No abstract

To determine the molecular genetic relationship between Melanesian strains of human T-lymphotropic virus type I (HTLV-I) and cosmopolitan prototype HTLV-I, we amplified by PCR, then cloned, and sequenced a 522-base-pair region of the HTLV-I env gene in DNA extracted from uncultured (fresh) and cultured peripheral blood mononuclear cells obtained from six seropositive Melanesian Papua New Guineans and Solomon Islanders, including a Solomon Islander with HTLV-I myeloneuropathy. Unlike isolates of HTLV-I from Japan, the West Indies, the Americas, and Africa, which share .97% sequence homology, the Melanesian strains of HTLV-I were only 91.8%-92.5% identical with a prototype Japanese HTLV-IATK-I. The nucleotide sequence of proviral DNA from the Solomon Islander with HTLV

There is now significant evidence that tumor necrosis factor (TNF) is involved in the pathogenesis of malaria. We have tested sera from patients presenting with a febrile illness admitted to hospital in Honiara, Solomon Islands, for the presence of TNF, interferon-gamma, and interleukin-1 (IL-1). This study differs from previous reports as the subjects were mainly adults from a semi-immune population living in an endemic area. The results from 2 different commercially-available assays for TNF were compared, and one was found to be superior to the other. Serum TNF concentrations correlated with malarial parasite density and the patients' temperatures, but not with interferon or IL-1. The results are discussed in the context of the immunopathology of this disease.

SUMMARY An investigation into the incidence of neurological disorder in 30 patients with adult coeliac disease has shown that three patients had severe depression, two had epileptiform convulsions, and one patient only had signs of involvement of the peripheral nervous system. Motor nerve conduction velocity was low in only one patient. When the nerve conduction velocities of the group on a gluten-free diet were compared with the group who were not on a gluten-free diet, there was no statistically significant difference. Similarly, nerve conduction velocities in patients with a low serum pyridoxal level were not significantly different from those with normal serum pyridoxal levels.