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Biomedical subjects

N Peter

Publications and source records attributed to N Peter.

3 recordsLinked to original sources
PubMed2003

Pegylated asparaginase in combination with high-dose methotrexate for consolidation in adult acute lymphoblastic leukaemia in first remission: a pilot study.

The German Multicentre acute lymphoblastic leukaemia (ALL) study group (GMALL) performed a pilot study using pegylated asparaginase (PEG-ASP) in combination with high-dose methotrexate as consolidation therapy in the 05/93 protocol. The aim of the study was an intra-individual comparison of two different doses of PEG-ASP in 26 patients, with regard to the depletion of asparagine in serum and toxicity. 'Pharmacokinetic' monitoring was performed to evaluate the effect of an intra-individual dose escalation of PEG-ASP from 500 to 1000 U/m2 intravenously in successive doses. Serum asparaginase activity was targeted at > or =100 U/l for 1 week and > or =50 U/l for 10 d. The second course of PEG-ASP was administered to 23 patients. Due to hypersensitivity reactions in five patients, only 18 patients were evaluable for pharmacokinetic monitoring. With respect to the PEG-ASP activity, an effective depletion of asparagine could be postulated in the majority of patients during 10 d after the first administration. The effect of an intraindividual dose escalation form 500 to 1000 U/m2 was evaluable in 17 of 22 patients. An increment in peak PEG-ASP activity >70% was observed in 65% of the patients. PEG-ASP was well tolerated. Despite the long half-life of PEG-ASP, neither pancreatic nor central nervous toxicities occurred among the 26 adult patients treated in this pilot study.

Adolescent↗
PubMed1994

Decrease in growth cone-neurite fasciculation by sensory or motor cells in vitro accompanies downregulation of Aplysia cell adhesion molecules by neurotransmitters.

Cell adhesion molecules play important roles in axon guidance and synapse formation. Recent studies suggest that the expression of some of these molecules can be regulated either by electrical activity or by specific neurotransmitters. The expression of neural cell adhesion molecule (NCAM)-like molecules in Aplysia, designated apCAM, is downregulated from the surface of sensory neurons by 5-HT, a transmitter known to evoke long-term changes in the structure and function of these neurons. We tested whether the distribution of apCAM on the surface of other neurons can be regulated by treatments with other neurotransmitters known to evoke long-term functional and structural changes in Aplysia neurons, and we examined the consequences of treatments with the neurotransmitters on the pattern of growth cone-neurite interactions. We report that applications of the neuropeptide Phe-Met-Arg-Phe-amide (FMRFamide) that evoke long-term synaptic depression also reduce apCAM expression on the surface of motor cell L7 via a mechanism that appears to be similar to the mechanism mediating the 5-HT-induced change in the sensory cells. Specific treatments that affect apCAM distribution on the surface of their respective cells, 5-HT on sensory cells or FMRFamide on motor cell L7, mimic treatment with monoclonal antibodies against apCAM by evoking a significant reduction in the fasciculation of growth cones with other neurites extending from homologous cells.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗