The curious nature of the hemispheric symmetry of the Earth’s water and energy balances

This paper presents new estimates of the hemispheric energy balance based on an assembly of radiative flux and ocean heat data. Further, it provides an overview of recent simulations with fully coupled climate models to investigate the role of its representation in causing tropical precipitation biases. The energy balance portrayed here features a small hemispheric imbalance with slightly more energy being absorbed by the Southern hemisphere. This yields a net transport of heat towards the NH composing of a northward crossequatorial heat transport by the oceans and a southward heat flow in the atmosphere. The turbulent fluxes and hemispheric precipitation balance to about 3 Wm−2 with slightly larger total accumulation occurring in the NH. CloudSat data indicate more frequent precipitation in the SH implying more intense precipitation in the NH. Fully coupled climate model simulations show that reducing hemispheric energy balance biases does little to reduce existing biases in tropical precipitation

Sustained calcium signalling and caspase-3 activation involve NMDA receptors in thymocytes in contact with dendritic cells

L-glutamate, the major excitatory neurotransmitter, also has a role in non-neuronal tissues and modulates immune responses. Whether NMDA receptor (NMDAR) signalling is involved in T-cell development is unknown. In this study, we show that mouse thymocytes expressed an array of glutamate receptors, including NMDARs subunits. Sustained calcium (Ca2+) signals and caspase-3 activation in thymocytes were induced by interaction with antigen-pulsed dendritic cells (DCs) and were inhibited by NMDAR antagonists MK801 and memantine. NMDARs were transiently activated, triggered the sustained Ca2+ signal and were corecruited with the PDZ-domain adaptor postsynaptic density (PSD)-95 to thymocyte-DC contact zones. Although T-cell receptor (TCR) activation was sufficient for relocalization of NMDAR and PSD-95 at the contact zone, NMDAR could be activated only in a synaptic context. In these T-DC contacts, thymocyte activation occurred in the absence of exogenous glutamate, indicating that DCs could be a physiological source of glutamate. DCs expressed glutamate, glutamate-specific vesicular glutamate transporters and were capable of fast glutamate release through a Ca2+-dependent mechanism. We suggest that glutamate released by DCs could elicit focal responses through NMDAR-signalling in T cells undergoing apoptosis. Thus, synapses between T and DCs could provide a functional platform for coupling TCR activation and NMDAR signalling, which might reflect on T-cell development and modulation of the immune response