Publications by authors named "A Kitani"
Background: Although interactions between amyloid-beta and tau proteins have been implicated in Alzheimer's disease (AD), the precise mechanisms by which these interactions contribute to disease progression are not yet fully understood. Moreover, despite the growing application of deep learning in various biomedical fields, its application in integrating networks to analyze disease mechanisms in AD research remains limited. In this study, we employed BIONIC, a deep learning-based network integration method, to integrate proteomics and protein-protein interaction data, with an aim to uncover factors that moderate the effects of the Aβ-tau interaction on mild cognitive impairment (MCI) and early-stage AD.
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- Alzheimer's disease research focuses on cognitive resilience (CR), which allows some individuals to maintain cognitive function despite typical AD brain changes like amyloid plaques and neurofibrillary tangles.
- To investigate CR, the study compared various machine learning models using RNA-seq data from two cohorts, finding that support vector regression (SVR) performed the best in predicting CR scores.
- The study introduced a tool called the resilience gene analyzer (REGA) that uses SHAP scores to visualize and interpret the genetic contributions to cognitive resilience, which is freely accessible online.
Article Synopsis
- - This study found that patient satisfaction and quality of life during dialysis treatment varied significantly among three different centers, indicating that local factors might affect these outcomes.
- - Although one center with better dialysis measures reported lower patient satisfaction, the relationship between satisfaction and quality of care remains complex and requires further research.
- - The findings suggest that patient demographics and experiences significantly influence satisfaction, which does not always align with clinical quality metrics like Kt/V, highlighting the need for a more comprehensive understanding of patient-centered care.
Article Synopsis
- The studies analyze how mutations in the NOD2 gene contribute to Blau syndrome by disrupting its normal signaling pathways, particularly affecting NF-κB activation and cross-regulation of innate immune responses.
- Key findings indicate that Blau-associated NOD2 mutations lead to impaired signaling, causing a loss of NOD2's ability to regulate inflammation effectively, which is vital in both Blau syndrome and Crohn's disease.
- The research suggests that the malfunctioning NOD2 signaling may be due to insufficient activation of the regulatory factor IRF4, which exacerbates inflammation in Blau syndrome.