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Biomedical subjects

G A Gresham

Publications and source records attributed to G A Gresham.

16 recordsLinked to original sources
PubMed1991

The ageing of bruises: a review and study of the colour changes with time.

This work was inspired by a recent case of child abuse where the question of the age of the bruises on the body was raised. The first part of this paper reviews published work on bruises. It illustrates the paucity of work in this field and the absence of studies of the colour changes in bruises of human skin with time. The second part of this paper consists of our own study of the appearance of bruises. The aim was to identify the colour changes which occur in bruises and over what time-scale, in order to determine whether bruises can be aged by appearance. A total of 369 photographs were obtained of bruises aged less than 6 h and up to 21 days old, in 89 subjects aged 10-100 years. It was found that the development of a yellow colour was the most significant change (subjects aged less than 65, P less than 0.001; subjects aged greater than or equal to 65 years, P less than 0.001). The development of a yellow colour occurred significantly faster in subjects aged less than 65 years. (P less than 0.001). The appearance of a blue and purple/black colour was of lesser significance. The appearance of a red colour did not alter significantly with time. From this study it was only possible to conclude that a bruise with a yellow colour was more than 18 h old.

Adolescent↗
PubMed1990

Rarity of synovitis in polymyalgia rheumatica.

The joints of 56 patients with polymyalgia rheumatica were examined for evidence of inflammatory synovitis. x Rays, isotope scans, and thermography supplemented clinical examination. Control sternoclavicular joints were examined at necropsy. Peripheral and axial synovitis were uncommon and the results contrast with the findings of several recent studies.

Aged↗
PubMed1990

Tennis elbow. A clinicopathologic study of 22 cases followed for 2 years.

Twenty-two elbows in 20 patients with persistent lateral pain due to epicondylitis had release of the common extensor origin and decortication of the lateral epicondyle. Specimens taken from the lateral epicondyle were examined histologically and compared with controls, and patients were reviewed clinically 2 (1/2-4) years after operation. Following surgery, symptoms were improved in 17 patients. Histologic examination of the bone-tendon junction revealed evidence of a repair response of variable degree, the most frequent features being mucopolysaccharide infiltration and bone formation. Fibrofatty degenerative changes were also present in some cases. There was no correlation between the intensity of the histologic reaction and the clinical outcome.

Adult↗
PubMed1979

Early bronchiolar damage following paraquat poisoning in mice.

Paraquat causes focal intracellular oedema of the terminal bronchiolar epithelial cells and focal subpleural atelectasis with thickening of the interalveolar septa 1 hr after the administration of an LD50. These changes are progressive, and lead to panacinar atelectasis with necrosis plus sloughing of epithelial cells in many terminal bronchioles. Radioactive phosphatidyl choline (PC) is recoverable by lavage within 90 s of the administration of tritiated palmitate, which supports previous suggestions that one source of pulmonary surfactant is rapid secretion by the terminal bronchiole. Paraquat causes a reduction in the relative amounts of radioactive PC that are recoverable from the airways within 90 s of giving tritiated palmitate. A deficiency of pulmonary surfactant of bronchiolar origin is implicated, at least in part, in the pathogenesis of the acute phase of the paraquat lesion in mice.

Animals↗
PubMed1975

Early events in atherogenesis.

Most of the factors that are thought to be involved in atherogenesis can act by producing increased endothelial permeability. They may cause damage in their own separate ways or through their effects on blood-platelets. Several constituents of platelets could produce vascular damage that may result in intimal oedema and subsequent atherosclerosis.

Animals↗
PubMed1975

Injury and repair of tracheobronchial cartilage following accidental exposure to ehtyleneimine.

A fatal case following ehtyleneimine inhalation is described. Profound destructive effects on tracheobronchial cartilage were found at necropsy after an interval of apparent recovery from early phases of poisoning. The pathogenesis of these cartilaginous changes is discussed. It is proposed that they may have been due to proteases liberated from liberated from mucosal granulation tissue.

Animals↗
PubMedDate not supplied

Is atheroma a reversible lesion?

In this review atherogenic factors are discussed in relation to the possibility of regression. Evidence for regression of human lesions comes mainly from postwar studies and observations on persons with chronic wasting diseases. The entry, exit and effects of lipids in the arterial wass are considered as important factors which might determine regression. A variety of experiments in different animals which have been done in order to study regression are described. Some involve cholesterol feeding and withdrawal, others are concerned with the effects of hyperoxia and drugs. It is concluded that certain forms of atheroma can be induced to regress.

Animals↗