Di-μ-pivalato-κ3 O,O′:O′;κ3 O:O,O′-bis­[(methanol-κO)bis­(2,2,6,6-tetra­methylhepta­ne-3,5-dionato)praseo­dymium(III)]

In the centrosymmetric dimeric title compound, [Pr2(C5H9O2)2(C11H19O2)4(CH3OH)2], the two praseodymium(III) atoms are eight-coordinate and are bridged by O atoms from the two pivalate anions. Each PrIII ion is further coordinated by two chelating 2,2,6,6-tetra­methyl-3,5-hepta­nedionate (thd−) ligands and one methanol mol­ecule. The distance between the two PrIII ions is 4.273 (5) Å. Intra­molecular hydrogen bonds exists between the methanol hy­droxy group on one PrIII atom and a chelating O atom of a thd− ligand coordinated to the symmetry-related PrIII atom

catena-Poly[1-butyl-3-methyl­imidazolium [[dichlorido(methanol-κO)(propan-2-ol-κO)lanthanate(III)]-di-μ-chlorido]]

The title compound, (C8H15N2)[LaCl4(CH3OH)(C3H7OH)], consists of one 1-butyl-3-methyl­imidazolium (BMI+) cation and one hexa­hedral tetra­chlorido(methanol)(propan-2-ol)lanthanate anion. The LaIII ion is eight-coordinate, with the LaIII ion bridged by a pair of Cl atoms, so forming chains propagating along the a-axis direction. Each LaIII ion is further coordinated by two isolated Cl atoms, one methanol and one propan-2-ol mol­ecule. The coordinated methanol and propan-2-ol mol­ecules of the anion form O—H⋯Cl hydrogen bonds with the Cl atoms of inversion-related anions. The BMI+ cation froms C—H⋯Cl hydrogen bonds with the Cl atoms of the anion. The anions are located in the C faces of the triclinic unit cell, with an inversion center in the middle of the La2Cl2 ring of the polymeric chain

Assortativity Decreases the Robustness of Interdependent Networks

It was recently recognized that interdependencies among different networks can play a crucial role in triggering cascading failures and hence system-wide disasters. A recent model shows how pairs of interdependent networks can exhibit an abrupt percolation transition as failures accumulate. We report on the effects of topology on failure propagation for a model system consisting of two interdependent networks. We find that the internal node correlations in each of the two interdependent networks significantly changes the critical density of failures that triggers the total disruption of the two-network system. Specifically, we find that the assortativity (i.e. the likelihood of nodes with similar degree to be connected) within a single network decreases the robustness of the entire system. The results of this study on the influence of assortativity may provide insights into ways of improving the robustness of network architecture, and thus enhances the level of protection of critical infrastructures

Association of ultra-rare coding variants with genetic generalized epilepsy: a case-control whole exome sequencing study

OBJECTIVE: We aimed to identify genes associated with genetic generalized epilepsy (GGE) by combining large cohorts enriched with individuals with a positive family history. Secondarily, we set out to compare the association of genes independently with familial and sporadic GGE. METHODS: We performed a case-control whole exome sequencing study in unrelated individuals of European descent diagnosed with GGE (previously recruited and sequenced through multiple international collaborations) and ancestry-matched controls. The association of ultra-rare variants (URVs; in 18 834 protein-coding genes) with epilepsy was examined in 1928 individuals with GGE (vs. 8578 controls), then separately in 945 individuals with familial GGE (vs. 8626 controls), and finally in 1005 individuals with sporadic GGE (vs. 8621 controls). We additionally examined the association of URVs with familial and sporadic GGE in two gene sets important for inhibitory signaling (19 genes encoding γ-aminobutyric acid type A [GABA(A)] receptors, 113 genes representing the GABAergic pathway). RESULTS: GABRG2 was associated with GGE (p = 1.8 × 10(-5)), approaching study-wide significance in familial GGE (p = 3.0 × 10(-6)), whereas no gene approached a significant association with sporadic GGE. Deleterious URVs in the most intolerant subgenic regions in genes encoding GABA(A) receptors were associated with familial GGE (odds ratio [OR] = 3.9, 95% confidence interval [CI] = 1.9-7.8, false discovery rate [FDR]-adjusted p = .0024), whereas their association with sporadic GGE had marginally lower odds (OR = 3.1, 95% CI = 1.3-6.7, FDR-adjusted p = .022). URVs in GABAergic pathway genes were associated with familial GGE (OR = 1.8, 95% CI = 1.3-2.5, FDR-adjusted p = .0024) but not with sporadic GGE (OR = 1.3, 95% CI = .9-1.9, FDR-adjusted p = .19). SIGNIFICANCE: URVs in GABRG2 are likely an important risk factor for familial GGE. The association of gene sets of GABAergic signaling with familial GGE is more prominent than with sporadic GGE

Fluctuation scaling in complex systems: Taylor's law and beyond

Complex systems consist of many interacting elements which participate in some dynamical process. The activity of various elements is often different and the fluctuation in the activity of an element grows monotonically with the average activity. This relationship is often of the form "$fluctuations \approx const.\times average^\alpha$", where the exponent $\alpha$ is predominantly in the range $[1/2, 1]$. This power law has been observed in a very wide range of disciplines, ranging from population dynamics through the Internet to the stock market and it is often treated under the names \emph{Taylor's law} or \emph{fluctuation scaling}. This review attempts to show how general the above scaling relationship is by surveying the literature, as well as by reporting some new empirical data and model calculations. We also show some basic principles that can underlie the generality of the phenomenon. This is followed by a mean-field framework based on sums of random variables. In this context the emergence of fluctuation scaling is equivalent to some corresponding limit theorems. In certain physical systems fluctuation scaling can be related to finite size scaling.Comment: 33 pages, 20 figures, 2 tables, submitted to Advances in Physic

Star polymers reduce IAPP toxicity via accelerated amyloid aggregation

Protein aggregation into amyloid fibrils is a ubiquitous phenomenon across the spectrum of neurodegenerative disorders and type 2 diabetes. A common strategy against amyloidogenesis is to minimize the populations of toxic oligomers and protofibrils by inhibiting protein aggregation with small molecules or nanoparticles. However, melanin synthesis in nature is realized by accelerated protein fibrillation to circumvent accumulation of toxic intermediates. Accordingly, we designed and demonstrated the use of star-shaped poly(2-hydroxyethyl acrylate) (PHEA) nanostructures for promoting the aggregation while ameliorating the toxicity of human islet amyloid polypeptide (IAPP), the peptide involved in glycemic control and the pathology of type 2 diabetes. The binding of PHEA elevated the beta-sheet content in IAPP aggregates while rendered a new morphology of ‘stelliform’ amyloids originating from the polymers. Atomistic molecular dynamics simulations revealed that the PHEA arms served as rod-like scaffolds for IAPP binding and subsequently accelerated IAPP aggregation by increased local peptide concentration. The tertiary structure of the star nanoparticles was found to be essential to drive the specific interactions required to impel the accelerated IAPP aggregation. This study shed new light on the structure-toxicity relationship of IAPP and points to the potential of exploiting star polymers as a new class of therapeutic agents against amyloidogenesis

Austerity, ageing and the financialisation of pensions policy in the UK

This article offers a detailed analysis of the recent history of pensions policy in the United Kingdom, culminating in two apparent ‘revolutions’ in policy now underway: the introduction of ‘automatic enrolment’ into private pensions, and proposals for a new ‘single-tier’ state pension. These reforms are considered exemplary of the ‘financialisation’ of UK welfare provision – typified in pensions policy by the notion that individuals must take personal responsibility for their own long-term financial security, and engage intimately with the financial services industry to do so. As such, the reforms represent the continuation of pensions policy between the Labour and coalition governments, despite the coalition government’s novel rhetorical commitment to austerity. In fact, the pensions revolutions will actually cost the state significantly more than current arrangements, yet the importance of fears about population ageing means that the government is both able to marshal the imagery of austerity to justify financialisation, but is also required to partly conceal the increased expenditure this requires. The article shows therefore how the financialisation agenda in pensions policy was evident before the financial crisis, but has evolved to both take advantage, and mitigate the constraints, of a post-crisis political climate