Robust stabilization of LPV systems with structured uncertainty using minimax controllers

This paper addresses a robust control scheduling scheme for uncertain linear parameter-varying systems with structured uncertainty. A gain-scheduled controller is proposed which employs a set of minimax optimal robust controllers and incorporates an interpolation rule to achieve continuity of the controller gain over a range of operating conditions. Novel weighted time-domain integral quadratic constraints are introduced to assist in the derivation of the controller. The key idea of the interpolation for the structured uncertainty case is to transform the parameterized algebraic Riccati inequalities into equivalent linear matrix inequalities. For every fixed value of the system parameter, the proposed controller guarantees robust stability and a certain bound on the worst-case performance of the corresponding uncertain closed loop system. Furthermore, a bound on the rate of parameter variations is obtained under which the closed loop LPV system is robustly stable. To obtain the proposed controller, a set of semi-definite programming problems are introduced; this enables an efficient numerical solution to the problem under consideration. © 2007 IEEE

Decentralized robust control of uncertain Markov jump parameter systems via output feedback

This paper addresses the problem of decentralized robust stabilization and control for a class of uncertain Markov jump parameter systems. Control is via output feedback and knowledge of the discrete Markov state. It is shown that the existence of a solution to a collection of mode-dependent coupled algebraic Riccati equations and inequalities, which depend on certain additional parameters, is both necessary and sufficient for the existence of a robust decentralized switching controller. A guaranteed upper bound on robust performance is also given. To obtain a controller which satisfies this bound, an optimization problem involving rank constrained linear matrix inequalities is introduced, and a numerical approach for solving this problem is presented. To demonstrate the efficacy of the proposed approach, an example stabilization problem for a power system comprising three generators and one on-load tap changing transformer is considered. © 2007 Elsevier Ltd. All rights reserved

Design of switching damping controllers for power systems based on a Markov jump parameter system approach

The application of a new technique, based on the theory of Markov Jump Parameter Systems (MJPS), to the problem of designing controllers to damp power system oscillations is presented in this paper. This problem is very difficult to address, mainly because these controllers are required to have an output feedback decentralized structure. The technique relies on the statistical knowledge about the system operating conditions to provide less conservative controllers than other modern robust control approaches. The influence of the system interconnections over its modes of oscillation is reduced by means of a proper control design formulation involving Integral Quadratic Constraints. The discrete nature of some typical events in power systems (such as line tripping or load switching) is adequately modeled by the MJPS approach, therefore allowing the controller to withstand such abrupt changes in the operating conditions of the system, as shown in the results. © 2006 IEEE

Few-shot Semantic Segmentation with Self-supervision from Pseudo-classes

Despite the success of deep learning methods for semantic segmentation, few-shot semantic segmentation remains a challenging task due to the limited training data and the generalisation requirement for unseen classes. While recent progress has been particularly encouraging, we discover that existing methods tend to have poor performance in terms of meanIoU when query images contain other semantic classes besides the target class. To address this issue, we propose a novel self-supervised task that generates random pseudo-classes in the background of the query images, providing extra training data that would otherwise be unavailable when predicting individual target classes. To that end, we adopted superpixel segmentation for generating the pseudo-classes. With this extra supervision, we improved the meanIoU performance of the state-of-the-art method by 2.5% and 5.1% on the one-shot tasks, as well as 6.7% and 4.4% on the five-shot tasks, on the PASCAL-5i and COCO benchmarks, respectively

Inhibition of the Bloom's and Werner's syndrome helicases by G-quadruplex interacting ligands.

G-Quadruplex DNAs are folded, non-Watson-Crick structures that can form within guanine-rich DNA sequences such as telomeric repeats. Previous studies have identified a series of trisubstituted acridine derivatives that are potent and selective ligands for G-quadruplex DNA. These ligands have been shown previously to inhibit the activity of telomerase, the specialized reverse transcriptase that regulates telomere length. The RecQ family of DNA helicases, which includes the Bloom's (BLM) and Werner's (WRN) syndrome gene products, are apparently unique among cellular helicases in their ability to efficiently disrupt G-quadruplex DNA. This property may be relevant to telomere maintenance, since it is known that the sole budding yeast RecQ helicase, Sgs1p, is required for a telomerase-independent telomere lengthening pathway reminiscent of the "ALT" pathway in human cells. Here, we show that trisubstituted acridine ligands are potent inhibitors of the helicase activity of the BLM and WRN proteins on both G-quadruplex and B-form DNA substrates. Inhibition of helicase activity is associated with both a reduction in the level of binding of the helicase to G-quadruplex DNA and a reduction in the degree to which the G-quadruplex DNA can support DNA-dependent ATPase activity. We discuss these results in the context of the possible utility of trisubstituted acridines as antitumor agents for the disruption of both telomerase-dependent and telomerase-independent telomere maintenance

Holomorphic anomaly equations and the Igusa cusp form conjecture

Let $S$ be a K3 surface and let $E$ be an elliptic curve. We solve the reduced Gromov-Witten theory of the Calabi-Yau threefold $S \times E$ for all curve classes which are primitive in the K3 factor. In particular, we deduce the Igusa cusp form conjecture. The proof relies on new results in the Gromov-Witten theory of elliptic curves and K3 surfaces. We show the generating series of Gromov-Witten classes of an elliptic curve are cycle-valued quasimodular forms and satisfy a holomorphic anomaly equation. The quasimodularity generalizes a result by Okounkov and Pandharipande, and the holomorphic anomaly equation proves a conjecture of Milanov, Ruan and Shen. We further conjecture quasimodularity and holomorphic anomaly equations for the cycle-valued Gromov-Witten theory of every elliptic fibration with section. The conjecture generalizes the holomorphic anomaly equations for ellliptic Calabi-Yau threefolds predicted by Bershadsky, Cecotti, Ooguri, and Vafa. We show a modified conjecture holds numerically for the reduced Gromov-Witten theory of K3 surfaces in primitive classes.Comment: 68 page

The DNA repair enzyme, aprataxin, plays a role in innate immune signaling.

Ataxia with oculomotor apraxia type 1 (AOA1) is a progressive neurodegenerative disorder characterized by a gradual loss of coordination of hand movements, speech, and eye movements. AOA1 is caused by an inactivation mutation in the APTX gene. APTX resolves abortive DNA ligation intermediates. APTX deficiency may lead to the accumulation of 5’-AMP termini, especially in the mitochondrial genome. The consequences of APTX deficiency includes impaired mitochondrial function, increased DNA single-strand breaks, elevated reactive oxygen species production, and altered mitochondrial morphology. All of these processes can cause misplacement of nuclear and mitochondrial DNA, which can activate innate immune sensors to elicit an inflammatory response. This study explores the impact of APTX knockout in microglial cells, the immune cells of the brain. RNA-seq analysis revealed significant differences in the transcriptomes of wild-type and APTX knockout cells, especially in response to viral infections and innate immune pathways. Specifically, genes and proteins involved in the cGAS-STING and RIG-I/MAVS pathways were downregulated in APTX knockout cells, which suggests an impaired immune response to cytosolic DNA and RNA. The clinical relevance of these findings was supported by analyzing publicly available RNA-seq data from AOA1 patient cell lines. Comparisons between APTX-deficient patient cells and healthy control cells also revealed altered immune responses and dysregulated DNA- and RNA-sensing pathways in the patient cells. Overall, this study highlights the critical role of APTX in regulating innate immunity, particularly in DNA- and RNA-sensing pathways. Our findings contribute to a better understanding of the underlying molecular mechanisms of AOA1 pathology and highlights potential therapeutic targets for this disease

The mRNA expression of SETD2 in human breast cancer: Correlation with clinico-athological parameters

BACKGROUND: SET domain containing protein 2 (SETD2) is a histone methyltransferase that is involved in transcriptional elongation. There is evidence that SETD2 interacts with p53 and selectively regulates its downstream genes. Therefore, it could be implicated in the process of carcinogenesis. Furthermore, this gene is located on the short arm of chromosome 3p and we previously demonstrated that the 3p21.31 region of chromosome 3 was associated with permanent growth arrest of breast cancer cells. This region includes closely related genes namely: MYL3, CCDC12, KIF9, KLHL18 and SETD2. Based on the biological function of these genes, SETD2 is the most likely gene to play a tumour suppressor role and explain our previous findings. Our objective was to determine, using quantitative PCR, whether the mRNA expression levels of SETD2 were consistent with a tumour suppressive function in breast cancer. This is the first study in the literature to examine the direct relationship between SETD2 and breast cancer. METHODS: A total of 153 samples were analysed. The levels of transcription of SETD2 were determined using quantitative PCR and normalized against (CK19). Transcript levels within breast cancer specimens were compared to normal background tissues and analyzed against conventional pathological parameters and clinical outcome over a 10 year follow-up period. RESULTS: The levels of SETD2 mRNA were significantly lower in malignant samples (p = 0.0345) and decreased with increasing tumour stage. SETD2 expression levels were significantly lower in samples from patients who developed metastasis, local recurrence, or died of breast cancer when compared to those who were disease free for > 10 years (p = 0.041). CONCLUSION: This study demonstrates a compelling trend for SETD2 transcription levels to be lower in cancerous tissues and in patients who developed progressive disease. These findings are consistent with a possible tumour suppressor function of this gene in breast cancer

The Role of Pre-Existing Diabetes Mellitus on Hepatocellular Carcinoma Occurrence and Prognosis: A Meta-Analysis of Prospective Cohort Studies

The impact of pre-existing diabetes mellitus (DM) on hepatocellular carcinoma (HCC) occurrence and prognosis is complex and unclear. The aim of this meta-analysis is to evaluate the association between pre-existing diabetes mellitus and hepatocellular carcinoma occurrence and prognosis.We searched PubMed, Embase and the Cochrane Library from their inception to January, 2011 for prospective epidemiological studies assessing the effect of pre-existing diabetes mellitus on hepatocellular carcinoma occurrence, mortality outcomes, cancer recurrence, and treatment-related complications. Study-specific risk estimates were combined by using fixed effect or random effect models.The database search generated a total of 28 prospective studies that met the inclusion criteria. Among these studies, 14 reported the risk of HCC incidence and 6 studies reported risk of HCC specific mortality. Six studies provided a total of 8 results for all-cause mortality in HCC patients. Four studies documented HCC recurrence risks and 2 studies reported risks for hepatic decomposition occurrence in HCC patients. Meta-analysis indicated that pre-existing diabetes mellitus (DM) was significantly associated with increased risk of HCC incidence [meta-relative risk (RR) = 1.87, 95% confidence interval (CI): 1.15-2.27] and HCC-specific mortality (meta-RR = 1.88, 95%CI: 1.39-2.55) compared with their non-DM counterparts. HCC patients with pre-existing DM had a 38% increased (95% CI: 1.13-1.48) risk of death from all-causes and 91% increased (95%CI: 1.41-2.57) risk of hepatic decomposition occurrence compared to those without DM. In DM patients, the meta-RR for HCC recurrence-free survival was 1.93(95%CI: 1.12-3.33) compared with non-diabetic patients.The findings from the current meta-analysis suggest that DM may be both associated with elevated risks of both HCC incidence and mortality. Furthermore, HCC patients with pre-existing diabetes have a poorer prognosis relative to their non-diabetic counterparts