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Biomedical subjects

B A Summers

Publications and source records attributed to B A Summers.

119 records · Page 7Linked to original sources
PubMed1982

Myoadenylate deaminase deficiency or not? Observations on two brothers with exercise-induced muscle pain.

This paper describes 2 brothers with increasingly severe exercise-induced muscle pain and stiffness, beginning in adolescence. Histochemical studies showed that myoadenylate deaminase activity was absent in the propositus, but present in his younger brother. Biochemical examination of muscle homogenates confirmed these findings, with enzyme activity approximately 60% of the mean control value in the younger sibling. Red cell adenylate deaminase activity was normal in both cases. The possible relationship between the clinical and biochemical findings in these patients is discussed.

AMP Deaminase↗
PubMed1982

Lymphocyte-mediated immune cytotoxicity in dogs infected with virulent canine distemper virus.

Immune lymphocyte-mediated cytotoxicity (ILMC) was evaluated in dogs after intranasal exposure to one of the following three virulent strains of canine distemper virus: Cornell A75/17, Ohio R252, and Snyder Hill. Cytotoxicity was tested with peripheral blood lymphocytes as effector cells and primary dog testicle cells that were matched for histocompatibility as target cells. A strong correlation was found between ILMC and the course of the infection. Dogs that succumbed to encephalitis with any of the strains had little or no ILMC, whereas dogs that recovered had the highest activity. In the intermediate range were dogs with a delayed or reduced ILMC which developed persistent but subclinical central nervous system infections. A significant difference in onset, peak, and duration of ILMC was observed in dogs infected with different strains of canine distemper virus. ILMC responses began at 14 days postinfection (p.i.), reached a peak at 21 to 28 days p.i., and returned to preinoculation levels by 63 to 70 days p.i. in canine distemper virus A75/17- and R252-infected dogs. In contrast, ILMC in canine distemper virus Snyder Hill-infected dogs began at 10 days p.i., peaked by 14 to 17 days p.i., and approached preinoculation levels by 28 days p.i. Antiviral immunity as measured by ILMC appears to be a critical factor in determining the outcome in canine distemper virus-infected hosts. Furthermore, for certain viral biotypes, a delayed ILMC response correlated with persistent infection of the central nervous system.

Animals↗
PubMed1982

Ultrastructure of the articular cartilage and synovium in the early stages of degenerative joint disease in canine hip joints.

A combined light and electron microscopic study recorded the developing degenerative changes in the hip joints of dogs with spontaneous joint disease. Synovium from joints with normal articular cartilage contained 33% type A and 64% type B cells. The 1st evidence of articular cartilage degeneration was loss of the surface amorphous layer and disruption of collagen fibrils. In the face of the earliest focal cartilage defects, the number of type A cells decreased (P less than 0.01) and remained low. Necrotic synoviocytes and synoviocytes of uncertain type increased as articular cartilage lesions progressed. The earliest pathologic changes in the synovium and the articular cartilage surface were evident only on ultrastructural examination.

Animals↗
PubMed1981

Laboratory diagnosis of Johne's disease: a potential source of error.

Gastrointestinal tract tissues from cattle with suspected clinical Johne's disease (JD), in which acid-fast bacilli were not identified in mucosal smears, were examined histopathologically. Twenty-two per cent were positive and 4 per cent were suggestive of JD. Failure to identify mycobacteria in mucosal smears appeared to result from the presence of mild, often focal mucosal lesions which contained relatively few bacilli. Ten of the 22 histopathologically positive cases had complement fixation titres for JD but several false-positive titres also occurred.

Animals↗
PubMed1981

Effect of beta-bungarotoxin on the release of endogenous amino aids from the sensorimotor cortex.

beta-Bungarotoxin, a snake neurotoxin purified from the venom of Bungarus multicinctus, caused a significant increase in the in vivo release of glutamate from the superfused sensorimotor cortex of awake animals. A smaller effect on GABA release was observed, but no change was detected in the release of six other amino acids measured. The effects on glutamate and GABA release were entirely blocked by tetrodotoxin (1 micrometer) and were reversible when the cortical tissue was washed with saline.

Amino Acids↗
PubMed1981

Early, asymptomatic stage of degenerative joint disease in canine hip joints.

The early stages of degenerative joint disease were investigated in coxofemoral joints from dogs with a hereditary predisposition to hip dysplasia. Alterations observed included mild nonsuppurative synovitis, increased volume of both synovial fluid and the ligamentum teres, and focal degenerative articular cartilage lesions. On radiologic examination, subluxation of the femoral head was seen, but only in the most severely affected joints. Synovial inflammation with increased synovial fluid and ligament volumes were indicators of early degenerative joint disease in dogs. These changes seemed to coincide with, or perhaps to precede, microscopic evidence for articular cartilage degeneration and occurred before radiologic abnormalities were detected.

Animals↗
PubMed1980

Studies on viral leukoencephalomyelitis and swayback in goats.

Six kid goats with CNS disease were studied by a variety of techniques. All had morphological evidence of Viral Leukoencephalomyelitis of Goats. (VLG) characterized by demyelinating encephalomyelitis and pneumonitis. Attempts were made to isolate a virus from 5 of these goats by direct culture of CNS and visceral tissues. Syncytial formation was found in some lung, spleen and bone marrow cultures but syncytia were found to be free of complete virus by electron microscopy. When newborn goats were inoculated with syncytia forming cells, a visna-like virus was found in bone marrow cultures of 1 goat 8 days post inoculation. Bone marrow cells from a twin goat 3 months after inoculation produced syncytia without complete virus. it is suggested that complete virus might be present in goats shortly after infection, while persisting in an incomplete form. Three of the 6 goats studied also had lesions of swayback with diffuse encephalomyelopathy and low liver copper levels. Control copper levels in kids with non-neurological disease were variable, occasionally being as low as swayback animals. The experience of others that swayback in the goat and low copper status are poorly correlated is confirmed. Discrepancies inherent in assaying formalin preserved tissues for copper are described.

Animals↗
PubMed1979

Early events in canine distemper demyelinating encephalomyelitis.

The early neuropathological development of demyelinating Canine Distemper Encephalomyelitis (CDE) was studied in SPF dogs. Neural tissues were examined up to 30 days post infection (PI). Three phases of activity were observed. The primary event (first observed 8 days PI) was a nonsuppurative encephalomyelitis associated with the initiation of central nervous system (CNS) infection by virus-laden lymphocytes. At 24 days PI noninflammatory demyelination occurred in well defined, subependymal foci. Cell fusion and syncytia formation accompanied this early demyelination. The third phase, found at day 30 PI in one dog showing signs of recovery, was a second wave of nonsuppurative inflammation. The initial encephalomyelitis was widely disseminated throughout the CNS but subsequent demyelination appeared to be initiated from within the ventricular system. Myelin was phagocytosed by endogeneous CNS macrophages often infected with Canine Distemper Virus (CDV). The possible importance of viral induced cell fusion as well as immune factors in the mechanism of demyelination are discussed.

Animals↗
PubMed1978

Possible initiation of viral encephalomyelitis in dogs by migrating lymphocytes infected with distemper virus.

The principal pathways by which viruses spread to the central nervous system (C.N.S.) are considered to be direct invasion along peripheral nerves or the haematogenous route. The latter is thought to involve passive transfer or active replication of virus in C.N.S. endothelial cells. In this study histological evidence of mild perivascular encephalomyelitis was found 8-10 days after infection of dogs with canine distemper virus (C.D.V.). C.D.V. antigen and viral nucleocapsids were detectable in the mononuclear cells infiltrating nervous tissue and C.D.V. was isolated from lymphoid tissue and buffy-coat cells. C.N.S. infection may thus be initiated by migrating virus-infected lymphocytes and this pathway may operate in other viral disorders of the C.N.S.

Animals↗