The Marine Microbial Eukaryote Transcriptome Sequencing Project (MMETSP): illuminating the functional diversity of eukaryotic life in the oceans through transcriptome sequencing.

Microbial ecology is plagued by problems of an abstract nature. Cell sizes are so small and population sizes so large that both are virtually incomprehensible. Niches are so far from our everyday experience as to make their very definition elusive. Organisms that may be abundant and critical to our survival are little understood, seldom described and/or cultured, and sometimes yet to be even seen. One way to confront these problems is to use data of an even more abstract nature: molecular sequence data. Massive environmental nucleic acid sequencing, such as metagenomics or metatranscriptomics, promises functional analysis of microbial communities as a whole, without prior knowledge of which organisms are in the environment or exactly how they are interacting. But sequence-based ecological studies nearly always use a comparative approach, and that requires relevant reference sequences, which are an extremely limited resource when it comes to microbial eukaryotes. In practice, this means sequence databases need to be populated with enormous quantities of data for which we have some certainties about the source. Most important is the taxonomic identity of the organism from which a sequence is derived and as much functional identification of the encoded proteins as possible. In an ideal world, such information would be available as a large set of complete, well curated, and annotated genomes for all the major organisms from the environment in question. Reality substantially diverges from this ideal, but at least for bacterial molecular ecology, there is a database consisting of thousands of complete genomes from a wide range of taxa, supplemented by a phylogeny-driven approach to diversifying genomics [2]. For eukaryotes, the number of available genomes is far, far fewer, and we have relied much more heavily on random growth of sequence databases, raising the question as to whether this is fit for purpose

Crosstalk between reactive oxygen species and pro-inflammatory markers in developing various chronic diseases: a review

The inflammation process in the human body plays a central role in the pathogenesis of many chronic diseases. In addition, reactive oxygen species (ROS) exert potentially a decisive role in human body, particularly in physiological and pathological process. The chronic inflammation state could generate several types of diseases such as cancer, atherosclerosis, diabetes mellitus and arthritis, especially if it is concomitant with high levels of pro-inflammatory markers and ROS. The respiratory burst of inflammatory cells during inflammation increases the production and accumulation of ROS. However, ROS regulate various types of kinases and transcription factors such nuclear factor-kappa B which is related to the activation of pro-inflammatory genes. The exact crosstalk between pro-inflammatory markers and ROS in terms of pathogenesis and development of serious diseases is still ambitious. Many studies have been attempting to determine the mechanistic mutual relationship between ROS and pro-inflammatory markers. Therefore hereby, we review the hypothetical relationship between ROS and pro-inflammatory markers in which they have been proposed to initiate cancer, atherosclerosis, diabetes mellitus and arthritis

Comparison of the non-linear spin dynamics in antiferromagnetic chain compounds Na2MnF5 and (ND4)2MnF5

Na2Mn0.98Fe0.02F5 and(ND4)(2)Mn0.98Fe0.02F5 was studied with the aid of Mossbauer spectroscopy. These results were interpreted on the basis of classical soliton theory. In order to confirm this concept, we have performed neutron scattering experiments on large single crystals of the pure compounds. We discuss the results obtained on a thermal and cold three-axis spectrometer, which probe the magnon spin wave excitations and the existence of the nonlinear excitations in the quasi 1-d antiferromagnetic chains of Na2MnF5 and (ND4)(2)MnF5, respectively. Additionally, we include elastic neutron diffraction and dc. single crystal susceptibility measurements to determine the magnetic structure. From the width of the quasielastic scattering signal the temperature dependence of the inverse magnetic correlation lengths was derived resulting in a soliton activation energy of E-s/k = 65(3) K and E-s/k - 81(3) K, respectively, which are in good agreement with the soliton energies obtained by our high resolution inelastic neutron scattering experiment. In contrast to these results the Mossbauer spectroscopy gives twice the value of the soliton energy caused by soliton pair or interband excitations