Effects of malaoxon on phosphatidylinositol signaling in convulsing and non-convulsing non-pregnant and pregnant female rats and their offspring.

Phosphatidylinositol (PI) signaling during organophosphate (OP) induced convulsions and tissue Ca2+ changes in 10 weeks old male, and 14 weeks old non-pregnant and pregnant female rats, and the offspring of the latter were explored. Brain inositol and inositol-1-phosphate (Ins1P) served as indices of alterations in brain PI signaling, and brain tissue Ca2+ as an index of early neuronal injury. A dose of malaoxon OP, which produced convulsions in about 60% of the exposed rats in different rat groups, was 39.2 for male, and 8.2 mg/kg for pregnant female rats, respectively. Malaoxon (8.2 mg/kg) did not produce convulsions in non-pregnant female rats. All the rats were followed for 1 or 4 hr subsequent to malaoxon. Malaoxon decreased cerebral inositol in both male and female rats, and the decrease was similar in spite of the dose difference. The decrease was larger in the convulsing than in the non-convulsing rats. A tendency towards a decrease of brain inositol also occurred in the offspring. Ins1P levels were markedly increased in male, and also in non-pregnant female rats, but not in the brains of pregnant female rats. Ins1P was not markedly changed in the brains of the offspring. Malaoxon elevated brain tissue Ca2+ in male but not in female rats or their offspring. Cholinergic systems and PI signaling in the brain seem to be associated with OP-induced convulsions both in male and female rats; females seem to be more sensitive than males. Malaoxon may also have slightly modified PI signaling in the offspring brain. Hormonal factors are likely to modify OP CNS toxicity and cholinergic stimulation of brain PI signaling.     

Bovine mesenteric vein graft (ProCol) in critical limb ischaemia with tissue loss and infection.

OBJECTIVES: Poor results have been reported following infrainguinal reconstructions using heterogenous grafts. The objective of this study was to assess the use of bovine mesenteric vein (ProCol) graft in patients with critical limb ischaemia (CLI), tissue loss/infection and no autologous vein available for reconstruction. METHODS: Prospective analysis of 32 patients with CLI and tissue loss/infection, in whom reconstruction with ProCol was undertaken between October 1999 and May 2002. RESULTS: The primary patency rate was 16% at 1 month. After thrombectomy, the secondary patency rate was 50% at 1 month and 26% at 14 months. No graft infections were seen. Aneurysmal dilatation of the graft occurred in 2 (6%). Limb salvage at 14 months was 47%. CONCLUSION: In patients with critical limb ischaemia, tissue loss/infection and no available vein, the ProCol graft may be an alternative. However, primary patency is a problem. In situations without tissue loss/infection, where the risk of graft infection is less, prosthetic material may be a better alternative.     

Dosimetric comparison at FiR 1 using microdosimetry, ionisation chambers and computer simulation.

Tissue equivalent proportional counter microdosimetry has been applied in the dosimetry of epithermal neutron beams as they can provide an independent and accurate method to determine gamma ray and neutron absorbed doses. Dosimetric comparison has been performed using a tissue equivalent proportional counter, dual ionisation chambers and DORT computer code at FiR 1 boron neutron capture therapy facility in Espoo, Finland. The three methods were applied to determine neutron and gamma ray absorbed doses at 25, 40, 60 and 120 mm depths along the beam centerline in a water-filled PMMA phantom. The determined absorbed doses were found to agree within the limits of the estimated uncertainties.     

Biochemical effects and monitoring of exposure of rats to 4-methylcyclohexyl-1,6-dicarboxylic acid anhydride vapour

Male Wistar rats exposed to 5, 10 or 20 p.p.m. 4-methylcyclohexyl-1,6-dicarboxylic acid anhydride vapour for 2-11 weeks showed dose-dependent blood anhydride concentrations. The maximum concentrations were found after two weeks. At five exposure weeks, they were smaller but they did not decrease further thereafter. The change was coincident with increased epoxide hydrase activity in liver. The excretion of 4-methylcyclohexyl-1,6-dicarboxylic acid was detected in the urine. The excretion was linearly related to the exposure in specimens collected during the 10th and 11th week. Brain acetylcholinesterase activity was transiently inhibited by the exposure at the two higher doses while decreased enzyme activity in the isolated spinal cord axons was only found after 11 weeks. This change was simultaneous with increased creatine kinase activity in the cerebellar homogenate. In the occupational setting, acetylcholinesterase activity might only be significantly inhibited in lungs because of the low exposure levels.