Abdominal Stab Wounds with Tension Pneumopericardium Confirmed by Autopsy and Postmortem Computed Tomography.

We present the first report of pneumopericardium observed by autopsy and on postmortem computed tomography (PMCT) images. The subject was a woman who died of self-inflicted stab wounds to the abdomen. The PMCT scan revealed air in the pericardial sac, a "flattened heart" sign, and retroperitoneal hemorrhage. Medicolegal autopsy revealed two abdominal stab wounds near the xiphoid process that had cut the apical pericardium and adjacent diaphragm and liver. Examination of the open thorax confirmed that the pericardial sac was distended with air. The wound extended to the abdominal aorta, causing retroperitoneal hemorrhage. PMCT images showed that the pneumopericardial volume was 133 mL. We believe that cardiac tamponade occurred resulting from the tension pneumopericardium; however, the effects were mitigated by hypovolemia secondary to the retroperitoneal hemorrhage as well as obstructive shock. Therefore, the cause of death appears to have been low-pressure cardiac tamponade.

Inflammatory responses to neutral fat and fatty acids in multiple organs in a rat model of fat embolism syndrome.

Fat embolism syndrome (FES) is a common complication of long bone fractures. FES is rare but with significant morbidity and occasional fatalities. Studies of animal models of FES are numerous; however, few studies compare inflammatory reactions in multiple organs. The present study investigated the effect of neutral fat and fatty acids, which cause changes in multiple organs and induce FES. Using rats we evaluated the ratio of lung-to-body weight and conducted histological analyses and quantitative analysis of inflammatory cytokine mRNAs in the lungs following intravenous administration of neutral fat or fatty acids. Neutral fat increased the ratio of lung-to-body weight, and neutral fat formed emboli in lung capillaries. The levels of interleukin-1 beta (IL-1ß), IL-6 and tumor necrosis factor-alpha (TNF-α) in the lungs increased after injection of neutral fat and oleic acid. Analysis of the histologic changes revealed that the highest numbers of fat droplets, occluding the capillaries of the lungs, kidney, heart, and brain formed 12h after the injection of neutral fat and fat droplets gradually diminished 48h later. Fat droplets were not detected in any organs after the injection of oleic acid. IL-1ß and TNF-α levels in the lungs were elevated 9-24h after the injection of neutral fat, although IL-6 levels peaked at 6h. After injection of oleic acid, peak levels of IL-1ß, IL-6, and TNF-α were detected at 6h, and IL-6 again increased in all organs and plasma at 15h. Neutral fat, but not fatty acids, formed emboli in the capillaries of multiple organs. These findings suggest that neutral fat increased inflammatory cytokine levels by forming emboli in organ capillaries, particularly in the lungs, while oleic acid augmented inflammatory cytokine levels by stimulating endothelial cells of multiple organs.

Interactions of human organic anion transporter 1 (hOAT1) with substances associated with forensic toxicology.

Renal excretion is an important elimination pathway for substances associated with forensic toxicology, such as medicines, agricultural chemicals, and industrial chemicals. This study aimed to elucidate the renal elimination pathway of substances using culture cells stably expressing the human organic anion transporter 1 (hOAT1) gene. Substances tested were diazepam, triazolam, haloperidol, amitriptyline, mianserin, bromovalerylurea, phenobarbital, acetaminophen, acetylsalicylic acid, lidocaine, aconitine, atropine, caffeine, nicotine, malathion, dichlorvos, fenitrothion, chlorpyrifosmethyl, paraquat, diquat, potassium cyanide, sodium arsenite, sodium azide, o-cresol, and probenecid (control, a representative inhibitor of hOAT1). Results demonstrated that diazepam, triazolam, amitriptyline, mianserin, malathion, fenitrothion, chlorpyrifosmethyl, and probenecid significantly inhibited representative substrates of hOAT1 and para-aminohippuric acid uptake by hOAT1. IC(50) values of the aforementioned substances were 133.3, 185.2, 354.1, 312.6, 114.2, 26.6, 191.5, and 7.9µM, respectively. Ki values were 83.5, 86.0, 573.9, 99.0, 134.0, 51.2, 324.6, and 9.1µM, respectively. In conclusion, the current results suggest that fenitrothion and chlorpyrifosmethyl are transported with pharmacokinetics indicative of hOAT1 involvement in the human kidney.