Serotonin 2A receptors modulate tail-skin temperature in two rodent models of estrogen deficiency-related thermoregulatory dysfunction.

Menopause-associated thermoregulatory dysfunction, including hot flushes and night sweats, is effectively treated by hormonal therapies that include estrogens. Evidence suggests that estrogen regulates serotonin 2A (5-HT(2A)) receptor expression and that 5-HT(2A) receptors are involved in thermoregulation. Therefore, the role of 5-HT(2A) receptors in thermoregulation was assessed in two rat models of ovariectomy-induced thermoregulatory dysfunction.

Glutamate mediates cell death and increases the Bax to Bcl-2 ratio in a differentiated neuronal cell line.

Excessive stimulation of the NMDA receptor by glutamate induces cell death and has been implicated in the development of several neurodegenerative diseases. While apoptosis plays a role in glutamate-mediated toxicity, the mechanisms underlying this process have yet to be completely determined. Recent evidence has shown that exposure to excitatory amino acids regulates the expression of the antiapoptotic protein, Bcl-2, and the proapoptotic protein, Bax, in neurons.

Decrements in nuclear glucocorticoid receptor (GR) protein levels and DNA binding in aged rat hippocampus.

Hippocampal glucocorticoid receptors (GRs) are believed to play a major role in age-related cognitive decline and cellular vulnerability. It has been proposed that these receptors mediate damaging effects of elevated glucocorticoid secretion on cellular function. In the present report we present evidence that intracellular trafficking of the GR is impaired with hippocampal aging, manifest as decreased nuclear translocation and deficient DNA binding.

Epidemiologic study of pulmonary obstruction in workers occupationally exposed to ethyl and methyl cyanoacrylate.

The association between pulmonary obstruction (e.g., asthma) and occupational exposure to methyl cyanoacrylate (MCA) and ethyl cyanoacrylate (ECA) was examined in an occupational cohort of 450 persons at an adhesive production facility in Puerto Rico.

Expression of the 75 kDA TNF receptor and its role in contact-mediated neuronal cell death.

We previously demonstrated TNF toxicity, at high TNF doses or in the presence of actinomycin D, in the N1E-115 neuronal cell line (N1Es), which expresses only the 55 kDa TNF receptor (TNFR). To determine whether presence of the 75 kDa TNFR increases N1E sensitivity to TNF toxicity, cells were transfected with a 75 kDa TNFR expression construct. However, 75 kDa TNFR protein expression was undetectable in stably transfected N1Es.