The role of case in A-bar extraction asymmetries

2014 ◽  
Vol 14 (2) ◽  
pp. 179-242 ◽  
Author(s):  
Jessica Coon ◽  
Pedro Mateo Pedro ◽  
Omer Preminger

Many morphologically ergative languages display asymmetries in the extraction of core arguments: while absolutive arguments (transitive objects and intransitive subjects) extract freely, ergative arguments (transitive subjects) cannot. This falls under the label “syntactic ergativity” (see, e.g. Dixon 1972, 1994; Manning 1996; Polinsky to appear(b)). These extraction asymmetries are found in many languages of the Mayan family, where in order to extract transitive subjects (for focus, questions, or relativization), a special construction known as the “Agent Focus” (AF) must be used. These AF constructions have been described as syntactically and semantically transitive because they contain two non-oblique DP arguments, but morphologically intransitive because the verb appears with only a single agreement marker and takes an intransitive status suffix (Aissen 1999; Stiebels 2006). In this paper we offer a proposal for (i) why some morphologically ergative languages exhibit extraction asymmetries, while others do not; and (ii) how the AF construction in Q’anjob’al circumvents this problem. We adopt recent accounts which argue that ergative languages vary in the locus of absolutive case assignment (Aldridge 2004, 2008a; Legate 2002, 2008), and propose that this variation is present within the Mayan family. Based primarily on comparative data from Q’anjob’al and Chol, we argue that the inability to extract ergative arguments does not reflect a problem with properties of the ergative subject itself, but rather reflects locality properties of absolutive case assignment in the clause. We show how the AF morpheme -on circumvents this problem in Q’anjob’al by assigning case to internal arguments.

Author(s):  
Navnit S. Makaram ◽  
Stuart H. Ralston

Abstract Purpose of Review To provide an overview of the role of genes and loci that predispose to Paget’s disease of bone and related disorders. Recent Findings Studies over the past ten years have seen major advances in knowledge on the role of genetic factors in Paget’s disease of bone (PDB). Genome wide association studies have identified six loci that predispose to the disease whereas family based studies have identified a further eight genes that cause PDB. This brings the total number of genes and loci implicated in PDB to fourteen. Emerging evidence has shown that a number of these genes also predispose to multisystem proteinopathy syndromes where PDB is accompanied by neurodegeneration and myopathy due to the accumulation of abnormal protein aggregates, emphasising the importance of defects in autophagy in the pathogenesis of PDB. Summary Genetic factors play a key role in the pathogenesis of PDB and the studies in this area have identified several genes previously not suspected to play a role in bone metabolism. Genetic testing coupled to targeted therapeutic intervention is being explored as a way of halting disease progression and improving outcome before irreversible skeletal damage has occurred.


2014 ◽  
Vol 10 (5) ◽  
pp. 392-399 ◽  
Author(s):  
Erin C. Accurso ◽  
Gregory J. Norman ◽  
Scott J. Crow ◽  
Cheryl L. Rock ◽  
Kerri N. Boutelle

2020 ◽  
Vol 29 (8) ◽  
pp. 2104-2116
Author(s):  
Elizabeth I. Johnson ◽  
Jennifer E. Copp ◽  
Anneliese C. Bolland ◽  
John M. Bolland

Circulation ◽  
2015 ◽  
Vol 131 (suppl_2) ◽  
Author(s):  
Taco W Kuijpers ◽  
Carline E Tacke ◽  
Sietse Q Nagelkerke ◽  
Willemijn B Breunis ◽  
Long T Hoang ◽  
...  

The human FCGR2/3 locus contains highly homologous genes encoding the five major receptors for IgG (Fc-gamma receptors, FcγRs). In two prior GWAS on Kawasaki disease (KD), a SNP in FCGR2A (131H>R; rs1801274) was identified to be associated with disease susceptibility. However, the FCGR2/3 locus contains multiple single nucleotide polymorphisms (SNPs) and copy number variations (CNVs), which were not covered by the detection platforms used in the GWAS. In this study we therefore focused on further fine-mapping of this locus to investigate the association of the different genetic variations with KD susceptibility. A highly accurate and validated multiplex ligation-dependent probe amplification (MLPA) assay was used to analyze all functionally relevant SNPs and CNVs within this locus. In a genetic association study involving case-control and family-based testing with 1028 patients with KD, the previous finding of FCGR2A-131H as a susceptibility marker for KD was confirmed (OR 1.16; 95%CI 1.08-1.32, meta-P = 0.01). In addition, we found a novel significant association of the FCGR2C-ORF haplotype with susceptibility to KD (OR 1.34; 95% confidence interval 1.11-1.62, meta-P = 0.003). FCGR2C-ORF leads to the expression of an extra, functionally activating FcγR (i.e. FcγRIIc) on myeloid cell types and NK cells. Being absent in Asian individuals, the FCGR2C-ORF haplotype only contributed to KD susceptibility in European subjects, independent of the established association with FCGR2A-H131R. We did not find any significant association of CNV of the locus with susceptibility to KD. Our data point to an important role of the activating FcγRs in KD pathology. We hypothesize that the identified functional SNPs might alter the balance between the activating and inhibitory FcγRs leading to unbalanced inflammation and KD.


2018 ◽  
pp. 359-374
Author(s):  
Debra K. Katzman ◽  
Tania Turrini ◽  
Seena Grewal

Adolescent health providers (AHPs) and nutritionists each have a unique role in the care of adolescents with eating disorders. Their respective roles and responsibilities are especially refined in the context of family-based therapy (FBT). The role of the AHP and nutritionist in the context of FBT requires a fundamental change in how these members of the interdisciplinary team think about and provide care to young people with eating disorders. This article focuses on the distinct roles of the AHP and nutritionist in FBT in the care of adolescents with eating disorders and their families.


Author(s):  
Sudie E. Back ◽  
Edna B. Foa ◽  
Therese K. Killeen ◽  
Katherine L. Mills ◽  
Maree Teesson ◽  
...  

This chapter provides the therapist with an outline of the COPE treatment and components of each session (e.g. check-in, review homework, post-traumatic stress disorder [PTSD] focus, substance use disorder focus). Questions regarding who can deliver the therapy are addressed, as well as questions regarding the role of medications. Finally, special considerations for delivering treatment to patients with PTSD and comorbid substance use disorders are reviewed for the therapist.


2006 ◽  
Vol 14 (4) ◽  
pp. 488-496 ◽  
Author(s):  
Francesco Paolo Schena ◽  
◽  
Giuseppina Cerullo ◽  
Diletta Domenica Torres ◽  
Francesco Scolari ◽  
...  

2000 ◽  
Vol 276 (15) ◽  
pp. 11545-11551 ◽  
Author(s):  
Stéphanie Gon ◽  
Marie-Thérèse Giudici-Orticoni ◽  
Vincent Méjean ◽  
Chantal Iobbi-Nivol

Reduction of trimethylamineN-oxide (E′0(TMAO/TMA)= +130 mV) inEscherichia coliis carried out by the Tor system, an electron transfer chain encoded by thetorCADoperon and made up of the periplasmic terminal reductase TorA and the membrane-anchored pentahemicc-type cytochrome TorC. Although the role of TorA in the reduction of trimethylamineN-oxide (TMAO) has been clearly established, no direct evidence for TorC involvement has been presented. TorC belongs to the NirT/NapCc-type cytochrome family based on homologies of its N-terminal tetrahemic domain (TorCN) to the cytochromes of this family, but TorC contains a C-terminal extension (TorCC) with an additional heme-binding site. In this study, we show that both domains are required for the anaerobic bacterial growth with TMAO. The intact TorC protein and its two domains, TorCNand TorCC, were produced independently and purified for a biochemical characterization. The reduced form of TorC exhibited visible absorption maxima at 552, 523, and 417 nm. Mediated redox potentiometry of the heme centers of the purified components identified two negative midpoint potentials (−177 and −98 mV) localized in the tetrahemic TorCNand one positive midpoint potential (+120 mV) in the monohemic TorCC. In agreement with these values, thein vitroreconstitution of electron transfer between TorC, TorCN, or TorCCand TorA showed that only TorC and TorCCwere capable of electron transfer to TorA. Surprisingly, interaction studies revealed that only TorC and TorCNstrongly bind TorA. Therefore, TorCCdirectly transfers electrons to TorA, whereas TorCN, which probably receives electrons from the menaquinone pool, is involved in both the electron transfer to TorCCand the binding to TorA.


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