[Determination of inorganic phosphates in a kinetic regimen].
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Biomedical subjects
Publications and source records attributed to P Stern.
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Lymphocytes from athymic and normal mice were tested and compared for cytotoxic activity after in vitro cultures supplemented with concanavalin A or T-cell growth factor (TCGF). Our results indicate that, in addition to cytotoxic T cells, natural killer (NK) activity can be recovered from lymphocytes cultured in the presence of TCGF and that this is not the result of contaminating interferon in the TCGF preparations. The NK nature of the effector cells was established by means of a panel of target cells, including a teratocarcinoma tumour cell, which enabled the distinction of T-cell- and NK-cell-mediated lysis.
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Natural killer (NK) cells from mice lyse murine teratocarcinoma stem cells in accordance with their appropriate cellular, genetic and interferon inducible features. In addition, rat and human putative NK cells were found to exhibit cytotoxicity of these embryonal carcinoma stem cells. By contrast, endodermal cells derived from such stem cells, either as cell lines or by recent induction with retinoic acid, were relatively resistant to effectors from all three mammalian species tested. Attempts to elicit a murine T-cell response to embryonal carcinoma by secondary in vitro stimulation failed. As previously shown, T killers directed to H-2 determinants were unable to lyse the MHC lacking embryonal carcinoma cells. The use of lectin "glues", a procedure supposedly capable of revealing the total cytotoxic. T-cell potential regardless of specificity, also failed to elicit lysis of these target cells. We have therefore failed to find evidence for T-cell recognition or lysis of embryonal carcinoma while NK cells from different species seemingly regard these latter cells as "universal" targets.
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The release of vasopressin (AVP) was assessed by measuring urinary excretion of the hormone in ten neonates who had an acute and symptomatic pneumothorax in the first three days after birth. AVP excretion rose significantly (paired t analysis) after the pneumothorax occurred. When apparent re-expansion of the lungs occurred after treatment, excretion of AVP returned to prepneumothorax levels within eight to 16 hours. If the pneumothorax persisted or worsened. AVP excretion remained elevated. Urine osmolality rose significantly (paired t analysis) after pneumothorax, presumably in response to the increased AVP levels. Two of the ten infants had hyponatremia in the period studied, while in a state of sodium balance. It was concluded that AVP release is increased after a pneumothorax occurs. This increase is apparently not due to osmoregulatory requirements. Fluid intake in these infants may need adjustment to prevent an inappropriate positive water balance.
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Small columns packed with octadecasilyl-silica were used to extract arginine-vasopressin in femtomole amounts from biological fluids for radioimmunoassay. This method is effective in isolating the peptide from substances in plasma and serum which interfere with its quantitation. Consistent and reproducible results and recoveries > 80% were obtained with this procedure. High pressure liquid chromatography and serial dilution of extracted samples confirm the identity of the extracted product.
Vasopressin increases the permeability of collecting ducts to water. Administration of this hormone is also associated with an increase in intramembranous particle clusters in rat collecting duct luminal membrane (CDLM) as revealed by freeze-fracture electron microscopy. To determine whether this morphologic alteration of CDLM is quantitatively related to the dose of vasopressin, anesthetized Brattleboro homozygous rats were given the hormone at different doses. CDLM from kidneys removed before and during infusion were examined by freeze-fracture electron microscopy. The frequency of CDLM clusters as well as the area of membrane occupied by them was related to the dose of vasopressin. In a separate experimental protocol, a decrease in intramembranous particle clusters accompanied a decrease in urinary osmolality when vasopressin was stopped. We conclude that CDLM intramembranous particle clusters represent a specific structural change related to the action of vasopressin. Accordingly, quantitation of CDLM clusters may serve as an end point for the study of vasopressin-induced water permeability.
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A rabbit antiserum to a mouse embryonal carcinoma cell line blocks compaction of cleaving mouse embryos. Cell division is not affected up to the 32-cell stage but intracellular junctions fail to develop. Removal of the antibody at this stage permits compaction to occur and a normal blastocyst develops. Prolonged decompaction beyond the 32-cell embryo results in an increasing proportion of malformed blastocysts in which trophectodermal cells predominate and functional inner cell mass (ICM) cells are reduced or absent. The relationship of compaction to the generation of ICM and trophectoderm lineages in the intact embryo is discussed.