ABSTRACT
The structure of graphite oxide (GO) has been systematically studied using various tools such as SEM, TEM, XRD, Fourier transform infrared spectroscopy (FT-IR), X-ray photoemission spectroscopy (XPS), (13)C solid-state NMR, and O K-edge X-ray absorption near edge structure (XANES). The TEM data reveal that GO consists of amorphous and crystalline phases. The XPS data show that some carbon atoms have sp(3) orbitals and others have sp(2) orbitals. The ratio of sp(2) to sp(3) bonded carbon atoms decreases as sample preparation times increase. The (13)C solid-state NMR spectra of GO indicate the existence of -OH and -O- groups for which peaks appear at 60 and 70 ppm, respectively. FT-IR results corroborate these findings. The existence of ketone groups is also implied by FT-IR, which is verified by O K-edge XANES and (13)C solid-state NMR. We propose a new model for GO based on the results; -O-, -OH, and -C=O groups are on the surface.
ABSTRACT
Polycystic ovarian syndrome (PCOS) is one of the most common human ovarian pathologies affecting women of reproductive age. Despite extensive investigation, the etiology of PCOS remains poorly understood. Experimentally, a PCO-like syndrome can be induced in rodents by a single dose of the long-acting estrogen, estradiol valerate (EV). We have used this model to examine the possibility that PCOS is associated with derangement of the sympathetic control of the ovary. The release of newly incorporated norepinephrine (NE) from ovarian nerve terminals in response to transmural stimulation of the gland increased significantly before the formation of cysts (30 days after EV injection) and remained elevated at the time when cysts form (60 days). The increase in evoked NE release was accompanied by an augmented NE content and enhanced incorporation of [3H]NE into ovarian tissue; both of these changes had been initiated by 30 days after EV treatment and became unambiguous at the time of cyst formation. The overall increase in ovarian sympathetic outflow suggested by these alterations in catecholamine homeostasis was accompanied by a thecal cell-interstitial tissue selective down-regulation of beta-adrenergic receptors; the beta-adrenergic receptor concentration in these sympathetically innervated ovarian compartments was significantly lower in PCO than during the estrous phase of the estrous cycle, a time at which the beta-adrenergic receptor concentration reaches its lowest levels in normal cycling ovaries. Tyrosine hydroxylase activity was found to increase only when expressed per mg ovary, but not in absolute terms (i.e. per total ovary), suggesting regulation of enzyme activity by the enhanced catecholamine content. The results demonstrate that an activation of the sympathetic neurons innervating the ovary precedes the development of cysts in EV-induced PCOS and raise the possibility that a derangement of sympathetic inputs to the ovary contributes to the etiology of PCOS.
