Gifu University of Medical Science

The purpose of this study is to identify image features in images with well-spread mammary glands, which are difficult to determine with human observation skills. We prepared images with sufficient mammary gland spread and images with insufficient mammary gland spread. We extracted image features from each and used statistical processing to examine the differences between the images. There were differences in 80 image features. There were many image features that differed in the high-frequency portion of the wavelet features.

Chronic peripheral inflammation triggered by adipokine release may extend to the brain, potentially influencing the pathological progression of Alzheimer's disease (AD) and neuropsychiatric symptoms (NPS). However, it remains unclear whether and how leptin contributes to the link between adipose tissue dysfunction and dementia. This study aims to investigate the role of leptin in the connection between adipose-derived inflammatory signaling and cognitive impairment/NPS.

Path analysis was employed to explore how leptin relates to the association between adipose-related metabolic dysfunction and dementia through inflammatory pathways in patients with AD pathology (n = 15). Variables included plasma leptin concentration, body mass index (BMI) as a marker of adiposity, and in vivo assessments of regional neuroinflammation using translocator protein (TSPO)-PET imaging with the tracer ¹¹C-DPA-713 (¹¹C-DPA-713-binding potential [¹¹C-DPA-713-BP_ND]). Cognitive function was measured using the Alzheimer's Disease Assessment Scale-Japanese Cognitive Subscale (ADAS-J cog), while NPS were assessed using the Neuropsychiatric Inventory Questionnaire (NPI-Q).

Regression analysis demonstrated that higher plasma leptin concentrations positively correlated with BMI and significantly predicted ¹¹C-DPA-713-BP_ND in the insula. Additionally, NPI-Q scores were associated with ¹¹C-DPA-713-BP_ND in the insula. Path analysis supported leptin's role linking adiposity to NPS through insular inflammation. The hypothesized model fit the data well under the null hypothesis [χ² (3) = 0.63, p = 0.89].

These findings underscore the relevance of exploring how leptin and adipose tissue dysfunction interact with neuroinflammatory processes in contributing to NPS in the patients in the AD continuum. Interventions targeting these interactions could represent promising avenues for managing NPS.

This study aimed to describe the natural history and genotype-phenotype associations concerning nonhematological complications in Epstein syndrome, a high-risk subtype of MYH9-related disease (MYH9-RD).

We conducted a nationwide cross-sectional study using data from congenital thrombocytopenia registries in Japan. Immunofluorescence analysis and gene testing identified patients with Epstein syndrome carrying high-risk MYH9 variants (R702C/H, S96L). We analyzed the onset and progression of nonhematological complications using Kaplan-Meier survival curves.

Among 177 MYH9-RD patients, 40 had Epstein syndrome with high-risk variants. Over 50 % developed renal failure, deafness, and proteinuria by age 19, increasing to 80 % by age 32. Immunofluorescence detected fine myosin-aggregated granules in neutrophils, which facilitated precise genetic diagnosis. Most cases (95 %) involved de novo variants, highlighting the need for early genetic screening.

Patients with Epstein syndrome are at high risk for developing progressive nonhematological complications. Early detection and intervention are critical for improving outcomes. This study highlights the importance of genetic testing and awareness among healthcare providers to prevent misdiagnosis and delayed treatment.