2,229 research outputs found

    Type-II heavy Fermi liquids and the magnetic memory of 4Hb-TaS2_2

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    The interplay of quantum spin liquids with itinerant conduction electrons is of crucial interest for understanding layered structures composed of frustrated magnet and metal monolayers. Using parton-mean-field theory, we here demonstrate that a type-II heavy Fermi liquid, which is characterized by a vortex lattice in the slave boson condensate, can occur in the vicinity of the quantum phase transition separating fractionalized and heavy Fermi liquid phases. The magnetic flux threading each such vortex is about vf/137c v_f/ 137 c times smaller than the magnetic flux threading vortices in type-II superconductors, where vfv_f is the speed of magnetic excitations and cc the speed of light. This makes a magnetic observation of this effect challenging. We propose scanning tunneling spectroscopy instead and investigate its signatures. If a type-II heavy Fermi liquid is cooled into a type-II superconductor, vortices in the slave boson condensate and in the superconducting condensate mutually attract. We argue that the type-II heavy Fermi liquid thereby provides a compelling explanation for the magnetic memory observed recently [Persky \textit{et al.}, Nature \textbf{609}, 692 (2022)] in thermal cycles of 4Hb-TaS2_2.Comment: 4+ϵ\epsilon pages, 9 pages supplement. 2 + 2 figures. Typos, formatting and reference list update

    The incidence of graft on developing-country firms

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    This paper measures the extent to which firms in developing countries are the target of bribes. Using new firm-level survey data from 33 African and Latin American countries, we first show that perceptions adjust slowly tofirms'experience with corrupt officials and hence are an imperfect proxy for the true incidence of graft. We then construct an experience-based index that reflects the probability that a firm will be asked for a bribe in order to complete a specified set of business transactions. On average, African firms are three times as likely to be asked for bribes as are firms in Latin America, although there is substantial variation within each region. Last, we show that graft appears to be more prevalent in countries with excessive regulation and where democracy is weak. In particular, our results suggest that the incidence of graft in Africa would fall by approximately 85 percent if countries in the region had levels of democracy and regulation similar to those that exist in Latin America.Public Sector Corruption&Anticorruption Measures,Corruption&Anitcorruption Law,Crime and Society,E-Business,Access to Finance

    ZN\mathbb{Z}_N lattice gauge theories with matter fields

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    Motivated by the exotic phenomenology of certain quantum materials and recent advances in programmable quantum emulators, we here study fermions and bosons in ZN\mathbb Z_N lattice gauge theories. We introduce a family of exactly soluble models, and characterize their orthogonal (semi-)metallic ground states, the excitation spectrum, and the correlation functions. We further study integrability breaking perturbations using an appropriately derived set of Feynman diagrammatic rules and borrowing physics associated to Anderson's orthogonality catastrophe. In the context of the ground states, we revisit Luttinger's theorem following Oshikawa's flux insertion argument and furthermore demonstrate the existence of a Luttinger surface of zeros in the fermionic Green's function. Upon inclusion of perturbations, we address the transition from the orthogonal metal to the normal state by condensation of certain excitations in the gauge sectors, so-called ``ee-particles''. We furthermore discuss the effect of dynamics in the dual ``mm-particle'' excitations, which ultimately leads to the formation of charge-neutral hadronic NN-particle bound states. We present analytical arguments for the most important phases and estimates for phase boundaries of the model. Specifically, and in sharp distinction to quasi-1D ZN\mathbb Z_N lattice gauge theories, renormalization group arguments imply that the phase diagram does not include an emergent deconfining U(1)U(1) phase. Therefore, in regards to lattice QED problems, ZN\mathbb Z_N quantum emulators with N<N<\infty can at best be used for approximate solutions at intermediate length scales

    The thanatophoric dysplasia type II mutation hampers complete maturation of fibroblast growth factor receptor 3 (FGFR3), which activates signal transducer and activator of transcription 1 (STAT1) from the endoplasmic reticulum

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    The K650E substitution in the fibroblast growth factor receptor 3 (FGFR3) causes constitutive tyrosine kinase activity of the receptor and is associated to the lethal skeletal disorder, thanatophoric dysplasia type II (TDII). The underlying mechanisms of how the activated FGFR3 causes TDII remains to be elucidated. FGFR3 is a transmembrane glycoprotein, which is synthesized through three isoforms, with various degrees of N-glycosylation. We have studied whether immature FGFR3 isoforms mediate the abnormal signaling in TDII. We show that synthesis of TDII-FGFR3 presents two phosphorylated forms: the immature non-glycosylated 98-kDa peptides and the intermediate 120-kDa glycomers. The mature, fully glycosylated 130-kDa forms, detected in wild type FGFR3, are not present in TDII. Endoglycosidase H cleaves the sugars on TDII intermediates thus indicating their intracellular localization in the endoplasmic reticulum. Accordingly, TDII-FGFR3-GFP co-localizes with calreticulin in the endoplasmic reticulum. Furthermore, following TDII transfection, signal transducer and activator of transcription 1 (STAT1) is phosphorylated in the absence of FGFR3 ligand and brefeldin A does not inhibit its activation. On the contrary, the cell membrane-anchored FRS2alpha protein is not activated in TDII cells. The opposite situation is observed in stable TDII cell clones where, despite the presence of phosphorylated mature receptor, STAT1 is not activated whereas FRS2alpha is phosphorylated. We speculate that the selection process favors cells defective in STAT1 activation through the 120-kDa TDII-FGFR3, thus allowing growth of the TDII cell clones. Accordingly, apoptosis is observed following TDII-FGFR3 transfection. These observations highlight the importance of the immature TDII-FGFR3 proteins as mediators of an abnormal signaling in TDII
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