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Biomedical subjects

M J Hamilton

Publications and source records attributed to M J Hamilton.

At least 73 records · Page 4Linked to original sources
PubMed1981

Inheritance of a neuromuscular disorder of Labrador retriever dogs.

A heritable neuromuscular disorder of Labrador Retrievers was demonstrated to be transmitted by a simple autosomal recessive mode. The pathologic changes were confined to affected dogs, and a method for identifying the unaffected carrier was not found. The disorder was first recognized in 4 litters submitted for clinical examination, then was studied in 6 additional litters to determine the mode of inheritance. Although the disorder appeared widespread, its prevalence was thought to be low.

Animals↗
PubMed1981

Salivary composition, phenytoin ingestion and gingival overgrowth.

Unstimulated and stimulated whole and unstimulated and stimulated parotid saliva were collected from subjected in three groups: I, control; II, seizure subjects ingesting phenytoin and without gingival overgrowth; III, seizure subjects receiving phenytoin and with grades 1 and 2 gingival overgrowth. Unstimulated whole saliva was obtained from mentally retarded donors with grade 3 phenytoin associated gingival overgrowth. The samples were analyzed for protein, lysozyme, lactoperoxidase, lactoferrin and aggregation capacity towards Streptococcus sanguis. Differences occurred in the salivary composition of patients ingesting phenytoin. No deficiencies of flow rate, protein or the specific proteins were found in subjects ingesting phenytoin. Instead, the only changes in these parameters were greater concentrations or secretion rates. Several differences occurred only in subjects with gingival overgrowth. These latter differences were prominent in unstimulated whole saliva. The data demonstrate changes in the oral cavity environment of patients ingesting phenytoin. These differences, however, do not have an obvious relationship to development of phenytoin associated gingival overgrowth. Some of the salivary changes occurred in patients undergoing therapy for seizures both with phenytoin and with other drugs. Increased amounts of unstimulated whole saliva components likely are due to excess tissue rather than a phenytoin effect on salivary gland secretions. In addition, most of the changes in salivary composition would not be expected to produce an environment the encourages plaque accumulation.

Adult↗
PubMed1979

Salivary and plasma IgA of seizure subjects receiving phenytoin.

Immunoglobulin A, phenytoin, and protein were determined in plasma, unstimulated and stimulated whole saliva and stimulated and unstimulated parotid saliva from seizure subjects, aged 18 or more, who had ingested phenytoin for 1 year or more from controls. Patient subgroups with low plasma IgA and with gingival overgrowth were evaluated separately. Plasma and salivary phenytoin and ratios of salivary to plasma phenytoin concentrations corresponded to published reports. Plasma IgA was significantly decreased in the total patient group. However, salivary IgA expressed as the concentration or as the proportion of salivary protein, with one exception, was not significantly decreased in any type of saliva from the total patient group or subgroups. Significant phenytoin induced increases in salivary IgA were noted. IgA secretion rate by the parotid gland was significantly increased in the total patient group. This investigation does not indicate a deficiency of oral IgA from chronic phenytoin ingestion. Thus, it appears unlikely that decreased oral IgA with a consequent enhanced susceptibility to inflammation contributes to phenytoin associated gingival overgrowth.

Adolescent↗
PubMed1976

Polyacrylamide gel electrophoresis of twin and nontwin parotid salivary proteins.

Parotid salivary proteins from monozygotic twins, dizygotic twins, nontwin sibs, and unrelated male and female subjects of the same age range as the twins were separated by polyacrylamide gel slab electrophoresis at pH 9.0. Variability of the stained protein patterns increased in the order: monozygotic twins; dizygotic twins and nontwin sibs; unrelated subjects. It is concluded that genetic factors are the major contributors to variability of parotid salivary proteins among subjects.

Adolescent↗
PubMed1976

Muscular dystrophy of mink: a new animal model.

Muscular dystrophies comprise an important group of inherited disorders of man. Although the disease has been studied extensively, little is known about the underlying primary pathomechanisms. Consequently, treatment of patients is difficult and prognosis is poor. An animal model of muscular dystrophy is a useful research tool for approaching the basic problems of pathogenesis in muscle diseases. An inherited progressive muscular dystrophy of mink which resembles the amyotonic forms of human muscular dystrophy is currently under study. Clinically, the earliest sign is progressive muscular weakness and atrophy. Muscle enzyme activities in serum are usually elevated to pathologic levels. Urinary creatine/creatinine ratio is elevated. Pathologic changes are limited to skeletal muscle and are typical of those seen in amyotonic forms of human muscular dystrophy. These changes include variation in diameter size of muscle fibers, centralized nuclei, floccular and hyaline degeneration of scattered muscle fibers, increase in connective tissue in endomysial and perimysial areas, and regenerative attempts. Both type I and type II muscle fibers are involved in the disease process. Genetic studies indicate an autosomal recessive mode of inheritance. Although the primary defect in muscular dystrophy is traditionally thought to reside in skeletal muscle, recent studies have produced theories of primary involvement of other tissues and organ systems. These theories are presented and relationships to the traditional theory are discussed.

Animals↗
PubMedDate not supplied

The revised Sign and Symptom Check-List for HIV (SSC-HIVrev).

Symptom management for persons living with HIV/AIDS is recognized as an extremely important component of care management. This article reports on the continuing validation of the revised Sign and Symptom Check-List for Persons With HIV Disease (SSC-HIVrev). The initial validation study used a combined sample of 933 HIV-positive persons and concluded that the validity and reliability of the instrument were adequate to measure patients' self-report of HIV-related signs and symptoms. The revised scale includes items to measure gynecological-related symptoms and the impact of lipodystrophy (body fat redistribution) due to antiretroviral therapy on patients' symptom experience. The scale structure (factor analysis) and reliability estimates were recalculated in a new sample of 372 HIV-positive persons. Based on reviewing the clusters of items, factor loadings, reliability estimates, and clinical interpretability, an 11-factor solution was determined that explained 73.3% of the variance. Of the retained factors, 4 had eigenvalues less than 1, yet they explained significant amounts of variance in the rotated sums of squares loading (5.0%, 4.3%, 4.3%, and 3.6%, respectively), the reliability estimates were good, and the factors had clinical meaning. The revised scale (SSC-HIVrev) has three parts: Part 1 consists of 45 items that clustered into 11 factor scores along with a total score, with reliability estimates ranging from .76 to .91; Part 2 consists of 19 HIV-related symptoms that do not cluster into factor scores but may be of interest from a clinical perspective; and Part 3 consists of 8 items related to gynecological symptoms for women. These 8 items were submitted to a principal components factor analysis with varimax rotation (n = 118 HIV-positive women), and a 1-factor solution explained 71.8% of the variance, with a reliability estimate of .94. The psychometric properties of the SSC-HIVrev are presented.

Adult↗
PubMedDate not supplied

Inheritance of congenital myasthenia gravis in smooth fox terrier dogs.

The phenotypes with respect to congenital myasthenia gravis of 132 smooth fox terrier dogs from 25 matings were analyzed. These included both prospective and retrospective matings. It was determined that congenital myasthenia gravis in the smooth fox terrier dog breed is inherited in an autosomal recessive manner with complete penetrance. We propose the symbol mg for the gene for congenital myasthenia gravis in the smooth fox terrier. Attempts to maintain live affected dogs to adulthood were unsuccessful and it is concluded that this is a lethal trait.

Animals↗