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Biomedical subjects

A Sonnenschein

Publications and source records attributed to A Sonnenschein.

4 recordsLinked to original sources
PubMed2005

Neutron detection via bubble chambers.

Research investigating the application of pressure-cycled bubble chambers to fast neutron detection is described. Experiments with a Halon-filled chamber showed clear sensitivity to an AmBe neutron source and insensitivity to a (137)Cs gamma source. Bubble formation was documented using high-speed photography, and a ceramic piezo-electric transducer element registered the acoustic signature of bubble formation. In a second set of experiments, the bubble nucleation response of a Freon-134a chamber to an AmBe neutron source was documented with high-speed photography.

Journal Article↗
PubMed2002

Novel mitochondrial DNA mutations in Parkinson's disease.

Despite the recent discovery of several chromosomal gene mutations in familial Parkinson's disease (PD) the genetic background for idiopathic PD remains to be elusive. Since the discovery of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) action on dopaminergic neuronal cells and the specific decrease of mitochondrial complex I activity in substantia nigra of PD patients mitochondrial biochemistry and genetics emerged to become Pandora's box in the pathogenesis of PD. One approach was to establish the potential role of defective mitochondrial DNA (mtDNA). As complex I genes are the most vulnerable part of mtDNA we analyzed the mitochondrial MTND1 and MTND2 genes of 10 substantia nigra and 85 platelet samples from PD patients. We were uneventful to detect heteroplasmic base changes even applying techniques able to visualize mutations with low percentage of heteroplasmy but here we report novel homoplasmic base changes. These results add further evidence that there are no inherited disease specific mtDNA mutations, hence individual homoplasmic mutations or very low grade heteroplasmic mutations in the vicinity of mitochondrial metabolism and oxidative stress may contribute to selective neuronal vulnerability in PD.

Base Sequence↗
PubMed1998

Metal ion requirement of bifunctional UDP-N-acetylglucosamine 2-epimerase/N-acetylmannosamine kinase from rat liver.

The metal ion requirement for both enzymatic activities of the bifunctional UDP-N-acetylglucosamine 2-epimerase/N-acetylmannosamine kinase (E.C. 5.1.3.14/2.7.1.60), the key enzyme of N-acetylneuraminic acid biosynthesis in rat liver, was investigated. UDP-N-acetylglucosamine 2-epimerase was active in imidazole/HCl buffer in the complete absence of any metal ion. 200 mM Na+, K+, Rb+ and Cs+ activated enzyme activity up to five-fold, whereas lower concentrations of these monovalent metal ions showed only a small effect on UDP-N-acetylglucosamine 2-epimerase activity. In sodium phosphate buffer the enzyme activity was increased by 0.5 mM Mg2+, Sr2+, Ba2+ and Mn2+, while in the presence of 200 mM NaCl UDP-N-acetylglucosamine 2-epimerase activity showed a stronger activation by these divalent metal ions. In imidazole/HCl buffer, UDP-N-acetylglucosamine 2-epimerase activity was partially inhibited by 0.5 mM Be2+, Mg2+, Ba2+, Mn2+, Sn2+ and Fe2+, and completely inhibited by 0.5 mM Zn2+ and Cd2+. Divalent metal ions were essential for N-acetylmannosamine kinase activity, the most effective being Mg2+, followed by Mn2+ and Co2+. The optimal concentration of these metal ions was 3 mM. Less effective were Ni2+ and Cd2+, whereas Ca2+, Ba2+, Cu2+, Fe2+ and Zn2+ showed no effect on enzyme activity.

Animals↗