| 281. |
- Afshari, Bahareh, 1981, et al.
(författare)
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Cyclic proofs for the first-order mu-calculus
- 2024
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Ingår i: Logic Journal of the IGPL. - : Oxford University Press (OUP). - 1367-0751 .- 1368-9894. ; 32:1, s. 1-34
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Tidskriftsartikel (refereegranskat)abstract
- We introduce a path-based cyclic proof system for first-order mu-calculus, the extension of first-order logic by second-order quantifiers for least and greatest fixed points of definable monotone functions. We prove soundness of the system and demonstrate it to be as expressive as the known trace-based cyclic systems of Dam and Sprenger. Furthermore, we establish cut-free completeness of our system for the fragment corresponding to the modal mu-calculus.
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| 282. |
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| 283. |
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| 284. |
- Afshari, Bahareh, 1981, et al.
(författare)
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Ill-Founded Proof Systems for Intuitionistic Linear-Time Temporal Logic
- 2023
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Ingår i: Automated Reasoning with Analytic Tableaux and Related Methods, 32nd International Conference, TABLEAUX 2023, Prague, Czech Republic, September 18–21, 2023, Proceedings / Editors: Revantha Ramanayake, Josef Urban. - Cham : Springer. - 0302-9743 .- 1611-3349. - 9783031435126
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Konferensbidrag (refereegranskat)
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| 285. |
- Afshari, Bahareh, 1981, et al.
(författare)
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Lyndon Interpolation forModal μ-Calculus
- 2022
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Ingår i: Language, Logic, and Computation, 13th International Tbilisi Symposium, TbiLLC 2019, Batumi, Georgia, September 16–20, 2019, Revised Selected Papers / editors: Aybüke Özgün, Yulia Zinova. - Cham : Springer International Publishing. - 0302-9743 .- 1611-3349. - 9783030984793
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Konferensbidrag (refereegranskat)
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| 286. |
- Afshari, Bahareh, 1981, et al.
(författare)
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PROOF SYSTEMS FOR TWO-WAY MODAL MU-CALCULUS
- 2023
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Ingår i: Journal of Symbolic Logic (JSL). - 0022-4812 .- 1943-5886.
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Tidskriftsartikel (refereegranskat)abstract
- We present sound and complete sequent calculi for the modal mu-calculus with converse modalities, aka two-way modal mu-calculus. Notably, we introduce a cyclic proof system wherein proofs can be represented as finite trees with back-edges, i.e., finite graphs. The sequent calculi incorporate ordinal annotations and structural rules for managing them. Soundness is proved with relative ease as is the case for the modal mu-calculus with explicit ordinals. The main ingredients in the proof of completeness are isolating a class of non-wellfounded proofs with sequents of bounded size, called slim proofs, and a counter-model construction that shows slimness suffices to capture all validities. Slim proofs are further transformed into cyclic proofs by means of re-assigning ordinal annotations.
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| 287. |
- Afshari, Bahareh, 1981, et al.
(författare)
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Uniform Interpolation from Cyclic Proofs: The Case of Modal Mu-Calculus
- 2021
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Ingår i: Automated Reasoning with Analytic Tableaux and Related Methods, 30th International Conference, TABLEAUX 2021, Birmingham, UK, September 6–9, 2021, Proceedings / Anupam Das, Sara Negri (eds.). - Cham : Springer. - 0302-9743 .- 1611-3349. - 9783030860585
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Konferensbidrag (refereegranskat)abstract
- We show how to construct uniform interpolants in the context of the modal mu-calculus. D’Agostino and Hollenberg (2000) were the first to prove that this logic has the uniform interpolation property, employing a combination of semantic and syntactic methods. This article outlines a purely proof-theoretic approach to the problem based on insights from the cyclic proof theory of mu-calculus. We argue the approach has the potential to lend itself to other temporal and fixed point logics.
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| 288. |
- Afshari, Mariam, 1989-, et al.
(författare)
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Development of an oral health-related quality of life questionnaire on neurosensory disturbances after orthognathic surgery - a pilot study.
- 2022
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Ingår i: Acta odontologica Scandinavica. - : Informa UK Limited. - 1502-3850 .- 0001-6357. ; 80:8, s. 635-640
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Tidskriftsartikel (refereegranskat)abstract
- Development of a new questionnaire, Oral Health-Related Quality of Life - Neurosensory Disturbances after Orthognathic Surgery (OHRQL-NDO), designed to measure the effects of neurosensory disturbance (NSD) on patients' oral health-related quality of life (OHRQL) and to evaluate reliability and validity of this questionnaire.A questionnaire including 11 items was constructed. Thirty patients with NSD affecting the lower lip and/or chin following orthognathic surgery were included. Convergent validity was assessed by comparing OHRQL-NDO with OHIP-14 and two global questions. Test-retest reliability was assessed by asking the patients to complete OHRQL-NDO at two different occasions with an interval of two to threeweeks.The internal consistency, measured with Cronbach's alpha, was 0.84. The test-retest reliability, measured with ICC, was 0.89 (95% CI 0.77-0.95). The correlation between the mean sum score for the OHRQL-NDO and the mean sum score for the OHIP-14 was r=0.75, using Pearson correlation coefficient. The correlations between the mean total score for the OHRQL-NDO and the global questions 1 and 2 were r=0.74 and r=0.72, respectively.The current instrument OHRQL-NDO is a promising test, but needs further development to better capture the different aspects of OHRQL. Further tests of the questionnaire must follow in other samples to finalize the instrument.
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| 289. |
- Afshari, Maryam K., et al.
(författare)
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Activation of PLAG1 and HMGA2 by gene fusions involving the transcriptional regulator gene NFIB
- 2020
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Ingår i: Genes Chromosomes & Cancer. - : Wiley. - 1045-2257 .- 1098-2264. ; 59:11, s. 652-660
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Tidskriftsartikel (refereegranskat)abstract
- The pleomorphic adenoma (PA), which is the most common salivary gland neoplasm, is a benign tumor characterized by recurrent chromosome rearrangements involving 8q12 and 12q14-15. We have previously shown that thePLAG1andHMGA2oncogenes are the targets of these rearrangements. Here, we have identified previously unrecognized subsets of PAs with ins(9;8)/t(8;9) (n = 5) and ins(9;12)/t(9;12) (n = 8) and breakpoints located in the vicinity of thePLAG1andHMGA2loci. RNA-sequencing and reverse transcriptase (RT)-PCR analyses of a case with an ins(9;8) revealed a novelNFIB-PLAG1fusion in whichNFIBexon 4 is linked toPLAG1exon 3. In contrast to the developmentally regulatedPLAG1gene,NFIBwas highly expressed in normal salivary gland, indicating thatPLAG1in this case, as in other variant fusions, is activated by promoter swapping. RT-PCR analysis of three PAs with t(9;12) revealed two tumors with chimeric transcripts consisting ofHMGA2exon 4 linked toNFIBexons 9 or 3 and one case with a fusion linkingHMGA2exon 3 toNFIBexon 9. TheNFIBfusion events resulted in potent activation ofPLAG1andHMGA2. Analysis of the chromatin landscape surroundingNFIBrevealed several super-enhancers in the 5 '- and 3 '-parts of theNFIBlocus and its flanking sequences. These findings indicate thatPLAG1andHMGA2, similar toMYBin adenoid cystic carcinoma, may be activated by enhancer-hijacking events, in which super-enhancers inNFIBare translocated upstream ofPLAG1or downstream ofHMGA2. Our results further emphasize the role ofNFIBas a fusion partner to multiple oncogenes in histopathologically different types of salivary gland tumors.
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| 290. |
- Afshari, Maryam K.
(författare)
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Transcriptomic and functional studies of fusion oncogene-driven salivary gland tumors
- 2020
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Doktorsavhandling (övrigt vetenskapligt/konstnärligt)abstract
- Fusion genes are potent oncogenic drivers resulting from exchange of regulatory/coding sequences between two genes. They were originally identified in leukemias but are now recognized as key oncogenic events also in many solid tumors, including salivary gland tumors (SGTs). Adenoid cystic carcinoma (ACC) is a highly malignant SGT with no effective treatment for patients with recurrent and/or metastatic disease. The MYB-NFIB fusion is the main genomic hallmark of ACC and a po- tential therapeutic target. Here, oncogenic signaling pathways as well as the molecular consequences and regulation of MYB-NFIB were assessed in cultured ACC cells and in ACC surgical samples. A combination of molecular and functional assays was used including RNAi, qPCR, western blot, phospho-receptor tyrosine kinase (RTK) arrays, proliferation/apoptosis/sphere assays, and gene expression microarrays. ACC patient- derived xenografts (PDX) were used to study the effects of RTK-inhibition on tumor growth. MYB-NFIB was shown to promote proliferation and spherogenesis of ACC cells. The fusion regulated expression of genes involved in DNA replication/repair, cell cycle, and RNA processing, and induced an MYC-like transcriptional program. MYB-NFIB was shown to be regulated by IGF1R through IGF2-activated AKT-signaling and phar- macological inhibition of IGF1R partially reversed the transcriptional program induced by MYB-NFIB. Moreover, IGF1R, EGFR, and MET were co-activated in ACC cells. Combined inhibition of these receptors in ACC cells and PDX-models induced differentiation and synergistic growth inhibition. The results provide new insights about the function and regulation of MYB-NFIB and are the first to show that a druggable cell surface receptor can regulate a fusion oncogene encoding a transcription factor. Importantly, the results also highlight novel potential treatment strategies for ACC patients. Pleomorphic adenoma (PA) is the most common SGT. Although it is a benign tumor, treatment may be complicated by recurrence and/or malignant transformation. Previous studies of PA have revealed recurrent chromosomal rearrangements that activate the key oncogenes PLAG1 and HMGA2 by gene fusion events. Here, detailed studies of previously uncharacterized subsets of PAs with 8;9- or 9;12-rearrangements revealed breakpoints within or in the proximity of either PLAG1 or HMGA2, and NFIB. Further analyses using RNA- seq, RT-PCR, qPCR, and arrayCGH revealed a novel NFIB-PLAG1 fusion in a PA with an ins(9;8) and HMGA2-NFIB fusions in cases with t(9;12). These findings highlight the role of NFIB as a fusion partner gene in both benign and malignant SGTs and indicate that NFIB can activate both PLAG1 and HMGA2 by gene fusion/enhancer hijacking events in PA. Furthermore, RNA-seq based transcriptomic analysis of PAs revealed a high frequency of PLAG1 and HMGA2 fusions (≈80% of the cases) and multiple novel fusion partner genes. The findings indicate that gene fusions are more common in PA than previously documented. Global gene expression and pathway analyses revealed several activated oncogenic signaling pathways and showed that the expression profile reflects certain morphological features typical of PA. Finally, the results showed that PLAG1 and HMGA2 drive tumorigenesis via shared signaling pathways. The results provide further insights into the pathogenesis of PA and reveal new potential therapeutic targets.
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