Haemophilus influenzae amnionitis with intact membranes: a case report.
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The ability of mouse amniotic fluid (MAF), alpha-foetoprotein (AFP) and MAF depleted of AFP (MAF - AFP) to suppress primary one-way MLR's was investigated. It was found that MAF, AFP and MAF - AFP were all suppressive of MLR's specific for MHC, K, D or I + S determinants. Suppression was observed when either lymph node or spleen cells were used as the responder cells. Nylon wool column passage of these cells did not significantly affect the immunosuppressive action of these substances. In contrast, MLR's specific for non-MHC/M-locus determinants demonstrated either diminished suppression or augmentation of the response, compared with the MHC stimulated MLR's. Our results show a differential effect of whole MAF and its fractions on the proliferative responses induced by various allogeneic stimuli and suggest that suppression is not due to a non-specific effect on proliferation regardless of the stimulus or cell type involved.
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UNLABELLED: In general intra-amniotic infection causes severe fetal compromise. Prematurity resulting from preterm labor, premature rupture of membranes, maternal fever, maternal or fetal septicemia and fetal tachycardia is the major problem of this clinical syndrome. Therefore early detection of chorioamnionitis gains high prospective value. Gram's staining method from amniotic fluid provides a quick and reliable diagnostic tool (sensitivity 63.8%, specificity 97.7%). A localized extra-amniotic abscess demonstrates the special case of a false negative amniocentesis performed for bacteriological reasons. CONCLUSION: In suspected amniotic infection the obstetrical management has always to take into account all different parameters--clinical symptoms, chemistry and microbiological analysis. Nevertheless Gram's stain is a reliable and quick method to verify amniotic infection syndrome.
The nitroblue tetrazolium (NBT) reduction of granulocytes from cord blood, when measured without in vitro stimulation with bacteria, was significantly higher than that of maternal granulocytes. This elevated activity may be an adequate response to the presence in cord blood of degradation products from the placenta but also of potentially pathogenic bacteria, found in cord blood of infants with high NBT values. On in vitro stimulation cord blood granulocytes displayed the same high NBT activity as those of the mothers and of healthy non-pregnant women. All but one blood culture from the infants 25--48 h after delivery were sterile. The only child with a low non-stimulated NBT activity of cord blood granulocytes was also the only one presenting a clinical picture of neonatal septicemia, though not bacteriologically verified.
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Whole pancreas or beta-cell transplantation has opened the way for the treatment of advanced stage of diabetes mellitus. However, it is always limited by the scarcity of transplantation materials. The amniotic membrane is part of the fetal membrane and is composed of amniotic epithelium (HAE) and mesenchymal (HAM) cells that are derived from the inner cell mass in the blastocyst. Thus, HAE and HAM cells may have the potential to differentiate into various organs. The aim of our study was to assess the possibility of HAE cells differentiating into insulin-producing cells. In vitro, HAE cells stimulated with nicotinamide induced insulin mRNA in the culture cells. In vivo, HAE cells were capable of normalizing the blood glucose level of diabetic mice after several weeks of implantation into streptozotocin-induced diabetic mice. The distribution of human cells and human insulin secretion in mouse tissue studied by immunohistochemistry for anti-human-specific beta-2-microglobulin and anti-human-specific insulin shows the same location in mouse tissue. These studies suggest that HAE cells have the potential to differentiate into beta-cells in vivo, and hence that HAE cells have therapeutic potential for the treatment of type I diabetes mellitus.
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