[Continuous subcutaneous desferrioxamine injection in primary idiopathic hemochromatosis with macrocytic anemia].
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Adult↗
Biomedical subjects
H Richter
Publications and source records attributed to H Richter.
[Estrogen and progesterone receptors in mesenchymal structures of the female urogenital tract].
In 37 women being operated on gynecologically small portions of mesenchymatic tissue have been sampled and analysed with respect to the presence and concentration of estrogen and progesterone receptors within the cytosol fraction. The proofs were taken from: ligamentum cardinale, ligamentum sacrouterinum, pubo-vesico-cervical fascia, paracolpium, ligamentum teres uteri, levator muscle and serving as a comparison tissue from fornix vaginae posterior. In the proofs of pubo-vesico-cervical fascia and paracolpium there were no progesterone receptors. In all the other tissues there were as a matter of principle estrogen and progesterone receptors. However from sample to sample there were wide differences with reference to the existence and the concentration of hormone receptors. There was no correlation to the age of life. The results are discussed and compared with those to be found in literature. MeSH: D 12.776.543.750.830.630 Receptors, estrogen G 6.184.154.803.817.349 Receptors, estrogen G 12.803.817.349 Receptors, estrogen D 12.776.543.750.830.700 Receptors, progesterone G 6.184.154.803.817.777 Receptors, progesterone G 12.803.817.777 Receptors, progesterone A 5.360.319.114.170 Broad ligament A 5.360.319.114.803 Round ligament
Adult↗
Free N-terminal fibronectin 30-kD-domain mediates binding of soluble fibrin to gelfiltered unstimulated thrombocytes.
Gelfiltered unstimulated human platelets neither bound 125-I-fibrinogen nor 125-I-fibrin. Fibrin-binding was, however, stimulated by N-terminal fibronectin 30 kD-and 70 kD-fragments while fibronectin was ineffective. The 30 kD-fragment also stimulated some platelet preparations to bind fibrinogen which, however, was suppressed by minute amounts of the thrombin inhibitor PPACK. PPACK hardly influenced fibrin-binding. Fragment-promoted fibrinogen-binding was also inhibited by a monoclonal antibody recognizing the membrane glycoprotein IIb/IIIa complex known to act as fibrinogen receptor. This antibody failed to influence fragment-stimulated fibrin-binding giving evidence that fibrinogen and fibrin were retained by different receptors. In contrast to 125-I-fibrin its plasmin-derived and 125-I-labelled fragment X was not recognized by the platelets in presence of the fibronectin 30 kD-fragment. Fragment-stimulated binding of 125-I-fibrin showed a lag phase and was completely inhibited by 0.25 mM putrescine as well as by 1 mM EDTA or 0.1 mM N-ethylmaleinimide. Evidently, a cell-attached transamidase was involved in fibrin-binding possibly by forming a ternary complex with fibrin and the fibronectin fragment.
Blood Platelets↗
Evidence for the presence of a free N-terminal fibronectin 30-kDa domain in human plasma by quantitative determination with an indirect immunosorbent assay.
The free N-terminal 30-kDa domain of the fibronectin subunit chains had previously been shown to mediate binding of soluble fibrin to phagocytic cells. In order to demonstrate whether the fragment is available in plasma in a suitable concentration, an indirect immunoassay procedure for its quantitative evaluation was developed. The free form of the 30-kDa domain was separated from fibronectin and the bulk of the plasma proteins by two-step affinity chromatography on gelatin- and heparin-Sepharose. In the eluate of the heparin-Sepharose the 30-kDa fragment was determined by its capacity to inhibit the immune reaction between a specific antiserum and the 30-kDa fragment immobilized on microtiter wells. The procedure offered reproductibility comparable with other immunoassays (coefficient of variation 4.0 to 8.0%); the lowest amount of detectable 30-kDa fragment was 0.1 microgram/ml. In human plasma this method detected for the first time ca. 5 micrograms/ml 30-kDa fragment. This concentration is in the range required for binding of fibrin to cells.
Buffers↗
An evaluation study of a health education programme for rural women in Bangladesh.
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Asia↗
[Results (in vitro and in vivo) of cryopreservation of human thrombocytes with glycerol].
The cryopreservation of human platelets was carried out with a final glycerol concentration of 0.38-0.48 mol/l (3.5-4.5%). The in-vitro-recovery (total platelets, aggregation, 14C-5-HT-uptake, clot retraction, total ATP, morphology) was in the range of 35-93% in comparison with freshly prepared platelet concentrates. The platelet survival was investigated by 51chrom labeling and autologous transfusion. A survival rate of 42% and a mean survival of 79% in comparison with freshly prepared platelets is concentrates are the results. In spite of reduced viability the cryopreservation of platelets is invaluable for providing compatible platelets for alloimmunized patients.
Blood Platelets↗
The role of fibronectin fragments and cell-attached transamidase on the binding of soluble fibrin to macrophages.
Proteolytic fragments from the N-terminus of the fibronectin subunit chains were shown to mediate the binding of 125-I-fibrin to macrophages. With increasing molecular weight of the fragments, binding activity decreased and intact plasma fibronectin was inactive. Fibrin binding to macrophages was a time dependent reaction and proceeded considerably faster than binding of fibrinogen. The binding reaction was inhibited by putrescine suggesting the involvement of a transamidase. Pericellular transamidase was demonstrated on macrophages by incorporation of 14-C-putrescine into fibronectin 30 kD-fragment. Expression of this enzyme appeared to be rate-limiting for the binding reaction which was accelerated after loading the cells with placental transamidase.
Acyltransferases↗
Effects of the phorbolester TPA and of the ionophore A 23187 on phospholipase A2 and C activities in the mouse epidermal cell line HEL-30.
The 12-O-tetradecanoylphorbol-13-acetate (TPA)- or ionophore A 23187-induced release of 14C-arachidonic acid from prelabeled murine HEL-30 keratinocytes was studied in vitro. Starting 8 min after drug treatment, a linear increase in the arachidonic acid content in the extracellular medium was observed with a concomitant loss of label in cellular phosphatidylcholine and phosphatidylinositol, but not in phosphatidylethanolamine and phosphatidylserine. No increase in intracellular diacylglycerol and phosphatidic acid was observed. The TPA-induced arachidonic acid release was inhibited by fluocinolone acetonide. The results indicate a direct activation of phosphatidylcholine- and phosphatidylinositol-specific phospholipases A2 by TPA and A23187. Cells prelabeled with 3H-choline released choline, choline phosphate and CDP-choline upon TPA but not upon A 23187 treatment. This could indicate activation of a phospholipase C-type enzyme by the phorbol ester. However, concomitant generation of diacylglycerol and phosphatidic acid was not detected.
Animals↗
Interaction of small dermatan sulfate proteoglycan from fibroblasts with fibronectin.
Immunogold labeling was used to localize the core protein of small dermatan sulfate proteoglycan (DS-PG) on the surface of cultured human fibroblasts. At 4 degrees C, DS-PG core protein was uniformly distributed over the cell surface. At 37 degrees C, gold particles either became rearranged in form of clusters or remained associated with fibrils. Double-label immunocytochemistry indicated the co-distribution of DS-PG core protein and fibronectin in the fibrils. In an enzyme-linked immunosorbent assay, binding of DS-PG from fibroblast secretions and of its core protein to fibronectin occurred at pH 7.4 and at physiological ionic strength. Larger amounts of core protein than of intact proteoglycan could be bound. Fibronectin peptides containing either the heparin-binding domain near the COOH-terminal end or the heparin-binding NH2 terminus were the only fragments interacting with DS-PG and core protein. Competition and replacement experiments with heparin and dermatan sulfate suggested the existence of adjacent binding sites for heparin and DS-PG core protein. It is hypothesized that heparan sulfate proteoglycans and DS-PG may competitively interact with fibronectin.
Cell Membrane↗
Chemotaxis of 3T3 and SV3T3 cells to fibronectin is mediated through the cell-attachment site in fibronectin and a fibronectin cell surface receptor.
Fibronectin (FN) is a multidomain extracellular matrix protein that induces attachment and chemotactic migration of fibroblastic cells. In this study we analyzed the molecular determinants involved in the FN-induced chemotactic migration of normal and SV40-transformed 3T3 cells. Two different monoclonal antibodies to the cell-binding site of FN blocked chemotaxis to a 140-kD FN fragment (Ca 140) containing the cell-binding domain. A monoclonal antibody to a determinant distant from the cell-binding site did not affect chemotaxis. A synthetic tetrapeptide, RGDS, which represents the major cell-attachment sequence, was able to compete with FN and the Ca 140 fragment in chemotaxis assays, but this peptide itself had no significant chemotactic activity. A larger peptide encompassing this sequence, GRGDSP, was chemotactic, while the peptide GRGESP, where a glutamic acid residue was substituted for aspartic acid, was inactive. Chemotactic migration could be prevented in a dose-dependent manner by a rabbit polyclonal antiserum to a 140-kD cell surface FN receptor. This antibody was more effective on normal than on transformed 3T3 cells. Neither the anti-FN receptor antiserum nor a monoclonal antibody to the cell-binding site of FN blocked migration induced by another potent chemoattractant, platelet-derived growth factor. These data indicate that FN-induced chemotaxis of 3T3 and SV3T3 cells is mediated via the RGDS cell-attachment site of FN and the 140-kD cell surface FN receptor. The interaction is specific and can be altered by transformation.
Animals↗
N-terminal fibronectin 30-kDa fragment mediates the immobilization of soluble fibrin by factor XIIIa-coated polystyrene beads.
Polystyrene beads coated with thrombin-activated Factor XIII (plasma transglutaminase, plasma transamidase) retained soluble 125I-fibrin, if a 30-kDa fragment of fibronectin was present. The fragment was obtained by proteolytic cleavage of plasma fibronectin with trypsin, but was also available with plasmin or thrombin. It represented a fibrin-binding domain at the N-terminus of each of the two subunit chains and contained close to its amino end a transamidase-reactive site. Fibronectin was unable to mediate the binding of 125I-fibrin to Factor XIIIa-coated beads. 125I-fibrinogen was hardly recognized by the beads even in presence of the fibronectin fragment. The relatively slow binding of 125I-fibrin was inhibited by 0.15 mM putrescine or by a pretreatment of the coated beads with EDTA or N-ethylmaleinimide indicating the involvement of a transamidation in the binding reaction. Immobilization of 125I-fibrin in presence of the fibronectin fragment is assumed to require a covalent cross-linking of the two ligands at the immobilized transamidase giving rise to a product which is retained strongly. The possibility is discussed that a surface-attached transamidase might act as a fibrin receptor which requires the fibronectin fragment as a cofactor.
Edetic Acid↗
[Aspects of drug supplies for veterinarians].
Problems of drug supply by veterinary doctors are discussed and explained. It has to be pointed out that the cancellation of drug substances needed for drugs and veterinary drugs, respectively, can lead to a sensible gap in the veterinary drug assortment, which is often difficult to compensate. Proposals to solve this problem are offered. In addition a growing demand on the treatment of small animals and pets, which are kept in increasing numbers, has to be considered. An adequate training and further education of pharmaceutical staff would be recommendable to meet the demands of an effective drug supply as well as a sufficient ability to give proper advice to proprietors of animals at the pharmacist's. This is already realised in Czechoslovakia in an exemplary way.
Germany, East↗
Radionuclide ventriculography: acute and chronic response to verapamil in patients with hypertrophic cardiomyopathy.
Eleven patients with hypertrophic cardiomyopathy were investigated by repeated radionuclide ventriculography. Nine of them were studied for the first time while under long-term treatment for 14 to 84 months. In all eleven patients radionuclide ventriculography was performed after a withdraw of verapamil for at least 14 days or before the onset of therapy respectively (control period). A third investigation was carried out 60 to 90 min after acute administration of 90 mg oral verapamil. A last radionuclide ventriculography was performed following 2 weeks of therapy with 480 mg oral verapamil. After acute administration heart rate significantly increased from 69 +/- 10 to 80 +/- 15/min. EDV was in the normal range. Left ventricular global ejection parameters showed no significant changes except for minimal decrease in ejection time from 309 +/- 29 to 278 +/- 50 ms after acute verapamil administration. The sectorial ejection fraction improved in apical sectors in relation to the basal one, while the global EF remained constant. The ventricular global peak filling rate increased significantly from 283 +/- 61 to 325 +/- 64%/EDV/s after acute administration of verapamil and the sectorial peak filling rate increased in apical sectors compared to basal sectors following acute administration as well as long-term therapy. After withdrawal of verapamil, six out of 11 patients showed a homogeneous left ventricular delay of contraction by means of the Fourier phases which were normalized under short- and long-term verapamil treatment. In conclusion, verapamil caused a marked improvement of the left ventricular contraction delay without significant changes in global systolic function.
Acute Disease↗
Models for the subunit arrangement in soluble and aggregated plasma fibronectin.
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Fibronectins↗
[Analysis of the shelf life and transfusion life of whole blood and erythrocyte concentrates].
The shelf life of 60,000 units of whole blood and red cell concentrates in the blood center were analysed before delivering to hospitals as well as the transfusion age of 18,000 units in relation to the stock-size and the outdated units. The mean transfusion age of whole blood units and red blood cell concentrates amounted to 11 to 12 days and 16 to 17 days, respectively. The shelf life of blood transfused within 24 hours after collection was 1.6% and 3.8% transfused within 48 hours according to the total number of whole blood and red blood cell concentrates. Washed red cell concentrates were prepared from buffy coat-free resuspended red cell concentrates on an average at the 7th day of storage. A high stock-size of about 1,000 units rather than of 600 units in the blood center increased the shelf life and also the number of outdated units from less than 0.5% up to more than 3%.
Blood Preservation↗
[Hepatitis B risk in dental personnel].
Dependent on the profession, medical personal is at different risk of hepatitis B infection. 505 staff members of 48 Berlin dental clinics were investigated for hepatitis B virus markers and demonstrated a significantly lower prevalence of HBsAg and its antibody than other hospital personal: anti-HBs positivity (EIA) was found in only 5.5 per cent of them (dental technicians: 1.6%, dental assistants: 3.8%, dentists: 8.0%). We conclude that in the GDR dental staff is not at higher risk of hepatitis B infection than other non-risk medical personal. Legal aspects of insurance and measures for hygienic prevention in dental practice are discussed.
Adult↗
[Course control and significance of circulating HBsAg-specific immune complexes in acute viral hepatitis B].
The occurrence and behaviour of circulating HBsAg-specific immune complexes were investigated in 52 patients suffering from acute viral hepatitis B. In 6 patients the illness took a chronic course. The determination was carried out by precipitation with polyethylene glycol 6,000 and the increase of HBsAg concentration after antibody splitting from the complexes by trypsin treatment. The results allow following conclusions: The early presence of immune complexes suggests a specific antibody response also against HBsAg before development of clinical illness. The timing and strength of this humoral immune reaction is sex dependent; females show anti-HBs earlier and in higher titers. The course of the concentration of circulating immune complexes depends on the immunoglobulin class of antibody and the quickness of virus elimination. The determination of circulating unspecific or HBsAg-specific immune complexes does not allow to draw any prognostic conclusion to the further course of acute hepatitis B. Only in chronificating cases, the future activity of the chronic HBV infection may be expected by the early behaviour of HBsAg immune complexes. Also patients developing chronic course of the HBV infection demonstrated a "peak" of the immune reaction 6-8 weeks after the beginning of disease, which could offer the point of time for starting an immunomodulating therapy.
Adolescent↗
SV40 transformed fibroblasts recognize the same 140 kD fibronectin chemotactic fragment as non-transformed cells.
SV40-virus-transformed human embryonal fibroblasts show an enhanced chemotactic response to the glycoprotein fibronectin. However, they recognize the same chemotactic active region as non-transformed fibroblasts. The result suggests that an enhancement of chemotaxis by fibroblasts which have been transformed with Simian Virus 40 is due not to the utilization of further chemotactic domains in the molecule, but to an increased sensitivity of the cells to the chemoattractant.
Cell Transformation, Viral↗