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Biomedical subjects

J A Render

Publications and source records attributed to J A Render.

At least 55 records · Page 3Linked to original sources
PubMed1988

Otic pathology of caprine beta-mannosidosis.

Caprine beta-mannosidosis is an autosomal recessive defect of glycoprotein catabolism with a deficiency of tissue and plasma beta-mannosidase activity and tissue accumulation of oligosaccharides within lysosomes. This rapidly fatal genetic disorder of Nubian goats is expressed at birth by a variety of clinical signs including deafness. Affected goats had folded pinnas, and the tympanic cavity was decreased due to multiple, polypoid projections of bone covered by middle ear mucosa which obstructed the view of the cochlear promontory. Numerous cells of the cochlear duct including mesothelial and epithelial cells of Reissner's membrane, mesothelial cells lining the scala tympani, cells of the stria vascularis, numerous supportive cells of the organ of Corti, cochlear hair cells, endothelial cells, perithelial cells, fibroblasts, macrophages, and neurons of the spiral ganglion contained numerous nonstaining intracytoplasmic vacuoles which resulted in distention of affected cells and caused thickening of involved structures. Ultrastructurally, the vacuoles were membrane-bound and consistent with lysosomes. Vacuolated cells were desquamated into the scala vestibuli and scala tympani. This is one of few reports describing light and electron microscopic otic alterations of a storage disease. Goats with beta-mannosidosis appear to be good models of hearing loss in patients with storage disease.

Animals↗
PubMed1987

Intraocular findings in three dogs and one cat with chronic glaucoma.

Intraocular neoplasia may cause secondary glaucoma. If an intraocular prosthesis is placed in an eye with glaucoma secondary to intraocular neoplasia, the neoplasm frequently regrows around the prosthetic ball, resulting in recurrence of buphthalmos and signs of pain. Histologic examination of eviscerated intraocular contents of 4 animals resulted in diagnosis of intraocular neoplasia in 2 glaucomatous eyes and ruled out neoplasia as the cause of glaucoma in 2 eyes.

Animals↗
PubMed1987

Glaucoma associated with a high number of mast cells in the uveal tract of an African lion cub.

An 8-week-old male lion cub (Panthera leo) was referred for evaluation of an enlarged and reddened left eye. Ocular examination revealed a buphthalmic left globe, with corneal edema, superficial neovascularization, moderate episcleral injection, a fixed dilated pupil, and an intraocular pressure of greater than 41.5 mm of Hg as measured by the Schiotz tonometer and a human conversion chart. A diagnosis of glaucoma was made. A silicone prosthesis was implanted after evisceration of the intraocular contents. Histologic examination of the eviscerated uveal tissue revealed numerous congested and dilated vessels of various sizes. Neutrophils were marginated along the vascular endothelium, and the uveal stroma was infiltrated by a few lymphocytes and numbers (3 to 30/hpf) of widely disseminated, well-differentiated mast cells with abundant, well-granulated cytoplasm.

Animals↗
PubMed1986

Axis determination in polyspermic Xenopus laevis eggs.

Polyspermic Xenopus laevis eggs can be identified easily because of regions of pigment accumulation and white stripes, which arise by a nocodazole-sensitive process. Eggs containing up to four sperm are capable of forming a single embryonic axis. Dispermic eggs display two regions of pigment accumulation, one around each sperm entry point (SEP), and one white stripe between the SEPs. Such eggs with a 180 degree separation between the SEPs were bisected before first cleavage along the white stripe, creating dorsal and ventral halves in many cases. Each half cleaved and formed a tadpole. When eggs were bisected early in the period of cytoplasmic reorganization (0.5-0.6 normalized time), each half could form a complete tadpole. When eggs were bisected after the period of reorganization (0.8-0.9), often one half formed a tadpole with a complete head but reduced or absent tail and the other half formed a tadpole with a complete tail but reduced or absent head. These results demonstrate that sperm cooperate to give a single embryonic axis in polyspermic eggs and the development of dorsal and ventral egg halves differs after egg reorganization before first cleavage.

Animals↗
PubMed1986

A neoplasm of globule leukocytes in a cat.

A neoplasm involving the ileo-cecal-colic junction, thymus, and tracheobronchial lymph nodes of a 7-year-old domestic cat was composed of dense sheets of round to oval mononuclear cells with oval to indented nuclei, moderate amounts of cytoplasm, and variable numbers of round eosinophilic granules. These granules are brown to black in phosphotungstic acid hematoxylin-stained sections and stain variably with the periodic acid-Schiff stain. They are 0.8 to 1.5 micron in diameter, limited by a single unit membrane, and have variable electron density. Light microscopic cellular morphology and staining characteristics as well as ultrastructural features of these cells are consistent with feline globule leukocytes. Morphologic features of the neoplastic cells in the present case are similar to those of the only other reported neoplasm of globule leukocytes which also involved the intestine of a cat.

Animals↗
PubMed1985

Pharyngeal polyps in two feline siblings.

Pharyngeal polyps were diagnosed in 2 sibling kittens referred for evaluation of chronic upper respiratory tract disease. Surgical excision of the masses was performed in both kittens after skull radiography and oral examination. One kitten had a recurrence of pharyngeal polyps 5 weeks after surgery and was euthanatized and necropsied. The clinical and histologic findings in these 2 cases suggested a congenital origin of this disease.

Animals↗
PubMed1985

Pathology of 6-aminonicotinamide toxicosis in the rabbit.

Daily doses of 6-aminonicotinamide (3-5 mg/kg) given by ip injection produced ataxia of the hind limbs progressing to an ascending paresis/paralysis, anorexia, diarrhoea and death in male and female New Zealand White and Dutch Belted rabbits. At autopsy, caecal and gastric distention were seen and the apex of the gall bladder had necrotic foci. Light microscopic lesions included atrophy and necrosis of the white lobe of Harder's gland and atrophy of seminiferous tubules with cellular necrosis, vacuolation and the presence of multinucleated giant cells. Cytoplasmic vacuolation was observed in epithelial cells from many tissues, usually in the basal portion of the cells. Vacuolation of the epithelium of the sacculus rotundus and vermiform appendix was found within the same time frame as histiocytic hyperplasia in these organs. Spongiosis and gliosis were seen in certain parts of the central nervous system. Ultrastructural alterations in the gall bladder epithelium consisted of distention of intercellular space, mild distention of perinuclear space and coalescing, intracytoplasmic, membrane-bound vacuoles, a few of which contained membranous debris. Some alterations of 6-aminonicotinamide toxicosis were prevented by simultaneous administration of nicotinamide with 6-aminonicotinamide.

6-Aminonicotinamide↗
PubMed1985

Ocular lesions of 6-aminonicotinamide toxicosis in rabbits.

6-Aminonicotinamide, an antimetabolite of nicotinamide, given by intraperitoneal injection produced diarrhea, ascending paresis/paralysis, death, and bilateral ocular alterations in both sexes of New Zealand white and Dutch belted rabbits. Ocular vascular lesions consisted of iridal congestion with iridal hemorrhage and associated acute iritis and aqueous flare in some rabbits. Cytoplasmic swelling, vacuolation, and loss of staining affinity that represented hydropic change were present in both layers of ciliary epithelium and the inner layer of iridal epithelium. Cells in the outer layer of the iridal processes and the ciliary ridge, were most severely affected. Vacuoles were also present in the retinal pigment epithelium and scattered throughout the outer plexiform layer of the retina with a few in the inner and outer nuclear layers. Ocular alterations were prevented by simultaneous administration of nicotinamide and their development appeared related to nicotinamide deficiency. No ocular alterations were caused by nicotinamide administration alone.

6-Aminonicotinamide↗
PubMed1985

Ultrastructural ocular lesions of 6-aminonicotinamide toxicosis in rabbits.

6-Aminonicotinamide, given by intraperitoneal injection to male and female Dutch belted rabbits, produced swelling and vacuolation of ciliary and iridal epithelium plus vacuolation of the retinal pigment epithelial and outer plexiform layers of the retina. By transmission electron microscopy, inner and outer ciliary epithelial cells and inner iridal epithelial cells contained numerous coalescing, membrane-bound vacuoles of the cytocavitary network. These vacuoles were viewed as numerous interconnecting, intracytoplasmic cavities in scanning electron micrographs. Swelling of vacuolated epithelial cells and the presence of fibrin and proteinaceous fluid in the ciliary stroma resulted in thickening of the anterior ciliary processes with the formation of surface alterations detectable by scanning electron microscopy. In transmission electron micrographs the vacuoles in the retinal pigment epithelium were large, electron-lucent spaces and the vacuoles in the outer plexiform layer of the retina appeared to be intracytoplasmic spaces in axons of photoreceptor cells. Distention of cytocavitary structures has been reported in glial cells of animals given 6-aminonicotinamide and this change was apparently due to alterations in ion and water movement across cellular membranes that resulted in intracellular edema.

6-Aminonicotinamide↗
PubMed1983

Giant cell tumor of soft parts in six horses.

Giant cell tumor of soft parts was diagnosed in 6 horses 3 to 12 years old (mean, 6.8 +/- 3.5 years): 3 Quarter Horse geldings, 2 Standardbred mares, and 1 Standardbred stallion. The neoplasms developed as raised, solitary masses, approximately 1 to 4 cm in diameter, which were firmly attached to subcutaneous tissue of the neck (1 horse), shoulder (1 horse), thigh (2 horses), or stifle (2 horses). Excision was followed by local recurrence in 3 horses within 1 to 1 1/2 months. The neoplasms were firm and cut with resistance. On cut surface, they were white, with mottled red hemorrhagic areas.

Animals↗
PubMed1983

Ocular, naso-maxillary, and neural anomalies in raccoons, Procyon lotor (L.).

Congenital ocular and related anomalies were studied in two unrelated young raccoons. One animal was anophthalmic and had severe anomalies of the central nervous system, consisting of meningoencephalocele, pachygyria, hydranencephaly, cerebellar cavitation, syringomyelia, and other defects. A second animal was microphthalmic with congenital defects of the nose, maxilla and teeth. Ocular lesions were severe and included chorioretinal coloboma, retinal folds, disorganized neuroectodermal cell layers, spherophakia, cataract and other defects. The nose had unilateral abnormal epithelium, hair follicles, sweat glands and sebaceous glands, and a lack of parietal cartilage on the affected side.

Abnormalities, Multiple↗
PubMed1982

Cerebrospinal nematodiasis and visceral larva migrans in an Australian (Latham's) brush turkey.

Cerebrospinal nematodiasis and visceral larva migrans were diagnosed in an Australian (Latham's) brush turkey (Alectura lathami) that died at the Indianapolis Zoo following a progressive neurologic disease. Histologically, multifocal areas of malacia, necrosis, and inflammation were seen in sections of cerebrum, cerebellum, and midbrain; lesions were most severe in the cerebellum. A large granuloma in a lung contained cross sections of a large ascarid larva identified as Baylisascaris. The CNS lesions were typical of larval migration, as documented in other avian species. An epizootiologic investigation indicated that Baylisascaris procyonis was the etiologic agent and that the bird had acquired the parasite through contact with fecal contamination from wild raccoons at the St Louis Zoo, where the bird had been raised.

Animals↗
PubMedDate not supplied

Insensitivity of the chicken embryo to the ototoxicity of aminoglycoside antibiotics and a loop diuretic.

Guinea pigs are routinely used in the histological evaluation of the cochlea as a method of testing for ototoxicity, but the procedures are very time-consuming. Because the avian cochlea is easier to examine and newly hatched chicks are sensitive to the ototoxic effects of gentamicin, birds may be useful in testing for ototoxicity. The use of chicken embryos would be even better for testing, but whether or not chicken embryos are sensitive to ototoxicants is unknown. In an attempt to determine whether or not chicken embryos may be used instead of guinea pigs in screening tests for ototoxicity, aminoglycoside antibiotics and a loop diuretic, ethacrynic acid, were administered to chicken embryos. A maximum-tolerated dose of gentamicin, kanamycin, streptomycin, ethacrynic acid, or a combination of gentamicin and ethacrynic acid was administered to fertile eggs of White Leghorn chickens on incubation days 10-17. To compare the effect of route of exposure on ototoxicity, gentamicin was administered by injection into the allantoic space, yolk sac, and air cell as well as by submerging the egg in gentamicin solution. With the preferred air cell route the effects of the ototoxic drugs kanamycin, streptomycin, ethacrynic acid, and a combination of ethacrynic acid and gentamicin were compared. On incubation day 18, cochleas were removed from the chicken embryos. Serial sections of these avian cochleas were examined and hair cells were counted. No significant difference was seen between the number of hair cells in cochleas of control chicken embryos and those from chicken embryos treated with drugs. Therefore, the chicken embryo appears to be insensitive to the ototoxicity of aminoglycoside antibiotics and a loop diuretic.

Animals↗