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•Homogeneous and heterogeneous iron species activation of PS and PMS are presented.•Synthetic ways for heterogeneous iron catalysts for PS/PMS activation are reviewed.•Influencing ...factors and synergistic methods for PS/PMS activation are introduced.•Further efforts related to iron-mediated activation of PS and PMS are proposed.
Various organic contaminants accumulated in the environment pose great threat to ecosystems and human health. Sulfate radical-based advanced oxidation processes (SR-AOPs) have attracted increasing attention for the removal of these contaminants in recent years. Iron species, including ferrous and ferric iron, zero-valent iron, iron oxides and oxyhydroxides, iron sulfides and various supported iron catalysts, are known to be effective in activating persulfate (PS) or peroxymonosulfate (PMS) to generate sulfate radicals. This review is dedicated to summarize the up-to-date research progresses of iron-mediated activation of PS and PMS mediated by these iron-based species in both homogeneous and heterogeneous ways. The activators are categorized based on their chemistry, and the up-to-date knowledge regarding the activation mechanisms are summarized and discussed. Then, a summary of frequently-used synthesis methods of heterogeneous iron catalysts is presented. In addition, the effects of anions, solution pH, dissolved oxygen, and external energy on the activation processes are discussed. Finally, future research perspectives on the iron-based PS/PMS activation method are proposed and how to further improve such a technology for practical application are also discussed.
As an outcome of chronic liver disease, liver fibrosis involves the activation of hepatic stellate cells (HSCs) caused by a variety of chronic liver injuries. It is important to explore approaches to ...inhibit the activation and proliferation of HSCs for the treatment of liver fibrosis. PLK1 is overexpressed in many human tumour cells and has become a popular drug target in tumour therapy. Therefore, further study of the function of PLK1 in the cell cycle is valid. In the present study, we found that PLK1 expression was elevated in primary HSCs isolated from CCl4‐induced liver fibrosis mice and LX‐2 cells stimulated with TGF‐β1. Knockdown of PLK1 inhibited α‐SMA and Col1α1 expression and reduced the activation of HSCs in CCl4‐induced liver fibrosis mice and LX‐2 cells stimulated with TGF‐β1. We further showed that inhibiting the expression of PLK1 reduced the proliferation of HSCs and promoted HSCs apoptosis in vivo and in vitro. Furthermore, we found that the Wnt/β‐catenin signalling pathway may be essential for PLK1‐mediated HSCs activation. Together, blocking PLK1 effectively suppressed liver fibrosis by inhibiting HSC activation, which may provide a new treatment strategy for liver fibrosis.
Microplastics (MPs) have the potential to interact with the toxicity of other common environmental contaminants, such as heavy metals. Here, we investigated the impacts of polystyrene-MPs (32–40 μm), ...cadmium (Cd) and their combination on early juveniles of the discus fish (Symphysodon aequifasciatus) in relation to Cd accumulation, antioxidant defence and innate immunity. Animals were exposed to three concentrations of MPs (0, 50 or 500 μg L−1) crossed with two levels of Cd (0 or 50 μg L−1) for 30 days. Our findings showed that MPs and Cd had no adverse effects on growth and survival. Under exposure to Cd, however, accumulation of Cd in the body of fish decreased with increasing MP concentrations as supported by a reduced metallothionein content. The activities of superoxide dismutase and glutathione peroxidase increased with MPs but decreased with Cd. MPs, Cd or the mixture increased catalase activity, despite an antagonistic interaction between the two stressors. Glutathione levels increased when exposed to high MP concentrations but decreased when co-exposed to Cd. Malondialdehyde content was only influenced by MPs and increased with elevated MPs. MPs or Cd alone did not increase protein carboxyl content but showed a synergistic effect and increased content. MPs or Cd alone showed no effect on lysozyme activity but had a synergistic effect and activated activity. Activities of both acid phosphatase and alkaline phosphatase were enhanced by MPs, Cd or their mixture, although there was an antagonistic interaction between the two stressors. In contrast, MPs, Cd or their mixture decreased complement 3 content, despite an antagonistic interaction between the two stressors. Collectively, this study suggests that exposure to Cd led to reduced Cd accumulation in the presence of MPs. Nevertheless, co-exposure could induce severe oxidative stress and stimulate innate immunity in the juvenile S. aequifasciatus.
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•MPs decreased the accumulation of Cd as supported by a reduced MT level.•The combination of MPs and Cd induced severe oxidative stress.•Co-exposure to MPs and Cd stimulated the innate immune system.
Necroptosis, a novel type of programmed cell death, is involved in stroke-induced ischemic brain injury. Although studies have sought to explore the mechanisms of necroptosis, its signaling pathway ...has not yet to be completely elucidated. Thus, we used oxygen-glucose deprivation (OGD) and middle cerebral artery occlusion (MCAO) models mimicking ischemic stroke (IS) conditions to investigate mechanisms of necroptosis. We found that OGD and MCAO induced cell death, local brain ischemia and neurological deficit, while zVAD-fmk (zVAD, an apoptotic inhibitor), GSK'872 (a receptor interacting protein kinase-3 (RIP3) inhibitor), and combined treatment alleviated cell death and ischemic brain injury. Moreover, OGD and MCAO upregulated protein expression of the triggers of necroptosis: receptor interacting protein kinase-1 (RIP1), RIP3 and mixed lineage kinase domain-like protein (MLKL). The upregulation of these proteins was inhibited by GSK'872, combination treatments and RIP3 siRNA but not zVAD treatment. Intriguingly, hypoxia-inducible factor-1 alpha (HIF-1α), an important transcriptional factor under hypoxic conditions, was upregulated by OGD and MCAO. Similar to their inhibitory effects on aforementioned proteins upregulation, GSK'872, combination treatments and RIP3 siRNA decreased HIF-1α protein level. These findings indicate that necroptosis contributes to ischemic brain injury induced by OGD and MCAO and implicate HIF-1α, RIP1, RIP3, and MLKL in necroptosis.
In this work, a novel three nitro‐group‐bearing monomer 3,6‐dinitro‐9‐(2‐trifluoromethyl‐4‐nitrophenyl)‐carbazole (Car‐3NO2‐CF3) via a CN coupling reaction between 3,6‐dinitro‐9H‐carbazole ...(Car‐2NO2) and 2‐chloro‐5‐nitrobenzotrifluoride is synthesized, and obtained single crystal and single crystal analysis data for this compound. The crystal system of Car‐3NO2‐CF3 is monoclinic and it has a P 21/c space group. This new monomer (Car‐3NO2‐CF3) is also utilized to synthesize a novel azo‐linked polymer (Azo‐Car‐CF3). The trifluoromethyl group has polar CF bonds, and thus it is an effective functional group for the capture of iodine. Azo‐Car‐CF3 has great thermal stability with a mass loss of only 10% at 414 °C, as well as good chemical stability as is demonstrated by its low solubility in common organic solvents such as tetrahydrofuran (THF), acetone, methanol, ethanol, and N,N‐dimethylformamide (DMF). The specific surface area of Azo‐Car‐CF3 can reach as high as 335 m2 g−1. Azo‐Car‐CF3 exhibits an excellent capacity for iodine adsorption and can reach up to 1198 mg g−1 in cyclohexane solution, and its adsorption capacity for iodine vapor can get to 2100 mg g−1. In addition, ethanol can be used to trigger the release of the captured iodine to be easily released from Azo‐Car‐CF3.
A three nitro‐group‐bearing monomer 3,6‐dinitro‐9‐(2‐trifluoromethyl‐4‐nitrophenyl)‐carbazole is synthesized and the single crystal analysis data is obtained. A robust and time‐efficient synthetic method based on a NaBH4‐mediated reductive coupling polymerization is utilized to synthesis a novel azo‐linked polymer (Azo‐Car‐CF3). Next, the Azo‐Car‐CF3 is used to conduct the adsorption and desorption experiment for iodine and the introduction of azo bond and trifluoromethyl is investigated in detail.
Noncoding RNAs in alcoholic liver disease Li, Hai‐Di; Du, Xiao‐Sa; Huang, Hui‐Min ...
Journal of cellular physiology,
September 2019, 2019-Sep, 2019-09-00, 20190901, Volume:
234, Issue:
9
Journal Article
Peer reviewed
Alcoholic liver disease (ALD) is a complex process with high morbitity and can cause liver dysfunction, which contains a wide spectrum of hepatic lesions, including steatohepatitis, fibrosis, ...cirrhosis, and eventually hepatocellular carcinoma. To date, the molecular mechanisms for ALD have not been fully explored and an effective therapy is still missing. Overwhelming evidence shows dysregulation of noncoding RNAs (ncRNAs), particularly microRNAs (miRNAs), is correlated with etiopathogenesis and progress of ALD including hepatocyte damage, disrupted lipid metabolism, aggressive inflammatory responses, oxidative stress, programmed cell death, fibrosis, and epigenetic changes induced by alcohol. For example, circulating miRNA‐122 is a marker of hepatocyte damage, and miRNA‐155 is a potential marker of inflammation, indicating their diagnosis therapeutic potential in ALD. In addition, roles for long noncoding RNAs (lncRNAs) and circular RNAs in ALD are being uncovered. Further, circulating ncRNAs and exosome‐derived ncRNAs have attracted more attention lately, suggesting a role in the prevention and treatment of ALD. This review covers the roles of ncRNAs in ALD, and the potential uses as markers for diagnosis and therapeutic options.
This review discusses the progress of noncoding RNAs (ncRNAs) in alcoholic liver disease and provides deeper insights into the biological functions and therapeutic potential of ncRNAs in disease.
Altered metabolic pathways have recently been considered as potential drivers of idiopathic pulmonary fibrosis (IPF) for the study of drug therapeutic targets. However, our understanding of the ...metabolite profile during IPF formation is lacking.
To comprehensively characterize the metabolic disorders of IPF, a mouse IPF model was constructed by intratracheal injection of bleomycin into C57BL/6J male mice, and lung tissues from IPF mice at 7 days, 14 days, and controls were analyzed by pathology, immunohistochemistry, and Western Blots. Meanwhile, serum metabolite detections were conducted in IPF mice using LC-ESI-MS/MS, KEGG metabolic pathway analysis was applied to the differential metabolites, and biomarkers were screened using machine learning algorithms.
We analyzed the levels of 1465 metabolites and found that more than one-third of the metabolites were altered during IPF formation. There were 504 and 565 metabolites that differed between M7 and M14 and controls, respectively, while 201 differential metabolites were found between M7 and M14. In IPF mouse sera, about 80% of differential metabolite expression was downregulated. Lipids accounted for more than 80% of the differential metabolite species with down-regulated expression. The KEGG pathway enrichment analysis of differential metabolites was mainly enriched to pathways such as the metabolism of glycerolipids and glycerophospholipids. Eight metabolites were screened by a machine learning random forest model, and receiver operating characteristic curves (ROC) assessed them as ideal diagnostic tools.
In conclusion, we have identified disturbances in serum lipid metabolism associated with the formation of pulmonary fibrosis, contributing to the understanding of the pathogenesis of pulmonary fibrosis.
Abstract
Background
Schools play an organizational role in managing myopia-related behavioral habits among students. We evaluated the effects of school myopia management measures on myopia onset and ...progression in a school-based prospective 1-year observational study.
Methods
In total, 8319 children from 26 elementary schools were included. Online questionnaire completed by a parent, in which school myopia management experience including outdoor activities in recess or physical education class, teachers’ supervision, and teaching facilities. Variables were defined as implemented well or poorly, according to the Comprehensive Plan to Prevent Myopia among Children and Teenagers. Children underwent ophthalmic examinations, and the incidence and progression of myopia from 2019 to 2020 were estimated. Multilevel logistic regression models were constructed to analyze the association between school management measures and myopia development in 8,9 years and 10,11 years students.
Results
From 2019 to 2020, the incidence of myopia among primary school students was 36.49%; the mean difference of spherical equivalent in myopic children was − 0.29 ± 1.22 diopters. The risk of incident myopia was reduced by 20% in 8,9 years participants with well-implemented class recess compared with those with poorly implemented class recess (adjusted odds ratio aOR: 0.80,
p
= 0.032). PE outdoor time was significantly associated with myopia incidence in 10,11 years students (aOR: 0.76,
p
= 0.043). Compared with poorly implemented reading and writing posture, desk and chair height, 10,11 participants with well-implemented desk and chair height were less likely to have rapid myopic progression (
p
= 0.029,
p
= 0.022).
Conclusion
In Shanghai, children’s myopia is associated with better implementation of school myopia management measures. The present findings suggest that outdoor activities during class recess or PE class, providing suitable desks and chairs, and adequate instruction in reading and writing postures might protect against pathological eye growth. An age-specific myopia prevention and control programs in school is of primary importance.
The frequency, duration and magnitude of drought are projected to increase in the next few decades, with consequences for community composition and nutrient utilization of plants. Nutrient ...resorption, a process facilitating plant nutrient conservation, is a crucial driver for ecosystem nutrient cycling. It remains unknown how would extreme drought affect nutrient resorption of plant communities through changing community composition.
We examined the contributions of different processes (richness and identity effect of species losses and species gains, as well as the context dependent effect) related with community compositional changes to the alterations of community‐level nutrient resorption efficiency after 4‐year treatments of chronic drought (66% rainfall reduction from May to August) and intense drought (100% rainfall reduction in June and July) in a temperate steppe in Hulun Buir, Inner Mongolia, China.
Both chronic and intense drought significantly reduced nutrient resorption efficiency in most of the common species, but did not affect that at the community level. Drought‐induced losses of species made positive contribution to the community‐level nutrient resorption, as they generally had lower nutrient resorption efficiency. Such positive contribution balanced the negative effect of drought on the nutrient resorption of the common species.
Our results indicate that drought‐induced changes in community composition, especially those species being lost, were important in mediating the community‐level responses of nutrient resorption to extreme drought in grasslands.
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概括
草原地区干旱事件的发生频率和强度在未来几十年中将不断增加，影响到植物群落组成及养分利用。作为植物养分利用的重要环节，植物器官枯萎过程中养分回收的改变对生态系统养分循环有重要影响。本研究基于中国呼伦贝尔草甸草原极端干旱控制实验平台，分析了连续4年缓慢干旱(减少5月至8月间66%的降水)和剧烈干旱(减少6月和7月100%的降水)后对植物群落水平氮磷回收效率的影响，并基于Price方程量化了干旱处理条件下丢失物种的属性、获得物种的多样性、获得物种的属性以及存留物种对于干旱导致的群落养分回收变化的贡献，旨在探讨极端干旱如何通过改变植物群落组成进而影响植物群落水平的养分回收状况。结果显示，两种干旱均显著降低了多数存留物种的养分回收效率，但是并没有改变群落水平的养分回收效率。在干旱过程中所丢失的物种，通常具有比其他物种更低的养分回收效率，因此它们的消失对于群落水平养分含量的变化具有正向贡献，即低回收效率物种的消失后群落平均回收效率与不进行干旱处理的对照群落相比得以提高。这种正向贡献在一定程度上能够抵消干旱对于存留物种养分回收效率的负面影响，因此使得干旱对于群落水平上的养分回收效率无显著影响。本研究揭示了干旱背景下丢失物种的属性如何作用于植物群落水平的养分利用特征，建立了群落构建关键过程与群落功能的联系。
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Alcohol-induced liver injury (ALI) is associated with inflammatory responses regulated by macrophages. Activation of macrophages plays a crucial role in ALI while DNA methylation-regulated gene ...silencing is associated with inflammation processes in macrophages. Proline-Serine-Threonine Phosphatase Interacting Protein 2 (PSTPIP2), which belongs to the Fes/CIP4 homology-Bin/Amphiphysin/Rvs domain family of proteins and plays a role in macrophages. Previous studies have shown that Pstpip2 can be methylated. Herein, its expression was found to be significantly downregulated in primary liver macrophages isolated from EtOH-fed mice and EtOH-induced RAW264.7 cells. Overexpression of PSTPIP2 using liver-specific recombinant AAV serotype 9 (rAAV9)-PSTPIP2 in EtOH-fed mice dramatically alleviated liver injury and inflammatory responses. In addition, silencing of PSTPIP2 aggravated the alcohol-induced inflammatory response in vitro. Mechanistically, PSTPIP2 might affect macrophage-induced inflammatory responses by regulating the STAT1 and NF-κB signaling pathways. The downregulation of PSTPIP2 in ALI may be associated with DNA methylation. Methylation-specific PCR and western blotting analyses showed that EtOH induced abnormal DNA methylation patterns and increased the protein expression levels of DNMT1, DNMT3a, and DNMT3b. The chromatin immunoprecipitation assay showed that DNMT3a could directly bind to the Pstpip2 promoter and act as a principal regulator of PSTPIP2 expression. Moreover, silencing of DNMT3a significantly restored the EtOH-induced low expression of PSTPIP2 and inhibited EtOH-induced inflammation. Overall, these findings provide a detailed understanding of the possible functions and mechanisms of PSTPIP2 in ALI, thus providing new substantive research to elucidate the pathogenesis of ALI and investigate potential targeted treatment strategies.
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