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T Friedrich

Publications and source records attributed to T Friedrich.

At least 127 records · Page 7Linked to original sources
PubMed1991

Primary structure and functional expression from complementary DNA of a brain calcium channel.

The primary structure of a voltage-dependent calcium channel from rabbit brain has been deduced by cloning and sequencing the complementary DNA. Calcium channel activity expressed from the cDNA is dramatically increased by coexpression of the alpha 2 and beta subunits, known to be associated with the dihydropyridine receptor. This channel is a high voltage-activated calcium channel that is insensitive both to nifedipine and to omega-conotoxin. We suggest that it is expressed predominantly in cerebellar Purkinje cells and granule cells.

Amino Acid Sequence↗
PubMed1991

Inhibition of the rat renal Na+/H+ exchanger by beta-adrenergic antagonists.

The beta-adrenergic antagonists, alprenolol and propranolol, inhibit the Na+/H+ exchanger in rat renal brush-border membrane vesicles. Half-maximal inhibition occurs at 86 microM alprenolol and 36 microM propranolol. Similar to amiloride and Na+, propranolol protects the Na+/H+ exchanger from irreversible inhibition by the carboxyl group reagent, N,N'-dicyclohexyl-carbodiimide (DCCD). Protection is incomplete, depends on propranolol concentration, and reaches a maximum at 0.4 mM propranolol. With a comparable dose dependence, propranolol protects a 65 kDa band from labeling with [14C]DCCD. The data indicate that beta-adrenergic antagonists specifically interact with the proximal tubular Na+/H+ exchanger.

Adrenergic beta-Antagonists↗
PubMed1991

[Serological diagnosis of cytomegalovirus-induced interstitial pneumonia in patients following bone marrow transplantation].

For diagnosis of the interstitial pneumonia conditioned by cytomegalovirus (CMV) an indirect immunofluorescence test was used to measure IgM and IgG antibodies to CMV in 369 serum specimens from 41 patients after bone marrow transplantation (BMT). An interstitial pneumonia conditioned by CMV was diagnosed in 5 patients either serological (4 patients) or by detection of cytomegaloviral infection typical inclusion bodies in lung cells (1 patient). The detection of antibodies to CMV for diagnosis of interstitial pneumonia conditioned by CMV is problematical in the phase immediately after BMT because bone marrow recipients are severely immunosuppressed by radiation and cytotoxic drugs received before transplantation. New method for detection of CMV-specific antigens are necessary.

Adolescent↗
PubMed1991

[Immunohistologic investigations of paraffin-embedded lymph nodes after bone marrow transplantation in autopsy samples].

A histological and immunohistochemical analysis of paraffin-embedded lymph nodes from 31 autopsies after bone marrow transplantation (BMT) was performed (20 allogeneic, 10 autologous, 1 syngeneic). Monoclonal antibodies against CD 45RB, CD 20, CD 21, CD 35. CD 43, CD 45RO, CD 76 and Ki-B3, and antisera for detection of S 100-protein and immunoglobulin isotypes were used. None of the lymph nodes showed a regular reconstitution. The lymphoid cells, scattered in a diffuse pattern, were mainly CD 43-positive. Most of them also expressed the CD 45RO antigen. CD 20- and Ki-B3 positive lymphoid cells were nearly absent within the first 100 days after BMT. After that time B cell follicles were detectable in a few cases. Surprisingly, in nearly all cases with infectious complications, numerous plasma cells could be found. The origin of this plasma cells is discussed.

Antibodies, Monoclonal↗
PubMed1990

The same domain motif for ubiquinone reduction in mitochondrial or chloroplast NADH dehydrogenase and bacterial glucose dehydrogenase.

The respiratory chain NADH:ubiquinone oxidoreductase (NADH dehydrogenase or Complex I) of mitochondria comprises some 30 different subunits, and one FMN and 4 or 5 iron-sulfur clusters as internal redox groups. The bacterial glucose dehydrogenase, which oxidizes glucose to gluconolactone in the periplasmatic space and transfers the electrons to ubiquinone, is a single polypeptide chain with pyrolloquinoline quinone as the only redox group. We report here that the two different enzymes have the same ubiquinone binding domain motif and we discuss the predicted membrane folding of this domain with regard to its role in the proton translocating function of the two enzymes.

Amino Acid Sequence↗
PubMed1989

A small isoform of NADH:ubiquinone oxidoreductase (complex I) without mitochondrially encoded subunits is made in chloramphenicol-treated Neurospora crassa.

In mitochondria of Neurospora crassa grown in the presence of chloramphenicol a small form of NADH:ubiquinone reductase is made in place of the normal electron-transfer-complex I. This smaller enzyme has a molecular mass of approximately 350 kDa and consists of (at least) 13 different subunits which are all synthesized in the cytoplasm. The complex I which is normally found in Neurospora has a molecular mass of approximately 700 kDa and consists of around 30 different subunits, of which at least six are made in the mitochondria. Immunoblotting and peptide mapping suggest that the subunits of the small enzyme are homologous to subunits of the large enzyme, one subunit might even be identical. The small and the large NADH:ubiquinone reductases have the same high-affinity binding site for NADH but the two enzymes differ in the affinity and inhibitor sensitivity of the ubiquinone-binding site. The possibility is discussed that the small NADH:ubiquinone reductase is primitive isoform of complex I.

Binding Sites↗
PubMed1989

Synthesis of shock proteins in cultured fetal mouse myocardial cells.

We examined the synthesis of shock proteins in cultured fetal mouse myocytes. The preparation is free from fibroblasts, and the cells are vital and morphologically intact with respect to beat frequency and electron microscopy. Cultured myocytes from fetal mouse heart respond to heat shock and cadmium chloride, H2O2, allylamine, cyclosporine, and azathioprine exposure with the synthesis of shock proteins. Heat shock induces the de novo synthesis of two proteins of 71 and 68 kDa; cadmium chloride induces, in addition, a protein of 30 kDa. The other substances tested provoke the synthesis only of the 30-kDa polypeptide. The formation of heat shock proteins is concentration-dependent: Cyclosporine provokes the de novo synthesis of the 30-kDa polypeptide at concentrations above 10 ng/ml, whereas azathioprine causes the same effect at concentrations above 50 micrograms/ml. Hence cyclosporine might be cardiotoxic already at concentrations below the pharmacological dosages while azathioprine influences the myocytes only at concentrations much higher than the therapeutic level. Our results indicate that heat shock protein expression in cultured myocytes may be a useful tool to monitor cardiotoxicity.

Animals↗
PubMed1989

Lethal complications in 30 patients after allogeneic BMT (BMT) and autografted (ABMT) patients (1980-1986) examined by autopsy.

Lethal and accompanying complications from 29 allogeneic, 8 autologous, and 1 syngeneic transplanted pts., died between 1980 and 1986 at the BMT-Center Leipzig were revisited. An important problem was that of systemic and local infections. We observed a predominance of bacterial and fungal infections within the first 3 weeks p.t., and later on a period of predominantly virus-associated infections. The most common early death (up to 3 months p.t.) was related to ICP, as a rule caused by CMV. GvHD was a common finding at autopsy, and GvHD of the bowel seems to facilitate infectious inflammations of the bowel. There was a positive correlation between severe GvHD and the occurrence of ICP. Neither of the died BMT pts. showed signs of relapse. After ABMT ICP did not occur. The lethal complications were septicaemia, local infections, relapse and haemorrhagic diathesis. A toxic effect of DMSO in 3 pts. must be taken into account. In conclusion, a rather small number of lethal factors indicates the steps in improving results of transplantation in the future.

Adolescent↗
PubMed1988

Inhibition and labeling of the rat renal Na+/H+-exchanger by an antagonist of muscarinic acetylcholine receptors.

A covalently binding label for muscarinic acetylcholine receptors, propylbenzilylcholine mustard (PrBCM), irreversibly inhibits the Na+/H+ exchanger in rat renal brush-border membrane vesicles. Substrates of the antiporter, Na+ and Li+, as well as inhibitors, amiloride, 5-(N-ethyl-N-isopropyl)amiloride (EIPA) and propranolol, protect the antiporter from inactivation by PrBCM. With [3H]PrBCM a band with an app. Mr of 65 kDa is predominantly labeled. Amiloride protects this band from labeling with [3H]PrBCM and [14C]-N,N'-dicyclohexylcarbodiimide (DCCD) proving its identity with the renal Na+/H+ exchanger. Our data reveal a specific interaction of PrBCM with the Na+/H+ exchanger and suggest structural relations between antiporter and receptors.

Acridine Orange↗
PubMed1988

[Testing of acute myeloid leukemia of humans using monoclonal antibodies BL-DR, BL-M/G, BL-T2 and BL-Ig-L/1].

The leukemic blasts of 22 patients with acute myelocytic and myelomonocytic leukemia were tested by indirect immunofluorescence with the monoclonal antibodies BL-DR (directed against HLA-DR-antigens), BL-M/G (react with both granulocytes and monocytes), BL-T2 (pan-T-lymphocyte-antibody CD 5), and BL-Ig-L/1 (anti-light-chains-antibody). The leukemic blasts showed no crossreaction with BL-DR and BL-Ig-L/1. Both the antibodies BL-DR and BL-M/G reacted mainly with the acute myelomonocytic leukemias FAB M4 and only seldom with the acute myelocytic leukemias FAB M1, M2, and M3. The antibodies BL-DR and BL-M/G are able to confirm the diagnosis of acute myelomonocytic leukemia and to classify some previously unclassifiable leukemias.

Antibodies, Monoclonal↗
PubMed1988

[Use of monoclonal antibodies in the diagnosis of acute leukemia].

Immunological analysis has demonstrated the heterogeneity of acute lymphoblastic leukemia (ALL). The use of classical immunological methods and monoclonal antibodies against human lymphoid cell surface antigens have made it possible to subdivide ALL into five major subclasses: null ALL, common ALL, T-ALL, pre-B-ALL and B-ALL. We have studied in this report 8 cases of adult ALL diagnosed on morphological and cytochemical criteria. Some conventional markers and a panel of monoclonal antibodies have been used to analyse the differentiation of those patients' blast cells. In a second part we report two cases in which myeloid and lymphoid cell markers were observed simultaneously when 22 patients with acute myeloid leukemia were phenotyped according to the French-American-British (FAB) classification system.

Antibodies, Monoclonal↗
PubMed1987

Inhibition of sodium-dependent transport systems in rat renal brush-border membranes with N,N'-dicyclohexylcarbodiimide.

Treatment of rat renal brush-border membrane vesicles with N,N'-dicyclohexylcarbodiimide (DCCD) causes irreversible inhibition of the Na+-coupled transport systems for D-glucose, L-phenylalanine, L-glutamate, and sulfate. The DCCD-reactive side groups of these transport systems differ in their sensitivity towards DCCD and protection by substrates. The D-glucose and L-glutamate transporters cannot be protected by their substrates. In contrast, Na+ protects the transport systems for L-phenylalanine and sulfate from inactivation by DCCD. The data suggest covalent modification by DCCD of D-glucose and L-glutamate transporters apart from their substrate binding sites and of L-phenylalanine and sulfate transporters within their Na+-binding regions.

Amino Acid Transport Systems↗
PubMed1987

Species differences between rat and rabbit renal Na+/H+ exchangers.

Amiloride, 5-ethylisopropylamiloride (EIPA), and 5-ethylisopropyl-6-bromo-amiloride (Br-EIPA) inhibit rabbit and rat renal Na+/H+ exchangers with comparable potency. Irreversible inhibitions by Br-EIPA after irradiation of rat and rabbit renal brush-border vesicles are also similar. In contrast, irreversible inhibition by N,N'-dicyclohexylcarbodiimide (DCCD) of the rabbit renal antiporter requires higher DCCD concentrations as compared to the rat. Rabbit renal brush-border membranes show highest [14C]DCCD incorporation at MW 80,000, 51,000 and 36,000 and lack the amiloride-protectable MW 65,000 protein previously identified as Na+/H+ exchanger in rat kidney cortex. The data indicate species differences with respect to renal Na+/H+ exchangers.

Amiloride↗
PubMed1987

Measurements of intracellular pH in single LLC-PK1 cells: recovery from an acid load via basolateral Na+/H+ exchange.

LLC-PK1 cells (a continuous epithelioid cell line with renal characteristics) are examined by microspectrofluorometry as single cells, in order to determine the mechanism of intracellular pH (pHi) recovery from an acid load imposed by ammonium preincubation and removal (NH4 prepulse). Initial experiments evaluate the intracellular K+ levels through a null point analysis of total cellular K+ with flame photometry. The response of BCECF (a pH-sensitive fluorescent dye) is then calibrated, using saturating concentrations of nigericin to cause defined changes in pH. For experiments with the microspectrofluorometer, LLC-PK1 cells were grown on either glass coverslips or filters (the latter attached to plastic coverslips with a hole under the filter). The cells on glass coverslips demonstrate a Na+-dependent recovery from an (NH4 prepulse) acid load which is sensitive to 1 microM ethylisopropylamiloride. They also demonstrate a 'set point' of activation of Na+/H+ exchange. When examined for changes in pH, due to changes in membrane potential, plasma membrane proton conductance could not be detected at resting pHi. Cells grown on filters also demonstrate a pHi recovery from an acid load which is Na+ dependent and ethylisopropylamiloride sensitive, but in this configuration, the majority of cells (22/23 preparations) require Na+ at the basolateral membrane for rapid pHi recovery. The morphology and polarity of the cells grown on permeable supports appears normal at the electron-microscopic level. The results are not affected by changes in cell seeding density or collagen treatment of the filters.

Animals↗