Results indicate that the role of social support seems important for drinking and depression but remains controversial for health care access. It raises the hypothesis that low social support may be one of the mechanisms for the increase in drinking that happens after immigration.

SummaryΔ41-52 hPRL (human prolactin with residues 41-52 removed) is a lead compound for a new class of hPRL antagonists. The deleted sequence contains residues that functionally couple sites 1 and 2, the two hormone surfaces that each bind receptors. Δ41-52 hPRL retains 0.03% agonist activity in FDC-1 cell bioassays, a 3,054-fold reduction in activity, and displays approximately 100-fold less agonist activity than G129R hPRL, an antagonist that reduces the binding of hPRL receptor at site 2 during the formation of the heterotrimeric hormone/receptor complex. Replacement of various numbers and types of residues into the gap created by the deletion of residues 41 through 52 created hPRLs with varying agonist activities, suggested that manipulation of the sequence connecting the C-terminal of helix 1 with the disulfide bond (cysteines 58 with 174) linking helices 1 and 4 modulates articulation of these helices and influences agonist activity. We have compared the antagonist activities of G129R and Δ41-52 hPRLs to induce apoptosis in Jurkat cells, a human lymphoid cell line displaying an autocrine/paracrine hPRL/receptor system. Δ41-52 hPRL induces apoptosis in a time and dose-dependent fashion. Under these same conditions G129R hPRL fails to induce apoptosis. We conclude Δ41-52 hPRL is a lead compound of a new class of hPRL antagonists capable at low concentrations of inducing apoptosis in human cells expressing an autocrine/paracrine hPRL/ receptor system.