Hypophyseal damage in persons with cerebrocranial injuries and who died in the hospital

The pituitary was examined in patients with craniocerebral injuries who died in hospital in various periods after treatment. Control group consisted of victims died at the site of accident. The results indicate the significance of examining the pituitary in craniocerebral injuries for the diagnosis of thanatogenesis, particularly in patients died in hospital. Causes of traumatic changes in the organ were determined, highly incident in the practice of forensic medical experts: directly during injury, as a result of skull bone fractures; during development of dislocation syndrome and in disorders of blood and lymph circulation in the brain matter; resultant from augmenting traumatic edema of the brain.     

Detecting Deception in Children's Testimony: Factfinders' Abilities to Reach the Truth in Open Court and Closed-Circuit Trials

This study examined the influence of closed-circuit television (CCTV) on jurors' abilities to detect deception in children's testimony. Children ages 7–9 individually played games and made a video movie with a male confederate. In the guilty condition, stickers were placed on exposed body parts (i.e., the child's arm, toes, and bellybutton). In the not-guilty and deception conditions, stickers were placed on the child's clothing rather than on bare skin. Approximately 3 weeks later, mock jurors recruited from the community viewed child participants testify either in a traditional courtroom setting or via one-way CCTV. The mock jurors responded to questions about the child witness and the defendant as well as deliberated to reach a verdict. Children in the deception condition were asked to testify as if the stickers had been placed on exposed body parts rather than on their clothing. Predeliberation, jurors were less likely to convict when a child testified in the deception condition as opposed to the guilty condition. These differences disappeared following deliberation. There was no support for the notion that jurors reach the truth better when children testify in open court versus via CCTV. Implications for jurors' abilities to reach the truth are discussed.     

Clinico-morphological parameters of heroin abuse and pathology connected with it

Morphological manifestations of narcomania in heroin users are described. Diseases associated with heroin narcomania and causes of death of heroin users are presented. Morphological manifestations at the site of injections and inflammatory reactions in parenchymatous organs are characterized. The authors pay special attention to the productive inflammation which can serve as one of the signs that confirm narcomania in cases with parenteral injections of crude heroin. The authors refer the granulomas to toxic allergic form of granulomatous hypersensitive inflammation.     

GHB. Club drug or confusing artifact?

GHB can be produced either as a pre- or postmortem artifact. The authors describe two cases in which GHB was detected and discuss the problem of determining the role of GHB in each case. In both cases, NaF-preserved blood and urine were analyzed using gas chromatography. The first decedent, a known methamphetamine abuser, had GHB concentrations similar to those observed with subanesthetic doses (femoral blood, 159 microg/ml; urine, 1100 microg/ml). Myocardial fibrosis, in the pattern associated with stimulant abuse, was also evident. The second decedent had a normal heart but higher concentrations of GHB (femoral blood, 1.4 mg/ml; right heart, 1.1 mg/ml; urine, 6.0 mg/ml). Blood cocaine and MDMA levels were 420 and 730 ng/ml, respectively. Both decedents had been drinking and were in a postabsorptive state, with blood to vitreous ratios of less than 0.90. If NaF is not used as a preservative, GHB is produced as an artifact. Therefore, the mere demonstration of GHB does not prove causality or even necessarily that GHB was ingested. Blood and urine GHB concentrations in case 1 can be produced by a therapeutic dose of 100 mg, and myocardial fibrosis may have had more to do with the cause of death than GHB. The history in case 2 is consistent with the substantial GHB ingestion, but other drugs, including ethanol, were also detected. Ethanol interferes with GHB metabolism, preventing GHB breakdown, raising blood concentrations, and making respiratory arrest more likely. Combined investigational, autopsy, and toxicology data suggest that GHB was the cause of death in case 2 but not case 1. Given the recent discovery that postmortem GHB production occurs even in stored antemortem blood samples (provided they were preserved with citrate) and the earlier observations that de novo GHB production in urine does not occur, it is unwise to draw any inferences about causality unless (1) blood and urine are both analyzed and found to be elevated; (2) blood is collected in NaF-containing tubes; and (3) a detailed case history is obtained.