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H Rieder

Publications and source records attributed to H Rieder.

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

Polymerase chain reaction analysis of BCR-ABL sequences in adult Philadelphia chromosome-negative acute lymphoblastic leukemia patients.

The Philadelphia (Ph) translocation is the most common cytogenetic abnormality in adult acute lymphoblastic leukemia (ALL) and is associated with an adverse prognosis. Using polymerase chain reaction (PCR) technology we recently observed a remarkably high incidence (55%) of BCR-ABL rearrangements in adult common ALL patients. In the present study we asked whether a subset of Ph-negative cALL, similarly to Ph-negative chronic myelocytic leukemia (CML) patients, exhibit BCR-ABL transcripts. PCR analysis of 58 adult Ph-negative cALL patients, including 47 cases with a normal karyotype revealed no evidence of chimeric BCR-ABL genes. We conclude that Ph-negative BCR/ABL-positive ALL is very rare entity if existing at all.

Adult↗
PubMed1991

Evidence for the identity of human scatter factor and human hepatocyte growth factor.

Scatter factor (SF), a secretory protein of fibroblasts, dissociates and increases the motility of epithelial cells and may be involved in cell migration processes during embryogenesis and tumor progression. Hepatocyte growth factor (HGF), a protein isolated from serum of patients with liver failure, is a potent mitogen for hepatocytes and is thought to play a role in liver regeneration. Here we present structural and functional evidence that human SF and human HGF (and also the human lung fibroblast-derived mitogen) are identical proteins encoded by a single gene, since (i) no major difference could be found by protein sequencing, by cDNA analysis, and by immunological comparison and (ii) SF in fact acts as a hepatocyte growth factor--i.e., stimulates DNA synthesis of activity--i.e., dissociates and induces invasiveness of various epithelial cells. The human SF/HGF gene was localized to chromosome bands 7q11.2-21. These results have important consequences for further studies on the involvement of SF/HGF as a modulator of cellular growth and motility in embryonal, malignant, and regenerative processes.

Amino Acid Sequence↗
PubMed1991

Sinusoidal endothelial liver cells in vitro release endothelin--augmentation by transforming growth factor beta and Kupffer cell-conditioned media.

Endothelin is the most potent vasoconstrictor peptide known today. Using a radioimmunoassay for endothelin, we measured immunoreactive endothelin in culture media of guinea pig sinusoidal endothelial liver cells and human umbilical vein endothelial cells. A time-dependent release of immunoreactive endothelin by confluent sinusoidal endothelial liver cells in culture was found. Sinusoidal endothelial liver cells produced similar amounts of immunoreactive endothelin as umbilical vein endothelial cells, about 900 pg/microgram DNA per 24 h. In the presence of transforming growth factor beta a dose-dependent increase of immunoreactive endothelin release was measured. The maximal increase of 50% was found at a concentration of 1 ng transforming growth factor per ml. To a similar extent Kupffer cell-conditioned media augmented the release of immunoreactive endothelin by sinusoidal endothelial liver cells, especially when Kupffer cells had been stimulated by endotoxin. Endotoxin itself did not alter the release of immunoreactive endothelin. Endothelin released by sinusoidal endothelial liver cells might influence the pericytes of the liver, i.e., the Ito-cells.

Animals↗
PubMed1991

[Pancreatitis associated with 5-aminosalicylic acid].

Acute pancreatitis with severe belt-like upper abdominal pain developed within 1-4 weeks of starting medication in three patients (29-year-old man with ulcerative colitis; 43-year-old woman and 22-year-old woman with Crohn's disease) treated, for the first time, with 5-aminosalicylic acid (mesalazine), 500 mg three times daily. Concentrations of lipase initially were 545, 1182 and 3000 U/l, and of amylase 243, 449 and 129 U/l, respectively. Symptoms receded within a few hours after the drug had been discontinued, enzyme levels returning to normal in the course of the next 2-3 weeks. On repeating the drug in two of the patients, in lower dosage, the pancreatitis recurred within a few days. These observations support the view that 5-aminosalicylic acid can cause acute pancreatitis, perhaps as an allergic reaction.

Acute Disease↗
PubMed1991

Dexamethasone modulates alpha 2-macroglobulin and apolipoprotein E gene expression in cultured rat liver fat-storing (Ito) cells.

Fat-storing (Ito) cells are perisinusoidal liver cells thought to play a central role in vitamin A metabolism and fibrongenesis. Glucocorticoids have been shown to be beneficial in the treatment of certain types of liver diseases by delaying the development of cirrhosis. To study the regulatory effects of dexamethasone on Ito cell gene expression, Ito cells were isolated from normal rat liver and primary cultures were established. The effect of dexamethasone on the synthesis of alpha 2-macroglobulin, apolipoprotein E, fibronectin and actin was examined. Protein synthesis was studied both at the protein level and at the RNA level by means of biosynthetic labeling, immunoprecipitation followed by sodium dodecyl sulfate-polyacrylamide gel electrophoresis and by Northern blot analysis of total RNA. After exposure to dexamethasone for 20 hr, alpha 2-macroglobulin protein synthesis was increased threefold, whereas apolipoprotein E expression was decreased 80%. Biosynthesis of fibronectin remained unaffected by hormone treatment. The dexamethasone effect became detectable 5 hr after beginning the exposure. Deinduction kinetic experiments showed that the glucocorticoid effect was detectable more than 12 hr after the replacement of the dexamethasone-containing culture medium by medium without the hormone. Corresponding to the data obtained at the protein level, dexamethasone increased the steady-state levels of alpha 2-macroglobulin-specific messenger RNA and reduced apolipoprotein E-specific transcripts, whereas fibronectin and actin messenger mRNA remained unchanged.(ABSTRACT TRUNCATED AT 250 WORDS)

Actins↗
PubMed1991

Tenascin gene expression in rat liver and in rat liver cells. In vivo and in vitro studies.

Tenascin is a major glycoprotein constituent of the extracellular matrix with a strong affinity to fibronectin; its distribution is believed to be temporarily and spatially limited. Tenascin gene expression is increased during wound healing processes. As repair mechanisms in chronic liver diseases resemble wound healing we studied tenascin gene expression in rat liver and in isolated rat liver cells. In normal rat liver a tenascin specific antiserum stains sinusoidal cells with fiber-like prolongations, which at the same time are desmin-positive (ITO-cells). In the CCl4-acutely-damaged liver a strong tenascin staining is detected in cells located among the mononuclear cells of the inflammatory infiltrates in the areas of necrosis and in cells of the sinusoids. In CCl4-chronically-damaged liver a strong tenascin staining is demonstrable in the connective tissue septa. In both cases, many of the tenascin-positive cells can be identified as desmin-positive by means of the double-staining fluorescence technique. The wall of larger vessels is always tensacin-negative. The staining pattern obtained with a fibronectin-specific antiserum is somewhat comparable with that of tenascin but the vessel wall was positive. hepatocytes, Kupffer cells, ITO-cells and endothelial cells were isolated from rat liver and studied for their capacity to express the tenascin gene. Biosynthetically labeled tenascin was immunoprecipated from supernatants and cell lysates obtained from cultured ITO-cells and to a much lesser extent from intracellular lysates obtained from endothelial cells; its synthesis in ITO-cells increased during the time in culture. Tenascin was also identified immuno-cytochemically in increasing amount in ITO-cells in culture.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1991

Serum hyaluronate and type III procollagen aminoterminal propeptide concentration in chronic liver disease. Relationship to cirrhosis and disease activity.

To analyse the relationship between the presence of liver cirrhosis and hepatic inflammation and the serum concentrations of the aminoterminal propeptide of procollagen type III (P-III-NP) and of hyaluronic acid (HA) in chronic liver disease, we measured P-III-NP and HA concentrations in paired serum samples from 133 patients with various chronic liver diseases, from 22 patients with acute hepatitis and from 50 healthy age-matched controls. In 24 (of the 133) patients with autoimmune chronic liver disease, follow-up determination was performed during therapeutic treatment with immunosuppressive drugs. Compared with controls P-III-NP concentrations (medians) were significantly elevated in 65% of patients with chronic active hepatitis (P = 0.00097) and in 79% of patients with active liver cirrhosis (P = 0.0126) but not in patients with chronic persistent hepatitis (P = 0.06). Serum concentrations (medians) of HA were increased (P = 0.0058) in 32% of patients with chronic active hepatitis and in 91% of patients with active cirrhosis (P less than 6 x 10(-7)). The difference of HA serum concentrations but not that of P-III-NP serum concentrations in patients with chronic active hepatitis and in patients with active cirrhosis was statistically significant. HA and P-III-NP serum concentrations were significantly elevated in 22 patients with acute hepatitis.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1991

[Genesis of fibronectin in ascites--detection of cellular and plasma fibronectin in portal and malignant ascites].

Measurement of fibronectin in ascites has been proposed for the differentiation of ascites either due to malignant growth in the peritoneal cavity or liver cirrhosis with portal hypertension. The high ascitic fibronectin concentration in patients with peritoneal carcinomatosis was thought to be due to the synthesis of this protein by neoplastic cells. Therefore in ascites of malignant origin cellular fibronectin should be present as it is synthesized by neoplastic cells. On the other side the transsudative ascites due to liver cirrhosis with portal hypertension should mainly contain plasma-fibronectin, which is secreted by hepatocytes into the bloodstream. With the aid of two different monoclonal antibodies and immunoblotting of partially digested or intact ascitic fibronectin, cellular fibronectin could be demonstrated in ascitic fluid of 10 patients with peritoneal carcinomatosis, 13 patients with liver cirrhosis, one patient with right-sided heart failure and one patient with Budd-Chiari-Syndrome. As determined by a specific ELISA 8 out of 10 samples of malignant ascites contained more than 30 mg/l of cellular fibronectin, whereas 10 out of 13 samples of ascites due to liver cirrhosis contained less than 10 mg/l. Whereas in ascites of malignant origin cellular fibronectin represented about 20% of total fibronectin, in portal ascites fibronectin represented sometimes more than 50% of total fibronectin. Cellular fibronectin of non-malignant origin is probably produced by mesothelial cells or peritoneal macrophages. Therefore, fibronectin accumulating in peritoneal carcinomatosis is only to some extent locally produced, but mainly caused by an unhindered exsudation of plasma-fibronectin.

Adult↗
PubMed1990

Chromosomal in situ hybridization of a Hodgkin's disease-derived cell line (L540) using DNA probes for TCRA, TCRB, MET, and rRNA.

The Hodgkin's lymphoma-derived cell line L540, which exhibits multiple marker chromosomes and a genotype characteristic of T-cell origin, showed expression of MET oncogene. L540 was studied by in situ hybridization for chromosomal rearrangements concerning the regions where genes for TCRA and TCRB chains, for MET oncogene, and for rRNA are located. All four genes were demonstrated to be involved in the formation of marker chromosomes. Especially remarkable was the participation of rDNA-bearing regions in two different translocations.

Cell Line↗
PubMed1990

Expression of the gene of the alpha-smooth muscle-actin isoform in rat liver and in rat fat-storing (ITO) cells.

Fat storing cells (FSCs) in the liver represent the main site of vitamin A deposition in the body. These cells are considered to play an important role during scar formation and fibrogenesis in the liver. The putative descent of FSCs from the fibroblastic or from the myofibroblastic system have not been determined yet by morphological or immunohistochemical studies. To further define the origin of these liver cells, we analysed the pattern of expression of three structural proteins: vimentin, desmin and the alpha-smooth muscle (SM)-actin isoform in FSCs of the rat liver, in smooth muscle cells (SMCs) from the aorta and in rat skin fibroblasts. FSCs were studied by immunohistochemical methods immediately after isolation, at days 3 and 7 after plating. FSC-gene-expression was also analysed by Northern blot analysis of total RNA extracted from cells in culture at days 3 and 7 after isolation. Arterial SMCs and skin fibroblasts were studied in a similar way. For comparison, isolated rat hepatocytes and Küpffer cells (Kc) were studied. Of freshly isolated FSCs, 100% were vimentin-positive, 50% were desmin-positive, but all were alpha-SM-actin negative. Three days after isolation, FSCs were clearly positive for vimentin and desmin and weakly alpha-SM-actin-positive, as demonstrated by indirect immunofluorescence as well as by the immunoperoxidase technique. Desmin, alpha-SM-actin and vimentin staining was further increased at day 7 after isolation, and alpha-actin specific transcripts in FSC-RNA were clearly detectable at day 7 after isolation. Passaged arterial SMCs were vimentin- and alpha-SM-actin-positive, but desmin-negative and fibroblasts were only vimentin-positive.(ABSTRACT TRUNCATED AT 250 WORDS)

Actins↗
PubMed1990

Prostanoid release of cultured liver sinusoidal endothelial cells in response to endotoxin and tumor necrosis factor. Comparison with umbilical vein endothelial cells.

Vascular endothelial cells release prostanoids, especially prostacyclin, when properly stimulated. In addition to short acting stimuli like thrombin and histamine an increased prostanoid release occurs in the presence of endotoxin, interleukin 1 or tumor necrosis factor (TNF). The response of sinusoidal endothelial liver cells to such stimuli - probably important in hepatic inflammatory disease - is unknown. Sinusoidal endothelial liver cells from the guinea pig were isolated by centrifugal elutriation and investigated as confluent monolayers. Their prostanoid release in response to endotoxin and human recombinant TNF was determined by radioimmunoassays and compared to that obtained with cultured human umbilical vein endothelial cells. A pronounced time- and dose-dependent release of prostanoids was found with both cell types in response to endotoxin. In contrast to umbilical vein cells, liver endothelial cells produced not only large amounts of 6-keto-PGF1 alpha and some PGE2 but also thromboxane B2. Only umbilical vein endothelial cells responded to TNF with an increased 6-keto-PGF1 alpha release, emphasising the metabolic differences between both cell types.

6-Ketoprostaglandin F1 alpha↗
PubMed1990

Sport activity and personality as elements in preventing cancer and coronary heart disease.

Results are reported for 3 groups of healthy male probands, 318 in each group, matched for age and personality type on the Personality-Stress Questionnaire. One group was actively engaged in sports, one had discontinued former sporting activities, and one group had never taken part in regular sports. Follow-up after 13 yr. showed lowest mortality in those actively engaged in sport, highest mortality in those who had given up sport, with those who had never been engaged in sport intermediate. Prophylactic behaviour therapy was shown to reduce mortality of those who had given up sport to a significant extent but not to affect degree of retinal sclerosis.

Adult↗
PubMed1989

Fat-storing (Ito) cells of rat liver synthesize and secrete apolipoproteins: comparison with hepatocytes.

Fat-storing cells of the liver store most of the vitamin A of the body. Vitamin A is present in a few large fat droplets within the cell. The aim of our study was to investigate apolipoprotein biosynthesis in isolated fat-storing cells from rat liver during the time in culture. Isolated rat hepatocytes were studied for comparison. Proteins were biosynthetically labeled and further identified by immunoprecipitation and sodium dodecyl sulfate-polyacrylamide gel electrophoresis analysis. Apoproteins in culture supernatants were identified by density gradient ultracentrifugation and by one- and two-dimensional sodium dodecyl sulfate-polyacrylamide gel electrophoresis analysis of aliquots of the gradient. Rat plasma was processed in the same way and used for comparison. Fat-storing cells synthesized and secreted apoprotein E, apoprotein A-I, apoprotein A-IV, and low amounts of apoprotein C. The synthesis of these proteins increased during the culture time, reaching a maximum at the fifth day after isolation. The proteins were identified mostly as apoproteins of high-density lipoprotein. Hepatocytes synthesized and secreted apoproteins of all classes of lipoproteins. The distribution of high-density lipoprotein apoproteins was similar to that of fat-storing cells but hepatocytes produced larger amounts of the apoproteins.

Animals↗
PubMed1989

Murine tissue macrophages synthesize and secrete amyloid proteins different to amyloid A (AA).

We recently demonstrated that serum amyloid A (SAA) gene expression can be induced in extrahepatic sites with exception of the brain. Furthermore we demonstrated that tissue macrophages express SAA-gene constitutively and that SAA-gene expression can be increased by endotoxin. Until now the protein corresponding to the SAA-specific mRNA contained in macrophages has not been identified. We compared proteins precipitated from endogenously labelled samples by three antisera against amyloid A (AA) raised in different laboratories. Radiolabelled samples were derived from murine hepatocyte cultures, from cell-free translation of acute phase liver RNA or hepatocytes RNA and from peritoneal macrophages as well as Kupffer cells. All three antisera recognize a protein of 12.5 kDa Mr produced by hepatocytes (SAA), and a major protein of 14.3 kDa Mr contained in the cell-free translation products; this is the precursor of the mature SAA as demonstrated by cleavage experiments with canine pancreas microsomal enzymes. The antisera also recognize two proteins--a major one of 14.5 kDa Mr and a second of 12.5 kDa Mr contained in the supernatants and cell lysates of liver and peritoneal macrophages. New antisera raised against the two proteins do not recognize any protein, either of hepatocyte or of cell-free translation samples; they specifically precipitate two proteins from macrophage samples with the same molecular mass as that of the proteins precipitated by the anti SAA antisera. Murine acute phase sera do not react with the new antisera. However, amyloid deposits of amyloidotic mice specifically react with the new antisera. We describe two new components of murine amyloid produced by tissue macrophages.

Acute-Phase Proteins↗