Orthogonal methods based ant colony search for solving continuous optimization problems

Research into ant colony algorithms for solving continuous optimization problems forms one of the most significant and promising areas in swarm computation. Although traditional ant algorithms are designed for combinatorial optimization, they have shown great potential in solving a wide range of optimization problems, including continuous optimization. Aimed at solving continuous problems effectively, this paper develops a novel ant algorithm termed "continuous orthogonal ant colony" (COAC), whose pheromone deposit mechanisms would enable ants to search for solutions collaboratively and effectively. By using the orthogonal design method, ants in the feasible domain can explore their chosen regions rapidly and e±ciently. By implementing an "adaptive regional radius" method, the proposed algorithm can reduce the probability of being trapped in local optima and therefore enhance the global search capability and accuracy. An elitist strategy is also employed to reserve the most valuable points. The performance of the COAC is compared with two other ant algorithms for continuous optimization of API and CACO by testing seventeen functions in the continuous domain. The results demonstrate that the proposed COAC algorithm outperforms the others

Mutually unbiased bases: tomography of spin states and star-product scheme

Mutually unbiased bases (MUBs) are considered within the framework of a generic star-product scheme. We rederive that a full set of MUBs is adequate for a spin tomography, i.e. knowledge of all probabilities to find a system in each MUB-state is enough for a state reconstruction. Extending the ideas of the tomographic-probability representation and the star-product scheme to MUB-tomography, dequantizer and quantizer operators for MUB-symbols of spin states and operators are introduced, ordinary and dual star-product kernels are found. Since MUB-projectors are to obey specific rules of the star-product scheme, we reveal the Lie algebraic structure of MUB-projectors and derive new relations on triple- and four-products of MUB-projectors. Example of qubits is considered in detail. MUB-tomography by means of Stern-Gerlach apparatus is discussed.Comment: 11 pages, 1 table, partially presented at the 17th Central European Workshop on Quantum Optics (CEWQO'2010), June 6-11, 2010, St. Andrews, Scotland, U

INPP4B protects from metabolic syndrome and associated disorders

A high fat diet and obesity have been linked to the development of metabolic dysfunction and the promotion of multiple cancers. The causative cellular signals are multifactorial and not yet completely understood. In this report, we show that Inositol Polyphosphate-4-Phosphatase Type II B (INPP4B) signaling protects mice from diet-induced metabolic dysfunction. INPP4B suppresses AKT and PKC signaling in the liver thereby improving insulin sensitivity. INPP4B loss results in the proteolytic cleavage and activation of a key regulator in de novo lipogenesis and lipid storage, SREBP1. In mice fed with the high fat diet, SREBP1 increases expression and activity of PPARG and other lipogenic pathways, leading to obesity and non-alcoholic fatty liver disease (NAFLD). Inpp4b−/− male mice have reduced energy expenditure and respiratory exchange ratio leading to increased adiposity and insulin resistance. When treated with high fat diet, Inpp4b−/− males develop type II diabetes and inflammation of adipose tissue and prostate. In turn, inflammation drives the development of high-grade prostatic intraepithelial neoplasia (PIN). Thus, INPP4B plays a crucial role in maintenance of overall metabolic health and protects from prostate neoplasms associated with metabolic dysfunction

Best practice recommendations for medically assisted reproduction in patients with known cardiovascular disease or at high risk of cardiovascular disease : A consensus statement supported by the UK Maternal Cardiology Society (UKMCS), British Fertility Society, MacDonald Obstetric Medicine Society (MOMS), British Cardiovascular Society (BCS), British Cardiovascular Intervention Society (BCIS), British Society for Heart Failure (BSH), Scottish Obstetric Cardiac Network (SOCN), Royal College of Obstetricians and Gynaecologists (RCOG), Association of Anaesthetists, Fertility UK, Primary Care Cardiovascular Society (PCCS), Obstetric Anaesthetists Association (OAA), Association of Inherited Cardiac Conditions (AICC)

\ua9 2024 The Author(s). Published by Informa UK Limited, trading as Taylor & Francis Group.Increasing numbers of people are seeking assisted conception. In people with known cardiac disease or risk factors for cardiac disease, assisted conception may carry increased risks during treatment and any subsequent pregnancy. These risks should be assessed, considered and minimized prior to treatment

Cytoplasmic p53 couples oncogene-driven glucose metabolism to apoptosis and is a therapeutic target in glioblastoma.

Cross-talk among oncogenic signaling and metabolic pathways may create opportunities for new therapeutic strategies in cancer. Here we show that although acute inhibition of EGFR-driven glucose metabolism induces only minimal cell death, it lowers the apoptotic threshold in a subset of patient-derived glioblastoma (GBM) cells. Mechanistic studies revealed that after attenuated glucose consumption, Bcl-xL blocks cytoplasmic p53 from triggering intrinsic apoptosis. Consequently, targeting of EGFR-driven glucose metabolism in combination with pharmacological stabilization of p53 with the brain-penetrant small molecule idasanutlin resulted in synthetic lethality in orthotopic glioblastoma xenograft models. Notably, neither the degree of EGFR-signaling inhibition nor genetic analysis of EGFR was sufficient to predict sensitivity to this therapeutic combination. However, detection of rapid inhibitory effects on [18F]fluorodeoxyglucose uptake, assessed through noninvasive positron emission tomography, was an effective predictive biomarker of response in vivo. Together, these studies identify a crucial link among oncogene signaling, glucose metabolism, and cytoplasmic p53, which may potentially be exploited for combination therapy in GBM and possibly other malignancies

Ki67 expression levels are a better marker of reduced melanoma growth following MEK inhibitor treatment than phospho-ERK levels

The loss of tumour phospho-extracellular responsive kinase (pERK) positivity is the major treatment biomarker for mitogen-activated protein kinase/extracellular responsive kinase (MEK) inhibitors. Here, we demonstrate that there is a poor correlation between pERK inhibition and the anti-proliferative effects of MEK inhibitors in melanoma cells. We suggest that Ki67 is a better biomarker for future clinical studies

Associations of common breast cancer susceptibility alleles with risk of breast cancer subtypes in BRCA1 and BRCA2 mutation carriers

Peer reviewedPublisher PD

“I had no idea this shame piece was in me”: couple and family therapists’ experience with learning an evidence-based practice

This study reports on the experience of shame while learning an evidence-based approach to working with couples or families. Couple and family therapists were interviewed about their experience with learning and using an evidence-based practice (EBP) and the data was analyzed using a phenomenological approach called interpretative phenomenological analysis. The theme of shame emerged from a number of research participants as part of their development with the EBP they were integrating into their practice. Starting with an exploration of the participants’ experiences and the impact of shame, the paper will then link these experiences with the psychological and sociological research literature about sham

TNF deficiency causes alterations in the spatial organization of neurogenic zones and alters the number of microglia and neurons in the cerebral cortex

•TNF deficiency alters the spatial organization of neurogenic zones.•TNF deficiency decreases WNT signaling-related proteins.•TNF deficiency alters neuronal and microglial numbers.•Long-term use of non-selective TNF inhibitors impairs learning and memory.•Long-term use of the soluble TNF selective inhibitor XPro1595 does not affect neurogenesis, learning and memory. Although tumor necrosis factor (TNF) inhibitors are used to treat chronic inflammatory diseases, there is little information about how long-term inhibition of TNF affects the homeostatic functions that TNF maintains in the intact CNS. To assess whether developmental TNF deficiency causes alterations in the naïve CNS, we estimated the number of proliferating cells, microglia, and neurons in the developing neocortex of E13.5, P7 and adult TNF knock out (TNF−/−) mice and wildtype (WT) littermates. We also measured changes in gene and protein expression and monoamine levels in adult WT and TNF−/− mice. To evaluate long-term effects of TNF inhibitors, we treated healthy adult C57BL/6 mice with either saline, the selective soluble TNF inhibitor XPro1595, or the nonselective TNF inhibitor etanercept. We estimated changes in cell number and protein expression after two months of treatment. We assessed the effects of TNF deficiency on cognition by testing adult WT and TNF−/− mice and mice treated with saline, XPro1595, or etanercept with specific behavioral tasks. TNF deficiency decreased the number of proliferating cells and microglia and increased the number of neurons. At the same time, TNF deficiency decreased the expression of WNT signaling-related proteins, specifically Collagen Triple Helix Repeat Containing 1 (CTHRC1) and Frizzled receptor 6 (FZD6). In contrast to XPro1595, long-term inhibition of TNF with etanercept in adult C57BL/6 mice decreased the number of BrdU+ cells in the granule cell layer of the dentate gyrus. Etanercept, but not XPro1595, also impaired spatial learning and memory in the Barnes maze memory test. TNF deficiency impacts the organization of neurogenic zones and alters the cell composition in brain. Long-term inhibition of TNF with the nonselective TNF inhibitor etanercept, but not the soluble TNF inhibitor XPro1595, decreases neurogenesis in the adult mouse hippocampus and impairs learning and memory after two months of treatment

Conflicting Interpretation of Genetic Variants and Cancer Risk by Commercial Laboratories as Assessed by the Prospective Registry of Multiplex Testing

Altres ajuts: Ambry Genetics, Myriad Genetics, Novartis (I), Pfizer (I)Massively parallel sequencing allows simultaneous testing of multiple genes associated with cancer susceptibility. Guidelines are available for variant classification; however, interpretation of these guidelines by laboratories and providers may differ and lead to conflicting reporting and, potentially, to inappropriate medical management. We describe conflicting variant interpretations between Clinical Laboratory Improvement Amendments-approved commercial clinical laboratories, as reported to the Prospective Registry of Multiplex Testing (PROMPT), an online genetic registry. Clinical data and genetic testing results were gathered from 1,191 individuals tested for inherited cancer susceptibility and self-enrolled in PROMPT between September 2014 and October 2015. Overall, 518 participants (603 genetic variants) had a result interpreted by more than one laboratory, including at least one submitted to ClinVar, and these were used as the final cohort for the current analysis. Of the 603 variants, 221 (37%) were classified as a variant of uncertain significance (VUS), 191 (32%) as pathogenic, and 34 (6%) as benign. The interpretation differed among reporting laboratories for 155 (26%). Conflicting interpretations were most frequently reported for CHEK2 and ATM, followed by RAD51C, PALB2, BARD1, NBN, and BRIP1. Among all participants, 56 of 518 (11%) had a variant with conflicting interpretations ranging from pathogenic/likely pathogenic to VUS, a discrepancy that may alter medical management. Conflicting interpretation of genetic findings from multiplex panel testing used in clinical practice is frequent and may have implications for medical management decisions