Ruddlesden-Popper Perovskite Nanocrystals as Interface Modification Layer for Efficient Perovskite Solar Cells.

Perovskite nanocrystals are advantageous for interfacial passivation of perovskite solar cells (PSCs), but the insulating long alkyl chain surface ligands impede the charge transfer, while the conventional ligand exchange would possibly introduce surface defects to the nanocrystals. In this work, we reported novel in situ modification of CsPbBr3 nanocrystals using a short chain conjugated molecule 2-methoxyphenylethylammonium iodide (2-MeO-PEAI) for interfacial passivation of PSCs. Transmission electron microscopy studies with atomic resolution unveil the transformation from cubic CsPbBr3 to Ruddlesden-Popper phase (RPP) nanocrystals due to halogen exchange. Synergic passivation by the RPP nanocrystals and 2-MeO-PEA+ has led to suppressed interface defects and enhanced charge carrier transport. Consequently, PSCs with in situ modified RPP nanocrystals achieved a champion power conversion efficiency of 24.39%, along with an improvement in stability. This work brings insights into the microstructural evolution of perovskite nanocrystals, providing a novel and feasible approach for interfacial passivation of PSCs.

Fetal overgrowth and weight trajectories during infancy and adiposity in early childhood.

BACKGROUND: Large-for-gestational age (LGA), a marker of fetal overgrowth, has been linked to obesity in adulthood. Little is known about how infancy growth trajectories affect adiposity in early childhood in LGA. METHODS: In the Shanghai Birth Cohort, we followed up 259 LGA (birth weight >90th percentile) and 1673 appropriate-for-gestational age (AGA, 10th-90th percentiles) children on body composition (by InBody 770) at age 4 years. Adiposity outcomes include body fat mass (BFM), percent body fat (PBF), body mass index (BMI), overweight/obesity, and high adiposity (PBF >85th percentile). RESULTS: Three weight growth trajectories (low, mid, and high) during infancy (0-2 years) were identified in AGA and LGA subjects separately. BFM, PBF and BMI were progressively higher from low- to mid-to high-growth trajectories in both AGA and LGA children. Compared to the mid-growth trajectory, the high-growth trajectory was associated with greater increases in BFM and the odds of overweight/obesity or high adiposity in LGA than in AGA children (tests for interactions, all P < 0.05). CONCLUSIONS: Weight trajectories during infancy affect adiposity in early childhood regardless of LGA or not. The study is the first to demonstrate that high-growth weight trajectory during infancy has a greater impact on adiposity in early childhood in LGA than in AGA subjects. IMPACT: Large-for-gestational age (LGA), a marker of fetal overgrowth, has been linked to obesity in adulthood, but little is known about how weight trajectories during infancy affect adiposity during early childhood in LGA subjects. The study is the first to demonstrate a greater impact of high-growth weight trajectory during infancy (0-2 years) on adiposity in early childhood (at age 4 years) in subjects with fetal overgrowth (LGA) than in those with normal birth size (appropriate-for-gestational age). Weight trajectory monitoring may be a valuable tool in identifying high-risk LGA children for close follow-ups and interventions to decrease the risk of obesity.

Activated carbon enhanced traditional activated sludge process for chemical explosion accident wastewater treatment.

With the development of industries, explosion accidents occur frequently during production, transportation, usage and storage of hazard chemicals. It remained challenging to efficiently treat the resultant wastewater. As an enhancement of traditional process, the activated carbon-activated sludge (AC-AS) process has a promising potential in treating wastewater with high concentrations of toxic compounds, chemical oxygen demand (COD) and ammonia nitrogen (NH4+-N), etc. In this paper, activated carbon (AC), activated sludge (AS) and AC-AS were used to treat the wastewater produced from an explosion accident in the Xiangshui Chemical Industrial Park. The removal efficiency was assessed by the removal performances of COD, dissolved organic carbon (DOC), NH4+-N, aniline and nitrobenzene. Increased removal efficiency and shortened treatment time were achieved in the AC-AS system. To achieve the same COD, DOC and aniline removal (90%), the AC-AS system saved 30, 38 and 58 h compared with the AS system, respectively. The enhancement mechanism of AC on the AS was explored by metagenomic analysis and three-dimensional excitation-emission-matrix spectra (3DEEMs). More organics, especially aromatic substances were removed in the AC-AS system. These results showed that the addition of AC promoted the microbial activity in pollutant degradation. Bacteria, such as Pyrinomonas, Acidobacteria and Nitrospira and genes, such as hao, pmoA-amoA, pmoB-amoB and pmoC-amoC, were found in the AC-AS reactor, which might have played important roles in the degradation of pollutants. To sum up, AC might have enhanced the growth of aerobic bacteria which further improved the removal efficiency via the combined effects of adsorption and biodegradation. The successful treatment of Xiangshui accident wastewater using the AC-AS demonstrated the potential universal characteristics of the process for the treatment of wastewater with high concentration of organic matter and toxicity. This study is expected to provide reference and guidance for the treatment of similar accident wastewaters.

Perfluorooctanoic acid disrupts thyroid-specific genes expression and regulation via the TSH-TSHR signaling pathway in thyroid cells.

Perfluorooctanoic acid (PFOA) is a highly persistent and widespread chemical in the environment with endocrine disruption effects. Although it has been reported that PFOA can affect multiple aspects of thyroid function, the exact mechanism by which it reduces thyroxine levels has not yet been elucidated. In this study, FRTL-5 rat thyroid follicular cells were used as a model to study the toxicity of PFOA to the genes related to thyroid hormone synthesis and their regulatory network. Our results reveal that PFOA interfered with the phosphorylation of the cyclic adenosine monophosphate (cAMP)-response element binding protein (CREB) induced by thyroid-stimulating hormone (TSH), as well as the transcription levels of paired box 8 (PAX8), thyroid transcription factor 1 (TTF1), sodium/iodide cotransporter (NIS), thyroglobulin (TG), and thyroid peroxidase (TPO). However, the above outcomes can be alleviated by enhancing cAMP production with forskolin treatment. Further investigations showed that PFOA reduced the mRNA level of TSH receptor (TSHR) and impaired its N-glycosylation, suggesting that PFOA has disrupting effects on both transcriptional regulation and post-translational regulation. In addition, PFOA increased endoplasmic reticulum (ER) stress and decreased ER mass in FRTL-5 cells. Based on these findings, it can be inferred that PFOA disrupts the TSH-activated cAMP signaling pathway by inhibiting TSHR expression and its N-glycosylation. We propose that this mechanism may contribute to the decrease in thyroid hormone levels caused by PFOA. Our study sheds light on the molecular mechanism by which PFOA can disrupt thyroid function and provides new insights and potential targets for interventions to counteract the disruptive effects of PFOA.

Effect of folic acid supplementation in the association between short sleep duration and gestational diabetes mellitus.

PURPOSE: To examine whether or not folic acid (FA) supplementation may modify the relationships between duration or quality of sleep and gestational diabetes mellitus (GDM) risk. METHODS: In a case-control study of patients with GDM and controls, mothers were interviewed face-to-face at enrollment. The Pittsburgh Sleep Quality Scale was used to assess duration and quality of sleep during early pregnancy, and information on FA supplementation and covariates was obtained using a semiquantitative questionnaire. RESULTS: Among 396 patients with GDM and 904 controls, GDM risk increased by 328% and 148% among women with short (< 7 h) and long (≥ 9 h) sleep durations, respectively, compared to those averaging 7-8.9 h sleep. Mothers with poor sleep quality increased their GDM risk by an average of 75% (all p < 0.05). The effect of short sleep duration on GDM risk was much weaker among women with adequate FA supplementation (taking supplements containing ≥ 0.4 mg FA daily for each day of the first three months of pregnancy) than that among women with inadequate FA supplementation, with a p-value for interaction = 0.003. There were no significant effects of FA on links among long duration and poor quality of sleep with GDM risk. CONCLUSIONS: Sleep duration and quality in early gestation were related to increased GDM risks. FA supplementation may reduce GDM risk associated with short sleep duration.

The association between maternal urinary Bisphenol A levels and neurodevelopment at age 2 years in Chinese boys and girls: A prospective cohort study.

The impact of maternal exposure to Bisphenol A on child cognitive development as well as its sex dimorphism remains uncertain. This study used data of 215 mothers and their children from a birth cohort in Shanghai. Urinary BPA were measured in spot urine samples of mothers at late pregnancy and children at age 2 years. Cognitive development was evaluated by Ages & Stages Questionnaires, Third Edition (ASQ-3) at age 2 years. Urinary BPA was detectable in 98.9% of mothers (geometric mean, GM: 2.6 µg/g. creatinine) and 99.8% children (GM: 3.4 µg/g. creatinine). Relative to the low and medium BPA tertiles, high tertile of maternal urinary BPA concentrations were associated with 4.8 points lower (95% CI: -8.3, -1.2) in gross motor and 3.7 points lower (95% CI: -7.4, -0.1) in problem-solving domain in girls only, with adjustment for maternal age, maternal education, pre-pregnancy BMI, passive smoking during pregnancy, parity, delivery mode, birth-weight for gestational age, child age at ASQ-3 test. This negative association remained with additional adjustment for child urinary BPA concentrations at age 2 years. No association was observed in boys. These results suggested the sex-dimorphism on the associations of maternal BPA exposure with gross motor and problem-solving domains in children at age 2 years. This study also indicated that optimal early child development should start with a healthy BPA-free "in utero" environment.

Effects of sleep duration and sleep quality in early pregnancy and their interaction on gestational diabetes mellitus.

PURPOSE: To examine the association of sleep duration and quality in early pregnancy with gestational diabetes mellitus (GDM), and explore their interaction effect on GDM. METHODS: Participants from 2 hospitals were enrolled in this case-control study between April 2018 and November 2020. Sleep duration and quality were measured using the Pittsburg Sleep Quality Index (PSQI). RESULTS: A total of 1300 participants (396 GDM and 904 controls) were included. After adjusting for potential confounders, higher global PSQI scores or poor sleep quality were associated with GDM with odds ratios of 1.13 (95% CI 1.07, 1.19, p < 0.001) and 1.75 (95% CI 1.29, 2.38, p < 0.001), respectively; sleep duration < 7 h, 9-9.9 h and ≥ 10 h were all associated with increased GDM with odds ratios of 4.28 (95% CI 2.51, 7.31, p < 0.001), 1.69 (95% CI 1.20, 2.39, p = 0.003), and 4.42 (95% CI 3.01, 6.50, p < 0.001), respectively. In the stratified analysis based on sleep duration, the effect of poor sleep quality on GDM in the < 7 h group (OR 5.47, 95% CI 2.57, 11.64, p < 0.001) was much stronger than that in the 7-8.9 h group (OR 1.24, 95% CI 0.81, 1.91, p = 0.327), and the p value of the interaction was 0.011. CONCLUSIONS: Poor sleep quality and short or long sleep duration in early pregnancy were all associated with GDM, and an interaction effect between short sleep duration and poor sleep quality on GDM was noted.

Perfluorooctanoic acid exposure increases both proliferation and apoptosis of human placental trophoblast cells mediated by ER stress-induced ROS or UPR pathways.

Perfluorooctanoate acid (PFOA) is a highly persistent and widespread chemical in the environment. PFOA serum levels in pregnant women are positively associated with an increased risk of placenta-related disorders. However, the mechanism of PFOA cytotoxicity involved in placental cells and cellular responses such as ER stress remains poorly understood. In this study, we studied the cellular toxicity of PFOA with a focus on proliferation and apoptosis in a human placental trophoblast cell line. Cell viability, number, apoptosis, stress response, activation of the involved signaling pathways were assessed. Our results showed PFOA affected cell viability, proliferation and also resulted in apoptosis. Besides, both pro-proliferation and pro-apoptosis effects were attenuated by endoplasmic reticulum (ER) stress inhibitors. Further experiments demonstrated that two different signaling pathways were activated by PFOA-induced ER stress and involved in PFOA toxicity: the reactive oxygen species (ROS)-dependent ERK signaling triggered trophoblast proliferation, while the ATF4-dependent C/EBP homologous protein (CHOP) signaling was the trigger of apoptosis. We conclude that PFOA-induced ER stress is the trigger of proliferation and apoptosis of trophoblast via ROS or UPR signaling pathway, which leads to the altered balance critical to the normal development and function of the placenta.

Total arsenic, dimethylarsinic acid, lead, cadmium, total mercury, methylmercury and hypertension among Asian populations in the United States: NHANES 2011-2018.

BACKGROUND: Non-Hispanic Asians (NHA) in USA have been reported with higher arsenic (As), lead (Pb), cadmium (Cd), mercury (Hg) and their specific species levels, comparing with non-NHA. This study aimed to investigate the associations of these metal/metalloid levels with blood pressure levels and prevalence of hypertension among general NHA using the 2011-2018 National Health and Nutrition and Examination Survey (NHANES) data. METHODS: The study included participants aged 20 years and older with determinations of As, Dimethylarsinic acid (DMA), Pb, Cd, Hg and methyl-Hg (MeHg) in blood (n = 10, 177) and urine (n = 5, 175). These metals/metalloid levels were measured by inductively coupled plasma mass spectrometry. Systolic (SBP) and diastolic blood pressure (DBP) levels were examined through a standardized protocol. Censored normal regression model and logistic regression model were employed to explore the associations of As, DMA, Pb, Cd, Hg and MeHg levels with blood pressure levels and prevalence of hypertension respectively, and potential confounders were adjusted in these regression models. Quantile-based g-computation approach was used to analysis joint effect of metals mixture on blood pressure level and hypertension. RESULTS: For NHA, urinary As and Hg levels were associated with increased DBP level; Higher blood Hg and MeHg levels were related to increased blood pressure levels and hypertension; However, negative association was observed between urinary Cd and SBP level; Blood metals mixture (including blood Pb, Cd and Hg) was associated with increased DBP level, but not for hypertension. For non-NHA, urinary As and DMA levels were associated with increased SBP level, but not DBP level and prevalence of hypertension; Urinary Pb level was associated with decreased DBP level; Nevertheless, positive associations were observed between blood Pb levels and SBP and prevalence of hypertension; Blood Hg level was associated with decreased DBP level and prevalence of hypertension; Furthermore, blood MeHg level was associated with decreased DBP level; Positive association was observed between blood metals mixture and increased SBP level among non-NHA. CONCLUSIONS: Highly exposed to Hg level among NHA was associated with increased blood pressure levels and prevalence of hypertension. Urinary As level was associated with increased DBP level among NHA. Furthermore, blood metals mixture was related to increased DBP level among NHA. Further prospective studies with larger sample size should be performed to warrant the results.

Maximizing electron flux, microbial diversity and gene abundance in MFC powered electro-Fenton system by optimizing co-addition of lysozyme and 2-bromoethanesulfonate.

In this study, a microbial fuel cell powered electro-Fenton system (MFCⓅEFs) was established in order to overcome the shortcomings of low electron flux and unexpected methane production, while simultaneously treating excess sludge (ES, substrate) and refractory syringic acid (SA). A strategy of co-adding lysozyme (LZ, as ES degradation catalyst) and 2-bromoethanesulfonate (BES, as methane inhibitor) into ES was optimized in MFCⓅEFs to maximize electron flux, microbial community diversity and functional gene abundance. The removal of sludge total chemical oxygen demand (TCOD) achieved 81.69% in 25 d under an optimal co-addition strategy (40.41 mg/gSS of LZ, 27.03 mmol/L of BES, adding on 22.8 h of the7th day), with a simultaneous high degradation of SA (99.30% in 25 h). Correspondingly, a maximum power density of 3.35 W/m3 was achieved (only 0.62 W/m3 from the control), which effectively realizes in-situ micro-electricity generation and utilization for bioelectric Fenton processes. Moreover, 42.25% of the total charges were employed for bio-electricity generation. The electricigens of Pseudomonas, Acinetobacter and Chlorobium showed effective enrichment, while the abundance of methanogenesis archaea was extremely decreased. Functional genes associated with methanogenesis including mtaA, hdra, and mcrA were effectively inhibited. The life cycle assessment along with an optimized co-addition strategy illustrated a beneficial environmental effect, particularly in terms of ecosystem quality and climate change. Above all, an enhanced synchronous degradation of excess sludge and refractory pollutants had been realized in a green and environmentally friendly way.

Effect of nighttime sleep duration and midday napping in early pregnancy on gestational diabetes mellitus.

PURPOSE: To explore the effect of nighttime sleep duration and midday napping in early pregnancy on gestational diabetes mellitus (GDM) among Chinese women. METHODS: Information on midday napping and nighttime sleep duration was assessed by a questionnaire. Diagnostic information of GDM was derived from the routine oral glucose tolerance test (OGTT) during the second trimester of pregnancy. RESULTS: A total of 500 pregnant women, including 196 patients with GDM and 304 controls, were included in the present study. In the case group, 47% of women took a midday nap > 1 h/day, and the proportion was 22% in the control group. Compared with women who had a midday nap ≤ 1 h/day, women who had a nap > 1 h/day had a significantly increased risk of GDM (OR 3.00, 95% CI 1.87, 4.82, p < 0.001). Compared with women who had a nighttime sleep of 7 to 8.9 h/night, women who slept < 7 or ≥ 9 h/night all had a significantly increased risk of GDM. Stratified analyses showed that compared with the nighttime sleep duration of 7 to 8.9 h/day, the GDM risk of the < 7 h/night group increased among mothers who had a midday nap ≤ 1 h/day. The impact was stronger than among women who had a nap > 1 h/day (p = 0.006). CONCLUSIONS: Shorter or longer nighttime sleep duration and longer midday napping duration in early pregnancy were all related to GDM. Midday napping would reduce the risk of GDM among mothers with shorter nighttime sleep duration.

The triclosan-induced shift from aerobic to anaerobic metabolism link to increased steroidogenesis in human ovarian granulosa cells.

Triclosan (TCS) is an endocrine-disrupting chemical (EDC), which is used ubiquitously as an antimicrobial ingredient in healthcare products and causes contamination in the environment such as air, water, and biosolid-amended soil. Exposure to TCS may increase the risk of reproduction diseases and health issues. Several groups, including ours, have proved that TCS increased the biosynthesis of steroid hormones in different types of steroidogenic cells. However, the precise mechanism of toxic action of TCS on increased steroidogenesis at a molecular level remains to be elucidated. In this study, we try to address the mode of action that TCS affects energy metabolism with increased steroidogenesis. We evaluated the adverse effects of TCS on energy metabolism and steroidogenesis in human ovarian granulosa cells. The goal is to elucidate how increased steroidogenesis can occur with a shortage of adenosine triphosphate (ATP) whereas mitochondria-based energy metabolism is impaired. Our results demonstrated TCS increased estradiol and progesterone levels with upregulated steroidogenesis gene expression at concentrations ranging from 0 to 10 µM. Besides, glucose consumption, lactate level, and pyruvate kinase transcription were increased. Interestingly, the lactate level was attenuated with increased steroidogenesis, suggesting that pyruvate fate was shifted away from the formation of lactate towards steroidogenesis. Our study is gathering evidence suggesting a mode of action that TCS changes energy metabolism by predominating glucose flow towards the biosynthesis of steroid hormones. To the best of our knowledge, this is the first report that TCS presents such toxic action in disrupting hormone homeostasis.

Long-term low-dose oxytetracycline potentially leads to neurobehavioural changes.

Trace levels of oxytetracycline (OTC)-a veterinary antibiotic and feed additive-are widespread in the environment. Studies revealed that OTC potentially impairs thyroid function, which may affect neurobehaviour; however, the impact of exposure to environmental concentrations of OTC on adult neurobehaviour is unknown. In this study, the effects of OTC on zebrafish after 30-day exposure were investigated. The total swimming distance was significantly increased under vibration and light/dark stimulation, while time spent in the white area was prolonged during the black/white preference test, indicating that the zebrafish became bolder and more impulsive under low OTC exposure. Additionally, monoamine neurotransmitter (5-hydroxytryptamine, dopamine, norepinephrine) levels were decreased and gene expression of monoamine oxidase (mao) involved in neurotransmitter metabolism was upregulated at the transcription level after OTC exposure. Because triiodothyronine (T3) levels were enhanced following exposure to OTC, we speculated that T3 may mediate OTC damage to the nervous system. Our simulated molecular docking analysis showed that OTC combined with the sodium iodide cotransporter protein may result in excessive T3 synthesis. We further exposed zebrafish to T3, and they exhibited similar behaviour to the OTC exposure group. In conclusion, environmental OTC may activate monoamine oxidase and enhance the metabolism of monoaminergic neurotransmitters via T3, thereby inducing abnormal neurobehaviour.

Adenylyl cyclase A mRNA localized at the back of cells is actively translated in live chemotaxing Dictyostelium.

Dictyostelium discoideum cells transport adenylyl cyclase A (ACA)-containing vesicles to the back of polarized cells to relay exogenous cAMP signals during chemotaxis. Fluorescence in situ hybridization (FISH) experiments showed that ACA mRNA is also asymmetrically distributed at the back of polarized cells. By using the MS2 bacteriophage system, we now visualize the distribution of ACA mRNA in live chemotaxing cells. We found that the ACA mRNA localization is not dependent on the translation of the protein product and requires multiple cis-acting elements within the ACA-coding sequence. We show that ACA mRNA is associated with actively translating ribosomes and is transported along microtubules towards the back of cells. By monitoring the recovery of ACA-YFP after photobleaching, we observed that local translation of ACA-YFP occurs at the back of cells. These data represent a novel functional role for localized translation in the relay of chemotactic signals during chemotaxis.

Perfluoroalkyl substances exposure in early pregnancy and preterm birth in singleton pregnancies: a prospective cohort study.

BACKGROUND: Preterm birth (PTB, < 37 completed weeks' gestation) is one of the global public health concerns. Epidemiologic evidence on the potential impact of perfluoroalkyl substances (PFAS) on PTB is still limited and inconsistent. We aimed to investigate the associations between prenatal PFAS exposure and PTB among singleton live births. METHODS: We studied 2849 mother-infant pairs in the Shanghai Birth Cohort (SBC) from 2013 to 2016. Ten PFAS in maternal plasma in early pregnancy (gestational age, median (interquartile range): 15 (13-16) weeks) were measured. Primary outcomes were duration of gestation, PTB, spontaneous PTB and clinically indicated PTB. A linear regression model was used to assess the associations between ln-transformed PFAS and duration of gestation (in weeks). Logistic regression models were applied to estimate the relative risks of these outcomes. RESULTS: The incidence of overall PTB was 4.8% (95% confidence limit: 4.0-5.6%, n = 136) in this study population. In the linear regression analyses, PFAS were not associated with the duration of gestation after controlling for potential confounders. In the multiple logistic models, no significant associations were observed between PFAS and overall PTB, spontaneous or indicated PTB. CONCLUSION: In this prospective cohort study, we did not observe significant associations between maternal plasma PFAS concentrations in early pregnancy and gestational length, overall PTB, spontaneous or indicated PTB.

Triclosan and Female Reproductive Health: A Preconceptional Cohort Study.

BACKGROUND: Triclosan (2,4,4'-trichloro-2'-hydroxy-diphenyl ether) is widely used in personal care and household products. Previous in vitro and in vivo studies showed that triclosan may affect female reproductive health. However, evidence from human studies is scarce. OBJECTIVES: To assess the potential effects of triclosan on women's reproductive health. METHODS: A prospective cohort study recruited 1,182 couples who planned to conceive and presented to preconception care clinics for physical examination in Shanghai, China, between 2013 and 2015. These couples were then prospectively followed every 2 months for 12 months. Triclosan was quantified in preconception urine samples at enrollment. The outcomes of interest included menstruation and fecundity. Normal menstruation was defined as a woman who had normal cycle duration between 21 and 35 days, duration of menstrual bleeding between 3 and 7 days, and self-reported normal amount of menstrual bleeding. RESULTS: A total of 698 women were included in the analysis on the association between triclosan and menstruation. Compared with low triclosan levels, high triclosan levels were associated with increased risks of abnormal menstruation [adjusted odds ratio (OR) = 1.47; 95% confidence interval = 1.05, 2.06] and prolonged menstrual cycle (OR = 2.08; 95% confidence interval = 1.00, 2.31). In the analysis on the association between triclosan and fecundability, 648 women were included. Compared with the lowest tertile of triclosan level (<1.1 ng/mL), the highest level (>4.5 ng/mL) was associated with a 23% of reduction in fecundability and there tended to be a dose-response pattern. CONCLUSION: Our findings suggest that triclosan may affect menstruation and reduce female fecundity.

[Role of PPARα in the oxidative damage of rat liver cells BRL-3A induced by perfluorooctanoic acid].

OBJECTIVE: To investigate the role of PPARα in oxidative damage of BRL-3A cells induced by perfluorooctanoic acid( PFOA) by inhibiting and activating gene expression. METHODS: In vitro culture of rat liver BRL-3A cells were divided into blank control group, PFOA experimental control group, PPARα inhibition group( GW6471), PPARα agonist group( WY14643), PPARα inhibitor pretreatment PFOA group( GW6471 + PFOA), PPARα agonist pretreatment PFOA group( WY14643 + PFOA). Fluorescence immunocytochemistry was used to detect the expression of PPARα. The expression of PPARα and its downstream target gene was detected by q PCR. The expression of related protein was detected by Western blot. RESULTS: The expression of PPARα in rat liver BRL-3A cells was successfully inhibited and stimulated by inhibitors and agonists( P < 0. 05). Compared with the blank control group and the PFOA experimental control group, there was a significant decrease in the content of ROS in the WY14643 + PFOA group compared with the blank control group and the PFOA experimental control group( P < 0. 05). The expression of PPARα and its downstream gene Cyp4a1 in GW6471 + PFOA group was higher than that in PPARα inhibitor group( P < 0. 05), but it was significantly lower than that in PFOA experimental control group( P < 0. 05). The expression of related genes in WY14643 + PFOA group was significantly lower than that in PPARα agonist group( P < 0. 05). The protein expression of PPARα in GW6471 + PFOA group was up-regulated compared with the inhibitor group, there was no difference compared with the blank control group. The protein expression of PPARα in WY14643 + PFOA group was not significantly different from that in agonist group, but it was significantly higher than that in PFOA experimental control group( P < 0. 05). CONCLUSION: PFOA exposure can activate the expression of PPARα, remove ROS, PPARα played a protective role in PFOA-induced rat liver cell oxidative damage.

Adenylyl cyclase mRNA localizes to the posterior of polarized DICTYOSTELIUM cells during chemotaxis.

BACKGROUND: In Dictyostelium discoideum, vesicular transport of the adenylyl cyclase A (ACA) to the posterior of polarized cells is essential to relay exogenous 3',5'-cyclic adenosine monophosphate (cAMP) signals during chemotaxis and for the collective migration of cells in head-to-tail arrangements called streams. RESULTS: Using fluorescence in situ hybridization (FISH), we discovered that the ACA mRNA is asymmetrically distributed at the posterior of polarized cells. Using both standard estimators and Monte Carlo simulation methods, we found that the ACA mRNA enrichment depends on the position of the cell within a stream, with the posterior localization of ACA mRNA being strongest for cells at the end of a stream. By monitoring the recovery of ACA-YFP after cycloheximide (CHX) treatment, we observed that ACA mRNA and newly synthesized ACA-YFP first emerge as fluorescent punctae that later accumulate to the posterior of cells. We also found that the ACA mRNA localization requires 3' ACA cis-acting elements. CONCLUSIONS: Together, our findings suggest that the asymmetric distribution of ACA mRNA allows the local translation and accumulation of ACA protein at the posterior of cells. These data represent a novel functional role for localized translation in the relay of chemotactic signal during chemotaxis.

A genetic variant in the placenta-derived MHC class I chain-related gene A increases the risk of preterm birth in a Chinese population.

Preterm birth (PTB) is a predominant contributor to neonatal mortality and morbidity worldwide. However, the pathophysiology of PTB is not well-understood. We tested the hypothesis that single-nucleotide polymorphisms (SNPs) in the placenta-derived MHC class I chain-related gene A (MICA) could disrupt placental development and hence result in PTB. Nineteen selected SNPs in MICA were genotyped in a case-control study of 127 premature infants and 634 term controls in a Chinese Han population. We found that significantly increased PTB risk was associated with homozygosity for the A variant of rs2256318 (adjusted odds ratio = 6.97 and 95% confidence interval = 2.34-20.74 for A/A, compared with G/G genotype, P = 0.001). In addition, the A/A genotype of rs2256318 was associated with decreased placental weight of neonates (ß = -25.331; P = 0.033). Furthermore, stratified analysis demonstrated that the A/A genotype of rs2256318 was associated with increased PTB risk in female group. In addition, we observed statistical interaction between the polymorphism rs2516448 and sex (P = 0.04). No significant differences in the distribution of haplotypes between cases and controls were detected. Our results indicate that the polymorphism of rs2256318 in MICA may contribute to the etiology of PTB through interfering with placental development. These findings need to be further validated in larger and multi-ethnic populations.

Urinary Bisphenol A Concentration and Gestational Diabetes Mellitus in Chinese Women.

BACKGROUND: Bisphenol A (BPA) has been associated with variable metabolic effects in animal models. It is unknown whether BPA exposure affects glucose tolerance in pregnancy. We aimed to investigate whether maternal urinary BPA concentration is associated with gestational diabetes mellitus (GDM). METHODS: This study included 620 pregnant women from Shanghai, China 2012-2013. Maternal urinary BPA concentration was measured by high-performance liquid chromatography-tandem mass spectrometry (HPLC-MS/MS). GDM (n = 79) was diagnosed according to the criteria of the International Association of Diabetes and Pregnancy Study Groups (IADPSG). Multivariate regressions were used to explore the relationships of urinary BPA with GDM, plasma glucose levels in the 75-g 2-hour oral glucose tolerance test (OGTT), birth weight, and ponder index. RESULTS: The geometric mean of BPA was 1.32 µg/L. After adjustment for maternal age, education, husband smoking status, prepregnancy body mass index (BMI), and urinary creatinine concentration, plasma glucose at 2 hours in the 75-g OGTT was 0.36 mmol/L lower (95% confidence index [CI] = -0.73, 0.01) for women with urine BPA in the high versus the low tertile. For each unit increase in natural log-transformed BPA, the odds of GDM was reduced by 27% (odds ratio (OR) = 0.73; 95% CI = 0.56, 0.97), the birth weight decreased by 25.70 g (95% CI = -54.48, 3.07), and ponder index was decreased by 0.02 (100 g/cm) (95% CI = -0.03, 0.00). CONCLUSIONS: Higher maternal urinary BPA concentrations were associated with reduced risk of GDM and marginally lower birth weight and ponder index.