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Biomedical subjects

B Voss

Publications and source records attributed to B Voss.

At least 73 records · Page 4Linked to original sources
PubMed1992

Cellular autofluorescent pigment and interstitial fibrosis in smoker's lung.

The mechanisms by which cigarette smoking lead to bronchopulmonary diseases are incompletely understood. The most characteristic lesion is a chronic macrophage-alveolitis accompanied by slight fibrosis and emphysema. The macrophages contain a ceroid-like granular autofluorescent pigment in their lysosomes. Using immunohistochemical methods, open lung-, transbronchial biopsies and cells obtained by broncho-alveolar lavage from cigarette smokers were studied: anti-human macrophage serum and anti-human elastase, immune sera against type I, type III collagens and fibronectin were used in the demonstration of the cellular components of alveolitis and the connective tissue constituents of fibrosis. The characteristic red-brown autofluorescent pigment of the macrophages was also found in an extra-alveolar location mainly in peribronchial, septal and pleural scars. Similar emission colour occurred focally in the elastic laminae of fibrotic alveoli and sclerotic arteries. Granular fluorescent pigment was found in many bronchial epithelial cells. The epithelial pigmentation was associated with increased transcription of nucleic acid proteins, revealed by colloid silver (AgNOR) reaction. The results suggest that the autofluorescent pigment substances in macrophages may indicate or also play a role in the development of pathological connective tissue and epithelial changes of smoker's lung, in addition to the known mediators and enzymes.

Adult↗
PubMed1991

Changes of DNA-acridine orange binding in monocytes and endothelial cells of hypertensive arteries.

The interactions of monocytes and endothelial cells were examined employing acridine orange (AO) binding to chromatin as an electron microscopic probe for studying changes in nuclear activity. The number of AO labeled nuclei were determined in adherent and sub-endothelial monocytes, and endothelial cells either associated with or devoid of monocytes in mesenteric arteries of renal hypertensive and normotensive rats. No AO-positive cell nuceli were found in the few adherent monocytes in the normotensive rats while in hypertensive rats 63% of the adherent monocytes and 86% of the subendothelial monocytes were labeled by AO. The number of AO-positive cell nuclei increased in the endothelium from 2% in normotensive rats to 17% in hypertensive animals. Fifty-seven percent of these endothelial cells were associated with monocytes adhering to their surfaces. Thirty-nine (52%) of AO-positive and 24 (52%) of AO-negative cell pairs represented 84% of cell pairs with identical nuclear activity. These findings indicate a sequential interaction of monocytes and adjacent endothelial cells recognized at the nuclear level. According to other experimental work the binding capacity of chromatin for AO increases as cell nuclei are reactivated by stimulation of cell proliferation. In addition, AO labeling of chromatin visualized electron microscopically is confined to three of the four stages of the cell cycle. Therefore AO labeling in the present experiments might indicate the reentrance of monocytes and endothelial cells into the cell cycle.

Acridine Orange↗
PubMed1991

Localization of elastase and tumor necrosis factor alpha mRNA by non-radioactive in situ hybridization in cultures of alveolar macrophages.

Digoxigenin is a new tool for labeling probes which can be detected with the help of specific antibodies in the cell by indirect or direct immunostaining. In contrast to the biotin-reaction, the advantage of digoxigenin is that it does not appear in animal or human cells in nature. In comparison to radioactive labeling methods it is favorable in terms of short exposure time and precise localization of signals in the cell. In this paper we describe the localization of elastase and tumor necrosis factor alpha (TNF alpha) mRNA by non-radioactive in situ hybridization of rat alveolar macrophages in cell culture after stimulation with welder steam dusts. Using digoxigenin labeled probes the determination of specific mRNA's expression and their precise localization in the cytoplasm of the cell could be achieved within one day.

Animals↗
PubMed1991

E-cadherin-mediated cell-cell adhesion prevents invasiveness of human carcinoma cells.

The ability of carcinomas to invade and to metastasize largely depends on the degree of epithelial differentiation within the tumors, i.e., poorly differentiated being more invasive than well-differentiated carcinomas. Here we confirmed this correlation by examining various human cell lines derived from bladder, breast, lung, and pancreas carcinomas. We found that carcinoma cell lines with an epithelioid phenotype were noninvasive and expressed the epithelium-specific cell-cell adhesion molecule E-cadherin (also known as Arc-1, uvomorulin, and cell-CAM 120/80), as visualized by immunofluorescence microscopy and by Western and Northern blotting, whereas carcinoma cell lines with a fibroblastoid phenotype were invasive and had lost E-cadherin expression. Invasiveness of these latter cells could be prevented by transfection with E-cadherin cDNA and was again induced by treatment of the transfected cells with anti-E-cadherin mAbs. These findings indicate that the selective loss of E-cadherin expression can generate dedifferentiation and invasiveness of human carcinoma cells, and they suggest further that E-cadherin acts as an invasion suppressor.

Antibodies, Monoclonal↗
PubMed1990

Extracellular matrix in preneoplastic lesions and early cancer of the lung.

Characterization of preneoplastic lesions mainly concentrated on cellular, nuclear and epithelial atypias. The extracellular matrix was almost neglected, although malignant tumour cells interact with extracellular matrix molecules during tumour invasion. Until now systematic investigations of extracellular matrix components in preneoplastic lesions and early stages of lung cancer are lacking. 150 preneoplastic lesions, 10 specimens of early cancer and 30 specimens of normal bronchial mucosa were examined by means of immunofluorescence microscopy. The distribution of collagen type I and III and the non-collagenous glycoproteins laminin and fibronectin have been investigated by an indirect immunohistochemical method. With an increasing degree of preneoplasia an increased matrix disarrangement of the basement membrane zone could be observed. In severe dysplasia and carcinoma in situ neosynthesis of collagen type III and especially laminin in close association to neoangiogenesis could be demonstrated besides a disintegration of extracellular matrix components. In early lung cancer numerous laminin positive basement membrane like structures are situated around tumour cells. An enhanced deposition of collagen type I and III fibres could be demonstrated around tumour cell islets. The results indicate a partial loss of function in preneoplastic basal cells in cases of dysplasia and carcinoma in situ. In early stages of invasive squamous cell carcinoma of the bronchus, extracellular matrix components obviously could be produced by tumour cells.

Basement Membrane↗
PubMed1990

Ultrastructural localization of extracellular matrix proteins in liver biopsies using ultracryomicrotomy and immuno-gold labelling.

We describe a technique for the localization of extracellular matrix proteins in wedge and needle biopsy specimens of human liver. Using ultra-thin (50-70 nm) sections of puncture perfusion fixed tissue, extracellular matrix proteins were localized using a protein A-gold labelling procedure. We obtained good preservation of ultrastructural detail and specific labelling for collagen types I, III and IV and fibronectin. The method represents a sensitive means of identifying the extracellular distribution and the cellular origin of these proteins in normal and diseased human liver.

Biopsy↗
PubMed1990

[The effect of endothelial interaction on the binding capacity of DNA acridine orange in hypertension].

Interaction of monocytes and endothelial cells were examined by acridine orange reaction in arteries of normotensive and hypertonic rats. The method is suitable for electron microscope study of DNA template activity. Activity of gen was compared in surface bound and subendothelial and in nonadhesive endothelial cells bound to monocyte. Acridine orange positivity, indicative of genic activity, was not found in few monocytes adhered in arteries of normotensive animals, while 62% of adhesive monocytes of hypertonic and 86% of ones accessed to endothelial space contained the products of acridine-orange-chromatin reaction in its nuclear, showing with it the gene derepression quickly ensuing in acute hypertensive vascular lesions. Only 2% of endothelial cells of pseudo-operated normotensive animals showed acridine orange positivity, while 17% of endothelial cells of hypertonic animals were positive. In the latter animals, 57% of endothelial cells showed acridine orange positivity, if monocytes adhered to their surface. In 84% of monocyte-endothelial pairs connected to each other, the nuclei have activity of same sign. Results show intensive activation of genes of monocytes in relation with adhesion and migration to vascular wall. Presumably, both hypertonia and monocyte adhesion have contributed to the increase of template activity of endothelial cells.

Acridine Orange↗
PubMed1989

Detection of an alteration of the alpha 2-macroglobulin gene in a patient with chronic lung disease and serum alpha 2-macroglobulin deficiency.

alpha 2-Macroglobulin (A2M) is a major human plasma protease inhibitor capable of inhibiting most endopeptidases tested so far. In the case of the other major plasma protease inhibitor, alpha 1-antitrypsin, genetically determined deficiency states are known to increase the risk of chronic obstructive pulmonary disease (COPD) 20- to 30-fold in affected individuals. No defects of the A2M gene have been described as yet, but A2M may play a role in the regulation of protease activity in the lung, especially with respect to those proteases not inhibited by alpha 1-antitrypsin. We report here the molecular genetic detection of an alteration of the A2M gene in a patient with serum A2M deficiency and chronic lung disease since childhood. The alteration involves restriction sites detected with 10 different enzymes and is most probably caused by a major deletion or rearrangement of the gene. Nine of the restriction enzymes used detected no polymorphisms in 40 healthy control subjects and 39 COPD patients. The polymorphism detected in this patient with the enzyme PvuII was different from another described previously, and was found in this patient only. The patient is heterozygous for an alteration in the A2M gene; this may be responsible for his serum A2M deficiency and may be relevant to the early onset of pulmonary disease in his case.

Adult↗
PubMed1989

Evaluation of serum laminin P1, procollagen-III peptides, and N-acetyl-beta-glucosaminidase for monitoring the activity of liver fibrosis.

Chronic liver diseases are characterized by an increase in connective tissue components in liver tissue. The determination of Col 1-3 peptide of type III procollagen (P-III-P) in serum of patients seems to be a useful parameter of hepatic fibroplasia. Specific radioimmunoassays are available for Col 1-3 (P-III-P) and the Col 1 and Col 1-3 (P-III-P-Fab) peptides of type III procollagen and for laminin P1 fragment. These proteins and the activity of N-acetyl-beta-glucosaminidase (beta-NAG) were measured in 94 patients with chronic liver diseases, and in 74 healthy controls. In addition, direct immunofluorescence studies were done for laminin P1 in normal and fibrotic liver tissues. In normal human liver, laminin was found in the basement membrane of bile ducts and in blood vessel walls. In fibrotic liver tissue, laminin additionally occurred in periportal areas and in sinusoids co-distributed with other connective tissue components. In serum concentrations of P-III-P, P-III-P-Fab and laminin were higher in patients than in healthy subjects. Laminin concentration was increased in early stages of chronic liver disease, possibly as a marker of regeneration; the highest concentrations were in active cirrhosis and chronic active hepatitis. The determination of P-III-P and P-III-P-Fab provided information on synthesis and degradation of type III collagen: In inactive cirrhosis, Col 1 peptide was increased in relation to Col 1-3 peptide.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylglucosaminidase↗
PubMed1988

Hydrocortisone-induced accumulation of fibronectin mRNA and cell surface-associated fibronectin.

A Morris hepatoma 7777-derived cell line, DTH-3, was used to study the control of fibronectin gene expression. In cultures of DTH-3 cells in conventional medium supplemented with serum or in chemically defined MX-83 medium supplemented with insulin no cell surface fibronectin was detectable by indirect immunofluorescence techniques using specific polyclonal antibodies. By Northern blot hybridization analysis a dose- and time-dependent accumulation of 8 kb fibronectin mRNA in response to hydrocortisone treatment was demonstrated. Furthermore, 24 h after addition of hydrocortisone an extensive fibrillar fibronectin network was established. The results suggest that the hydrocortisone-dependent induction of fibronectin production might, at least in part, be controlled at the transcriptional level.

Animals↗
PubMed1988

Characterization of human extrahepatic biliary duct epithelial cells in culture.

In order to study human bile duct cells in vitro, cystic ducts were obtained during cholecystectomy and treated with collagenase and mechanical abrasion to isolate biliary epithelial cells. The culture medium was supplemented with 50% of a bovine bile duct conditioned medium obtained by incubating minced bovine extrahepatic bile ducts for 24 hr in Dulbecco's modified Eagle's medium. Cells grew in monolayer and showed contact inhibition at confluency. The epithelial origin of primary cultures was verified by their growth pattern, ultrastructure, and indirect immunofluorescence for cytokeratin. The cultures showed specific immunofluorescence for lysozyme, collagen types I, III, and IV, fibronectin, and laminin, but were negative for collagen type V and factor VIII-associated antigen. Thus, these cultures provide an experimental model for the in vitro study of biliary atresia and other bile duct diseases.

Animals↗
PubMed1987

Asbestos induced fibrosis in the omentum of rats. Immunofluorescence microscopical demonstration of collagens types I and III; laminin and fibronectin.

Fibrosis and neoplasia are evoked by asbestos fibres. Different experimental models have been used to elucidate the cellular mechanism of their pathogenesis but there is no report available dealing with the role of structural glycoproteins and collagens in the development of the fibrosis. The omentums of 20 female SPF-Sprague-Dawley rats were investigated 1, 2 and 6 months after intraperitoneal injection of 15 mg UICC reference samples of crocidolite, by light- and immunofluorescence microscopy. Using monospecific antibodies, laminin, collagens types I and III and fibronectin were localized. After 6 months typical asbestos bodies were detected. By indirect marking of the basal lamina with anti-laminin-antibodies the marked degree of vessel proliferation occurring during the development of granuloma became visible. The deposition of connective tissue which was already established after 4 weeks was mainly due to collagen type III. After 4 and 8 weeks an accumulation of fibronectin associated with larger asbestos fibres was observed. The results suggest that fibrogenesis is promoted by the opsonic activity of fibronectin for long asbestos fibres. The fibrosis may derive from activated resident fibroblasts.

Animals↗
PubMed1987

Serum concentration of N-terminal procollagen peptide of collagen type III in schistosomal liver fibrosis.

The major cause of mortality in human schistosomiasis is the chronic granulomatous reaction of the liver tissue to Schistosoma mansoni eggs. Liver biopsy still provides the best evaluation of the degree of liver damage. However, liver biopsy does not provide an image of the dynamic process of fibrogenesis. Variations of concentrations of procollagen type III peptide in sera have been proposed to be significant markers of liver fibrosis. Thus, liver function tests in relation to histopathological diagnosis and procollagen type III peptide concentrations were studied in patients with schistosomiasis and revealed a high correlation between the serum procollagen type III peptide and the degree of fibrosis in liver tissue.

Adult↗
PubMed1986

Concentrations of 7S collagen and laminin P1 in sera of patients with diabetes mellitus.

Specific radioimmunoassays were used to quantify two basement membrane components, 7S collagen and laminin P1, in sera of 70 patients suffering from diabetes mellitus types I and II with and without clinical signs of chronic diabetic complications. Serum levels of both antigens were increased in diabetics compared to controls (p less than 0.001). Concentrations of 7S collagen were significantly different in diabetics with signs of microvascular damage compared to those without small vessel disease (p less than 0.05). The difference between laminin P1 concentrations in the two groups of diabetics was not significant (p less than 0.2). The augmented levels of circulating 7S collagen and laminin P1 may reflect alterations of basement membrane metabolism. Thus, the measurement of concentrations of these basement membrane components in serum may be a useful tool for monitoring the development of chronic diabetic complications.

Adolescent↗
PubMed1986

Immunogold localization of procollagen III, fibronectin and heparan sulfate proteoglycan on ultrathin frozen sections of the normal rat liver.

In the present study, we have localized by immunocytochemistry at the LM and EM level, procollagen type III (PIIIP), fibronectin (FN) and heparan sulfate proteoglycan (HSPG). Intracellularly, PIIIP was observed in both parenchymal and endothelial cells. In parenchymal cells, PIIIP was found in Golgi derived vesicles. This observation suggests that PIIIP synthesis is a normal function of liver parenchymal cells. In endothelial cells, vesicles, which could not be identified, were seen to contain PIIIP. This result does not allow to conclude, whether sinusoidal endothelial cells secrete or take up PIIIP. Extracellularly, PIIIP was present around portal and central veins, in the space of Disse and between adjacent parenchymal cells. In the space of Disse, almost all interstitial collagen fibrils reacted with the anti PIIIP antibodies. This observation leads to the conclusion that most fibrils of the space of Disse contain type III in addition to type I collagen molecules. By immunofluorescence, FN was seen mainly along the sinusoids in discrete dots. By EM, FN was found to be present in diffuse material closely associated with the sinusoidal membrane of the parenchymal cells and in strands connecting adjacent parenchymal cells, parenchymal and endothelial cells or parenchymal cells and collagen fibrils. FN was also present in vascular and ductular basal laminae. Strong HSPG reaction was observed around bile ducts. Moderate reaction was seen around blood vessels and in the space of Disse. In the latter location, the ultrastructural distribution of HSPG resembles that of FN, i.e. HSPG is present in diffuse material and in strands.

Animals↗