Short-term general recidivism risk of juvenile sex offenders: validation of the Washington State Juvenile Court Prescreen Assessment.

It is important to examine whether general risk-assessment instruments developed for nonsex offenders can also be applied to sex offenders, because juvenile sex offenders are much more likely to reoffend with a nonsexual offense than a sexual offense. This study examined to what extent the Washington State Juvenile Court Prescreen Assessment (WSJCPA) can be used to assess the risk for general recidivism among different types of juvenile sex offenders. The predictive validity of the WSJCPA was examined separately for the following subgroups: boys convicted for a misdemeanor sexual offense against a peer (n = 381), boys convicted for a felony sexual offense against a peer (n = 282), boys convicted for a sexual offense against a younger child (n = 521), and girls convicted for a sexual offense (n = 71) and two comparison groups of male (n = 15,155) and female (n = 5,811) juvenile nonsex offenders. The area under the receiver operating characteristic curve scores for general recidivism ranged between .64 and .73. The WSJCPA proved to be at least equally predictive of general offending among juvenile sex and nonsex offenders groups.

Omental milky spots in the local immune response in the peritoneal cavity of rats.

BACKGROUND: Milky spots have been described as reactive structures, their classification varying from inflamed or haematopoietic tissue to lymphoid organs. In this study we investigated the reactivity of the milky spots in the omentum of rats upon induction of a chronic immune response in the peritoneal cavity. METHODS: At different time points after intraperitoneal administration of Bacillus Calmette-Guérin (BCG), a peritoneal lavage was made, and the omentum and the draining parathymic lymph nodes were taken out. The cellular composition of these tissues was examined on the light microscopic level, using a panel of monoclonal antibodies, and also by electron microscopy. RESULTS: During the first 4 months after administering BCG, the number and size of the milky spots increased enormously. Separate macrophage, T, and B cell areas were formed, but interdigitating cells and follicular dendritic cells were not observed. The number of cells in the peritoneal cavity also increased, and the cellular composition showed a strong similarity with that of the milky spots. Especially during the onset of the experiment, most bacteria were observed in the macrophages in the milky spots rather than in the draining lymph nodes. A cellular immune response was observed in the parathymic lymph nodes but not in the milky spots. CONCLUSIONS: Milky spots, either unstimulated or stimulated, should be classified as perivascular infiltrates. They play a role in the initial clearance of bacteria from the peritoneal cavity. Although the large increase in cell number is predominantly caused by immigration of cells, the results do support the role of milky spots as a site for local proliferation and maturation of especially macrophages and also B cells. The obtained data, however, do not support the earlier made assumption that milky spots function as a secondary lymphoid organ in the peritoneal cavity.

T cell-derived antigen binding molecules play a role in the induction of airway hyperresponsiveness.

We previously demonstrated that tracheal hyperreactivity (in vitro) and altered lung functions (in vivo) were induced during a delayed-type hypersensitivity (DTH) reaction in murine lungs. These alterations were transferable with T cells, suggesting that this animal model could be used as a model for cellular IgE-independent immunity. In the present study we demonstrated that depletion of T suppressor/cytotoxic cells failed to abolish the ability of transferred cells to induce hyperresponsiveness. Depletion of T helper cells partially inhibited the induction of hyperreactivity. Depletion of 14-30+ cells (the monoclonal antibody 14-30 reacts with a common isotype of T cell-derived antigen binding molecules [TABM] that can arm mast cells) completely abolished the ability to transfer hyperreactivity. The cromoglycate-like antiasthmatic drug nedocromil, which stabilizes mast cells, inhibited the induction of T cell-mediated hyperresponsiveness. Moreover, in mast cell-deficient mice, T cell-mediated hyperresponsiveness can be less induced compared with normal littermates. These experiments indicate that mast cells play at least a partial role in the induction of airway hyperresponsiveness in this model. Dexamethasone, a well-known inhibitor of phospholipase A2, inhibited the T cell-mediated hyperresponsiveness, whereas the cyclooxygenase inhibitor suprofen did not. This indicated that arachidonic acid metabolites, but not cyclooxygenase products, play a role in the induction of T cell-mediated hyperreactivity. Pretreatment with the lipoxygenase inhibitor AA-861 significantly inhibited the induction of tracheal hyperreactivity. Platelet-activating factor appeared not to be involved in the induction of hyperresponsiveness in this model, because the platelet-activating factor antagonist WEB 2170 failed to abolish the induction of T cell-mediated hyperreactivity. Intravenous injection of purified mast cell-arming TABM, followed by intranasal hapten challenge 30 min later, resulted in increased vascular permeability 2 h after challenge, which is characteristic of the early initiating phase of DTH. In addition, tracheal hyperreactivity (in vitro) and altered lung functions (in vivo) were observed 2 h after challenge. From these data we conclude that airway hyperreactivity and altered lung functions are induced by early steps in the cellular cascade of DTH.

Induction of an increased number of dendritic cells in the peritoneal cavity of rats by intraperitoneal administration of Bacillus Calmette-Guérin.

Recently we described the presence of a small number of DC among the peritoneal cells of steady state rats. These DC had the same morphological characteristics and a similar antigen-presenting capacity as DC isolated from the spleen. This study shows that in the peritoneal cavity, which is a non-lymphoid microenvironment, the number of DC increases after i.p. administration of BCG. Next to this relatively small influx of DC, the approximately three-fold increase of the total number of cells is predominantly caused by an enormous influx of neutrophilic granulocytes, and to a lesser extent by an influx of macrophages. The phenotype and the antigen-presenting capacity of peritoneal DC has not changed, while the number of Ia-positive M phi has increased. Nevertheless, due to a suppressive effect of the peritoneal M phi, the total peritoneal cell suspension is no longer capable of presenting antigen.

Morphological and functional characteristics of rat steady state peritoneal dendritic cells.

Dendritic cells (DC) are present in lymphoid organs and also in many non-lymphoid tissues. In this study, DC in the steady state peritoneal cavity of rats were identified morphologically and functionally. Approximately 1% of the peritoneal cells are DC. On cytocentrifuge preparations these cells had the same characteristics as lymph node and spleen DC: they had an irregular outline, all were strongly MHC class II positive and had acid phosphatase activity in a spot in a juxtanuclear position. Also ultrastructurally, peritoneal DC were similar to DC isolated from lymph node and spleen. Enrichment of peritoneal DC, using overnight culture and a Nycodenz gradient, resulted in a highly purified DC fraction. Functionally, peritoneal DC appeared to be very potent antigen-presenting cells, far more potent than peritoneal macrophages, which had an inhibitory rather than an accessory function.