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Biomedical subjects

D W Hayden

Publications and source records attributed to D W Hayden.

At least 55 records · Page 3Linked to original sources
PubMed1985

High dose intravenous glucose tolerance test and serum insulin and glucagon levels in diabetic and non-diabetic cats: relationships to insular amyloidosis.

The high dose intravenous glucose tolerance test and concurrent immunoreactive serum insulin and glucagon levels were measured and the results related to the presence or absence of pancreatic insular amyloid in 16 cats, seven of which were known to be diabetic. Control values for all parameters were established using seven additional clinicopathologically normal cats. Nine of the 16 cats had normal fasting blood glucose levels (less than 120 mg/dl) and impaired glucose tolerance. These cats had attenuated (3/9) or normal (6/9) 0 to 5 minute glucose-stimulated insulin secretion, rising 45 to 60 minute insulin secretion (7/9), low mean insulin/glucose ratio, and normal mean serum glucagon. Three of the nine cats with impaired glucose tolerance had insular amyloidosis. These three cats had significantly higher mean blood glucose levels during the glucose tolerance test than did cats with impaired glucose tolerance and no insular amyloid deposits. Also, these three cats accounted for three of the four longest glucose disappearance one-half times (T1/2S), three of the four lowest glucose disappearance coefficients, and three of the four lowest 0 to 5 minute insulin responses. The seven diabetic cats (fasting blood glucose levels greater than 120 mg/dl) had either low to low normal (6/7) or above normal (1/7) fasting insulin levels, no insulin response to intravenous glucose stimulation (6/7), and elevated mean serum glucagon levels. Insular amyloid was present in six of the seven diabetic cats. Three diabetic cats with marked insular amyloid deposits had glucose disappearance T1/2 and K (coefficient) values, serum insulin levels, serum glucagon levels, and insulin/glucose ratios which were not significantly different from the other three diabetic cats with slight to moderate insular amyloidosis. These results confirm a strong association between the occurrence, but not the extent of insular amyloidosis and diabetes mellitus in adult diabetic cats, although amyloid replacement of pancreatic islets does not appear to be the primary diabetogenic event. Rather, these results appear to be consistent with our hypothesis that insular amyloid deposition is a morphologic marker of primary B-cell dysfunction that is basic to the pathogenesis of the diabetic condition, and is reflected clinically by impaired glucose tolerance.

Amyloidosis↗
PubMed1985

Feline insular amyloid: immunohistochemical and immunochemical evidence that the amyloid is insulin-related.

Utilizing islet amyloid-laden pancreatic tissues from six diabetic cats, we demonstrated substantial immunoreactivity (peroxidase-antiperoxidase technique) of the islet amyloid with antiserum to a B chain-rich insulin fraction, but no reactivity with antisera to insulin, glucagon, or somatostatin. Islet amyloid was purified from two cats and a protein unique to the diabetic and islet amyloid-laden cats was separated by sodium dodecyl sulfate polyacrylamide gel electrophoresis. Immunoreactivity of this protein with antiserum to the B chain-rich insulin fraction was also shown by immunoblotting. Attempts to obtain the amino acid composition of the purified unique protein (represented by a single 25,000 dalton band on gel electrophoresis) were not successful because the amount of protein was too small. These results provide important additional evidence that an insulin-related protein is involved in the formation of islet amyloid. Our study also shows that the diabetic cat provides several advantages for the continued study of the etiopathogenic relationship of islet amyloid and diabetes mellitus.

Amino Acids↗
PubMed1985

Pancreatic ganglioneuronal amyloid. Occurrence in diabetic cats with islet amyloidosis.

Amyloid in pancreatic ganglia and nerves (ganglioneuronal amyloid) was demonstrated in 4 of 8 diabetic cats with islet amyloid deposits. Eighteen nondiabetic cats (including 4 with islet amyloid) did not have detectable amyloid in pancreatic nerves or ganglia. Ganglioneuronal amyloid had staining characteristics identical to those previously reported for islet amyloid, including 1) congophilia, 2) resistance to oxidation by KMnO4, 3) immunoreactivity (PAP technique) with antiserum to a B-chain-rich insulin fraction, and 4) no reactivity with antisera to insulin, glucagon, or somatostatin. Nonneuronal cells with insulin, glucagon, and somatostatin immunoreactivity were seen in many pancreatic ganglia and nerves; and in a few instances, B cells were found near ganglioneuronal amyloid deposits. The premise that these ganglioneuronal amyloid deposits (like islet amyloid) are insulin-related is supported by their immunoreactivity with antiserum to B-chain-rich insulin and the demonstration of B cells in pancreatic ganglia and nerves.

Amyloid↗
PubMed1985

Pathophysiologic effects of experimentally induced Fascioloides magna infection in sheep.

The pathophysiologic responses of 13 sheep inoculated orally with 100 metacercariae of Fascioloides magna were monitored for 4 months after inoculation. There were no differences in weight gains between these and a number of noninoculated control sheep throughout the experiment. Complete blood cell counts showed an increase only in the absolute number of eosinophils. Serum preparations (2 times a week) from 7 inoculated and 7 noninoculated sheep did not identify any significant changes in alkaline phosphatase, aspartate aminotransferase, alanine aminotransferase, and gamma-glutamyl transferase activities. There were no changes in total bilirubin, BUN, creatinine, inorganic phosphorus, calcium, albumin, chloride, potassium, and sodium values. Four months after they were inoculated, all sheep were necropsied, and flukes were recovered. Gross lesions attributed to fluke migration were found in the liver and portal lymph nodes, diaphragm, lungs, kidneys, and spleen. Microscopically, liver lesions in inoculated sheep occurred in the portal areas, veins, and Glisson's capsule and were characterized by both active and chronic forms of inflammation. Abundant infiltrates of eosinophils and plasma cells often marked the portal areas. Endophlebitis, with or without thrombosis, was the predominate vascular lesion. The flukes recovered varied greatly in size (6.5 to 48.0-mm long) and demonstrated some sexual development, but none was sexually mature.

Animals↗
PubMed1984

Lipogranulomatous lymphangitis in canine intestinal lymphangiectasia.

Lipogranulomatous lymphangitis of the intestine occurred in four dogs with intestinal lymphangiectasia. All four presented with chronic diarrhea; three had ascites and two had hypoalbuminemia. Lipogranulomas appeared in lymphatics, often at the point of mesenteric attachment, of small intestine, ileum, or ileum and colon. Mesenteric lymphatics were obstructed and villous lacteals were distended. Mesenteric lymph nodes of one dog contained large lipid spaces and that same animal had a solitary subcapsular lipogranuloma of the liver. This disorder is one of several that result in protein-losing enteropathy in dogs.

Animals↗
PubMed1984

Progesterone receptors in feline mammary adenocarcinomas.

Estradiol and progesterone receptors were measured in tumor cytosols from 3 intact and 4 neutered female cats with spontaneously occurring mammary adenocarcinomas. Serum from 2 of the intact cats which had been in estrus 4 and 4 to 6 weeks before tumor excision contained progesterone concentrations of 16.2 and 2.2 ng/ml, respectively; serum progesterone in the other cats was less than 2 ng/ml. Estradiol receptors were not detected in any cytosols. Progesterone receptors were detected in all of the cytosols, in concentrations ranging from 4.0 to 11.7 (mean = 7.2) fmol/mg of protein. Scatchard plot analysis of tumor cytosol from an 8th cat with mammary adenocarcinoma revealed presence of high affinity progesterone binding with a dissociation constant (Kd) of 3.47 nM. Tumor receptor content could not be correlated with stage of the estrous cycle nor with whether the cat was intact or neutered.

Adenocarcinoma↗
PubMed1984

Influence of reduced protein diets on morbidity, mortality, and renal function in dogs with induced chronic renal failure.

The influence of a maintenance diet containing 44.4% dry weight protein and 2 reduced protein diets containing 8.2% and 17.2% dry weight protein on morbidity, mortality, and renal function of dogs with induced chronic renal failure was studied for 40 weeks. The diets differed in mineral and electrolyte composition in addition to differences in protein, carbohydrate, and fat content. Dogs fed the 44.4% protein diet had a higher mortality (6 of 11) than did dogs fed the 8.2% (1 of 6) or 17.2% (0 of 6) protein diets. Dogs fed the 44.4% protein diet died of uremic complications. An occlusive portal vein thrombus caused death of the nonsurvivor fed the 8.2% protein diet. Clinical signs of uremia were detected only in nonsurvivors fed the 44.4% protein diet. Surviving dogs fed the maintenance diet were less active and had poorer hair than did dogs fed reduced protein diets. Inulin clearance rate and urinary protein excretion were lower in most dogs fed reduced protein diets than in dogs fed the maintenance diet. Despite the greater decrease in renal function, serum urea nitrogen concentrations were markedly lower in dogs fed the 8.2% and 17.2% protein diets than in dogs fed the 44.4% protein diet. Seemingly, the reduced protein renal failure diets were of benefit in preventing or reducing morbidity and mortality associated with the uremic syndrome and in reducing serum urea nitrogen concentrations as compared with that of the higher protein diet. The potential benefits of dietary protein restriction in dogs with chronic renal failure prevailed over potential adverse affects of excessive protein consumption.

Animals↗
PubMed1983

Effects of modified protein diets in dogs with chronic renal failure.

A maintenance diet containing 44.4% dry weight protein and 2 reduced protein diets containing 17.2% and 8.2% dry weight protein were studied in dogs with induced chronic renal failure to determine effects on their (1) clinical status, (2) renal function, (3) electrolyte and acid-base balance, (4) divalent ion balance, (5) nutritional status, (6) hematologic status, and (7) hemostasis. A cross-over design of feeding was utilized so that the effect of diet could be studied in each dog at a known state of renal dysfunction and so that reversibility of effects could be determined. The inulin clearance rate was higher when the 44.4% protein diet was fed than when the 8.2% or 17.2% protein diets were fed. However, consumption of lower protein diets was associated with greater physical activity and reduction in serum urea nitrogen concentrations, compared with consumption of the 44.4% protein maintenance diet. Varying degrees of hyperchloremic metabolic acidosis developed in dogs fed the 8.2% and 17.2% protein diets. Reduced total serum protein and albumin concentrations, and hypercholesterolemia developed in dogs fed the 8.2% protein diet. All effects were reversible after diets were changed. It was concluded that diet-induced alterations in renal function associated with moderate dietary protein restriction did not adversely effect clinical and biochemical status of dogs with renal failure. It was unclear whether the clinical and biochemical changes observed with more severe protein restriction resulted from diet-induced changes in renal function.

Animal Feed↗
PubMed1983

Ultrastructure of feline mammary hypertrophy.

The ultrastructure of feline mammary hypertrophy was studied in a five-month-old female which had aborted recently, a ten-year-old female which was one month postestrus, and a four-year-old progestin-treated neutered male. Morphologic comparisons were made to normal mammary tissue from a one-year-old female cat. Hypertrophied mammary tissue had the same cell types and spatial relationships as did the normal gland. Major differences included a more highly developed duct system composed of metabolically active cells which often were arranged in multiple cell layers, and periductular stroma with increased fibroblasts and vascularization. Hypertrophied epithelial cells were characterized generally by smooth-contoured nuclear membranes, more evenly dispersed heterochromatin, prominent nucleoli, increased polyribosomes, and elongated mitochondria. Secretory activity was developed significantly only in the cat that had aborted recently. Modifications in myoepithelial cells included: more evenly dispersed nuclear heterochromatin, thicker bundles of cytoplasmic filaments, more straight plasma membranes along the basal lamina, and elongated hemidesmosomes. Multilayering of the basal lamina was accentuated. Stromal fibroblasts had nuclear heterochromatin distributed similarly to that of epithelial and myoepithelial cells, and increased rough endoplasmic reticulum. Myoepithelial cells did not contribute to the increased stromal cellularity. No significant ultrastructural differences were noted between mammary hypertrophy in young, old, and progestin-treated cats.

Abortion, Veterinary↗
PubMed1983

Influence of modified protein diets on the nutritional status of dogs with induced chronic renal failure.

The influence of a canine maintenance diet containing 44.4% protein (dry weight) and 2 reduced-protein renal-failure diets containing 8.2% or 17.2% protein (dry weight) on the nutritional status of dogs with induced chronic renal failure was evaluated for 40 weeks. Nutritional status was assessed by changes in serially determined body weights, hindlimb circumferences, serum protein concentrations, complete blood cell counts, serum cholesterol concentrations, glucose tolerance tests, and blood glucose concentrations. Evidence of suboptimum nutritional status was observed in dogs fed the 8.2% or 44.4% protein diets, but not in dogs fed the 17.2% protein diet. Only a small reduction in hindlimb circumference developed in dogs fed the 17.2% protein diet. Reduced body weight and hindlimb circumference and normocytic normochromic anemia developed in dogs fed the 44.4% protein diet. Reduced body weight and hindlimb circumference, hypoalbuminemia, hypoproteinemia, hypercholesterolemia, and normocytic normochromic anemia developed in dogs fed the 8.2% protein diet. A beneficial effect of moderate dietary protein restriction (17.2% protein) on the nutritional status of the dogs was observed. In contrast, excessive intake or restriction of dietary protein was associated with detrimental effects.

Animals↗
PubMed1982

Influence of modified protein diets on electrolyte, acid base, and divalent ion balance in dogs with experimentally induced chronic renal failure.

The influence of a maintenance diet (44.4% dry weight protein) and 2 reduced protein diets (8.2 and 17.2% dry weight protein) on acid-base, electrolyte, and divalent ion balance of dogs with experimentally induced chronic renal failure was studied for 40 weeks. Moderate-to-severe hyperchloremic metabolic acidosis developed in dogs fed the 8.2% protein diet, but not in the groups fed the 17.2% and 44.4% protein diets. Serum sodium and potassium concentrations were not altered significantly by the diets. Mean serum calcium concentrations increased significantly in the 3 groups after renal failure was induced; however, serum calcium concentration generally did not exceed the normal range. Dogs fed reduced protein diets had smaller serum magnesium and phosphorus concentrations than did the dogs fed the maintenance diet. Microscopic alterations in bone morphology consistent with canine renal osteodystrophy were not detected after 40 weeks of renal failure in dogs fed the 17.2% and 44.4% protein diets. Examination of skull radiographs of the dogs prepared 40 weeks after renal failure was induced revealed that the lamina dura dentes were visible in all groups. It was concluded that the 8.2% protein diet was of therapeutic benefit in management of altered divalent ion metabolism in dogs with chronic renal failure. However, the high frequency of concomitant acidosis indicated that appropriate alkalinization therapy should be included with this diet. Adverse effects of feeding the 17.2% protein diet were not detected. However, it was less effective than the 8.2% protein diet in minimizing development of hypermagnesemia and skeletal changes consistent with renal osteodystrophy.

Acid-Base Equilibrium↗
PubMed1981

Feline insular amyloid: histochemical distinction from secondary systemic amyloid.

Amyloid in islets of Langerhans from 48 domestic cats, one human, one non-human primate, and one raccoon was compared with secondary systemic amyloid from three domestic cats, one dog, one human, and one cow to determine affinity for Congo red dye after treatment of paraffin-embedded tissue sections with potassium permanganate and dilute sulfuric acid. Insular amyloid from all six species was resistant to pretreatment with potassium permanganate, i.e., affinity for Congo red was retained, whereas secondary systemic amyloid from all species was sensitive to the potassium permanganate pretreatment. Other stains did not distinguish between insular and secondary systemic amyloid. The potassium permanganate-Congo red staining procedure thus can be used to differentiate insular from secondary systemic amyloid in the cat and other species. The results also indicate that insular amyloid and secondary systemic amyloid are of different chemical composition and pathogenesis.

Adrenal Glands↗
PubMed1981

Feline insular amyloid: incidence in adult cats with no clinicopathologic evidence of overt diabetes mellitus.

Pancreatic tissues from 93 adult domestic cats with no clinicopathologic evidence of overt diabetes mellitus were examined for islet amyloid. Amyloid deposits were found in the pancreatic islets of 44 cats. Approximately one-third of these deposits were not seen with HE, but subsequently were identified with Congo red stain. The proportion of islets with amyloid, the intra-islet location of amyloid, and the amount of amyloid in individual islets also were characterized. In this select population of adult cats, the presence or absence of islet amyloid was not linked significantly (p = greater than 0.05) to age, breed, sex or primary anatomic diagnosis. Results of this study indicate that: the incidence of islet amyloid in cats is higher than previously recognized; as in man, islet amyloid can occur in cats without concurrent overt diabetes mellitus; and islet amyloid should not be considered pathognomonic for diabetes mellitus.

Amyloid↗
PubMed1981

Feline insular amyloid: association with diabetes mellitus.

Of 31 domestic cats with diabetes mellitus, 20 (65%) had amyloid deposits in their pancreatic islets (i.e., insular amyloid). The incidence of insular amyloidosis (p = 0.34) was not significantly different between diabetic and age-matched, non-diabetic cats from our previous study. Diabetic cats, however, had a significantly higher mean percentage of islets with amyloid (p = less than .005) and a significantly higher mean percentage of islets with abundant amyloid deposits (p = less than .005) than did non-diabetic cats. These results suggest that insular amyloidosis and diabetes are causally related and are not simply concurrent diseases associated with aging. Although the specific relationship of insular amyloidosis to the pathogenesis of diabetes mellitus was not determined, a functional islet cell abnormality probably precedes the diabetic state and the deposition of insular amyloid.

Amyloidosis↗
PubMed1981

Feline insular amyloid. Ultrastructural evidence for intracellular formation by nonendocrine cells.

The objective of this ultrastructural study in cats was to investigate the early relationship of pancreatic islet cells with amyloid deposits. We used pancreatic islets from six domestic cats with minimal and apparently early amyloid deposits. Although amyloid deposits were occasionally arranged perpendicularly to beta cells, and rarely within deep invaginations of these cells, there was no consistent or convincing relationship of extracellular fibrils to any of the major islet stricted to, nongranulated perivascular cells in islets from two of the cats. Small and relatively electron-dense amyloid inclusions contained compact arrays of parallel fibrils. Larger inclusions were more electron-lucent and had loosely and randomly arranged fibrils. Indirect evidence strongly suggested that the fibril-laden inclusions resulted from intracellular production rather than from phagocytosis. The definitive identity of these amyloid-containing cells was not determined. However, these calls lacked secretory granules specific for known islet endocrine cell types and were topographically always located in close proximity to capillaries. The results of our study, therefore, do not directly support a morphologic association of amyloid fibril formation with typical islet endocrine cells. Our results do, however, draw attention to the possibility that nonendocrine cells play a key role in the pathogenesis of insular amyloidosis in the cat.

Amyloid↗
PubMed1981

Feline mammary hypertrophy/fibroadenoma complex: clinical and hormonal aspects.

Abnormal mammary enlargement, characterized microscopically by hyperplasia of both epithelial and mesenchymal tissues, was studied in 26 cats which were mostly young, sexually intact females. Clinicopathologic data indicated that mammary hypertrophy was likely progesterone-dependent. Administration of progestins preceded this condition in 5 cats, 4 of which were neutered. Serum progesterone concentrations (6.7 ng/ml) were increased in 1 of the 3 cats tested. Estrogen receptors were not found in the cytosols or nuclei of mammary tissues in the 2 cats studied. However, there were convincing 4S [3H]progesterone or 5S [3H]R5020 binding peaks which were suppressible by nonlabeled progestins. Progesterone receptors were measured at 14.9 and 8.6 fm/mg of protein, respectively. The apparent influence of progesterone, whether present as exogenous therapy in the male or female or as endogenous steroid of ovarian origin, has thus been demonstrated directly and indirectly in cats with mammary hypertrophy.

Adenofibroma↗