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Biomedical subjects

D F Patterson

Publications and source records attributed to D F Patterson.

At least 73 records · Page 4Linked to original sources
PubMed1983

Short-limbed dwarfism and ocular defects in the Samoyed dog.

A syndrome of short-limbed dwarfism and ocular defects was found in Samoyed dogs. The most prominent abnormalities were small stature and valgus deformity of the carpi. Radiographic evidence of retarded growth at the distal ulnar physis was apparent by 12 weeks of age. Ocular defects included cataracts and retinal detachment. Family studies and limited breeding experiments were consistent with an autosomal recessive mode of inheritance.

Animals↗
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

Defects in collagen fibrillogenesis causing hyperextensible, fragile skin in dogs.

Two unrelated mixed-breed dogs were donated for studies of their fragile, hyperextensible skin. Breeding of these dogs to bitches with normal skin showed that half of their male and female offspring also had fragile, hyperextensible skin, indicating that the defect was transmitted as an autosomal dominant trait in both dogs. Electron microscopy showed distinct abnormalities in the packing of collagen into fibrils and fibers in affected skin. These packing defects in dermal collagen were identical in related dogs, but were slightly different in unrelated animals. A clinical test, the skin extensibility index, was used to quantitate the extensibility of affected and unaffected skin. This index ranged from 8% to 15% in normal dogs and from 17% to 25% in newborn pups and adult dogs with collagen packing defects. The tensile strength of dorsolateral thoracic skin of affected pups was only 5% to 10% of that of matched specimens of paired littermates. The hyperextensibility and fragility of skin were the only clinical signs, but radiographic and microradiographic studies revealed subclinical involvement of bone.

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↗
PubMed1981

Evolution of the electrocardiogram in young dogs during the first 12 weeks of life.

In 36 normal pups the evolution of the ECG during the first 12 weeks was studied. Sixteen pups were randomly selected, healthy pups; 20 were normal littermates from dog families with congenital heart disease. The direction of P, QRS, and T vectors was determined, and the modal QRS axis (vector) was constructed from lead I and AVF in the frontal, from lead I and V10 in the transverse, and from lead AVF and V10 in the sagittal plane. Except for the T wave directly after birth, no marked difference in the ECG evolution between the two groups was found. After birth the modal QRS vector was almost exclusively directed to the right. The modal QRS vectors in the first, second, and third weeks were significantly different from each other. By the twelfth week all vectors were directed to the left and the majority was oriented leftward and caudally. In the serial ECG tracings the change from right ventricular to left ventricular dominance was seen to be progressive. The R/S ratio in the left chest leads increased from less than 1.0 at week 1 to a multiple of 1.0 after the sixth week. The changes occurring in scaler ECG's were mirrored in VCG's recorded in selected pups.

Aging↗
PubMed1981

Evolution of the electrocardiogram in young dogs with congenital heart disease leading to right ventricular hypertrophy.

In 18 pups obtained from a breeding colony established for investigation of hereditary heart disease, ECG's were recorded shortly after birth. The ECG's, as well as clinical examinations, were repeated weekly in pups surviving the first week of life. The QRS modal axis was constructed in the frontal, transverse and sagittal planes. Cardiac catheterization was performed on all pups reaching the age of 8 to 12 weeks. VCG's were taken on selected pups. All dogs were necropsied terminally. In pups with severe pulmonic stenosis a pathological right ventricular hypertrophy was recognized immediately after birth. No evolution to a left ventricular dominance occurred in the serial tracings. Pups with milder grades of right ventricular outflow obstruction showed a normal evolution pattern or some minor deviations from the normal QRS complex evolution. In pups with patent ductus arteriosus (PDA) and left-to-right shunt, there was no difference from the normal ECG evolution within the first 12 weeks of life, except for some increase in amplitude. Two cases of PDA and right-to-left shunt were not different from the "physiologic right ventricular hypertrophy" at birth, but developed a severe right ventricular hypertrophy pattern within the first 12 weeks of life without any clinical signs of a left-to-right shunting within the period.

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↗