The periodic topography of ice stream beds: Insights from the Fourier spectra of mega-scale glacial lineations

Ice stream bed topography contains key evidence for the ways ice streams interact with, and are potentially controlled by, their beds. Here we present the first application of two-dimensional Fourier analysis to 22 marine and terrestrial topographies from 5 regions in Antarctica and Canada, with and without mega-scale glacial lineations (MSGLs). We find that the topography of MSGL-rich ice stream sedimentary beds is characterized by multiple, periodic wavelengths between 300 and 1200 m and amplitudes from decimeters to a few meters. This periodic topography is consistent with the idea that instability is a key element to the formation of MSGL bedforms. Dominant wavelengths vary among locations and, on one paleo ice stream bed, increase along the direction of ice flow by 1.7 ± 0.52% km−1. We suggest that these changes are likely to reflect pattern evolution via downstream wavelength coarsening, even under potentially steady ice stream geometry and flow conditions. The amplitude of MSGLs is smaller than that of other fluvial and glacial topographies but within the same order of magnitude. However, MSGLs are a striking component of ice stream beds because the topographic amplitude of features not aligned with ice flow is reduced by an order of magnitude relative to those oriented with the flow direction. This study represents the first attempt to automatically derive the spectral signatures of MSGLs. It highlights the plausibility of identifying these landform assemblages using automated techniques and provides a benchmark for numerical models of ice stream flow and subglacial landscape evolution.The research was funded by the NE/J004766/1 UK NERC New Investigator and a SAGES 728 PECRE grants awarded to MS

Direct observations of evolving subglacial drainage beneath the Greenland Ice Sheet

Seasonal acceleration of the Greenland Ice Sheet is influenced by the dynamic response of the subglacial hydrologic system to variability in meltwater delivery to the bed [1,2] via crevasses and moulins (vertical conduits connecting supraglacial water to the bed of the ice sheet). As the melt season progresses, the subglacial hydrologic system drains supraglacial meltwater more efficiently [1–4], decreasing basal water pressure [4] and moderating the ice velocity response to surface melting [1,2]. However, limited direct observations of subglacial water pressure [4–7] mean that the spatiotemporal evolution of the subglacial hydrologic system remains poorly understood. Here we show that ice velocity is well correlated with moulin hydraulic head but is out of phase with that of nearby (0.3–2 kilometres away) boreholes, indicating that moulins connect to an efficient, channelized component of the subglacial hydrologic system, which exerts the primary control on diurnal and multi-day changes in ice velocity. Our simultaneous measurements of moulin and borehole hydraulic head and ice velocity in the Paakitsoq region of western Greenland show that decreasing trends in ice velocity during the latter part of the melt season cannot be explained by changes in the ability of moulin-connected channels to convey supraglacial melt. Instead, these observations suggest that decreasing late-season ice velocity may be caused by changes in connectivity in unchannelized regions of the subglacial hydrologic system. Understanding this spatiotemporal variability in subglacial pressures is increasingly important because melt-season dynamics affect ice velocity beyond the conclusion of the melt season [8–10]

Characteristics and critical function of CD8+ T cells in the Toxoplasma-infected brain

The rise of the AIDS epidemic made the requirement for T cells in our continuous protection from pathogens critically apparent. The striking frequency with which AIDS patients exhibited profound neurological pathologies brought attention to many chronic infections that are latent within theimmune-privileged CNS. One of the most common lethal opportunistic infections of these patients was with the protozoan parasite, Toxoplasma gondii. Reactivation of Toxoplasma cysts within the brain causes massive tissue destruction evidenced as multiple ring-enhancing lesions on MRI and is called Toxoplasmic encephalitis (TE). TE is not limited to AIDS patients, but rather is a risk for all severely immunocompromised patients, including recipients of chemotherapy or transplant recipients. The lessons learned from these patient populations are supported by T cell depletion studies in mice. Such experiments have demonstrated that CD4+ and CD8+ T cells are required for protection against TE. Although it is clear that these T cell subsets work synergistically to fight infection, much evidence has been generated that suggests CD8+ T cells play a dominant role in protection during chronic toxoplasmosis. . In other models of CNS inflammation, such as intracerebral infection with LCMV and experimental autoimmune encephalomyelitis (EAE), infiltration of T cells into the brain is harmful and even fatal. In the brain of the immunocompetent host, the well-regulated T cell response to Toxoplasma gondii is therefore an ideal model to understand a controlled inflammatory response to CNS infection. This review will examine our current understanding of CD8+ T cells in the CNS during T. gondii infection in regards to the 1) mechanisms governing entry into the brain, 2) cues that dictate behavior within the brain, and 3) the functional and phenotypic properties exhibited by these cell