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Biomedical subjects

D F Patterson

Publications and source records attributed to D F Patterson.

At least 55 records · Page 3Linked to original sources
PubMed1989

Ultrastructural and immunohistochemical changes of the extracellular matrix during intimal cushion formation in the ductus arteriosus of the dog.

The changes of the intima during subendothelial edema formation were studied by ultrastructural and immunohistochemical methods in the ductus arteriosus (DA) of the dog. Subendothelial edema formation is the first stage in the development of intimal cushions in the DA. Development of intimal cushions is a physiological process preceding normal spontaneous closure after birth. The material consisted of normal canine DA and DA from a strain of dogs with hereditary persistence of the DA (PDA). In the normal DA intimal thickening starts with separation of the endothelial cells from the internal elastic lamina by a widened subendothelial region (SR). Initially this SR is, at the ultrastructural level, composed of granular and amorphous material. Collagen fibrils and elastin are not detected. During the formation of the SR a shedding of the basal lamina underneath the endothelial cells is observed. In the PDA the endothelial cells remain attached to the internal elastic lamina. The topography of the extracellular matrix components collagen type I, III, IV, fibronectin and laminin were studied immunohistochemically. These are important factors in the adherence of the endothelial cells to the underlying intimal layers. Laminin and collagen type I are diffusely present before but absent after detachment of the endothelial cells. Collagen type III, barely detectable before detachment, becomes visible underneath the detached cells. No changes are observed in the distribution of collagen type IV and fibronectin. Comparison of the normal DA with the various types of the PDA strain and controls allowed the conclusion that the observed changes in the extracellular matrix components were confined to those parts of the vessel wall that showed development of intimal thickening. The observed alterations both at the ultrastructural and immunohistochemical level do not explain the initiation of the process of endothelial cell detachment, which have been shown in a previous study to be related to an increase in hyaluronic acid.

Animals↗
PubMed1989

X-linked severe combined immunodeficiency in the dog.

This study documents the occurrence of a form of X-linked severe combined immunodeficiency (SCID) in the dog with clinical, immunologic, and pathologic features similar to those of X-linked SCID with B cells in man. The disease in the dog is characterized by growth retardation and increased susceptibility to bacterial and viral infections in young pups. Affected pups have all died or were euthanatized by 5 months with signs of canine distemper, infectious hepatitis, or bacterial pneumonia. Laboratory findings include normal numbers of circulating B lymphocytes and normal concentrations of serum IgM, but low to absent concentrations of serum IgG and IgA, indicating a defect in the terminal differentiation of IgG and IgA B cells into immunoglobulin-secreting plasma cells. This is supported by the failure of peripheral lymphocytes to produce IgG or IgA plaque-forming cells in response to polyclonal activation. There are low-to-normal numbers of circulating T cells, but a severely depressed blastogenic response to T cell mitogens. Postmortem findings include thymic dysplasia and hypoplasia of lymphoid tissue. Family studies and breeding experiments are consistent with an X-linked recessive mode of inheritance.

Animals↗
PubMed1989

Müllerian inhibiting substance is present in testes of dogs with persistent müllerian duct syndrome.

Breeding studies in a strain of miniature schnauzer dogs with Persistent Müllerian Duct Syndrome (PMDS) indicate this syndrome is inherited as an autosomal recessive trait, as it is in man. Testes of neonatal dogs affected with PMDS and normal male littermates were examined for Müllerian Inhibiting Substance (MIS) production by immunohistochemistry and bioassay. MIS immunoactivity was detected in Sertoli cells of normal and affected pups using an avidin-biotin complex-enhanced method. Rat embryonic Müllerian ducts regressed when cocultured with testis fragments of both normal and affected pups in a graded organ culture bioassay, demonstrating that the MIS produced was bioactive. These findings indicate that Müllerian duct persistence in affected dogs is not due to a mutation in the structural gene for MIS, but rather, by inference, to a failure of response to MIS at the receptor level.

Animals↗
PubMed1989

Distribution of prostacyclin synthase, 6-keto-prostaglandin F1 alpha, and 15-hydroxy-prostaglandin dehydrogenase in the normal and persistent ductus arteriosus of the dog.

The presence of prostacyclin synthase (PGI2 synthase), 6-keto-prostaglandin F1 alpha (6k-PGF1 alpha), and the stable hydrolysis product of prostacyclin (PGI2), prostaglandin E2 (PGE2), as well as the activity of 15-hydroxy-prostaglandin dehydrogenase (PGDH) were studied in the aorta, pulmonary artery, the normal ductus arteriosus (DA), and persistent DA (PDA) of the dog using histochemical and immunohistochemical techniques. The normal DA is characterized by the development of intimal thickening, a process that does not occur in the persistent DA. Distribution of PGI2 synthase was identical in the aorta, pulmonary artery, and persistent DA. In these vessels endothelial cells contained higher levels of PGI2 synthase as compared with medial smooth muscle cells. In the normal DA, levels of PGI2 synthase were clearly higher in smooth muscle cells at the sites of intimal thickening than at other sites. Distribution of 6-keto-PGF1 alpha resembled the localization of PGI2 synthase. Presence of PGE2 and activity of PGDH could not be demonstrated. The results demonstrated existence of a clear relationship between ductal morphology and the presence of PGI2 synthase. This finding suggests a more important role for PGI2 in regulating ductal patency than has heretofore been appreciated. It was assumed that the role of PGI2 in regulating ductal patency is, at birth, at least overruled by the constrictive effect of the cytochrome P450 mono-oxygenase mechanism. It is still possible to attribute a role to PGI2 in the regulation of cushion formation. Once smooth muscle cell activity has been enhanced by the presence of a glycosaminoglycan rich environment, increase in PGI2 may produce a concurrent inhibition of smooth muscle cell growth.

6-Ketoprostaglandin F1 alpha↗
PubMed1988

XX sex reversal in the American cocker spaniel dog: phenotypic expression and inheritance.

This study was conducted to define the range of phenotypic expression and mode of inheritance of XX sex reversal in the cocker spaniel dog. Breeding experiments produced F1, F1BC, and F2 generations in which 29 XX true hermaphrodites and 3 XX males were defined by chromosome constitution, serial histologic sections of the gonads, and examination of the internal and external genitalia. In XX true hermaphrodites, the most common combination of gonads was bilateral ovotestes, followed by ovotestis and ovary, then ovotestis and testis. The amount of testicular tissue in the two gonads was closely correlated within each true hermaphrodite. The distribution of testicular tissue within ovotestes of true hermaphrodites was consistent with the hypothesis that testicular differentiation is initiated in the center of the gonad and spreads outward. XX males had bilateral aspermatogenic testes and the internal ducts and external genitalia were more masculinized than in true hermaphrodites. Results of breeding experiments are consistent with autosomal recessive inheritance, the affected phenotype being expressed only in dogs with an XX chromosome constitution. The phenotypic expression and mode of inheritance of this disorder is compared to XX sex reversal in humans and other animals.

Animals↗
PubMed1988

Insulin-like growth factor I levels in proportionate dogs, chondrodystrophic dogs and in giant dogs.

Plasma insulin-like growth factor I concentrations from proportionate, chondrodystrophic and giant breeds were evaluated and compared with body size. IGF-I plasma concentrations were 91.2 +/- 10.9 micrograms/l in Keeshounds (proportionate dog), 122.6 +/- 25.4 micrograms/l in Bassethounds (chondrodystrophic dog) and 280 +/- 22.8 micrograms/l in German Shepherds (proportionate dog). The highest IGF-I level (389.6 +/- 24.2 micrograms/l) was found in the New Foundland, a giant breed (mean +/- SEM). The mean body weight was 11.8 +/- 0.4 kg in Keeshounds, 15.4 +/- 1.4 kg in Bassethounds, 32 +/- 1.5 kg in German Shepherds, and 45.6 +/- 1.7 kg in New Foundlands (mean +/- SEM). Body weight and plasma IGF-I concentration were significantly correlated (y (IGF-I) = -7.43 + 8.7 X (body weight); P less than 0.0001.

Animals↗
PubMed1988

Hyaluronic acid accumulation and endothelial cell detachment in intimal thickening of the vessel wall. The normal and genetically defective ductus arteriosus.

The closing ductus arteriosus (DA) was studied as a model for the development of intimal thickening of vessel walls using ultrastructural and immunohistochemical techniques. The material consisted of DA from neonatal dogs of three types: normal beagles, DA-defective pups from a line of mixed poodles with a genetic defect in the closure of the DA leading to persistent ductus arteriosus (PDA line), and normal litter-mates of DA-defective pups in the PDA line. The DA of the normal litter-mates of DA-defective pups did not differ from those of normal beagles. In the DA of normal beagles and normal PDA-line pups, closure is preceded by intimal thickening characterized by formation of a widened subendothelial region (SR), detachment of endothelial cells, invagination of endothelial cells, and migration of smooth muscle cells into the SR. It was observed that immediately before and after endothelial cell detachment, there was an increase in hyaluronic acid (HA) in the SR and inner media. In the DA-defective pups, the increase in hyaluronic acid failed to occur and there was no intimal thickening. The SR failed to expand, endothelium remained attached to the internal elastic membrane, and there was no invagination of endothelium or migration of smooth muscle cells. It is hypothesized that the increased synthesis of HA is an important early event leading to intimal thickening in the normal DA and perhaps to abnormal intimal thickening of other vessels. By its hygroscopic properties, HA may be directly involved in the formation of a wide SR, inducing endothelial cell detachment and favoring smooth muscle cell migration. In affected pups of the PDA line, there is a genetically-determined "block" in the normal process of intimal thickening at or before the initiation of increased HA synthesis.

Animals↗
PubMed1987

Müllerian inhibiting substance in sex-reversed dogs.

In normal males, Müllerian Inhibiting Substance (MIS), produced by testes during an embryonic critical period, is thought to induce regression of the Müllerian duct system, including the oviducts and uterus. In XX sex-reversed dogs, an apparent contradiction has been reported: The uterus persists in the presence of testes or ovotestes. The objective of this study is to determine whether testes of XX male and ovotestes of true hermaphrodite dogs produce MIS, and to examine the anatomy of Müllerian duct derivatives of affected dogs for evidence of regression. Gonadal samples were tested for MIS activity in a bioassay. The mean MIS activity score of XX males was similar to that of normal XY males and significantly greater than that of normal XX females. The mean MIS activity score of XX true hermaphrodites was intermediate between normal XX females and XY males. Within the true hermaphrodite group, ovotestes in which the proportion of testicular tissue was greater than or equal to 1/2 had higher MIS scores than those in which the proportion of testicular tissue was less than 1/2. XX males had a well-developed epididymis adjacent to each testis, but no oviducts. In true hermaphrodites, the oviduct regressed and an epididymis was present when greater than or equal to 1/2 of the adjacent ovotestis was testicular, and MIS activity in that gonad was high. A few ovotestes with intermediate levels of MIS activity had both an oviduct and an epididymis. Regression of the oviductal portion of the Müllerian duct system was positively correlated to the amount of testicular tissue and the MIS activity of the gonad, as would be predicted by Jost's original hypothesis.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1986

Lethal acrodermatitis in bull terriers.

A lethal syndrome characterized clinically by growth retardation, progressive acrodermatitis, chronic pyoderma and paronychia, diarrhea, pneumonia, and abnormal behavior was observed in 17 related Bull Terrier pups. Median survival time was 7 months. Laboratory evaluation revealed non-degenerative neutrophilia, consistently low activities of serum alkaline phosphatase and alanine transaminase, and frequently, hypercholesterolemia. Lymphocyte blastogenic responses were decreased and there was dysgammaglobulinemia in pups in which quantitative studies of immunoglobulins were made. The mean of plasma zinc concentrations in 5 affected pups was significantly lower than the mean of age- and breed-matched controls. Pathologic findings included parakeratosis, hyperkeratosis, and superficial bacterial infections of the skin. There was severe reduction of lymphocytes in T-lymphocyte areas of lymphoid tissue. Bronchopneumonia and dilatation of the cerebral ventricles were found in most affected pups. Family studies indicated that the syndrome is inherited as an autosomal recessive trait. In spite of its similarities to lethal trait A46 in Black Pied Danish cattle and acrodermatitis enteropathica in man, oral or parenteral treatment with zinc failed to ameliorate the clinical signs of the syndrome.

Acrodermatitis↗
PubMed1985

Histologic studies on normal and persistent ductus arteriosus in the dog.

The process of anatomic closure of the ductus arteriosus was studied at the ultrastructural level in 15 normal beagles (age 0 hour to 13 days) and in 18 specimens from a strain of dogs with hereditary persistent ductus arteriosus (age 4 hours to 27 days). Normal ductal closure takes place from the pulmonary artery to the aortic end. It is accompanied by a series of histologic changes: 1) separation of the endothelial cells from the internal elastic lamina resulting in a wide region of subendothelial edema; 2) ingrowth and infolding of endothelial cells and migration of undifferentiated smooth muscle cells from the inner media into the subendothelial region; 3) apposition of endothelial cells bordering the lumen; and 4) degenerative changes. In persistent ductus arteriosus, these changes do not occur. The endothelial cells remain closely adhered to the internal elastic lamina and the underlying media is abnormal in structure. In the case of partial persistent ductus arteriosus (ductus diverticulum), both the normal and the abnormal type of wall are found in a single ductus arteriosus. The histologic features of the normal and the persistent ductus arteriosus in the dog resemble those of the normal and the persistent ductus arteriosus in humans, suggesting a similar pathogenesis.

Animals↗
PubMed1984

Inherited XX sex reversal in the cocker spaniel dog.

Nine XX true hermaphrodites and two XX males were discovered in a family of American cocker spaniels. The true hermaphrodites were partially-masculinized females with ovotestes; the XX males had malformed male external genitalia and cryptorchid aspermatogenic testes. Wolffian and Mullerian duct derivatives were present in both true hermaphrodites and XX males. All four sires of sex-reversed dogs were normal XY males; five of the dams were anatomically normal females and one was an XX true hermaphrodite. A second true hermaphrodite reproduced as a female, producing anatomically normal offspring. All matings that produced sex-reversed offspring were consanguineous. Matings of the parents of sex-reversed cocker spaniels to normal beagles with no family history of intersexuality produced only normal offspring. Examination of G-banded karyotypes of the affected animals, their parents, and siblings, revealed no structural anomalies of the chromosomes that were consistently associated with sex-reversal. In assays for serologically-detectable H-Y antigen, the group of XX true hermaphrodites and the group of XX males had mean levels of the antigen not significantly different from that in normal male controls. Female parents of sex-reversed dogs and some of their female siblings were typed H-Y antigen positive, but the mean level of the antigen in this group was less than that of normal male controls. It is proposed that XX sex reversal in cocker spaniels is due to a mutant gene which when homozygous in females, results in a level of H-Y antigen similar to that found in normal males and the gonads develop as ovotestes or testes. When the gene is heterozygous in females, the level of serologically-detectable H-Y antigen is lower than that found in normal males and the gonads develop as normal ovaries. The persistence of Mullerian structures in the presence of testicular tissue suggests that Mullerian inhibiting substance is deficient or ineffective in its action in this condition.

Animals↗
PubMed1984

Beta-glucuronidase deficiency in a dog: a model of human mucopolysaccharidosis VII.

This report describes a third mucopolysaccharidosis in animals: canine mucopolysaccharidosis VII. The affected dog was the offspring of a father-daughter mating. Weakness in the rear legs was evident at 8 weeks of age and became progressively worse. He had a large head, a shortened maxilla, and corneal granularities. Most joints were extremely lax, easily subluxated, with joint capsules that were swollen and fluctuant. The dog was alert and had apparently normal pain perception. At 13 months of age, there was radiographic evidence of extensive skeletal disease including bilateral femoral head luxation, abnormalities in the shape and density of the carpal and tarsal bones, radiolucent lesions of the epiphyseal regions of most long bones, and cervical vertebral dysplasia and platyspondylia. The electrophoretic pattern of precipitated glycosaminoglycans indicated a predominance of chondroitin sulfate. The animal died suddenly from gastric dilatation. There was generalized hepatomegaly, thickening of the atrioventricular heart valves, and generalized polyarthropathy. Vacuolated cytoplasm was observed in hepatocytes, keratocytes, fibroblasts, chondrocytes and cells of the synovial membrane, retinal pigment epithelium, and cardiac valves. Neurons had cytoplasmic vacuoles. Electron microscopy demonstrated membrane-bound cytoplasmic inclusions in polymorphonuclear leukocytes, hepatocytes, synovium, heart valves and spleen. The activities of 12 lysosomal hydrolases were determined in liver from the affected and control dogs: beta-glucuronidase (EC 3.2.1.31), beta-hexosaminidases A and B (EC 3.2.1.30), alpha-hexosaminidase (EC 3.2.1.-), alpha-L-iduronidase (EC 3.2.1.76), alpha-galactosidase A (EC 3.2.1.22), beta-galactosidase (EC 3.2.1.23), arylsulfatases A and B (EC 3.1.6.1), acid alpha-mannosidase (EC 3.2.1.24), acid beta-mannosidase (EC 3.2.1.25), and N-acetyl-D-galactosamine-6-sulfate sulfatase (EC 3.1.6.-).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1984

Insulin-like growth factor I in the dog: a study in different dog breeds and in dogs with growth hormone elevation.

A radioimmunoassay (RIA) devised for the measurement of human insulin-like growth factor I (IGF I) was employed for the measurement of canine IGF I. Canine IGF I was extracted from plasma specimens by gel chromatography. Columns were eluted with 1 M acetic acid and the fractions representing the 55 to 85% bed volume were pooled, lyophilized and reconstituted with assay buffer. Serial dilutions of canine IGF I from both normal and acromegalic dogs when added to the RIA system gave a similar displacement pattern of human [125I]IGF I as the one obtained by the addition of unlabelled human IGF I. The dose-response curve obtained by canine IGF I paralleled the one obtained by human IGF I. Logit-log transformation and least squares fitting resulted in straight line fitting of the standard curve between 0.039 and 5 ng IGF I added per tube. The within-assay coefficient of variation (CV) was 16.7% and the between-assay CV was 21.8%. Plasma IGF I concentrations in normal dogs appeared to be a function of body size. The concentrations were 36 +/- 27 ng/ml in Cocker Spaniels, 87 +/- 33 ng/ml in Beagles, 117 +/- 34 ng/ml in Keeshonds, and 280 +/- 23 ng/ml in German Shepherds (mean +/- SEM). The mean IGF I level in a group of dogs with growth hormone (GH) elevation was 700 +/- 90 ng/ml. Though this group of dogs comprised both small and large dogs, the mean IGF I level significantly differed from the one found in German Shepherds, the largest breed studied (P less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Acromegaly↗
PubMed1984

Body size parallels insulin-like growth factor I levels but not growth hormone secretory capacity.

The relationships between body size, growth hormone (GH) secretory capacity and circulating insulin-like growth factor I (IGF I) levels were studied in genetically-determined subgroups of disparate size within one breed of dogs, the Poodle. Standard (large) Poodles exhibited six times the mean plasma IGF I concentration found in Toy Poodles. The mean IGF I level found in Standard Poodles significantly differed from the one found in Miniature and Toy Poodles (P less than 0.001). The correlation between circulating IGF I levels and body size was found to be highly significant (P less than 0.001; r = 0.88). All dogs secreted similar, normal amounts of GH in response to clonidine administration. The results show that body weight is correlated with IGF I levels rather than with the GH secretory capacity, thus providing indirect evidence for IGF I as an important in vivo growth-promoting principle.

Animals↗