Biomedical subjects

C McCollum

Publications and source records attributed to C McCollum.

At least 37 records · Page 2Linked to original sources

PubMed1998

Avoiding the consequences of deep vein thrombosis. Elevation and compression are important-and too often forgotten.

Explore the source record for details and available documents.

Bandages↗

PubMed1998

Calcification in atherosclerotic plaque of human carotid arteries: associations with mast cells and macrophages.

Calcification has been examined in 250 samples of atherosclerotic lesions (types II to VI) of human carotid arteries using von Kossa and haematoxylin staining. Early calcification described as 'stippling' was first noted in stage III specimens, with intermediate and solid calcifications becoming increasingly prominent within advanced plaques, especially stages Vb and VI. Although the relative frequencies of stippling, intermediate and large calcified deposits varied between plaques of the same stage, the prevalent sites of calcification were recognized as the deeper regions of the intima and the atheroma. Immunolocalization and histochemical techniques were used to identify the associations of mast cells (MCs), macrophages, smooth muscle cells (SMCs), and elastin with the different stages of calcification. Early, dispersed stippling was commonly associated with local accumulations of macrophages (HAM56 and CD68-positive), MCs and extracellular MC tryptase, the presence of immunoreactive elastin, but the relative absence of SMCs. Intermediate stages of calcification described as 'morula' deposits were also associated with local increases in the numbers of macrophages and MCs. Larger calcified deposits, even within the same plaque specimen, showed no regular pattern of cellular or elastin associations. However, in the vast majority of specimens, macrophages represented the predominant cell type associated with different phases of calcification. By contrast, the calcification less frequently observed in the media beneath advanced plaques was commonly associated with SMCs and elastin; only rarely were macrophages or MCs present. These studies are the first to demonstrate that macrophages, MCs, and extracellular tryptase frequently occupy micro-environmental loci showing the first stages of calcification within the atherosclerotic plaque; similar associations with more advanced mineral deposits are discussed in relation to plaque rupture.

Aged↗

PubMed1998

Observations on bone formation and remodelling in advanced atherosclerotic lesions of human carotid arteries.

Immunolocalisation and histochemical techniques were used to examine mineralised bone deposits within late stage atherosclerotic plaques of human carotid arteries. These specimens showed characteristic features of osteogenesis. Large calcifications were often observed in close association with or integrated within mineralised bone. Smooth muscle cells (alpha-actin positive) were often located around osteoid-like matrix, together with focal accumulations of macrophages (CD68 and HAM56 positive). Local accumulations of mast cells (tryptase positive) were consistently observed in close association with the bone. Multinucleated giant cells in close apposition with mineralised bone demonstrated typical osteoclastic morphology, and were positively stained for acid phosphatase and the macrophage marker CD68. Thus, all the normal features of bone formation and resorption were observed in this microcosm of osteogenesis within atherosclerotic plaque; the term 'osteosome' seems appropriate for the structure. These osteosomes have numerous advantages for experimental studies of the various osteogenic factors responsible for bone metabolism, especially following short-term tissue culture. This ex vivo technique was used to demonstrate the distribution and the multiple cellular sources of bone morphogenetic protein 6.

Acid Phosphatase↗

PubMed1998

von Willebrand factor, fibrinogen and other plasma proteins as determinants of plasma viscosity.

Plasma viscosity and fibrinogen are risk factors for cardiovascular disease and on rheological grounds, it is widely believed that the latter is a major determinant of the former. However, other plasma constituents may also be important determinants of plasma viscosity. Our aim was to determine whether or not levels of von Willebrand factor contributed to plasma viscosity. We measured plasma viscosity, fibrinogen, von Willebrand factor, immunoglobulins G, A and M, total, HDL- and LDL-cholesterol, triglycerides and albumin in 95 patients with peripheral arterial disease and in 120 healthy controls. A stepwise multivariate analysis was performed to determine the major influences of plasma viscosity. We also measured fibrinogen, von Willebrand factor, immunoglobulins G, A and M, total, HDL- and LDL-cholesterol, triglycerides, albumin and viscosity in 32 smokers as they successfully progressed to being non-smokers. The level of von Willebrand factor was an independent influence on plasma viscosity in the controls (P < 0.05), patients (P < 0.01) and in the combined group (P < 0.001). von Willebrand factor, fibrinogen and plasma viscosity, but not the immunoglobulins, lipoproteins or albumin, fell (P < 0.05) in smokers as they became non-smokers. We find that von Willebrand factor contributes to plasma viscosity, hence a reduction in levels of von Willebrand factor should result in a reduction in viscosity. These data may have implications for the pathogenesis of cardiovascular disease.

Adult↗

PubMed1997

Mast cell distribution, activation, and phenotype in atherosclerotic lesions of human carotid arteries.

Immunohistochemical staining for mast cell tryptase and chymase was used to examine the distribution, activation, and tryptase/chymase phenotype of mast cells (MCs) in 250 samples of atherosclerotic lesions (type I to VI) of human carotid arteries. Dual immunolocalization and histochemical techniques were used to identify the associations of MCs with macrophages, smooth muscle cells, and extracellular matrix components. Whereas normal carotid arteries contained very few MCs within the intima, atherosclerotic lesions showed increased MC numbers with variable focal accumulations. MCs were identifiable from the earliest stages of atherosclerosis, and especially at the shoulder regions of the fully formed atheroma. They were observed in close association with macrophages (HAM56 positive) and extracellular lipid, as well as at sites of foam cell formation. MCs and diffuse tryptase staining were also evident within sites of new calcification and around small calcified deposits. Extensive MC activation/degranulation, as judged by diffuse extracellular tryptase staining, was a common feature of the advanced atherosclerotic plaques complicated by fissure, haemorrhage, and thrombus formation. Moreover, such sites of extracellular MC tryptase were often associated with localized oedema and disruption of the stromal matrix. MCs which contained both tryptase and chymase (the MCTC phenotype) represented approximately 80-95 per cent of all MCs. These studies are the first to demonstrate significant numbers and focal accumulations of MCs in all developmental stages of atherosclerotic carotid arteries. Since MCs contain or express a variety of potent mediators, their release could profoundly influence the development and pathological complications of atherosclerotic plaques.

Aged↗

PubMed1997

Single-layer and multilayer bandaging in the treatment of venous leg ulcers.

This study compares levels of compression achieved in the application of both multilayer compression bandage systems and single-layer bandages by practitioners who are experienced with levels achieved by those who are inexperienced. Nineteen practitioners experienced in compression bandaging (13 nurses, six doctors) and 18 inexperienced (12 nurses, six doctors) participated in the study. Both experienced and inexperienced practitioners achieved a pressure of 40 mmHg more consistently when applying multilayer compression bandage systems than in the application of single-layer bandages. Compression bandaging experience does not result in significantly better sub-bandage pressure when using a multilayer system. Inexperienced practitioners are more likely to apply dangerously high levels of pressure with single-layer bandages than with a multilayer system. Single-layer compression bandages should be applied only by those health-care professionals with extensive experience of applying compression bandages.

Bandages↗

PubMed1997

Up-regulation of elastase in acute wounds of healthy aged humans and chronic venous leg ulcers are associated with matrix degradation.

Chronic wound healing states are often associated with aging, and despite the increased number of aged patients with nonhealing wounds, controversy still exists concerning the effects of age on wound repair. Our previous work showed that in both venous ulcers in humans and acute wounds in aged animals, fibronectin, an early component in granulation tissue, is deficient compared to normal skin and acute wounds in healthy young animals, respectively. In the present study, we have determined the protease responsible for fibronectin degradation by analyzing tissue taken from the margins of chronic venous ulcers and standardized acute cutaneous wounds collected from a large cohort of "Health status"-defined aged human subjects (screened as per the SENIEUR protocol). When tissue samples were subjected to fibronectin zymography, the main protease involved in the breakdown of fibronectin in both venous ulcers and acute wounds of elderly subjects was found to be a serine protease with a molecular weight of approximately 30 kd. This protease was identified as neutrophil elastase by immunoblotting. In tissue biopsies, elastase was localized to granulocytes by immunocytochemical techniques and shown to be present in greater quantities in venous ulcers and Day-7 and -14 healing acute wounds of healthy aged subjects relative to those of young subjects. The highest quantities were found in acute wounds of elderly women. Our results suggest that the process of aging in healthy human subjects is associated with an up-regulation of elastase during acute wound healing and that an abnormality in down-regulation of this protease could be partially responsible for the transition to chronic wound healing states in the aged.

Acute Disease↗

PubMed1996

Soluble L-selectin in peripheral arterial disease: relationship with soluble E-selectin and soluble P-selectin.

Soluble L-selectin, E-selectin and P-selectin were measured in a small case control study of 42 patients with peripheral arterial disease and 42 age and sex matched controls. Levels of soluble L-selectin were 1204 +/- 221 ng/ml (mean +/- S.D.) in the patients compared to 1256 +/- 271 ng/ml in the controls (P = 0.37). There was also no difference in levels of soluble E-selectin (57 +/- 17 ng/ml versus 51 +/- 20 ng/ml, P = 0.15) but levels of soluble P-selectin were increased (249 +/- 101 ng/ml versus 198 +/- 98 ng/ml, P = 0.011). There were no significant correlations between any of the selectins and the risk factors for atherosclerosis or with any leucocyte index. The data point to different mechanisms of release of the soluble selectins in peripheral atherosclerosis and may have important implications for leukocyte/endothelial cell interactions.

Arteriosclerosis↗

PubMed1996

Community leg ulcer clinics: a comparative study in two health authorities.

OBJECTIVE: To compare the outcome and cost of care for leg ulcers in community leg ulcer clinics in Stockport District Health authority with Trafford District Health Authority as a control. DESIGN: Detailed cost and efficacy studies conducted prospectively over a three month period in both districts both before and one year after the introduction of five leg ulcer clinics in Stockport. SETTING: Two large district health authorities of broad socioeconomic mix and total population of 540,000. PATIENTS: All patients receiving treatment for an active leg ulcer, irrespective of the profession or location of their carer. MAIN OUTCOME MEASURES: The proportion of ulcerated limbs completely healed within three months and total cost of leg ulcer care. RESULTS: The introduction of community clinics in Stockport improved healing of leg ulcers from 66/252 (26%) in 1993 to 99/233 (42%) in 1994 (P < 0.001) compared with in Trafford, where 47/203 (23%) healed in 1993 and only 43/213 (20%) in 1994. This improved result in Stockport was achieved while the annual expenditure on care of leg ulcers was reduced from 409,991 pounds to only 253,371 pounds. In the same year the cost of leg ulcer care in Trafford increased from 556,039 pounds to 673,318 pounds. CONCLUSION: In the first year after the introduction of community clinics, before most patients in Stockport had access to these clinics, healing of leg ulcers was already improved whereas costs were reduced.

Community Health Centers↗

PubMed1996