The victim, a 63-year-old prosperous businessman from Labasa, of the Northern Island (Vanua Levu) of Fiji Islands, was found completely decapitated in the early hours of morning in 2004. Initial police investigation did not reveal any history of any medical or family calamity. Further inquiry by the police revealed that on the previous day the deceased had visited all his friends and relatives, and his behavior was not out of the ordinary. The police suspected it to be a case of homicide. On visit to the scene, a completely decapitated body was found in a van on a downhill road. Tire marks were found on the road. A nylon rope was used for ligature strangulation. At autopsy, the decapitation wound of the head and the torso articulated well. The face was congested, and there was tongue bite. Wound margins were clear-cut, with well-demarcated abrasion and multiple imprints of the nylon rope on the neck. The upper one third of the larynx was attached to the head. No other injuries were found on the body. From the findings, it was obvious that asphyxiation was involved in the death before decapitation.
Introduction: This study examined the association of losartan induced changes in urinary
metabolomic profile with the changes in blood pressure (BP) and renin-angiotensinaldosterone system (RAAS) in spontaneously hypertensive rats (SHR). Methods: Male SHR
were administered with either 0.5 mL of distilled water (control group, n=6) or 10 mg.kg-1 of
losartan (group 2, n=6) daily by oral gavage for 4 weeks. Body weight, BP, food and water
intake were measured weekly. At week 4, urine was collected for urinary electrolyte analysis
and metabolite profiling, after which the animals were euthanised by decapitation and blood
was collected for analysis of components of RAAS and electrolyte concentrations. Urine
metabolite profile of SHR was determined using proton nuclear magnetic resonance (
1H-NMR)
spectrometry combined with multivariate data analysis. Results: At week 4, losartan-treated
SHR had significantly lower BP than non-treated SHR. There were no differences in water
and food intake, body weight, serum and urinary electrolyte concentrations or in their urinary
excretions between the two groups. No differences were evident in the components of RAAS
except that the angiotensinogen level was significantly higher in losartan-treated SHR
compared to non-treated SHR. Orthogonal partial least squares discriminant analysis (OPLSDA) showed clear separation of urinary metabolites between control and losartan-treated
SHR. Losartan-treated SHR group was separated from the control group by changes in the
intermediates involved in glycine, serine and threonine metabolism. Conclusion:
Antihypertensive effect of losartan in SHR seems to be associated with changes in urinary
metabolite profile, particularly involving the metabolism of glycine, serine and threonine.