Relationships between feeding behaviors and emotions : an electroencephalogram (EEG) frequency analysis study

Feeding behaviors may be easily affected by emotions, both being based on brain activity; however, the relationships between them have not been explicitly defined. In this study, we investigated how emotional environments modulate subjective feelings, brain activity, and feeding behaviors. Electroencephalogram (EEG) recordings were obtained from healthy participants in conditions of virtual comfortable space (CS) and uncomfortable space (UCS) while eating chocolate, and the times required for eating it were measured. We found that the more participants tended to feel comfortable under the CS, the more it took time to eat in the UCS. However, the EEG emergence patterns in the two virtual spaces varied across the individuals. Upon focusing on the theta and low-beta bands, the strength of the mental condition and eating times were found to be guided by these frequency bands. The results determined that the theta and low-beta bands are likely important and relevant waves for feeding behaviors under emotional circumstances, following alterations in mental conditions

Geographic Inequalities in All-Cause Mortality in Japan: Compositional or Contextual?

Background: A recent study from Japan suggested that geographic inequalities in all-cause premature adult mortality have increased since 1995 in both sexes even after adjusting for individual age and occupation in 47 prefectures. Such variations can arise from compositional effects as well as contextual effects. In this study, we sought to further examine the emerging geographic inequalities in all-cause mortality, by exploring the relative contribution of composition and context in each prefecture. Methods We used the 2005 vital statistics and census data among those aged 25 or older. The total number of decedents was 524,785 men and 455,863 women. We estimated gender-specific two-level logistic regression to model mortality risk as a function of age, occupation, and residence in 47 prefectures. Prefecture-level variance was used as an estimate of geographic inequalities in mortality, and prefectures were ranked by odds ratios (ORs), with the reference being the grand mean of all prefectures (value = 1). Results: Overall, the degree of geographic inequalities was more pronounced when we did not account for the composition (i.e., age and occupation) in each prefecture. Even after adjusting for the composition, however, substantial differences remained in mortality risk across prefectures with ORs ranging from 0.870 (Okinawa) to 1.190 (Aomori) for men and from 0.864 (Shimane) to 1.132 (Aichi) for women. In some prefectures (e.g., Aomori), adjustment for composition showed little change in ORs, while we observed substantial attenuation in ORs in other prefectures (e.g., Akita). We also observed qualitative changes in some prefectures (e.g., Tokyo). No clear associations were observed between prefecture-level socioeconomic status variables and the risk of mortality in either sex. Conclusions: Geographic disparities in mortality across prefectures are quite substantial and cannot be fully explained by differences in population composition. The relative contribution of composition and context to health inequalities considerably vary across prefectures

Canagliflozin reduces epicardial fat in patients with type 2 diabetes mellitus

Background: It is unknown whether canagliflozin, a selective sodium glucose co-transporter 2 inhibitor, reduces epicardial adipose tissue (EAT) thickness, which is associated with insulin resistance and is a risk factor for coronary artery disease. Methods and results: We administered 100 mg of canagliflozin for 6 months to 13 patients with type 2 diabetes mellitus. We evaluated glycemic control, visceral adipose tissue (VAT) area and subcutaneous adipose tissue (SAT) area, and skeletal muscle mass by using impedance methods, and EAT thickness by using echocardiography. Canagliflozin treatment for 6 months decreased hemoglobin A1c level from 7.1 ± 0.5% to 6.7 ± 0.6% (P < 0.05) and decreased EAT thickness from 9.3 ± 2.5 to 7.3 ± 2.0 mm (P < 0.001), along with a trend of decreasing VAT and SAT area. No association was found between any of these changes. Conclusion: Canagliflozin reduced EAT thickness in patients with type 2 diabetes mellitus independent of its effect on lowering blood glucose, suggesting that canagliflozin may have an effect in preventing cardiovascular events in these patients (UMIN000021327)

MEF/ELF4 transactivation by E2F1 is inhibited by p53

Myeloid elf-1-like factor (MEF) or Elf4 is an E-twenty-six (ETS)-related transcription factor with strong transcriptional activity that influences cellular senescence by affecting tumor suppressor p53. MEF downregulates p53 expression and inhibits p53-mediated cellular senescence by transcriptionally activating MDM2. However, whether p53 reciprocally opposes MEF remains unex-plored. Here, we show that MEF is modulated by p53 in human cells and mice tissues. MEF expression and promoter activity were suppressed by p53. While we found that MEF promoter does not contain p53 response elements, intriguingly, it contains E2F consensus sites. Subsequently, we determined that E2F1 specifically binds to MEF promoter and transactivates MEF. Nevertheless, E2F1 DNA binding and transactivation of MEF promoter was inhibited by p53 through the association between p53 and E2F1. Furthermore, we showed that activation of p53 in doxorubicin-induced senescent cells increased E2F1 and p53 interaction, diminished E2F1 recruitment to MEF promoter and reduced MEF expression. These observations suggest that p53 downregulates MEF by associating with and inhibiting the binding activity of E2F1, a novel transcriptional activator of MEF. Together with previous findings, our present results indicate that a negative regulatory mechanism exists between p53 and MEF

Monkeys mutant for PKD1 recapitulate human autosomal dominant polycystic kidney disease.

Autosomal dominant polycystic kidney disease (ADPKD) caused by PKD1 mutations is one of the most common hereditary disorders. However, the key pathological processes underlying cyst development and exacerbation in pre-symptomatic stages remain unknown, because rodent models do not recapitulate critical disease phenotypes, including disease onset in heterozygotes. Here, using CRISPR/Cas9, we generate ADPKD models with PKD1 mutations in cynomolgus monkeys. As in humans and mice, near-complete PKD1 depletion induces severe cyst formation mainly in collecting ducts. Importantly, unlike in mice, PKD1 heterozygote monkeys exhibit cyst formation perinatally in distal tubules, possibly reflecting the initial pathology in humans. Many monkeys in these models survive after cyst formation, and cysts progress with age. Furthermore, we succeed in generating selective heterozygous mutations using allele-specific targeting. We propose that our models elucidate the onset and progression of ADPKD, which will serve as a critical basis for establishing new therapeutic strategies, including drug treatments

Examination of Usefulness of Simulation Education in Collaboration with Clinical Nurses in Adult Nursing －From Student Self Assessments－

本研究は臨床看護師と連携したシミュレーション教育の有用性を検討することを目的とした。方法は、１．シナリオ作成、２．シミュレーションの実施、３．シミュレーション教育の有用性の検討とした。研究対象者は看護学科３年生６名で術後急性期にある患者の観察を実施した。２人１組で観察した後全員で振り返りを実施した。シミュレーション実施後に無記名自記式質問紙調査を行った。内容は５段階のリッカート尺度を用いた目標達成度の自己評価、自由記述による演習の感想とし、単純集計と自由記述の内容から有用性を検討した。臨床看護師はシナリオ作成およびデブリファーとしてシミュレーシに参加した。質問紙調査の結果、目標達成度の項目平均値は 3.0～4.8 であった。臨床看護師の指導により、観察の視点や観察方法、アセスメントの根拠や報告の方法の理解が深まっていたことから、本シミュレーション教育は学習の動機付けとなっており有用であることが示唆された。This study examined the usefulness of simulation education in collaboration with nursing guidance in nursing education. Clinical nurses participated in the simulation by formulating scenarios and acting as de-briefing supporters. For the execution of the simulation, six third-year nursing students worked in pairs to observe acute post-operative patients, and all students reflected on their observations. They assessed the usefulness of simulation education via a self-administered, anonymous questionnaire distributed after the simulation. The content was the self-evaluation of goal achievement using a five-point Likert scale, and impressions of the exercise were provided through free writing. The results demonstrated that the mean value of the items for goal attainment ranged from 3.0 to 4.8. Meanwhile, the guidance of clinical nurses helped the students deepen their understanding of observation perspectives, observation methods, assessment rationale, and reporting methods. The findings indicated that simulation education was beneficial because it provided motivation for learning.departmental bulletin pape

The ARID1B spectrum in 143 patients: from nonsyndromic intellectual disability to Coffin–Siris syndrome

Purpose: Pathogenic variants in ARID1B are one of the most frequent causes of intellectual disability (ID) as determined by large-scale exome sequencing studies. Most studies published thus far describe clinically diagnosed Coffin–Siris patients (ARID1B-CSS) and it is unclear whether these data are representative for patients identified through sequencing of unbiased ID cohorts (ARID1B-ID). We therefore sought to determine genotypic and phenotypic differences between ARID1B-ID and ARID1B-CSS. In parallel, we investigated the effect of different methods of phenotype reporting. Methods: Clinicians entered clinical data in an extensive web-based survey. Results: 79 ARID1B-CSS and 64 ARID1B-ID patients were included. CSS-associated dysmorphic features, such as thick eyebrows, long eyelashes, thick alae nasi, long and/or broad philtrum, small nails and small or absent fifth distal phalanx and hypertrichosis, were observed significantly more often (p < 0.001) in ARID1B-CSS patients. No other significant differences were identified. Conclusion: There are only minor differences between ARID1B-ID and ARID1B-CSS patients. ARID1B-related disorders seem to consist of a spectrum, and patients should be managed similarly. We demonstrated that data collection methods without an explicit option to report the absence of a feature (such as most Human Phenotype Ontology-based methods) tended to underestimate gene-related features