Low Intake of Vegetables, High Intake of Confectionary, and Unhealthy Eating Habits are Associated with Poor Sleep Quality among Middleaged Female Japanese Workers: Ryoko KATAGIRI, et al. Department of Social and Preventive Epidemiology, Graduate School of Medicine, the University of Tokyo—Objectives: Although workers with poor sleep quality are reported to have problems with work performance, few studies have assessed the association between dietary factors and sleep quality using validated indexes. Here, we examined this association using information acquired from validated questionnaires.Methods: A total of 3,129 female workers aged 34 to 65 years were analyzed. Dietary intake was assessed using a self‐administered diet history questionnaire (DHQ), and subjective sleep quality was assessed using the Pittsburgh Sleep Quality Index (PSQI). The relationship between the intake of several food groups and nutrients and sleep quality was examined using multivariable logistic regression models. The effect of eating habits on sleep quality was also examined.Results: Poor sleep quality was associated with low intake of vegetables (p for trend 0.002) and fish (p for trend 0.04) and high intake of confectionary (p for trend 0.004) and noodles (p for trend 0.03) after adjustment for potential confounding factors (age, body mass index, physical activity, depression score, employment status, alcohol intake and smoking status). Poor sleep quality was also significantly and positively associated with consumption of energy drinks and sugar‐sweetened beverages, skipping breakfast, and eating irregularly. In addition, poor sleep quality was significantly associated with high carbohydrate intake (p for trend 0.03).Conclusions: A low intake of vegetables and fish, high intake of confectionary and noodles and unhealthy eating habits were independently associated with poor sleep quality. Poor sleep quality was also associated with high carbohydrate intake in free‐living Japanese middle‐aged female workers.

Background: Protein intake has been inversely associated with frailty. However, no study has examined the effect of the difference of protein sources (animal or plant) or the amino acid composing the protein on frailty. Therefore, we examined the association of protein and amino acid intakes with frailty among elderly Japanese women. Methods: A total of 2108 grandmothers or acquaintances of dietetic students aged 65 years and older participated in this cross-sectional multicenter study, which was conducted in 85 dietetic schools in 35 prefectures of Japan. Intakes of total, animal, and plant protein and eight selected amino acids were estimated from a validated brief-type self-administered diet history questionnaire and amino acid composition database. Frailty was defined as the presence of three or more of the following four components: slowness and weakness (two points), exhaustion, low physical activity, and unintentional weight loss. Results: The number of subjects with frailty was 481 (23%). Adjusted ORs (95% CI) for frailty in the first, second, third, fourth, and fifth quintiles of total protein intake were 1.00 (reference), 1.02 (0.72, 1.45), 0.64 (0.45, 0.93), 0.62 (0.43, 0.90), and 0.66 (0.46, 0.96), respectively (P for trend = 0.001). Subjects categorized to the third, fourth, and fifth quintiles of total protein intake (>69.8 g/d) showed significantly lower ORs than those to the first quintile (all P <0.03). The intakes of animal and plant protein and all selected amino acids were also inversely associated with frailty (P for trend <0.04), with the multivariate adjusted OR in the highest compared to the lowest quintile of 0.73 for animal protein and 0.66 for plant protein, and 0.67-0.74 for amino acids, albeit that the ORs for these dietary variables were less marked than those for total protein. Conclusions: Total protein intake was significantly inversely associated with frailty in elderly Japanese women. The association of total protein with frailty may be observed regardless of the source of protein and the amino acid composing the protein.

Background: Multiple early gastric cancers (EGCs) may develop in 6–14% of patients even after achieving curative endoscopic submucosal dissection (ESD); however, a useful biomarker for predicting recurrence is not available. The present study investigated whether the expression of CD44 variant 9 (CD44v9), a functional cancer stem cell marker, in the primary gastric cancer tissue represents an indicator of recurrence. Methods: Eighty-eight patients who underwent ESD for EGC from 2008 to 2010 were enrolled and monitored for recurrence for 3 years. The expression levels of CD44v9 in the tissue of initial EGCs were evaluated by immunohistochemistry, and the recurrence rate was compared between CD44v9-positive and CD44v9-negative groups. The mucin phenotype and expression of microRNA-21 (miR-21) and programmed cell death protein 4 (PDCD4) were also analysed. Results: The recurrence rate of EGC was significantly higher in the CD44v9-positive group than in the CD44v9-negative group (hazard ratio (HR), 21.8; 95% confidence interval (CI), 5.71–83.1). However, mucin phenotypes and the expression of miR-21 and PDCD4 did not predict recurrence after ESD. Meanwhile, grade of gastric atrophy was also identified as a significant marker of multiple recurrence (HR, 4.95; 95% CI, 1.30–18.8). Conclusion: CD44 variant 9 expression represents a potential predictive marker for recurrence in EGC.

Emodin is an active component of a traditional Chinese and Japanese medicine isolated from the root and rhizomes of Rheum palmatum L. Here, we show that emodin significantly induces cytotoxicity in the human myeloma cells through the elimination of myeloid cell leukemia 1 (Mcl-1). Emodin inhibited interleukin-6–induced activation of Janus-activated kinase 2 (JAK2) and phosphorylation of signal transducer and activator of transcription 3 (STAT3), followed by the decreased expression of Mcl-1. Activation of caspase-3 and caspase-9 was triggered by emodin, but the expression of other antiapoptotic Bcl-2 family members, except Mcl-1, did not change in the presence of emodin. To clarify the importance of Mcl-1 in emodin-induced apoptosis, the Mcl-1 expression vector was introduced into the human myeloma cells by electroporation. Induction of apoptosis by emodin was almost abrogated in Mcl-1–overexpressing myeloma cells as the same level as in parental cells, which were not treated with emodin. In conclusion, emodin inhibits interleukin-6–induced JAK2/STAT3 pathway selectively and induces apoptosis in myeloma cells via down-regulation of Mcl-1, which is a good target for treating myeloma. Taken together, our results show emodin as a new potent anticancer agent for the treatment of multiple myeloma patients. [Mol Cancer Ther 2007;6(3):987–94]