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Biomedical subjects

B Gromoll

Publications and source records attributed to B Gromoll.

7 recordsLinked to original sources
PubMed1998

Topographic pattern of advanced atherosclerotic lesions in carotid arteries.

Ulcers in extracranial carotid arteries are a known source of cerebral embolism. However, there are no data available on the prevalence of ulcerations located at the origin of these vessels in the aortic arch. Therefore, in this pathological study the topographic distribution of ulcerated lesions were determined in these arteries. One hundred and one consecutively autopsied patients composed the study group. Ulcerated plaques were sought for in both carotid arteries, from their origin in the arch up to the carotid canal, and also in the aortic arch and ascending aorta. The two anatomical sites mostly affected by atherosclerosis were the region of the carotid sinus and the orifices of cervical arteries in the aortic arch. More than one third of all ulcers were at the orifices of cervical arteries in the arch. Interestingly, ulcers at the orifice of the left common carotid artery in the arch were accompanied with other ulcers located elsewhere in the remaining segments of the left carotid system, whereas ulcerations at the orifice of brachiocephalic trunk were not accompanied with other concomitant lesions in the right carotid system. Furthermore, there was no symmetric distribution of ulcerated plaques in both carotid systems.

Adult↗
PubMed1996

Aortic atherosclerotic plaques as a source of systemic embolism.

OBJECTIVES: Our study was designed to determined the significance of aortogenic embolism in an unselected autopsy collective. BACKGROUND: Although embolism arising from atherosclerotic plaques in the aorta has been acknowledged, the role of aortic atheromatosis among other well known sources of embolism remains to be further clarified. METHODS: We examined the proximal part of the arterial system with regard to the presence of atherosclerotic lesions as well as cardiac changes in 120 consecutive necropsy studies. Pathologic evidence of embolic events was recorded. Clinical and neuropathologic data were also surveyed in all patients. RESULTS: Among atherosclerotic lesions, fibrous plaques (p < 0.05) and calcified (p < 0.0001) and ulcerated lesions (p < 0.0001) as well as thrombi (p < 0.005) were observed significantly more frequently in the aortic arch and in the descending aorta than in the ascending aorta, whereas fatty streaks were distributed uniformly. In 40 (33%) of the 120 patients, we found pathologic evidence of arterial embolization. Multiple logistic regression analysis revealed a significant correlation between embolism and complicated atherosclerotic plaques in the aortic arch (odds ratio [OR] 5.8, 95% confidence interval [CI] 1.1 to 31.7, p < 0.05), severe ipsilateral carotid artery disease (OR 3.1, 95% CI 3.1 to 45.3, p < 0.001) and atrial fibrillation (OR 3.5, 95% CI 1.1 to 9.9, p < 0.05). CONCLUSIONS: Complicated atherosclerotic plaques in the aortic arch represent an independent risk factor for systemic embolism similar to atrial fibrillation and severe atherosclerosis of the carotid arteries.

Adult↗
PubMed1995

[Arteriosclerosis of the thoracic aorta as a source of systemic emboli. A clinico-pathologic study].

The significance of the thoracic aorta as a source of systemic emboli in addition to other sources of embolism remains unexplained. A study of 120 consecutive necropsies (65 men, 55 women; mean age 71 [29-94] years) analysed the possible correlation of the severity of arteriosclerosis of the aorta, the carotid arteries and the arteries at the base of the brain as well as cardiac changes, with potential sources of emboli and with proven emboli (n = 39). Complex and fibrous plaques in the arch of the aorta, ipsilateral carotid artery stenoses, a history of atrial fibrillation and heart weight correlated significantly with emboli on both uni- and multivariant analysis. But the presence of calcified and complex plaques in the descending aorta, as well as moderate and severe arteriosclerosis in the arteries at the base of the brain, correlated significantly only on univariant analysis. Ischaemic brain lesions had been clinically silent in twelve of 32 cases, while visceral emboli had been silent in nine out of ten cases. -It is concluded from these data that, in addition to the cardiac chambers and arteriosclerosis of the arteries at the base of the brain, advanced arteriosclerosis of the aortic arch is an important source of systemic emboli. As many of the emboli remain silent, their incidence is probably underestimated clinically.

Adult↗
PubMed1993

Binding sites for short-term glycated albumin on peritoneal cells of the rat.

The interaction of in vitro short-term glycated rat serum albumin with rat peritoneal cells (40% macrophages) was investigated. Using 125I-labeled albumins the following results were obtained. Glycated albumins showed a binding reaction at 4 degrees C, which appeared to reach equilibrium within 2 h. The concentration-dependent binding of glycated albumin showed saturation. Binding data evaluated for glycated albumin using the Sips equation are: average association constant Ko = 3.15 x 10(7) M-1 with a heterogeneity index of a = 0.8 and 1.12 x 10(4) binding sites per cell. Such binding sites were identified in 40% of the peritoneal cell preparations studied. Native albumins, maleylated albumin, chondroitinsulfates, polylysine, lysine, fructose, glucose and hexitol-lysine could not compete with radio-labeled glycated rat albumin for its binding site on peritoneal cells. Effective competitors were glycated human serum albumin, glycated polylysine and fructose-lysine. Although the contamination with minute amounts of advanced glycosylation end products (AGE) could not be excluded, short-term glycated albumin was found to be bound to membranes of peritoneal phagocytotic cells by fructose-lysine specific proteins, whose approximately defined molecular masses of 290 kDa are distinct from hitherto described binding proteins for AGE- and aldehyde-modified proteins or for the scavenger receptors.

Animals↗
PubMed1990

Complement component 3 (C3) genetics and diabetes mellitus.

Complement component 3 (C3) phenotype and allele frequencies were defined in 312 patients with type-1 diabetes (insulin-dependent diabetes mellitus), 256 patients with type-2 diabetes (non-insulin-dependent diabetes mellitus), 114 apparently non-diabetic first-degree relatives of type-1 diabetics, in 10 families (29 members) with a familial history of type-1 or type-2 diabetes, in 181 patients with coronary heart disease and 255 subjects with arterial hypertension. 512 blood donors served as controls. All persons investigated were Europeans. There is no evidence that genes linked to C3 influence susceptibility to type-1 and type-2 diabetes and to their late complications as well as to atherosclerosis and essential hypertension. The distribution of apolipoprotein E phenotypes in patients and controls was likewise not significantly different. The combined evaluation of data from linked genes (C3 and apo E) could not improve the results. Deductions of C3 as a genetic disease marker have to be interpreted with caution.

Alleles↗
PubMed1989

[Methodologic studies of the isolation of VLDL using the lipoprotein precipitation reaction in the preparation of apolipoprotein E (Apo E)].

Several lipoprotein precipitation reactions were examined in the isolation of VLDL for apo E phenotyping in comparison to ultracentrifugation. MgCl2-Heparin- and phosphotungstic acid precipitation revealed the best results, although an apo E phenotyping was possible in only 40% of the samples. Ultracentrifugation was unequivocally superior to lipoprotein precipitation reactions.

Apolipoproteins E↗