Quantum planes and quantum cylinders from Poisson homogeneous spaces

Quantum planes and a new quantum cylinder are obtained as quantization of Poisson homogeneous spaces of two different Poisson structures on classical Euclidean group E(2).Comment: 13 pages, plain Tex, no figure

Quantum symmetric pairs and representations of double affine Hecke algebras of type C∨CnC^\vee C_n

We build representations of the affine and double affine braid groups and Hecke algebras of type $C^\vee C_n$, based upon the theory of quantum symmetric pairs $(U,B)$. In the case $U=U_q(gl_N)$, our constructions provide a quantization of the representations constructed by Etingof, Freund and Ma in arXiv:0801.1530, and also a type $BC$ generalization of the results in arXiv:0805.2766.Comment: Final version, to appear in Selecta Mathematic

Free q-Schrodinger Equation from Homogeneous Spaces of the 2-dim Euclidean Quantum Group

After a preliminary review of the definition and the general properties of the homogeneous spaces of quantum groups, the quantum hyperboloid qH and the quantum plane qP are determined as homogeneous spaces of Fq(E(2)). The canonical action of Eq(2) is used to define a natural q-analog of the free Schro"dinger equation, that is studied in the momentum and angular momentum bases. In the first case the eigenfunctions are factorized in terms of products of two q-exponentials. In the second case we determine the eigenstates of the unitary representation, which, in the qP case, are given in terms of Hahn-Exton functions. Introducing the universal T-matrix for Eq(2) we prove that the Hahn-Exton as well as Jackson q-Bessel functions are also obtained as matrix elements of T, thus giving the correct extension to quantum groups of well known methods in harmonic analysis.Comment: 19 pages, plain tex, revised version with added materia

Prenatal smoke exposure induces persistent Cyp2a5 methylation and increases nicotine metabolism in the liver of neonatal and adult male offspring

Prenatal smoke exposure (PSE) is a risk factor for nicotine dependence. One susceptibility gene for nicotine dependence is Cytochrome P450 (CYP) 2A6, an enzyme responsible for the conversion of nicotine to cotinine and nicotine clearance in the liver. Higher activity of the CYP2A6 enzyme is associated with nicotine dependence, but no research has addressed the PSE effects on the CYP2A6 gene or its mouse homologue Cyp2a5. We hypothesized that PSE affects Cyp2a5 promoter methylation, Cyp2a5 mRNA levels, and nicotine metabolism in offspring. We used a smoke-exposed pregnant mouse model. RNA, DNA, and microsomal protein were isolated from liver tissue of foetal, neonatal, and adult offspring. Enzyme activity, Cyp2a5 mRNA levels, and Cyp2a5 methylation status of six CpG sites within the promoter region were analysed via HPLC, RT-PCR, and bisulphite pyrosequencing. Our data show that PSE induced higher cotinine levels in livers of male neonatal and adult offspring compared to controls. PSE-induced cotinine levels in neonates correlated with Cyp2a5 mRNA expression and promoter methylation at CpG-7 and CpG+45. PSE increased methylation in almost all CpG sites in foetal offspring, and this effect persisted at CpG-74 in male neonatal and adult offspring. Our results indicate that male offspring of mothers which were exposed to cigarette smoke during pregnancy have a higher hepatic nicotine metabolism, which could be regulated by DNA methylation. Given the detected persistence into adulthood, extrapolation to the human situation suggests that sons born from smoking mothers could be more susceptible to nicotine dependence later in life

Postnatal Smoke Exposure Further Increases the Hepatic Nicotine Metabolism in Prenatally Smoke Exposed Male Offspring and Is Linked with Aberrant Cyp2a5 Methylation

Prenatal smoke exposure (PreSE) is a risk factor for nicotine dependence, which is further enhanced by postnatal smoke exposure (PostSE). One susceptibility gene to nicotine dependence is Cytochrome P450 (CYP) 2A6, an enzyme responsible for the conversion of nicotine to cotinine in the liver. Higher CYP2A6 activity is associated with nicotine dependence and could be regulated through DNA methylation. In this study we investigated whether PostSE further impaired PreSE-induced effects on nicotine metabolism, along with Cyp2a5, orthologue of CYP2A6, mRNA expression and DNA methylation. Using a mouse model where prenatally smoke-exposed adult offspring were exposed to cigarette smoke for 3 months, enzyme activity, mRNA levels, and promoter methylation of hepatic Cyp2a5 were evaluated. We found that in male offspring, PostSE increased PreSE-induced cotinine levels and Cyp2a5 mRNA expression. In addition, both PostSE and PreSE changed Cyp2a5 DNA methylation in male groups. PreSE however decreased cotinine levels whereas it had no effect on Cyp2a5 mRNA expression or methylation. These adverse outcomes of PreSE and PostSE were most prominent in males. When considered in the context of the human health aspects, the combined effect of prenatal and adolescent smoke exposure could lead to an accelerated risk for nicotine dependence later in life.</p

Maintaining friendships in early stage dementia: Factors to consider

Friendships and the importance of social connectiveness play a critical role in aging well, regardless of gender, race, social class, or impairment. Yet, dementia takes its toll on social relationships, and many friends withdraw and ‘disappear’, because they can no longer bear to see the changes that are taking place in their diagnosed friend. The dementia care literature documents this abandonment; however, this study examines the opposite occurrence. In order to understand more clearly the role of long-term friendships and how such friendships remain and continue, despite the diagnosis of dementia, this qualitative study examines in depth eight people in the early stages of dementia who have been able to maintain strong friendships despite the diagnosis. Factors that seem to play important roles are: (1) the importance of the friendships, (2) factors affecting the quality of the relationships, (3) mutually beneficial relationships, (4) core values, (5) acceptance and disclosure, and (6) recognition of strengths and understanding of limitations

TAB2 deletions and variants cause a highly recognisable syndrome with mitral valve disease, cardiomyopathy, short stature and hypermobility

Deletions that include the gene TAB2 and TAB2 loss-of-function variants have previously been associated with congenital heart defects and cardiomyopathy. However, other features, including short stature, facial dysmorphisms, connective tissue abnormalities and a variable degree of developmental delay, have only been mentioned occasionally in literature and thus far not linked to TAB2. In a large-scale, social media-based chromosome 6 study, we observed a shared phenotype in patients with a 6q25.1 deletion that includes TAB2. To confirm if this phenotype is caused by haploinsufficiency of TAB2 and to delineate a TAB2-related phenotype, we subsequently sequenced TAB2 in patients with matching phenotypes and recruited patients with pathogenic TAB2 variants detected by exome sequencing. This identified 11 patients with a deletion containing TAB2 (size 1.68-14.31 Mb) and 14 patients from six families with novel truncating TAB2 variants. Twenty (80%) patients had cardiac disease, often mitral valve defects and/or cardiomyopathy, 18 (72%) had short stature and 18 (72%) had hypermobility. Twenty patients (80%) had facial features suggestive for Noonan syndrome. No substantial phenotypic differences were noted between patients with deletions and those with intragenic variants. We then compared our patients to 45 patients from the literature. All literature patients had cardiac diseases, but syndromic features were reported infrequently. Our study shows that the phenotype in 6q25.1 deletions is caused by haploinsufficiency of TAB2 and that TAB2 is associated not just with cardiac disease, but also with a distinct phenotype, with features overlapping with Noonan syndrome. We propose the name "TAB2-related syndrome"

Accessible and reliable neurometric testing in humans using a smartphone platform

Tests of human brain circuit function typically require fixed equipment in lab environments. We have developed a smartphone-based platform for neurometric testing. This platform, which uses AI models like computer vision, is optimized for at-home use and produces reproducible, robust results on a battery of tests, including eyeblink conditioning, prepulse inhibition of acoustic startle response, and startle habituation. This approach provides a scalable, universal resource for quantitative assays of central nervous system function.</p