73 research outputs found

    UWB-based early breast cancer existence prediction using artificial intelligence for large data set

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    Breast cancer is the most often identified cancer among women and the main reason for cancer-related deaths worldwide. The most effective methods for controlling and treating this disease through breast screening and emerging detection techniques. This paper proposes an intelligent classifier for the early detection of breast cancer using a larger dataset since there is limited researcher focus on that for better analytic models. To ensure that the issue is tackled, this project proposes an intelligent classifier using the Probabilistic Neural Network (PNN) with a statistical feature model that uses a more significant size of data set to analyze the prediction of the presence of breast cancer using Ultra Wideband (UWB). The proposed method is able to detect breast cancer existence with an average accuracy of 98.67%. The proposed module might become a potential user-friendly technology for early breast cancer detection in domestic use

    Existing and emerging breast cancer detection technologies and its challenges: a review

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    Breast cancer is the most leading cancer occurring in women and is a significant factor in female mortality. Early diagnosis of breast cancer with Artificial Intelligent (AI) developments for breast cancer detection can lead to a proper treatment to affected patients as early as possible that eventually help reduce the women mortality rate. Reliability issues limit the current clinical detection techniques, such as Ultra-Sound, Mammography, and Magnetic Resonance Imaging (MRI) from screening images for precise elucidation. The capability to detect a tumor in early diagnosis, expensive, relatively long waiting time due to pandemic and painful procedure for a patient to perform. This article aims to review breast cancer screening methods and recent technological advancements systematically. In addition, this paper intends to explore the progression and challenges of AI in breast cancer detection. The next state of the art between image and signal processing will be presented, and their performance is compared. This review will facilitate the researcher to insight the view of breast cancer detection technologies advancement and its challenges

    Optimized intelligent classifier for early breast cancer detection using ultra-wide band transceiver

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    Breast cancer is the most common cancer diagnosed in women and the leading cause of cancer-related deaths among women worldwide. The death rate is high because of the lack of early signs. Due to the absence of a cure, immediate treatment is necessary to remove the cancerous cells and prolong life. For early breast cancer detection, it is crucial to propose a robust intelligent classifier with statistical feature analysis that considers parameter existence, size, and location. This paper proposes a novel Multi-Stage Feature Selection with Binary Particle Swarm Optimization (MSFS–BPSO) using Ultra-Wideband (UWB). A collection of 39,000 data samples from non-tumor and with tumor sizes ranging from 2 to 7 mm was created using realistic tissue-like dielectric materials. Subsequently, the tumor models were inserted into the heterogeneous breast phantom. The breast phantom with tumors was imaged and represented in both time and frequency domains using the UWB signal. Consequently, the dataset was fed into the MSFS–BPSO framework and started with feature normalization before it was reduced using feature dimension reduction. Then, the feature selection (based on time/frequency domain) using seven different classifiers selected the frequency domain compared to the time domain and continued to perform feature extraction. Feature selection using Analysis of Variance (ANOVA) is able to distinguish between class-correlated data. Finally, the optimum feature subset was selected using a Probabilistic Neural Network (PNN) classifier with the Binary Particle Swarm Optimization (BPSO) method. The research findings found that the MSFS–BPSO method has increased classification accuracy up to 96.3% and given good dependability even when employing an enormous data sample

    The Human Phenotype Ontology in 2024: phenotypes around the world.

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    The Human Phenotype Ontology (HPO) is a widely used resource that comprehensively organizes and defines the phenotypic features of human disease, enabling computational inference and supporting genomic and phenotypic analyses through semantic similarity and machine learning algorithms. The HPO has widespread applications in clinical diagnostics and translational research, including genomic diagnostics, gene-disease discovery, and cohort analytics. In recent years, groups around the world have developed translations of the HPO from English to other languages, and the HPO browser has been internationalized, allowing users to view HPO term labels and in many cases synonyms and definitions in ten languages in addition to English. Since our last report, a total of 2239 new HPO terms and 49235 new HPO annotations were developed, many in collaboration with external groups in the fields of psychiatry, arthrogryposis, immunology and cardiology. The Medical Action Ontology (MAxO) is a new effort to model treatments and other measures taken for clinical management. Finally, the HPO consortium is contributing to efforts to integrate the HPO and the GA4GH Phenopacket Schema into electronic health records (EHRs) with the goal of more standardized and computable integration of rare disease data in EHRs

    The Political Economy of Taxation: Positive and Normative Analysis when Collective Choice Matters

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    Convalescent plasma in patients admitted to hospital with COVID-19 (RECOVERY): a randomised controlled, open-label, platform trial

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    SummaryBackground Azithromycin has been proposed as a treatment for COVID-19 on the basis of its immunomodulatoryactions. We aimed to evaluate the safety and efficacy of azithromycin in patients admitted to hospital with COVID-19.Methods In this randomised, controlled, open-label, adaptive platform trial (Randomised Evaluation of COVID-19Therapy [RECOVERY]), several possible treatments were compared with usual care in patients admitted to hospitalwith COVID-19 in the UK. The trial is underway at 176 hospitals in the UK. Eligible and consenting patients wererandomly allocated to either usual standard of care alone or usual standard of care plus azithromycin 500 mg once perday by mouth or intravenously for 10 days or until discharge (or allocation to one of the other RECOVERY treatmentgroups). Patients were assigned via web-based simple (unstratified) randomisation with allocation concealment andwere twice as likely to be randomly assigned to usual care than to any of the active treatment groups. Participants andlocal study staff were not masked to the allocated treatment, but all others involved in the trial were masked to theoutcome data during the trial. The primary outcome was 28-day all-cause mortality, assessed in the intention-to-treatpopulation. The trial is registered with ISRCTN, 50189673, and ClinicalTrials.gov, NCT04381936.Findings Between April 7 and Nov 27, 2020, of 16 442 patients enrolled in the RECOVERY trial, 9433 (57%) wereeligible and 7763 were included in the assessment of azithromycin. The mean age of these study participants was65·3 years (SD 15·7) and approximately a third were women (2944 [38%] of 7763). 2582 patients were randomlyallocated to receive azithromycin and 5181 patients were randomly allocated to usual care alone. Overall,561 (22%) patients allocated to azithromycin and 1162 (22%) patients allocated to usual care died within 28 days(rate ratio 0·97, 95% CI 0·87–1·07; p=0·50). No significant difference was seen in duration of hospital stay (median10 days [IQR 5 to >28] vs 11 days [5 to >28]) or the proportion of patients discharged from hospital alive within 28 days(rate ratio 1·04, 95% CI 0·98–1·10; p=0·19). Among those not on invasive mechanical ventilation at baseline, nosignificant difference was seen in the proportion meeting the composite endpoint of invasive mechanical ventilationor death (risk ratio 0·95, 95% CI 0·87–1·03; p=0·24).Interpretation In patients admitted to hospital with COVID-19, azithromycin did not improve survival or otherprespecified clinical outcomes. Azithromycin use in patients admitted to hospital with COVID-19 should be restrictedto patients in whom there is a clear antimicrobial indication

    The genetics of the mood disorder spectrum:genome-wide association analyses of over 185,000 cases and 439,000 controls

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    Background Mood disorders (including major depressive disorder and bipolar disorder) affect 10-20% of the population. They range from brief, mild episodes to severe, incapacitating conditions that markedly impact lives. Despite their diagnostic distinction, multiple approaches have shown considerable sharing of risk factors across the mood disorders. Methods To clarify their shared molecular genetic basis, and to highlight disorder-specific associations, we meta-analysed data from the latest Psychiatric Genomics Consortium (PGC) genome-wide association studies of major depression (including data from 23andMe) and bipolar disorder, and an additional major depressive disorder cohort from UK Biobank (total: 185,285 cases, 439,741 controls; non-overlapping N = 609,424). Results Seventy-three loci reached genome-wide significance in the meta-analysis, including 15 that are novel for mood disorders. More genome-wide significant loci from the PGC analysis of major depression than bipolar disorder reached genome-wide significance. Genetic correlations revealed that type 2 bipolar disorder correlates strongly with recurrent and single episode major depressive disorder. Systems biology analyses highlight both similarities and differences between the mood disorders, particularly in the mouse brain cell-types implicated by the expression patterns of associated genes. The mood disorders also differ in their genetic correlation with educational attainment – positive in bipolar disorder but negative in major depressive disorder. Conclusions The mood disorders share several genetic associations, and can be combined effectively to increase variant discovery. However, we demonstrate several differences between these disorders. Analysing subtypes of major depressive disorder and bipolar disorder provides evidence for a genetic mood disorders spectrum

    Genetic Overlap Between Alzheimer’s Disease and Bipolar Disorder Implicates the MARK2 and VAC14 Genes

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    Background: Alzheimer's disease (AD) and bipolar disorder (BIP) are complex traits influenced by numerous common genetic variants, most of which remain to be detected. Clinical and epidemiological evidence suggest that AD and BIP are related. However, it is not established if this relation is of genetic origin. Here, we applied statistical methods based on the conditional false discovery rate (FDR) framework to detect genetic overlap between AD and BIP and utilized this overlap to increase the power to identify common genetic variants associated with either or both traits. Methods: We obtained genome wide association studies data from the International Genomics of Alzheimer's Project part 1 (17,008 AD cases and 37,154 controls) and the Psychiatric Genetic Consortium Bipolar Disorder Working Group (20,352 BIP cases and 31,358 controls). We used conditional QQ-plots to assess overlap in common genetic variants between AD and BIP. We exploited the genetic overlap to re-rank test-statistics for AD and BIP and improve detection of genetic variants using the conditional FDR framework. Results: Conditional QQ-plots demonstrated a polygenic overlap between AD and BIP. Using conditional FDR, we identified one novel genomic locus associated with AD, and nine novel loci associated with BIP. Further, we identified two novel loci jointly associated with AD and BIP implicating the MARK2 gene (lead SNP rs10792421, conjunctional FDR=0.030, same direction of effect) and the VAC14 gene (lead SNP rs11649476, conjunctional FDR=0.022, opposite direction of effect). Conclusions: We found polygenic overlap between AD and BIP and identified novel loci for each trait and two jointly associated loci. Further studies should examine if the shared loci implicating the MARK2 and VAC14 genes could explain parts of the shared and distinct features of AD and BIP

    Bipolar multiplex families have an increased burden of common risk variants for psychiatric disorders.

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    Multiplex families with a high prevalence of a psychiatric disorder are often examined to identify rare genetic variants with large effect sizes. In the present study, we analysed whether the risk for bipolar disorder (BD) in BD multiplex families is influenced by common genetic variants. Furthermore, we investigated whether this risk is conferred mainly by BD-specific risk variants or by variants also associated with the susceptibility to schizophrenia or major depression. In total, 395 individuals from 33 Andalusian BD multiplex families (166 BD, 78 major depressive disorder, 151 unaffected) as well as 438 subjects from an independent, BD case/control cohort (161 unrelated BD, 277 unrelated controls) were analysed. Polygenic risk scores (PRS) for BD, schizophrenia (SCZ), and major depression were calculated and compared between the cohorts. Both the familial BD cases and unaffected family members had higher PRS for all three psychiatric disorders than the independent controls, with BD and SCZ being significant after correction for multiple testing, suggesting a high baseline risk for several psychiatric disorders in the families. Moreover, familial BD cases showed significantly higher BD PRS than unaffected family members and unrelated BD cases. A plausible hypothesis is that, in multiplex families with a general increase in risk for psychiatric disease, BD development is attributable to a high burden of common variants that confer a specific risk for BD. The present analyses demonstrated that common genetic risk variants for psychiatric disorders are likely to contribute to the high incidence of affective psychiatric disorders in the multiplex families. However, the PRS explained only part of the observed phenotypic variance, and rare variants might have also contributed to disease development
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