Nicotine and cotinine levels in body fluids of smokers who committed suicide

Cigarette smoking is associated with a higher risk for suicide. The present study was conducted on the hypothesis that suicide smokers show higher nicotine and cotinine levels in blood and urine than non-suicide smokers. We determined nicotine and cotinine levels in blood and urine of 87 deceased individuals (18 suicides and 69 non-suicides) by gas chromatography. The smoking rate was 77.8% for individuals who committed suicide and 42.0% for those who did not commit suicide. Average nicotine and cotinine levels in blood were significantly higher in the suicide smokers than in the non-suicide smokers (nicotine: 93.2+/-46.6 ng/ml versus 25.8+/-14.4 ng/ml, p<0.0001 and cotinine: 378+/-235 ng/ml versus 201+/-137 ng/ml, p<0.005). Average levels of urinary nicotine and cotinine were also significantly higher in the suicide smokers than in the non-suicide smokers (nicotine: 1980+/-2210 ng/ml versus 394+/-376 ng/ml, p<0.005 and cotinine: 1170+/-1330 ng/ml versus 414+/-290 ng/ml, p<0.05). Twenty-six decedents were intoxicated with alcohol, and they included 7 suicides (7 smokers) and 19 non-suicides (15 smokers). Our data suggest that cigarette smokers who commit suicide smoke more heavily than other cigarette smokers.     

Discrimination of transparent polyethylene films based on identification of inorganic antiblocking agents

Several nondestructive and semidestructive analyses were used to discriminate colorless transparent polyethylene bags. Transparent plastic bags made from low-density and linear low-density polyethylene usually contain antiblocking agents to prevent sticking of the film, which makes it difficult to open the mouths of plastic bags. Inorganic antiblocking agents are uniformly dispersed in polyethylene films, so they are easily observed using optical microscopy. The particle size distributions of the antiblocking agents were compared by statistical tests. Particle composition was examined by elemental analysis using energy-dispersive X-ray spectrometry with a scanning electron microscope and by molecular vibration analysis using a sensitive microscopic Raman spectrometer. The compositions could be determined nondestructively on the basis of the results. These data reinforce the morphological discrimination. Morphological discrimination of the dispersed antiblocking agent powders, statistical comparison of particle size distributions, and compositional analysis of the antiblocking agents strengthen the ability to discriminate polyethylene films.     

Adipocere formation via hydrogenation of linoleic acid in a victim kept under dry concealment

Adipocere formation is well known as a later post-mortem change. We experienced a female victim who had been sealed up in a clothes box for approximately 4 years. We collected several subcutaneous fats as well as visceral fats from the victim to investigate adipocere formation. Fresh subcutaneous fats of one female and five male victims who suddenly died were used as the control. These samples were homogenized and the lipids were extracted with chloroform and methanol followed by injection into gas chromatography-mass spectrometry and gas chromatography. We detected a hydroxy fatty acid in the fat of the case, but not in the controls. Using standard synthetic hydroxy fatty acid, the lipid extract component was identified as 10-hydroxyoctadecanoic acid (10-OH 18:0) and this concentration was quantified. Consequently we confirmed that adipocere was formed much slowly in dry concealment. In addition, the fatty acid composition was compared with the control. Most of the linoleic acid (18:2) disappeared and a peak developed instead. Using standard synthetic fatty acid, this peak was identified as cis-12-octadecenoic acid (cis-12-18:1). This suggests that linoleic acid is hydrogenated to cis-12-octadecenoic acid in the process of adipocere formation.     

Experimental studies on the mechanism of ethanol formation in corpses

Various in vitro experiments were performed for the purpose of clarifying the mechanism of ethanol production in corpses. Whereas a negligible quantity of ethanol was produced in the blood alone, which was left at room temperature, the quantity of ethanol was slightly increased by addition of glucose to the blood. When saprogens were further added, the quantity was markedly increased. Various materials were added to blood-liver homogenates as specimens, and the mixtures were stored in an incubator at 37 degrees C. As a result of the addition of an antibiotic to the mixture every day, there was hardly any production of ethanol. When alcohol dehydrogenase (ADH) and reduced nicotinamide adenine dinucleotide (NADH) were added, ethanol production was slightly increased. When acetaldehyde was added first, ethanol production was inhibited the next day, but on and after day 2, the quantity of ethanol was more than that in the control material. When pyruvic acid was added first, the results were similar to the above. Pyrazole, cyanamide, and disulfiram completely inhibited the production of ethanol. Ethanol production in corpses is believed to take place through a pathway opposite to that of ethanol metabolism in the living body, under the influence of ADH, ALDH, etc., in saprogens using carbohydrates as substrates.     

Next task for the WTO system and the APEC process

With the “globalization” of production, firms need to be able to operate in other economies, exploiting their advantages, enabling them to remain internationally competitive. Today, the focus of attention, in the international trading system, is shifting to measures that affect the ability of foreign firms to invest and conduct business in national economies, to the openness of markets to global competition. However such measures are broached, governments cannot get away from deciding unilaterally whether, when, and how to deregulate, creating an internationally attractive business environment. Asia has benefited much from foreign direct investment, not regional trade negotiations, and APEC should adhere to non-discrimination as its guiding principle. Ryutaro Hashimoto has been minister of international trade and industry in the government of Japan since 1994, having earlier been minister of finance (1989–1991) and minister of transport (1986–1987).     

Tissue distribution of intubation-related lidocaine in brain-dead patients

Tissue distribution of lidocaine that was used for endotracheal intubation during cardiopulmonary resuscitation (CPR) was measured in 3 patients who were brain-dead or near brain death. Case 1 was a 69-year-old female whose heartbeat was restored by CPR but stopped 10 hours later. The lidocaine ratios of cerebrum to blood (2.04) and diencephalon to blood (1.01) were within ranges of those found in non-brain-dead patients. Case 2 was a 77-year-old female whose heart resumed beating after CPR but stopped 66 hours later. The lidocaine ratios of cerebrum to blood (5.69), diencephalon to blood (18.7), and cerebellum to blood (11.3) were much higher than those in non-brain-dead patients. Case 3 was a 48-year-old male who had cardiopulmonary arrest following an acute subarachnoid hemorrhage. His heart resumed beating after resuscitation but ceased beating 114 hours after admission. Lidocaine was detected only from the cerebrum, cerebellum, and blood clots in the superior sagittal sinus at levels of 0.028, 0.024, and 0.007 mug/g, respectively. Tissue distribution of intubation-related lidocaine in brain-dead patients is useful as supplementary data for reviewing hemodynamic changes in their brains during medical treatment.     

Central monoamines and the death process time (antemortem time) during asphyxia. An experimental study in the mouse brain

The changes of the brain monoamines, norepinephrine (NE), dopamine (DA), and serotonin (5-HT), during acute asphyxia, caused by strangulation, anoxia, and drowning, were studied in the mouse. In several asphyxiated animal groups significant linear correlation was found between the level of monoamines, NE, DA, and 5-HT, and the death process times or antemortem times were r = 0.50, 0.98 (P less than 0.05), and 0.57, respectively. It is concluded that the level of brain NE and DA increased in the mouse that died of asphyxia, and the level of 5-HT showed only an apparent decrease in anoxia groups as compared with the control group and showed a twice as high increase in drowning groups. Especially, there was a tendency that the longer the death process times or antemortem times, the higher was the level of DA.     

Postmortem diffusion of drugs from the bladder into femoral venous blood.

We describe significantly elevated drug concentrations in the femoral venous blood due probably to postmortem diffusion from the bladder. A 16-year-old deceased male was found in a shallow ditch in winter. The estimated postmortem interval was 9 days and putrefaction was not advanced. The cardiac chambers contained fluid and coagulated blood and a small amount of buffy coat clots. Diffused hemorrhages were found in the gastric mucosa. The bladder contained approximately 600 ml of clear urine. Gas chromatographic-mass spectrometric analysis of the urine disclosed allylisopropylacetylurea (a fatty acid ureide sedative), diphenhydramine, chlorpheniramine and dihydrocodeine. The cause of death was considered to be drowning due to a drug overdose and cold exposure. The concentrations of diphenhydramine, free dihydrocodeine and total dihydrocodeine in the femoral venous blood (1.89, 3.27 and 3.30 microg/ml, respectively) were much higher than those in blood from the right cardiac chambers (0.294, 0.237 and 0.240 microg/ml, respectively). Urine concentrations of diphenhydramine, free dihydrocodeine and total dihydrocodeine were 22.6, 37.3 and 43.1 microg/ml, respectively. The stomach contained negligible amounts of diphenhydramine, free dihydrocodeine and total dihydrocodeine (0.029, 0.018 and 0.024 mg, respectively); concentrations of these drugs in the femoral muscle were 0.270, 0.246 and 0.314 microg/g, respectively. These results indicate that postmortem diffusion of diphenhydramine and dihydrocodeine from the bladder resulted in the elevated concentrations of these drugs in the femoral venous blood. Not only high urinary drug concentrations but also a large volume of urine in the bladder might accelerate the postmortem diffusion.