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D H Percy

Publications and source records attributed to D H Percy.

At least 73 records · Page 4Linked to original sources
PubMed1982

Comparison of biologic behavior and histology of transplanted mammary tumors in GR mice.

Mammary tumors that arose spontaneously in inbred GR mice were transplanted into syngeneic castrated males. The hormone responsiveness of the transplants was studied in mice treated with estrone and progesterone and was compared with the hormone responsiveness in mice that received no hormone treatment. Microscopic examination of hormone-responsive and hormone-independent tumors revealed similar histologic patterns in both groups. It was evident that pale cells, which are classically associated with hormone-responsive tumors, may also be present in transplanted hormone-independent tumors in this strain. No correlation was found between the histologic pattern of these transplanted tumors and the biologic behavior, hormonal status, or presence of a specific murine mammary tumor virus (MuMTV) proviral fragment. Mammary tumors also appeared capable of undergoing differentiation into more than one morphologic type. Two cotransplanted tumors (derived from the same parental tumor) had markedly different histologic patterns; however, analysis of MuMTV proviral fragments indicated that the MuMTV-infected cells were of the same parentage.

Adenocarcinoma↗
PubMed1981

Feline histoplasmosis with ocular involvement.

A 12-year-old, castrated male cat with a history of respiratory disease developed bilateral endophthalmitis, retinal detachment, and granulomatous choroiditis, and unilateral glaucoma, and was killed. Other lesions included granulomatous optic neuritis, myositis involving extraocular muscles, and focal retinitis. Light and electron microscopy showed many intracellular organisms, interpreted to be Histoplasma. Granulomatous inflammatory lesions and organisms were present in lung, liver, lymphoid tissues, and adrenals.

Animals↗
PubMed1981

Suppression of experimental allergic encephalomyelitis in guinea/pigs by liposome-associated human myelin basic protein.

Human myelin basic protein (MBP) was inserted into phosphatidyl-serine liposomes and Hartley guinea pigs were treated with 1 or 2 injections of MBP-liposomes mixture by the intracardial route before an encephalitogenic challenge with MBP in CFA. Other groups of guinea pigs were pretreated with equivalent amounts of MBP in saline or of MBP in IFA. Of 24 untreated animals, 22 developed EAE and died or had to be sacrificed within 15 days after challenge. Only 4 of 29 guinea pigs treated with either 75 microgram or 112 microgram MBP-liposomes developed clinical signs of the disease. In the group pretreated with MBP in saline, 11 of 15 animals died, whereas in the MBP-IFA group, only 4 out of 10 died. Histologic modifications were also decreased in the MBP-liposomes and MBP-IFA groups, but in many instances, clinical normal guinea pigs showed disseminated perivascular infiltrates in the brain and spinal cord. Delayed hypersensitivity reactions to MBP were positive in all but 1 animal tested. Early T-rosette levels followed essentially the clinical course of the disease: they were drastically decreased 7 days after challenge in the untreated and MBP-saline-treated groups, but remained essentially normal in the MBP-liposomes group throughout the experiment. Lymphocyte transformation tests carried out in parallel with soluble MBP and with MBP-liposomes indicated that animals in certain groups responded preferentially to 1 form or the other of the antigen. Compared with prevailing procedures, the single i.v. injection of a relatively small amount of liposome-associated MBP appears to represent a promising approach for the antigen-specific suppression of EAE.

Animals↗
PubMed1980

Experimental type 2 herpes simplex ophthalmitis in the newborn rat.

An animal model for the study of type 2 herpes simplex virus (HSV2) ophthalmitis is described. Wistar rats were inoculated intracerebrally with HSV2 at 0, 5, 10, 15, 20, or 30 days of age. Eyes and brain from all animals, whether they survived or succumbed with encephalitis, were collected for microscopic and virologic studies. Up to 20% or more of the HSV2-inoculated rats had lesions in the cornea, uveal tract, and/or retina. Herpetic keratiis occurred in a few animals while the eyelids were still fused, indicative of internal spread of HSV2. Intranuclear inclusions were observed in corneal epithelium and neural retina, and herpesvirus particles were demonstrated in the cornea, iris, and retina. Lesions of the cornea and iris were also visualized by scanning electron microscopy. Virus was isolated from over 40% of the eyes tested. In general, titers of the virus in the eyes were less than those in the brains of HSV2-inoculated rats. The newborn rat thus represents another animal model to study herpetic ophthalmitis. Unlike most studies, ocular lesions were produced by a route other than the usual topical or intraocular inoculation of the virus.

Animals↗
PubMed1978

Globular bodies: a primary cause of the opacity in senile and diabetic posterior cortical subcapsular cataracts?

We examined 9 cataracts from maturity onset diabetics and 4 senile posterior subcapsular cataracts by scanning electron microscopy, transmission electron microscopy, immunofluorescence for crystallin proteins and actin, histochemical methods and x-ray diffraction. The cataractous regions contained spherical globules up to 20 mu in diameter, often in a fibrous matrix. Some were extracellular Morgagnian globules, apparently formed by blebbing from the cell surface; others appeared to have been formed intracellularly. The area of globular degeneration was usually 300 mu deep, but had deeper fusiform extensions. Morphological changes in the cell cytoplasm varied according to their depth in the cataract. Electron microscopy showed intracellular and extracellular globules, many of them were bounded by lipid bilayer membranes. Immunofluorescent staining showed that all the globules contained gamma-crystallin; some contained alpha- and beta-crystallins and actin. All the globules contained higher concentrations of cysteine or cystine than the surrounding lens tissue but they did not react to stains for carbohydrate or calcium. X-ray diffraction studies showed that crystalline calcium salts were absent. Globules and cavities averaged 45% of the total area in cross section. Assuming an area of cataract to be 300 micron thick and that globules 1 mu in diameter scattered, while 2--20 mu in diameter reflected light, we calculated that light passing through such a thickness would be reduced by 65%. Thus the globules could account for most of the opacity of the cataractous area. Presumably the fibrous degeneration of the cells causes enough light scattering to account for the remainder of the reduction. Cataract patients complain of decreased visual acuity, a golden halo around objects, and difficulties when driving while facing oncoming traffic at night. These probably result from light scattering. In our previous experiments, globular bodies containing gamma-crystallin were found in cells grown in tissue culture, and blebs with increased acitn content similar to Morgagnian globules were formed in tissue culture by treating differentiated rat lens cells of stage 2 by cytochalasin D (which impaired microfilament function). These results suggest the possibility of simulating in tissue culture the morphological alterations seen in the cataractous cell.

Aged↗
PubMed1977

Ocular abnormalities in the myopathic hamster (UM-X7.1 strain).

Eyes from cardiomyopathic hamsters (UM-X7.1 strain) were examined histologically for evidence of ocular defects. Changes observed included microphthalmia, scleral ectasia, scleral rupture, keratoconus, retinal detachment, retinal dysplasia, retinal fragmentation, retinal thinning, fibrosis of iris and ciliary body, ectopia lentis, and cataract formation. Lesions characteristic of cardiomyopathic hamsters were observed in the myocardium and skeletal muscle. This strain may be a suitable animal model to study the pathogenesis of ocular changes seen in certain congenital connective tissue disorders in man.

Age Factors↗
PubMed1977

Experimental retinal dysplasia due to cytosine arabinoside.

Retinal dysplasia was produced in newborn rats treated postnatally with the antimitotic substance, cytosine arabinoside (ara-C). In rats examined from 6 to 60 days, there were numerous retinal rosettes surrounded by photoreceptor cells and bipolar cells containing photoreceptor cell processes, displaced nuclei, and cellular debris. Abnormal development and alignment of photoreceptor cell processes were commonly observed. Cellular degeneration was evident at all ages, and infiltrating phagocytic cells were especially numerous in the retina of treated rats examined at 60 days. Characteristic features of ara-C-induced retinal dysplasia included the scattering of bipolar cell nuclei in the inner and outer nuclear layers and marked reduction in the width of the affected retina. Considerable retinal and cerebellar development occurs postnatally in the rat, thus newborn animals might be useful in the testing of possible teratogenic drugs.

Animals↗
PubMed1976

Malignant teratoid medulloepithelioma in a dog.

A malignant teratoid medulloepithelioma that arose from the ciliary body was found in an adult Beagle. The anterior part contained relatively well-differentiated tumor cells, cartilage, and ganglion cells. These structures were interpreted as teratoid formations derived from the embryonic anlage of the medullary epithelium. The more posterior part was highly anaplastic and invasive. A transitional area contained neural rosettes of the Flexner-Wintersteiner type. This tumor is rare in both man and animals.

Animals↗
PubMed1976

Canine herpes-induced retinal dysplasia and associated ocular anomalies.

Thirty-eight newborn Beagle puppies from eight litters of a specific pathogen-free colony maintained in isolation were inoculated with canine herpesvirus. Pups were killed between one and 30 days after inoculation. Histopathologic studies were carried out on the eyes and other tissues in conjunction with fluorescent antibody and viral isolation studies. Evidence of ocular inflammation manifested by panuveitis with the presence of intranuclear inclusion bodies was usually seen by the fourth day after infection. Eyes with severe inflammation showed peripheral anterior synechiae, cataract, and keratitis. The presence of the virus was confirmed by viral isolation from ocular tissues and fluorescent antibody studies. Developmental anomalies included retinal dysplasia with fold and tube formation of the neural retina, retardation of retinal maturation, and areas of necrosis and reorganization were seen. The retinal pigment epithelium showed initially patchy depigmentation and vacuolization and, subsequently, folding hypertrophy and duplication as well as areas of widespread atrophy and patchy loss. In some animals ectopic retina was found within cystic spaces of the optic nerve. These experiments confirm the ability of canine herpes infection in neonatal pups to produce severe ocular inflammation with subsequent retinal dysplasia and associated ocular anomalies.

Animals↗
PubMed1975

Taratogenic effects of the pyrimidine analogues 5-iododeoxyuridine and cytosine arabinoside in late fetal mice and rats.

Pregnant mice and rats were treated daily with 5-iododeoxyuridine (IUDR) or cytosine arabinoside (CA) on 3 consecutive days, beginning on day 16 and 18 of pregnancy, respectively. Offspring were killed at 10 and 20 days of age and the cerebellum, eye, and kidney examined histologically. All offspring of mice treated with 400 mg/kg IUDR were stillborn or died within the first 48 h of life, and deaths occurred at other dosages in both species. In IUDR-exposed mice and rats there was persistence of granule cells in the external granular layer, and scattered foci of microcystic tubular change in the renal cortices. In both species CA produced segmental cerebellar hypoplasia and focal microcystic renal cortical dysplasia. Retinal dysplasia occurred in rats exposed to 50 mg/kg. Lesions were concentrated in the central retina, corresponding with the stage of development at the time of administration of CA. The teratogenic effects of IUDR were minimal and were induced by dosages much higher than normally used in human medicine. On the other hand, lesions were more extensive in mice and rats exposed to CA. Thus, in addition to other known causes of congenital retinal dysplasia, defective development may be drug induced, in this case by the prenatal administration of CA.

Abnormalities, Drug-Induced↗
PubMed1975

Experimental infection with herpes simplex virus type 2 in newborn rats: Effects of treatment with iododeoxyuridine and cytosine arabinoside.

Sprague-Dawley rats were inoculated, within 36 hr of birth, with either of two strains of herpes simplex virus type 2. The effects of treatment for five days with either 5-iododeoxyuridine or cytosine arabinoside in near toxic doses were studied. Evaluation of treatment based on rate of survival, incidence of lesions, and isolation of virus from the central nervous system showed no appreciable difference between treated and untreated littermates. Drug-related effects of retardation of growth and defective development of the cerebellum and retina were found. The validity of therapy with either of these drugs in generalized herpetic infections is questioned because activity was minimal against the infecting agent even when the dosage of the drug was sufficient to produce serious defects in certain developing tissues.

Animals↗