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Biomedical subjects

C W Adams

Publications and source records attributed to C W Adams.

At least 73 records · Page 4Linked to original sources
PubMed1977

Regression of atheroma in the rabbit.

Ten studies in the literature concerning regression of rabbit atheroma were re-examined. In studies where cholesterol content was referred to weight, a degree of regression was noted in 3/4 studies. Such regression might at least partly have resulted from the dilution effect of the atheroma contents when results were expressed on a weight basis. By contrast, when results were referred to length or protein, partial regression was seen in only 1/4 studies. Mild atheroma induced by short-term cholesterol feeding did seem to regress in 2/2 studies.

Animals↗
PubMed1977

Permeability of inner and outer layers of rat and rabbit aortic wall. Two new microscopic test with trypan blue.

Two new permeability tests are described for use with intravenously injected trypan blue. One depends on the demonstration of trypan blue by its specific red fluorescence in green light at 570 nm, while the other is a surface microscopy technique at low magnification, using illumination from a fibre-optics light source. The routes of entry of the trypan blue-albumin complex into the rat and rabbit aorta appear to be from both the inner and outer surfaces. Over the period 1/4-24 h after injection of the dye, more entered from the outer surface than the inner surface in the rat aorta and rather more in the rabbit thoracic aorta. The arch of the rabbit aorta showed in general rather greater entry from the inner surface. Trypan blue that has entered the aortic wall is partly taken up by the elastic lamellae. Elastic competes successfully for the dye and captures it from the trypan blue-albumin complex; this uptake is blocked by deamination with nitrous acid.

Animals↗
PubMed1976

Ganglion cells in achalasia of the cardia.

The histopathology of 40 cases of achalasia of the cardia, 6 cases of oesophageal spasm-incoordination and 4 cases of scleroderma was examined. Three cases of carcinoma and 6 cases of reflux oesophagitis were used as a control group. A nearly complete loss of myenteric ganglion cells was found in the upper thickened segment in achalasia. Some surviving ganglion cells were found in the lower segments in half the cases of achalasia; in two cases counts were normal in this segment. The occurrence of neuronal chromatolysis in 9 biopsies of achalasia supports the view that an active disease process was involved. The preganglionic parasympathetic fibres in two cases of achalasia were normal in appearance and number; this somewhat limited evidence tends to count against a primary disorder of the preganglionic neurone in this condition. The 6 cases of oesophageal spasm-incoordination showed similar neuronal loss to that in the lower segment in achalasia. Possibly "oesophageal spasm" represent an early stage or incomplete expression of achalasia. One cases of scleroderma showed loss of ganglion cells, but the myenteric plexus was here involved by the disease process. None of the 9 cases in the control group showed any loss of ganglion cells or chromatolysis. Acute and chronic inflammation was not convincingly associated with loss of ganglion cells in either achalasia or oesophageal spasm.

Autonomic Fibers, Preganglionic↗
PubMed1976

Dietary restriction and regression of atherosclerosis.

Rabbits were fed a cholesterol-enriched diet to render them atheromatous. After 3 months on this diet they were switched to a low-lipid stock diet. Some animals were killed at this point, while the rest were divided into (a) a group allowed to eat ad-libitum and (b) a resticted group allowed to eat half by weight of what the ad-libitum group consumed. Most animals were killed at 9 months (i.e. after 6 months' regression). The group allowed the restricted diet showed a 27% weight loss, but their serum cholesterol fell slightly more slowly than that of the ad-libitum animals. Likewise, atherosclerosis was slightly worse in the restricted than in the ad-libitum group. The results do not support the view that severe dietary restriction causes atherosclerosis to regress.

Animals↗
PubMed1976

Detection of macrophages in atherosclerotic lesions with cytochrome oxidase.

The anaerobic metabolism of the arterial wall allows macrophages to be demonstrated therein by the cytochrome oxidase histochemical method. Monocytes (macrophages) in human fatty streaks (WHO grade I) or fibrofatty (WHO grade II) human atherosclerotic lesions are normally confined to subendothelial regions. Lesions complicated by ulceration, mural thrombosis or intimal haemorrhage (WHO grade III) showed numerous monocytes (macrophages) around newly-formed capillaries in focal areas of organization. By contrast with grades I and II atherosclerotic lesions, macrophages in lipid granulomas induced by subcutaneous injection of cholesterol oleate are more numerous and distributed throughout the lesion. The slow or absent resorption of lipid from atheromatous lesions may in part result from the paucity of macrophages therein.

Adult↗
PubMed1975

Phagocytes, lipid-removal and regression of atheroma.

Reticuloendothelial (RE) phagocytes (macrophages and histiocytes) can be distinguished from locally-derived lipid-containing cells (e.g., arterial smooth muscle) or locally derived phagocytes (e.g., Schwann cells and microglia) by the demonstration of a diffuse catalase reaction in a proportion of these RE cells with a short incubation modification of the Novikoff-Golfischer diaminobenzidine histochemical methods. Even though only a proportion of an RE population is catalase-positive, the results accord with the majority of current opinion that most of the cells in atherosclerotic lesions are derived locally, whereas the phagocytes in lipid implants and xanthomas are of RE origin. The phagocytes in the peripheral nerve undergoing Wallerian degeneration appear to be of mixed RE and endogenous origin, whereas microglia around multiple sclerosis plaques seem to be derived locally. Lipid in lesions with RE phagocytes (subcutaneous lipid implants and xanthomas) is relatively rapidly resorbed, whereas lipid in lesions with few RE phagocytes (atherosclerosis) or phagocytes of endogenous origin (CNS degeneration) is more slowly resorbed or partly retained within the tissue. Wallerian degeneration in the peripheral nerve, with its mixed population of RE and endogenous phagocytes, occupies an intermediate position in the speed of lipid removal.

Adult↗
PubMed1975

The onset and progression of the lesion in multiple sclerosis.

The active established plaque in multiple sclerosis is characterized by hypercellularity at its edge and lipid phagocytosis (gitter cells). The hyperactive early plaque shows cells throughout the lesion. Active plaques seems to extend at their edges; proteolysis of myelin basic protein is perhaps an important factor in the myelin breakdown at the rim of these lesions. The hyperactive early plaque usually shows infiltration with monocytes, lymphocytes and plasma cells around its central vein. The phagocytic element is presumably a response to myelin breakdown but the significance of the lymphocytes in these lesions in uncertain. Perivenular infiltrates that are predominantly composed of lymphocytes are seen around veins and venules in the vicinity of established lesions in some patients who died during an acute episode...

Adolescent↗