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To investigate the dynamic interplay between human immunodeficiency virus type I (HIV-1) replication and the extent of immune destruction in HIV-1-infected children, virus burden in lymphoid tissues (LN) and peripheral blood was compared with changes in LN architecture and cytokine levels constitutively expressed in LN. In agreement with results of a preliminary study, the plasma HIV-1 RNA level correlated with the amount of provirus in LN. However, the level was also associated with a degree of destruction of lymphoid follicular architecture and an alteration of immune cytokine expression. Expression of interleukin (IL)-4 was higher in LN with higher virus replication. Reduction of plasma viremia was associated with an increase in IL-2 mRNA levels in LN. These findings suggest that measurable virus burden in the peripheral blood is not a simple reflection of viral replication in LN but is also influenced by the extent of progressive immune destruction.

When isolated rat liver cells were incubated for 15 min in the presence of vasoactive intestinal peptide, secretin, gastrin, caerulein or glucagon at concentrations ranging from 0.2 microgram to 2 microgram per ml, glycogenolysis was stimulated. Among the gastrointestinal hormones or peptides tested, vasoactive intestinal peptide had the highest stimulatory activity. However, somatostatin was inhibitory for liver glycogenolysis. Combination experiments showed that somatostatin also inhibited the stimulatory effects of vasoactive intestinal peptide and secretin, but not that of glucagon, while glucagon and vasoactive intestinal peptide, or glucagon and secretin showed additive effects on glycogenolysis, but secretin and vasoactive intestinal peptide did not. The results suffest that the receptor site of glucagon is different from those of secretin and vasoactive intestinal peptide. Slight but significant stimulation of gluconeogenesis was also observed by vasoactive intestinal peptide and secretin. The evidence presented in this paper indicates that the so-called enterohepatic axis, in which a part of serum glucose levels is regulated directly by gastrointestinal hormones, exists and that the axis is inhibited by somatostatin.

Nucleosomes isolated from Yoshida sarcoma chromatin by micrococcal nuclease treatment were relatively inactive as templates for in vitro DNA synthesis. However, the template activity increased by trypsin digestion of nucleosomes or addition of heparin to the reaction mixture. This indicates that the nucleosomal template activity is masked. A crude extract of Yoshida sarcoma cells stimulated the nucleosomal template activity. The stimulatory factor was separated into three peaks by DEAE cellulose column chromatography. The same three peaks were observed in normal rat liver extract with much lower activities, but enhanced in regenerating liver. The factors seem to stimulate DNA synthesis by activating DNA template in nucleosomes without degrading histones or changing the primary structure of nucleosomal DNA.

Three kinds of deoxyribonucleases (peaks A, B, and C) were separated from purified rat liver nuclei on DEAE-cellulose column chromatography, and their characteristics were partially studied. Peaks A and B had endonuclease activities under acidic conditions with low substrate specificity and did not require divalent metal ions. Peak C had an exonuclease activity under alkaline conditions with substrate specificity for denatured DNA or single stranded homopolymer and required divalent cations. Peak C degraded 3'-terminally mismatched substrate much faster than 3'-terminally matched substrate.