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Biomedical subjects

R Buder

Publications and source records attributed to R Buder.

12 recordsLinked to original sources
PubMed2003

A randomized study comparing interferon (IFN alpha) plus low-dose cytarabine and interferon plus hydroxyurea (HU) in early chronic-phase chronic myeloid leukemia (CML).

This multicenter randomized phase III study was designed to compare the efficacy and toxicity of IFN alpha-2c (3.5 MU/d) in combination with either araC (10 mg/m(2) d1-10) or hydroxyurea (HU: 25 mg/kg per day) in newly diagnosed CML patients. A total of 114 patients were randomized. Following a median observation period of 36 (range 1-73) months the major cytogenetic response rates were 25 and 27% and the 4-year survival probabilities 62.5 and 63% for the araC and HU group, respectively. While the overall toxicity profile was comparable between both groups, patients in the HU arm exhibited a slightly higher degree of WHO grades 3 and 4 non-hematological toxicities.

Adult↗
PubMed1996

[Effect of prostaglandin E1 on extravascular lung water in patients with severe heart failure].

Prostaglandin E1 (PGE1) is a physiologic vasodilator, which is broadly used in the therapy of peripheral arterial occlusive disease. In addition, the successful use of PGE1 in patients with severe heart failure has been described in several studies, where a decrease in pulmonary artery pressure and an increase in cardiac output were observed. In contrast to these positive effects, the development of lung edema was reported in individual cases after the infusion of PGE1 in patients with heart disease. We therefore conducted a double-blind study to evaluate the effect of PGE1 on extravascular lung water (EVLW) in patients with heart failure (NYHA III-IV) and borderline increased EVLW. Seven patients received an infusion of PGE1 (Prostavasin) at a dosage of 60 micrograms over 2 hours, while in 6 patients (control group) isotonic saline was given as placebo. EVLW was measured using a double indicator method at time points -15 h, -9 h before and at the start of the infusion, 1 h and 2 h during infusion, as well as +1 h, +4 h, +7 h, and +22 h after termination of the infusion. Infusion of PGE1 did not alter EVLW both in comparison to pre-study values (9.8 +/- 4.3 ml/kg bw preinfusion. 9.3 +/- 3.2 ml/kg bw after 1 hour and 9.4 +/- 3.5 ml/kg bw after 2 hours) or to the control group (6.5 +/- 3.3 ml/kg bw preinfusion, 7.1 +/- 2.7 ml/kg bw after 1 hour and 7.0 +/- 3.2 ml/kg bw after 2 hours). We conclude that there is no evidence that PGE1 might contribute to the development, or worsening of lung edema by inducing extravascular lung water accumulation and can, thus, be savely given to patients with even a severe degree of heart failure (NYHA III-IV).

Alprostadil↗
PubMed1990

2-Aminobenzoyl-CoA monooxygenase/reductase, a novel type of flavoenzyme. Identification of the reaction products.

In a previous report we have described some properties of a novel flavoenzyme from a denitrifying Pseudomonas species which catalyzes the oxygen- and NAD(P)H-dependent conversion of 2-aminobenzoyl-CoA [Buder, R., Ziegler, K., Fuchs, G., Langkau, B. & Ghisla, S. (1989) Eur. J. Biochem. 185, 637-634]. In this paper, we report on the identification of the three products formed from 2-aminobenzoyl-CoA in this reaction. The spectroscopic data and the chemical properties of these compounds and those of their degradation products are compatible with the structures of 2-amino-5-hydroxybenzoyl-CoA, 2-amino-5-hydroxycyclohex-1-enecarboxyl-CoA and of 2-amino-5-oxocyclohex-1-enecarboxyl-CoA. The latter is the main product and was found to be rather unstable since it hydrolyzes and decarboxylates readily at pH less than 5. Ammonia is released from the decarboxylation product in the neutral pH range to yield 1,4-cyclohexanedione. Conditions were optimized such that the CoA thioester of 2-amino-5-hydroxybenzoate is the product obtained at greater than 98% yield. 2-amino-5-hydroxycyclohex-1-enecarboxyl-CoA is the product which is formed when the mixture of the reaction products is treated with sodium borohydride before separation.

Chemical Phenomena↗
PubMed1989

2-Aminobenzoyl-CoA monooxygenase/reductase, a novel type of flavoenzyme. Purification and some properties of the enzyme.

A novel aerobic mechanism of 2-aminobenzoate metabolism was proposed in a denitrifying Pseudomonas species. 2-Aminobenzoic acid is activated in a coenzyme-A-ligase reaction to 2-aminobenzoyl-CoA and this intermediate is dearomatized by a unique enzyme, tentatively named 2-aminobenzoyl-CoA monooxygenase/reductase. This paper describes the purification and some molecular, kinetic and spectral properties of this flavoenzyme which catalyzes the hydroxylation and reduction of 2-aminobenzoyl-CoA to an unknown non-aromatic compound. 2-Aminobenzoyl-CoA monooxygenase/reductase was purified 25-fold to a specific activity of 25 mumol.min-1.mg-1 protein using ammonium sulfate precipitation, DEAE-cellulose anion-exchange, hydroxylapatite and Mono Q FPLC anion-exchange chromatography. Superose 6 gel filtration for estimation of molecular mass resulted in one symmetrical protein peak corresponding to a molecular mass of 170 kDa. Several experimental data suggest that the protein is probably an alpha 2 dimer; however, it may exist in three dimeric forms, alpha alpha, alpha alpha' and alpha' alpha', where alpha' may be a subunit with a different conformation. Approximately 2 mol noncovalently bound FAD/mol enzyme was found, which in the absence of O2 was reduced by NADH. The enzyme was specific for the substrates 2-aminobenzoyl-CoA (Km less than or equal to 25 microM) and O2 (Km less than or equal to 5 microM), but less specific for the reduced pyridine nucleotides NADH (Km = 42 microM) or NADPH [Km = 500 microM; Vmax (NADH)/Vmax (NADPH) = 1.7:1]. The turnover number was 4250 min-1. The enzyme also reduced N-ethylmaleimide and maleimide with NAD(P)H. The substrate, the products and the reaction stoichiometry are described in two following papers.

Catalysis↗
PubMed1989

2-Aminobenzoyl-CoA monooxygenase/reductase, a novel type of flavoenzyme. Studies on the stoichiometry and the course of the reaction.

The reaction catalyzed by 2-aminobenzoyl-coenzyme-A monooxygenase/reductase from a denitrifying Pseudomonas sp. has been investigated. 2-Aminobenzoyl-CoA and 2-amino[carboxy-14C]benzoyl-CoA were synthesized enzymatically using 2-aminobenzoyl-CoA synthetase from the same organism. The product was purified by chromatography and characterized by ultraviolet/visible and 1H-NMR spectroscopy. The conversion of 2-aminobenzoyl-CoA catalyzed by the monooxygenase/reductase requires NADH and oxygen, and yields at least two different products depending on the relative concentration of NADH. At [NADH] less than Km (40 microM), i.e. [NADH]/[2-aminobenzoyl-CoA] approximately 0.02-0.05, the main product is probably a hydroxylated derivative of 2-aminobenzoyl-CoA, which is characterized by an absorbance maximum around 375 nm. When [NADH]/[2-aminobenzoyl-CoA] approximately 2-5, the predominant product is a non-aromatic coenzyme A thioester (lambda max approximately 320 nm). The stoichiometry in this case is 2.1-2.4 mol NADH oxidized (mol oxygen consumed)-1 (mol 2-aminobenzoyl-CoA metabolized)-1. The product is extremely unstable in the acidic pH range and undergoes decarboxylation in a few minutes at pH less than 5. Some degree of stabilisation is obtained upon reduction with sodium borohydride, probably resulting in a further reduced non-aromatic coenzyme-A thioester.

Catalysis↗
PubMed1982

[A comparison of cinoxacin and nalidixic acid in the treatment of chronic urinary tract infections].

A total of 60 patients with chronic urinary tract infections were included in this comparative study. 29 patients received cinoxacin and 31 nalidixic acid for a period of ten days. There were five therapy failures in the cinoxacin group and nine in the nalidixic acid group. Drug-related side-effects were reported by 11 patients in the cinoxacin group and by 13 patients in the nalidixic acid group. Gastrointestinal and central nervous disturbances were the adverse reactions which occurred most frequently. In all cases side-effects disappeared quickly after therapy was discontinued.

Bacteriuria↗
PubMedDate not supplied

Effect of prostaglandin E1 on extravascular lung water in patients with severe heart failure.

Prostaglandin E ( 1 ) (PGE ( 1 ) ) is a naturally occurring paracrine hormone that is used pharmacologically for treatment of peripheral occlusive arterial disease and to maintain ductus-arteriosus patency in neonates with congenital heart disease until the primary condition is operable. PGE ( 1 ) treatment also has been associated with reduction in pulmonary arterial pressure and increase in cardiac output in patients with left ventricular failure. In contrast, in isolated cases, patients with heart failure reportedly have developed pulmonary edema while receiving PGE ( 1 ). Therefore, to better define the effect of PGE ( 1 ) in heart failure, this double-blind study investigated the effect of PGE ( 1 ) on extravascular lung water in intensive-care patients with severe heart failure (New York Heart Association [NYHA] classes III and IV) and slightly above-normal extravascular lung water. Intravenous infusion of 60 microg PGE ( 1 ) (Prostavasin; Schwarz Pharma, Monheim, Germany) over a period of 2 hours caused no significant change in lung water relative to the baseline values (9.8 +/- 4.3 mL/kg before the infusion, 9.3 +/- 3.2 mL/kg after 1 hour, and 9.4 +/- 3.5 mL/kg after 2 hours) or to values observed in placebo-treated patients (6.5 +/- 3.3 mL/kg before the infusion, 7.1 +/- 2.7 mL/kg after 1 hour, and 7.0 +/- 3.2 mL/kg after 2 hours). Thus, administration of PGE ( 1 ) is unlikely to cause or worsen pulmonary edema in patients with severe heart failure (NYHA classes III and IV).

Adult↗