Clinicians should remain mindful that one out of every six individuals with a psychotic disorder reports being a victim of violence in the previous year. Models of care that address issues related to symptom relief, accommodation, and exposure to high-crime areas may reduce the rates of victimisation amongst those with psychotic disorders.

SummaryCyclosporin A (CSA), FK506, and glucocorticosteroids all inhibit the production of lymphokines by decreasing lymphokine gene expression. Previous experiments have defined six different sites that may contribute to the transcriptional control of the interleukin 2 (IL2) promoter, and for each, active nuclear binding factors are induced upon mitogenic stimulation. While dexamethasone markedly blocks the increase in IL2 mRNA in stimulated human blood T cells, we found that the drug does not block the appearance of factors that bind to the transcriptional control sites termed AP-1, AP-3, NF-kB, OCT 1, B site, and NF-AT. In contrast, both CSA and FK506 have similar effects : the drugs cause modest decreases in AP-3 and NF-kB, and marked decreases in the activity of AP-1 and NF-AT Therefore, CSA and FK506, while chemically different, seem to act upon a similar pathway that leads to IL2 gene expression, whereas glucocorticoids do not affect this pathway.variety of immunosuppressants block T cell prolifera A tion and lymphokine production. A major site of action of these immunosuppressive drugs is at the level of lym phokine gene expression . This was noted first for cyclosporin A (CSA) (1-4), which acts primarily at the level of lymphokines rather than other components of T cell activation, such as the p55 IL2R and cfos (2) . Two other drugs, dexamethasone and FK506, also act primarily at the level of 11,2 gene expression (5-7). It is likely that glucocorticoids have a different mechanism of action than CSA and FK506, since steroids affect many cell types, whereas CSA and FK506 are more T cell restricted .To gain more insight into the mechanism ofaction of immunosuppressive drugs, we have taken advantage of recent progress in defining nuclear factors that bind to the IL2 promoter. An activation-dependent enhancer within sequences -326 to -52 of the 5' flanking region of the IL2 gene has been identified (for review see reference 8). In this enhancer reside several elements common to other genes, like the NFkB, AP-1, AP-3, and OCT-1 sites, as well as a site that seems restricted to activated lymphoid cells and is called the nuclear factor for activated T cells (NF-AT) (9) . Here, we report the induction of these nuclear factors in primary populations of human blood T cells . We show that FK-506 and CSA markedly inhibit the activation of factors that bind to the AP-1 and NF-AT sites, whereas dexamethasone has no effect on all six nuclear binding factors tested . 1869 Materials and MethodsCell Cultures. Briefly, human mononuclear cells were isolated from huffy coats on Ficoll-Hypaque density gradients, washed in PBS, and rosetted with neuraminidase-treated sheep erythrocytes. The rosette-positive fraction was further purified by passage over a nylon wool column and used as a source of T cells. T cells were cultured at 5 x 106/ml in RPMI 1640 supplemented with 10% heatinactivated FCS, 20,ug/ml gentamicin sulfate, and 5 x 10-5 M 2-ME. Cells were stimulated with PHA (Gibco Laboratories, Grand Island, NY) at 1 Rg/ml and ...

We report on 2 infants with the DiGeorge anomaly born to diabetic mothers treated with insulin. Both infants had unilateral renal agenesis. One of the mothers has manifestations suggestive of velo-cardio-facial syndrome (VCFS). Cytogenetic studies on both patients and the mother with apparent VCFS were normal. Molecular studies utilizing probes from the DiGeorge critical region did not demonstrate a 22q11 microdeletion in either patient or the mother with apparent VCFS. We conclude that maternal diabetes is a pathogenetic factor in the DiGeorge anomaly, and infants of diabetic mothers who have this anomaly should also be screened for renal agenesis.

30,1159 (1981)] appeared which identified the same compound to be the most active isomer to inhibit calf intestinal ADA. Only the (+)-and (-)-EHNA's were prepared, and they were synthesized from two different precursors.