Polyurethane elastomer with PEO-PTMO-PEO soft segment for sustained release of drugs.

Blood-compatible segmented polyurethanes and polyurethaneureas were evaluated as drug delivery matrices using crystal violet and benzethonium chloride as model drugs. These polymers were synthesized from ABA-type triblock copolyether as a prepolymer, where A stands for poly(ethylene oxide) and B for poly(tetramethylene oxide). Microphase separation was observed in segmented polyurethaneureas, including drug-doped films. Crystal violet dissolved more in the hard segment domain than in the soft segment matrix, whereas benzethonium chloride was easily dissolved in the soft segment matrix. The drug release behaviours from these films were analysed by the exponent relation Mt/M infinity = ktn, where k and n are constants and Mt/M infinity is the fraction of drug released until time, t. The constant k grew with increasing poly(ethylene oxide) content in the prepolymer, i.e. increased swelling. The constant n was found to be close to 0.5 in many samples, which suggests the release of drug from these polymers is explained by the Fickian diffusion model. However, the mechanism became non-Fickian with increased swelling of the devices.

Apoptosis in placentas from human T-lymphotropic virus type I-seropositive pregnant women: a possible defense mechanism against transmission from mother to fetus.

OBJECTIVE: The mechanism by which the placenta serves as the barrier against mother-to-fetus transmission of microorganisms remains to be elucidated. Programmed cell death, apoptosis, is considered a cellular defense mechanism against infection. The hypothesis of this study is that apoptosis of human T-lymphotropic virus type I (HTLV-I)-infected placental villous cells is involved in the defense mechanism against mother-to-fetus transmission of HTLV-I. METHODS: Apoptosis was compared in term placentas from eight HTLV-I-seropositive pregnant women and eight HTLV-I-seronegative pregnant women by the terminal deoxynucleotidyl transferase-mediated deoxyuridine nick end-labeling method. In addition, an in vitro cocultivation with an HTLV-I-infected lymphocyte cell line (MT-2 cells) was performed to examine whether placental villous cells were infected with HTLV-I and apoptosis was induced. RESULTS: The incidence of apoptosis-positive cells (nuclei) in placentas from the HTLV-I-seropositive pregnant women was higher than in the HTLV-I-seronegative pregnant women (P < .02). Cocultivation with MT-2 cells showed that trophoblast cells were able to be infected with HTLV-I and that apoptosis was induced in the placental villous cells. CONCLUSION: HTLV-I infection induces apoptosis in the placenta. We speculate that apoptosis may be involved in the defense mechanism of the placenta against mother-to-fetus transmission of HTLV-I.

Immunotherapy with husband's leukocytes to primary habitual aborters and autoantibodies in their sera.

OBJECTIVE: This study was performed to determine whether primary habitual aborters have an autoimmunological tendency and whether immunotherapy with leukocytes induces autoantibodies in their sera. METHODS: We measured the levels of antiphospholipid antibodies (APAs) and antinuclear antibodies (ANAs) in the sera of 65 primary habitual aborters. Among them, 8 primary habitual aborters received immunotherapy with their respective husband's leukocytes; these 8 patients were followed up for autoantibodies in their sera before immunotherapy, at the time of pregnancy permission, during the first trimester of pregnancy, at delivery, and postpartum. RESULTS: Sixty-nine percent of the 65 primary habitual aborters were positive for IgG or IgM antibodies to at least 1 of 6 phospholipids, and 29% of them were positive for ANAs. Although the pregnancy outcomes of the 8 primary habitual aborters after immunotherapy were good, their APAs and ANAs converted to positive after the immunotherapy. CONCLUSION: Immunotherapy with leukocytes should be performed after checking and confirming the absence of autoantibodies in the sera of a habitual aborter.