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Biomedical subjects

G Stewart

Publications and source records attributed to G Stewart.

At least 145 records · Page 8Linked to original sources
PubMed1984

Pretibial myxoedema.

This paper reviews the clinical, endocrine and lymphatic status of 6 patients with pretibial myxoedema. The lymphatics were studied to determine whether they were involved in the pathogenesis of the disease. The main lymph trunks were normal although there was occasionally some collateral flow and some of the lymph nodes had small irregular filling defects. These changes suggest compression of the lymphatics by the myxomatous material and the deposition of mucinous material in the lymph nodes. There was no evidence of a primary lymphatic abnormality.

Female↗
PubMed1984

Abnormal fibrinolysis: the cause of lipodermatosclerosis or "chronic cellulitis" in patients with primary lymphedema.

Blood fibrinolytic activity was measured in 20 patients with primary lymphedema, ten without and ten with skin changes usually attributed to "chronic cellulitis". The patients with abnormal skin showed reduced fibrinolytic activity, a finding previously described in patients with chronic venous disease and lipodermatosclerosis . It is postulated that changes of "chronic cellulitis" are identical to lipodermatosclerosis and are produced by a similar mechanism, namely reduced fibrinolysis.

Adult↗
PubMed1981

Galvanic vestibular tests in the assessment of coma and brain death.

Galvanic stimulation over the mastoid process elicits oculovestibular responses that provide a measure of brainstem function. The equipment is simple and is available in most neurodiagnostic laboratories. This type of test provides an advantage over caloric testing in the presence of external and middle ear disease and basal skull fracture and can be a useful adjunct in the evaluation of coma and brain death.

Adult↗
PubMed1979

Mental health treatment and referral practices of clergy and physician caregivers.

Consistent with previous literature, the results of a detailed survey mailed to clergy and physicians from a community known for its longstanding, excellent mental health system indicated extensive treatment and referral of mental health problems by clergy and physicians. Clergy and physicians, though, displayed very limited knowledge of mental health services and personnel, particularly innovative approaches and workers. Receiving mental health training was identified as a key factor, particularly for physicians, in terms of knowledge of services and personnel, referral to a mental health center, and treatment of serious mental health problems. Strategies were, therefore, outlined to provide more accurate information to this natural treatment and referral system.

Clergy↗
PubMed1979

Sialidosis type 1: cherry red spot-myoclonus syndrome with sialidase deficiency and altered electrophoretic mobilities of some enzymes known to be glycoproteins. 1. Clinical findings.

A family is described with three affected brothers, two of whom were examined, born to consanguineous parent, who in early adult life began to experience ataxia, intention myoclonus, and progressive visual failure. The brothers examined had cherry red spots at the maculae and cataracts. They were of normal intelligence. The intention myoclonus responded partially to treatment with clonazepam and pheneturide, but not to 5-hydroxytryptophan in combination with carbidopa or to sodium valproate. Studies in one patient showed the excretion of large quantities of sialylated oligosaccharides in the urine. Both patients showed deficient sialidase activity in their cultured fibroblasts. Further studies on cultured skin fibroblasts revealed increased electrophoretic mobility of six glycoprotein enzymes that was returned approximately to normal by treatment with sialidase. The clinical and biochemical findings indicate that these patients are further cases of the newly described condition sialidosis type 1.

Adult↗
PubMed1979

Sialidosis type 1: cherry red spot-myoclonus syndrome with sialidase deficiency and altered electrophoretic mobility of some enzymes known to be glycoproteins. II. Enzymes studies.

Observations have been made on two brothers who had progressive ataxia, intention myoclonus and visual failure starting early in the third decade of life. Their parents were consanguineous. The brothers showed bilateral cherry red spots at the maculae and bilateral perinuclear cataracts; their intelligence was preserved. Urine was found to contain large amounts of sialylated oligosaccharides; cultured skin fibroblasts showed deficiency of the enzyme sialidase (neuraminidase). Studies on leucocytes and cultured skin fibroblasts showed aberrant electrophoretic mobilities of six enzymes all of which are known to be glycoproteins, and this has been attributed to excessive amounts of sialic acid on the enzyme molecules. The clinical features together with the biochemical findings indicate that these are further cases of the newly described condition Sialidosis Type 1 and it is suggested that the electrophoretic findings might be typical of the condition.

Adult↗
PubMed1977

Reduction of ischemic myocardial damage in the dog by lidocaine infusion.

The effects of lidocaine infusion on the ultrastructural damage induced in cardiac muscle by normothermic cardiopulmonary bypass were assessed in 15 dogs. Six dogs received no medication other than sodium pentobarbital (25 mg/kg, intravenously) while 9 dogs were treated with lidocaine after anesthesia. Lidocaine was given as a 2-mg/kg loading dose 10 minutes prior to ischemic arrest and a 2-mg/min continuous infusion during the entire experimental period. Biopsy samples of the left ventricular apex were taken 15 and 45 minutes after the start of ischemic arrest and 5 minutes after resumption of coronary blood flow. Biopsy samples were also obtained from 4 animals after thoracotomy to serve as controls for experimental procedures. Myocardial ultrastructure in the 4 control animals was comparable to that reported by other investigators. Five of 6 of the nontreated dogs and 8 of 9 lidocaine-treated dogs survived the entire period of ischemia and 5 minutes of coronary reperfusion. However, the extent of ultrastructural damage varied considerably between the two groups. In the experimental dogs receiving no lidocaine, mitochondria were swollen, cristae were absent, the mitochondrial matrix was cleared, and sarcomeres were disrupted. Myelin figures and contraction bands were also observed. None of the surviving lidocaine-treated animals had ultrastructural changes comparable to the worst ones in nontreated dogs. Damage was limited to some swelling of mitochondria with focal clearing of matrix. Most cristae remained intact. There were no myelin figures and few contraction bands. The results suggest that lidocaine protects the integrity of ischemic myocardium. It is suggested that this protection resulted from stabilization of plasma and/or mitochondrial membranes. (Am J Pathol 87:399-414, 1977).

Animals↗
PubMed1975

Morphological features in a neutral lipid storage disease.

The morphological changes in a patient with a generalized storage disease characterized by the intracellular deposition of neutral lipid are described. There is widespread accumulation of lipid in the cytoplasm of many cells and in occasional nuclei. Diagnosis may be facilitated by the recognition of clear vacuoles in the cytoplasm of granulocytes in blood films. In jejunal biopsies vacuolation of the epithelial cells may simulate the appearances of a-betalipoproteinaemia. The lipid inclusions consist largely of normal triglycerides and are free in the cytoplasm, unassociated with any organelle. The biochemical basis of the lesions is uncertain. Although there are lipoprotein abnormalities the primary defect appears to be intrinsic to the cell and may involve either a defective cytoplasmic lipase or an impaired uptake and utilization of fatty acids by mitochondria.

Adult↗