Concept of death in a sample of Israeli kibbutz children.

The study of children's concept of death and factors that affect its acquisition continue to evolve. In this study, the concept of death of 22 Israeli children (aged 5-12 years), were assessed using vignettes. Participants' understanding of finality, universality, inevitability, and total concept of death were explored using the Concept of Death Assessment (CODA). The child's developmental level was assessed using an interactive developmental tool based on a Piagetian/constructivist framework (R. B. Sund, 1976). Development was scored as a continuous, rather than as a dichotomous variable. In this sample, age was the only significant predictor of concept of death (p less than .01). Children had an accurate concept of death as young as 6 years, however, it was not possible to determine an upper age limit by which children had an accurate concept of death. The mean developmental score was 64.8% +/-18.7. Still, 45% of this sample had an accurate concept of death, and 95.5% had an accurate understanding of finality. Environmental factors unique to an Israeli sample that might affect concept acquisition are explored. Questions remain about the interrelationship of development and concept acquisition.

Hepatitis C virus in the etiology of chronic hepatitis and liver cirrhosis: possibility of mixed viral infections due to parenteral transmission.

Sera obtained from 381 patients with chronic liver disease from four cities within the USSR were studied for HBV, HDV, and HCV markers of infection. Anti-HCV activity was detected in 41.2% of non-A, non-B cases. The etiological distribution of chronic hepatitis in Moscow and Dushanbe was similar with an approximate 20% prevalence for HBV, HDV, and HCV infections, whereas in Yakutsk 40% of cases were caused by HDV infections. The etiology of disease remained unrecognized in approximately 40% of patients with chronic liver disease in Moscow and Dushanbe and in 15% in Yakutsk. Anti-HCV activity was detected in 18.8% of patients with chronic HBV infections and in 8.3% of patients with chronic HDV infections. Anti-HCV activity was detected in 41% of patients without markers of HBV or HDV infections. The reasons for the observed differences in HCV prevalence among patients chronically infected with HDV are discussed.

[Hepatitis B virus antigens and antibodies in acute infection]. / Antigeny virusa hela gepatita B i antitela k nim pri ostrom zabolevanii.

Investigations of hepatitis B virus antigens (HBsAg and HBeAg) and antibody (anti-HBc, anti-HBe, anti-HBs) and DNA-polymerase activity in 136 patients with acute virus hepatitis B revealed their different diagnostic value depending on the severity of the process. The rate of finding of hepatitis B virus antigens declines in regression of the clinical symptoms of the disease. However, when hepatodystrophy develops, HBsAg and HBeAg concentration decreases, anti-HBc persist, and in one third of the patients anti-HBs are found. In moderately severe and mild forms of hepatitis, anti-HBs were detected in the convalescent period, as a rule.

Analysis of DNA from human adenovirus type 6 with restriction endonucleases HindIII, BglIII and BamHI.

The genome of the type 6 human adenovirus has three restriction sites for R.BamHI, thirteen for R.HindIII and ten for R.BglII. The terminal fragments of DNA cleaved by each of the enzymes have been determined by means of terminal nucleotidyl transferase and by analysis of the DNA-terminal protein complex. The sequence of the cleaved fragments has been determined by partial cleavage of DNA, simultaneous digestion of DNA with various combinations of enzymes and secondary digestion of individual isolated fragments with other enzymes. The following order of the cleaved fragments in the adenovirus type 6 genome has been found (the figures in brackets are the weights in mega-daltons): for R.BamHI-B(7.1)-D(3.0)-C(4.05)-A(8.5); for R.HindIII-F(1.7)-C1(2.14)-A(3.44)-M(0.046)-I(1.24)-J(0.77)-D(2.1)-E(1.96)-B(3.18)-H(1.36)-L(0.18)-C2(2.14)-G(1.44)-K(0.16); for R.BglII-E(2.07)-B(3.58)-A(4.8)-C(3.36)-I(0.78)-D(3.25)-G(1.37)-J(0.21)-F(1.85)-K(0.17)-H(0.94).