Interest groups or incentives: the political economy of fiscal decay

One view is that concessions demanded by and granted to interests groups are responsible for steady fiscal decline, and delay in reforms. We argue that negative supply shocks combined with the political objective of protecting the poor can build in incentives leading to these results. Pricing rules for government services, generated in such circumstances, would be equivalent to a fixed price contract that left the government with negative rent. A decline in investment in and quality of government services would follow, since price controls in the presence of cost shocks would lead to systematic incentives to lower quality and investment. Tax capacity and the ability to reduce poverty in the future would fall. The framework helps to understand the Indian experience. Time series based tests of causality support the causal priority of positive cost shocks. If it is accepted that incentives, and not only interest groups are responsible for fiscal decay, a concerted attempt to rationalize user charges and improve quality may be politically feasible

Manas Kr. Mondal

ABSTRACT: A total of 18 lactating multiparous cows (4-6 years aged) were selected from the out patients at the Addl. Block Animal Health Center, Matiali Block, Jalpaiguri, West Bengal, India and divided into three group, i.e normally cyclic (C), repeat breeder (RB) and post partum anoestrous (A). Blood samples were collected from all these cows for haematological and biochemical parameters. Erythrocyte sedimentation rate (ESR) and total leukocyte count (TEC) count were higher (P<0.05) in repeat breeder and anoestrous cows compared to cyclic ones; however the Hb and PCV values were low (P<0.05). Serum glucose and protein levels were low (P<0.05) repeat breeding cows than the normally cyclic cows. The results indicate that there may not be any specific haemato-biochemical marker for common reproductive disorders in cows

Inter-Landau-level Andreev Reflection at the Dirac Point in a Graphene Quantum Hall State Coupled to a NbSe2 Superconductor

Superconductivity and quantum Hall effect are distinct states of matter occurring in apparently incompatible physical conditions. Recent theoretical developments suggest that the coupling of quantum Hall effect with a superconductor can provide a fertile ground for realizing exotic topological excitations such as non-abelian Majorana fermions or Fibonacci particles. As a step toward that goal, we report observation of Andreev reflection at the junction of a quantum Hall edge state in a single layer graphene and a quasi-two dimensional niobium diselenide (NbSe2) superconductor. Our principal finding is the observation of an anomalous finite-temperature conductance peak located precisely at the Dirac point, providing a definitive evidence for inter-Landau level Andreev reflection in a quantum Hall system. Our observations are well supported by detailed numerical simulations, which offer additional insight into the role of the edge states in Andreev physics. This study paves the way for investigating analogous Andreev reflection in a fractional quantum Hall system coupled to a superconductor to realize exotic quasiparticles.Comment: published verio

Augmentation of smad‐dependent BMP signaling in neural crest cells causes craniosynostosis in mice

Craniosynostosis describes conditions in which one or more sutures of the infant skull are prematurely fused, resulting in facial deformity and delayed brain development. Approximately 20% of human craniosynostoses are thought to result from gene mutations altering growth factor signaling; however, the molecular mechanisms by which these mutations cause craniosynostosis are incompletely characterized, and the causative genes for diverse types of syndromic craniosynostosis have yet to be identified. Here, we show that enhanced bone morphogenetic protein (BMP) signaling through the BMP type IA receptor (BMPR1A) in cranial neural crest cells, but not in osteoblasts, causes premature suture fusion in mice. In support of a requirement for precisely regulated BMP signaling, this defect was rescued on a Bmpr1a haploinsufficient background, with corresponding normalization of Smad phosphorylation. Moreover, in vivo treatment with LDN‐193189, a selective chemical inhibitor of BMP type I receptor kinases, resulted in partial rescue of craniosynostosis. Enhanced signaling of the fibroblast growth factor (FGF) pathway, which has been implicated in craniosynostosis, was observed in both mutant and rescued mice, suggesting that augmentation of FGF signaling is not the sole cause of premature fusion found in this model. The finding that relatively modest augmentation of Smad‐dependent BMP signaling leads to premature cranial suture fusion suggests an important contribution of dysregulated BMP signaling to syndromic craniosynostoses and potential strategies for early intervention.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/98343/1/jbmr1857.pdfhttp://deepblue.lib.umich.edu/bitstream/2027.42/98343/2/jbmr1857-0008-sm-SupplFigS8.pdfhttp://deepblue.lib.umich.edu/bitstream/2027.42/98343/3/jbmr1857-0004-sm-SupplFigS4.pdfhttp://deepblue.lib.umich.edu/bitstream/2027.42/98343/4/jbmr1857-0009-sm-SupplFigS9.pdfhttp://deepblue.lib.umich.edu/bitstream/2027.42/98343/5/jbmr1857-0005-sm-SupplFigS5.pdfhttp://deepblue.lib.umich.edu/bitstream/2027.42/98343/6/jbmr1857-0001-sm-SupplFigS1.pdfhttp://deepblue.lib.umich.edu/bitstream/2027.42/98343/7/jbmr1857-0006-sm-SupplFigS6.pdfhttp://deepblue.lib.umich.edu/bitstream/2027.42/98343/8/jbmr1857-0002-sm-SupplFigS2.pdfhttp://deepblue.lib.umich.edu/bitstream/2027.42/98343/9/jbmr1857-0007-sm-SupplFigS7.pdfhttp://deepblue.lib.umich.edu/bitstream/2027.42/98343/10/jbmr1857-0003-sm-SupplFigS3.pd

F-box protein FBXO16 functions as a tumor suppressor by attenuating nuclear beta-catenin function

Aberrant activation of beta-catenin has been implicated in a variety of human diseases, including cancer. In spite of significant progress, the regulation of active Wnt/beta-catenin-signaling pathways is still poorly understood. In this study, we show that F-box protein 16 (FBXO16) is a putative tumor suppressor. It is a component of the SCF (SKP1-Cullin1-F-box protein) complex, which targets the nuclear beta-catenin protein to facilitate proteasomal degradation through the 26S proteasome. FBXO16 interacts physically with the C-terminal domain of beta-catenin and promotes its lysine 48-linked polyubiquitination. In addition, it inhibits epithelial-to-mesenchymal transition (EMT) by attenuating the level of beta-catenin. Therefore, depletion of FBXO16 leads to increased levels of beta-catenin, which then promotes cell invasion, tumor growth, and EMT of cancer cells. Furthermore, FBXO16 and beta-catenin share an inverse correlation of cellular expression in clinical breast cancer patient samples. In summary, we propose that FBXO16 functions as a putative tumor suppressor by forming an SCF(FBXO16) complex that targets nuclear beta-catenin in a unique manner for ubiquitination and subsequent proteasomal degradation to prevent malignancy. This work suggests a novel therapeutic strategy against human cancers related to aberrant beta-catenin activation