Publications by authors named "Junichi Abe"

Aim: This study leveraged standard-of-care CT scans of patients receiving unilateral radiotherapy (RT) for early tonsillar cancer to detect volumetric changes in the carotid arteries, and determine whether there is a dose-response relationship.

Methods: Disease-free cancer survivors (>3 months since therapy and age > 18 years) treated with intensity modulated RT for early (T1-2, N0-2b) tonsillar cancer with pre- and post-therapy contrast-enhanced CT scans available were included. Patients treated with definitive surgery, bilateral RT, or additional RT before the post-RT CT scan were excluded.

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Modulating immune function is a critical strategy in cancer and atherosclerosis treatments. For cancer, boosting or maintaining the immune system is crucial to prevent tumor growth. However, in vascular disease, mitigating immune responses can decrease inflammation and slow atherosclerosis progression.

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The functional and structural integrity of the endothelium is essential for vascular homeostasis. Loss of barrier function in quiescent and migratory capacity in proliferative endothelium causes exuberant vascular permeability, a cardinal feature of many inflammatory diseases including acute lung injury (ALI). However, the signals governing these fundamental endothelial cell (EC) functions are poorly understood.

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Article Synopsis
  • Researchers aimed to create models to predict major adverse cardiovascular and cerebrovascular events (MACCE) in lung and breast cancer patients after chest radiation therapy (RT).
  • The study analyzed data from patients treated at Mayo Clinic between 2010 and 2014, identifying key risk factors and developing two predictive models: one for use before therapy (C2AD) and another following treatment (C2AD2).
  • Both models effectively categorized patients into low, intermediate, and high-risk groups for post-RT MACCE, showing significant correlations with patient survival outcomes and making them useful tools for clinical decisions.
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Radiation therapy (RT) is a cornerstone in cancer treatment (used in 50% of cases), yet challenges persist because damage to normal tissue through direct impact of radiation or bystander effects is inevitable. Injury of macrovessels by RT manifests as obstructive disease, which is akin to atherosclerotic disease. Historically observed in coronary arteries of patients treated for breast cancer and lymphoma, it also affects patients receiving contemporary therapy for lung and chest cancers.

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Purpose Of Review: Major Depressive Disorder (MDD) is characterized by persistent symptoms such as fatigue, loss of interest in activities, feelings of sadness and worthlessness. MDD often coexist with cardiovascular disease (CVD), yet the precise link between these conditions remains unclear. This review explores factors underlying the development of MDD and CVD, including genetic, epigenetic, platelet activation, inflammation, hypothalamic-pituitary-adrenal (HPA) axis activation, endothelial cell (EC) dysfunction, and blood-brain barrier (BBB) disruption.

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Exposure to cancer therapies is associated with an increased risk of clonal hematopoiesis (CH). The objective of our study was to investigate the genesis and evolution of CH after cancer therapy. In this prospective study, we undertook error-corrected duplex DNA sequencing in blood samples collected before and at 2 time points after chemoradiation in patients with esophageal or lung cancer recruited from 2013 to 2018.

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  • The study investigates radiation induced carotid artery disease (RICAD) in survivors of oropharyngeal cancer, focusing on changes in carotid artery volume after unilateral radiotherapy for early tonsillar cancer.
  • Researchers analyzed pre- and post-therapy CT scans from disease-free patients to assess the effects of differing radiation doses on carotid artery volumes, aiming to identify early imaging markers for RICAD.
  • Results from 46 patients revealed significant volume decrease in irradiated carotid arteries but no clear dose-response relationship, suggesting the need for further research on factors influencing carotid artery changes post-radiation therapy.
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Background: Traf2 and Nck-interacting kinase (TNIK) is known for its regulatory role in various processes within cancer cells. However, its role within endothelial cells (ECs) has remained relatively unexplored.

Methods: Leveraging RNA-seq data and Ingenuity Pathway Analysis (IPA), we probed the potential impact of TNIK depletion on ECs.

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  • Cardio-oncology and emergency medicine work together closely since cancer patients often face cardiac issues that need emergency treatment, especially those receiving immune checkpoint inhibitors (ICIs) for head and neck cancer (HNC).
  • A study analyzed cardiovascular problems in 610 HNC patients treated with ICIs from April 2016 to December 2020, finding that 25.7% had pre-existing cardiovascular disease (CVD) and 31.5% of those without it developed new CVD diagnoses post-treatment; the most common was tachyarrhythmias.
  • The research shows that myocarditis and tachyarrhythmias required visits to the emergency department, indicating that the cardiovascular side effects of ICIs are significant and not yet
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The histone H3 lysine 4 (H3K4) methyltransferase KMT2D (also called MLL4) is one of the most frequently mutated epigenetic modifiers in medulloblastoma (MB) and other types of cancer. Notably, heterozygous loss of KMT2D is prevalent in MB and other cancer types. However, what role heterozygous KMT2D loss plays in tumorigenesis has not been well characterized.

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Article Synopsis
  • * CVD risk may increase for cancer survivors due to long-term complications from cancer and its treatments, with cellular senescence playing a significant role in this relationship.
  • * The article seeks to explore the mechanisms connecting premature cellular aging to CVD in cancer survivors and suggests future research directions for a deeper understanding of this complex issue.
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  • SENP2 is a crucial protein that helps protect against atherosclerosis; however, when phosphorylated at T368 under disturbed flow, it loses its function and leads to endothelial cell activation.
  • Researchers developed a specific antibody and used CRISPR/Cas9 to create mice with a mutation at the S344 phosphorylation site of SENP2 and studied its effects on endothelial cell behavior under different flow conditions.
  • The study found that normal flow (L-flow) causes phosphorylation of SENP2 at S344, which inhibits harmful endothelial cell activation, while mutations in this site lead to increased inflammation, migration, and cell proliferation, making atherosclerosis worse, especially in female mice.
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This study aimed to prepare anti- inclusion complexes (ICs) of Hinoki essential oil (HEO) with β-cyclodextrin (β-CD) and 2-hydroxypropyl-β-cyclodextrin (2-HP-β-CD). An ultrasound-assisted kneading method was applied for the complexation for the first time. The recovery yield, embedding fraction and loading capacity of the HEO/β-CD ICs were 92.

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Cancer survivors undergone treatment face an increased risk of developing atherosclerotic cardiovascular disease (CVD), yet the underlying mechanisms remain elusive. Recent studies have revealed that chemotherapy can drive senescent cancer cells to acquire a proliferative phenotype known as senescence-associated stemness (SAS). These SAS cells exhibit enhanced growth and resistance to cancer treatment, thereby contributing to disease progression.

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Exercise changes the tumor microenvironment by remodeling blood vessels and increasing infiltration by cytotoxic immune cells. The mechanisms driving these changes remain unclear. Herein, we demonstrate that exercise normalizes tumor vasculature and upregulates endothelial expression of VCAM1 in YUMMER 1.

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Background: ERK5 (extracellular signal-regulated kinase 5) is a dual kinase transcription factor containing an N-terminal kinase domain and a C-terminal transcriptional activation domain. Many ERK5 kinase inhibitors have been developed and tested to treat cancer and inflammatory diseases. However, recent data have raised questions about the role of the catalytic activity of ERK5 in proliferation and inflammation.

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Cellular metabolic dysregulation is a consequence of SARS-CoV-2 infection that is a key determinant of disease severity. However, how metabolic perturbations influence immunological function during COVID-19 remains unclear. Here, using a combination of high-dimensional flow cytometry, cutting-edge single-cell metabolomics, and re-analysis of single-cell transcriptomic data, we demonstrate a global hypoxia-linked metabolic switch from fatty acid oxidation and mitochondrial respiration towards anaerobic, glucose-dependent metabolism in CD8Tc, NKT, and epithelial cells.

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RNA velocity provides an approach for inferring cellular state transitions from single-cell RNA sequencing (scRNA-seq) data. Conventional RNA velocity models infer universal kinetics from all cells in an scRNA-seq experiment, resulting in unpredictable performance in experiments with multi-stage and/or multi-lineage transition of cell states where the assumption of the same kinetic rates for all cells no longer holds. Here we present cellDancer, a scalable deep neural network that locally infers velocity for each cell from its neighbors and then relays a series of local velocities to provide single-cell resolution inference of velocity kinetics.

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Radiation therapy (RT) to the chest increases the patients' risk of cardiovascular disease (CVD). A complete understanding of the mechanisms by which RT induces CVD could lead to specific preventive, therapeutic approaches. It is becoming evident that both genotoxic chemotherapy agents and radiation induce mitochondrial dysfunction and cellular senescence.

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We have shown that membrane-associated guanylate kinase with inverted domain structure-1 (MAGI1), a scaffold protein with six PSD95/DiscLarge/ZO-1 (PDZ) domains, is involved in the regulation of endothelial cell (EC) activation and atherogenesis in mice. In addition to causing acute respiratory disease, influenza A virus (IAV) infection plays an important role in atherogenesis and triggers acute coronary syndromes and fatal myocardial infarction. Therefore, the aim of this study is to investigate the function and regulation of MAGI1 in IAV-induced EC activation.

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Article Synopsis
  • - Numerous studies show that cancer treatments can cause premature cell aging, leading to age-related diseases, primarily through a process called senescence-associated secretory phenotype (SASP) triggered by telomere damage.
  • - Telomere dysfunction from cancer therapies can lead to lasting cellular issues such as mitochondrial dysfunction and increased reactive oxygen species, contributing to the side effects experienced by cancer survivors.
  • - The interaction between cellular mechanisms involving p90 ribosomal S6 kinase and ERK5 signaling is crucial in connecting telomere damage, mitochondrial problems, persistent SASP, and the risk of developing cardiovascular diseases in individuals who have survived cancer.
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This study aims to develop an antibacterial agent that can be used for food packaging. Essential oils of Thunb., a well-known medical herb, were extracted by two methods: multi-solvent consecutive extraction method and single ethanol extraction with a pre-heating method.

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