Machine Learning Analysis of Gaze Data for Enhanced Precision in Diagnosing Oral Mucosal Diseases

Uchida S., Hiraoka S.I., Kawamura K., et al. Machine Learning Analysis of Gaze Data for Enhanced Precision in Diagnosing Oral Mucosal Diseases. Journal of Clinical Medicine 13, 136 (2024); https://doi.org/10.3390/jcm13010136.The diagnosis of oral mucosal diseases is a significant challenge due to their diverse differential characteristics. Risk assessment of lesions by visual examination is a complex process due to the lack of definitive guidelines. This study aimed to improve this process by creating a diagnostic algorithm using gaze data acquired during oral mucosal disease examinations. A total of 78 dentists were included in this study. Tobii Pro Nano® (Tobii Technology) was used to acquire gaze data during clinical photographic visual examinations. Advanced analysis tools such as support vector machines and heatmaps were used to visualize the gazing tendencies of a group of skilled oral surgeons, focusing on the number of gazes per region and the gazing time ratios. The preliminary findings showed the possibility of visualizing gazing tendencies and identifying areas of importance for diagnosis. The classification of intraoral photographs based on gross features revealed the existence of an optimal examination method for each category and diagnostically significant areas. This novel approach to analyzing gaze data has the potential to refine diagnostic techniques and increase both accuracy and efficiency

Error-Prone Translesion DNA Synthesis by Escherichia coli DNA Polymerase IV (DinB) on Templates Containing 1,2-dihydro-2-oxoadenine

Escherichia coli DNA polymerase IV (Pol IV) is involved in bypass replication of damaged bases in DNA. Reactive oxygen species (ROS) are generated continuously during normal metabolism and as a result of exogenous stress such as ionizing radiation. ROS induce various kinds of base damage in DNA. It is important to examine whether Pol IV is able to bypass oxidatively damaged bases. In this study, recombinant Pol IV was incubated with oligonucleotides containing thymine glycol (dTg), 5-formyluracil (5-fodU), 5-hydroxymethyluracil (5-hmdU), 7,8-dihydro-8-oxoguanine (8-oxodG) and 1,2-dihydro-2-oxoadenine (2-oxodA). Primer extension assays revealed that Pol IV preferred to insert dATP opposite 5-fodU and 5-hmdU, while it inefficiently inserted nucleotides opposite dTg. Pol IV inserted dCTP and dATP opposite 8-oxodG, while the ability was low. It inserted dCTP more effectively than dTTP opposite 2-oxodA. Pol IV's ability to bypass these lesions decreased in the order: 2-oxodA > 5-fodU~5-hmdU > 8-oxodG > dTg. The fact that Pol IV preferred to insert dCTP opposite 2-oxodA suggests the mutagenic potential of 2-oxodA leading to A:T→G:C transitions. Hydrogen peroxide caused an ~2-fold increase in A:T→G:C mutations in E. coli, while the increase was significantly greater in E. coli overexpressing Pol IV. These results indicate that Pol IV may be involved in ROS-enhanced A:T→G:C mutations

Repression of interleukin-4 in T helper type 1 cells by Runx/Cbfβ binding to the Il4 silencer

Interferon γ (IFNγ) is the hallmark cytokine produced by T helper type 1 (Th1) cells, whereas interleukin (IL)-4 is the hallmark cytokine produced by Th2 cells. Although previous studies have revealed the roles of cytokine signaling and of transcription factors during differentiation of Th1 or Th2 cells, it is unclear how the exclusive expression pattern of each hallmark cytokine is established. The DNaseI hypersensitivity site IV within the mouse Il4 locus plays an important role in the repression of Il4 expression in Th1 cells, and it has been named the Il4 silencer. Using Cbfβ- or Runx3-deficient T cells, we show that loss of Runx complex function results in derepression of IL-4 in Th1 cells. Binding of Runx complexes to the Il4 silencer was detected in naive CD4+ T cells and Th1 cells, but not in Th2 cells. Furthermore, enforced expression of GATA-3 in Th1 cells inhibited binding of Runx complexes to the Il4 silencer. Interestingly, T cell–specific inactivation of the Cbfβ gene in mice led to elevated serum immunoglobulin E and airway infiltration. These results demonstrate critical roles of Runx complexes in regulating immune responses, at least in part, through the repression of the Il4 gene

Disease-Free Interval Length Correlates to Prognosis of Patients Who Underwent Metastasectomy for Esophageal Lung Metastases

BackgroundPulmonary metastasectomy is a standard method for treatment of selected pulmonary metastases cases. Nevertheless, because prognosis for patients with lung metastases from esophageal cancer who have undergone pulmonary metastasectomy is poor, candidates for this method of treatment are rare. Therefore, the efficacy of surgical treatment for pulmonary metastatic lesions from esophageal cancer has not been thoroughly examined.MethodsBetween March 1984 and May 2006, 57 patients underwent resection of pulmonary metastases from primary esophageal cancer. These cases were registered in the database developed by the Metastatic Lung Tumor Study Group of Japan and were retrospectively reviewed from the registry. After excluding eight cases because of missing information, we reviewed the remaining 49 cases and examined the prognostic factors for pulmonary metastasectomy for metastases from esophageal cancer.ResultsThere were no perioperative deaths. After pulmonary metastasectomy, disease recurred in 16 (33%) of the 49 patients. The overall 5-year survival was 29.6%. Median survival time was 18 months. The survival of patients with a disease-free interval (DFI) less than 12 months was significantly lower than patients with a DFI greater than 12 months. Through multivariate analysis, we identified DFI as a clinical factor significantly related to overall survival (p = 0.04).ConclusionsWe identified that patients with a DFI less than 12 months who underwent pulmonary metastasectomy for metastases from esophageal cancer had a worse prognosis. Pulmonary metastasectomy for esophageal cancer should be considered for selected patients with a DFI ≥12 months

Concentrated Ambient Particles Alter Myocardial Blood Flow During Acute Ischemia in Conscious Canines

Background: Experimental and observational studies have demonstrated that short-term exposure to ambient particulate matter (PM) exacerbates myocardial ischemia. Objectives: We conducted this study to investigate the effects of concentrated ambient particles (CAPs) on myocardial blood flow during myocardial ischemia in chronically instrumented conscious canines. Methods: Eleven canines were instrumented with a balloon occluder around the left anterior descending coronary artery and catheters for determination of myocardial blood flow using fluorescent microspheres. Telemetric electrocardiographic and blood pressure monitoring was available for four of these animals. After recovery, we exposed animals by inhalation to 5 hr of either filtered air or CAPs (mean concentration ± SD, 349.0 ± 282.6 μg/m$^{3}$) in a crossover protocol. We determined myocardial blood flow during a 5-min coronary artery occlusion immediately after each exposure. Data were analyzed using mixed models for repeated measures. The primary analysis was based on four canines that completed the protocol. Results: CAPs exposure decreased total myocardial blood flow during coronary artery occlusion by 0.12 mL/min/g (p < 0.001) and was accompanied by a 13% (p < 0.001) increase in coronary vascular resistance. Rate–pressure product, an index of myocardial oxygen demand, did not differ by exposure (p = 0.90). CAPs effects on myocardial blood flow were significantly more pronounced in myocardium within or near the ischemic zone versus more remote myocardium (p interaction < 0.001). Conclusions: These results suggest that PM exacerbates myocardial ischemia by increased coronary vascular resistance and decreased myocardial perfusion. Further studies are needed to elucidate the mechanism of these effects