Dorsomedial hindbrain participation in glucoprivic feeding response to 2DG but not 2DG-induced hyperglycemia or activation of the HPA axis.

2-Deoxy-d-glucose (2DG) is a glucose analogue that inhibits intracellular utilization of glucose and produces a characteristic behavioral response known as glucoprivic feeding. The area postrema (AP) is a caudal hindbrain structure shown previously to be involved in 2DG-induced glucoprivic feeding. In addition, peripheral administration of 2DG is known to elicit activation of both the hypothalamic-pituitary-adrenal (HPA) axis and the sympathoadrenomedullary system. The neural substrates for these neuroendocrine and neural responses to 2DG are not known although they may also involve the AP. The possible role of the AP in 2DG-induced feeding, activation of the HPA axis and hyperglycemia was investigated in Sprague-Dawley rats with lesions centered on the area postrema (APX) and sham-operated (SHM) rats administered 2DG (200 mg/kg) or physiological saline (1 ml/kg). Peripheral administration of 2DG evoked a feeding response in SHM rats that was abolished in APX animals. Interestingly, 2DG administered at this dose produced a significant increase in plasma corticosterone and plasma glucose in both SHM and APX rats for up to 4 h after drug treatment. Collectively, these findings suggest that the AP is involved in the behavioral (feeding) response to peripheral administration of 2DG, but does not appear to be a common neural substrate for the neuroendocrine (HPA axis) and sympathoadrenal (hyperglycemic) responses to this agent.

The area postrema is involved in paraquat-induced conditioned aversion behavior and neuroendocrine activation of the hypothalamic-pituitary-adrenal axis.

Paraquat is a herbicide capable of eliciting conditioned taste aversion (CTA), a behavioral response characteristic of toxicosis. The area postrema (AP) is a hindbrain circumventricular organ previously shown to be important in mediating signs of paraquat-induced toxicity, namely CTA and weight loss. The relationship between neural substrates for paraquat-induced CTA and activation of the hypothalamic-pituitary-adrenal (HPA) axis was investigated in Sprague-Dawley rats with lesions centered on the AP (APX) and sham-operated (SHM) rats administered paraquat (25 mumol/kg) or saline (1 ml/kg). Injection of paraquat at a dose sufficient to condition taste aversion, but produce no other signs of overt toxicity, significantly increased plasma corticosterone concentrations in SHM rats up to 4 h after administration. Paraquat-induced activation of the HPA axis was significantly attenuated in AP-lesioned rats as compared to sham-operated controls. These findings suggest the area postrema is a common neural substrate for the behavioral and neuroendocrine responses to paraquat.

Serum concentrations of retinol, d-alpha-tocopherol and beta-carotene: effects of storage at -70 degrees C for five years.

To investigate the effects of prolonged storage of serum samples at -70 degrees C on concentrations of micronutrients, we measured concentrations of retinol, d-alpha-tocopherol, and beta-carotene in serum samples drawn in 1986. We compared values we measured in 1991 to values we obtained in 1986, using the same analytical methods. The relative concentrations obtained in 1991 (mean +/- S.D.) were: retinol 99.7 +/- 12.6% (n = 23), d-alpha-tocopherol 100.7 +/- 6.4% (n = 19), and beta-carotene 103.4 +/- 13.7% (n = 28). Using these techniques of sample preparation and high-performance liquid chromatographic analysis, we found that the effects of storage of serum at -70 degrees C for five years appear insignificant in a small population of patients. However, we did identify clinically important changes in concentration (> 20% difference) in several individual subjects.

Alpha 1-antitrypsin deficiency-associated panniculitis: case report and review of the literature.

Alpha 1-antitrypsin is the primary serum proteinase inhibitor. Alpha 1-antitrypsin deficiency, especially the ZZ genotype, has been linked mainly to emphysema and cirrhosis; it is also associated with paniculitis. A case of alpha 1-AT-associated panniculitis was documented in a 13-year-old girl in whom a deficiency of the enzyme was known to be present from infancy. This is unusual, since alpha 1-AT panniculitis previously was described in older patients without prior knowledge of the duration of the deficiency. Our patient developed erythematous, subcutaneous nodules subsequent to trauma, which later developed into deep, painless ulcers. We report this case so that the condition may be suspected in patients with panniculitis. The diagnosis may be confirmed by measuring quantitative alpha 1-AT serum levels and by enzyme genotyping. The treatment of choice is dapsone.