Fatal human herpes virus 6B myocarditis: Postmortem diagnosis of HHV-6B based on CD134+ T-cell tropism.

Human herpes virus 6 (HHV-6) is one of the most important pathogens of viral myocarditis, and is often responsible for sudden death in young adults. A 59-year-old immunocompetent man died of serious lymphocytic myocarditis, and his peripheral blood sample showed HHV-6 DNAemia. Recently, HHV-6 cell entry and reactivation have been suggested to be regulated by the expression of specific CD receptors on T lymphocytes. Here, we report a case of HHV-6 myocarditis diagnosed using an experimental method focused on this unique cell tropism. The interaction between HHV-6 and CD expression was assessed using an immunofluorescence assay. Colocalization between HHV-6B and CD134 was detected in lymphocytes infiltrating the myocardium, which was highly suggestive of an active HHV-6B infection and could be a useful criterion for postmortem diagnosis of HHV-6B myocarditis in the acute phase.

Pre-administration of low-dose methamphetamine enhances movement and neural activity after high-dose methamphetamine administration in the striatum.

Methamphetamine (METH) is a powerful stimulant drug of abuse, with potent addictive and neurotoxic properties. In this study, the effects of low-dose METH administration prior to high-dose METH administration on movement and neural activity in rats were examined. Rats were administered low-dose (1 mg/kg/day) METH or saline for 5 consecutive days (m5 and s5, respectively), followed by high-dose (10 mg/kg) METH on day 6 (m5M and s5M, respectively). An accelerometer was used to evaluate the frequency of movement when rats were placed in a cage for 30 min. The expression of c-fos, a neuronal activity marker, in the striatum was analyzed using immunohistochemistry. Striatal protein expression of neuronal markers, including vesicular glutamate transporter 2 (VGLUT2), glutamate decarboxylase 67 (GAD67), tyrosine hydroxylase (TH), tryptophan hydroxylase 2 (TPH2), and the glial marker, glial fibrillary acidic protein (GFAP), was analyzed by western blot. Accelerometer counts and the numbers of c-fos-positive cells in the striatum were significantly higher in the m5M than in the s5, m5, and s5M groups. The expression levels of VGLUT2 and GAD67, but not those of TH, TPH2, or GFAP, were significantly higher in the m5M than in the s5M group. These results suggest that pre-administration of low-dose METH prior to high-dose METH administration in rats may alter excitatory and inhibitory neurons in the striatum, thereby affecting movement and neural activity in rats.

An autopsy report of accidental burial in a beach sand hole.

We present a 23-year-old married couple who died by accidental burial in a beach sand hole. The victims fell into a hole that had been covered with a plastic sheet, and were buried suddenly by sand that had been piled on the top of the sheet. At autopsy, facial congestion; petechial hemorrhages in the conjunctivae and the oral mucosa; skin petechiae at the face, neck and upper chest; congestion and hemorrhages in the cervical lymph nodes; and some minor hemorrhages in the cervical muscles were found in both victims. Little sand was evident in the airway, while sand debris was found in the oral cavity. Prior reports suggest that aspiration of sand is a major contributing factor in asphyxia after accidental burials. However, neck and chest compression and face coverage by sand masses could induce lethal asphyxia without airway obstruction caused by sand aspiration. Asphyxia was deemed to be the cause of death in both individuals and was considered to result from chest compression by sand. In addition, compression of the neck may also have contributed to asphyxia. In this instance, the sand beach hole was excavated for recreational purposes. The potentially life-threatening implications of beach sand hole excavations should be recognized and highlighted to prevent lethal accidents such as those described in this report.