Midbrain serotonin transporter binding potential measured with [11C]DASB is affected by serotonin transporter genotype.

BACKGROUND: Homozygote carriers of two long (L) alleles of the serotonin transporter (5-HTT) regulatory region displayed in vitro a twofold increase in 5-HTT expression compared with carriers of one or two short (S) alleles. However, in vivo imaging studies yielded contradictory results. Recently, an A > G exchange leading to differential transcriptional activation of 5-HTT mRNA in lymphobalstoid cell lines was discovered in the 5-HTT regulatory region. In vitro and in vivo evidence suggests that [(11)C]DASB, a new 5-HTT ligand offers some advantages over the ligands used in previous studies in measuring 5-HTT density independent of synaptic levels of serotonin. METHOD: We assessed 5-HTT binding potential (BP (2)) in the midbrain of 19 healthy subjects with positron emission tomography and [(11)C]DASB. Accounting for the hypothesized functional similarity of L (G) and S in driving 5-HTT transcription, we assessed whether L (A) L (A) homozygotes display increased midbrain BP (2) compared with carriers of at least one S allele. RESULTS: BP (2) in the midbrain was significantly increased in L (A) L (A) homozygotes compared with carriers of at least one S allele. Interestingly, the genotype effect on the midbrain was significantly different from that on the thalamus and the amygdala where no group differences were detected. CONCLUSIONS: This in vivo study provides further evidence that subjects homozygous for the L (A) allele display increased expression of 5-HTT in the midbrain, the origin of central serotonergic projections.

[Determination of residues of 20 kinds of organochlorinated pesticides in oils, fruits and vegetables by wide-bore capillary gas chromatographic column].

A rapid and high performance gas chromatographic method for the determination of 20 organchlorinated pesticides in oils, fruits and vegetables has been developed. The samples of fruits and vegetables were extracted with petroleum ether-acetone, while those of oils were extracted with acetonitrile-hexane. The extract was purified by Florisil column with ethyl ether-hexane(15:85, V/V) or ethyl ether-petroleum ether(15:85, V/V) as eluent. Chromatographic analysis was performed on wide-bore capillary column with ECD detector. Satisfactory separation and detection of these organchlorinated pesticides are presented with the proposed method. The detection limits of this method were 1.0 ng/g-20.0 ng/g(S/N = 5), the recoveries 83.2%-106.8% and the relative standard deviations 2.0%-9.5%.

[Effects of selenium deficiency and supplementation on tumor immune response in mice].

DBA/2 mice were fed for 16 weeks with Torula yeast-based synthetic diet containing various concentrations of selenium (Se). At 13th week, the mice were immunized with syngenetic L5178 Y lymphoma cells and their specific and non-specific tumor immune responses were examined 3 weeks after immunization. The results indicated that in mice fed with a diet containing 0.007 ppm Se, the serum Se level was extremely low (0.02 micrograms/ml). These Se-deficient mice were unable to elicit normal tumor-specific immune responses. Both the specific proliferation of T cells in MLTC and tumoricidal activity of CTL were very much depressed. In addition, these mice also showed impaired NK and LAK cell activity. The effects of Se supplementation varied depending on the amount of Se given. When 0.170 ppm Se was added to the low Se diet, all the immune parameters examined were restored to the normal level. When 0.567 ppm Se was added, however, the tumor immune responses remained as low as those in Se-deficient mice. This study implies that the prevalence of primary hepatocellular carcinoma in areas where Se is deficient has a profound immunological basis. Se supplementation is obviously indicated for cancer prevention in these areas but the amount of Se supplied is crucial.