Kanae Mure

Introduction: The accessory navicular (AN) is an accessory ossicle located on the medial side of the navicular bone and is often associated with sports-related overuse injuries during adolescence. However, little is known about the natural history of AN. This study aimed to clarify the natural course of AN, including symptomatic cases, in children through a longitudinal epidemiological investigation. Methods: Data from the KID Locomo Study, a prospective cohort study aimed at elucidating musculoskeletal disorders in childhood, were used. Of the 834 children recruited in the 2022 baseline survey, 66 children (109 feet) aged 11–13 years with AN were enrolled in this 2-year longitudinal analysis. The presence of AN was assessed using ultrasonography. Data on sex, age, height, weight, presence of pain at the AN site, laterality, flatfoot (based on footprint analysis), and participation in athletic clubs were collected. The natural history of AN, including painful presentations, was evaluated. Multivariable logistic regression analysis was performed to identify risk factors for non-fusion of the AN with the navicular bone. Results: Among the 109 feet with AN at baseline, 38 (34.9%) demonstrated fusion with the navicular bone at the 2-year follow-up. Of the 21 feet with painful AN at baseline, pain had resolved in 15 (71.4%) after 2 years. Multivariable logistic regression analysis revealed that female sex (odds ratio: 3.00; 95% confidence interval: 1.26–7.45; p = 0.01) and higher body mass index (BMI) (odds ratio: 1.20; 95% confidence interval: 1.02–1.43; p = 0.02) were significant risk factors for non-fusion. Conclusions: This study provides epidemiological data on the natural history of AN, including symptomatic cases, in children. To our knowledge, this is the first study to report the natural course of painful AN. These findings may offer fundamental insights into prevention and management strategies for painful AN in children.

Introduction Age-related spinal sagittal malalignment is commonly attributed to factors such as disc degeneration, osteoporotic vertebral fractures, and paraspinal muscle degeneration. These factors often coexist, making it challenging to discern their relative contributions to spinal malalignment in the elderly population. Understanding these contributions is crucial for both prevention and treatment strategies for spinal deformities in aging individuals. Methods A cross-sectional analysis was conducted within the second survey of the Wakayama Spine Study (2012–2013). A total of 952 participants were recruited, and 794 (239 men, 555 women; mean age, 63.5 ± 13.1 years) were eligible for magnetic resonance imaging (MRI) and standing radiographic evaluation of spinal alignment. Primary outcome measures included the C7 sagittal vertical axis (SVA), pelvic incidence (PI), and pelvic tilt (PT) from standing lateral radiographs. Secondary outcomes included MRI-based assessments of disc degeneration using the Pfirrmann classification, vertebral fractures via the semi-quantitative (SQ) method, and paraspinal muscle fatty infiltration ratio at the L1/L2 level. Spinal sagittal malalignment was defined as C7 SVA ≥ 50 mm. Statistical analyses, including logistic regression, were performed to identify significant factors associated with spinal malalignment. Results Spinal sagittal malalignment was observed in 98 participants (12%), with 53 (55%) reporting low back pain in the past month. Significant factors associated with sagittal malalignment included age ≥ 70 years (odds ratio [OR], 2.48; 95% confidence interval [CI], 1.33–4.69), PT ≥ 18.7° (OR, 3.12; 95% CI, 1.77–5.63), vertebral fracture (morphometric fracture index ≥ 4; OR, 2.01; 95% CI, 1.15–3.51), and paraspinal muscle fatty infiltration ratio ≥ 10.6% (OR, 4.98; 95% CI, 2.74–9.27). Conclusion Paraspinal muscle fatty infiltration was the most significant factor associated with spinal malalignment in the general population. Among the identified risk factors, paraspinal muscle degeneration is potentially reversible, underscoring its importance in postural correction strategies and surgical planning. These findings suggest that interventions targeting muscle quality may be crucial in managing spinal malalignment in elderly individuals.

Introduction: The accessory navicular (AN) is an accessory ossicle located on the medial side of the navicular bone and is often associated with sports-related overuse injuries during adolescence. However, little is known about the natural history of AN. This study aimed to clarify the natural course of AN, including symptomatic cases, in children through a longitudinal epidemiological investigation. Methods: Data from the KID Locomo Study, a prospective cohort study aimed at elucidating musculoskeletal disorders in childhood, were used. Of the 834 children recruited in the 2022 baseline survey, 66 children (109 feet) aged 11 to 13 years with AN were enrolled in this 2-year longitudinal analysis. The presence of AN was assessed using ultrasonography. Data on sex, age, height, weight, presence of pain at the AN site, laterality, flatfoot (based on footprint analysis), and participation in athletic clubs were collected. The natural history of AN, including painful presentations, was evaluated. Multivariable logistic regression analysis was performed to identify risk factors for non-fusion of the AN with the navicular bone. Results: Among the 109 feet with AN at baseline, 38 (34.9%) demonstrated fusion with the navicular bone at the 2-year follow-up. Of the 21 feet with painful AN at baseline, pain had resolved in 15 (71.4%) after 2 years. Multivariable logistic regression analysis revealed that female sex (odds ratio: 3.00; 95% confidence interval: 1.26–7.45; p = 0.01) and higher body mass index (BMI) (odds ratio: 1.20; 95% confidence interval: 1.02–1.43; p = 0.02) were significant risk factors for non-fusion. Conclusions: This study provides epidemiological data on the natural history of AN, including symptomatic cases, in children. To our knowledge, this is the first study to report the natural course of painful AN. These findings may offer fundamental insights into prevention and management strategies for painful AN in children.

Multiple development of esophageal squamous-cell carcinoma is explained by field cancerization and is associated with alcohol consumption and smoking. We investigated the association between the development of second primary esophageal squamous-cell carcinoma after endoscopic resection for esophageal squamous-cell carcinoma and genetic polymorphisms related to alcohol and nicotine metabolism. The study group comprised 56 patients with esophageal squamous-cell carcinoma after endoscopic resection. The main variables were the following: (i) cumulative incidence and total number of second primary esophageal squamous-cell carcinoma according to genetic polymorphisms in alcohol dehydrogenase 1B, aldehyde dehydrogenase 2 and cytochrome P450 2A6; and (ii) risk factors of second primary esophageal squamous-cell carcinoma identified using a multivariate Cox proportional-hazards model. The frequencies of alcohol dehydrogenase 1B, aldehyde dehydrogenase 2 and cytochrome P450 2A6 genetic polymorphisms in the buccal mucosa were analyzed. The median follow-up was 92.8 months (range: 2.7–134.2). Slow-metabolizing alcohol dehydrogenase 1B was associated with a higher 7-year cumulative incidence of second primary esophageal squamous-cell carcinoma (fast-metabolizing alcohol dehydrogenase 1B vs slow-metabolizing alcohol dehydrogenase 1B: 20.5% vs 71.4%, P = 0.006). Slow-metabolizing alcohol dehydrogenase 1B (relative risk [95% confidence interval]: 3.17 [1.49–6.73]), inactive aldehyde dehydrogenase 2 (2.17 [1.01–4.63]) and poorly-metabolizing cytochrome P450 2A6 (4.63 [1.74–12.33]) had a significantly higher total number of second primary esophageal squamous-cell carcinoma per 100 person-years. In the multivariate Cox proportional-hazards model, slow-metabolizing alcohol dehydrogenase 1B was a significant risk factor of the development of second primary esophageal squamous-cell carcinoma (hazard ratio 9.92, 95% confidence interval: 2.35–41.98, P = 0.0018). Slow-metabolizing alcohol dehydrogenase 1B may be a significant risk factor for the development of second primary esophageal squamous-cell carcinoma. In addition, inactive aldehyde dehydrogenase 2 and poorly-metabolizing cytochrome P450 2A6 may be important factors.

Aspirin has gained great attention as a cancer preventive agent. Our previous study revealed that the low-dose aspirin prevents colorectal tumor recurrence in Japanese patients with colorectal adenomas and/or adenocarcinomas, whereas aspirin increases risks in smokers and has no effects on regular drinkers. Our recent study revealed that aspirin reduces polyp growth in Japanese patients with familial adenomatous polyposis (FAP). In this study, we have studied the association of genotypes of alcohol metabolizing enzymes (ADH1B and ALDH2) on aspirin's efficacy of suppressing polyp growth (≥5 mm) in a total of 81 Japanese patients with FAP. Our study revealed that aspirin showed significant preventive effects for patients with ADH1B-AA and AA+GA types [OR = 0.21; 95% confidence interval (CI), 0.05–0.95, and OR = 0.31; 95% CI, 0.10–0.95, respectively], and for patients with ALDH2-GG and GG+GA types (OR = 0.10; 95% CI, 0.01–0.92, and OR = 0.29; 95% CI, 0.09–0.94, respectively), but not for patients with ADH1B-GG and GA+GG types, and ALDH2-AA and GA+AA types. In addition, substantial preventive effects of aspirin were seen for patients with ADH1B-AA type who do not drink regularly (<3 times/week, OR = 0.11; 95% CI, 0.02–0.78), where a statistically significant interaction between aspirin and ADH1B was observed (Pinteraction = 0.036). Results from this exploratory study strongly indicate that aspirin is beneficial in prevention of polyp growth for patients with FAP with ADH1B-AA and AA+GA types, and ALDH2-GG and GG+GA types. Taken together, we propose ADH1B and ALDH2 as candidate markers for the personalized prevention by aspirin.Significance:Aspirin is beneficial to patients with FAP with ADH1B-AA and AA+GA types or ALDH2-GG and GG+GA types. ADH1B and ALDH2 genotypes can be the markers for the personalized prevention of colorectal cancer by aspirin.

Aspirin has gained great attention as a cancer preventive agent. Our previous study revealed that the low-dose aspirin prevents colorectal tumor recurrence in Japanese patients with colorectal adenomas and/or adenocarcinomas, whereas aspirin increases risks in smokers and has no effects on regular drinkers. Our recent study revealed that aspirin reduces polyp growth in Japanese patients with familial adenomatous polyposis (FAP). In this study, we have studied the association of genotypes of alcohol metabolizing enzymes (ADH1B and ALDH2) on aspirin's efficacy of suppressing polyp growth (≥5 mm) in a total of 81 Japanese patients with FAP. Our study revealed that aspirin showed significant preventive effects for patients with ADH1B-AA and AA+GA types [OR = 0.21; 95% confidence interval (CI), 0.05–0.95, and OR = 0.31; 95% CI, 0.10–0.95, respectively], and for patients with ALDH2-GG and GG+GA types (OR = 0.10; 95% CI, 0.01–0.92, and OR = 0.29; 95% CI, 0.09–0.94, respectively), but not for patients with ADH1B-GG and GA+GG types, and ALDH2-AA and GA+AA types. In addition, substantial preventive effects of aspirin were seen for patients with ADH1B-AA type who do not drink regularly (<3 times/week, OR = 0.11; 95% CI, 0.02–0.78), where a statistically significant interaction between aspirin and ADH1B was observed (Pinteraction = 0.036). Results from this exploratory study strongly indicate that aspirin is beneficial in prevention of polyp growth for patients with FAP with ADH1B-AA and AA+GA types, and ALDH2-GG and GG+GA types. Taken together, we propose ADH1B and ALDH2 as candidate markers for the personalized prevention by aspirin.Significance:Aspirin is beneficial to patients with FAP with ADH1B-AA and AA+GA types or ALDH2-GG and GG+GA types. ADH1B and ALDH2 genotypes can be the markers for the personalized prevention of colorectal cancer by aspirin.

Aspirin has gained great attention as a cancer preventive agent. Our previous study revealed that the low-dose aspirin prevents colorectal tumor recurrence in Japanese patients with colorectal adenomas and/or adenocarcinomas, whereas aspirin increases risks in smokers and has no effects on regular drinkers. Our recent study revealed that aspirin reduces polyp growth in Japanese patients with familial adenomatous polyposis (FAP). In this study, we have studied the association of genotypes of alcohol metabolizing enzymes (ADH1B and ALDH2) on aspirin's efficacy of suppressing polyp growth (≥5 mm) in a total of 81 Japanese patients with FAP. Our study revealed that aspirin showed significant preventive effects for patients with ADH1B-AA and AA+GA types [OR = 0.21; 95% confidence interval (CI), 0.05–0.95, and OR = 0.31; 95% CI, 0.10–0.95, respectively], and for patients with ALDH2-GG and GG+GA types (OR = 0.10; 95% CI, 0.01–0.92, and OR = 0.29; 95% CI, 0.09–0.94, respectively), but not for patients with ADH1B-GG and GA+GG types, and ALDH2-AA and GA+AA types. In addition, substantial preventive effects of aspirin were seen for patients with ADH1B-AA type who do not drink regularly (<3 times/week, OR = 0.11; 95% CI, 0.02–0.78), where a statistically significant interaction between aspirin and ADH1B was observed (Pinteraction = 0.036). Results from this exploratory study strongly indicate that aspirin is beneficial in prevention of polyp growth for patients with FAP with ADH1B-AA and AA+GA types, and ALDH2-GG and GG+GA types. Taken together, we propose ADH1B and ALDH2 as candidate markers for the personalized prevention by aspirin.Significance: Aspirin is beneficial to patients with FAP with ADH1B-AA and AA+GA types or ALDH2-GG and GG+GA types. ADH1B and ALDH2 genotypes can be the markers for the personalized prevention of colorectal cancer by aspirin.

Cigarette smoking and alcohol consumption are major risk factors for lifestyle-related diseases. Although it has been reported that the combination of these habits worsens risks, the underlying mechanism remains elusive. Reactive carbonyl species (RCS) cause chemical modifications of biological molecules, leading to alterations in cellular signaling pathways, and total RCS levels have been used as a lipid peroxidation marker linked to lifestyle-related diseases. In this study, at least 41 types of RCS were identified in the lipophilic fraction of plasma samples from 40 subjects using liquid chromatography/electrospray ionization tandem mass spectrometry (LC/ESI-MS/MS). Higher levels of 10 alkanals, 5 trans-2-alkenals, 1 cis-4-alkenal, and 3 alkadienals were detected in the smoking/drinking group (N = 10) as compared to those with either habit (N = 10 each) or without both habits (N = 10) in the analysis of covariances adjusted for age and BMI. The levels of 3 alkanals, 1 trans-2-alkenal, 1 alkadienal, and 1 4-hydroxy-2-alkenal in the smoking/drinking group were significantly higher than those in the no-smoking/drinking and no-smoking/no-drinking groups. These results strongly indicate that the combination of cigarette smoking and alcohol drinking synergistically increases the level and variety of RCS in the circulating blood, and may further jeopardize cellular function.