Projectively and conformally invariant star-products

We consider the Poisson algebra S(M) of smooth functions on T^*M which are fiberwise polynomial. In the case where M is locally projectively (resp. conformally) flat, we seek the star-products on S(M) which are SL(n+1,R) (resp. SO(p+1,q+1))-invariant. We prove the existence of such star-products using the projectively (resp. conformally) equivariant quantization, then prove their uniqueness, and study their main properties. We finally give an explicit formula for the canonical projectively invariant star-product.Comment: 37 pages, Latex; minor correction

Dual-sPLS: a family of Dual Sparse Partial Least Squares regressions for feature selection and prediction with tunable sparsity; evaluation on simulated and near-infrared (NIR) data

Relating a set of variables X to a response y is crucial in chemometrics. A quantitative prediction objective can be enriched by qualitative data interpretation, for instance by locating the most influential features. When high-dimensional problems arise, dimension reduction techniques can be used. Most notable are projections (e.g. Partial Least Squares or PLS ) or variable selections (e.g. lasso). Sparse partial least squares combine both strategies, by blending variable selection into PLS. The variant presented in this paper, Dual-sPLS, generalizes the classical PLS1 algorithm. It provides balance between accurate prediction and efficient interpretation. It is based on penalizations inspired by classical regression methods (lasso, group lasso, least squares, ridge) and uses the dual norm notion. The resulting sparsity is enforced by an intuitive shrinking ratio parameter. Dual-sPLS favorably compares to similar regression methods, on simulated and real chemical data. Code is provided as an open-source package in R: \url{https://CRAN.R-project.org/package=dual.spls}

Étude de l'impact des microARNs sur la carcinogenèse des cancers colorectaux instables sur les séquences répétées microsatellites du génome

La progression tumorale MSI (Microsatellite Instable) est un processus multi-étapes résultant de mutations générées par un processus d'instabilité génétique qui affecte en majorité les motifs répétés en tandem de l'ADN (microsatellites). Ces mutations contribuent à l'oncogenèse lorsqu'elles perturbent la fonction d'oncogènes ou de gènes suppresseurs de tumeurs. Le trait phénotypique MSI est consécutif à l'inactivation du système de réparation des mésappariements de l'ADN (système MMR). Dans ce travail, je me suis intéressé au rôle des microARNs dans l'oncogenèse MSI. Les microARNs régulent l'expression de nombreux gènes pouvant avoir un rôle clé dans le cancer. J'ai donc fait l'hypothèse d'un rôle de ces microARNs lors des différentes étapes du processus tumorigénique MSI. Tout d'abord nous avons mis en évidence une surexpression du miR-155 (ciblant les principales protéines MMR) au niveau de la muqueuse colique non transformée des malades atteints d'une Maladie Inflammatoire Chronique Intestinale, qui pourrait constituer un évènement pré-tumoral favorisant l'émergence de clones MMR-déficients (notion d'effet de champs). Dans une deuxième partie, nous avons pu identifier la première mutation somatique touchant un microARN. Il s'agit du miR-3613 dont la répétition microsatellite est entièrement localisée dans le miR mature. L'instabilité au niveau de ce miR conduit à des changements de séquence à l'extrémité 3' du miR (notion d'IsomiRs). Les isomiRs produits ont un répertoire de cibles qui pour certaines sont communes à la forme sauvage et pour d'autres spécifiques à chacun des variants.MSI tumor progression (Microsatellite Instability) is depicted as a multistage process that results from mutations generated by a process of genetic instability affecting mostly DNA tandem repeats (known as microsatellites). These mutations contribute to tumorigenesis when they disrupt the function of oncogenes or tumor suppressor genes. As a phenotypic trait, MSI is the consequence of DNA mismatch repair inactivation (MMR). This work focused on the role microRNAs might play in MSI tumorigenesis. MicroRNAs regulate the expression of numerous genes and are deregulated in cancer. I have hypothesized a role of theses microRNAs during the various stages of the MSI tumorigenic process, choosing colorectal cancers (CRC) as a working model. First we demonstrated that overexpression of miR-155 (targeting core MMR proteins) in the non-transformed colonic mucosa of patients with Inflammatory Bowel Disease, might constitute a pre-tumoral event promoting the emergence of MMR-deficient clones (a concept known as ?field effect?). In a second part, we were able to identify the first somatic mutation affecting a mature microRNA sequence. A DNA microsatellite repeat is indeed fully embedded within the mature sequence of miR-3613. Instability at this DNA repeat leads to sequence modifications at the 3?end of miR-3613-5p (IsomiRs). IsomiRs display a signature among which some mRNA targets are common to the wild form, while others are specific to each variant.PARIS-JUSSIEU-Bib.électronique (751059901) / SudocSudocFranceF

Computing the Real Isolated Points of an Algebraic Hypersurface

Let $\mathbb{R}$ be the field of real numbers. We consider the problem of computing the real isolated points of a real algebraic set in $\mathbb{R}^n$ given as the vanishing set of a polynomial system. This problem plays an important role for studying rigidity properties of mechanism in material designs. In this paper, we design an algorithm which solves this problem. It is based on the computations of critical points as well as roadmaps for answering connectivity queries in real algebraic sets. This leads to a probabilistic algorithm of complexity $(nd)^{O(n\log(n))}$ for computing the real isolated points of real algebraic hypersurfaces of degree $d$. It allows us to solve in practice instances which are out of reach of the state-of-the-art.Comment: Conference paper ISSAC 202

A Federated Search and Social Recommendation Widget

This paper presents a federated search and social recommen- dation widget. It describes the widget’s interface and the un- derlying social recommendation engine. A preliminary eval- uation of the widget’s usability and usefulness involving 15 subjects is also discussed. The evaluation helped identify us- ability problems that will be addressed prior to the widget’s usage in a real learning context

Capabilities of GPT-4 in ophthalmology: an analysis of model entropy and progress towards human-level medical question answering

Background: Evidence on the performance of Generative Pre-trained Transformer 4 (GPT-4), a large language model (LLM), in the ophthalmology question-answering domain is needed. // Methods: We tested GPT-4 on two 260-question multiple choice question sets from the Basic and Clinical Science Course (BCSC) Self-Assessment Program and the OphthoQuestions question banks. We compared the accuracy of GPT-4 models with varying temperatures (creativity setting) and evaluated their responses in a subset of questions. We also compared the best-performing GPT-4 model to GPT-3.5 and to historical human performance. // Results: GPT-4–0.3 (GPT-4 with a temperature of 0.3) achieved the highest accuracy among GPT-4 models, with 75.8% on the BCSC set and 70.0% on the OphthoQuestions set. The combined accuracy was 72.9%, which represents an 18.3% raw improvement in accuracy compared with GPT-3.5 (p<0.001). Human graders preferred responses from models with a temperature higher than 0 (more creative). Exam section, question difficulty and cognitive level were all predictive of GPT-4-0.3 answer accuracy. GPT-4-0.3’s performance was numerically superior to human performance on the BCSC (75.8% vs 73.3%) and OphthoQuestions (70.0% vs 63.0%), but the difference was not statistically significant (p=0.55 and p=0.09). // Conclusion: GPT-4, an LLM trained on non-ophthalmology-specific data, performs significantly better than its predecessor on simulated ophthalmology board-style exams. Remarkably, its performance tended to be superior to historical human performance, but that difference was not statistically significant in our study

MiRNA Genes Constitute New Targets for Microsatellite Instability in Colorectal Cancer

Mismatch repair-deficient colorectal cancers (CRC) display widespread instability at DNA microsatellite sequences (MSI). Although MSI has been reported to commonly occur at coding repeats, leading to alterations in the function of a number of genes encoding cancer-related proteins, nothing is known about the putative impact of this process on non-coding microRNAs. In miRbase V15, we identified very few human microRNA genes with mono- or di-nucleotide repeats (n = 27). A mutational analysis of these sequences in a large series of MSI CRC cell lines and primary tumors underscored instability in 15 of the 24 microRNA genes successfully studied at variable frequencies ranging from 2.5% to 100%. Following a maximum likelihood statistical method, microRNA genes were separated into two groups that differed significantly in their mutation frequencies and in their tendency to represent mutations that may or may not be under selective pressures during MSI tumoral progression. The first group included 21 genes that displayed no or few mutations in CRC. The second group contained three genes, i.e., hsa-mir-1273c, hsa-mir-1303 and hsa-mir-567, with frequent (≥80%) and sometimes bi-allelic mutations in MSI tumors. For the only one expressed in colonic tissues, hsa-mir-1303, no direct link was found between the presence or not of mono- or bi-allelic alterations and the levels of mature miR expression in MSI cell lines, as determined by sequencing and quantitative PCR respectively. Overall, our results provide evidence that DNA repeats contained in human miRNA genes are relatively rare and preserved from mutations due to MSI in MMR-deficient cancer cells. Functional studies are now required to conclude whether mutated miRNAs, and especially the miR-1303, might have a role in MSI tumorigenesis

NMD inhibition fails to identify tumour suppressor genes in microsatellite stable gastric cancer cell lines

BACKGROUND: Gastric cancers frequently show chromosomal alterations which can cause activation of oncogenes, and/or inactivation of tumour suppressor genes. In gastric cancer several chromosomal regions are described to be frequently lost, but for most of the regions, no tumour suppressor genes have been identified yet. The present study aimed to identify tumour suppressor genes inactivated by nonsense mutation and deletion in gastric cancer by means of GINI (gene identification by nonsense mediated decay inhibition) and whole genome copy number analysis. METHODS: Two non-commercial gastric cancer cell lines, GP202 and IPA220, were transfected with siRNA directed against UPF1, to specifically inhibit the nonsense mediated decay (NMD) pathway, and with siRNA directed against non-specific siRNA duplexes (CVII) as a control. Microarray expression experiments were performed in triplicate on 4 × 44 K Agilent arrays by hybridizing RNA from UPF1-transfected cells against non-specific CVII-transfected cells. In addition, array CGH of the two cell lines was performed on 4 × 44K agilent arrays to obtain the DNA copy number profiles. Mutation analysis of GINI candidates was performed by sequencing. RESULTS: UPF1 expression was reduced for >70% and >80% in the GP202 and IPA220 gastric cancer cell lines, respectively. Integration of array CGH and microarray expression data provided a list of 134 and 50 candidate genes inactivated by nonsense mutation and deletion for GP202 and IPA220, respectively. We selected 12 candidate genes for mutation analysis. Of these, sequence analysis was performed on 11 genes. One gene, PLA2G4A, showed a silent mutation, and in two genes, CTSA and PTPRJ, missense mutations were detected. No nonsense mutations were detected in any of the 11 genes tested. CONCLUSION: Although UPF1 was substantially repressed, thus resulting in the inhibition of the NMD system, we did not find genes inactivated by nonsense mutations. Our results show that the GINI strategy leads to a high number of false positives

Symplectic Fluctuations for Electromagnetic Excitations of Hall Droplets

We show that the integer quantum Hall effect systems in plane, sphere or disc, can be formulated in terms of an algebraic unified scheme. This can be achieved by making use of a generalized Weyl--Heisenberg algebra and investigating its basic features. We study the electromagnetic excitation and derive the Hamiltonian for droplets of fermions on a two-dimensional Bargmann space (phase space). This excitation is introduced through a deformation (perturbation) of the symplectic structure of the phase space. We show the major role of Moser's lemma in dressing procedure, which allows us to eliminate the fluctuations of the symplectic structure. We discuss the emergence of the Seiberg--Witten map and generation of an abelian noncommutative gauge field in the theory. As illustration of our model, we give the action describing the electromagnetic excitation of a quantum Hall droplet in two-dimensional manifold.Comment: 23 page