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Biomedical subjects

B J Cooper

Publications and source records attributed to B J Cooper.

At least 55 records · Page 3Linked to original sources
PubMed1986

Mice heterozygous for the mld mutation have intermediate levels of myelin basic protein mRNA and its translation products.

Myelin-deficiency (mld) is an autosomal recessive mutation in mice exhibiting a severe deficit in the synthesis of myelin basic protein (MBP). In order to understand the mechanisms involved in the regulation of MBP synthesis in the mld mutation, we examined the amount of MBP and MBP-specific mRNA in control, heterozygous and homozygous mld brains. In vitro translation of poly(A)+ RNA in a cell-free system, in situ hybridization, and filter hybridization with a radiolabelled probe pMBP-1 after dot or Northern blotting were used in this study. The levels of MBP and MBP-specific mRNA were very low but detectable in mld homozygotes, and intermediate in heterozygotes. MBP specific mRNA from mutants, and its translation products, were of normal size. These results show that the mld mutation is expressed co-dominantly in heterozygotes and affects a cis-acting regulatory element controlling the MBP gene.

Animals↗
PubMed1985

Pathogenesis of canine parvovirus enteritis: the importance of viremia.

The clinical signs, hematologic changes, serum and fecal virus titers, specific antibody production and the occurrence of histologic lesions were studied in 22 nine-week-old seronegative beagle dogs inoculated by the oral and intravenous route with canine parvovirus. Approximately 30% of the dogs had clinical signs of pyrexia, depression, vomiting, and diarrhea irrespective of the route of inoculation. Events in the dogs inoculated intravenously preceded those in dogs inoculated orally by approximately two days. Only one dog died. Lymphopenia was the most consistent hematologic change. Viremia always preceded the initiation of fecal virus shedding. Viral titers in the serum and feces were significantly greater in symptomatic dogs compared to asymptomatic dogs. Termination of the plasma viremia coincided with the onset of the humoral immune response, but viremia persisted one day longer in symptomatic dogs. The severity of lymphoid tissue and intestinal infection, assessed by tissue immunofluorescence and histology, was also greater in symptomatic dogs. The severity of intestinal disease was highly correlated with the magnitude and duration of viremia.

Animals↗
PubMed1985

Canine laryngeal rhabdomyoma.

Three canine laryngeal tumors were diagnosed as oncocytomas by light microscopy, but were determined to be rhabdomyomas following ultrastructural and immunocytochemical examination. Tumors consisted of large eosinophilic cells interspersed with smaller dark cells. Large tumor cells had a granular, intensely eosinophilic cytoplasm. Scattered through the tumors were a few elongated cells with cytoplasmic cross striations and multiple nuclei. Tumor cells from all three dogs contained numerous mitochondria and bundles of myofibrils with electron-dense Z-lines typical of striated muscle cells. Intracellular myoglobin and desmin were detected in the tumors by immunocytochemistry. Comparisons are made with a previous report of canine laryngeal oncocytomas.

Adenoma↗
PubMed1985

Pathogenesis of canine parvovirus enteritis: sequential virus distribution and passive immunization studies.

After oral inoculation, the sequential distribution of canine parvovirus was studied in 14 nine-week-old seronegative beagle dogs. Two or three dogs were necropsied on days 1 through 6 after inoculation. Tissues were collected for virus isolation, immunofluorescence testing, and light microscopy. Virus was isolated from, and fluorescent cells were seen in the tonsil, retropharyngeal and mesenteric lymph nodes one and two days after inoculation. Virus infection of systemic and intestinal lymphoid tissues occurred as early as three days after inoculation and was associated with viremia. Intestinal epithelial infection was first seen four days after oral inoculation. All dogs were viremic before intestinal epithelial infection was found. Fecal virus excretion first occurred four days after oral virus inoculation. Intestinal virus infection and lesions became progressively more severe between four and six days after inoculation. The severity of intestinal lesions was variable and related to the severity of systemic lymphoid tissue lesions and the magnitude and duration of viremia. Four littermates of virus-infected dogs were passively immunized against canine parvovirus with convalescent canine serum 24 hours after oral virus inoculation. Neither clinical signs, lymphopenia, nor fecal virus excretion occurred in passively immunized dogs. Intestinal epithelial infection was not demonstrable by immunofluorescence testing when passively immunized dogs were necropsied four, five, and six days after virus inoculation.

Animals↗
PubMed1984

Defective Schwann cell function in canine inherited hypertrophic neuropathy.

Segments of peripheral nerve from dogs with canine inherited hypertrophic neuropathy ( CIHN ) were transplanted to the transected sciatic nerve of immuno incompetent mice. Regenerating mouse axons penetrated the grafts and were myelinated by dog Schwann cells. In grafts collected 3 or more months after transplantation, filamentous or granular material, identical to that occurring in nerves of affected dogs, accumulated in myelinating Schwann cells. Demyelinated fibers were only rarely found in grafted segments of affected nerve. Neither filamentous accumulations nor demyelination were observed in grafts of control canine nerve. These results indicate that CIHN is associated with a defect in Schwann cell function, and the abnormal accumulations of filaments suggest that the defect may be in the cytoskeleton. The rarity of demyelination in grafts suggests that some factor in addition to the Schwann cell defect is required to precipitate myelin destruction.

Animals↗
PubMed1984

Myelination in the CNS of mld mutant mice: comparison between composition and structure.

Myelination was studied between 15 and 135 days postnatally in the brain and optic nerves of myelin deficient (mld) mutant mice. Between 15 and 30 days almost no myelin basic protein (MBP) could be detected in mld myelin. The axons were loosely wrapped by membranes which only fused at the extracellular sites forming the intraperiod line. At this age the major dense line was absent. At 25-30 days, purified myelin contained extremely high 2',3'-cyclic nucleotide 3'-phosphodiesterase (CNP) (EC 3.1.4.37) activities which could be related to the redundant paranodal-like structures observed at this age in mld CNS. Therefore, it can be suggested that CNP is probably localized in such paranodal loops. After the active phase of myelin deposition was completed in controls, mld mutants showed important increases of MBP concentration in myelin with the concomitant appearance of the major electron dense line and better compaction of the myelin lamellae. The yield of myelin increased from 5 to 14% of control values during the period of 30 to 135 days. Since the recovery phase occurred at the time when myelin lipid synthesizing enzymes are at low residual activities, the myelin deficit could only be partially corrected. This study indicates that there is a delay of MBP synthesis in mld mice and the decrease of other myelin proteins could be secondary to the assumed primary defect involving MBP.

2',3'-Cyclic-Nucleotide Phosphodiesterases↗
PubMed1984

Experimental viral myocarditis: parvoviral infection of neonatal pups.

Myocarditis was produced in seronegative five-day-old pups by oral and by intraperitoneal inoculation of canine parvovirus. The disease was subclinical. Histologic lesions were compatible with, but less extensive than, those seen in naturally occurring canine parvoviral myocarditis. In pups necropsied 23 days after inoculation, scattered cardiac myocytes contained intranuclear inclusion bodies, and virus-infected myocytes were demonstrated by immunofluorescence. Degeneration and loss of cardiac myocytes usually was not associated with a cellular infiltrate. At 51 days after inoculation, the myocardium contained an extensive lymphocytic infiltrate which was sometimes associated with fragmented myocytes, and was often contiguous with areas of interstitial fibrosis. At 108 days after inoculation, inflammatory lesions had regressed, and there were multifocal areas of myocardial fibrosis.

Animals↗
PubMed1984

Canine inherited hypertrophic neuropathy: clinical and electrodiagnostic studies.

Clinical and electrodiagnostic features of acute and chronic canine-inherited hypertrophic neuropathy were studied in 20 affected dogs. The age of onset was consistently between 7.5 and 10 weeks of age. Affected pups had rapidly developing limb weakness accompanied by muscle hypotonia and hyporeflexia. There was no clinical evidence of cranial nerve dysfunction. Pups that did not develop limb contractures later regained some strength and became clinically stable for long periods, although they always remained weak. Progressive slowing of nerve conduction velocities occurred during the development of clinical signs of limb weakness. Temporal dispersion of evoked muscle action potentials was present in more chronically affected dogs. Transient spontaneous activity was present in muscles of affected dogs examined by electromyography. An autosomal recessive mode of inheritance was supported by the results of breeding studies.

Animals↗
PubMed1983

Hypoglycemic seizures in a Shetland pony.

A 12-year-old, 195 kg Shetland pony broodmare had eight seizures between May 29 and August 7, 1979. Plasma glucose levels during three of these seizures were markedly depressed (16, 18 and 19 mg/100 ml). Serum insulin levels were elevated during two of the seizures (86.0 and 97.7 microU/ml). Although a fasting hypoglycemia was not demonstrated, plasma glucose values during a normal day were abnormal; a plasma glucose level of 42 mg/100 ml was noted eight hours post-feeding. Serum insulin values obtained during an oral glucose tolerance test and intravenous glucagon tolerance test were consistent with organic hyperinsulinism of a pancreatic origin. An intravenous glucose tolerance test and a twenty-four hour fast failed to differentiate between the subject and control ponies with respect to plasma glucose and serum insulin levels. Gross and microscopic pathological evaluation of the pancreas revealed a single 2.0 mm adenoma of pancreatic islet cell origin and hyperplasia of islet cells, predominantly beta cells. This is the first report of hypoglycemic seizures in a horse as a result of a pancreatic neoplasm and associated hyperinsulinism.

Adenoma, Islet Cell↗
PubMed1982

Canine intestinal carcinoids.

Intestinal carcinoids were diagnosed in three aged dogs. Two of the neoplasms occurred in the rectum and one at the cecocolic junction. Judged by histologic criteria, all three carcinoids were considered to be malignant. Amyloid was present in both rectal tumors. In each tumor the diagnosis was confirmed by the finding of electron-dense intracytoplasmic secretory granules in the neoplastic cells.

Amyloid↗
PubMed1982

Ultrastructural evaluation of adenocarcinomas derived from apocrine glands of the anal sac associated with hypercalcemia in dogs.

Adenocarcinomas derived from apocrine glands of the anal sac and associated with persistent hypercalcemia in dogs were composed of tumor cells with numerous profiles of rough endoplasmic reticulum, clusters of free ribosomes, and a prominent Golgi apparatus. Neoplastic cells contained microtubules, microfilaments, tonofibrils, and had two types of electron-dense granules. Large lysosomelike dense bodies ranged from 0.6 to 2.2 microns in diameter and had a poorly delineated limiting membrane. Small granules (150-400 nm in diameter) had a sharply delineated limiting membrane with a narrow submembranous space and a homogeneous dense core. These smaller granules usually were located near the apexes of neoplastic cells, whereas the larger granules were situated near the base of cells. Apocrine cells in glands of the anal sac from control dogs that were in the secretory phase were columnar and had large dilated profiles of rough endoplasmic reticulum. Membranes of the endoplasmic reticulum fused with the plasmalemma and appeared to secrete their product directly into the lumens of acini, characteristic of merocrine secretion. Apical blebs of electron-lucent cytoplasm pinched off from nonneoplastic aprocine cells and were released into glandular lumens. Similar electron-lucent cytoplasmic blebs were present at the apexes of tumor cells. Myoepithelial cells were present between the epithelial cells and basement membrane in normal apocrine glands and were absent in neoplasms derived from these glands. Identification of the contents of the secretory-like granules in tumor cells and characterization of the hypercalcemic factor in the plasma or tumor tissue from dogs with this syndrome will help explain the pathogenesis of hypercalcemia associated with malignancy in animals and man.

Adenocarcinoma↗
PubMed1981

Canine inherited hypertrophic neuropathy.

A recessively inherited hypertrophic neuropathy was discovered in Tibetan Mastiff dogs. Affected pups developed a generalized weakness with hyporeflexia shortly after weaning. Diagnostic findings in 10-18-week-old pups included: moderate to severe reduction in nerve conduction velocities, infrequent denervation potentials, and inconstant elevation in CSF protein. Light- and electron-microscopic studies of peripheral nerves and roots revealed widespread demyelination and primitive onion bulb formation with relatively little degeneration of axons. Myelin changes often were most striking in the cytoplasmic regions of the sheaths and consisted of separations at the major dense lines, anomalous incisure patterns, and marked filamentous accumulations in the inner spirals and adaxonal cytoplasm. The results of these initial studies suggest an inborn defect in the Schwann cell's ability to form or maintain a stable myelin sheath.

Animals↗
PubMed1981

Hypercalcemia associated with an adenocarcinoma derived from the apocrine glands of the anal sac.

Clinical, gross, and light microscopic findings are described for 36 dogs, 33 females and three males, with adenocarcinomas arising from the apocrine glands of the anal sac. All tumors had light microscopic features of malignancy and 22 of 23 metastasized to iliac and lumbar lymph nodes. Nine dogs had disseminated metastases, but bone metastases were found in only one dog. Differentiated neoplasms formed secretory acini and tubules lined by tall columnar or cuboidal epithelium. Most neoplasms were histologically bimorphic, with glandular areas and solid nests. Parathyroid glands were atrophic. Hypercalcemia (mean = 16.1 mg/dl) was present in 20 of 22 dogs (90%) and hypophosphatemia (mean = 3.2 mg/dl) in 12 of 17 (71%). Remission of hypercalcemia by tumor ablation and recurrence of hypercalcemia with tumor regrowth suggested that the tumor produced a substance that caused hypercalcemia. This unique clinicopathologic syndrome is characterized by hypercalcemia in old, predominantly female, dogs with an adenocarcinoma arising from the apocrine glands of the anal sac.

Adenocarcinoma↗
PubMed1980

Canine laryngeal oncocytomas.

Solitary, protruding tumors were found in the wall of the larynx in three adult dogs with clinical upper respiratory obstruction. They were composed of cells with abundant granular acidophilic cytoplasm, the granularity caused by an unusually large number of mitochondria. The lesions were considered to be neoplasms arising from oncocytes as described in man. Oncocytomas have not been reported previously in domestic animals.

Adenoma↗
PubMed1979

Canine viral enteritis. I. Status report on corona- and parvo-like viral enteritides.

This report attempts to provide the most recent information on salient features of two newly recognized viral enteritides of dogs. The viruses, a corona-like virus and canine parvo-like virus, are distinct but the disease manifestations in a particular outbreak often are similar. Laboratory study is therefore required. The parvoviral infection generally is more severe, with leukopenia (relative lymphopenia) a most prominent feature. Knowledge of the pathogenesis, epizootiology and the host's immune response is fragmentary at the present time, but research now in progress will doubtless expand knowledge of both diseases and of the viruses that cause them.

Animals↗