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Biomedical subjects

P F Jezyk

Publications and source records attributed to P F Jezyk.

At least 37 records · Page 2Linked to original sources
PubMed1983

Spinal cord compression and hindlimb paresis in cats with mucopolysaccharidosis VI.

Six cats with mucopolysaccharidosis VI had hindlimb paresis and other clinical signs associated with compression of the thoracolumbar spinal cord. In 5 cats, the neurologic abnormality progressed over 2 to 4 weeks to loss of thoracolumbar spinal cord function. In 1 cat, the hindlimb paresis remained stable for 18 months. In the cats with progressive worsening of hindlimb function, the abnormality was caused by compression of the spinal cord from proliferation of bony tissue in the thoracolumbar region. In all affected cats, the compression occurred from T12 to L2. In 1 cat, an attempt to relieve the clinical signs by surgery was unsuccessful.

Animals↗
PubMed1983

Potentiation of the canine lymphocyte blastogenic response by indomethacin.

Cultivation of normal canine peripheral blood lymphocytes in the presence of indomethacin, a potent prostaglandin synthetase inhibitor, produced a consistent potentiation of their in vitro response to mitogenic stimulation as compared to cultures without indomethacin. The enhancing effect of indomethacin increased with decreasing concentrations of mitogens. Indomethacin had to be added to the cultures during the first four hours for the potentiating effect to be observed. These data suggest that prostaglandins may play an important role in the regulation of the dog's immune response.

Animals↗
PubMed1983

The pathology of the feline model of mucopolysaccharidosis I.

Five cats with feline alpha-L-iduronidase-deficient mucopolysaccharidosis were studied. Membrane-bound cytoplasmic inclusions were present in central nervous system neurons, hepatocytes, chondrocytes, vascular and splenic smooth muscle cells, bone marrow leukocytes, and fibroblasts of the skin, eye, and cardiac valves. The lesions in these cats closely resemble those described in human patients with mucopolysaccharidosis I H (Hurler syndrome).

Animals↗
PubMed1980

Myocarditis induced by parvoviral infection in weanling pups in the United States.

In a nationwide survey from January 1978 through September 1979, acute parvovirus-induced myocarditis was identified in 76 of 147 (52%) pups in 19 litters. The affected pups were from 12 states. Birth of all pups registered with the American Kennel Club during this period increased during the spring months, peaking in May, which was correlated in 4 to 8 weeks with the greatest number of cases in the study. Serologic data available for 4 dams, for 6 of their surviving pups, and for 3 contact pups indicated that all had been exposed to parvovirus. In 2 kennels, cases of acute myocarditis were preceded within 2 months by cases of severe gastroenteritis in older litters on the same premises.

Animals↗
PubMed1980

Pseudoachondroplastic dysplasia in miniature poodles: clinical, radiologic, and pathologic features.

The clinical, radiologic, and pathologic features of pseudoachondroplastic dysplasia were studied in 13 affected Miniature Poodles. The disease became evident when pups were about 3 weeks old. Normal-appearing and affected pups were in the same litter, and both sexes were affected. Abnormal locomotion with abducted hindlimbs and flattened rib cages were accompanied by short, bent limbs and enlarged joints. Radiographically, areas of stippling and patchy densities were evident in the epiphyses. Histologically, these densities were identified as areas of bone associated with retarded ossification. After growth is completed, the epiphyses, ossify, but the bones are shortened and deformed. General health appears normal, except for restricted locomotion due to secondary arthritis and difficult breathing in dogs with a deformed thorax.

Achondroplasia↗
PubMed1980

The pathology of the feline model of mucopolysaccharidosis VI.

Three cats with feline arylsulfatase-B--deficient mucopolysaccharidosis were studied by light and transmission electron microscopy. Membrane-bound cytoplasmic inclusions were present in hepatocytes, bone marrow granulocytes, vascular smooth muscle cells, and fibroblasts in skin, cornea, and cardiac valves. Central nervous system lesions were restricted to mild ventricular dilatation, perithelial cell vacuolation, and, in one animal, cord compression by vertebral exostoses. The lesions in these cats closely resembled those described in human patients with mucopolysaccharidosis VI (Maroteaux-Lamy syndrome).

Animals↗
PubMed1979

Mucopolysaccharidosis in a domestic short-haired cat--a disease distinct from that seen in the Siamese cat.

A 10-month-old male domestic short-haired cat was examined because of progressive lameness, a broad face with depressed nasal bridge, small ears, corneal clouding, and multiple bone dysplasia. The cat excreted excessive amounts of glycosaminoglycan (a component of connective tissue) in its urine and had evidence of lysosomal storage of glycosaminoglycans in fibroblasts and neurons. Activity of alpha-L-iduronidase, a lysosomal enzyme involved in glycosaminoglycan degradation, was deficient in cultured fibroblasts and leukocytes. The mucopolysaccharidosis was distinct from that seen in Siamese cats in terms of the pathologic changes and the specific enzyme deficiency.

Animals↗
PubMed1979

Myocarditis of probable viral origin in pups of weaning age.

Myocarditis in 4- to 8-week-old pups from 10 litters was characterized by sudden death. Histopathologic findings included mononuclear cellular infiltration and interstitial fibrosis in the myocardium of the left ventricle. Basophilic intranuclear inclusion bodies were seen in myocardial cells in 4 of 18 pups necropsied, suggesting a viral origin of the disease. Other pathologic changes were variable, but all were attributable to cardiac failure. Of 8 surviving pups examined, 7 had evidence of cardiac failure, including pulmonary edema, cardiomegaly, and cardiac arrhythmias.

Animals↗
PubMed1979

Free amino acids in the plasma and urine of dogs from birth to senescence.

Plasma and urinary amino acid concentrations were determined from a cross-sectional sample of dogs of all ages. Reference or base line values for these components were established for five different age groups. A general decrease in urinary excretion of amino acids for each gram of creatinine was found during the developmental period. This decrease was not correlated to changes in plasma concentrations, which varied for the individual amino acids. The decrease did appear to be related to the functional maturation of the kidney. Several methylated basic amino acids were identified in the urine. Of these, NG, NG- and NG,N'G-dimethylarginine, and trimethyllysine had not been previously reported as constituents of dig urine, but are major components of the urinary amino acids, expecially in newborn animals. The 3-methylhistidine is also excreted in large amounts by dogs and measurable quantities of this compound appear in the plasma. These findings suggest an active metabolic function for methylated amino acids in the dog.

Aging↗