kidneys) collected from these fish show an average of about 11 ppm selenium (fresh weight) for both organs; other metals were not detected in the liver (or kidneys) of these fish. Ultrastructural examination of livers from fish of this group showed focal necrosis, areas of granular cytoplasm, fatty infiltration, increased numbers of Kupffer cells, and disorganized liver architecture--compared with those of controls. The presence of massive levels of selenium in the liver and concomitant hepatocyte changes suggests a causal relationship between these phenomena.
Subject(s)
Liver/ultrastructure , Selenium/metabolism , Animals , Female , Fishes/physiology , Kidney/ultrastructure , Liver/drug effects , Liver/metabolism , Male , Microscopy, Electron , Neutron Activation Analysis , Selenium/pharmacologyABSTRACT
A group of green sunfish was collected from a selenium-rich lake and compared with a similar group collected from a control lake upstream in the same drainage system in east Texas. Since the level of selenium in kidneys of these fish was relatively high (averaging 11 ppm on a fresh weight basis), histopathological and ultrastructural data were collected. Kidneys from fish from the selenium-rich lake showed proliferative glomerulonephritis and hematuria as well as vacuolation and necrosis of cells of the convoluted tubules.
