Strong quasi-particle tunneling study in the paired quantum Hall states

The quasi-particle tunneling phenomena in the paired fractional quantum Hall states are studied. A single point-contact system is first considered. Because of relevancy of the quasi-particle tunneling term, the strong tunneling regime should be investigated. Using the instanton method it is shown that the strong quasi-particle tunneling regime is described as the weak electron tunneling regime effectively. Expanding to the network model the paired quantum Hall liquid to insulator transition is discussed

The edge state network model and the global phase diagram

The effects of randomness are investigated in the fractional quantum Hall systems. Based on the Chern-Simons Ginzburg-Landou theory and considering relevant quasi-particle tunneling, the edge state network model for the hierarchical state is introduced and the plateau-plateau transition and liquid-insulator transition are discussed. This model has duality which corresponds to the relation of the quantum Hall liquid phase and the Hall insulating phase and reveals a mechanism in the weak coupling regime.Comment: 5 page RevTe

Quasi-Particle Tunneling in Anti-Pfaffian Quantum Hall State

We study tunneling phenomena at the edge of the anti-Pfaffian quantum Hall state at the filling factor $\nu=5/2$. The edge current in a single point-contact is considered. We focus on nonlinear behavior of two-terminal conductance with the increase in negative split-gate voltage. Expecting the appearance of the intermediate conductance plateau we calculate the value of its conductance by using the renormalization group (RG) analysis. Further, we show that non-perturbative quasi-particle tunneling is effectively described as perturbative electron tunneling by the instanton method. The two-terminals conductance is written as a function of the gate voltage. The obtained results enable us to distinguish the anti-Pfaffian state from the Pfaffian state experimentally.Comment: 5 pages, 4 figure

The electronic properties of bilayer graphene

We review the electronic properties of bilayer graphene, beginning with a description of the tight-binding model of bilayer graphene and the derivation of the effective Hamiltonian describing massive chiral quasiparticles in two parabolic bands at low energy. We take into account five tight-binding parameters of the Slonczewski-Weiss-McClure model of bulk graphite plus intra- and interlayer asymmetry between atomic sites which induce band gaps in the low-energy spectrum. The Hartree model of screening and band-gap opening due to interlayer asymmetry in the presence of external gates is presented. The tight-binding model is used to describe optical and transport properties including the integer quantum Hall effect, and we also discuss orbital magnetism, phonons and the influence of strain on electronic properties. We conclude with an overview of electronic interaction effects.Comment: review, 31 pages, 15 figure

Phosphate and Klotho

Klotho is a putative aging suppressor gene encoding a single-pass transmembrane co-receptor that makes the fibroblast growth factor (FGF) receptor specific for FGF-23. In addition to multiple endocrine organs, Klotho is expressed in kidney distal convoluted tubules and parathyroid cells, mediating the role of FGF-23 in bone–kidney–parathyroid control of phosphate and calcium. Klotho–/– mice display premature aging and chronic kidney disease-associated mineral and bone disorder (CKD-MBD)-like phenotypes mediated by hyperphosphatemia and remediated by phosphate-lowering interventions (diets low in phosphate or vitamin D; knockouts of 1α-hydroxylase, vitamin D receptor, or NaPi cotransporter). CKD can be seen as a state of hyperphosphatemia-induced accelerated aging associated with Klotho deficiency. Humans with CKD experience decreased Klotho expression as early as stage 1 CKD; Klotho continues to decline as CKD progresses, causing FGF-23 resistance and provoking large FGF-23 and parathyroid hormone increases, and hypovitaminosis D. Secreted Klotho protein, formed by extracellular clipping, exerts FGF-23-independent phosphaturic and calcium-conserving effects through its paracrine action on the proximal and distal tubules, respectively. We contend that decreased Klotho expression is the earliest biomarker of CKD and the initiator of CKD-MBD pathophysiology. Maintaining normal phosphate levels with phosphate binders in patients with CKD with declining Klotho expression is expected to reduce mineral and vascular derangements

Klotho and the Aging Process

The klotho gene was originally identified as a putative age-suppressing gene in mice that extends life span when overexpressed. It induces complex phenotypes resembling human premature aging syndromes when disrupted. The gene was named after a Greek goddess Klotho who spun the thread of life. Since then, various functional aspects of the klotho gene have been investigated, leading to the identification of multiple novel endocrine axes that regulate various metabolic processes and an unexpected link between mineral metabolism and aging. The purposes of this review were to overview recent progress on Klotho research and to discuss a novel aging mechanism

Klotho Lacks a Vitamin D Independent Physiological Role in Glucose Homeostasis, Bone Turnover, and Steady-State PTH Secretion In Vivo

Apart from its function as co-receptor for fibroblast growth factor-23 (FGF23), Klotho is thought to regulate insulin signaling, intracellular oxidative stress, and parathyroid hormone (PTH) secretion in an FGF23 independent fashion. Here, we crossed Klotho deficient (Kl−/−) mice with vitamin D receptor (VDR) mutant mice to examine further vitamin D independent functions of Klotho. All mice were fed a rescue diet enriched with calcium, phosphorus, and lactose to prevent hyperparathyroidism in VDR mutants, and were killed at 4 weeks of age after double fluorochrome labeling. Kl−/− mice displayed hypercalcemia, hyperphosphatemia, dwarfism, organ atrophy, azotemia, pulmonary emphysema, and osteomalacia. In addition, glucose and insulin tolerance tests revealed hypoglycemia and profoundly increased peripheral insulin sensitivity in Kl−/− mice. Compound mutants were normocalcemic and normophosphatemic, did not show premature aging or organ atrophy, and were phenocopies of VDR mutant mice in terms of body weight, bone mineral density, bone metabolism, serum calcium, serum phosphate, serum PTH, gene expression in parathyroid glands, as well as urinary calcium and phosphate excretion. Furthermore, ablation of vitamin D signaling in double mutants completely normalized glucose and insulin tolerance, indicating that Klotho has no vitamin D independent effects on insulin signaling. Histomorphometry of pancreas islets showed similar beta cell volume per body weight in all groups of animals. In conclusion, our findings cast doubt on a physiologically relevant vitamin D and Fgf23 independent function of Klotho in the regulation of glucose metabolism, bone turnover, and steady-state PTH secretion in vivo

Serumproteinbindung von ACTH

3H- 1–23-Corticotropin wurde an Dextrangel (Sephadex G-25) gebunden und konnte durch Serumproteine, Albumin oder 0,1 N HCl eluiert werden. Mittels Dextrangelfiltration wurde gefunden, daß3H-ACTH kompetitiv an Serumproteine (Albumin) und Dextrangel gebunden wurde. Auch für natürliches Schweine-ACTH und endogenes ACTH in Patientenplasma (Adrenalektomie) wurde mittels biologischer ACTH-Bestimmung die Bindung von ACTH an Proteine bestätigt.3H- 1–23 corticotropin was bound to dextran gel (sephadex G-25) and was eluted by either serum proteins, albumin or 0.1 N HCl. Competitive binding of3H-ACTH to serum proteins (albumin) and dextran gel was shown by dextran gel filtration. Likewise natural ACTH (pig) and endogenous ACTH from plasma of an adrenalectomized patient were shown to be partly protein bound using biological ACTH-assay

Identification of TNF-alpha-Responsive Promoters and Enhancers in the Intestinal Epithelial Cell Model Caco-2

The Caco-2 cell line is one of the most important in vitro models for enterocytes, and is used to study drug absorption and disease, including inflammatory bowel disease and cancer. In order to use the model optimally, it is necessary to map its functional entities. In this study, we have generated genome-wide maps of active transcription start sites (TSSs), and active enhancers in Caco-2 cells with or without tumour necrosis factor (TNF)-α stimulation to mimic an inflammatory state. We found 520 promoters that significantly changed their usage level upon TNF-α stimulation; of these, 52% are not annotated. A subset of these has the potential to confer change in protein function due to protein domain exclusion. Moreover, we locate 890 transcribed enhancer candidates, where ∼50% are changing in usage after TNF-α stimulation. These enhancers share motif enrichments with similarly responding gene promoters. As a case example, we characterize an enhancer regulating the laminin-5 γ2-chain (LAMC2) gene by nuclear factor (NF)-κB binding. This report is the first to present comprehensive TSS and enhancer maps over Caco-2 cells, and highlights many novel inflammation-specific promoters and enhancers