We investigate whether a heat-shock protein gene (HSP70-2) is involved in determining susceptibility to systemic lupus erythematosus (SLE) in a Spanish population. A HSP70-2 PstI polymorphism was characterized by restriction fragment length polymorphism analysis of polymerase chain reaction-amplified genomic DNA in 90 SLE patients and 117 controls. The PstI site containing allele (B) was significantly increased in SLE patients compared to healthy controls. This was due to a significant increase in the BB homozygous genotype in patients, particularly in those with diffuse proliferative nephritis. Neither allelic nor genotypic differences were detected when compared by the presence or absence of DR3. The HSP70-2 B allele seems tightly linked to the human leucocyte antigen (HLA) haplotypes carrying susceptibility to SLE in our population. An independent role for this gene cannot be confirmed due to its linkage with HLA DR3.

Objective. To determine whether clonally expanded B cells are present in the early infiltrates of minor labial salivary glands (LSG) of Sjogren's syndrome (SS) patients.Methods. Available paraffin-embedded LSG biopsies from 14 patients with primary SS were studied. DNA from LSG tissue was amplified by a polymerase chain reaction directed toward rearranged immunoglobulin gene DNA.Results. All LSG specimens showed oligoclonal or monoclonal B cell expansion. In one patient with plasma cell neoplasm, tumor and LSG specimens obtained at the same operation displayed different immunoglobulin gene rearrangements.Conclusion. Clonal expansion is characteristic of primary SS, and it is uniformly found in the early LSG infiltrates of patients who do not experience further progression to pseudolymphoma or lymphoma (mean followup 4.1 years after biopsy). This feature, together with the clonal discordance between the LSG and the B cell neoplasm found in one patient, suggests that additional steps are critical for the progression to malignancy.

The absorption, deposition, and excretion of zinc65 was studied in mice, rats, and dogs. When zinc65 was fed to the animals it was poorly absorbed, but its long biologic half-life made even the small portion absorbed physiologically significant. Absorption was obviated by feeding large quantities of nonradioactive carrier zinc. Injected zinc65 chloride first was deposited, preferably in the pancreas, liver, and spleen, with only minor deposition in muscle and in the brain. Subsequently, a large proportion was transferred to bone. The chief means of excretion was in feces, presumably via pancreatic secretion. Injected nonradioactive zinc or treatment with 2,3-dimercaptopropanol (BAL), Versene, or cadmium ion failed to alter body burden significantly. Cadmium, however, decreased soft tissue zinc65 deposition and increased accretion by the skeleton. Blood activity fell rapidly and less than .01% of the dose injected remained in the blood after 1 day. Renal excretion of zinc65 rose as plasma concentration fell and clearance ratios in excess of 1.0 were noted, indicating probable renal secretion.

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