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Let $\Omega $ be a compact subset of $\mathbb {C}$ and let A be a unital simple, separable $C^*$-algebra with stable rank one, real rank zero, and strict comparison. We show that, given a Cu-morphism ${\alpha :\mathrm { Cu}(C(\Omega ))\to \mathrm {Cu}(A)}$ with , there exists a homomorphism $\phi : C(\Omega )\to A$ such that $\mathrm {Cu}(\phi )=\alpha $. Moreover, if $K_1(A)$ is trivial, then $\phi $ is unique up to approximate unitary equivalence. We also give classification results for maps from a large class of $C^*$-algebras to A in terms of the Cuntz semigroup.
We introduce and study the weak Glimm property for $\mathrm{C}^{*}$-algebras, and also a property we shall call (HS$_0$). We show that the properties of being nowhere scattered and residual (HS$_0$) are equivalent for any $\mathrm{C}^{*}$-algebra. Also, for a $\mathrm{C}^{*}$-algebra with the weak Glimm property, the properties of being purely infinite and weakly purely infinite are equivalent. It follows that for a $\mathrm{C}^{*}$-algebra with the weak Glimm property such that the absolute value of every nonzero, square-zero, element is properly infinite, the properties of being (weakly, locally) purely infinite, nowhere scattered, residual (HS$_0$), residual (HS$_{\text {t}}$), and residual (HI) are all equivalent, and are equivalent to the global Glimm property. This gives a partial affirmative answer to the global Glimm problem, as well as certain open questions raised by Kirchberg and Rørdam.
Inhibitory control plays an important role in children’s cognitive and socioemotional development, including their psychopathology. It has been established that contextual factors such as socioeconomic status (SES) and parents’ psychopathology are associated with children’s inhibitory control. However, the relations between the neural correlates of inhibitory control and contextual factors have been rarely examined in longitudinal studies. In the present study, we used both event-related potential (ERP) components and time-frequency measures of inhibitory control to evaluate the neural pathways between contextual factors, including prenatal SES and maternal psychopathology, and children’s behavioral and emotional problems in a large sample of children (N = 560; 51.75% females; Mage = 7.13 years; Rangeage = 4–11 years). Results showed that theta power, which was positively predicted by prenatal SES and was negatively related to children’s externalizing problems, mediated the longitudinal and negative relation between them. ERP amplitudes and latencies did not mediate the longitudinal association between prenatal risk factors (i.e., prenatal SES and maternal psychopathology) and children’s internalizing and externalizing problems. Our findings increase our understanding of the neural pathways linking early risk factors to children’s psychopathology.
The clay fractions of Jurassic marls in the Great Estuarine Group in southern Isle of Skye are composed of mixed-layered illite-smectite (I-S) with large percentages (>85%) of illite layers, kaolinite, and generally smaller amounts of chlorite. These marls have not been buried to the depths normally required to convert smectite to illite-rich I-S, so it is possible that the conversion was in response to heat and hydrothermal fluids from nearby early Tertiary igneous activity ∼55 Ma ago. The large percentages of illite layers in I-S, the Środoń intensity ratios, and the Kübler index values appear to be consistent with the formation of diagenetic I-S as a result of relatively brief heating caused by igneous activity. The Jurassic rocks in southern Skye contain a secondary chemical remanent magnetization (CRM) that resides in magnetite and formed at approximately the same time as the Tertiary igneous rocks on Skye. K-Ar age values for I-S based on illite age analysis have been determined to test the hypothesis that the CRM was acquired coincidently with the smectite-to-illite conversion. However, linear extrapolation of K-Ar age vs. percentage of 2M1 polytype (detrital illite) from one marl (EL-6) yields an estimate for the age of diagenetic illite of 106 Ma, which is close to the measured age of the finest subfraction (108 Ma). These estimated and measured age values, however, could be substantially greater than the true age of the diagenetic illite in I-S because of the presence of detrital 1Md illite that was recycled from early Paleozoic shales and whose abundance relative to the diagenetic I-S may have been enhanced because the diagenetic fluid had a low K/Na ratio, limiting the amount of diagenetic illite formed. Nevertheless, most of the illite in the Elgol marls (80% or more in the finest fractions) must be diagenetic and probably formed in response to the early Tertiary magmatism.
Presidential elections can be forecast using information from political and economic conditions, polls, and a statistical model of changes in public opinion over time. However, these “knowns” about how to make a good presidential election forecast come with many unknowns due to the challenges of evaluating forecast calibration and communication. We highlight how incentives may shape forecasts, and particularly forecast uncertainty, in light of calibration challenges. We illustrate these challenges in creating, communicating, and evaluating election predictions, using the Economist and Fivethirtyeight forecasts of the 2020 election as examples, and offer recommendations for forecasters and scholars.
It is shown that the colored isomorphism class of a unital, simple, $\mathcal {Z}$-stable, separable amenable C$^*$-algebra satisfying the universal coefficient theorem is determined by its tracial simplex.
Individuals with schizophrenia are at higher risk of physical illnesses, which are a major contributor to their 20-year reduced life expectancy. It is currently unknown what causes the increased risk of physical illness in schizophrenia.
Aims
To link genetic data from a clinically ascertained sample of individuals with schizophrenia to anonymised National Health Service (NHS) records. To assess (a) rates of physical illness in those with schizophrenia, and (b) whether physical illness in schizophrenia is associated with genetic liability.
Method
We linked genetic data from a clinically ascertained sample of individuals with schizophrenia (Cardiff Cognition in Schizophrenia participants, n = 896) to anonymised NHS records held in the Secure Anonymised Information Linkage (SAIL) databank. Physical illnesses were defined from the General Practice Database and Patient Episode Database for Wales. Genetic liability for schizophrenia was indexed by (a) rare copy number variants (CNVs), and (b) polygenic risk scores.
Results
Individuals with schizophrenia in SAIL had increased rates of epilepsy (standardised rate ratio (SRR) = 5.34), intellectual disability (SRR = 3.11), type 2 diabetes (SRR = 2.45), congenital disorders (SRR = 1.77), ischaemic heart disease (SRR = 1.57) and smoking (SRR = 1.44) in comparison with the general SAIL population. In those with schizophrenia, carrier status for schizophrenia-associated CNVs and neurodevelopmental disorder-associated CNVs was associated with height (P = 0.015–0.017), with carriers being 7.5–7.7 cm shorter than non-carriers. We did not find evidence that the increased rates of poor physical health outcomes in schizophrenia were associated with genetic liability for the disorder.
Conclusions
This study demonstrates the value of and potential for linking genetic data from clinically ascertained research studies to anonymised health records. The increased risk for physical illness in schizophrenia is not caused by genetic liability for the disorder.
Schizophrenia is a highly heritable disorder with undetermined neurobiological causes. Understanding the impact on brain anatomy of carrying genetic risk for the disorder will contribute to uncovering its neurobiological underpinnings.
Aims
To examine the effect of rare copy number variants (CNVs) associated with schizophrenia on brain cortical anatomy in a sample of unaffected participants from the UK Biobank.
Method
We used regression analyses to compare cortical thickness and surface area (total and across gyri) between 120 unaffected carriers of rare CNVs associated with schizophrenia and 16 670 participants without any pathogenic CNV. A measure of cortical thickness and surface area covariance across gyri was also compared between groups.
Results
Carrier status was associated with reduced surface area (β = −0.020 mm2, P < 0.001) and less robustly with increased cortical thickness (β = 0.015 mm, P = 0.035), and with increased covariance in thickness (carriers z = 0.31 v. non-carriers z = 0.22, P < 0.0005). Associations were mainly present in frontal and parietal areas and driven by a limited number of rare risk alleles included in our analyses (mainly 15q11.2 deletion for surface area and 16p13.11 duplication for thickness covariance).
Conclusions
Results for surface area conformed with previous clinical findings, supporting surface area reductions as an indicator of genetic liability for schizophrenia. Results for cortical thickness, though, argued against its validity as a potential risk marker. Increased structural thickness covariance across gyri also appears related to risk for schizophrenia. The heterogeneity found across the effects of rare risk alleles suggests potential different neurobiological gateways into schizophrenia's phenotype.
A category structure for ordered Bratteli diagrams is proposed in which isomorphism coincides with the notion of equivalence of Herman, Putnam, and Skau. It is shown that the natural one-to-one correspondence between the category of Cantor minimal systems and the category of simple properly ordered Bratteli diagrams is in fact an equivalence of categories. This gives a Bratteli–Vershik model for factor maps between Cantor minimal systems. We give a construction of factor maps between Cantor minimal systems in terms of suitable maps (called premorphisms) between the corresponding ordered Bratteli diagrams, and we show that every factor map between two Cantor minimal systems is obtained in this way. Moreover, solving a natural question, we are able to characterize Glasner and Weiss’s notion of weak orbit equivalence of Cantor minimal systems in terms of the corresponding C*-algebra crossed products.
Around 30% of individuals with schizophrenia remain symptomatic and significantly impaired despite antipsychotic treatment and are considered to be treatment resistant. Clinicians are currently unable to predict which patients are at higher risk of treatment resistance.
Aims
To determine whether genetic liability for schizophrenia and/or clinical characteristics measurable at illness onset can prospectively indicate a higher risk of treatment-resistant psychosis (TRP).
Method
In 1070 individuals with schizophrenia or related psychotic disorders, schizophrenia polygenic risk scores (PRS) and large copy number variations (CNVs) were assessed for enrichment in TRP. Regression and machine-learning approaches were used to investigate the association of phenotypes related to demographics, family history, premorbid factors and illness onset with TRP.
Results
Younger age at onset (odds ratio 0.94, P = 7.79 × 10−13) and poor premorbid social adjustment (odds ratio 1.64, P = 2.41 × 10−4) increased risk of TRP in univariate regression analyses. These factors remained associated in multivariate regression analyses, which also found lower premorbid IQ (odds ratio 0.98, P = 7.76 × 10−3), younger father's age at birth (odds ratio 0.97, P = 0.015) and cannabis use (odds ratio 1.60, P = 0.025) increased the risk of TRP. Machine-learning approaches found age at onset to be the most important predictor and also identified premorbid IQ and poor social adjustment as predictors of TRP, mirroring findings from regression analyses. Genetic liability for schizophrenia was not associated with TRP.
Conclusions
People with an earlier age at onset of psychosis and poor premorbid functioning are more likely to be treatment resistant. The genetic architecture of susceptibility to schizophrenia may be distinct from that of treatment outcomes.
Rare copy number variants (CNVs) are associated with risk of neurodevelopmental disorders characterised by varying degrees of cognitive impairment, including schizophrenia, autism spectrum disorder and intellectual disability. However, the effects of many individual CNVs in carriers without neurodevelopmental disorders are not yet fully understood, and little is known about the effects of reciprocal copy number changes of known pathogenic loci.
Aims
We aimed to analyse the effect of CNV carrier status on cognitive performance and measures of occupational and social outcomes in unaffected individuals from the UK Biobank.
Method
We called CNVs in the full UK Biobank sample and analysed data from 420 247 individuals who passed CNV quality control, reported White British or Irish ancestry and were not diagnosed with neurodevelopmental disorders. We analysed 33 pathogenic CNVs, including their reciprocal deletions/duplications, for association with seven cognitive tests and four general measures of functioning: academic qualifications, occupation, household income and Townsend Deprivation Index.
Results
Most CNVs (24 out of 33) were associated with reduced performance on at least one cognitive test or measure of functioning. The changes on the cognitive tests were modest (average reduction of 0.13 s.d.) but varied markedly between CNVs. All 12 schizophrenia-associated CNVs were associated with significant impairments on measures of functioning.
Conclusions
CNVs implicated in neurodevelopmental disorders, including schizophrenia, are associated with cognitive deficits, even among unaffected individuals. These deficits may be subtle but CNV carriers have significant disadvantages in educational attainment and ability to earn income in adult life.
We show that the property of a C*-algebra that all its Hilbert modules have a frame, in the case of σ-unital C*-algebras, is preserved under Rieffel–Morita equivalence. In particular, we show that a σ-unital continuous-trace C*-algebra with trivial Dixmier–Douady class, all of whose Hilbert modules admit a frame, has discrete spectrum. We also show this for the tensor product of any commutative C*-algebra with the C*-algebra of compact operators on any Hilbert space.
A category structure for Bratteli diagrams is proposed and a functor from the category of $\text{AF}$ algebras to the category of Bratteli diagrams is constructed. Since isomorphism of Bratteli diagrams in this category coincides with Bratteli’s notion of equivalence, we obtain in particular a functorial formulation of Bratteli’s classification of $\text{AF}$ algebras (and at the same time, of Glimm’s classification of $\text{UHF}$ algebras). It is shown that the three approaches to classification of $\text{AF}$ algebras, namely, through Bratteli diagrams, $\text{K}$-theory, and a certain natural abstract classifying category, are essentially the same from a categorical point of view.
Let $\theta \,\in \,\left[ 0,\,1 \right]$ be any irrational number. It is shown that the extended rotation algebra ${{B}_{\theta }}$ introduced by the authors in J. Reine Angew. Math. 665(2012), pp. 1–71, is always an $\text{AF}$ algebra.
Copy number variants (CNVs) are structural changes in chromosomes that result in deletions, duplications, inversions or translocations of large DNA segments. Eleven confirmed CNV loci have been identified as rare but important risk factors in schizophrenia. These CNVs are also associated with other neurodevelopmental disorders and medical/physical comorbidities. Although the penetrance of the CNVs for schizophrenia (the chance that CNV carriers will develop the disorder) is modest, the penetrance of CNVs for any early-onset developmental disorder (e.g. intellectual disability or autism) is much higher. Testing for CNVs is now affordable and being used in clinical genetics and neurodevelopmental disorders clinics. It is possible that testing will be expanded to psychiatric clinics. This article provides a clinically relevant overview of recent CNV findings in schizophrenia and related disorders.
A number of copy number variants (CNVs) have been suggested as susceptibility factors for schizophrenia. For some of these the data remain equivocal, and the frequency in individuals with schizophrenia is uncertain.
Aims
To determine the contribution of CNVs at 15 schizophrenia-associated loci (a) using a large new data-set of patients with schizophrenia(n = 6882) and controls (n = 6316), and (b) combining our results with those from previous studies.
Method
We used Illumina microarrays to analyse our data. Analyses were restricted to 520 766 probes common to all arrays used in the different data-sets.
Results
We found higher rates in participants with schizophrenia than in controls for 13 of the 15 previously implicated CNVs. Six were nominally significantly associated (P<0.05) in this new data-set: deletions at 1q21.1, NRXN1, 15q11.2 and 22q11.2 and duplications at 16p11.2 and the Angelman/Prader–Willi Syndrome (AS/PWS) region. All eight AS/PWS duplications in patients were of maternal origin. When combined with published data, 11 of the 15 loci showed highly significant evidence for association with schizophrenia(P<4.1×10−4).
Conclusions
We strengthen the support for the majority of the previously implicated CNVs in schizophrenia. About 2.5% of patients with schizophrenia and 0.9% of controls carry a large, detectable CNV at one of these loci. Routine CNV screening may be clinically appropriate given the high rate of known deleterious mutations in the disorder and the comorbidity associated with these heritable mutations.
Let $X$ be a compact metric space. A lower bound for the radius of comparison of the ${{\text{C}}^{*}}$-algebra $\text{C}\left( X \right)$ is given in terms of ${{\dim}_{\mathbb{Q}}}\,X$, where ${{\dim}_{\mathbb{Q}}}\,X$ is the cohomological dimension with rational coefficients. If ${{\dim}_{\mathbb{Q}}}\,X\,=\,\dim\,X\,=\,d$, then the radius of comparison of the ${{\text{C}}^{*}}$-algebra $C\left( X \right)$ is $\max \left\{ 0,\,\left( d\,-\,1 \right)/\,2\,-\,1 \right\}$ if $d$ is odd, and must be either ${d}/{2}\;\,-\,1$ or ${d}/{2}\;\,-\,2$ if $d$ is even (the possibility ${d}/{2}\;\,-\,1$ does occur, but we do not know if the possibility ${d}/{2}\;\,-\,2$ can also occur).