Diethyl 2-amino-5-[(E)-(furan-2-yl­methyl­idene)amino]­thio­phene-3,4-di­carboxyl­ate

In the crystal structure of the title compound, C15H16N2O5S, the azomethine adopts the E configuration. The two heterocyclic rings adopt an anti­periplanar orientation. The mean planes of the thio­phene and furan rings are twisted by 2.51 (4)°. The crystal structure exhibits inter­molecular N—H⋯O hydrogen bonding. π–π stacking is also observed, the centroid-to-centroid distance being 3.770 (4) Å

Diethyl 2,5-bis­[(E)-2-furylmethyl­ene­amino]thio­phene-3,4-dicarboxyl­ate

The title compound, C20H18N2O6S, crystallizes as two independent mol­ecules that are disposed about a pseudo-inversion center (1/2, 1/4, 1/8). The mean planes of the two terminal furyl rings are twisted with respect to the central thio­phene ring by 7.33 (4) and 21.74 (5)° in one mol­ecule, and by 6.91 (4) and 39.80 (6)° in the other

(E)-5-(2-Thienylmethyl­eneamino)quinolin-8-ol

Two mol­ecules of the title compound, C14H10N2OS, are hydrogen bonded about a center of inversion. In the mol­ecule, the two aromatic rings are twisted by 37.27 (5)° with respect to one another. The azomethine bond is in the E configuration

Diethyl 2-[(1-methyl-1H-pyrrol-2-yl)methyl­ene­amino]-5-(2-thienylmethyl­ene­amino)thio­phene-3,4-dicarboxyl­ate

Both imine bonds of the title compound, C21H21N3O4S2, were found to be in the E configuration. The terminal pyrrole and thio­phene rings are twisted by 2.5 (3) and 2.3 (2)°, respectively, from the mean plane of the central thio­phene to which they are attached. The structure is disordered by exchange of the terminal heterocyclic rings; the site occupancy factors are ca 0.8 and 0.2. The crystal packing involves some π–π stacking [3.449 (4) Å between pyrrole and terminal thio­phene rings]

Diethyl 2,5-bis­[(1E)-(1H-pyrrol-2-yl­methyl­idene)amino]­thio­phene-3,4-dicarboxyl­ate

In the crystal structure of the title compound, C20H20N4O4S, the azomethine group adopt E conformations. The pyrrole units are twisted by 10.31 (4) and 18.90 (5)° with respect to the central thio­phene ring. The three-dimensional network is close packed and involves N—H⋯O, N—H⋯N, C—H⋯N and C—H⋯O hydrogen bonding

Multidimensional Dynamics of the Proteome in the Neurodegenerative and Aging Mammalian Brain

Neurodegenerative diseases are characterized by the abnormal accumulation of aggregated proteins in the brain. Using in vivo pulse isotope labeling, we screened the proteome for changes in protein turnover and abundance in multiple mouse models of neurodegeneration. These data suggest that the disease state of pathologically affected tissue is characterized by a proteome-wide increase in protein turnover and repair. In contrast, in healthy wild-type mice, aging in the mammalian brain is associated with a global slowdown in protein turnover.Peer reviewe

A Networks-Science Investigation into the Epic Poems of Ossian

In 1760 James Macpherson published the first volume of a series of epic poems which he claimed to have translated into English from ancient Scottish-Gaelic sources. The poems, which purported to have been composed by a third-century bard named Ossian, quickly achieved wide international acclaim. They invited comparisons with major works of the epic tradition, including Homer's Iliad and Odyssey, and effected a profound influence on the emergent Romantic period in literature and the arts. However, the work also provoked one of the most famous literary controversies of all time, colouring the reception of the poetry to this day. The authenticity of the poems was questioned by some scholars, while others protested that they misappropriated material from Irish mythological sources. Recent years have seen a growing critical interest in Ossian, initiated by revisionist and counter-revisionist scholarship and by the two-hundred-and-fiftieth anniversary of the first collected edition of the poems in 1765. Here we investigate Ossian from a networks-science point of view. We compare the connectivity structures underlying the societies described in the Ossianic narratives with those of ancient Greek and Irish sources. Despite attempts, from the outset, to position Ossian alongside the Homeric epics and to distance it from Irish sources, our results indicate significant network-structural differences between Macpherson's text and those of Homer. They also show a strong similarity between Ossianic networks and those of the narratives known as Acallam na Sen\'orach (Colloquy of the Ancients) from the Fenian Cycle of Irish mythology.Comment: Accepted for publication in Advances in Complex system

Extrinsic and intrinsic determinants of nerve regeneration

After central nervous system (CNS) injury axons fail to regenerate often leading to persistent neurologic deficit although injured peripheral nervous system (PNS) axons mount a robust regenerative response that may lead to functional recovery. Some of the failures of CNS regeneration arise from the many glial-based inhibitory molecules found in the injured CNS, whereas the intrinsic regenerative potential of some CNS neurons is actively curtailed during CNS maturation and limited after injury. In this review, the molecular basis for extrinsic and intrinsic modulation of axon regeneration within the nervous system is evaluated. A more complete understanding of the factors limiting axonal regeneration will provide a rational basis, which is used to develop improved treatments for nervous system injury

Defending the genome from the enemy within:mechanisms of retrotransposon suppression in the mouse germline

The viability of any species requires that the genome is kept stable as it is transmitted from generation to generation by the germ cells. One of the challenges to transgenerational genome stability is the potential mutagenic activity of transposable genetic elements, particularly retrotransposons. There are many different types of retrotransposon in mammalian genomes, and these target different points in germline development to amplify and integrate into new genomic locations. Germ cells, and their pluripotent developmental precursors, have evolved a variety of genome defence mechanisms that suppress retrotransposon activity and maintain genome stability across the generations. Here, we review recent advances in understanding how retrotransposon activity is suppressed in the mammalian germline, how genes involved in germline genome defence mechanisms are regulated, and the consequences of mutating these genome defence genes for the developing germline