Problem gambling and family violence: prevalence and patterns in treatment-seekers.

The primary aim of this study was to explore the prevalence and patterns of family violence in treatment-seeking problem gamblers. Secondary aims were to identify the prevalence of problem gambling in a family violence victimisation treatment sample and to explore the relationship between problem gambling and family violence in other treatment-seeking samples. Clients from 15 Australian treatment services were systematically screened for problem gambling using the Brief Bio-Social Gambling Screen and for family violence using single victimisation and perpetration items adapted from the Hurt-Insulted-Threatened-Screamed (HITS): gambling services (n=463), family violence services (n=95), alcohol and drug services (n=47), mental health services (n=51), and financial counselling services (n=48). The prevalence of family violence in the gambling sample was 33.9% (11.0% victimisation only, 6.9% perpetration only, and 16.0% both victimisation and perpetration). Female gamblers were significantly more likely to report victimisation only (16.5% cf. 7.8%) and both victimisation and perpetration (21.2% cf. 13.0%) than male gamblers. There were no other demographic differences in family violence prevalence estimates. Gamblers most commonly endorsed their parents as both the perpetrators and victims of family violence, followed by current and former partners. The prevalence of problem gambling in the family violence sample was 2.2%. The alcohol and drug (84.0%) and mental health (61.6%) samples reported significantly higher rates of any family violence than the gambling sample, while the financial counselling sample (10.6%) reported significantly higher rates of problem gambling than the family violence sample. The findings of this study support substantial comorbidity between problem gambling and family violence, although this may be accounted for by a high comorbidity with alcohol and drug use problems and other psychiatric disorders. They highlight the need for routine screening, assessment and management of problem gambling and family violence in a range of services.

beta-Cyclodextrin: 52-week toxicity studies in the rat and dog.

A 52-wk toxicity study by dietary administration was performed in Sprague-Dawley rats and in pure-bred beagle dogs with beta-cyclodextrin, a starch derivative that acts as a molecular inclusion agent. Doses of 0 (control), 12,500, 25,000 and 50,000 ppm were selected for the rat study, and 0 (control), 6200, 12,500 and 50,000 ppm were selected for the dog study. The liver and kidney were identified at the histopathological examination as target organs for toxicity in the rat at doses of 50,000 and 25,000 ppm, with the hepatic changes associated with increased plasma liver enzyme and reduced plasma triglyceride concentrations. In the dog study, there was no pathological evidence of systemic toxicity, although there were minor changes in urinalysis and biochemical parameters and a slightly higher incidence of liquid faeces. These changes were considered to be of no toxicological importance. The results in these studies, therefore, indicate that the non-toxic effect level was 12,500 ppm in the rat (equivalent to 654 or 864 mg/kg/day for males or females, respectively) and 50,000 ppm in the dog (equivalent to 1831 or 1967 mg/kg/day for males or females, respectively).

Ampicillin inhibits the movement of biliary secretory vesicles in rat hepatocytes.

A number of biliary secretory processes are inhibited by administration of ampicillin to isolated perfused rat livers. Reduction in output was observed for phospholipid, cholesterol, the endogenous protein rat serum albumin and the exogenous protein bovine serum albumin, whilst secretin of bile salts was virtually unaffected. All of the affected materials are secreted by processes involving vesicles which are brought to the appropriate pole of the hepatocyte, and the observed inhibitory effects of ampicillin may, therefore, possibly be due to a blockage in the transport of these substances. The effects of ampicillin were much less marked on materials secreted at the sinusoidal pole of the cell.

Sodium valproate inhibits the movement of secretory vesicles in rat hepatocytes.

Sodium valproate (VPA), a simple 8-carbon branched chain fatty acid, is an effective anti-epileptic drug with an occasional serious side effect of liver damage, including the accumulation of triacylglycerols within hepatocytes, and reductions in serum protein concentrations. By investigating the effects of VPA, using biliary fistula rats and isolated perfused rat livers, we have shown that secretion of triacylglycerols and rat serum albumin at the sinusoidal pole of hepatocytes, and of phospholipids, lysosomal contents, and IgA at their biliary pole, are all reduced, to somewhat different extents, by acute VPA administration. In addition, the vesicular transcytosis of exogenous protein (i.e. bovine serum albumin) from the perfusion fluid into bile is also decreased by VPA administration. To determine whether the phenomena were specific to VPA, a control series of experiments was also performed using octanoate (a straight-chain analogue of VPA). With the biliary fistula rats, octanoate did not show inhibition of secretion as compared with the saline controls; with the isolated perfused livers, however, octanoate did show such an inhibition. These phenomena suggest that VPA inhibition of secretion may be a factor in its hepatotoxicity, as the effects are apparent in both the whole animal and the isolated perfused liver, whereas octanoate is not hepatotoxic in the whole animal. Since when octanoate is administered to the isolated liver it causes an inhibition in secretion similar to that caused by VPA, it may be that the large dose of this compound reaching the liver affects a key step in liver metabolism or vesicle transport under these circumstances. Since octanoate does not normally reach the liver in such amounts, as it will normally be metabolized by other tissues, it is not hepatotoxic in the whole animal as is VPA.