The Earth's 'hum' is driven by ocean waves over the continental shelves

Observations show that the seismic normal modes of the Earth at frequencies near 10 mHz are excited at a nearly constant level in the absence of large earthquakes. This background level of excitation has been called the 'hum' of the Earth, and is equivalent to the maximum excitation from a magnitude 5.75 earthquake. Its origin is debated, with most studies attributing the forcing to atmospheric turbulence, analogous to the forcing of solar oscillations by solar turbulence. Some reports also predicted that turbulence might excite the planetary modes of Mars to detectable levels. Recent observations on Earth, however, suggest that the predominant excitation source lies under the oceans. Here I show that turbulence is a very weak source, and instead it is interacting ocean waves over the shallow continental shelves that drive the hum of the Earth. Ocean waves couple into seismic waves through the quadratic nonlinearity of the surface boundary condition, which couples pairs of slowly propagating ocean waves of similar frequency to a high phase velocity component at approximately double the frequency. This is the process by which ocean waves generate the well known 'microseism peak' that dominates the seismic spectrum near 140 mHz (refs 11, 12), but at hum frequencies, the mechanism differs significantly in frequency and depth dependence. A calculation of the coupling between ocean waves and seismic modes reproduces the seismic spectrum observed. Measurements of the temporal correlation between ocean wave data and seismic data have confirmed that ocean waves, rather than atmospheric turbulence, are driving the modes of the Earth.     

Pathogenesis and therapy of psoriasis

Psoriasis is one of the most common human skin diseases and is considered to have key genetic underpinnings. It is characterized by excessive growth and aberrant differentiation of keratinocytes, but is fully reversible with appropriate therapy. The trigger of the keratinocyte response is thought to be activation of the cellular immune system, with T cells, dendritic cells and various immune-related cytokines and chemokines implicated in pathogenesis. The newest therapies for psoriasis target its immune components and may predict potential treatments for other inflammatory human diseases.     

Missing lithotroph identified as new planctomycete.

With the increased use of chemical fertilizers in agriculture, many densely populated countries face environmental problems associated with high ammonia emissions. The process of anaerobic ammonia oxidation ('anammox') is one of the most innovative technological advances in the removal of ammonia nitrogen from waste water. This new process combines ammonia and nitrite directly into dinitrogen gas. Until now, bacteria capable of anaerobically oxidizing ammonia had never been found and were known as "lithotrophs missing from nature". Here we report the discovery of this missing lithotroph and its identification as a new, autotrophic member of the order Planctomycetales, one of the major distinct divisions of the Bacteria. The new planctomycete grows extremely slowly, dividing only once every two weeks. At present, it cannot be cultivated by conventional microbiological techniques. The identification of this bacterium as the one responsible for anaerobic oxidation of ammonia makes an important contribution to the problem of unculturability.     

Linear ubiquitination prevents inflammation and regulates immune signalling

Members of the tumour necrosis factor (TNF) receptor superfamily have important functions in immunity and inflammation. Recently linear ubiquitin chains assembled by a complex containing HOIL-1 and HOIP (also known as RBCK1 and RNF31, respectively) were implicated in TNF signalling, yet their relevance in vivo remained uncertain. Here we identify SHARPIN as a third component of the linear ubiquitin chain assembly complex, recruited to the CD40 and TNF receptor signalling complexes together with its other constituents, HOIL-1 and HOIP. Mass spectrometry of TNF signalling complexes revealed RIP1 (also known as RIPK1) and NEMO (also known as IKKγ or IKBKG) to be linearly ubiquitinated. Mutation of the Sharpin gene (Sharpin(cpdm/cpdm)) causes chronic proliferative dermatitis (cpdm) characterized by inflammatory skin lesions and defective lymphoid organogenesis. Gene induction by TNF, CD40 ligand and interleukin-1β was attenuated in cpdm-derived cells which were rendered sensitive to TNF-induced death. Importantly, Tnf gene deficiency prevented skin lesions in cpdm mice. We conclude that by enabling linear ubiquitination in the TNF receptor signalling complex, SHARPIN interferes with TNF-induced cell death and, thereby, prevents inflammation. Our results provide evidence for the relevance of linear ubiquitination in vivo in preventing inflammation and regulating immune signalling.