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Neurotensin and its high affinity receptor (NTSR1) localise within dopaminergic neurones in the mesocortical, mesolimbic and nigrostriatal systems12345 and it is now clear that neurotensin can selectively modulate dopaminergic neurotransmission.2367891011 This has led to the hypothesis that altered neurotensin function contributes to the pathogenesis of schizophrenia and other psychoses. This hypothesis has been supported circumstantially by a number of lines of evidence. (1) Central administration of neurotensin produces effects similar to those produced by the peripheral administration of atypical antipsychotics.12131415 (2) Observations of low levels of neurotensin in the CSF of schizophrenics.1617 (3) Reduced numbers of neurotensin receptors in the brains of schizophrenics.1819 Given the above link between neurotensin and dopamine, and the evidence implicating altered neurotensin function in psychosis, we20 have postulated that DNA sequence variation in neurotensin or its receptors might be associated with schizophrenia. In keeping with this hypothesis, an association has recently been reported21 between schizophrenia and the gene encoding the neurotensin high affinity receptor (NTSR1). However, caution is required because the associated marker, a tetranucleotide repeat, is located 3 kb away from the 3' end of the gene and there is no evidence that it is functional. Therefore, as a follow-up to our earlier work on neurotensin,20 we have now sought to test the hypothesis that DNA sequence variants that alter the structure or expression of the NTSR1 gene (VAPSEs)22 are associated with schizophrenia. However, while we found 14 novel sequence variants in 28 probands with psychosis, none resulted in an amino acid change, and neither direct nor indirect association studies suggested these are involved in susceptibility to schizophrenia.

Aromatic L-amino acid decarboxylase (AADC) is a relatively non specific enzyme involved in the biosynthesis of several classical neurotransmitters including dopamine and 5-hydroxytryptamine (5HT; serotonin).1 AADC does not catalyse the rate limiting step in either pathway, but is rate limiting in the synthesis of 2-phenylethylamine (2PE) which is a positive modulator of dopaminergic transmission and a candidate natural psychotogenic compound.1 We and others have proposed that polymorphism in AADC resulting in altered 2PE activity might contribute to the pathogenesis of psychosis.1,2 In order to test this hypothesis, we have used denaturing high performance liquid chromatography (DHPLC)3 to screen 3943 bases of the aadc gene and its promoter regions for variants that might affect protein structure or expression in 15 unrelated people with schizophrenia, and 15 unrelated people with bipolar disorder. three polymorphisms were identified by dhplc: a insertion/deletion polymorphism in the 5' utr of the neuronal specific mrna (g.-33-30delagag, bases 586-589 of genbank m77828), a t>a variant in the non-neuronal exon 1 (g.-67t>a, genbank m88070), and a g>a polymorphism within intron 8 (g.ivs8 +75g>A, GenBank M84598). Case-control analysis did not suggest that genetic polymorphism in the AADC gene is associated with liability for developing schizophrenia or bipolar disorder.

This review presents an analysis of research published by Irish nurses during the period 1990–2005. The analysis is the first effort made to identify the main characteristics of Irish nursing research. Overall, 213 published studies were identified for consideration, from which, 152 were included in the review. The studies were published in 60 journals, 4 books, and 8 research reports. Journal articles selected from 6 journals accounted for 52%. Inclusion criteria were quality of research design, sampling (including sample size), data analysis, scientific merit, and authorship. Each article was analyzed based on this schema. The major areas of research identified included clinical practice (56%) (e.g., medical surgical, mental health, intellectual disability, and maternal and child), nursing management and professional issues (19%), and nursing education (25%).

A number of studies using the repeat expansion detection (RED) technique have suggested an association between unknown large CAG/CTG repeats and schizophrenia. The polymorphic CAG/CTG repeat loci CTG18.1 and ERDA1 have been reported to account for a high proportion (approximately 90%) of the large repeats detected by RED and may therefore be responsible for the cited association. The recently described locus TGC13-7a contains a highly polymorphic CTA/TAG and CAG/CTG composite repeat, and is thus another authentic candidate. In the present investigation, each locus was analysed for association with schizophrenia in a sample of 206 patients and 219 group-matched controls. No evidence for association of CTG18.1, ERDA1 and/or TGC13-7a with schizophrenia was found. The combined data accounted for only 54% of the CAG/CTG arrays of > 40 repeats found in our previous RED analysis.