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 investigate the efficacy of dapagliflozin administration time using light-dark cycle-disrupted mice. Five-week-old male C57BL/6J mice were fed a control diet or high-fat diet (HFD) for 8-weeks under a disrupted light-dark cycle. During the final 2-weeks of the study, the mice were administered dapagliflozin at a fixed time (8:00) or 2-h after the light phase, respectively. An olive oil-ethanol emulsion was used as the vehicle. At the end of the experiment, the mice were euthanized after an 18-hour fasting period, and plasma and tissue samples (epididymal white adipose tissue, liver, and kidney) were collected. Dapagliflozin administration significantly reduced the HFD-induced body weight gain in both treatment groups. However, the effect of dapagliflozin on body weight reduction was stronger at a fixed time than 2-h after the disrupted light phase. In addition, the administration of dapagliflozin at a fixed time significantly decreased HFD-induced affects such as hyperglycemia and hyperinsulinemia. Although dapagliflozin administration 2-h after the light phase tended to be effective, the levels were lower than those at the fixed time. Our findings suggest that the time to take medicines such as dapagliflozin in shift workers should be fixed at a regular time rather than after waking up.