[Not Available]. / Hysterie und Borderline - Einige empirische Annäherungen an den "Paradiesvogel"/ Hysteria and Borderline - Some empirical approaches to the "bird of paradise".

The intention of the study is the empirical differentiation between "mature" and "immature" (borderline-) hysterics. 366 inpatients of the Department of Psychoso-matic Medicine of the Central Institute of Mental Health in Mannheim (university of Heidelberg) were diagnosed with regard to the existence of hysterical personality traits. 146 patients shared the criteria of the DOPSY-system for hysteria. This group was divided by assistance of the Bordcrlinc-Syndromc-Index (BSI) into a subgroup of n = 79 "mature" and a subgroup of n=67 "immature" Borderline hysterics. The distri-bution was validated by the Freiburger Personality inventure (FPI). Both groups are similar referring to age, gender and schooleducation. On the level of symptomatology we found the same feature of diagnoses in the area F40-45 in the ICD-10. Two third of the patients with hysterical personality traits have got an additional classification of personality disorder, but only 48% in the group of mature hysterics and 37% in the group of immature hysterics were classified by experienced psychoanalysists as his-trionic personality disorder (F60.4, ICD-10). With respect to risk factors in the life history we found that mature hysterics much more often were characterized by a loss of father in the first three years and the position of the eldest (and sometimes only) child. The results pointed to distinct developmental lines, which suggest, that the two hysterical groups can be differentiated by the style of coping and defense.

Activation of thiamin diphosphate and FAD in the phosphatedependent pyruvate oxidase from Lactobacillus plantarum.

The phosphate- and oxygen-dependent pyruvate oxidase from Lactobacillus plantarum is a homotetrameric enzyme that binds 1 FAD and 1 thiamine diphosphate per subunit. A kinetic analysis of the partial reactions in the overall oxidative conversion of pyruvate to acetyl phosphate and CO2 shows an indirect activation of the thiamine diphosphate by FAD that is mediated by the protein moiety. The rate constant of the initial step, the deprotonation of C2-H of thiamine diphosphate, increases 10-fold in the binary apoenzyme-thiamine diphosphate complex to 10(-2) s-1. Acceleration of this step beyond the observed overall catalytic rate constant to 20 s-1 requires enzyme-bound FAD. FAD appears to bind in a two-step mechanism. The primarily bound form allows formation of hydroxyethylthiamine diphosphate but not the transfer of electrons from this intermediate to O2. This intermediate form can be mimicked using 5-deaza-FAD, which is inactive toward O2 but active in an assay using 2,6-dichlorophenolindophenol as electron acceptor. This analogue also promotes the rate constant of C2-H dissociation of thiamine diphosphate in pyruvate oxidase beyond the overall enzyme turnover. Formation of the catalytically competent FAD-thiamine-pyruvate oxidase ternary complex requires a second step, which was detected at low temperature.

RNA aptamers specifically interact with the prion protein PrP.

We have isolated RNA aptamers which are directed against the recombinant Syrian golden hamster prion protein rPrP23-231 (rPrPc) fused to glutathione S-transferase (GST). The aptamers did not recognize the fusion partner GST or the fusion protein GST::rPrP90-231 (rPrP27-30), which lacks 67 amino acids from the PrP N terminus. The aptamer-interacting region of PrPc was mapped to the N-terminal amino acids 23 to 52. Sequence analyses suggest that the RNA aptamers may fold into G-quartet-containing structural elements. Replacement of the G residues in the G quartet scaffold with uridine residues destroyed binding to PrP completely, strongly suggesting that the G quartet motif is essential for PrP recognition. Individual RNA aptamers interact specifically with prion protein in brain homogenates from wild-type mice (C57BL/6), hamsters (Syrian golden), and cattle as shown by supershifts obtained in the presence of anti-PrP antibodies. No interaction was observed with brain homogenates from PrP knockout mice (prn-p(0/0)). Specificity of the aptamer-PrP interaction was further confirmed by binding assays with antisense aptamer RNA or a mutant aptamer in which the guanosine residues in the G tetrad scaffold were replaced by uridine residues. The aptamers did not recognize PrP27-30 in brain homogenates from scrapie-infected mice. RNA aptamers may provide a first milestone in the development of a diagnostic assay for the detection of transmissible spongiform encephalopathies.