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In “The value of nothing: asymmetric attention to opportunity costs drives intertemporal decision making” Read, Olivola and Hardisty (2017) proposed an asymmetric subjective opportunity cost (ASOC) effect to explain and predict why impatience can be detected in intertemporal choice. This work deserves to be replicated and extended for its novel and potentially important findings. The present study aimed to examine the reliability and robustness of the evidence presented by Read et al. by conducting precise replications of their key findings in Study 1. The ASOC effect (Read, et al., 2017) was important for expanding its application and reported to be typically stronger when baseline larger-but-later option (LL) and smaller-but-sooner option (SS) preferences were closer to 50% in the authors’ original condition. Therefore, the present study also aimed to replicate and test the ASOC effect when baseline LL preferences were higher or lower than those in the original condition. We intended to set two additional conditions wherein either LL or SS is more obviously favored (i.e., baseline LL preferences were higher or lower than those in the original condition) by respectively applying the common difference effect (Kirby & Herrnstein, 1995) and the unit effect (Burson, Larrick & Lynch Jr., 2009; Pandelaere, Briers & Lembregts, 2011). Having successfully generated two more obviously favored conditions, the ASOC effect was replicated and confirmed under the original condition and one additional condition wherein SS was more obviously favored. However, the ASOC effect was not detected under the other additional condition wherein LL was more obviously favored. The implications of these findings were discussed.
This study evaluated the association between inflammatory diets as measured by the Dietary Inflammatory index (DII), inflammation biomarkers and the development of preeclampsia among the Chinese population. We followed the reporting guidelines of the Strengthening the Reporting of Observational Studies in Epidemiology statement for observational studies. A total of 466 preeclampsia cases aged over 18 years were recruited between March 2016 and June 2019, and 466 healthy controls were 1:1 ratio matched by age (±3 years), week of gestation (±1 week) and gestational diabetes mellitus. The energy-adjusted DII (E-DII) was computed based on dietary intake assessed using a seventy-nine item semiquantitative FFQ. Inflammatory biomarkers were analysed by ELISA kits. The mean E-DII scores were −0·65 ± 1·58 for cases and −1·19 ± 1·47 for controls (P value < 0·001). E-DII scores positively correlated with interferon-γ (rs = 0·194, P value = 0·001) and IL-4 (rs = 0·135, P value = 0·021). After multivariable adjustment, E-DII scores were positively related to preeclampsia risk (Ptrend < 0·001). The highest tertile of E-DII was 2·18 times the lowest tertiles (95 % CI = 1·52, 3·13). The odds of preeclampsia increased by 30 % (95 % CI = 18 %, 43 %, P value < 0·001) for each E-DII score increase. The preeclampsia risk was positively associated with IL-2 (OR = 1·07, 95 % CI = 1·03, 1·11), IL-4 (OR = 1·26, 95 % CI = 1·03, 1·54) and transforming growth factor beta (TGF-β) (OR = 1·17, 95 % CI = 1·06, 1·29). Therefore, proinflammatory diets, corresponding to higher IL-2, IL-4 and TGF-β levels, were associated with increased preeclampsia risk.
Findings for the roles of dairy products, Ca and vitamin D on ovarian cancer risk remain controversial. We aimed to assess these associations by using an updated meta-analysis. Five electronic databases (e.g. PubMed and Embase) were searched from inception to 24 December 2019. Pooled relative risks (RR) with 95 % CI were calculated. A total of twenty-nine case–control or cohort studies were included. For comparisons of the highest v. lowest intakes, higher whole milk intake was associated with increased ovarian cancer risk (RR 1·35; 95 % CI 1·15, 1·59), whereas decreased risks were observed for higher intakes of low-fat milk (RR 0·84; 95 % CI 0·73, 0·96), dietary Ca (RR 0·71; 95 % CI 0·60, 0·84) and dietary vitamin D (RR 0·80; 95 % CI 0·67, 0·95). Additionally, for every 100 g/d increment, increased ovarian cancer risks were found for total dairy products (RR 1·03; 95 % CI 1·01, 1·04) and for whole milk (RR 1·07; 95 % CI 1·03, 1·11); however, decreased risks were found for 100 g/d increased intakes of low-fat milk (RR 0·95; 95 % CI 0·91, 0·99), cheese (RR 0·87; 95 % CI 0·76, 0·98), dietary Ca (RR 0·96; 95 % CI 0·95, 0·98), total Ca (RR 0·98; 95 % CI 0·97, 0·99), dietary vitamin D (RR 0·92; 95 % CI 0·87, 0·97) and increased levels of circulating vitamin D (RR 0·84; 95 % CI 0·72, 0·97). These results show that whole milk intake might contribute to a higher ovarian cancer risk, whereas low-fat milk, dietary Ca and dietary vitamin D might reduce the risk.
For the prevention and control of newly emergent or sudden infectious diseases, we built an on-site, modularized prevention and control system and tested the equipment by using the clustering analysis method. On the basis of this system, we propose a modular equipment allocation method and 4 applications of this method for different types of infectious disease prevention and control. This will help to improve the efficiency and productivity of anti-epidemic emergency forces and will provide strong technical support for implementing more universal and serialized equipment in China. (Disaster Med Public Health Preparedness. 2017;11:375–382)
Fusion of nucleoli or nucleolus precursor bodies (NPBs) has been observed during somatic cell interphase and pronuclear development of human zygotes; however, the underlying mechanism is unknown. NPB fusion and its regulation by mitogen-activated protein kinase (MAPK) and maturation-promoting factor (MPF) were studied in activated mouse oocytes. Small NPBs appeared about 4 h after ethanol activation, and took about 1.5 h to fuse into a large NPB, which persisted for about 10 h before disappearance. Analysis of the temporal windows for kinase action indicated that a high MAPK activity during the first 2 h and a low MPF activity during the first 3–4 h after activation were essential for subsequent NPB fusion. A preactivation decline in MAPK activity was associated with decreased NPB fusion following activation of aged oocytes. While MAPK inactivation by regulator U0126 prevented NPB fusion in oocytes activated by ethanol or 5 min Sr2+ treatments, it had no effect on oocytes fertilized or activated by 6 h Sr2+ treatment. In most cases, while rates of pronuclear formation did not differ, rates of NPB fusion differed significantly between different treatments. Our results suggest that: (i) the MAPK and MPF activities at the initial stage of activation regulate NPB fusion after pronuclear formation; (ii) pronuclear assembly and NPB fusion are two separable events that might be controlled by different mechanisms; and (iii) high MAPK activity and low MPF activity at the initial stage of activation is essential for NPB fusion when only one calcium rise is induced by ethanol, while inhibition of MAPK activity does not affect NPB fusion when the repetitive intracellular Ca2+ rises are induced after fertilization.
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