Drought and waterlogging seriously affect the growth of plants and are considered severe constraints on agricultural and forestry productivity; their frequency and degree have increased over time due to global climate change. The morphology, photosynthetic activity, antioxidant enzyme system and hormone levels of plants could change in response to water stress. The mechanisms of these changes are introduced in this review, along with research on key transcription factors and genes. Both drought and waterlogging stress similarly impact leaf morphology (such as wilting and crimping) and inhibit photosynthesis. The former affects the absorption and transportation mechanisms of plants, and the lack of water and nutrients inhibits the formation of chlorophyll, which leads to reduced photosynthetic capacity. Constitutive overexpression of 9-cis-epoxydioxygenase (NCED) and acetaldehyde dehydrogenase (ALDH), key enzymes in abscisic acid (ABA) biosynthesis, increases drought resistance. The latter forces leaf stomata to close in response to chemical signals, which are produced by the roots and transferred aboveground, affecting the absorption capacity of CO2, and reducing photosynthetic substrates. The root system produces adventitious roots and forms aerenchymal to adapt the stresses. Ethylene (ETH) is the main response hormone of plants to waterlogging stress, and is a member of the ERFVII subfamily, which includes response factors involved in hypoxia-induced gene expression, and responds to energy expenditure through anaerobic respiration. There are two potential adaptation mechanisms of plants (“static” or “escape”) through ETH-mediated gibberellin (GA) dynamic equilibrium to waterlogging stress in the present studies. Plant signal transduction pathways, after receiving stress stimulus signals as well as the regulatory mechanism of the subsequent synthesis of pyruvate decarboxylase (PDC) and alcohol dehydrogenase (ADH) enzymes to produce ethanol under a hypoxic environment caused by waterlogging, should be considered. This review provides a theoretical basis for plants to improve water stress tolerance and water-resistant breeding.
MicroRNAs (miRNAs) are involved in the progression of many cancers through largely unelucidated mechanisms. The results of our present study identified a gene cluster, miR‐221/222, that is constitutively upregulated in serum exosome samples of patients with colorectal carcinoma (CRC) with liver metastasis (LM); this upregulation predicts a poor overall survival rate. Using an in vitro cell coculture model, we demonstrated that CRC exosomes harboring miR‐221/222 activate liver hepatocyte growth factor (HGF) by suppressing SPINT1 expression. Importantly, miR‐221/222 plays a key role in forming a favorable premetastatic niche (PMN) that leads to the aggressive nature of CRC, which was further shown through in vivo studies. Overall, our results show that exosomal miR‐221/222 promotes CRC progression and may serve as a novel prognostic marker and therapeutic target for CRC with LM.
Toward improving the selective adsorption performance of molecularly imprinted polymers in strong polar solvents, in this work, a new ionic liquid functional monomer, 1‐butyl‐3‐vinylimidazolium bromide, was used to synthesize sulfamethoxazole imprinted polymer in methanol. The resulting molecularly imprinted polymer was characterized by Fourier transform infrared spectra and scanning electron microscopy, and the rebinding mechanism of the molecularly imprinted polymer for sulfonamides was studied. A static equilibrium experiment revealed that the as‐obtained molecularly imprinted polymer had higher molecular recognition for sulfonamides (e.g., sulfamethoxazole, sulfamonomethoxine, and sulfadiazine) in methanol; however, its adsorption of interferent (e.g., diphenylamine, metronidazole, 2,4‐dichlorophenol, and m‐dihydroxybenzene) was quite low. 1H NMR spectroscopy indicated that the excellent recognition performance of the imprinted polymer was based primarily on hydrogen bond, electrostatic and π‐π interactions. Furthermore, the molecularly imprinted polymer can be employed as a solid phase extraction sorbent to effectively extract sulfamethoxazole from a mixed solution. Combined with high‐performance liquid chromatography analysis, a valid molecularly imprinted polymer‐solid phase extraction protocol was established for extraction and detection of trace sulfamethoxazole in spiked soil and sediment samples, and with a recovery that ranged from 93–107%, and a relative standard deviation of lower than 9.7%.
Mesenchymal stem cells (MSCs) are a promising cellular vehicle for transferring anti-cancer factors to malignant tumors. Currently, a variety of anti-cancer agents, including the tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL), have been loaded into MSCs derived from a range of sources through different engineering methods. These engineered MSCs exhibit enormous therapeutic potential for various cancers. To avoid the intrinsic defects of MSCs derived from tissues and the potential risk of viral vectors, TRAIL was site-specifically integrated into the ribosomal DNA (rDNA) locus of human-induced pluripotent stem cells (iPSCs) using a non-viral rDNA-targeting vector and transcription activator-like effector nickases (TALENickases). These genetically modified human iPSCs were differentiated into an unlimited number of homogeneous induced MSCs (TRAIL-iMSCs) that overexpressed TRAIL in both culture supernatants and cell lysates while maintaining MSC-like characteristics over continuous passages. We found that TRAIL-iMSCs significantly induced apoptosis in A375, A549, HepG2, and MCF-7 cells in vitro. After intravenous infusion, TRAIL-iMSCs had a prominent tissue tropism for A549 or MCF-7 xenografts and significantly inhibited tumor growth through the activation of apoptotic signaling pathways without obvious side effects in tumor-bearing mice models. Altogether, our results showed that TRAIL-iMSCs have strong anti-tumor effects in vitro and in vivo on a range of cancers. This study allows for the development of an unlimited number of therapeutic gene-targeted MSCs with stable quality and high homogeneity for cancer therapy, thus highlighting a universal and safe strategy for stem cell-based gene therapy with high potential for clinical applications.
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