The longitudinal variation of equatorial waves due to propagation on a varying zonal flow

The general 1-D theory of waves propagating on a zonally varying flow is developed from basic wave theory, and equations are derived for the variation of wavenumber and energy along ray paths. Different categories of behaviour are found, depending on the sign of the group velocity (cg) and a wave property, B. For B positive the wave energy and the wave number vary in the same sense, with maxima in relative easterlies or westerlies, depending on the sign of cg. Also the wave accumulation of Webster and Chang (1988) occurs where cg goes to zero. However for B negative they behave in opposite senses and wave accumulation does not occur. The zonal propagation of the gravest equatorial waves is analysed in detail using the theory. For non-dispersive Kelvin waves, B reduces to 2, and analytic solution is possible. B is positive for all the waves considered, except for the westward moving mixed Rossby-gravity (WMRG) wave which can have negative as well as positive B. Comparison is made between the observed climatologies of the individual equatorial waves and the result of pure propagation on the climatological upper tropospheric flow. The Kelvin wave distribution is in remarkable agreement, considering the approximations made. Some aspects of the WMRG and Rossby wave distributions are also in qualitative agreement. However the observed maxima in these waves in the winter westerlies in the eastern Pacific and Atlantic are not consistent with the theory. This is consistent with the importance of the sources of equatorial waves in these westerly duct regions due to higher latitude wave activity.

Calcium Flux in Neuroblastoma Cells Is a Coupling Mechanism between Non-Genomic and Genomic Modes of Estrogens

Estrogens have been demonstrated to rapidly modulate calcium levels in a variety of cell types. However, the significance of estrogen-mediated calcium flux in neuronal cells is largely unknown. The relative importance of intra- and extracellular sources of calcium in estrogenic effects on neurons is also not well understood. Previously, we have demonstrated that membrane-limited estrogens, such as E-BSA given before an administration of a 2-hour pulse of 17beta-estradiol (E(2)), can potentiate the transcription mediated by E(2) from a consensus estrogen response element (ERE)-driven reporter gene. Inhibitors to signal transduction cascades given along with E-BSA or E(2) demonstrated that calcium flux is important for E-BSA-mediated potentiation of transcription in a transiently transfected neuroblastoma cell line. In this report, we have used inhibitors to different voltage-gated calcium channels (VGCCs) and to intracellular store receptors along with E-BSA in the first pulse or with E(2) in the second pulse to investigate the relative importance of these channels to estrogen-mediated transcription. Neither L- nor P-type VGCCs seem to play a role in estrogen action in these cells; while N-type VGCCs are important in both the non-genomic and genomic modes of estrogen action. Specific inhibitors also showed that the ryanodine receptor and the inositol trisphosphate receptor are important to E-BSA-mediated transcriptional potentiation. This report provides evidence that while intracellular stores of calcium are required to couple non-genomic actions of estrogen initiated at the membrane to transcription in the nucleus, extracellular sources of calcium are also important in both non-genomic and genomic actions of estrogens. Copyright (c) 2005 S. Karger AG, Basel.