Search PubMed⌕ Search

Biomedical subjects

R Brandl

Publications and source records attributed to R Brandl.

35 records · Page 2Linked to original sources
PubMed1999

[Surgical aortic fenestration in acute thoracoabdominal aortic dissection with abdominal malperfusion and end organ ischemia].

Intestinal, renal, spinal or peripheral arterial ischemia or failure of branch artery recanalization following initial prosthetic repair of thoracoabdominal aortic dissection is still a problem, with high morbidity and mortality. Five consecutive patients with acute thoracoabdominal aortic dissection (two type A dissections, three type B dissections) suffering from concomitant intestinal, renal, spinal and acute peripheral arterial ischemia are reported. Considering the anatomical and pathophysiological basis of thoracoabdominal aortic dissection and concomitant organ ischemia, the aortic fenestration procedure as a primary or secondary operative approach succeeded in restoring blood flow in all cases without complications. Assessment of the long-term results after 3 years revealed that all patients are doing well without any residual complaints. We conclude that in the case of persistent or secondary onset of aortic branch artery ischemia following initial prosthetic repair of either type A or type B dissection, aortic fenestration can be recommended immediately as a staged operative approach. Primary abdominal aortic fenestration is justified in acute type B dissection when end-organ ischemia becomes the focus of clinical deterioration.

Acute Disease↗
PubMed1997

Topographic analysis of proliferative activity in carotid endarterectomy specimens by immunocytochemical detection of the cell cycle-related antigen Ki-67.

BACKGROUND: On the basis of contradictory results found in animal experiments and coronary atherectomy tissue, there is an ongoing debate about the significance of cellular proliferation in human atherosclerosis. In the present prospective study, the cell cycle-related antigen Ki-67 was detected for topographic determination of cell turnover in distinct regions of human carotid endarterectomy specimens harvested en bloc by surgical biopsy. METHODS AND RESULTS: After en bloc resection, serial sections of 26 consecutive carotid lesions were analyzed by histomorphological examination and immunohistochemistry. Thereby, 319 high-power fields were attributed to separate plaque regions defined as follows: distal boundary of the lesion with normal intima, plaque shoulder, core region, and diffuse intimal thickening. Endothelial cells, smooth muscle cells, T cells, and macrophages were identified by immunostaining of factor VIII-related protein, alpha-actin, CD68, and CD45R0. An overall proliferation index of 0.49+/-1.05% was yielded by positive anti-Ki-67 immunolabeling, predominantly in macrophage-rich areas characterized by high cell density (>1000 cells/mm2) as well as in reparative sites in the perimeter of atheroma, intramural thrombosis, plaque hemorrhage, and neovascularization (P<.01). Few or no signs of proliferation activity were found in normal intima, in areas of dense alpha-actin positivity, or adjacent media. As shown by double immunostaining, macrophages and unspecified mesenchymal cells represented the prevailing proliferating cell type. CONCLUSIONS: Our results suggest that proliferation in advanced human carotid lesions is confined to the intima and focally concentrated in central plaque regions negative for alpha-actin. Furthermore, it apparently occurs primarily as part of inflammatory processes and structural repair predominantly involving macrophages, as well as unspecific mesenchymal cells.

Aged↗
PubMed1997

Pattern formation triggered by rare events: lessons from the spread of rabies.

Understanding of large-scale spatial pattern formation is a key to successful management in ecology and epidemiology. Neighbourhood interactions between local units are known to contribute to large-scale patterns, but how much do they contribute and what is the role of regional interactions caused by long-distance processes? How much long-distance dispersal do we need to explain the patterns that we observe in nature? There seems to be no way to answer these questions empirically. Therefore, we present a modelling approach that is a combination of a grid-based model describing local interactions and an individual-based model describing dispersal. Applying our approach to the spread of rabies, we show that in addition to local rabies dynamics, one long-distance infection per 14000 km2 per year is sufficient to reproduce the wave-like spread of this disease. We conclude that even rare ecological events that couple local dynamics on a regional scale may have profound impacts on large-scale patterns and, in turn, dynamics. Furthermore, the following results emerge: (i) Both neighbourhood infection and long-distance infection are needed to generate the wave-like dispersal pattern of rabies; (ii) randomly walking rabid foxes are not sufficient to generate the wave pattern; and (iii) on a scale of less than 100 km x 100 km, temporal oscillations emerge that are independent from long-distance dispersal.

Animals↗
PubMed1996

Activated transcription factor nuclear factor-kappa B is present in the atherosclerotic lesion.

Nuclear factor-kappa B (NF-kappaB)/Rel transcription factors play an important role in the inducible regulation of a variety of genes involved in the inflammatory and proliferative responses of cells. The present study was designed to elucidate the implication of NF-kappaB/Rel in the pathogenesis of atherosclerosis. Activation of the dimeric NF-kappaB complex is regulated at a posttranslational level and requires the release of the inhibitor protein IkappaB. The newly developed mAb alpha-p65mAb recognizes the IkappaB binding region on the p65 (RelA) DNA binding subunit and therefore selectively reacts with p65 in activated NF-kappaB. Using immunofluorescence and immunohistochemical techniques, activated NF-kappaB was detected in the fibrotic-thickened intima/media and atheromatous areas of the atherosclerotic lesion. Activation of NF-kappaB was identified in smooth muscle cells, macrophages, and endothelial cells. Little or no activated NF-kappaB was detected in vessels lacking atherosclerosis. Electrophoretic mobility shift assays and colocalization of activated NF-kappaB with NF-kappaB target gene expression suggest functional implications for this transcription factor in the atherosclerotic lesion. This study demonstrates the presence of activated NF-kappaB in human atherosclerotic tissue for the first time. Atherosclerosis, characterized by features of chronic inflammation and proliferative processes, may be a paradigm for the involvement of NF-kappaB/Rel in chronic inflammatory disease.

Animals↗
PubMed1995

Migration behavior of human smooth muscle cells cultivated from restenotic and primary lesions.

Subintimal smooth muscle cell (SMC) migration is considered an essential determinant of arteriosclerosis and neointimal formation. In this study, a cell culture model was established to characterize migration activity of SMCs originating from restenotic and primary lesions. Plaques from symptomatic stenoses of 32 patients (19 men, 13 women; 4 carotid, 17 peripheral, 11 coronary lesions) were removed by percutaneous atherectomy or direct operative approach. Ten patients suffered from recurrent stenosis. Cell cultures were established by explantation of tissue samples. By indirect immunofluorescence microscopy, SMCs were shown to be the predominant cell type of all advanced lesions irrespective of their origin. The spontaneous cellular motility of SMCs was analyzed in vitro by means of a computer-assisted observation system. Cells of all groups exhibited random motility. SMC migratory velocity was found to be significantly (P < 0.001) greater in cells from restenotic lesions than in those from primary plaques. In conclusion, migration behavior of human SMCs originating from arteriosclerotic lesions may be quantified in vitro as a functional determinant characterizing restenotic versus primary lesions.

Aged↗
PubMed1991

[The migration behavior of human vascular myocytes in culture--the screening potential of anti-arteriosclerosis active endogenous and exogenous substances].

Besides proliferation, migration of smooth muscle cells (SMC) is considered to be an essential cellular mechanism involved in plaque formation. Human SMCs were cultured from 14 arteriosclerotic lesions of coronary (n = 5), femoral (n = 7) and aortic (n = 2) arteries. By a semi-automatic standardized video analysis system SMC migratory activity was quantified to be 21.7 +/- 2.1 microns/h (n = 14; x +/- SD). Addition of drugs, such as calcium antagonists (10(-5) - 10(-7) M), heparin (100 micrograms/ml), SIN-1 (10(-5) M) and colchicine (10(-7) M) resulted in a significant decrease of SMC migratory velocity. Exposure to endogenous extracellular matrix proteins (5 micrograms/cm2) showed no effect for collagen I and a significant reduction of SMC migratory activity for fibronectin, respectively. Our results indicate SMC migratory velocity to be a parameter of potential interest to screen various substances for an anti-arteriosclerotic effect.

Arteriosclerosis↗
PubMed1991

[Increased in vitro motility of human vascular wall myocytes from restenotic lesions of peripheral and coronary vessels].

In this study we report on the successful cultivation of human peripheral and coronary plaque specimens selectively retrieved by percutaneous Simpson atherectomy and obtained by direct operative approach. A total of 32 patients in whom plaque tissue was excised from 22 primary and 10 restenotic lesions comprise the study population. Irrespective of their origin or location, all advanced lesions showed smooth muscle cells (SMC) to be their predominant cell type proven by indirect immunofluorescence technique. Cultured endothelial cells were only identified in 2/6 surgically removed samples. Locomotion analysis of cultured smooth muscle cells was performed with a standardized computer-assisted video system. Cells of all groups exhibited random motility. However, SMC migratory velocity of restenotic origin amounted to 47.4 +/- 3.4 microns/h (n = 10, x +/- SD) and thereby was found 2.4 times (p less than 0.001) increased as compared to primary lesion values of 22.0 +/- 3.7 microns/h (n = 22, x +/- SD). This highly significant difference was seen for both peripheral and coronary lesions. Our data suggest increased SMC migratory activity to represent a basic biological mechanism involved in human accelerated arteriosclerosis and restenosis formation.

Aged↗
PubMed1990

[Early and late results of subclavian transposition].

The subclavian-carotid transposition presents nowadays an elegant procedure for the treatment of the steal syndrome in subclavian stenosis. In 85 patients we were able to establish normal blood pressure without operative mortality. Follow-up examination after a mean time interval of 48 months revealed no reocclusion and 81% had complete relief of symptoms, whereas 18% were improved. The low operative morbidity, combined with the favorable late results demonstrate, that transposition is the method of choice for the treatment of subclavian steal syndrome. The operative procedure and the potential difficulties are described extensively, based on our experiences.

Adult↗