Quasiparticle Interactions in Two and Three Dimensional Superconductors

I investigate the difference between the quasiparticle properties in two dimensional(2D)and three dimensional(3D) s-wave superconductors. Using the original BCS model for the pairing interaction and direct Coulomb interaction I show that quasiparticle interactions lead to a stronger energy dependence in the single-particle self-energies in 2D than in 3D superconductors. This difference arises from the presence of the low lying collective mode of the order parameter in the 2D case which ensures that oscillator strength in the response function is at low frequencies, $\sim \Delta$. This strong quantitative difference between 2D and 3D superconductors points to the importance of treating quasiparticle interactions in low dimensional superconductors rather than assuming that renormalizations remain unchanged from the normal state.Comment: version of original paper accepted for publication in Europhysics Letter

Deletion of Gpr27 in vivo reduces insulin mRNA but does not result in diabetes.

Gpr27 is a highly conserved, orphan G protein coupled receptor (GPCR) previously implicated in pancreatic beta cell insulin transcription and glucose-stimulated insulin secretion in vitro. Here, we characterize a whole-body mouse knockout of Gpr27. Gpr27 knockout mice were born at expected Mendelian ratios and exhibited no gross abnormalities. Insulin and Pdx1 mRNA in Gpr27 knockout islets were reduced by 30%, but this did not translate to a reduction in islet insulin content or beta cell mass. Gpr27 knockout mice exhibited slightly worsened glucose tolerance with lower plasma insulin levels while maintaining similar insulin tolerance. Unexpectedly, Gpr27 deletion reduced expression of Eif4e3, a neighboring gene, likely by deleting transcription start sites on the anti-sense strand of the Gpr27 coding exon. Our data confirm that loss of Gpr27 reduces insulin mRNA in vivo but has only minor effects on glucose tolerance

Molecular medicine of microRNAs: structure, function and implications for diabetes

MicroRNAs (miRNAs) are a family of endogenous small noncoding RNA molecules, of 19–28 nucleotides in length. In humans, up to 3% of all genes are estimated to encode these evolutionarily conserved sequences. miRNAs are thought to control expression of thousands of target mRNAs. Mammalian miRNAs generally negatively regulate gene expression by repressing translation, possibly through effects on mRNA stability and compartmentalisation, and/or the translation process itself. An extensive range of in silico and experimental techniques have been applied to our understanding of the occurrence and functional relevance of such sequences, and antisense technologies have been successfully used to control miRNA expression in vitro and in vivo. Interestingly, miRNAs have been identified in both normal and pathological conditions, including differentiation and development, metabolism, proliferation, cell death, viral infection and cancer. Of specific relevance and excitement to the area of diabetes research, miRNA regulation has been implicated in insulin secretion from pancreatic β-cells, diabetic heart conditions and nephropathy. Further analyses of miRNAs in vitro and in vivo will, undoubtedly, enable us determine their potential to be exploited as therapeutic targets in diabetes

Integrating the inputs that shape pancreatic islet hormone release.

The pancreatic islet is a complex mini organ composed of a variety of endocrine cells and their support cells, which together tightly control blood glucose homeostasis. Changes in glucose concentration are commonly regarded as the chief signal controlling insulin-secreting beta cells, glucagon-secreting alpha cells and somatostatin-secreting delta cells. However, each of these cell types is highly responsive to a multitude of endocrine, paracrine, nutritional and neural inputs, which collectively shape the final endocrine output of the islet. Here, we review the principal inputs for each islet-cell type and the physiological circumstances in which these signals arise, through the prism of the insights generated by the transcriptomes of each of the major endocrine-cell types. A comprehensive integration of the factors that influence blood glucose homeostasis is essential to successfully improve therapeutic strategies for better diabetes management

Nuclear factor κB-inducing kinase activation as a mechanism of pancreatic β cell failure in obesity

The nuclear factor κB (NF-κB) pathway is a master regulator of inflammatory processes and is implicated in insulin resistance and pancreatic β cell dysfunction in the metabolic syndrome. Whereas canonical NF-κB signaling is well studied, there is little information on the divergent noncanonical NF-κB pathway in the context of pancreatic islet dysfunction. Here, we demonstrate that pharmacological activation of the noncanonical NF-κB-inducing kinase (NIK) disrupts glucose homeostasis in zebrafish in vivo. We identify NIK as a critical negative regulator of β cell function, as pharmacological NIK activation results in impaired glucose-stimulated insulin secretion in mouse and human islets. NIK levels are elevated in pancreatic islets isolated from diet-induced obese (DIO) mice, which exhibit increased processing of noncanonical NF-κB components p100 to p52, and accumulation of RelB. TNF and receptor activator of NF-κB ligand (RANKL), two ligands associated with diabetes, induce NIK in islets. Mice with constitutive β cell-intrinsic NIK activation present impaired insulin secretion with DIO. NIK activation triggers the noncanonical NF-κB transcriptional network to induce genes identified in human type 2 diabetes genome-wide association studies linked to β cell failure. These studies reveal that NIK contributes a central mechanism for β cell failure in diet-induced obesity.</p

Entre sistemas de protección social: inmigrantes filipinos en Europa y su (in)movilidad socio-espacial

With the aim to better understand how “care regimes” (that is, social protection systems) affect migrants’ lives, the present article draws from three separate studies on migrant Filipinas in Europe. The cases of three of these women unveil the important characteristic of the care regime in their country of origin and that in their respective receiving countries, which particularly shapes their lives. Interview data analysis suggests that insufficient care resources in the Philippines partly motivated these women’s migration as well as that of their offspring. In Europe, they experienced spatial and social class (im)mobilities due to the pro-undocumented migrant, family-focused, and transmigrant-friendly care regimes in their receiving countries, respectively France, Belgium and the Netherlands. Their encounters with the social protection systems “here” and “there” highlight their lives betwixt interacting care regimes in their social spaces.Con el objetivo de comprender mejor cómo los “regímenes de cuidado” (es decir, los sistemas de protección social) afectan la vida de los migrantes, el presente artículo se basa en tres estudios separados sobre las migrantes filipinas en Europa. Los casos de tres de estas mujeres desvelan la importante característica del régimen asistencial en su país de origen y que en sus respectivos países receptores, que en particular moldea sus vidas. El análisis de los datos de las entrevistas sugiere que los insuficientes recursos de atención en filipinas motivaron en parte la migración de estas mujeres, así como la de sus hijos. En Europa, experimentaron movilidad espacial y de clase social debido a los regímenes migratorios pro-indocumentados migrantes en sus países receptores, respectivamente, Francia, Bélgica y los Países Bajos. Sus encuentros con los sistemas de protección social “aquí” y “allí” resaltan sus vidas entre regímenes de atención interactivos en sus espacios sociales

Biological characteristics and mortality of western butterfish (Pentapodus vitta), an abundant bycatch species of prawn trawling and recreational fishing in a large subtropical embayment

The western butterfish (Pentapodus vitta) is numerous in the bycatch of prawn trawling and recreational fishing in Shark Bay, Western Australia. We have thus determined crucial aspects of its biological characteristics and the potential impact of fishing on its abundance within this large subtropical marine embayment. Although both sexes attained a maximum age of 8 years, males grow more rapidly and to a larger size. Maturity is attained at the end of the first year of life and spawning occurs between October and January. The use of a Bayesian approach to combine independent estimates for total mortality, Z, and natural mortality, M, yielded slightly higher point estimates for Z than M. This result indicates that P. vitta is lightly impacted by fishing. It is relevant that, potentially, the individuals can spawn twice before recruitment into the fishery and that 73% of recreationally caught individuals are returned live to the water

A Gpr120-selective agonist improves insulin resistance and chronic inflammation in obese mice.

It is well known that the ω-3 fatty acids (ω-3-FAs; also known as n-3 fatty acids) can exert potent anti-inflammatory effects. Commonly consumed as fish products, dietary supplements and pharmaceuticals, ω-3-FAs have a number of health benefits ascribed to them, including reduced plasma triglyceride levels, amelioration of atherosclerosis and increased insulin sensitivity. We reported that Gpr120 is the functional receptor for these fatty acids and that ω-3-FAs produce robust anti-inflammatory, insulin-sensitizing effects, both in vivo and in vitro, in a Gpr120-dependent manner. Indeed, genetic variants that predispose to obesity and diabetes have been described in the gene encoding GPR120 in humans (FFAR4). However, the amount of fish oils that would have to be consumed to sustain chronic agonism of Gpr120 is too high to be practical, and, thus, a high-affinity small-molecule Gpr120 agonist would be of potential clinical benefit. Accordingly, Gpr120 is a widely studied drug discovery target within the pharmaceutical industry. Gpr40 is another lipid-sensing G protein-coupled receptor, and it has been difficult to identify compounds with a high degree of selectivity for Gpr120 over Gpr40 (ref. 11). Here we report that a selective high-affinity, orally available, small-molecule Gpr120 agonist (cpdA) exerts potent anti-inflammatory effects on macrophages in vitro and in obese mice in vivo. Gpr120 agonist treatment of high-fat diet-fed obese mice causes improved glucose tolerance, decreased hyperinsulinemia, increased insulin sensitivity and decreased hepatic steatosis. This suggests that Gpr120 agonists could become new insulin-sensitizing drugs for the treatment of type 2 diabetes and other human insulin-resistant states in the future

Strong-Coupling Features Due to Quasiparticle Interaction in Two Dimensional Superconductors

I calculate the effect of interactions among superconducting quasiparticles in two-dimensional(2D) a superconductor at T=0. The strength of the effective interaction among the quasiparticles is essentially given by the screened Coulomb interaction which has strength at low frequency because of the gapless nature of the plasmon. This is in contrast to three dimensions where the effective interaction has negligible weight at frequencies $\sim \Delta$, the superconducting gap. The quasiparticle interactions give rise to strong-coupling effects in experimental quantities which are beyond the conventional Eliashberg treatment of superconductivity. The present calculation offers an explanation of why these effects are much larger in 2D than in 3D superconductors and, in particular, why the analogous strong-coupling effects due to quasiparticle interactions are seen in data on the quasi-2D cuprate superconductors. the strong-coupling features seen in data on the cuprates are discussed in light of the present calculation.Comment: 18 pages including 11 figures Revte