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How does market power affect consumer perceptions and purchase behavior? In the theoretically and pragmatically important context of price increases, we theorize that (i) consumer price fairness perceptions decline with market power when a price increase is due to costs; and (ii) this fairness difference arises due to greater perceptions of controllability and, in turn, exploitation by firms with higher market power. Consistent with our theorizing, we further argue that market power does not affect fairness (iii) when prices rise due to demand (which is perceived as equally exploitative and unfair regardless of firm power) or (iv) when price increases are clearly beyond the firm’s control (and perceived as equally fair for firms with high and low market power). We provide empirical support for these predictions in a series of behavioral experiments combined with an analysis of retail scanner data. Together, our findings shed light on how market power and pricing actions jointly drive consumer perceptions of unfairness, with implications for firms’ pricing strategies, competition in the retail marketplace, and the principle of dual entitlement as a community standard of fairness in pricing.

Background: While socioeconomic position (SEP) is consistently related to pregnancy and birth outcome disparities, relevant biological mechanisms are manifold, thus necessitating more comprehensive characterization of SEP-exposome associations during pregnancy. Objectives: We implemented an exposomic approach to systematically characterize the socioeconomic landscape of prenatal exposures in a setting where social segregation was less distinct in a hypotheses-generating manner. Methods: We described the correlation structure of 134 prenatal exogenous and endogenous sources (e.g., micronutrients, hormones, immunomodulatory metabolites, environmental pollutants) collected in a diverse, population-representative, urban, high-income longitudinal mother-offspring cohort (N = 1341; 2009–2011). We examined the associations between maternal, paternal, household, and areal level SEP indicators and 134 exposures using multiple regressions adjusted for precision variables, as well as potential effect measure modification by ethnicity and nativity. Finally, we generated summary SEP indices using Multiple Correspondence Analysis to further explore possible curved relationships. Results: Individual and household SEP were associated with anthropometric/adiposity measures, folate, omega-3 fatty acids, insulin-like growth factor-II, fasting glucose, and neopterin, an inflammatory marker. We observed paternal education was more strongly and consistently related to maternal exposures than maternal education. This was most apparent amongst couples discordant on education. Analyses revealed additional non-linear associations between areal composite SEP and particulate matter. Environmental contaminants (e.g., per- and polyfluoroalkyl substances) and micronutrients (e.g., folate and copper) showed opposing associations by ethnicity and nativity, respectively. Discussion: SEP-exposome relationships are complex, non-linear, and context specific. Our findings reinforce the potential role of paternal contributions and context-specific modifiers of associations, such as between ethnicity and maternal diet-related exposures. Despite weak presumed areal clustering of individual exposures in our context, our approach reinforces subtle non-linearities in areal-level exposures. Agency for Science, Technology and Research (A*STAR) National Medical Research Council (NMRC) National Research Foundation (NRF) Published version This research is supported by the Singapore National Research Foundation under the Translational and Clinical Research (TCR) Flagship, and Open Fund Large Collaborative Grant (OFLCG) Programmes and administered by the Singapore Ministry of Health’s National Medical Research Council (NMRC), Singapore - NMRC/TCR/004-NUS/2008; NMRC/TCR/012-NUHS/2014; OFLCG/MOH-000504. Additional funding is provided by the Singapore Institute for Clinical Sciences, Agency for Science Technology and Research (A*STAR), Singapore.

Phthalate exposure is related to the development of allergic diseases; however, studies regarding its effect on lung function are limited. Our study aims to identify an association between phthalate exposure at different ages and lung function in children at age 9 by conducting a cohort study. The Taiwan Birth Panel Study (TBPS) was established from April 2004 to January 2005. Urine samples were collected from children in the TBPS cohort at ages 2, 5, and 9years. Urinary phthalate metabolite concentrations were measured via ultrahigh-performance liquid chromatography coupled with tandem mass spectrometry. Questionnaires, lung function tests and serum IgE levels were obtained from children at the age of 9. Multiple linear regressions adjusted for confounding factors were applied to investigate the associations between phthalate exposure at different ages and lung function at age 9. Our results demonstrate that in children with allergic diseases, a per log unit increase in the urinary phthalate metabolite mono-ethyl phthalate (MEP) concentration at age 9 was associated with a decreasing forced expiratory volume in 1 sec (FEV1) (β=-25.22; 95% CI: -47.53 to -2.91 per log ml/ln-μg/g cr) and forced vital capacity (FVC) (β=-32.3; 95% CI: -63.51 to -1.09 per log ml/ln-μg/g cr). For children with high serum IgE levels (>100kU/L) at age 9, the urinary MEP concentrations at the same age were negatively associated with the FEV1 (β=-30.4; 95% CI: -56.8 to -4.0 per log ml/ln-μg/g cr), FVC (β=-47.6; 95% CI: -84.2 to -11.0 per log ml/ln-μg/g cr) and peak expiratory flow (PEF) (β=-102.4; 95% CI: 180.2 to -24.7 per log ml/ln-μg/g cr). Phthalate exposure at ages 2 and 5 had little effect on lung function at age 9. Our study suggests that concurrent exposure to phthalates, such as MEP, is negatively associated with lung function in children. Further investigation is required to elaborate on this correlation.

Sun-induced chlorophyll fluorescence (SIF) from spaceborne sensors is a promising tool for global carbon cycle monitoring, but its application is constrained by insufficient understanding of the drivers underlying diurnal SIF dynamics. SIF measurements from ground-based towers can reveal diurnal SIF dynamics across biomes and environmental conditions; however, meaningful interpretation of diurnal variations requires disentangling impacts from canopy structure, plant physiology, instrument configuration and retrieval methods, which often interact with and confound each other. This study aims to unpack these drivers using 1) concurrent ground and airborne canopy-scale and leaf-scale measurements at a corn field, 2) a mechanistic SIF model that explicitly considers the dynamics of photochemistry (via the fraction of open photosystem II reaction centers, qL) and photoprotection (via nonphotochemical quenching, NPQ) as well as their interactive dependence on the sub-canopy light environment, and 3) cross-comparison of SIF instrument configurations and retrieval methods. We found that crop row orientations and sun angles can introduce a distinctive midday dip in SIF in absence of stress, due to a midday drop of absorbed photosynthetically active radiation (APAR) when crop rows are north-south oriented. Canopy structure caused distinctive responses in both qL and NPQ at different positions within the vertical canopy that collectively influenced fluorescence quantum yield (ΦF) at the leaf scale. Once integrated at the canopy scale, diurnal dynamics of both APAR and canopy escape probability (e) are critical for accurately shaping diurnal SIF variations. While leaf-level qL and NPQ exhibited strong diurnal dynamics, their influence was attenuated at the canopy scale due to opposing effects on SIF at different canopy layers. Furthermore, different system configurations (i.e., bi-hemispherical vs. hemispherical-conical) and retrieval methods can bias the SIF magnitude and distort its diurnal shapes, therefore confounding the interpretation of inherent strength and dynamics of SIF emission. Our findings demonstrate the importance of crop row structures, interactive variations in canopy structure and plant physiology, instrument configuration, and retrieval method in shaping the measured dynamics of diurnal SIF. This study highlights the necessity to account for these factors to accurately interpret satellite SIF, and informs future synthesis work with different SIF instrumentation and retrieval methods across sites.

Background Perfluoroalkyl substances (PFASs) are wildly distributed environmental pollutants. Laboratory mice exposed prenatally to PFASs develop smaller birth weight but are more likely to become obese in adulthood. The evidences in human studies are still inconclusive. Methods The participants were 429 mother-infant pairs from Taiwan Birth Panel Study. These children were followed serially and growth data were collected through face to face interviews and records in Child Healthcare Handbooks until 108 months of age. The age-specific z-scores for weight (WAZ), length/height (LAZ/HAZ) and BMI (BMIAZ) were calculated. PFASs in umbilical cord blood were analyzed by ultra-high-performance liquid chromatography/tandem mass spectrometry. Results At birth, perfluorooctyl sulfonate (PFOS) levels were negatively associated with weight and height [per ln unit: adjusted β (95% confidence interval, CI) = − 0.14 (− 0.26, − 0.01) for WAZ and − 0.16 (− 0.31, − 0.02) for LAZ]. However, these adverse impacts diminished as children grow up. When stratified the analysis by gender, the effects of prenatal PFOS exposure were more obvious for girls especially during the time span of 6 to 12 and 12 to 24 months of age [per ln unit: adjusted β (95% CI) = − 0.25 (− 0.47, − 0.04) and − 0.24 (− 0.41, − 0.04) for WAZ, respectively; per ln unit: adjusted β (95% CI) = − 0.33 (− 0.59, − 0.08) and − 0.25 (− 0.45, − 0.05) for BMIAZ, respectively]. Later in the period of 60 to 108 months of age, positive association between prenatal PFOS exposure and girls' BMI was observed [per ln unit: adjusted β (95% CI) = 0.34 (0.007, 0.68) for BMIAZ]. There was little evidence in these data for a consistent association of perfluorooctanoic acid (PFOA) with any of the indicators. Conclusions Our study had shown that higher prenatal PFOS exposure was associated with decreased fetal growth, but the effects were diminished as children grow up. Modest effect of gender specific manner was observed.

Numerous studies have explored the associations between environmental pollutants and pediatric health. Recent studies have investigated the issue in Asia, but no systematic review has been published to date. This study aims to elucidate the issue by summarizing relevant epidemiologic evidence for cohorts in Asia, using information from the Birth Cohort Consortium of Asia (BiCCA). Environmental pollutants include mercury, environmental tobacco smoke (ETS), polychlorinated biphenyls (PCB), perfluoroalkyl substances (PFAS) and phthalates. This study sought to classify the effects of such compounds on fetal growth and pregnancy outcomes, neurodevelopment and behavioral problems, allergic disease and immune function and the endocrine system and puberty. These evidences showed ETS has been associated with infant birth weight, children's neurodevelopment and allergy disease; mercury and PCB have been shown to affect children's neurodevelopment; phthalate has effects on endocrine function; PFAS alters children's neurodevelopment, the endocrine system, and the allergic response. However, more consistent and coordinated research is necessary to understand the whole picture of single environmental and/or co-exposure and children's health. Therefore, harmonization and international collaboration are also needed in Asia.

Background: Prenatal tobacco exposure (maternal active and passive smoking) has been associated with childhood obesity. It is unclear whether this is directly attributable to in utero exposure, with a graded effect across exposure groupings, or to associated lifestyle factors. Methods: In 971 maternal-offspring pairs from the GUSTO cohort, maternal plasma cotinine at 26-28 weeks' gestation and smoking history were used to categorise mothers into prenatal tobacco exposure groups. Offspring anthropometry was obtained longitudinally from birth and at ages 3, 6, 9, 12, 15, 18, 24, 36 months (m). Multiple linear regression, mixed linear models and counterfactual-based analysis were conducted, adjusting for ethnicity, maternal age, education, 1st trimester BMI, parity and gestational age. Findings: All results were compared with unexposed offspring (undetectable maternal cotinine and no history of tobacco exposure). Infants with low maternal cotinine (0·17-13·99 ng/ml) had a similar birthweight, while those with high maternal cotinine (≥14ng/ml) had a lower birthweight [β(95%CI) -162·0g (-291·8,-32·2)]. Low maternal cotinine was associated with higher offspring weight z-score at 18m [0·24 SDs (0·01,0·47)] and 36m [0·27 SDs (0·03,0·52)], and higher BMI z-score at 6m and across 15-36m [36m: 0·45 SDs (0·20,0·70)]. Over the 36m period high maternal cotinine was associated with accelerated gain in weight zscore [0·17 SDs/year (0·03,0·31)]. There was a dose-dependent BMI z-score acceleration, with offspring of mothers with low and high cotinine showing 0·09 (0·01,0·17) SDs/year and 0·17 (0·02,0·32) SDs/year gain, respectively. The association of prenatal tobacco exposure with 36m BMI was not explained by reduced breast-feeding, poor diet and increased screen time. Interpretation: Avoiding even low levels of prenatal tobacco exposure may reduce the risk of early childhood obesity. In utero programming by tobacco exposure directly influences childhood BMI rather than through unhealthy childhood lifestyle factors. Funding Statement: Singapore's National Medical Research Council and Singapore Institute for Clinical Sciences, A*STAR. Declaration of Interests: KMG is supported by the UK Medical Research Council (MC_UU_12011/4), the National Institute for Health Research (NIHR Senior Investigator (NF-SI-0515-10042) and the NIHR Southampton Biomedical Research Centre) and the European Union (Erasmus+ Programme Early Nutrition eAcademy Southeast Asia-573651-EPP-1-2016-1- DE-EPPKA2-CBHE-JP). KMG, Y-SC, and YSL have received reimbursement for speaking at conferences sponsored by companies selling nutritional products. KMG, S-YC and Y-SC are part of an academic consortium that has received research funding from Abbott Nutrition, Nestec and Danone. The other authors have no financial or personal conflict of interest to declare. Ethics Approval Statement: The study was ethically-approved by the Institutional Review Boards of the KK Women’s and Children’s Hospital, and the National University Health System. Informed written consent was obtained from all participants

CD8 + cells from healthy, asymptomatic HIV-1-infected individuals can inhibit HIV-1 replication in naturally or acutely infected CD4 + cells in the absence of cell killing. This CD8 + cell noncytotoxic anti-HIV response (CNAR) is mediated by a soluble CD8 + cell antiviral factor (CAF). CNAR/CAF inhibits HIV-1 replication by blocking viral RNA transcription. HIV transcription is regulated by a variety of cis -acting DNA sequence elements within the proviral long terminal repeat (LTR). We hypothesized that one of the HIV-1 LTR proviral DNA sequence elements that binds host cell transcriptional factors is involved in this antiviral activity. To assess this possibility, we constructed full-length infectious HIV-1 molecular clones with mutations in the LTR elements NFAT, AP-1, IL-2 homology region, and the downstream ISRE. We also tested full-length infectious molecular clones that had deletions of either the NF-κB or Sp1 sites of the LTR or lacked functional Tat and TAR elements. Viruses generated from these molecular clones were used to acutely infect CD4 + cells that subsequently were either co-cultured with CD8 + cells from individuals that exhibited strong CNAR or cultured with CAF-containing fluids. The replication of all of the mutant HIV-1 viruses tested was substantially reduced in the presence of CNAR/CAF. These findings suggest that other regions in the viral LTR or other host cell processes are involved in the transcriptional block elicited by CNAR/CAF.

Marketing a destination requires an understanding of vacationer perception. The gap analysis provided by normal pre- and post-visit surveys represents a good starting point in evaluating how the visitor feels about the destination, but yields only part of the story. This paper suggests that two additional gaps should be evaluated: the gap between the general public and the purchaser, and that which exists between one-time and repeat visitors. Using Bintan Resorts, Indonesia, a relatively new self-contained resort development near Singapore, this paper provides a tool for evaluating these gaps, and at the same time provides an interesting view of Bintan, a destination that has set its sights upon becoming the “Hawaii of the Orient” (Yeow, [Singapore] The Straits Times , 17 September 1993, Money Section 47).