PubMed Health⌕ Search

Biomedical subjects

D J Prieur

Publications and source records attributed to D J Prieur.

At least 91 records · Page 5Linked to original sources

Lysozyme activity in gastrointestinal and lymphoreticular tissues of rabbits genetically deficient in lysozyme.

Lysozyme activities in gastrointestinal and lymphoreticular tissues and in macrophage culture products of normal and genetically lysozyme-deficient rabbits were measured and compared. The supernatants of homogenates of 18 gastrointestinal and lymphoreticular tissues were assayed for lysozyme. In the gastrointestinal tract, there were no major differences in lysozyme activities between the two groups of rabbits. Ascending colon and orad gastrointestinal tissues had low activities, whereas descending colon and rectum had very high lysozyme activities in both types of rabbits. In the lymphoreticular tissues, lysozyme-deficient rabbits had graded lysozyme deficiencies: slight or no deficiency was present in thymus, partial deficiency in gut-associated lymphoid tissues, and near total deficiencies in secondary lymphoid tissues and bone marrow. Both macrophage culture cells and fluids from lysozyme-deficient rabbits were completely deficient in lysozyme. The results indicate that in the lysozyme-deficient rabbits there is tissue-specific lysozyme activity expressed and when considered along with other observations suggest that the lysozyme-deficient condition may be due to a deficiency of an isozyme or isozymes of lysozyme.

Animals↗

Ocular manifestations of the Chédiak-Higashi syndrome in four species of animals.

Ocular examinations were performed on cattle, cats, mink, and mice affected with Chédiak-Higashi syndrome (CHS). Bovine eyes were examined grossly and with an indirect ophthalmoscope, and Schirmer tear tests were performed. Feline eyes were examined grossly as well as with an indirect opthalmoscope and a slit lamp biomicroscope, and Schirmer tear tests were done on them. Postrotatory nystagmus was induced and measured in clinically normal Siamese cats, in clinically normal Persian and domestic short-haired cats, and in cats with CHS. Mink and mouse eyes were examined grossly with focal illumination. The animals with CHS had photophobia, pale irises, and fundic hypopigmentation associated with red fundic light reflections. Cats with CHS also had cataracts. Spontaneous nystagmus was observed in four of nine cats with CHS, and the duration of induced nystagmus was longer in the cats with CHS and in Siamese cats than in clinically normal cats that were not Siamese. Tear secretion appeared to be normal in all species of animals with CHS. The ocular manifestations of CHS in these animals were compared with those reported in man and were found to be similar.

Animals↗

Partial oculocutaneous albinism in Mystromys albicaudatus: nonhomology with the Chediak-Higashi syndrome.

Partially albinic Mystromys albicaudatus were examined to determine if the condition in these animals was homologous with the Chediak-Higashi syndrome. Tissues and cells from partially albinic and normal Mystromys albicaudatus were studied by light and electron microscopy. No evidence of cytoplasmic granule enlargement, which is characteristic of the Chediak-Higashi syndrome, was detected in the cells of the partially albinic rats when compared to controls. It was concluded that the inherited condition of partial albinism of Mystromys albicaudatus was not homologous with the inherited partially albinic disease known as the Chediak-Higashi syndrome.

Albinism↗

Plasma and synovial fluid lysozyme activity in horses with experimental cartilage defects.

Cartilaginous defects were created in the radiocarpal joints of 12 horses. Synovial fluid cytologic features, lysozyme activity, and beta-glucuronidase activity were monitored for 16 days. A comparison was made of plasma lysozyme and beta-glucuronidase activity and of synovial fluid lysozyme, beta-glucuronidase, and leukocyte concentrations. Plasma lysozyme was found to be independent of synovial fluid lysozyme activity. Synovial fluid lysozyme was significantly increased (P less than 0.001) in all joints with surgically induced defects (group I) compared with controls (arthrocentesis done; group III). However, there was no significant difference in lysozyme activity in group I joints and sham-operated controls (cartilage exposed only; group II). Increased lysozyme concentration was found to be positively correlated with increased numbers of leukocytes in the synovial fluid. Parallel changes were noted in synovial fluid beta-glucuronidase activity, indicating that much of the observed synovial fluid lysozyme activity was of lysosomal origin and not from cartilage destruction. Lysozyme activity in synovial fluid was found to be a very sensitive indicator of acute joint injury or inflammation (or both).

Animals↗

The Chediak-Higashi syndrome of cats.

Initial clinical, genetic, cytochemical and ultrastructural studies have characterized the Chediak-Higashi syndrome in cats. Three cats with Chediak-Higashi syndrome were found in a single line of 27 Persian cats, and three additional affected cats were produced from two prospective breedings of the original line. The disorder was characterized genetically as an autosomal recessive condition. All cats in the line with the combination of yellow eye color and "blue smoke" hair color exhibited the disorder. Four of the five cats examined had bilateral nuclear cataracts as early in life as 3 months of age. No increased susceptibility to infectious disease was observed. A bleeding tendency was noted. Abnormally large eosinophilic, sudanophilic, peroxidase-containing granules were observed in the neutrophils of the granulocytic series of blood and bone marrow by electron and light microscopy. Granules of eosinophils and basophils were also enlarged. Light microscopic studies of hair and skin revealed enlarged melanin granules. These manifestations were similar to those in man, mink, cattle, mice, and the killer whale with Chediak-Higashi syndrome. Cats are the sixth species in which this genetic disease has been reported.

Animals↗

A choroid plexus papilloma in an elasmobranch (Squalus acanthias).

A choroid papilloma in the choroid plexus of the ala of the fourth ventricle in a mature male elasmobranch, Squalus acanthias, was described. This is apparently the first report of a neoplasm of the central nervous system in a member of the class Chondrichthyes.

Animals↗

Hypercalcemic VX-2 carcinoma in rabbits: a clinicopathologic study.

Rabbits receiving intramuscular injections of VX-2 carcinoma cells in biceps femoris muscles developed rapidly progressive neoplastic growths at 14 to 21 days associated with a significant hypercalcemia. The biologic behavior of the VX-2 carcinoma was characterized by local infiltration and metastases to regional lymph nodes and lungs. No metastases to skeletal tissues were evident. Femora from intramuscularly injected rabbits had varying degrees of osteophytosis and lysis evident roentgenographically. Histopathologic evaluation of femoral sections revealed periosteal new bone growth, cortical osteolysis, endosteal new bone growth, and in a few long term rabbits, pathologic fractures. Bone lesions were evident histologically in the vicinity of neoplastic growth (i.e., femora, tibiae) but not at distant sites (i.e., humeri and vertebrae). Mineral analyses of VX-2 carcinoma tissues and kidneys from VX-2-bearing rabbits revealed concentrations of calcium 83 and 3 times greater, respectively, than those of skeletal muscle and kidneys from controls. These findings correlated well with histochemical evidence of excessive amounts of calcium in sections of kidneys and VX-2 carcinoma tissues. Rabbits receiving intraperitoneal injections of VX-2 carcinoma cells did not develop hypercalcemia despite an extensive, progressive neoplastic burden with metastases to abdominal and thoracic viscera. Roentgenographic, histopathologic, and physiochemical analyses of selected bones from these rabbits revealed no significant alterations. These findings indicate that VX-2 carcinoma cells need to be in close proximity to skeletal tissues in order to induce hypercalcemia. The development of a significant hypercalcemia in intramuscularly injected rabbits precedes the invasion of osseous tissues by VX-2 carcinoma cells. Therefore, it appears that VX-2 carcinoma cells have the ability to alter skeletal morphology and physiochemistry through a dual humoral/cellular mechanism. The clinicopathologic characteristics of the VX-2 carcinoma in the rabbit suggest that the neoplasm is a good experimental model to study osseous-mediated hypercalcemia of malignancy.

Animals↗

Decreased nucleotide and serotonin storage associated with defective function in Chediak-Higashi syndrome cattle and human platelets.

Prolonged mean template bleeding time of 14 min observed in seven cattle with the Chediak-Higashi syndrome (CHS) prompted the examination of platelet function in these animals. There was no distinguishable difference in concentration of circulating platelets between CHS and control cattle. CHS bovine platelets failed to aggregate in vitro in response to concentrations of acid-soluble collagen which induced aggregation in all normal samples. The primary platelet response to 5 muM ADP was normal in CHS cattle. A markedly decreased amount of serotonin (1.2% of normal) was detected in CHS bovine platelets. Bovine CHS platelet ATP and ADP contents were significantly less than normal, and the ATP/ADP ratios were 5.04 in normal and 29.38 in CHS platelets. Results of these animal investigations prompted a similar study of two patients with CHS. In humans, an increased bleeding time greater than 15 min and an in vitro impaired aggregation response to acid-soluble collagen and 5 muM adrenaline were discovered. Both ATP and ADP were reduced in CHS human platelets, and the ATP/ADP ratio was 3.96, compared to a ratio of 1.52 for platelets of two normal subjects. These findings suggested the presence of a "storage pool disease" of CHS platelets.

Adenosine Diphosphate↗

Chemical and morphologic alterations of rabbit bone induced by adriamycin.

Long term, low dose administration of adriamycin (ADR) to young growing rabbits resulted in significant alterations in bone structure and chemistry. Morphologic changes were most pronounced at epiphyseal and metaphyseal areas of long bones. Epiphyseal cartilage plates were thin and there was derangement of growth zones. Areas of primary and secondary spongiosa were deficient in trabeculae, osteoblasts and osteoclasts. Analysis of femora, humeri and lumbar vertebrae from ADR-treated rabbits revealed increased water and fat content and significant decreases in bone density compared to age-matched controls. Cortices of long bones were roentgenographically thin and contained large irregular spaces evident microscopically. Evaluation of bone ash from ADR treated rabbits revealed significant increases in the percentage of calcium and phosphorus, although Ca/P ratios were not different from controls. Results of in vitro studies indicate that ADR binds readily to nondemineralized, but not demineralized, fresh cortical bone powder. The findings of decreased bone density, histopathologic alterations, and a paucity of osteogenic cells in ADR treated rabbits are interpreted as retardation of bone maturation. It is suggested that ADR affects adversely both the organic and inorganic fractions of bone. Due to its unique characteristics of cytostatic action, binding to metal cations and orange-red fluorescence, ADR is a novel chemical agent that may be useful in experimental bone studies.

Animals↗

Composition of cartilage from lysozyme-deficient rabbits.

Costal and auricular cartilage obtained from mutant rabbits exhibiting lysozyme deficiency has been found to be identical to similar tissue from control animals in a variety of biochemical parameters. These data seriously question the putative role of lysozyme as a structural component of cartilage.

Age Factors↗

Electrolyte and morphologic alterations of myocardium in adriamycin-treated rabbits.

Rabbits receiving adriamycin (ADR) on a chronic schedule developed significant histopathologic, ultrastructural and tissue electrolyte alterations of the ventricular myocardium. Rabbits that developed clinicopathologic evidence of cardiomyopathy with ADR had histologic lesions of the myocardium, including perivascular fibrosis, interstitial fibrosis and edema and myocytolysis. Ultrastructurally, large vacuoles resembling distended sarcoplasmic reticulum displaced the contractile elements and mitochondria, which were diminished in number within affected myocytes. Frequently, mitochondria appeared as electron-dense structures surrounded by layers of membranes resembling myelin figures. In addition, rabbits with cardiomyopathy had marked elevations in ventricular Ca, Na and H(2)O concentrations. Serum electrolytes were not significantly elevated, but lactic dehydrogenase (LDH) and creatine phosphokinase (CPK) were significantly increased, indicative of a cardiomyopathy. Rabbits receiving ADR but not developing clinicopathologic evidence of heart failure also had significant elevations in ventricular Ca, Na and H(2)O. Rabbits with no cardiomyopathy had no increases either in serum electrolyte concentrations or CPK and LDH levels. These studies indicate that marked increases in ventricular tissue Ca precede and accompany morphologic evidence of chronic myocardial degeneration and may be instrumental in the development of the ADR-induced cardiomyopathy.

Animals↗