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Digital Frequency Customized Relieving Sound for Chronic Subjective Tinnitus Management: Prospective Controlled Study.
J Med Internet Res
January 2025
ENT Institute and Department of Otorhinolaryngology, Eye & ENT Hospital, Fudan University, Shanghai, China.
Background: Tinnitus is a major health issue, but currently no tinnitus elimination treatments exist for chronic subjective tinnitus. Acoustic therapy, especially personalized acoustic therapy, plays an increasingly important role in tinnitus treatment. With the application of smartphones, personalized acoustic stimulation combined with smartphone apps will be more conducive to the individualized treatment and management of patients with tinnitus.
View Article and Find Full Text PDFArtificial Intelligence-Powered Human Epidermal Growth Factor Receptor 2 and Tumor Microenvironment Analysis in Human Epidermal Growth Factor Receptor 2-Amplified Metastatic Colorectal Cancer: Exploratory Analysis of Phase II TRIUMPH Trial.
JCO Precis Oncol
January 2025
Translational Research Support Office, National Cancer Center Hospital East, Chiba, Japan.
Purpose: Human epidermal growth factor receptor 2 (HER2)-targeted therapies have shown promise in treating -amplified metastatic colorectal cancer (mCRC). Identifying optimal biomarkers for treatment decisions remains challenging. This study explores the potential of artificial intelligence (AI) in predicting treatment responses to trastuzumab plus pertuzumab (TP) in patients with -amplified mCRC from the phase II TRIUMPH trial.
View Article and Find Full Text PDFBreast Cancer Specificities of Patients With Anti-Ri Paraneoplastic Neurologic Syndromes.
Neurol Neuroimmunol Neuroinflamm
March 2025
MeLis Institute, SynatAc Team, Inserm U1314/ UMR CNRS5284, France.
Background And Objectives: Breast cancers (BCs) of patients with paraneoplastic neurologic syndromes and anti-Yo antibodies (Yo-PNS) overexpress human epidermal growth factor receptor 2 (HER2) and display genetic alterations and overexpression of the Yo-onconeural antigens. They are infiltrated by an unusual proportion of B cells. We investigated whether these features were also observed in patients with PNS and anti-Ri antibodies (Ri-PNS).
View Article and Find Full Text PDFDysregulation of the Kynurenine Pathway in Relapsing Remitting Multiple Sclerosis and Its Correlations With Progressive Neurodegeneration.
Neurol Neuroimmunol Neuroinflamm
March 2025
Macquarie Medical School, Faculty of Medicine, Health and Human Sciences, Macquarie University, Sydney.
Background And Objectives: Despite the absence of acute lesion activity in multiple sclerosis (MS), chronic neurodegeneration continues to progress, and a potential underlying mechanism could be the kynurenine pathway (KP). Prolonged activation of the KP from chronic inflammation is known to exacerbate the progression of neurodegenerative diseases through the production of neurotoxic metabolites. Among the 8 KP metabolites, six of them, namely kynurenine (KYN), 3-hydroxylkynurenine (3HK), anthranilic acid (AA), kynurenic acid (KYNA), and quinolinic acid (QUIN), have been associated with neurodegeneration.
View Article and Find Full Text PDFSquamocin Suppresses Tumor Growth through Triggering an Endoplasmic Reticulum Stress-Associated Degradation of EZH2/MYC Axis.
Adv Sci (Weinh)
January 2025
School of Laboratory Medicine and Biotechnology, Southern Medical University, Guangzhou, 510515, China.
Despite substantial advances in the antitumor effects of annonaceous acetogenins (ACGs), the absence of a defined biological action mechanism remains a major barrier to their clinical application. Here, it is found that squamocin effectively depletes both EZH2 and MYC in multiple cancer cell lines, including head and neck squamous cell carcinoma, and gastric and colorectal cancer, demonstrating potent efficacy in suppressing these in vivo tumor models. Through the combination of surface plasmon resonance (SPR), differential scanning fluorimetry (DSF), and cellular thermal shift assay (CETSA), heat shock protein 90α (HSP90α) is identified as the direct binding target of squamocin.
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