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Biomedical subjects

E Vollmer

Publications and source records attributed to E Vollmer.

At least 55 records · Page 3Linked to original sources
PubMed1993

A probably familial saccular aneurysm of the anterior communicating artery in a neonate.

A 32-day-old boy died of recurring cerebral hemorrhages starting on the 4th day of life. Autopsy disclosed a remittingly ruptured saccular aneurysm of the anterior communicating artery. A 7-day-old brother of his had previously died of recurring subarachnoid hemorrhages as well. The young age of the patient, the site of the aneurysm, and its probably familial occurrence make this case a unique one. Nonaneurysmatic basal cerebral arteries showed remarkable histological changes partly resembling those seen in fibromuscular dysplasia, some of them probably representing preaneurysmatic alterations. A known underlying systemic disease could not be found, and immunohistochemical detection of type III collagen revealed no identifiable deficiency.

Aneurysm, Ruptured↗
PubMed1993

Divergent and co-localization of the two small proteoglycans decorin and proteoglycan-100 in human skeletal tissues and tumors.

The core protein of a recently described small proteoglycan, proteoglycan-100, was localized in fetal human tissues by indirect immunocytochemistry and compared with the localization of known members of the small proteoglycan family. Co-localization of decorin and proteoglycan-100 was seen in bone tissue but decorin and proteoglycan-100 exhibited a substantially divergent distribution in fetal skin, cartilage and in the mineralization zone of the growth plate. Proteoglycan-100 was also found in striated muscle, nerve fibers, and synovial tissue. Immunostaining of a chondroblastic osteosarcoma demonstrated chondroid cells selectively expressing either proteoglycan-100 or decorin. Co-expression of both small proteoglycans was observed in sections from a chordoma. In fetal bone and in the two tumors, colocalization of proteoglycan-100 and of biglycan was also found. These results provide evidence of the wide and characteristic distribution of proteoglycan-100.

Bone Neoplasms↗
PubMed1991

Distribution patterns of apolipoproteins A1, A2, and B in the wall of atherosclerotic vessels.

Atherosclerotic vessels were analysed histochemically for distribution, quantity, and composition of apolipoprotein (Apo) types in the vascular wall. The specimens comprised all stages of atherosclerosis, from very discrete intimal changes to complicated lesions. The vessel specimens were marked with antibodies against human Apo A1, A2, and B. Apo A1 can be demonstrated in even the earliest stage of atherosclerosis, and increases with the progression of the disease. In the initial stage, Apo A1 is found first in lumen-adjacent layers of the intima, and is evident in deeper layers of the wall as the disease progresses. Arteries of muscular type show accumulation of Apo in an earlier stage (or in greater quantity at the same stage) than arteries of elastic type. At all stages, the amount of Apo A1 always exceeds that of A2 and B. In the intima, Apo B is higher than Apo A2, the media contains hardly any Apo B, and the adventitia has less B than A2. Within the intimal layer, Apo A1 and A2 are found in an intracellular (mainly in foam cells) or in an extracellular location, according to the stage of atherosclerosis. Apo B is almost exclusively extracellular; only cases of advanced atherosclerosis show some intracellular localization (mostly in foam cells), visualized as electron dense lamellar organelles, probably of lysosomal origin. In the media, Apo A1 and A2 are accumulated in intracellular deposits, whereas the extracellular storage of Apo A1, A2 and B is observed only in cases with the most severe damage. Our investigations suggest that the accumulation of apolipoproteins in the vascular wall is affected not only by insudation from the plasma, but also by neosynthesis and/or metabolism by locally derived cells or cells immigrating in the process of atherosclerosis. The presence of Apo A1 and A2 in the vessel wall is now documented, and their role at this site apparently differs from that in the plasma.

Aorta↗
PubMed1991

Histogenesis of clear cell chondrosarcoma. An immunohistochemical study with osteonectin, a non-collagenous structure protein.

The histogenesis of clear cell chondrosarcoma is still unclear: Apart from typical clear cell tumor areas, extensive production of woven bone formation suggests within the clear cell cartilagenous stroma is an intriguing phenomenon. Three cases of clear cell chondrosarcoma documented in the Bone Tumor Registry of Westphalia were examined for their patterns of osteonectin expression, and compared with other bone tumors of either osseous or cartilaginous origin, and with normal cartilage tissue. Found predominantly in osseous structures, the protein osteonectin takes part in the formation of new bone. The three clear cell chondrosarcomas showed a strong immunoexpression of osteonectin in clear cell, chondroid and in osseous tumor areas. Similarly, evidence of osteonectin was also found in osteoblastic and in chondroblastic osteosarcomas as well as in osteoblastomas. In contrast, osteonectin could not be demonstrated in the chondrosarcomas and mesenchymal chondrosarcomas from our registry that were analysed for comparison, and was found only minimally in the fibroblastic areas of dedifferentiated chondrosarcomas. The chondroblastic tumor components were always negative. There was no immunoexpression of osteonectin either in fetal or adult intervertebral disc tissue. The present immunohistochemical study of osteonectin has distinctly separated clear cell chondrosarcoma from the other variants of chondrosarcoma, and aptly verified the specificity of this entity. Moreover, the study would call for further histogenetic evaluation of clear cell chondrosarcoma, since the pattern of osteonectin expression in that tumor seems to indicate an osteogenic rather than a chondrogenic origin.

Adenocarcinoma↗
PubMed1991

Immunohistochemical double labeling of macrophages, smooth muscle cells, and apolipoprotein E in the atherosclerotic plaque.

To find out which cell types in the atherosclerotic plaque are actively involved in apolipoprotein-secretion, we stained tissue samples from the ascending aorta of patients undergoing coronary bypass surgery. We used monoclonal antibodies against macrophages, smooth muscle cells and apolipoprotein E. The present in situ-study of the atherosclerotic plaque has shown that apolipoprotein synthesis is predominantly secreted by macrophages transformed into foam cells. Besides this, there are obviously some smooth muscle cells equally transformed to foam cells, which also carry apolipoprotein E in their cytoplasm. Our data suggest that both cell types in the atherosclerotic plaque are actively involved in apolipoprotein secretion.

Apolipoproteins E↗
PubMed1991

Apolipoproteins and immunohistological differentiation of cells in the arterial wall of kidneys in transplant arteriopathy. Morphological parallels with atherosclerosis.

22 nephrectomy specimens of renal allografts in chronic rejection after periods between 3 and 96 months, were studied immunohistologically. Various cell types in the arterial wall were characterized with antibodies specific against different cells of the mononuclear phagocyte system, against smooth muscle cells, and against differentiating lymphoid cells. In addition, the metabolism of lipoproteins was investigated using appropriate antibodies against several apolipoproteins. Subendothelial plaques of foam cells were found to consist of macrophages in foamy transformation. At the stage of intimal fibrosis the smooth muscle cells are more prominent. Lymphatic infiltration consists almost exclusively of T-lymphocytes. Apolipoprotein analysis reveals deposits of Apo A1, A2 and B1, most of them extracellular. According to these results, it is not only immunologic factors that are involved in arterial wall reactions during chronic transplant arteriopathy, but disorders of the lipoprotein metabolism--probably due to endothelial dysfunction--are also playing an important role like in atherosclerosis.

Adolescent↗
PubMed1990

The impact of osteonectin for differential diagnosis of bone tumors. An immunohistochemical approach.

75 osteosarcoma at various grades of histologic differentiation, including chondroblastic and small cell variants, and 5 fibrosarcomas of bone, 5 Ewing's sarcomas, 5 malignant fibrous histiocytomas of bone, 8 chondrosarcomas, and 2 dedifferentiated chondrosarcomas, were investigated immunohistochemically for evidence of osteonectin. According to the results of our study, osteonectin is present in all osteosarcomas, with special topographic preponderance in the osteoblastic and chondroblastic variants. Evidence of osteonectin was also found in all other bone tumors we had analysed so far. In chondrosarcomas, positive reactions appeared only in the vicinity of trabeculae and in dedifferentiated areas. Thus, osteonectin cannot be regarded as a bone-specific protein. Although a high affinity for the osseous matrix is one of its undoubted features, it is therefore unsuitable for differential diagnostic purposes.

Bone Neoplasms↗
PubMed1990

In situ detection of basic fibroblast growth factor by highly specific antibodies.

Basic fibroblast growth factor (bFGF) is thought to be of major importance for fibrosis and angiogenesis. Despite intensive studies dealing with the biochemistry and multiple biologic effects of bFGF, the cellular distribution is virtually unknown. Therefore, using the indirect immunoperoxidase technique, we examined the effect of bFGF on a large pattern of normal, inflammatory, and tumorous human tissues. Staining was performed on cryostat sections with a highly specific affinity-purified antiserum. In normal tissues, especially those of the thymus and placenta, mainly dendritic cells contained the growth factor. High levels of bFGF were also detected in basal cells and gland epithelial cells of skin biopsies. A conspicuous expression was observed in chronic inflammatory tissues corresponding to a generally pronounced proliferation of fibroblasts and endothelial cells in these situations. Tumors revealed a very heterogenous staining pattern. In some lesions, bFGF was predominantly present in infiltrating and endothelial cells. In several, neoplasms tumor cells exhibited an intensive staining. In some, especially vascular tumors, bFGF could not be detected. From the staining results it is concluded that angiogenesis is not simply controlled by the presence of bFGF but is mediated by a balance of several angiogenic inducers and inhibitors.

Blood Cells↗
PubMed1990

Proliferation kinetics of bone tumors.

We investigated bone tumors of various grades of malignancy as well as tumor-like lesions with regard to proliferation kinetic parameters immunohistologically, autoradiographically, and flow cytophotometrically. Good correlation of the established tumor kinetic parameters with the prognostic expectations of the tumor entities was found. Apart from this, possibilities concerning the differential diagnostic analysis of the proliferation rate in a given tumor and its possible grading as well as the possible practical impact of these modern methods on pre- and/or post-therapeutic monitoring of patients are demonstrated.

Antigens, Surface↗
PubMed1989

The proliferation behavior of bone tumors investigated with the monoclonal antibody Ki-67.

Specimens of several tumor entities at various grades of malignancy were selected from the Bone Tumor Registry of Westphalia for an immunohistological study of their proliferation behavior. Using the monoclonal antibody Ki-67 directed against a nuclear antigen present in all active phases of the cell cycle (G1, S, G2, and M), we were able to demonstrate the growth fractions in tissues with an atypical rate of proliferation, implying an increased risk of malignant transformation. In the 97 cases examined we found a good correlation of the biological proliferation behavior with the expression of the nuclear antigen Ki-67. Moreover, our immunohistological results are comparable with the data from the same tumor entities obtained by other methods such as flow cytometry and autoradiography. Thus the monoclonal antibody Ki-67 provides an excellent marker for labeling the growth fraction in a human tissue. Its practical impact lies in the differential diagnostic analysis of the proliferation rate in a given tumor and its possible grading, and in pre- or posttherapeutic monitoring of patients and the establishment of a prognosis.

Adolescent↗
PubMed1989

Immunohistochemical investigation of chordomas: histogenetic and differential diagnostic aspects.

Chordomas are rare tumors of neuroectodermal origin and often show a very heterogeneous histological picture. In a combined histochemical and immunohistochemical study of 32 chordomas collected in the Bone Tumor Registry of Westphalia we were able to show that the immunoreactivity of the cells in both chordoma and notochordal structures are in close relationship with the extracellular matrix and depends more on the metabolic activity of these cells than on the origin of the cells of the neuroectoderm. All tumor cells show a bimodal immunoreaction with cytokeratin and vimentin, as well as a strong immunoreaction with the oncofetal markers CEA and AFP. The differentiation of chordomas from other malignant tumors, mainly the myxoid variant of chondrosarcoma, may cause major difficulties, especially if only a little biopsy material is available. Here we can see that in tumors with bimodal immunoexpression of vimentin and cytokeratin, as can be found in chordomas, the further use of antibodies offers a reliable differential diagnostic tool. The positive reaction of chordomas with all epithelial tumor markers offers a clear differentiation from chondrosarcomas, which, unlike chordomas, do not express cytokeratin. The identification of a marker profile by employing common antisera is of major value in the differentiation of chordoma from other epithelial or mesenchymal tumors.

Adult↗