Economic benefits of implementing trading zones for Australian livestock disease outbreaks of limited duration.

OBJECTIVE: The objective is to estimate the economic benefits of trading zones as part of foot-and-mouth disease (FMD) control measures for limited duration outbreaks. DESIGN: The proposed trading zones for FMD at the state level are determined using multiple tools. Eleven individual incursion scenarios in six Australian states are simulated within the Australian Animal Disease Spread epidemiological model to identify the potential geographic extent of outbreaks, as well as the number of animals infected and the duration of outbreaks. The disease spread information is used to identify the boundaries of trading zones. The outbreak duration data are combined with historical export data to estimate the share of Australian exports that could be embargoed. The market impacts of the potential export embargoes including changes in equilibrium quantities, prices and revenue are simulated within the Australian Bureau of Agricultural and Resource Economics and Sciences' AgEmissions partial equilibrium model of Australian agriculture. RESULTS: Results emphasize the importance of jurisdictional and outbreak characteristics in determining trading zones. Should Australia effectively implement trading zones at the state level in response to small FMD outbreaks, the potential reductions of embargoed exports lead to a reduction in estimated producer revenue losses compared with losses under a national embargo. Producer revenue losses are reduced between $3 billion and $9 billion estimated in present value terms over 10 years at a 7% discount rate. CONCLUSION: Economic analysis of the implications of trading zones identifies additional investments that would be of value to livestock industries.

Randomized trial of ligation versus combined ligation and sclerotherapy for bleeding esophageal varices.

BACKGROUND: Endoscopic band ligation combined with sclerotherapy has been postulated to be superior to ligation alone for the treatment of esophageal variceal bleeding. METHODS: A randomized trial of ligation versus combined ligation and sclerotherapy was designed to determine whether combined therapy results in faster eradication of varices compared to ligation alone. Sixty patients were randomized to undergo band ligation or ligation combined with injection of 1 to 2 mL of polidocanol (1%) into each variceal column immediately proximal to the previously placed bands. Therapy was repeated at 1- or 2-week intervals until variceal eradication was achieved. Follow-up endoscopy was performed at 3 months and then at 6-month intervals. RESULTS: The demographic and clinical characteristics of the 31 patients who underwent ligation were similar to those of the 29 who received combined treatment. Sixty percent of the patients had cirrhosis due to viral hepatitis. No significant differences were found between the combined and ligation alone groups in arresting active bleeding [9 of 9 (100%) vs. 6 of 7 (86%)], units of blood transfusion (3 +/- 0.8 vs. 2 +/- 0.6), number of sessions required to eradicate varices (3.8 +/- 0.5 vs. 3.6 +/- 0.4), treatment failure [2 (17%) vs. 4 (14%)], esophageal varix recurrence [6 (21.%) vs. 2 (6%)], gastric varices formation [4 (14%) vs. 1 (3%)], stricture [1 (3%) vs. 0 (0%)], recurrent bleeding [5 (17%) vs. 7 (23%)], other complications [10 (34%) vs. 9 (29%)], or death [3 (10%) vs. 7 (23%)] during a follow-up period of up to 36 months. CONCLUSIONS: Combined ligation and sclerotherapy does not reduce the number of endoscopic treatment sessions required for variceal eradication and offers no benefit over ligation alone. Because of the lack of benefit, the added procedure time, and the cost, we do not advocate combination therapy, and ligation alone remains the best endoscopic treatment.

Post-transplantation polyomavirus infections.

Increasing attention has been recently accorded to BK and JC viruses (BKV and JCV). Both these human polyomavirus (HPV) are members of the papovavirus family which includes the simian virus SV 40. BKV and JCV infect more than 60% of the population worldwide. After primary infection, they remain harboured in the kidneys and may become reactivated in situations of immune impairment. HPV were first described in 1971. BKV was isolated in a renal transplant patient with ureteral stricture and JCV in a patient with progressive multifocal leukoencephalopathy (PML). BKV was known to be involved in post-bone marrow transplantation (BMT) hemorrhagic cystitis. In renal transplantation, BKV and JCV were initially found in the post-transplant ureteric stricture and PML. They are now recognised as a possible cause of transplant interstitial nephritis, mimicking rejection (satisfying the Banff criteria for acute rejection) or drug toxicity. In HPV nephritis there is a mixed interstitial inflammatory infiltrate with focal tubular injury; the tubular epithelium shows marked anisonucleosis, nuclear atypia and basophilic or amphophilic intranuclear inclusions. Tubulitis is frequent. DNA hybridisation or gene amplification by polymerase chain reaction usually demonstrate HPV. Although histology with viral nucleic acid detection may be helpful in differentiating viral infection and rejection, confusion between these complications may lead to either anti-rejection therapy, with the risk of over-immunosuppression, or reduction of immunosuppression, with the risk of graft loss. Confusion may also arise with inclusions of other viruses, such as cytomegalovirus, herpes virus and adenovirus. Reactivation of BKV and JCV infection was demonstrated in respectively 22.2% and 10.9% of renal transplant recipients and 55% and 6.7% of BMT patients. Unfortunately, no routine screening is available for these viruses, so this complication is probably underestimated. No specific therapy of HPV infection is currently available.

[Voluntary drug poisoning cases admitted to an emergency care unit]. / Intoxications médicamenteuses volontaires reçues dans un service d'accueil des urgences.

OBJECTIVES: The aim of this study was to ascertain the specific nature of voluntary drug intoxications seen in emergency wards receiving adult patients. METHODS: From July 1992 to June 1993, all patients presenting at the emergency room with voluntary drug intoxication were assessed retrospectively. There were 727 patients (482 females and 245 males, mean age 33.3 +/- 12 years, age range 15-92) admitted for 804 episodes of voluntary drug intoxication. RESULTS: A past history of psychiatric problems or drug abuse was found in 42.8 and 9.1% of the patients respectively. The time laps between ingestion and consultation was noted for 43% (5 h 30 +/- 9 h, range 15-4320 min). The drug ingested was identified in 89% of the cases and 1.7 drugs were ingested per episode (range 1-8). Generally, only 1 (52%) or 2 (21%) drugs were ingested. Nonbarbituric psychotropic agents were ingested in 79.7% of the cases. Alcohol had also been consumed in 36.5% of the cases. Treatment was gastric lavage in 34.4%, activated carbon in 16.7%, flumazenil in 16.9%, naloxone and N-acetyl-cysteine in 3.4%. Twelve patients required intubation. Patients were admitted to a medical (n = 156) or psychiatric (n = 67) ward or an intensive care unit (n = 61). Nearly 25% of the patients left hospital either against medical advice or left without notice. CONCLUSION: Voluntary drug intoxications seen in emergency rooms require care by a well coordinated team of clinicians and psychiatrists.

Lead effect on the oxidation resistance of erythrocyte membrane in rat triton-induced hyperlipidemia.

The anemia observed in severe chronic lead poisoning is in part attributable to alterations in the erythrocyte physicochemical properties. Since they are partly related to the membrane lipid composition, the aim of the present study was to determine the effects of a triton-induced hyperlipidemia on the resistance to oxidation of erythrocyte membranes in lead-treated Wistar rats. Our results showed that triton administration to lead-treated rats induced an increase in erythrocyte choline phospholipid levels together with a significant decrease in the erythrocyte membrane lipid resistance to oxidation. These results led us to suggest that anemia in lead poisoning is linked to interactions between lead present in the membrane and plasma phospholipids. Their increase in rat hyperlipidemia induced by triton resulted in a decrease in the membrane resistance to oxidation and finally in an erythrocyte fragility leading to their destruction.

Comparison of production of volatile hydrocarbons by phenylhydrazine-induced peroxidation in rats chronically treated with lead.

We have studied the effect of a chronic pretreatment by lead on the peroxidation processes by measuring the production of the four main volatile hydrocarbons: ethane and pentane as index of lipid peroxidation; propane as marker of protein peroxidation and ethylene as index of both lipid and protein peroxidations. Our results have shown that: 1) lead alone did not increase the physiological formation of alkanes indicating that lead is not able per se to initiate the peroxidative processes; 2) after phenylhydrazine injection, lipid peroxidation makers were not modified, except pentane in male lead-treated rats. Conversely, ethylene and propane exhalation were increased 45 min after phenylhydrazine injection in lead-treated rats indicating a potentialisation of the oxidative effect of phenylhydrazine, mainly on proteins, by lead.

The effects of chronic administration of morphine on the levels of brain and adrenal catecholamines and neuropeptide Y in rats.

1. Monoamine turnover and neuropeptide Y (NPY) levels were investigated in the central and peripheral nervous systems in adult male rats chronically treated with morphine. 2. The well-recognized biochemical alterations (serotoninergic turnover increased in the hypothalamus, hippocampus and striatum; dopaminergic turnover increased in the striatum and cortex; adrenaline levels decreased in the adrenal glands) were observed. 3. In addition, we observed a significant decrease of the NPY levels in the hypothalamus, the striatum and the adrenal glands. The observed changes were not reflected in plasma. 4. Our results contribute to the evidence that brain and adrenal monoamines and NPY could be involved in the mechanism of morphine tolerance and/or dependence.