The magic nature of (132)Sn explored through the single-particle states of (133)Sn.

Atomic nuclei have a shell structure in which nuclei with 'magic numbers' of neutrons and protons are analogous to the noble gases in atomic physics. Only ten nuclei with the standard magic numbers of both neutrons and protons have so far been observed. The nuclear shell model is founded on the precept that neutrons and protons can move as independent particles in orbitals with discrete quantum numbers, subject to a mean field generated by all the other nucleons. Knowledge of the properties of single-particle states outside nuclear shell closures in exotic nuclei is important for a fundamental understanding of nuclear structure and nucleosynthesis (for example the r-process, which is responsible for the production of about half of the heavy elements). However, as a result of their short lifetimes, there is a paucity of knowledge about the nature of single-particle states outside exotic doubly magic nuclei. Here we measure the single-particle character of the levels in (133)Sn that lie outside the double shell closure present at the short-lived nucleus (132)Sn. We use an inverse kinematics technique that involves the transfer of a single nucleon to the nucleus. The purity of the measured single-particle states clearly illustrates the magic nature of (132)Sn.

Alpha:2n:alpha molecular band in 10Be.

The 10.15 MeV resonance in 10Be has been probed via resonant 6He+4He elastic scattering. It is demonstrated that it is the Jpi=4+ member of a rotational band built on the 6.18 MeV 0+ state. A Gammaalpha of 0.10-0.13 MeV and Gammaalpha/Gamma=0.35-0.46 were deduced. The corresponding reduced alpha width, gamma2alpha, indicates one of the largest alpha-cluster spectroscopic factors known. The deformation of the band, including the 7.54 MeV, 2+ member, is large (h2/2I=200 keV). Such a deformation and the significant degree of clusterization signals a well-developed alpha:2n:alpha molecular structure.

Altered adrenal steroid production in term infants having respiratory acidosis.

Prior studies have provided evidence for reduced fetal adrenal production of dehydroepiandrosterone sulfate and normal or increased production of cortisol in association with pregnancy complications believed to result in fetal stress. In the present study, we sought to determine the status of adrenal steroidogenesis in 36 term infants having respiratory acidosis and to compare acidotic infants to (i) non-acidotic infants matched for pregnancy complications, gestational age, and method and indications for delivery (control infants), and (ii) non-acidotic infants of non-complicated pregnancies who were also matched for gestational age and delivery method (normal infants). Umbilical cord serum levels of dehydroepiandrosterone sulfate were lowest in acidotic infants, intermediate in the condition matched control infants and highest in the non-acidotic infants of normal pregnancies. On the other hand, cortisol levels were highest in acidotic infants, intermediate in control infants and lowest in the normal infants. These data suggest that various pregnancy complications give rise to significant alterations in adrenal steroidogenesis (decreased dehydroepiandrosterone sulfate and increased cortisol). Intrauterine deterioration during labor with resultant respiratory acidosis has an additional effect on fetal adrenal function.

Adrenocorticotropin interferes with transforming growth factor-beta-induced growth inhibition of neocortical cells from the human fetal adrenal gland.

The effects of transforming growth factor-beta (TGF-beta) and ACTH on growth, as indicated by [3H]thymidine incorporation into DNA, of primary cultures of neocortical cells from the human fetal adrenal gland were studied. TGF-beta inhibited, in a dose- and time-dependent manner, the growth of fetal neocortical cells, and ACTH significantly blunted the inhibitory effects of TGF-beta on growth of these cells. ACTH did not block the inhibitory effects of TGF-beta on growth of fetal adrenal fibroblasts or liver cells; neither ACTH nor TGF-beta had any effect on growth of fetal kidney cells. Thus, it appears that growth regulation of the neocortex may differ strikingly from that of the fetal zone of the human fetal adrenal, in which ACTH and TGF-beta have been reported recently to have additive inhibitory effects on cell proliferation.

Investigation of the effect of interleukin-1 beta on steroidogenesis in the human fetal adrenal gland.

Interleukin-1 beta (IL-1 beta) has been shown by several investigators to be a stimulator of adrenal glucocorticoid production in vivo. However, little evidence exists for direct actions of IL-1 beta on the adrenal gland. We sought to elucidate the direct effects, if any, of IL-1 beta on human fetal adrenal steroidogenesis in the presence and absence of ACTH in both cell and organ cultures. We studied the effects of several doses of recombinant human IL-1 beta (0.05, 0.5, and 5 U/ml), in the presence and absence of two doses of ACTH (0.1 and 1 microgram/ml). With all doses of IL-1 beta, we were unable to demonstrate alterations in basal adrenal steroidogenesis as measured by dehydroepiandrosterone sulfate and cortisol production. Whereas both doses of ACTH induced significant increases in steroid production over control values (P less than 0.05), there was no additional effect on steroidogenesis when IL-1 beta was added to cultures containing ACTH. We conclude that although IL-1 beta may act in conjunction with other products of the immune system to modulate adrenal cortisol production, IL-1 beta alone does not directly influence human fetal adrenal steroidogenesis. Rather, it is likely that this cytokine acts via stimulation of pituitary ACTH production.