The cortisol rhythm analysis indicated a circadian rhythm pattern for only one premature infant, all others of the neonates showed no circadian or ultradian rhythm in cortisol. Cortisol level of the premature neonates was significantly higher during the first day of the study period at night-time (median: 17.1 nmol/L, IQR=9.7-24.4 nmol/L) than on days 7 (median: 9.6 nmol/L, IQR=4.7-14.6 nmol/L; Tukey-HSD, z=4.12, p<0.001) and 14 (IQR=5.8-13.7 nmol/L; Tukey-HSD, z=2.89, p<0.05). No significant effect of acoustic stimulation was observed on the cortisol concentration and sleep-wake behavior. The activity-sleep rhythm of preterm neonates was dominated by ultradian rhythm patterns with a prominent period length of 4 h (30.5%). Activity frequencies of neonates were also significantly higher overnight on the first study day (mean: 329±185.1 U) than of night seven (mean: 260.2±132.4 U; Tukey-HSD, z=2.50, p<0.05). Quiet-activity patterns increased, whereas high-activity patterns decreased during the observation period. Average sleep time increased significantly during the study time from day 1 to day 7 (Tukey-HSD, z=2.51, p<0.05). In conclusion, premature infants showed higher cortisol levels - without a circadian rhythmicity - and higher activity frequencies in the first days after birth which may reflect an adaptation process of neonates after birth. Cortisol concentrations and the activity patterns were not influenced by music interventions.
Standardized acoustic stimulation with recorded lullabies and taped maternal voice led to a decrease in heart rate and respiratory rate, and was associated with lower activity. Whether this indicates a reduced stress reaction needs to be investigated in further studies.
The effects of murine oncostatin M (mOSM) are specifically mediated by the heterodimeric oncostatin M receptor (OSMR)/gp130 receptor complex. In the current study we demonstrate that murine adrenocortical Y-1 tumor cells express the OSMR/gp130 complex. Incubation of Y-1 cells with 1 and 10 ng/ml mOSM induces cell death due to specific induction of apoptosis. Western blot analysis of Y-1 cells incubated with mOSM for 24 h revealed caspase-3 cleavage and poly(ADP-ribase) polymerase (PARP) cleavage. In a proliferation assay system, incubation of Y-1 cells with 0·01, 0·1, 1 and 10 ng/ml mOSM for 24 h resulted in a decrease in cell numbers to 99 2%, 84 9%, 50 7% and 43 5% respectively of untreated control (defined as 100%). Pretreatment of Y-1 cells with the Jak2 inhibitor AG490 (100 µM) rescued Y-1 cells from OSM-induced (10 ng/ml) cell death.
Objective: This comparative in vitro study examined the effects of all known gp130 cytokines on murine corticotroph AtT-20 cell function. Methods: Cytokines were tested at equimolar concentrations from 0.078 to 10 nM. Tyrosine phosphorylation of the signal transducer and activator of transcription (STAT)3 and STAT1, the STAT-dependent suppressor of cytokine signaling (SOCS)-3 promoter activity, SOCS-3 gene expression, STAT-dependent POMC promoter activity and adrenocorticotropic hormone (ACTH) secretion were determined. Results: Leukemia inhibitory factor (LIF), human oncostatin M (OSM) and cardiotrophin (CT)-1 (LIFR/gp130 ligands), as well as ciliary neurotrophic factor (CNTF) and novel neurotrophin-1/B-cell stimulating factor-3 (CNTFRα/LIFR/gp130 ligands) are potent stimuli of corticotroph cells in vitro. In comparison, interleukin (IL)-6 (IL-6R/gp130 ligand) and IL-11 (IL-11R/gp130 ligand) exhibited only modest direct effects on corticotrophs, while murine OSM (OSMR/gp130 ligand) showed no effect. Conclusion: (i) CNTFR complex ligands are potent stimuli of corticotroph function, comparable to LIFR complex ligands; (ii) IL-6 and IL-11 are relatively weak direct stimuli of corticotroph function; (iii) differential effects of human and murine OSM suggest that LIFR/gp130 (OSMR type I) but not OSMR/gp130 (OSMR type II) are involved in corticotroph signaling. (iv) CT-1 has the hitherto unknown ability to stimulate corticotroph function, and (v) despite redundant immuno-neuroendocrine effects of different gp130 cytokines, corticotroph cells are preferably activated through the LIFR and CNTFR complexes.
Bei der durch Mg-arme Ernährung erzeugten Arteriosklerose von Ratten waren im Serum die Konzentrationen von Cholesterin, Triglyceriden und Phosphatiden sowie das Spektrum der verschiedenen Lipoproteine gegenüber Kontrolltieren nicht verändert. Der Gehalt des Serum an freien Fettsäuren war erhöht. Der Serumproteingehalt war besonders durch eine Abnahme der Albumine und y-Globuline verringert. Diese Ergebnisse sind unabhängig vom Gehalt der Mg-armen Nahrung an mehrfach ungesättigten Fettsäuren. Der Gehalt von Cholesterin, Triglyceriden und Phosphatiden in den Aorten und Lebern wurde durch die Mg-arme Ernährung nicht beeinflußt. Eine Störung im Lipidstoffwechsel konnte als Ursache der durch Mg-Mangel bedingten Arteriosklerose ausgeschlossen werden. Lipid metabolism during a dietary magnesium deficiency. Studies on artherosclerosis induced by magnesium deficiencyArtherosclerosis was induced in rats by a diet deficient in magnesium. Compared with the non-artherosclerotic controls, the serum concentrations of cholesterol, triglycerides and phospholipids and the spectrum of various lipoproteins were unchanged in the artherosclerotic animals. The concentration of free fatty acids was increased. The serum protein concentration showed a decrease, which was due mainly to decreases in the albumin and y-globulin fractions. These results were not influenced by changes in the levels of polyunsaturated fatty acids in the Mg-deficient diet. The concentrations of cholesterol, triglycerides and phospholipids in the aortas and livers of Mg-deficient rats were the same as in the controls. These results show that Mg-deficiency artherosclerosis cannot be correlated with a disturbance in lipid metabolism.
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