Psychotic symptoms and disorders and the risk of violent behaviour in the community

This study uses data from the Epidemiologic Catchment Area (ECA) surveys to examine the strength of the association between psychotic symptoms and violent behaviour, controlling for underlying mental disorder, substance abuse, sociodemographic characteristics and use of mental health services, in a representative sample of community residents. A replication is conducted of a study that found an increased risk of violence associated with a particular cluster of psychotic symptoms involving perceived threat and internal control-override (TCO). Respondents who reported TCO symptoms were about twice as likely to engage in assaultive behaviour as those with hallucinations or other psychotic symptoms, and about five times as likely as those with no mental disorder. The combination of substance use disorders with TCO symptoms added significantly to the risk of violent behaviour. Those with a history of using mental health services also posed a higher risk of violence, probably due to the differential selection of more severely ill and ‘dangerous’ individuals into treatment settings. Copyright © 1996 Whurr Publishers Ltd.     

Glycine modulation of the phencyclidine binding site in mammalian brain

Neurophysiological studies have shown that glycine potentiates the NMDA response in cultured neurons by a strychnine-insensitive mechanism. Autoradiographic data have demonstrated a correspondence between strychnine-insensitive [3H]glycine binding sites and NMDA-sensitive [3H]glutamate binding sites. Here we report that in synaptic plasma membranes from rat brain, the binding of a PCP analog, [3H]TCP, was enhanced more than 5-fold by 1 microM glycine. This glycine stimulation of binding of [3H]TCP was blocked by the competitive NMDA-receptor antagonist, D-AP7. These data provide support for the hypothesis that a unique amino acid recognition site is associated with the proposed NMDA/PCP receptor complex in brain.     

Image-directed percutaneous biopsies with a biopsy gun

Core tissue for histologic study is believed by many pathologists to be more diagnostic than material from needle aspiration. Recently, a biopsy "gun" has been introduced, which simplifies core biopsies. With this device, 182 biopsies of multiple anatomic sites were performed with ultrasonic, computed tomographic, and fluoroscopic guidance and 18-gauge needles. High-quality histopathologic specimens were obtained in 177 of the biopsies, and diagnostic target tissue was obtained in 167. Only three significant complications occurred: one bleeding complication that required transfusion and two cases of pneumothorax that necessitated placement of chest tubes. The biopsy gun eliminated the disjointed movements of conventional "skinny" needle biopsies, and none of the samples demonstrated significant "crush" artifact or obscuring blood, problems that are commonly associated with manual biopsy techniques. Patient discomfort was decreased with this system compared with that of manual biopsies, and the total procedure time was reduced. Because of these distinct advantages, the authors now use the biopsy gun exclusively for all percutaneous biopsies and recommend that other institutions consider the use of this biopsy method.     

Membrane alteration responsible for the induction of gamma interferon.

Induction of gamma interferon in human lymphoid cells cultures appears to be dependent upon specific membrane-mediated events and calcium flux. Since blastic response had been observed after enzymic oxidation of membrane-bound galactose residues, we used this system to study the nature of membrane alterations responsible for the activation of interferon induction. The results of these experiments suggest that a membrane oxidation is essential for interferon induction and depletion of calcium abolishes interferon production. In addition, we have shown that interferon induction by concanavalin A, phytohemagglutinin, and staphylococcal enterotoxin A, but not by galactose oxidase is prevented by cleavage of N-acetylneuraminic acid residues. Thus, interferon induction in human lymphoid cell cultures by galactose oxidase, concanavalin A, phytohemagglutinin, staphylococcal enterotoxin A, and NaIO4 appears to reside in terminal oligosaccharides of the cell membrane. How this specific membrane event relates to the derepression of the interferon locus is being actively pursued.     

Vesicular uptake of eosinophil peroxidase by guinea pig basophils and by cloned mouse mast cells and granule-containing lymphoid cells.

Guinea pig basophils, cloned mouse mast cells, and cloned mouse granule-containing lymphoid cells were found to utilize a vesicular transport system to internalize eosinophil peroxidase (EPO) added in vitro. Kinetic analysis indicated that EPO internalization involved the binding of EPO to the plasma membrane, the formation of complex surface invaginations, and the movement of EPO-laden vesicles, tubules, and vacuoles toward the center of the cells. EPO became associated with multivesicular bodies in granule-containing lymphoid cells and mast cells, with immature granules in mast cells, and with mature granules in basophils. In other cells, the endogenous production of granule peroxidases (neutrophils and eosinophils) or the prior uptake of exogenous peroxidatic substances (some basophils) precluded cytochemical analysis of granules for EPO. Vesicular transport of EPO provides a possible explanation for the variable detection of peroxidase activity in mast cells or basophils. It also provides a mechanism for sequestration of this potentially toxic material or for its storage for possible future use.     

Effect of acute and chronic ascorbic acid on flow-mediated dilatation with sedentary and physically active human ageing

Peripheral conduit artery flow-mediated dilatation decreases with ageing in humans. The underlying mechanisms and efficacy of preventive strategies are unknown. Brachial artery flow-mediated dilatation was determined at baseline and after ascorbic acid (vitamin C) intravenous infusion and chronic supplementation (500 mg day⁻¹ for 30 days) in three groups of healthy men: young sedentary ( n = 11; 25 ± 1 years, mean ± s.e.m. ), older sedentary ( n = 9; 64 ± 2), and older endurance-exercise trained ( n = 9; 64 ± 2). At baseline, flow-mediated dilatation (normalized for the hyperaemic stimulus) was ∼45% lower in the older (0.015 ± 0.001) versus young (0.028 ± 0.004) sedentary men ( P < 0.01), but was preserved in older exercising men (0.028 ± 0.004). Ascorbic acid infusion increased plasma concentrations > 15-fold in all groups and restored flow-mediated dilatation in the sedentary older men (to 0.023 ± 0.002; P > 0.1 versus other groups), with no effects in the other two groups. Oral ascorbic acid supplementation did not affect flow-mediated dilatation in any group. Brachial artery endothelium-independent dilatation (sublingual nitroglycerin) did not differ among the groups at baseline nor change with ascorbic acid administration. These results provide the first evidence for an important role of oxidative stress in both the impairment in peripheral conduit artery flow-mediated dilatation with sedentary human ageing and the preservation of flow-mediated dilatation with physically active ageing.