Isolation of n-decyl-alpha(1-->6) isomaltoside from a technical APG mixture and its identification by the parallel use of LC-MS and NMR spectroscopy.

The identification of n-decyl alpha(1-->6)isomaltoside as a main component of technical alkyl polyglucoside (APG) mixtures by the parallel use of liquid chromatography-mass spectrometry (LC-MS) and nuclear magnetic resonance (NMR) spectroscopy is described. Following enrichment on a styrene-divinylbenzene-based solid-phase extraction material, unknown components were separated by reversed-phase liquid chromatography (LC). Chemical characterization was achieved by both mass spectrometry and NMR spectroscopy.

[Investigation of hematologic and clinical chemical parameters in serum of newborn fallow deer calves (Dama dama L.). Clinical chemical parameters].

59 blood samples from newborn fallow deer calves were clinical-chemically investigated at day of birth. To estimate the metabolic situation post natum we measured the concentration of glucose (6.8 +/- 2.

[Investigations on hematologic and clinical chemical parameters in blood serum of newborn fallow deer calves (Dama dama L.). 1: Birth weight and hematologic parameters].

59 newborn fallow deer calves were caught, marked, clinically investigated and weighed within 24 hours after parturition. Simultaneously a blood sample was taken from the jugular vein for hematological investigation. Mean birth weight was 4.

Prolactin and glucocorticoid hormones control transcription of the beta-casein gene by kinetically distinct mechanisms.

Transcription of the beta-casein milk protein gene in the HC11 mouse mammary epithelial cell line is induced synergistically by the hormones glucocorticoid and PRL. Sequential treatment of HC11 cells with glucocorticoid and PRL demonstrated that the two hormones had different modes of action on beta-casein transcription. Pretreatment with dexamethasone enhanced the response to subsequent induction by PRL, but not vice versa.

Oncogene mediated repression of glucocorticoid hormone response elements and glucocorticoid receptor levels.

We have previously described the inhibition of glucocorticoid-dependent transcription from the mouse mammary tumor virus long terminal repeat promoter by products of the H-ras and v-mos oncogenes. We have studied the effects of conditional oncogenes on expression of glucocorticoid-dependent indicator genes. Expression of the glucocorticoid-dependent transcription of the tyrosine aminotransferase gene was monitored in FTO-2B rat hepatoma cells during Mr 21,000 protein (p21) H-ras induction.