Environmental exposures during pregnancy have been associated with adverse obstetric outcomes. However, limited and inconsistent evidence exists regarding the association between air temperature exposure and the risk of preeclampsia (PE). This study aimed to evaluate the correlation between ambient temperature exposure during pregnancy and PE risk, as well as identify the specific time window of temperature exposure that increases PE risk. A population-based cohort study was conducted from January 2012 to April 2022 in Guangzhou, China. Pregnant women were recruited in early pregnancy and followed until delivery. A total of 3,314 PE patients and 114,201 normal pregnancies were included. Ambient temperature exposures at different gestational weeks were recorded for each participant. Logistic regression models were used to evaluate the correlation between ambient temperature exposure and PE risk. Stratified analyses were conducted based on maternal age and pre-pregnancy BMI. Distributed lag models were employed to identify the time window of temperature exposure related to PE. Exposure to extreme high temperature (aOR = 1.24, 95 % CI 1.12–1.38) and moderate high temperature (aOR = 1.22, 95 % CI 1.10–1.35) during early pregnancy was associated with an increased risk of PE. Furthermore, women with higher pre-pregnancy BMI had a higher risk of developing PE when exposed to high temperature during early pregnancy compared to normal-weight women. The time window of temperature exposure related to PE was identified as pregnancy weeks 1 to 8. This study provides evidence for the association of high temperature exposure during early pregnancy with the risk of PE, as well as identifies the specific time window of temperature exposure related to PE. These findings have implications for developing potential strategies to protect pregnant women, particularly those with higher pre-pregnancy BMI, from the adverse effects of extreme temperatures during early pregnancy.
Sun-induced chlorophyll fluorescence (SIF) has shown potential in quantifying plant responses to environmental changes by which abiotic drivers are dominated. However, SIF is a mixed signal influenced by factors such as leaf physiology, canopy structure, and sun-sensor geometry. Whether the physiological information contained in SIF can better quantify crop disease stresses dominated by biological drivers, and clearly explain the physiological variability of stressed crops, has not yet been sufficiently explored. On this basis, we took winter wheat naturally infected with stripe rust as the research object and conducted a study on the responses of physiological signals and reflectivity spectrum signals to crop disease stress dominated by biological drivers, based on in situ canopy-scale and leaf-scale data. Physiological signals include SIF, SIFyield (normalized by absorbed photosynthetically active radiation), fluorescence yield (ΦF) retrieved by NIRvP (non-physiological components of canopy SIF) and relative fluorescence yield (ΦF-r) retrieved by near-infrared radiance of vegetation (NIRvR). Reflectance spectrum signals include normalized difference vegetation index (NDVI) and near-infrared reflectance of vegetation (NIRv). At the canopy scale, six signals reached extremely significant correlations (P < 0.001) with disease severity levels (SL) under comprehensive experimental conditions (SL without dividing the experimental samples) and light disease conditions (SL < 20%). The strongest correlation between NDVI and SL (R = 0.69) was observed under the comprehensive experimental conditions, followed by NIRv (R = 0.56), ΦF-r (R = 0.53) and SIF (R = 0.51), and the response of ΦF (R = 0.45) and SIFyield (R = 0.34) to SL was weak. Under lightly diseased conditions, ΦF-r (R = 0.62) showed the strongest response to disease, followed by SIFyield (R = 0.60), SIF (R = 0.56) and NIRv (R = 0.54). The weakest correlation was observed between ΦF and SL (R = 0.51), which also showed a result approximating NDVI (R = 0.52). In the case of a high level of crop disease severity, NDVI showed advantages in disease monitoring. In the early stage of crop diseases, which we pay more attention to, compared with SIF and reflectivity spectrum signals, ΦF-r estimated by the newly proposed ‘NIRvR approach’ (which uses SIF together with NIRvR (i.e., SIF/ NIRvR) as a substitute for ΦF) showed superior ability to monitor crop physiological stress, and was more sensitive to plant physiological variation. At the leaf scale, the response of SIF to SL was stronger than that of NDVI. These results validate the potential of ΦF-r estimated by the NIRvR approach to monitoring disease stress dominated by biological drivers, thus providing a new research avenue for quantifying crop responses to disease stress.
Electrocatalytic water splitting suffers from sluggish kinetics towards the hydrogen evolution reaction (HER). Balancing the adsorption/desorption ability towards H* and OH* is considered to be an efficient way to enhance the HER efficiency, but it is too hard at one activity site. In this work, the HER activity of the single 3d transition metal atom-anchored BC2N monolayer (M@BC2N, M = Fe, Co, and Ni) was investigated by a density functional theory approach. Our calculation suggests that an efficient dual-active site is formed on M@BC2N towards the HER, i.e., the metal center M as the OH* active site and its adjacent C atoms as the H* active site. The combination of single M atoms with the BC2N monolayer can effectively tune the electronic structure of dual active sites to optimize the adsorption of H* and OH*, resulting in a HER activity sequence of Fe@BC2N < Co@BC2N < Ni@BC2N. Notably, the HER exchange current density of Ni@BC2N reaches up to 0.53 mA cm-2, which is close to the value for commercial Pt/C, suggesting its huge potential in the HER.
Radiotherapy (RT) has been shown to cause immunogenic cell death (ICD) of cancer cells, which promote the release of tumor-associated antigens, and trigger the cancer-immunity cycle (CIC). However, ICD induced by RT usually does not occur in hypoxic tumor cells due to their resistance to radiation. Moreover, RT also induces programmed death ligand 1 (PD-L1) upregulation on tumor cells, which has an inhibitory effect on T lymphocytes. Therefore, therapy based on CIC must selectively target the restricted steps of antitumor immunity. Herein, the authors design a versatile three-in-one assembling nanoparticle that can simultaneously execute these obstacles. The amphiphilic peptide drug conjugate NIA-D1, containing the hydrophobic radio-sensitizer 2-(2-nitroimidazol-1-yl) acetic acid (NIA), a peptide substrate of matrix metalloproteinase-2, and a hydrophilic PD-L1 antagonist D PPA-1, is constructed and co-assembled with hydrophobic Toll-like receptor (TLR) 7/8 agonist R848 to form nanoparticle NIA-D1@R848. The NIA-D1@R848 nanoparticles combined with RT can trigger the apoptosis of tumor cells and initiate the CIC. In the presence of R848, it promotes the maturation of dendritic cells, which together with protein programmed cell death protein 1 (PD-1) and its ligand PD-L1 blockade to relieve T cell suppression, and amplify the antitumor immune cycle. In conclusion, a functionalized three-in-one nanoparticle NIA-D1@R848 is successfully constructed, which can induce strong systemic antitumor immune response.
Abstract An immunoaffinity chromatographic method was developed for the purification of 9 sulfonamides (sulfamethazine, sulfadimethoxine, sulfamerazine, sulfathiazole, sulfamethoxazole, sulfamethizole, sulfadiazine, sulfamonomethoxine, and sulfapyridine) from chicken tissue (muscle and liver) samples. Two monoclonal antibodies (antisulfamethazine and antisulfamethoxazole) were simultaneously covalently coupled to CNBr-activated Sepharose 4B for the preparation of a re-usable immunoaffinity column. After extraction with methanolwater and purification by immunoaffinity column, the sulfonamides were determined by reversed-phase liquid chromatography and UV detection at 270 nm. The recoveries for each drug at fortification levels of 1050 ng/g ranged from 74.1 to 108.9 with relative standard deviations from 1.9 to 11.5. The limits of detection were 2 ng/g for each drug.
The molecular mechanisms underlying arsenic-induced neurotoxicity have not been completely elucidated. Our study aimed to determine the role of the Fas-FasL-FADD signaling pathway in arsenic-mediated neuronal apoptosis. Pathological and molecular biological tests were performed on the cerebral cortex of arsenic-exposed rats and SH-SY5Y neuroblastoma cells. Arsenic induced apoptosis in the cortical neurons, which corresponded to abnormal ultrastructural changes. Mechanistically, arsenic activated the Fas-FasL-FADD signaling pathway and the downstream caspases both in vivo and in vitro. ZB4 treatment reversed the apoptotic effects of arsenic on the SHSY5Y cells. Taken together, arsenic induces neurotoxicity by activating the Fas-FasL-FADD signaling pathway.