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In view of the low computational efficiency and the limitations of the platform of the unsharp masking image enhancement algorithm, an unsharp masking image enhancement parallel algorithm based on Open Computing Language (OpenCL) is proposed. Based on the analysis of the parallel characteristics of the algorithm, the problem of unsharp masking processing is implemented in parallel. Making use of the characteristics of data reuse in the algorithm, the effective allocation and optimization of global memory and constant memory are realized according to the access attributes of data and the characteristics of the OpenCL storage model, and the use efficiency of off-chip memory is improved. Through the data storage access mode, the fast computing local memory access mode is discovered, and the logical data space transformation is used to convert the storage access mode, so as to improve the bandwidth utilization of the on-chip memory. The experimental results show that, compared with the CPU serial algorithm, the OpenCL accelerated unsharp masking image enhancement parallel algorithm greatly reduces the execution time of the algorithm while maintaining the same image quality, and achieves a maximum speedup of 16.71 times. The high performance and platform transplantation of the algorithm on different hardware platforms are realized. It provides a reference method for real-time processing of a large amount of data of high-resolution images for image enhancement.

p-Alkoxyphenols (AOPs) are a class of ethers that are widely used in industrial and agricultural productions and daily necessities. p-Phenoxyphenol (PhOP) and p-pentyloxyphenol (PeOP) belong to this class and have been reported to be estrogenic in vitro. However, their in vivo estrogenic activities have rarely been of concern. In this study, we performed an immature mouse uterotrophic assay and studied the estrogenic effects of these two compounds in mice. The results revealed that the uterine weights of the animals treated with PhOP significantly increased at doses of 30 and 300 mg kg-1 bw day-1 for 3 days (P β-estradiol (E2)-treated specimens. In particular, some estrogen-responsive genes, such as the Sprr2 gene family, Apoa1, Prap1, and Ahsg, displayed a regulation trend similar to that of E2. In addition, molecule docking analysis revealed that both PhOP and PeOP could be well docked into the active site of hERα, with potential of mean force (PMF) values of − 58.68 and − 52.67 kcal mol-1 for PhOP and PeOP, respectively. The results of this study indicate that PhOP exhibits relatively strong in vivo estrogenic activity, which could be of future concern.

Microalgae are the most abundant microorganisms in aquatic environments, and many possess the ability to remove organic contaminants. The presence of endocrine disruption compounds (EDCs) in many coastal marine systems and their associated risks have elicited great concern, especially in the case of nonylphenol (NP), which is classified as a priority contaminate by the U.S. EPA. In this context, batch experiments were conducted to investigate the intracellular absorption, extracellular adsorption and biodegradation of NP by four species of marine microalgae: Phaeocystis globosa, Nannochloropsis oculata, Dunaliella salina and Platymonas subcordiformis. The results showed a sharp reduction of NP in medium containing the four microalgal species during the first 24 h of incubation, and the four species exhibited the greatest capacity for NP adsorption and absorption within 24 h of culture. However, the amount of NP absorbed and adsorbed by all four microalgae decreased with increasing time in culture, and intracellular absorption was greater than extracellular adsorption. After 120 h of exposure to NP, the four species could biodegrade most of the NP in the medium, with efficiencies ranging from 43.43 to 90.94%. In sum, we found that the four microalgae have high biodegradation percentages and can thus improve the bioremediation of NP-contaminated water.

Fertilisation datasets collected from field experiments (n = 21) in tea-producing areas from 2016 to 2018 were used to build a quantitative evaluation of the fertility of tropical soils (QUEFTS) model to estimate nutrient uptake of tea plants, and to investigate relationships between tea yield and nutrient accumulation. The production of 1000 kg spring tea (based on one bud with two young expanding leaves) required 12.2 kg nitrogen (N), 1.2 kg phosphorus (P), and 3.9 kg potassium (K), and the corresponding internal efficiencies (IEs) for N, P, and K were 82.0, 833.3, and 256.4 kg kg−1. To produce 1000 kg summer tea, 9.1 kg N, 0.8 kg P, and 3.1 kg K were required, and the corresponding IEs for N, P, and K were 109.9, 1250.0, and 322.6 kg kg−1. For autumn tea, 8.8 kg N, 1.0 kg P, and 3.2 kg K were required to produce 1000 kg tea, and the corresponding IEs for N, P, and K were 113.6, 1000.0, and 312.5 kg kg−1. Field validation experiments performed in 2019 suggested that the QUEFTS model can appropriately estimate nutrient uptake of tea plants at a certain yield and contribute to developing a fertiliser recommendation strategy for tea production.

We study the synchronization behaviors of two indirectly coupled mechanical oscillators of different frequencies in a doublecavity optomechanical system. It is found that quantum synchronization is roughly vanishing though classical synchronization seems rather good when each cavity mode is driven by an external field in the absence of temporal modulations. By periodically modulating cavity detunings or driving amplitudes, however, it is possible to observe greatly enhanced quantum synchronization accompanied with nearly perfect classical synchronization. The level of quantum synchronization observed here is, in particular, much higher than that for two directly coupled mechanical oscillators. Note also that the modulation on cavity detunings is more appealing than that on driving amplitudes when the robustness of quantum synchronization is examined against the bath’s mean temperature or the oscillators’ frequency difference.

The global spread of Zika virus (ZIKV) as well as its unexpected link to infant microcephaly have resulted in serious public health concerns. No antiviral drugs against ZIKV is currently available, and vaccine development is of high priority to prepare for potential ZIKV pandemic. In the present study, a truncated E protein with the N-terminal 90% region reserved (E90) from a contemporary ZIKV strain was cloned and expressed in Escherichia coli, purified by a Ni-NTA column, and characterized by Western blotting assays. Immunization with recombinant E90 induced robust ZIKV-specific humoral response in adult BALB/c mice. Passive transfer of the antisera from E90-immunized mice conferred full protection against lethal ZIKV challenge in a neonatal mice model. Our results indicate that recombinant ZIKV E90 described here represents as a promising ZIKV subunit vaccine that deserves further clinical development.

Our previous study showed that prenatal caffeine exposure (PCE) could induce intrauterine growth retardation (IUGR) and glucocorticoid elevation in the fetus. Researchers suggested that IUGR is a risk factor for T helper cell (Th)1/Th2 deviation. However, whether PCE can induce these immune disorders and the underlying mechanisms of that induction remain unknown. This study aimed to observe the effects of PCE on the Th1/Th2 balance in offspring and further explore the developmental origin mechanisms from the perspective of glucocorticoid overexposure-induced thymocyte apoptosis. An IUGR model was established by caffeine administration from gestational day (GD) 9 to GD 18, and the offspring were immunized on postnatal day (PND) 42. The results show that maternal glucocorticoid overexposure increased fetal thymocyte apoptosis by activating both the Fas-mediated and the Bim-regulated apoptotic pathways. After birth, accelerated thymocyte apoptosis and Th1 suppression were also found in the PCE offspring at PND 14 and PND 49. Moreover, the PCE offspring showed immune disorders after immunization, manifesting as increased IgG1/IgG2a ratio and IL-4 production in the serum. In conclusion, PCE could induce fetal overexposure to maternal glucocorticoids and increase thymocyte apoptosis, which could persist into postnatal life and be implicated in Th1 inhibition and further immune disorders.

Metformin is a widely used first-line antidiabetic drug that has been shown to protect against a variety of specific diseases in addition to diabetes, including cardiovascular disorders, polycystic ovary syndrome and cancer. However, the precise mechanisms underlying the diverse therapeutic effects of metformin remain elusive. Here, we report that transforming growth factor-β1 (TGF-β1), which is involved in the pathogenesis of numerous diseases, is a novel target of metformin. Using a surface plasmon resonance-based assay, we identified the direct binding of metformin to TGF-β1 and found that metformin inhibits [125I]-TGF-β1 binding to its receptor. Furthermore, based on molecular docking and molecular dynamics simulations, metformin was predicted to interact with TGF-β1 at its receptor-binding domain. Single-molecule force spectroscopy revealed that metformin reduces the binding probability but not the binding force of TGF-β1 to its type II receptor. Consequently, metformin suppresses type II TGF-β1 receptor dimerization upon exposure to TGF-β1, which is essential for downstream signal transduction. Thus, our results indicate that metformin is a novel TGF-β suppressor with therapeutic potential for numerous diseases in which TGF-β1 hyperfunction is indicated.

The estrogenicity of parabens at human exposure levels has become a focus of concern due to the debate over whether the estrogenicity of parabens is strong enough to play a role in the increased incidence of breast cancer. In this study, the uterotrophic activities of methylparaben (MP) and ethylparaben (EP) at doses close to the acceptable daily intake as allocated by JECFA were demonstrated in immature Sprague-Dawley rats by intragastric administration, and up-regulations of estrogen-responsive biomarker genes were found in uteri of the rats by quantitative real-time RT–PCR (Q-RT-PCR). At the same time, the urinary concentrations of MP and EP, as measured by gas chromatography–mass spectrometry (GC-MS) in rats that received the same doses of MP and EP, were found to be near the high urinary levels reported in human populations in recent years. These results show the in vivo estrogenicity of MP and EP at human exposure levels, and indicate that populations exposed to large amounts of MP and EP may have a high burden of estrogenicity-related diseases. In addition, a molecular docking simulation showed interaction between the parabens and the agonist-binding pocket of human estrogen receptor α (hERα).

Overexpression of folate receptor alpha (FRα) and high telomerase activity are considered to be the characteristics of ovarian cancers. In this study, we developed FRα-targeted lipoplexes loaded with an hTERT promoter-regulated plasmid that encodes a matrix protein (MP) of the vesicular stomatitis virus, F-LP/pMP(2.5), for application in ovarian cancer treatment. We first characterized the pharmaceutical properties of F-LP/pMP(2.5). The efficient expression of the MP-driven hTERT promoter in SKOV-3 cells was determined after an in-vitro transfection assay, which was significantly increased compared with a non-modified LP/pMP(2.5) group. F-LP/pMP(2.5) treatment significantly inhibited the growth of tumors and extended the survival of mice in a SKOV-3 tumor model compared with other groups. Such an anti-tumor effect was due to the increased expression of MP in tumor tissue, which led to the induction of tumor cell apoptosis, inhibition of tumor cell proliferation and suppression of tumor angiogenesis. Furthermore, a preliminary safety evaluation demonstrated a good safety profile of F-LP/pMP(2.5) as a gene therapy agent. Therefore, FRα-targeted lipoplexes with therapeutic gene expression regulated by an hTERT promoter might be a promising gene therapy agent and a potential translational candidate for the clinical treatment of ovarian cancer.