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Biomedical subjects

B Goldschmidt

Publications and source records attributed to B Goldschmidt.

At least 19 recordsLinked to original sources
PubMed2006

The chromosomes of Rodentolepis nana (Siebold, 1852) Spasskii, 1954 obtained from naturally infected mice conventionally maintained in a Braziuan laboratory animal house.

The karyotype of Rodentolepis nana obtained from mice in Rio de Janeiro, Brazil, was described. The diploid chromosome number obtained by the division of embryonic cells was 2n = 12. The first and the third pairs presented subterminal centromeres and the other pairs were all acrocentric. The studied species differed in chromosome morphology when compared to previous description by Mutafova and Gergova (1994) in Bulgaria, suggesting an intraspecific variation.

Animals↗
PubMed1994

Suboptimal control of fed-batch bioprocesses using phase properties.

A new method for the evaluation of suboptimal feeding strategies for fed-batch bioprocesses is introduced. This method is based on a time-local optimization of the process dynamics. To include global effects into the optimization, the process has to be partitioned into several phases with different local extremality conditions. The penicillin bioprocess is used to illustrate the method. One advantage of the proposed method is that the evaluated control function appears as a feedback law. Simultaneously, the new method allows the inclusion of constraints on the process states and the use of very complex models. Due to the simplicity and stability of the numerical procedure the method is robust against external perturbation. Therefore, it is suited for use in on-line controls.

Algorithms↗
PubMed1992

Metabolites formed during anaerobic transformation of toluene and o-xylene and their proposed relationship to the initial steps of toluene mineralization.

Strain T1 is a facultative bacterium that is capable of anaerobic toluene degradation under denitrifying conditions. While 80% of the carbon from toluene is either oxidized to carbon dioxide or assimilated into cellular carbon, a significant portion of the remainder is transformed into two dead-end metabolites. These metabolites were produced simultaneous to the mineralization of toluene and were identified as benzylsuccinic acid and benzylfumaric acid. Identification was based on comparison of mass spectra of the methyl esters of the metabolites and authentic compounds that were chemically synthesized. Strain T1 is also capable of o-xylene transformation during growth on toluene. o-Xylene does not serve as a source of carbon and is not mineralized. Rather, it is transformed to analogous dead-end metabolites, (2-methylbenzyl)-succinic acid and (2-methylbenzyl)-fumaric acid. o-Xylene transformation also occurred during growth on succinic acid, which suggests that attack of the methyl group by succinyl-coenzyme A is a key reaction in this transformation. We reason that the main pathway for toluene oxidation to carbon dioxide involves a mechanism similar to that for the formation of the metabolites and involves an attack of the methyl group of toluene by acetyl-coenzyme A.

Anaerobiosis↗
PubMed1990

[Vitamin K 1 concentration and vitamin K-dependent clotting factors in newborn infants after intramuscular and oral administration of vitamin K 1].

Serum concentration of vitamin K1 and activity of vitamin-K-dependent factors II, VII, IX and X were determined before and after vitamin K1 administration in infants. The babies received vitamin K1 intramuscularly or orally. 12 hours after vitamin K1 treatment the mean concentration was increased in the groups receiving vitamin K1 intramusculary or orally, respectively. Serum level of vitamin K1 fell exponentially, the mean half life was about 30 hours in both groups. Activity of vitamin K-dependent clotting factors did not change significantly after intramuscular or oral vitamin K1 administration during the first four-five days of life. It was no direct correlation between the concentration of vitamin K1 and the activity of vitamin-K-dependent clotting factors. This study suggest that oral administration of vitamin K1 is as effective as the intramuscular route.

Administration, Oral↗
PubMed1990

[Prothrombin and acarboxyprothrombin activity in neonates after oral and intramuscular administration of vitamin K].

The effect of prophylaxis with oral or intramuscular vitamin K1 (Konakion) on the hypoprothrombinaemia and on the rate of detectable acarboxyprothrombin of full-term newborns was investigated. Factor II clotting activity, factor II activity by Echis carinatus venom, factor II protein concentration and acarboxyprothrombin were determined in four groups of breast-fed infants. In the untreated group and in the group where the babies received vitamin K1 orally at birth the factor, II clotting activity was decreased and the rate of acarboxyprothrombin positive cases was increased significantly (from 30% and 28% to 55% and 52% respectively) at the 3d and 5-7th days of age. By the other two groups where 1 mg vitamin K1 was given intramusculary or 2-3 mg vitamin K1 was given orally with the first milk-feed, the factor II clotting activity increased at 3d and 5-7th days of life. In these groups the rate of acarboxyprothrombin positive babies was reduced at 3d day of life from 36% and 35% (cord blood values) to 16% and 13% respectively, and there was found acarboxyprothrombin in none of the babies at 5-7th days of life. These findings support that vitamin K1 given orally at birth is ineffective to prevent vitamin K deficiency, but when it was given with the first feed orally to well, mature babies it seems to be enable to protect the early haemorrhagic disease of the newborns.

Administration, Oral↗
PubMed1990

[Latent vitamin K deficiency in breast-fed infants].

Quick test, coagulation activity of vitamin K-dependent clotting factors, factor II activity by ecarin, levels of factor II immunoreactive antigen and acarboxyprothrombin were examined in two groups of infants, breast-fed and bottle-fed at the ages of one month and 3 months. None of them received vitamin K at birth and later. Acarboxyprothrombin could be demonstrated in about 14% at the both age of life of breast-fed children, but not in the groups of bottle-fed infants. The activity of coagulation factors was significantly lower in the acarboxyprothrombin-positive group compared to the acarboxyprothrombin-negative group. In none of the infants manifest bleeding was observed. No difference in the activities of factors could be detected in the acarboxyprothrombin-negative groups of breast- and bottle-fed children. These data suggest a frequent latent deficiency of vitamin K in breast-fed infants.

Breast Feeding↗
PubMed1984

Metabolism of fibrinogen in children with acute lymphoblastic leukaemia.

The metabolism and in vivo kinetics of fibrinogen were studied using homologous 125I-labelled fibrinogen in 21 children with acute lymphoblastic leukaemia (ALL). Ten patients were undergoing induction therapy, 11 children were in complete remission on maintenance therapy. Results in the patients undergoing induction therapy were: plasma fibrinogen levels were normal in all except one patient, the plasma fibrinogen pool was elevated in six cases, seven patients had a shortened fibrinogen half-life and increased fractional catabolic rate for fibrinogen. The absolute catabolic rate for fibrinogen was elevated in six cases. This shortened fibrinogen half-life together with the correcting effect of heparinisation on the fibrinogen turnover indicated that fibrinogen was consumed by chronic disseminated intravascular coagulation. Inhibition of the fibrinolytic system with epsilon-aminocaproic acid in five patients had no influence on the fibrinogen half-life in three of them but resulted in its prolongation in two patients. All except two children in complete remission had normal fibrinogen levels. Six patients had elevated plasma fibrinogen pools and in all of the cases survival and fractional catabolic rate of fibrinogen were normal. The absolute catabolic rate for fibrinogen was normal in eight, elevated in three of the patients. This observation indicates that fibrinogen synthesis remains accelerated in some cases of ALL in complete remission, but the cause of this is not known.

Adolescent↗