Preparation and specificities of antisera to beta 1 leads to 4 linked N-acetyl-D-glucosamine oligosaccharides.
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Biomedical subjects
Publications and source records attributed to D Paul.
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Various hormonal and non-hormonal agents were tested for their ability to induce ornithine decarboxylase (EC 4.1.1.17) in primary cultures of fetal rat liver cells that retain many of the differentiated functions of hepatocytes. The only agents to induce ornithine decarboxylase in this cell type were fetal calf serum, prostaglandin E1 and cyclic AMP derivatives. Also, the amino acid arginine would induce ornithine decarboxylase in this cell type following arginine starvation for 24 h. These observations are in contrast to the wide range of hormones, e.g. insulin, hydrocortisone, glucagon and growth hormone, than can induce ornithine decarboxylase in vivo in the adult rat liver but which are all without effect on fetal rat liver cells.
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Growth stimulation of either fetal rat liver cells or rat embryo fibroblasts in culture results in considerable increases in intracellular polyamine levels as cells proceed through the cell cycle. Treatment of such cell cultures with appropriate levels of two inhibitors of polyamine synthesis, namely alpha-hydrazino ornithine and methylglyoxal bis (guanylhydrazone), can essentially completely block these increases in cellular polyamine content. Under such conditions, where the elevation in intracellular polyamine content is prevented, cell cultures are nevertheless able to initiate DNA synthesis and subsequently synthesize DNA at rates comparable to untreated control cultures that have been growth-stimulated. These two cell types therefore contain sufficient polyamines when in a resting state (G1) to enable them to enter from G1 into S phase and traverse S phase at normal rates in the absense of further polyamine synthesis. The recruitment of cells into the first cell cycle, through serum stimulation of growth, therefore appears not to be mediated or regulated by the increases in intracellular levels of polyamines that occurs under these conditions. Conversely, the arrest of growth of these cell types resulting from serum deprivation is not mediated by a limitation of intracellular polyamine content.
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The serum-induced transition of 3T3 fibroblasts from resting to growing state is characterized by a marked increase in cellular ATP content, the maximal level of which is reached at the onset of DNA replication. This increase in cellular ATP during the G 1 period of the cell cycle is correlated with about 3-fold stimulation of transcription of rRNA measured in permeabilized cell in vitro. Addition of hypoxanthine to serum-depleted quiescent 3T3 cells gives rise to an increase in both the ATP pool and the rate of rRNA synthesis. The expansion of cellular ATP pools after growth induction by serum seems to be a prerequisite for initiation of DNA synthesis since inhibition of purine de novo biosynthesis by azaserine inhibits both ATP pool expansion and DNA replication. This effect of azaserine can be abolished by addition of hypoxanthine to the culture medium. It is concluded that (a) the increase of the rate of rRNA synthesis in 3T3 cells in response to growth factors or serum is controlled by the cellular purine nucleoside triphosphate concentration and (b) an increased ATP level is necessary for initiation of DNA synthesis but is not sufficient to trigger the events that lead to DNA replication.
The negative effects of fractures of paralyzed and partially paralyzed lower extremities are described. A good result to a certain extent restoring the condition from before the accident can only obtained by early osteosynthesis. Only the AO-method and intramedullary nailing should be applied for osteosynthesis.
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The specific demand of sodium hydroxide is determined for the dissolution of sunflower seed globulin, casein and a mixture of them to equal parts. In low protein-containing solutions it depends for sunflower seed globulin very much on the sodium chloride concentration. From sunflower seed globulin, casein and a mixture of them to equal parts are prepared with sodium hydroxide high protein-containing alkaline solutions. Sunflower seed globulin forms temporally a gel phase. After this phase the solution of sunflower seed globulin shows like casein and a mixture of sunflower seed globulin/casein (I:I) pseudoplastic flow. The flow curves of the pseudoplastic solutions are described mathematically with the OSWALDian power statement. By alkaline solutions of casein and sunflower seed globulin/casein (I:I) the flow exponent n is distributed statistically about 0.9, by solutions of sunflower seed globulin a distribution exists about the mean values n = 0.85 and n = 0.50. lg k depends in all protein solutions on the concentration of protein, sodium chloride, sodium hydroxide and on the temperature and time. For all protein solutions exists a linear relation between the logarithm of viscosity and the reciprocal temperature for lg k and I/T, which is derived normally for NEWTONian flow behaviour. In a suitable scope of spinning for all protein solutions are carried out complete factorial experiment, which guide to regression equations of lg k; in the case of sunflower seed globulin are calculated also a regression equation of the flow exponent n. Going out from the parameters of the spinning process the properties of the spun sunflower seed globulin/casein (I:I) fibers are described.
The effects of the newly synthesized neuromuscular blocking agent, chandonium iodide (17a-methyl-3beta-pyrrolidino-17a-aza-D-homo-5-androstene dimethiodide) have been investigated on guinea-pig isolated ileum and vas deferens preparations. On the ileum, chandonium (0-1-10-0 mug ml(-1); 1-6 X 10(-7) M-1-6 X 10(-5) M) had weak muscarinic receptor blocking action (pA2 is 5-7), but no antihistamine properties at the concentration tested. No evidence for anticholinesterase actions was found. On the vas deferens, chandonium (10-50 mug ml(-1); 1-6-8-1 X 10(-5) M) potentiated responses to exogenous noradrenaline; responses to electrical stimulation were potentiated only in the presence of 50 mug ml(-1) chandonium. No adrenoceptor or adrenergic neuron blockade was found. The results provide evidence that chandonium acts selectively at acetylcholine receptors and that it is more active as a nicotinic receptor antagonist than as a muscarinic receptor antagonist.