The geranylgeranyl moiety but not the methyl moiety of the smg-25A/rab3A protein is essential for the interactions with membrane and its inhibitory GDP/GTP exchange protein.

The smg-25A/rab3A protein (smg p25A), a member of the small GTP-binding protein superfamily, has a C-terminal structure of Cys-Ala-Cys which is post-translationally processed: both cysteine residues are geranylgeranylated followed by the carboxyl methylation of the C-terminal cysteine residue. We reported previously that this posttranslational processing is essential for the interactions of smg p25A with membrane and its inhibitory GDP/GTP exchange protein, named smg p25A GDP dissociation inhibitor (GDI). In this study, we examined which posttranslational modification of smg p25A is necessary for these interactions. The smg p25A which was not posttranslationally processed was produced in Escherichia coli and purified. This protein was then geranylgeranylated at both of the 2 cysteine residues by use of a bovine brain geranylgeranyltransferase in a cell-free system (recombinant smg p25A-GG). By use of this recombinant smg p25A-GG, its membrane-binding activity and its sensitivity to smg p25A GDI were compared with those of the fully posttranslationally processed form of bovine brain smg p25A (smg p25A-GG-Me) and the posttranslationally unprocessed form of bacterial smg p25A (recombinant smg p25A). The membrane-binding activity and sensitivity to smg p25A GDI were similar between the recombinant smg p25A-GG and smg p25A-GG-Me, although recombinant smg p25A lacked both activities. These results indicate that the geranylgeranyl moiety of smg p25A is essential and sufficient for its interactions with membrane and smg p25A GDI and that the methyl moiety is not essential for these interactions.     

Transfusion-induced immunomodulation and its possible role in cancer recurrence and perioperative bacterial infection

Over the last decade, it has become evident that homologous transfusions carry immunologic consequences beyond the well-understood ones of alloimmunization to blood cell antigens. Transfusions constitute temporary transplants of large amounts of allogeneic antigen given intravenously and cause down-regulation of many cellular immune functions. These changes may explain in part the association of transfusion with such clinically important events as (1) improved survival of renal allografts, (2) decreased recurrence rates for autoimmune disease, (3) increased frequency and earlier recurrences of solid tumors, (4) increased frequency of post-operative bacterial infection, and (5) increased severity of viral infection. Preliminary data suggest that, in animal models and clinical settings, syngeneic or autologous transfusions are not associated with such events. This finding supports the hypothesis that these associations are cause and effect and involve immunologic mechanisms.     

Development of long-term post-tetanic potentiation and changes in S-100 protein contents in hippocampal slices of rats in different functional states]

Male rats of the strains with low (LE) high excitability (HE) of the nervous system have been used in this study. Half of the animals of each strain were neurotized in accordance with the Hecht's scheme. In the hippocampal slices of the non-neurotized LE rats there was a significant increase of the populational spike amplitude during development of LTP as compared with the opposite group of the animals. The LTP formation in the LE strain of rats caused a decrease in the S-100 protein content in the water-soluble, and an increase in the membrane-bound fraction of the protein. Similar results we have observed with the non-inbred Wistar rats but not with the HE strain of the animals. The levels of the water-soluble S-100 protein fraction were also higher in the hippocampuses and entorenal cortices, but not in the cerebellae of the LE strain, as compared with the HE strain of the rats. No differences have been found in the membrane-bound fraction of S-100 protein.     

Psychiatrically hospitalized children: a critical review

The high cost of inpatient hospitalization and the rise in the number of private psychiatric beds for children and adolescents prompt several questions about who is using these services. To examine these issues, a review focusing on the use of psychiatric inpatient services by children was undertaken. The history of inpatient care of children is briefly outlined, recent public policies contributing to the rise in the number of psychiatric beds are considered, and findings from available studies are reviewed. We conclude that the data base is inadequate to draw many conclusions about who is using child psychiatric inpatient services. There appear, however, to be important differences in use of inpatient services according to age and perhaps by institutional type and geographic region. Suggestions for future research and some of the social policy implications are discussed as well.