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Intermetallic (Co-Sn, Ni-Sn, Co-Ni) nanoparticles have been synthesized through a borohydride reduction with NaBH4 in aqueous solutions of the chloride salts of Co, Ni, Sn at room temperature using a template technique with a carbon support. As a result nanocomposite materials have been obtained in situ. The ratio of the metallic components has been chosen according the phase diagrams of the relevant binary (Co-Sn, Ni-Sn, Co-Ni) systems: Co:Sn=35:65, Ni:Sn=45:55, Co:Ni=50:50. As carbon supports have been used graphite and carbon powder. To avoid the nanoparticle’s aggregation b-cyclodextrin has been added to the reaction solutions. To study the influence of the supports used on the morphology, specific surface area, elemental and phase composition of the synthesized intermetallic nanoparticles and their carbon nanocomposites SEM, EDS, BET, and XRD investigation techniques have been used. The particle’s morphology varies with the different supports, but in the all cases it is typical for alloyed materials. The nanoparticles are different in shape and size and exhibit a tendency to aggregate. The last-one is due to the unsaturated nanoparticle’s surface and the existing magnetic forces. Regardless of the elemental composition, the nanosized particles are characterized by a relatively high specific surface area (SSA). The Ni-Sn nanoparticle have the largest SSA (80 m2/g), while the Co-Sn particles have the lowest SSA (69 m2/g). The use of a carrier modifies the SSA of the resulting nanocomposites differently depending on the size and shape of the carrier’s particles. The studies conducted on the intermetallic nanoparticles synthesized with various carriers demonstrate that the particle’s morphology, size, and specific surface area for the different supports are suitable for use as catalysts, electrode materials in Li-ion batteries and as magnetic materials for biomedical applications.

Schizophrenia is one of the major psychiatric disorders. It is a disorder of complex inheritance, involving both heritable and environmental factors. DNA methylation is an inheritable epigenetic modification that stably alters gene expression. We reasoned that genetic modifications that are a result of environmental stimuli could also make a contribution.

Tyrosine hydroxylase (TH), the rate-limiting enzyme in the metabolism of catecholamines, is considered a candidate gene in bipolar affective disorder (BPAD) and has been the subject of numerous linkage and association studies. Taken together, most results do not support a major gene effect for the TH gene in BPAD. Genetic and phenotypic heterogeneity may partially explain the difficulty of confirming the exact role of this gene using both association and linkage methods. Four hundred one BPAD patients and 401 unrelated matched controls were recruited within a European collaborative project (BIOMED1 project in the area of brain research, European Community grant number CT 92-1217, project leader: J. Mendlewicz) involving 14 centers for a case-control association study with a tetranucleotide polymorphism in the TH gene. Patients and controls were carefully matched for geographical origin. Phenotypic heterogeneity was considered and subgroup analyses were performed with relevant variables: age at onset, family history, and diagnostic stability. No association was observed in the total sample or for subgroups according to age at onset (n=172), family history alone (n=159), or high degree of diagnostic stability and a positive family history (n=131). The results of this association study do not confirm the possible implication of TH polymorphism in the susceptibility to BPAD. Am. J. Med. Genet. (Neuropsychiatr. Genet.) 88:527–532, 1999. © 1999 Wiley-Liss, Inc.

Despite strong evidence provided by genetic epidemiology of genetic involvement in the aetiology of bipolar and unipolar affective disorders, the exact nature of the predisposing genes is still being investigated through linkage and association studies. The interaction of susceptibility genes and environmental factors in these diseases is also of fundamental importance and requires proper investigation. Interesting theories have recently been proposed examining the possible role of various chromosomal regions, candidate genes and mutations in affective disorders. Reliable multicentrebased methodology is currently being employed to examine these theories, with attention given to statistical analysis and the statistical power of the sample. The present article describes the European Collaborative Project on Affective Disorders ECPAD ‘Interactions between genetic and psychosocial vulnerability factors’, involving 15 European centres. A description is given of the association and family samples collected for the project and also the methodology used to analyse interactions in the genepsychosocial environment. This material provides a powerful tool in the search for susceptibility genes in affective disorders and takes into account nongenetic aetiological factors. Psychiatr Genet 8197205 © 1998 Lippincott Williams & Wilkins.

Available data on gamma amino butyric acid (GABA) support the hypothesis that a dysfunction in the brain GABAergic system activity contributes to vulnerability to affective disorders (AD), including bipolar disorder (BPAD) and unipolar disorder (UPAD). The localization of the a3 subunit GABA receptor (GABRA3) gene in Xq28, a region of interest for BPAD suggests that GABRA3 may be a relevant candidate gene. In the present study, we tested the genetic contribution of the GABRA3 dinucleotide polymorphism in a European multicentre UPAD case-control sample [UPAD (n = 106), controls (n = 212)]. Our negative results suggest that GABRA3 does not confer susceptibility nor is it in linkage disequilibrium with another close gene involved in the genetic aetiology of UPAD.