A significant ONSD response to acute postural change and to spaceflight was demonstrated in this preliminary study. Increases in Doppler peak flow velocities correlated with increases in ONSD. Further investigations are warranted to corroborate the relationship between ONSD, intracranial pressure, and central retinal blood flow for occupational surveillance and research purposes.

Six patients with acromegaly at examination were found to have pituitary adenomas composed of cells that secreted GH and PRL. This was demonstrated by the elevated serum hormone concentrations, by immunoperoxidase staining of 5 specimens, and by electron microscopic examination of 4. Ultrastructural characteristics, described in detail, suggest that these adenomas were mixed adenomas consisting of 2 well-defined, distinct cell types, each secreting one hormone. By immunoperoxidase staining some cells were found to contain immunoreactive growth hormone, other cells immunoreactive prolactin. No cells were detected exhibiting immunostaining for both growth hormone and prolactin. Eelctron microscopy, consistent with the results of immunostaining, revealed the presence of two distinct cell types, distinguishable from each other by their characteristic fine structural features. No intermediate forms were noted. Thus there was no evidence to suggest that one cell type might transform to the other. Present findings seem to indicate that mixed adenomas secreting growth hormone as well as prolactin and consisting of somatotrophs as well as lactotrophs do occur in the human pituitary gland. Although all the results obtained so far suggest that these tumors are composed of two distinct cell types and thus can be interpreted as representing real mixed adenomas, further work is required to establish whether or not they derive from one common progenitor.

Hypothalamic-pituitary-adrenal (HPA) axis hyperactivity occurs in type 2 diabetes, and stress is assumed to play a causal role. However, intermittent restraint stress, a model mimicking some mild stressors, delays development of hyperglycemia in Zucker diabetic fatty (ZDF) rats. We examine whether such stress delays hyperglycemia independent of stress-induced reductions in hyperphagia and is due to adaptations in gene expression of HPA-related peptides and receptors that ameliorate corticosteronemia and thus hyperglycemia. ZDF rats were intermittently restraint stressed (1 h/d, 5 d/wk) for 13 wk and compared with obese control, pair fed, and lean ZDF rats. After 13 wk, basal hormones were repeatedly measured over 24 h, and HPA-related gene expression was assessed by in situ hybridization. Although restraint initially induced hyperglycemia, this response habituated over time, and intermittent restraint delayed hyperglycemia. This delay was partly related to 5-15% decreased hyperphagia, which was not accompanied by decreased arcuate nucleus NPY or increased POMC mRNA expression, although expression was altered by obesity. Obese rats demonstrated basal hypercorticosteronemia and greater corticosterone responses to food/water removal. Basal hypercorticosteronemia was further exacerbated after 13 wk of pair feeding during the nadir. Importantly, intermittent restraint further delayed hyperglycemia independent of food intake, because glycemia was 30-40% lower than after 13 wk of pair feeding. This may be mediated by increased hippocampal MR mRNA, reduced anterior pituitary POMC mRNA levels, and lower adrenal sensitivity to ACTH, thus preventing basal and stress-induced hypercorticosteronemia. In contrast, 24-h catecholamines were unaltered. Thus, rather than playing a causal role, intermittent stress delayed deteriorations in glycemia and ameliorated HPA hyperactivity in the ZDF rat.