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Ozone (O3) in the troposphere, an air pollutant with phytotoxicity, is considered as a driver of global warming, because it reduces plant carbon fixation. Recently, a process-based plant growth model has been used in evaluating the O3 impacts on plants (Schauberger et al., 2019). To make the evaluation more rigorous, we developed a plant growth model and clarified the key factors driving O3-induced change in the whole-plant carbon fixation amount (Cfix). Fagus crenata seedlings were exposed to three O3 levels (charcoal-filtered air or 1.0- or 1.5-folds ambient [O3]) with three soil fertilization levels (non-, low-, or high-fertilized), i.e., a total of nine treatments. The Cfix was reduced in non- and low-fertilized treatments but was unaffected in high-fertilized treatment by O3 fumigation. Our plant growth model could simulate Cfix accurately ( less then 10% error) by considering the impacts of O3 on plant leaf area and photosynthetic capacities, including maximum velocities of carboxylation and electron transport (Vcmax and Jmax, respectively), and the initial slope and convexity of the curve of the electron transport velocity response to photosynthetic photon flux density (φ and θ, respectively). Furthermore, the model revealed that changes in Vcmax and Jmax, φ and θ, or leaf area, caused by 1.5-folds the ambient [O3] fumigation resulted in the following Cfix changes -1.6, -5.8, or -16.4% in non-fertilized seedlings, -4.1, -4.4, or -9.3% in low-fertilized seedlings, and -4.6, -7.6, or +5.8% in high-fertilized seedlings. Therefore, photosynthetic capacities (particularly φ and θ) and leaf area are important factors influencing the impact of O3 on Cfix of F. crenata seedlings grown under various fertilization levels. Further, the impacts of O3 and soil nutrient on these photosynthetic capacities and plant leaf area should be considered to predict O3-induced changes in carbon fixation by forest tree species using the process-based plant growth model. There is clear evidence of severe honeybee declines in recent years, and parallel declines of plant community and crop productivity that rely on them. Different stresses, including heat stress, are among the primary drivers of this decline. However, the mechanisms by which honeybees respond to heat stress are elusive. Though heat shock proteins (Hsps) play important roles in heat stress response, the function of DnaJs (a subfamily of Hsps) is unclear. Here, we aimed to determine the underlying regulatory mechanism of honeybees to heat stress mediated by DnaJs. We found that several DnaJ genes, including DnaJA1, DnaJB12 and DnaJC8, are key for honeybee heat tolerance. DnaJA1 and DnaJB12 are cytoplasmic proteins, and DnaJC8 is a nuclear protein. The expression of DnaJA1, DnaJB12 and DnaJC8 was induced at different levels under short-term and long-term heat stress. Phenotypic analysis indicated that DnaJA1, DnaJB12 and DnaJC8 knockdown attenuated honeybee heat resistance. In addition, DnaJA1 participated in the heat stress response by upregulating many heat-inducible genes at the transcriptome-wide level, especially LOC108002668 and LOC107995148. Importantly, the upregulation of LOC108002668 and LOC107995148 was significantly repressed under heat stress when DnaJA1 was knocked down. We also found that knockdown of DnaJA1, DnaJB12 and DnaJC8 decreased antioxidant defense ability and increased the degree of oxidative damage in the honeybee. Taken together, our results indicate that DnaJ genes play important roles under heat stress in the honeybee. Overexpression of DnaJ genes may protect honeybees from heat stress-induced injuries and increase their survival rate. V.A novel photocatalyst (Cu-TiO2@HQ) had been synthesized by combining Cu-doped TiO2 nanoparticles with 8-Hydroxyquinoline (HQ) via hydrothermal method. The photocatalytic activities of Cu-TiO2@HQ were investigated by using phenol and tetrabromobisphenol A (TBBPA) as target pollutants, respectively. 1-Methylnicotinamide The results indicated that the degradation efficiencies of phenol and TBBPA by Cu-TiO2@HQ were 99.2% (in 30 min) and 99.4% (in 10 min) under visible light irradiation. Both of them were much better than that of pure TiO2 (8.63% in 30 min) and Cu-TiO2 (14.74% in 30 min). When phenol or TBBPA were degraded together with the reduction of Cr (VI), the reaction rate of each pollutant was significantly increased, and the cyclic stability of photocatalyst Cu-TiO2@HQ was greatly improved. Based on the spectroscopic and photoelectric characteristic analysis we found that in the mixture of phenol-Cr (VI) or TBBPA-Cr (VI) both photo-generated electrons and holes can be consumed simultaneously, thus preventing their recombination. The possible degradation products of phenol and TBBPA including its degradation path way were also analyzed by high resolution liquid chromatography-mass spectrometry-mass spectrometry. Gestational diabetes mellitus (GDM) is a temporary form of diabetes during pregnancy which influences the health of both mother and child. Both inflammation and oxidative stress have been implicated in the pathophysiology of GDM. Apocynin, acetophenone with anti-oxidative and anti-inflammation activities, has been shown to protect against insulin resistance. In the current study, the effects of apocynin on GDM symptoms, productive outcomes, oxidative stress, and inflammation were evaluated and the underlying mechanisms were explored. We administrated apocynin to GDM mice and monitored the GDM symptoms including body weight, serum levels of glucose, insulin, lipid profile, and the fetal outcomes in GDM mice. We also evaluated the effects of apocynin on placental oxidative stress, inflammation, and activation of TLR4/NF-κB signaling pathway in GDM mice. Here, we reported that apocynin treatment significantly reduced serum levels of glucose, cholesterol, triglyceride, and low-density lipoprotein in GDM mice, while significantly increased serum level of insulin and high-density lipoprotein. Apocynin improved fetal outcomes in GDM mice. Apocynin ameliorated placental oxidative stress and inflammation and inhibited TLR4/NF-κB signaling pathway activation in GDM mice. We concluded that apocynin suppressed oxidative stress and inflammation in GDM by inhibiting the TLR4/NF-κB signaling pathway.We recently reported that human herpesvirus 6 (HHV-6) infection is frequently present in endometrial tissue of women with unexplained infertility, and that virus infection induces a profound remodulation of miRNA expression in human cells of different origin. Since specific miRNA patterns have been associated with specific pregnancy outcomes, we aimed to analyze the impact of HHV-6A infection on miRNAs expression and trophoblast receptivity in human endometrial cells. To this purpose, a human endometrial cell line (HEC-1A) was infected with HHV-6A and analyzed for alterations in the expression of miRNAs and for permissiveness to the attachment of a human choriocarcinoma trophoblast cell line (JEG-3). The results showed that HHV-6A infection of endometrial cells up-modulates miR22 (26-fold), miR15 (19.5-fold), and miR196-5p (12.1 fold), that are correlated with implant failure, and down-modulates miR18 (11.4 fold), miR101-3p (4.6 fold), miR181-5p (4.9 fold), miR92 (3.3 fold), and miR1207-5p (3.9 fold), characterized by a low expression in preeclampsia. Moreover, HHV-6A-infected endometrial cells infected resulted less permissive to the attachment of trophoblast cells. In conclusion, collected data suggest that HHV-6A infection could modify miRNA expression pattern and control of trophoblast cell adhesion of endometrial cells, undermining a correct trophoblast cell attachment on endometrial cells.We aimed to study the association between the number of placentas with vascular malperfusion lesions in dichorionic twin pregnancies complicated by preeclampsia and the severity of the disease and pregnancy outcomes. Dichorionic twin pregnancies with preeclampsia (n = 125), from January 2007-June 2018, were reviewed. Affected placenta was defined as the presence of maternal/fetal vascular malperfusion lesions. Maternal demographics, pregnancy characteristics, and neonatal outcomes were compared between three groups no pathological placentas, one pathological placenta, and two pathological placentas. Composite adverse neonatal outcome was defined as ≥ 1 early neonatal complication. Regression analysis models were used to recognize independent associations with the number of involved placentas. The two pathological placenta group (n = 57 pregnancies), the one pathological placenta group (n = 40 pregnancies), and the no pathological placenta group (n = 28 pregnancies) differed in terms of gestational age (GA) ath SGA and adverse neonatal outcome.A consistent body of in vitro evidence supports a detrimental effect of endometriosis on ovarian steroidogenesis, in particular the synthesis of estrogens. However, clinical evidence is scanty and methodologically weak. This study aimed at clarifying whether peripheral 17-β-estradiol during IVF are influenced by the presence of endometriosis. Women undergoing IVF were retrospectively reviewed. Cases were women with a diagnosis of endometriosis. Controls were matched to cases in a 11 ratio by study period, age, total number of developed follicles on the day of hCG administration, protocol of hyperstimulation, gonadotropin used, and starting dose. The primary outcome was the ratio between serum levels of 17-β-estradiol and the total number of developed follicles. Fifty-three women with endometriosis and 53 controls were selected. The median ratio (interquartile range) between serum 17-β-estradiol and the total number of developed follicles in the two groups was 207 (164-282) and 201 (144-268) pg/ml, respectively (p = 0.46). Sensitivity analyses on the magnitude of the follicular response, the history of surgery for endometriomas, and the presence of endometriomas did not show any subgroup at increased risk of peripheral estrogens impairment. Endometriosis does not influence peripheral levels of 17-β-estradiol during IVF. Our findings argue against a biologically relevant effect of the disease on ovarian estrogen-synthesis.Antenatal steroids suppress growth in the fetus and newborn. Although weight deficits are regained by weaning, studies show that intrauterine growth restriction with postnatal "catch-up" growth is a risk factor for hypertension, insulin resistance, and ischemic heart disease in adult life, with multigenerational consequences. We tested the hypothesis that fetal exposure to betamethasone suppresses fetal growth in the F1 pups and their untreated F2 offspring. Timed pregnant rats received a single two-dose course of intramuscular betamethasone (0.25 mg/kg/day) on days 17 and 18 of gestation. Matched controls received equivalent volumes sterile normal saline. The first-generation (F1) offspring were studied at term, P21, and P70, or mated at P60 to produce the following subgroups (1) saline male/saline female (SM/SF), (2) betamethasone (B) male/BFemale (BM/BF), (3) BM/SF, and (4) SM/BF. The unexposed second-generation (F2) offspring were examined at birth and P70. Growth, neurological outcomes, and growth factors were determined.