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D V Parums

Publications and source records attributed to D V Parums.

At least 19 recordsLinked to original sources
PubMed1998

Tricuspid valve repair in a mountaineer.

Lord Hunt of Everest presented with aortic stenosis but predominant right ventricular failure. He was found to have signs of pulmonary hypertension with a dilated right ventricle, severe tricuspid regurgitation, and right atrial hypertrophy in the absence of elevated pulmonary artery pressures. He is a lifelong mountaineer and we attribute these findings to intermittent prolonged exposure to high altitude.

Adaptation, Physiological↗
PubMed1997

Unrestricted usage of immunoglobulin heavy chain genes in B cells infiltrating the wall of atherosclerotic abdominal aortic aneurysms.

The aim of this study was to provide evidence for the hypothesis that the B cell rich infiltrate concentrated in the adventitia of atherosclerotic abdominal aortic aneurysms is an autoimmune response to specific tissue antigens. Detailed histological examination of biopsies from 26 atherosclerotic abdominal aortic aneurysms showed in the adventitia, the presence of lymphoid follicles in 7/26 (27%) and of plasma cells in all cases. DNA prepared from the outer aneurysm wall (n = 25) was amplified using the polymerase chain reaction to investigate the repertoire of the immunoglobulin heavy chain (VH) genes used. Amplification of the VDJ region of VH, using both framework 2 and 3 primers, revealed unrestricted usage of the VH gene in 24/25 cases. The only case where restricted usage of the VH genes was observed, might have been attributable to severe virally-induced tissue inflammation. These results indicate that, in the vast majority of atherosclerotic abdominal aortic aneurysms, the B cell rich adventitial infiltrates are not an autoimmune response to a limited repertoire of tissue antigens.

Aged↗
PubMed1996

Inducible nitric oxide synthase is present within human atherosclerotic lesions and promotes the formation and activity of peroxynitrite.

Inflammatory cytokines associated with atherosclerosis may be capable of stimulating the synthesis and activity of inducible nitric oxide synthase (iNOS), which could further influence the pathologic features associated with the disease. Although there is a certain amount of indirect evidence to support the presence of iNOS in atherosclerosis, there has been no definitive study to confirm this. This study has assessed the localization of iNOS within human normal and atherosclerotic vessels by immunocytochemistry, Western blotting, and in situ hybridization. Further, activity of NO synthase has been assessed by detection of nitrotyrosine, which is a marker indicative of the formation and activity of the nitric oxide-derived oxidant, peroxynitrite. In Western blots of crude homogenates of atherosclerotic aorta, the iNOS antiserum reacted with a band of approximately 130 kd (the known molecular weight for iNOS), but no such band was seen in normal aorta. Immunostaining and in situ hybridization confirmed the presence of iNOS in atherosclerotic vessels, in which it was specifically localized to (CD68-positive) macrophages, foam cells, and the vascular smooth muscle. The antiserum to nitrotyrosine reacted with a wide range of protein bands (approximately 180 to 30 kd) in Western blots of atherosclerotic aorta. The distribution of immunostaining for nitrotyrosine was virtually identical to that seen for iNOS and was present in macrophages, foam cells, and the vascular smooth muscle. In conclusion, these studies have demonstrated that stimulated expression of iNOS is associated with atherosclerosis and that the activity of this enzyme under such conditions preferentially promotes the formation and activity of peroxynitrite. This may be important in the pathology of atherosclerosis, which contributes to lipid peroxidation and to vascular damage.

Adult↗
PubMed1994

The arteritides.

This article reviews the histopathological, clinical and immunological features of the arteritides. Based on these criteria, a classification scheme is proposed that includes infectious and non-infectious causes. Included in the non-infectious arteritides are: hypersensitivity vasculitis including serum sickness. Henoch-Schönlein purpura, mixed cryoglobulinaemia, hypocomplementaemia, drug and malignancy-associated vasculitis; arteritides of small and medium-sized arteries including polyarteritis nodosa, Kawasaki's disease, Wegener's granulomatosis, Churg-Strauss syndrome, necrotizing sarcoid granulomatosis, thromboangiitis obliterans (Buerger's disease) and localized forms of arteritis; arteritides involving large, medium and small-sized arteries which includes giant cell (temporal) arteritis, Takayasu's disease and arteritis of collagen-vascular disease (rheumatoid arthritis, rheumatic fever, Behçet's disease, Sjörgren's syndrome, systemic lupus erythematosis and systemic sclerosis.

Arteritis↗
PubMed1994

The distribution of adhesion molecules in chronic periaortitis.

Chronic periaortitis is a local complication of human atherosclerosis. It is defined as the triad of advanced atherosclerosis, medical thinning and aortic adventitial chronic inflammation. It is present to a variable degree in association with atherosclerotic abdominal aortic aneurysms. These aortic adventitial infiltrates differ from those described solely within the atheroma itself, in that they consist predominantly of B lymphocytes. Many of the lymphocytes are activated and proliferating, and germinal centres are common. In this study, an immunohistochemical analysis was carried out on fresh surgical aortic aneurysm tissue in order to investigate the presence and distribution of activation-inducible adhesion molecules, and to correlate this with the degree of inflammation. A consistent finding was the presence of E-selectin on endothelial cells in up to 50% of the vessels throughout the aortic wall and at the base of the atheroma, independent of the severity of inflammation. ICAM-1 expression was abundant on many cell types and increased with the severity of chronic inflammation, being strongest in the germinal centres. VCAM-1 expression was predominant on follicular dendritic cells and also increased with severity of inflammation. VCAM-1 expression was also detected on vessels within lymphoid follicles. The pattern of expression of the adhesion molecules suggests a role in the initiation and progression of chronic inflammation associated with advanced atherosclerosis.

Aged↗
PubMed1994

Cytokine gene expression in aortic adventitial inflammation associated with advanced atherosclerosis (chronic periaortitis).

AIMS: To determine whether aortic adventitial chronic inflammation associated with advanced atherosclerosis ("chronic periaortitis") is associated with any detectable cytokine gene expression. METHODS: RNA was extracted from six fresh surgical specimens of atherosclertic aortic aneurysm wall showing a spectrum of chronic periaortitis. Controls included four normal aortas and an HUT 78 T cell line. Reverse transcriptase and the polymerase chain reaction (PCR) were used to amplify mRNA for interleukins-1 alpha (IL-1 alpha), -2 (IL-2), -4 (IL-4), IL-2 receptor-alpha (IL-2R-alpha), tumour necrosis factor alpha (TNF-alpha) and gamma interferon (IFN-gamma) with beta-actin as an internal control. RESULTS: No TNF-alpha mRNA was detected in any of the inflamed aortic tissue samples, in contrast to the aortic T lymphocytes propagated in culture in IL-2 conditioned medium (aortic cultured T cells) and peripheral blood mononuclear cells from these patients. In contrast, IFN-gamma, IL-1 alpha, IL-2, IL-2 receptor and IL-4 PCR products were detected for each inflamed aortic tissue RNA sample with IFN-gamma mRNA expression increasing with increasing degrees of adventitial inflammation. Only beta-actin mRNA was present in the normal aorta. CONCLUSIONS: These findings indicate the active nature of aortic adventitial chronic inflammation associated with human advanced atherosclerosis ("chronic periaortitis") and show its possible progressive potential to the clinically important diseases termed "idiopathic retroperitoneal fibrosis" and "inflammatory aneurysm".

Adult↗
PubMed1993

The distribution of adhesion molecules in human atherosclerosis.

Chronic inflammatory cells are a recognized component of atherosclerotic plaques at all stages of development. As adhesion molecules play a fundamental role in inflammatory processes, we have carried out an immunohistochemical investigation of the distribution of endothelial leucocyte adhesion molecule-1 (ELAM-1)*, intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) in human atherosclerotic lesions. Autopsy specimens from abdominal aorta and coronary arteries were obtained from 21 cases within 24 h of death. ELAM-1 and ICAM-1 were consistently expressed by the entire intimal endothelium of normal coronary arteries and also by the intimal endothelium overlying aortic fatty streaks. Both coronary artery and aortic lesions showed strong staining for ICAM-1 on and around macrophages. VCAM-1 was not detected on intimal endothelial cells, but strong staining of adventitial lymphoid aggregates for this molecule was seen. This work suggests a role for ELAM-1 and ICAM-1 in mononuclear cell recruitment during atherogenesis.

Adult↗
PubMed1993

Quantification of specific mRNA by flatbed scintillation counting of dual-labeled dot blots.

A dual-labeling technique was developed for direct quantification of specific mRNA using a flatbed liquid scintillation counter. This method simultaneously measures cpm of 32P- and 35S-labeled probes bound to RNA dot blots and subtracts counts due to nonspecific background radioactivity bound to the filter. Probes for T-cell receptor and beta-actin (as the internal standard) were hybridized both separately and simultaneously to RNA isolated from five different sources. There was concordance between the radioactivity measured from single- and dual-hybridizations for each combination of 35S- and 32P-labeled probes. This methodology directly quantifies specific mRNA sequences bound to membranes and has potential for measuring gene dosage, without the need for re-probing or densitometric analysis.

Actins↗
PubMed1992

Combined immunohistochemical and immunofluorescence method to determine the phenotype of proliferating cell populations.

AIMS: To determine the phenotype of proliferating cell populations. METHODS: The double immunostaining technique combines the autofluorescent properties of alkaline phosphatase substrate naphthol/Fast Red with immunofluorescence using fluorescein. Fresh human tonsil and fresh atherosclerotic aortic aneurysm wall tissue were studied using a panel of monoclonal antibodies including Ki-67, CD4, CD8, CD19, CD22, HLA-DR alpha, CD68 and CD31. RESULTS: This double immunostaining method permitted simultaneous colocalisation of different markers on the same cell and could be used to identify HLA-DR positive cells as well as proliferation associated Ki-67 positive cells in human tonsil tissue and in chronic periaortitis associated with advanced atherosclerosis. CONCLUSION: This technique is simple and the results may be viewed using a single fluorescence filter. The Fast Red reaction product is stable and does not fade under storage. The staining works particularly well with markers for nuclear antigens in combination with markers for cytoplasmic or surface antigens.

Aortic Aneurysm, Abdominal↗
PubMed1992

Fatal case of disseminated infection with the turtle bacillus Mycobacterium chelonae.

An apparently immunocompetent 78 year old woman presented with confusion, subcutaneous abscesses, and lesions of the nasopharynx. Gram positive, acid fast bacilli were isolated from her blood after 10 days' incubation. She was treated with trimethoprim-sulphamethoxazole for presumed disseminated nocardiasis but deteriorated and died. A post mortem examination showed skin and pulmonary lesions and endomyocardial fibrous plaques. Organisms isolated from the skin and lung were indistinguishable from those cultured from the blood. The organism was subsequently identified as Mycobacterium chelonae. Primary pulmonary infection and disseminated disease are rarely caused by this organism and bacteraemia is seldom documented. The clinical presentation and bacteriological and histological findings are difficult to differentiate from those of disseminated nocardiasis. Isolation of the organism may fail without prolonged incubation of initial cultures and there is a danger of its being dismissed as medically unimportant. Diagnosis is further hampered because large pulmonary foci may be poorly revealed by conventional radiological examination of the chest.

Aged↗
PubMed1991

Characterisation of inflammatory cells associated with "idiopathic retroperitoneal fibrosis".

During ureterolysis in a patient with "idiopathic retroperitoneal fibrosis", fresh samples of peri-ureteric and peri-aortic tissue were obtained. An abdominal CT scan confirmed the peri-aortic distribution of the inflammation associated with advanced abdominal aortic atherosclerosis. Histology confirmed the presence of fibrosis and a variable chronic inflammatory cell infiltrate. Monoclonal antibodies were used to identify the inflammatory cells. B and T lymphocytes were present with the majority of T lymphocytes of the T helper phenotype. The majority of lymphocytes and macrophages and most vascular endothelial cells were HLA-DR positive. Ki67 and BerH2 staining was found in B cells and T helper cells, indicating that these cells were proliferating and activated. These findings compare with the characterisation of inflammatory cells associated with "inflammatory aneurysms" and with the inflammatory cells present in the spectrum of inflammation seen as a complication of advanced atherosclerosis--conditions known as "chronic peri-aortitis". It is suggested that our findings support the view that idiopathic retroperitoneal fibrosis represents clinical chronic peri-aortitis seen in an undilated aorta.

Antibodies, Monoclonal↗
PubMed1990

Extent of mesorectal spread and involvement of lateral resection margin as prognostic factors after surgery for rectal cancer.

The extent of tumour growth beyond the muscularis propria (mesorectal spread) was measured in specimens from 167 consecutive patients with rectal cancer. The 5-year survival was significantly greater in patients with slight mesorectal spread (4 mm or less) than in those with more extensive mesorectal spread (55% [95% confidence interval 42-66%] vs 25% [13-38%]). The prognostic value for survival of mesorectal spread was independent of the presence of lymphnode metastases. There were also significant differences in survival between patients with slight and extensive mesorectal spread among patients with Dukes' stage B tumours (66% [41-82%] vs 37% [14-60%]) and those with Dukes' stage C tumours (30% [12-52%] vs 18% [6-34%]). Thus mesorectal spread of rectal cancer is an important determinant of survival, and its accurate measurement may serve to subdivide Dukes' B and C cases. In this study tumour involvement of the lateral resection margin was not a useful predictor of local recurrence, but it did correlate with poor prognosis.

Actuarial Analysis↗
PubMed1990

Immunohistochemical characterization of inflammatory cells associated with advanced atherosclerosis.

During repair of 12 atherosclerotic abdominal aortic aneurysms, fresh samples of aneurysm wall were obtained. Histology confirmed the presence of advanced atherosclerosis associated with medial thinning and a variable aortic adventitial chronic inflammatory cell infiltrate. Monoclonal antibodies were used to identify the inflammatory cells throughout the aortic wall. The majority of lymphocytes in the aortic adventitia were B-cells. B-cells were not present in atheromatous plaques. T-cells, predominantly T-helper cells, were found in atheromatous plaques and in aortic adventitia. The majority of lymphocytes and macrophages in aortic adventitia and most vascular endothelial cells were HLA-DR positive. Ki-67 staining was found in B-cells and T-helper cells, indicating that these cells were proliferating. Occasional lymphocytes were BerH2 positive, indicating that some lymphocytes were activated. These findings suggest that chronic periaortitis is an active, immunologically mediated, local complication of advanced human atherosclerosis.

Aged↗
PubMed1990

The spectrum of chronic periaortitis.

A review of the histology of 440 sections of atherosclerotic aortas and arteries showed that 85% contained advanced atherosclerotic plaques. Of these, 92% showed some degree of adventitial inflammation with subclinical chronic periaortitis in 49%. A review of 20 cases of clinical chronic periaortitis, which included 12 cases of inflammatory aneurysm and 8 cases of idiopathic retroperitoneal fibrosis, showed that there were no significant differences between them apart from an increase in aortic diameter in the former. The term chronic periaortitis is appropriate for the spectrum of subclinical and clinical forms of chronic adventitial inflammation associated with advanced atherosclerosis and medial thinning.

Aged↗