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  • 11
    Electronic Resource
    Electronic Resource
    Pharmacological profile of AA-861, A 5-lipoxygenase inhibitor
    Amsterdam : Elsevier
    Prostaglandins 26 (1983), S. 955-972 
    Details
    ISSN: 0090-6980
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Medicine
    Type of Medium: Electronic Resource
    URL: http://linkinghub.elsevier.com/retrieve/pii/0090-6980(83)90157-0
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  • 12
    Electronic Resource
    Electronic Resource
    Differentiability of the cost functions is equivalent to strict quasiconcavity of the production functions
    Amsterdam : Elsevier
    Economics Letters 12 (1983), S. 135-139 
    Details
    ISSN: 0165-1765
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Economics
    Type of Medium: Electronic Resource
    URL: http://linkinghub.elsevier.com/retrieve/pii/0165-1765(83)90124-6
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  • 13
    Electronic Resource
    Electronic Resource
    Antiinflammatory, analgesic, and antipyretic activities of methyl 7-butyl-4,5,6,7-tetrahydro-3-methylamino-4,6-dioxo-5-propyl-2H-pyrazolo[3,4-d]pyrimidine-2-carboxylate (AA-2379), a novel non-acidic agent (1988)
    Springer
    Inflammation research 25 (1988), S. 385-393 
    Details
    ISSN: 1420-908X
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The antiinflammatory, analgesic, and antipyretic activities of methyl 7-butyl-4,5,6,7-tetrahydro-3-methylamino-4,6-dioxo-5-propyl-2H-pyrazolo[3,4-d] pyrimidine-2-carboxylate (AA-2379), a novel nonacidic agent, were examined. 1. AA-2379 had a potent antiinflammatory activity; 3–25 mg/kg, p.o. of the compound inhibited rat carrageenin-, bradykinin-, trypsin-, formalin-, dextran-, and nystatin-induced paw edema; mouse traumatic edema; and rat croton oil pouch inflammation by about 30%. The compound at 25–50 mg/kg, p.o. also inhibited the vascular permeability induced by histamine, serotonin, and bradykinin. 2. AA-2379 had an analgesic activity; the ID50 values in mouse phenylquinone-induced writhing were 10.1 mg/kg, p.o. and the compound at 12.5 mg/kg, p.o. inhibited dog urate arthritis. 3. AA-2379 at 3–10 mg/kg, p.o. showed antipyretic activity in febrile rats and rabbits. 4. AA-2379, at 500 mg/kg, p.o. was not ulcerogenic in rats. 5. These data show that AA-2379 is more active than non-acidic antiinflammatory agents, such as tiaramide and aminopyrine.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01965047
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  • 14
    Electronic Resource
    Electronic Resource
    Thiamine-responsive lactic acidaemia: role of pyruvate dehydrogenase complex (1998)
    Springer
    European journal of pediatrics 157 (1998), S. 648-652 
    Details
    ISSN: 1432-1076
    Keywords: Key words Lactic acidaemia ; Thiamine ; Pyruvate dehydrogenase complex ; Thiamine pyrophosphate ; Sodium dichloroacetate
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Lactic acidaemia is sometimes associated with a defect of the pyruvate dehydrogenase complex (PDHC), catalysing the thiamine-dependent decarboxylation of pyruvate. The activity of PDHC for different thiamine pyrophosphate (TPP) concentrations was determined in 13 patients with lactic acidaemia, clinically responsive to thiamine treatment in order to assess the role of PDHC in the aetiology of thiamine-responsive lactic acidaemia. Culture of lymphoblastoid cells and skin fibroblasts and muscle biopsies were performed in these 13 patients. The activity of PDHC to sodium dichloroacetate (DCA), known as the activator of PDHC, was also examined. Three groups were identified according to PDHC activity. Group 1 (two patients) displayed very low PDHC activity, which was not increased by DCA. This PDHC activity increased at high TPP concentrations. Group 2 (five patients) displayed below normal PDHC activity at low TPP concentrations, increased by DCA. This PDHC activity became normal at high TPP concentrations. PDHC deficiency in these patients of groups 1 and 2 was due to a decreased affinity of PDHC for TPP. Group 3 included six patients with normal PDHC activity at low as well as high TPP concentrations. This PDHC activity was increased by DCA. Conclusion High concentrations of TPP may be required for maximal activity of PDHC in some patients with lactic acidaemia. The assay of PDHC activity, performed at a low concentration of TPP (1 × 10−4 mM) allows selection of patients with thiamine-responsive lactic acidaemia.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004310050903
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  • 15
    Electronic Resource
    Electronic Resource
    Book reviews (1994)
    Springer
    Journal of economics 60 (1994), S. 209-228 
    Details
    ISSN: 1617-7134
    Source: Springer Online Journal Archives 1860-2000
    Topics: Economics
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01227868
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  • 16
    Electronic Resource
    Electronic Resource
    Effects of deoxyadenosine on ribonucleotide reductase in adenosine deaminase-deficient lymphocytes (1991)
    Springer
    Journal of inherited metabolic disease 14 (1991), S. 87-95 
    Details
    ISSN: 1573-2665
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary To explore the relationship between ribonucleotide reductase and immunodysfunction in adenosine deaminase deficiency, the effects of deoxyadenosine on ribonucleotide reductase in ADA-deficient lymphocytes was investigated. An assay system for ribonucleotide reductase in intact permeabilized lymphocytes was developed to approximate physiological conditions. The activity of cytidine diphosphate (CDP) reductase in resting but not in proliferating lymphocytes in culture was inhibited by 1 to 10 µmol/L deoxyadenosine. The resting cells were protected from the toxicity of 1 µmol/L deoxyadenosine by 5 mmol/L nicotinamide or 30 µmol/L deoxycytidine and from that of 10 µmol/L deoxyadenosine by 30 µmol/L deoxycytidine. These findings suggest that depletion of nicotinamide adenine dinucleotide might be the principal cause of death in resting lymphocytes with ADA deficiency. It is concluded that the mechanism of deoxyadenosine toxicity on non-replicating lymphocytes, which may not be mediated by ribonucleotide reductase inhibition, is closely related to the mechanism of immunodysfunction in patients with ADA deficiency.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01804395
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  • 17
    Electronic Resource
    Electronic Resource
    Mutation of E1α gene in a female patient with pyruvate dehydrogenase deficiency due to rapid degradation of E1 protein (1992)
    Springer
    Journal of inherited metabolic disease 15 (1992), S. 848-856 
    Details
    ISSN: 1573-2665
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary A mutation of an insertion of 4 bp in the gene for the α subunit of pyruvate dehydrogenase (E1α) was found in a female with pyruvate dehydrogenase deficiency due to the rapid degradation of α and β subunit proteins of pyruvate dehydrogenase. This mutation caused a frameshift that altered the amino acid sequence and created a premature stop codon. This 4-bp insertion has been found in an unrelated female patient with E1α deficiency. It is rare that the same mutation is found in unrelated patients with this rare inborn error of metabolism. Furthermore, short deletions or duplications in the E1α gene of patients with E1α deficiency have been found only in exons 10 and 11. These exons may be hot spots for the mutations by the recombinational processes. This patient was heterozygous for the normal and a mutant allele. However, in most of the cultured skin fibroblasts from this patient, the mutant allele was expressed. These observations suggest that the X chromosome containing the normal allele was predominantly inactivated so that she developed lactic acidaemia and neurological abnormalities despite being heterozygous. The mutant α subunit protein failed to form a stable structure of pyruvate dehydrogenase, so that both α and β subunit proteins were degraded rapidly.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01800220
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  • 18
    Electronic Resource
    Electronic Resource
    Biochemical and molecular analysis of an X-linked case of Leigh syndrome associated with thiamin-responsive pyruvate dehydrogenase deficiency (1997)
    Springer
    Journal of inherited metabolic disease 20 (1997), S. 539-548 
    Details
    ISSN: 1573-2665
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract We report molecular analysis of thiamin-responsive pyruvate dehydrogenase complex (PDHC) deficiency in a patient with an X-linked form of Leigh syndrome. PDHC activity in cultured lymphoblastoid cells of this patient and his asymptomatic mother were normal in the presence of a high thiamin pyrophosphate (TPP) concentration (0.4 mmol/L). However, in the presence of a low concentration (1 X 10-4 mmol/L) of TPP, the activity was significantly decreased, indicating that PDHC deficiency in this patient was due to decreased affinity of PDHC for TPP. The patient's older brother also was diagnosed as PDHC deficiency with Leigh syndrome, suggesting that PDHC deficiency in these two brothers was not a de novo mutation. Sequencing of the X-linked PDHC E1 α subunit revealed a C → G point mutation at nucleotide 787, resulting in a substitution of glycine for arginine 263. Restriction enzyme analysis of the E1α gene revealed that the mother was a heterozygote, indicating that thiamin-responsive PDHC deficiency associated with Leigh syndrome due to this mutation is transmitted by X-linked inheritance.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1005305614374
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  • 19
    Electronic Resource
    Electronic Resource
    Clinical and biochemical findings in parents of children with vitamin D-dependent rickets type II (1991)
    Springer
    Journal of inherited metabolic disease 14 (1991), S. 231-240 
    Details
    ISSN: 1573-2665
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Vitamin D-dependent rickets type II is a rare disease caused by a disorder of the receptor for 1, 25-dihydroxyvitamin D (1, 25(OH)2D). Several parameters of this receptor-effector system were investigated to obtain biochemical information on the presumed heterozygotes of vitamin D-dependent rickets type II in parents of five patients and in their age-matched controls. It was found that the serum concentrations of 1,25-(OH)2D and 24,25-dihydroxy-vitamin D (24, 25(OH)2D), and the ratio of 1,25-(OH)2D/24,25-(OH)2D differed significantly in the parents from those of the patients and the respective control groups. In the parents' cultured skin fibroblasts, the activity of 25-hydroxyvitamin D-24-hydroxylase induced by 10−8 mol/L 1, 25-(OH)2D3 ranged from 50 to 82% of that of their controls (versus 1–13% of controls for the patients). The binding capacity of the parents' [3H]1, 25-(OH)2D3 to the nucleus was 38–54% of that of their control subjects (versus 7–27% of controls for the patients). The parents' values were thus in a range between those of the patients and the control groups. These findings suggest that, in the parents, a partial impairment of the receptor system for 1,25-(OH)2D led to an imbalance of vitamin D metabolism, thus confirming that vitamin D-dependent rickets type II is an autosomal recessive inherited disease. Serum concentrations of 1, 25-(OH)2D and 24,25-(OH)2D may provide useful parameters for detecting heterozygotes of this disease.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01800596
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