In Support of the Matrix Language Frame Model: Evidence from Igbo-English Intrasentential Codeswitching

This paper explores the morphosyntactic features of mixed nominal expressions in a sample of empirical Igbo-English intrasentential codeswitching data (i.e. codeswitching within a bilingual clause) in terms of the Matrix Language Frame (MLF) model. Since both Igbo and English differ in the relative order of head and complement within the nominal argument phrase, the analysed data seem appropriate for testing the veracity of the principal assumption underpinning the MLF model: the notion that the two languages (in our case Igbo and English) participating in codeswitching do not both contribute equally to the morphosyntactic frame of a mixed constituent. As it turns out, the findings provide both empirical and quantitative support for the basic theoretical view that there is a Matrix Language (ML) versus Embedded Language (EL) hierarchy in classic codeswitching as predicted by the MLF model because both Igbo and English do not simultaneously satisfy the roles of the ML in Igbo-English codeswitching

Assumptions behind grammatical approaches to code-switching: when the blueprint is a red herring

Many of the so-called ‘grammars’ of code-switching are based on various underlying assumptions, e.g. that informal speech can be adequately or appropriately described in terms of ‘‘grammar’’; that deep, rather than surface, structures are involved in code-switching; that one ‘language’ is the ‘base’ or ‘matrix’; and that constraints derived from existing data are universal and predictive. We question these assumptions on several grounds. First, ‘grammar’ is arguably distinct from the processes driving speech production. Second, the role of grammar is mediated by the variable, poly-idiolectal repertoires of bilingual speakers. Third, in many instances of CS the notion of a ‘base’ system is either irrelevant, or fails to explain the facts. Fourth, sociolinguistic factors frequently override ‘grammatical’ factors, as evidence from the same language pairs in different settings has shown. No principles proposed to date account for all the facts, and it seems unlikely that ‘grammar’, as conventionally conceived, can provide definitive answers. We conclude that rather than seeking universal, predictive grammatical rules, research on CS should focus on the variability of bilingual grammars

Cardiopulmonary Exercise Testing as a Longitudinal Clinical Tool in Interstitial Lung Disease Management

This is an abstract from International Conference of the American-Thoracic-Society Location: Dallas, TX Date: MAY 17-22, 2019Royal Devon & Exeter Hospita

A patient with limb girdle muscular dystrophy carries a TRIM32 deletion, detected by a novel CGH array, in compound heterozygosis with a nonsense mutation

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Operationalising and measuring language dominance

The paper offers a new way to measure language ability in bilinguals, based on measures of lexical richness. The validity of proposed approach is tested in a variety of ways

Two-neutron transfer in 7 Be + 9 Be collisions

Elastic scattering and transfer cross sections for the 7 Be + 9 Be system have been measured at E lab = 23.1 MeV using the 7 Be radioactive secondary beam produced at Radioactive Ion Beams in Brazil facility at the University of São Paulo. The elastic scattering has been measured by detecting the 7 Be scattered at forward angles in the laboratory system. The transfer reaction 9 Be ( 7 Be , 9 Be ) 7 Be was identified by detecting the 9 Be scattered at the same laboratory angles. The elastic angular distribution has been analyzed by optical model calculations using a Woods-Saxon form factor whose parameters have been varied to best reproduce the experimental data at forward angles. Coupled reaction channels calculations (CRC) have been performed to describe the transfer, considering the coupling to the transfer channel and including contributions to the ground state and to the first excited state of 7 Be ( 1 / 2 − ; 429 keV ) in the final state. The spectroscopic amplitudes used in the CRC calculation have been derived from shell-model calculations. Similar CRC calculations were applied to existing 9 Be ( p , t ) 7 Be data to check the consistency of our results results for the ( 7 Be , 9 Be ) transfer reaction.Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq) de Brasil, Fundação de Amparo à Pesquisa do Estado do Rio de Janeiro (FAPERJ) de Brasil y Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP) de Brasil. 2013/22100-7 y 2016/21434-

Multimodal MRI can identify perfusion and metabolic changes in the invasive margin of glioblastomas.

PURPOSE: To use perfusion and magnetic resonance (MR) spectroscopy to compare the diffusion tensor imaging (DTI)-defined invasive and noninvasive regions. Invasion of normal brain is a cardinal feature of glioblastomas (GBM) and a major cause of treatment failure. DTI can identify invasive regions. MATERIALS AND METHODS: In all, 50 GBM patients were imaged preoperatively at 3T with anatomic sequences, DTI, dynamic susceptibility perfusion MR (DSCI), and multivoxel spectroscopy. The DTI and DSCI data were coregistered to the spectroscopy data and regions of interest (ROIs) were made in the invasive (determined by DTI), noninvasive regions, and normal brain. Values of relative cerebral blood volume (rCBV), N-acetyl aspartate (NAA), myoinositol (mI), total choline (Cho), and glutamate + glutamine (Glx) normalized to creatine (Cr) and Cho/NAA were measured at each ROI. RESULTS: Invasive regions showed significant increases in rCBV, suggesting angiogenesis (invasive rCBV 1.64 [95% confidence interval, CI: 1.5-1.76] vs. noninvasive 1.14 [1.09-1.18]; P < 0.001), Cho/Cr (invasive 0.42 [0.38-0.46] vs. noninvasive 0.35 [0.31-0.38]; P = 0.02) and Cho/NAA (invasive 0.54 [0.41-0.68] vs. noninvasive 0.37 [0.29-0.45]; P = < 0.03), suggesting proliferation, and Glx/Cr (invasive 1.54 [1.27-1.82] vs. noninvasive 1.3 [1.13-1.47]; P = 0.028), suggesting glutamate release; and a significantly reduced NAA/Cr (invasive 0.95 [0.85-1.05] vs. noninvasive 1.19 [1.06-1.31]; P = 0.008). The mI/Cr was not different between the three ROIs (invasive 1.2 [0.99-1.41] vs. noninvasive 1.3 [1.14-1.46]; P = 0.68). In the noninvasive regions, the values were not different from normal brain. CONCLUSION: Combining DTI to identify the invasive region with perfusion and spectroscopy, we can identify changes in invasive regions not seen in noninvasive regions.This study was funded from a National Institutes of Health Research Clinician Scientist FellowshipThis is the final version of the article. It first appeared from Wiley via http://dx.doi.org/10.1002/jmri.2499

Telomere length and risk of idiopathic pulmonary fibrosis and chronic obstructive pulmonary disease:a mendelian randomisation study

Background: Idiopathic pulmonary fibrosis (IPF) is a fatal lung disease accounting for 1% of UK deaths. In the familial form of pulmonary fibrosis, causal genes have been identified in about 30% of cases, and a majority of these causal genes are associated with telomere maintenance. Prematurely shortened leukocyte telomere length is associated with IPF and chronic obstructive pulmonary disease (COPD), a disease with similar demographics and shared risk factors. Using mendelian randomisation, we investigated evidence supporting a causal role for short telomeres in IPF and COPD. Methods: Mendelian randomisation inference of telomere length causality was done for IPF (up to 1369 cases) and COPD (13 538 cases) against 435 866 controls of European ancestry in UK Biobank. Polygenic risk scores were calculated and two-sample mendelian randomisation analyses were done using seven genetic variants previously associated with telomere length, with replication analysis in an IPF cohort (2668 cases vs 8591 controls) and COPD cohort (15 256 cases vs 47 936 controls). Findings: In the UK Biobank, a genetically instrumented one-SD shorter telomere length was associated with higher odds of IPF (odds ratio [OR] 4·19, 95% CI 2·33–7·55; p=0·0031) but not COPD (1·07, 0·88–1·30; p=0·51). Similarly, an association was found in the IPF replication cohort (12·3, 5·05–30·1; p=0·0015) and not in the COPD replication cohort (1·04, 0·71–1·53; p=0·83). Meta-analysis of the two-sample mendelian randomisation results provided evidence inferring that shorter telomeres cause IPF (5·81 higher odds of IPF, 95% CI 3·56–9·50; p=2·19 × 10−12). There was no evidence to infer that telomere length caused COPD (OR 1·07, 95% CI 0·90–1·27; p=0·46). Interpretation: Cellular senescence is hypothesised as a major driving force in IPF and COPD; telomere shortening might be a contributory factor in IPF, suggesting divergent mechanisms in COPD. Defining a key role for telomere shortening enables greater focus in telomere-related diagnostics, treatments, and the search for a cure in IPF. Investigation of therapies that improve telomere length is warranted. Funding: Medical Research Council.</p