Purpose: We aimed to comprehensively analyze the immune cell and stromal components of tumor microenvironment at the single-cell level and identify tumor heterogeneity among the major top-derived oncogene mutations in non-small cell lung cancer (NSCLC) using single-cell RNA sequencing (scRNA-seq) data. Materials and Methods: The scRNA-seq dataset utilized in this study comprised 64369 primary tumor tissue cells from 21 NSCLC patients, focusing on mutations in EGFR, ALK, BRAF, KRAS, TP53, and the wild-type. Results: Tumor immune microenvironment (TIM) analysis revealed differential immune responses across NSCLC mutation subtypes. TIM analysis revealed different immune responses across the mutation subtypes. Two mutation clusters emerged: KRAS, TP53, and EGFR+TP53 mutations (MC1); and EGFR, BRAF, and ALK mutations (MC2). MC1 showed higher tertiary lymphoid structures signature scores and enriched populations of C2-T-IL7R, C3-T/NK-CXCL4, C9-T/NK-NKG, and C1-B-MS4A1 clusters than cluster 2. Conversely, MC2 cells exhibited higher expression levels of TNF, IL1B, and chemokines linked to alternative immune pathways. Remarkably, co-occurring EGFR and TP53 mutations were grouped as MC1. EGFR+TP53 mutations showed upregulation of peptide synthesis and higher synthetic processes, as well as differences in myeloid and T/NK cells compared to EGFR mutations. In T/NK cells, EGFR+TP53 mutations showed a higher expression of features related to cell activity and differentiation, whereas EGFR mutations showed the opposite. Conclusion Our research indicates a close association between mutation types and tumor microenvironment in NSCLC, offering insights into personalized approaches for cancer diagnosis and treatment.

Purpose: We aimed to comprehensively analyze the immune cell and stromal components of tumor microenvironment at the single-cell level and identify tumor heterogeneity among the major top-derived oncogene mutations in non-small cell lung cancer (NSCLC) using single-cell RNA sequencing (scRNA-seq) data. Materials and Methods: The scRNA-seq dataset utilized in this study comprised 64369 primary tumor tissue cells from 21 NSCLC patients, focusing on mutations in EGFR, ALK, BRAF, KRAS, TP53, and the wild-type. Results: Tumor immune microenvironment (TIM) analysis revealed differential immune responses across NSCLC mutation subtypes. TIM analysis revealed different immune responses across the mutation subtypes. Two mutation clusters emerged: KRAS, TP53, and EGFR+TP53 mutations (MC1); and EGFR, BRAF, and ALK mutations (MC2). MC1 showed higher tertiary lymphoid structures signature scores and enriched populations of C2-T-IL7R, C3-T/NK-CXCL4, C9-T/NK-NKG, and C1-B-MS4A1 clusters than cluster 2. Conversely, MC2 cells exhibited higher expression levels of TNF, IL1B, and chemokines linked to alternative immune pathways. Remarkably, co-occurring EGFR and TP53 mutations were grouped as MC1. EGFR+TP53 mutations showed upregulation of peptide synthesis and higher synthetic processes, as well as differences in myeloid and T/NK cells compared to EGFR mutations. In T/NK cells, EGFR+TP53 mutations showed a higher expression of features related to cell activity and differentiation, whereas EGFR mutations showed the opposite. Conclusion Our research indicates a close association between mutation types and tumor microenvironment in NSCLC, offering insights into personalized approaches for cancer diagnosis and treatment.

Purpose: We aimed to comprehensively analyze the immune cell and stromal components of tumor microenvironment at the single-cell level and identify tumor heterogeneity among the major top-derived oncogene mutations in non-small cell lung cancer (NSCLC) using single-cell RNA sequencing (scRNA-seq) data. Materials and Methods: The scRNA-seq dataset utilized in this study comprised 64369 primary tumor tissue cells from 21 NSCLC patients, focusing on mutations in EGFR, ALK, BRAF, KRAS, TP53, and the wild-type. Results: Tumor immune microenvironment (TIM) analysis revealed differential immune responses across NSCLC mutation subtypes. TIM analysis revealed different immune responses across the mutation subtypes. Two mutation clusters emerged: KRAS, TP53, and EGFR+TP53 mutations (MC1); and EGFR, BRAF, and ALK mutations (MC2). MC1 showed higher tertiary lymphoid structures signature scores and enriched populations of C2-T-IL7R, C3-T/NK-CXCL4, C9-T/NK-NKG, and C1-B-MS4A1 clusters than cluster 2. Conversely, MC2 cells exhibited higher expression levels of TNF, IL1B, and chemokines linked to alternative immune pathways. Remarkably, co-occurring EGFR and TP53 mutations were grouped as MC1. EGFR+TP53 mutations showed upregulation of peptide synthesis and higher synthetic processes, as well as differences in myeloid and T/NK cells compared to EGFR mutations. In T/NK cells, EGFR+TP53 mutations showed a higher expression of features related to cell activity and differentiation, whereas EGFR mutations showed the opposite. Conclusion Our research indicates a close association between mutation types and tumor microenvironment in NSCLC, offering insights into personalized approaches for cancer diagnosis and treatment.

Purpose: We aimed to comprehensively analyze the immune cell and stromal components of tumor microenvironment at the single-cell level and identify tumor heterogeneity among the major top-derived oncogene mutations in non-small cell lung cancer (NSCLC) using single-cell RNA sequencing (scRNA-seq) data. Materials and Methods: The scRNA-seq dataset utilized in this study comprised 64369 primary tumor tissue cells from 21 NSCLC patients, focusing on mutations in EGFR, ALK, BRAF, KRAS, TP53, and the wild-type. Results: Tumor immune microenvironment (TIM) analysis revealed differential immune responses across NSCLC mutation subtypes. TIM analysis revealed different immune responses across the mutation subtypes. Two mutation clusters emerged: KRAS, TP53, and EGFR+TP53 mutations (MC1); and EGFR, BRAF, and ALK mutations (MC2). MC1 showed higher tertiary lymphoid structures signature scores and enriched populations of C2-T-IL7R, C3-T/NK-CXCL4, C9-T/NK-NKG, and C1-B-MS4A1 clusters than cluster 2. Conversely, MC2 cells exhibited higher expression levels of TNF, IL1B, and chemokines linked to alternative immune pathways. Remarkably, co-occurring EGFR and TP53 mutations were grouped as MC1. EGFR+TP53 mutations showed upregulation of peptide synthesis and higher synthetic processes, as well as differences in myeloid and T/NK cells compared to EGFR mutations. In T/NK cells, EGFR+TP53 mutations showed a higher expression of features related to cell activity and differentiation, whereas EGFR mutations showed the opposite. Conclusion Our research indicates a close association between mutation types and tumor microenvironment in NSCLC, offering insights into personalized approaches for cancer diagnosis and treatment.

Purpose: We aimed to comprehensively analyze the immune cell and stromal components of tumor microenvironment at the single-cell level and identify tumor heterogeneity among the major top-derived oncogene mutations in non-small cell lung cancer (NSCLC) using single-cell RNA sequencing (scRNA-seq) data. Materials and Methods: The scRNA-seq dataset utilized in this study comprised 64369 primary tumor tissue cells from 21 NSCLC patients, focusing on mutations in EGFR, ALK, BRAF, KRAS, TP53, and the wild-type. Results: Tumor immune microenvironment (TIM) analysis revealed differential immune responses across NSCLC mutation subtypes. TIM analysis revealed different immune responses across the mutation subtypes. Two mutation clusters emerged: KRAS, TP53, and EGFR+TP53 mutations (MC1); and EGFR, BRAF, and ALK mutations (MC2). MC1 showed higher tertiary lymphoid structures signature scores and enriched populations of C2-T-IL7R, C3-T/NK-CXCL4, C9-T/NK-NKG, and C1-B-MS4A1 clusters than cluster 2. Conversely, MC2 cells exhibited higher expression levels of TNF, IL1B, and chemokines linked to alternative immune pathways. Remarkably, co-occurring EGFR and TP53 mutations were grouped as MC1. EGFR+TP53 mutations showed upregulation of peptide synthesis and higher synthetic processes, as well as differences in myeloid and T/NK cells compared to EGFR mutations. In T/NK cells, EGFR+TP53 mutations showed a higher expression of features related to cell activity and differentiation, whereas EGFR mutations showed the opposite. Conclusion Our research indicates a close association between mutation types and tumor microenvironment in NSCLC, offering insights into personalized approaches for cancer diagnosis and treatment.

Purpose: By utilizing both protein and mRNA expression patterns, we can identify more detailed and diverse immune cells, providing insights into understanding the complex immune landscape in cancer ecosystems. Materials and Methods: This study was performed by obtaining publicly available Cellular Indexing of Transcriptomes and Epitopes by Sequencing (CITE-seq) data of peripheral blood mononuclear cells (PBMCs) from the Gene Expression Omnibus database. A total of 94674 total cells were analyzed, of which 32412 were T cells. There were 228 protein features and 16262 mRNA features in the data.The Seurat package was used for quality control and preprocessing, principal component analysis was performed, and Uniform Manifold Approximation and Projection was used to visualize the clusters. Protein and mRNA levels in the CITE-seq were analyzed. Results: We observed that a subset of T cells in the clusters generated at the protein level divided better. By identifying mRNA markers that were highly correlated with the CD4 and CD8 proteins and cross-validating CD26 and CD99 markers using flow cytometry, we found that CD4 + and CD8+ T cells were better discriminated in PBMCs. Weighted Nearest Neighbor clustering results identified a previously unobserved T cell subset. Conclusion In this study, we used CITE-seq data to confirm that protein expression patterns could be used to identify cells more precisely. These findings will improve our understanding of the heterogeneity of immune cells in the future and provide valuable insights into the complexity of the immune response in health and disease.

Lance-Adams syndrome (LAS) is a rare neurological disorder that may occur after cardiopulmonary resuscitation. The LAS is usually caused by hypoxic changes.Neuroimaging studies show that the brain pathology of LAS patients is not uniform, and the pathophysiology of the myoclonus can vary from patient to patient. Our case study contributes to this etiological heterogeneity by neuroimaging and transcranial magnetic stimulation (TMS). In patients with rare brain conditions such as LAS, a combination of brain stimulation methods, such as TMS, and diffusion tensor imaging can provide insights into this condition's pathophysiology. These insights can facilitate the development of more effective therapies.

Objective: To verify the pharyngeal width at rest as a measurement that could be used to assess changes in the degree of dysphagia over time in stroke patients. Methods: In a cohort of stroke patients, we performed serial measurements of the pharyngeal width at the midpoints of the second (C2) and third (C3) cervical vertebral bodies using lateral neck X-rays while the patients were at rest. The JOSCYL width, a parameter named after the first initial of each developers’ surname and defined as the average value of the upper and lower pharyngeal widths, was used to formulate the JOSCYL scale, which was calculated as the JOSCYL width × 100eck circumference. All patients also underwent serial videofluoroscopic swallowing studies (VFSSs). The Spearman correlation analysis was used to detect correlations between the serial VFSS results, JOSCYL widths, and JOSCYL scale values. Results: Over time, we observed significant positive and negative correlations of change in the JOSCYL width and scale with changes in the Penetration-Aspiration Scale and the Dysphagia Outcome and Severity Scale scores, respectively. Conclusion The JOSCYL width and JOSCYL scale clearly reflected changes in dysphagia in stroke patients over time. These parameters may provide an easier method for evaluating whether post-stroke dysphagia has been alleviated.

Traumatic brain injury is a main cause of long-term neurological disability, and many patients suffer from cognitive impairment for a lengthy period. Cognitive impairment is a fatal malady to that limits active rehabilitation, and functional recovery in patients with traumatic brain injury. In severe cases, it is impossible to assess cognitive function precisely, and severe cognitive impairment makes it difficult to establish a rehabilitation plan, as well as evaluate the course of rehabilitation. Evaluation of cognitive function is essential for establishing a rehabilitation plan, as well as evaluating the course of rehabilitation. We report a case of the analysis of electroencephalography with global synchronization index and low-resolution brain electromagnetic tomography applied, for evaluation of cognitive function that was difficult with conventional tests, due to severe cognitive impairment in a 77-year-old male patient that experienced traumatic brain injury.
Aged ; Brain ; Brain Injuries ; Cognition Disorders ; Cognition ; Electroencephalography ; Humans ; Magnets ; Male ; Rehabilitation

OBJECTIVE: To develop a new tool for aspiration risk prediction based on pharyngeal width at rest in older adults with symptoms of aspiration. METHODS: Lateral cervical spine roentgenograms were obtained from 33 older adult patients who complained of dysphagia and from 33 healthy, age-matched controls. Pharyngeal width at rest was measured at two points. We named the average of these two pharyngeal widths ‘JOSCYL Width’, calculated ‘JOSCYL Scale’, and compared these parameters between dysphagia and control groups. Correlations of individual JOSCYL Width and JOSCYL Scale, with Penetration Aspiration Scale (PAS) and Dysphagia Outcome and Severity Scale (DOSS) scores were analyzed for the dysphagia group. To determine optimal cutoff points for predicting aspiration, a receiver operating characteristic curve analysis was performed on JOSCYL Width and JOSCYL Scale. RESULTS: Both JOSCYL Width and JOSCYL Scale of the dysphagia group were larger than those of the control group (p<0.001). The correlation between JOSCYL Width and severity of dysphagia was significant for the dysphagia group (PAS p=0.007; DOSS p=0.012). The correlation between JOSCYL Scale and the severity of dysphagia was also significant for the dysphagia group (PAS p=0.009; DOSS p=0.011). Optimal cutoffs for JOSCYL Width and JOSCYL Scale for predicting aspiration were 20.0 mm and 5.9, respectively. CONCLUSION: JOSCYL Width and JOSCYL Scale can be new indicators for predicting aspiration in older adults. They are both precise and easy to use.
Adult ; Aged ; Deglutition Disorders ; Dioctyl Sulfosuccinic Acid ; Humans ; Pharynx ; ROC Curve ; Spine