Transcriptomic and Functional Analyses of Two Cadmium Hyper-Enriched Duckweed Strains Reveal Putative Cadmium Tolerance Mechanisms.

Cadmium (Cd) is one of the most toxic metals in the environment and exerts deleterious effects on plant growth and production. Duckweed has been reported as a promising candidate for Cd phytoremediation. In this study, the growth, Cd enrichment, and antioxidant enzyme activity of duckweed were investigated. We found that both high-Cd-tolerance duckweed (HCD) and low-Cd-tolerance duckweed (LCD) strains exposed to Cd were hyper-enriched with Cd. To further explore the underlying molecular mechanisms, a genome-wide transcriptome analysis was performed. The results showed that the growth rate, chlorophyll content, and antioxidant enzyme activities of duckweed were significantly affected by Cd stress and differed between the two strains. In the genome-wide transcriptome analysis, the RNA-seq library generated 544,347,670 clean reads, and 1608 and 2045 differentially expressed genes were identified between HCD and LCD, respectively. The antioxidant system was significantly expressed during ribosomal biosynthesis in HCD but not in LCD. Fatty acid metabolism and ethanol production were significantly increased in LCD. Alpha-linolenic acid metabolism likely plays an important role in Cd detoxification in duckweed. These findings contribute to the understanding of Cd tolerance mechanisms in hyperaccumulator plants and lay the foundation for future phytoremediation studies.

Influence of cadmium and microplastics on physiological responses, ultrastructure and rhizosphere microbial community of duckweed.

The combined contamination of heavy metals and microplastics is widespread in freshwater environments. However, there are few researches on their combined effects on aquatic plants. In this study, the effects of single and combined stress of 0.01 mg L-1 cadmium (Cd), 50 mg L-1 polyethylene and 50 mg L-1 polypropylene for 15 days on the physiological response, ultrastructure and rhizosphere microbial community of duckweed were investigated. The results showed that Cd and microplastics single or combined stress inhibited the growth of duckweed, shortened the root length and decreased the chlorophyll content. Compared with single Cd treatments, the combination of microplastics and Cd increased duckweed growth rate and increased superoxide dismutase activity and malondialdehyde content and reduced chloroplast structural damage, indicating that the combined stress could reduce the toxicity of heavy metals to duckweed. Through the study of rhizosphere microbial diversity, 1381 Operational Taxonomic Unit (OTUs) were identified and rich microbial communities were detected in the duckweed rhizosphere. Among them, the main microbial communities were Proteobacteria, Bacteroidetes, and Cyanobacteria. Compared with Cd single stress, the ACE and chao index of rhizosphere microbial community increased under combined stress, indicating that the diversity and abundance of microbial communities were improved after combined stress treatment. Our study revealed the effects of heavy metals and microplastics on aquatic plants, providing a theoretical basis for duckweed applications in complex water pollution.

Duckweed Is a Promising Feedstock of Biofuels: Advantages and Approaches.

With the growing scarcity of traditional sources of energy and the accompanying acute environmental challenges, biofuels based on biomass are favored as the most promising alternative. As one of the core raw materials for biomass energy, research on its production methods and synthesis mechanisms is emerging. In recent years, duckweed has been used as a high-quality new biomass feedstock for its advantages, including fast biomass accumulation, high starch content, high biomass conversion efficiency, and sewage remediation. This study provides a systematic review of the growth characteristics, starch metabolism pathways, and methods to improve starch accumulation in the new energy plant, duckweed. The study also presents a prospect that might be used as a reference for the development of duckweed as a new energy-providing plant.

Inhibition of intracranial hemangioma growth and hemorrhage by TNFSF15.

Hemangioblastoma (HB) is an abnormal intracranial buildup of blood vessels that exhibit a great potential for hemorrhage. Surgical options are limited, and few medications are available for treatment. We show here by immunohistochemical analysis that HB lesions display highly increased levels of VEGF expression and macrophage/microglia infiltration compared with those in normal brain tissues. In the meantime, TNF superfamily 15 (TNFSF15) (also known as vascular endothelial growth inhibitor), an antiangiogenic cytokine, is highly expressed in normal brain blood vessels but diminished in HB lesions. We set up a brain hemangioma model by using mouse bEnd.3 cells of a T antigen-transformed endothelial cell line that produce a large amount of VEGF. When implanted in mouse brains, these cells form lesions that closely resemble the pathologic characteristics of HB. Retroviral infection of bEnd.3 cells with TNFSF15 leads to inhibition of VEGF production and retardation of hemangioma formation. Similar results are obtained when wild-type bEnd.3 cells are implanted in the brains of transgenic mice overexpressing TNFSF15. Additionally, TNFSF15 treatment results in enhanced pericyte coverage of the blood vessels in the lesions together with reduced inflammatory cell infiltration and decreased hemorrhage. These findings indicate that the ability of TNFSF15 to counterbalance the abnormally highly angiogenic and inflammatory potential of the microenvironment of HB is of therapeutic value for the treatment of this disease.-Yang, G.-L., Han, Z., Xiong, J., Wang, S., Wei, H., Qin, T.-T., Xiao, H., Liu, Y., Xu, L.-X., Qi, J.-W., Zhang, Z.-S., Jiang, R., Zhang, J., Li, L.-Y. Inhibition of intracranial hemangioma growth and hemorrhage by TNFSF15.

Frond transformation system mediated by Agrobacterium tumefaciens for Lemna minor.

The Lemnaceae, known as duckweed, the smallest flowering aquatic plant, shows promise as a plant bioreactor. For applying this potential plant bioreactor, establishing a stable and efficient genetic transformation system is necessary. The currently favored callus-based method for duckweed transformation is time consuming and genotype limited, as it requires callus culture and regeneration, which is inapplicable to many elite duckweed strains suitable for bioreactor exploitation. In this study, we attempted to establish a simple frond transformation system mediated by Agrobacterium tumefaciens for Lemna minor, one of the most widespread duckweed species in the world. To evaluate the feasibility of the new transformation system, the gene CYP710A11 was overexpressed to improve the yield of stigmasterol, which has multiple medicinal purposes. Three L. minor strains, ZH0055, D0158 and M0165, were transformed by both a conventional callus transformation system (CTS) and the simple frond transformation system (FTS). GUS staining, PCR, quantitative PCR and stigmasterol content detection showed that FTS can produce stable transgenic lines as well as CTS. Moreover, compared to CTS, FTS can avoid the genotype constraints of callus induction, thus saving at least half of the required processing time (CTS took 8-9 months while FTS took approximately 3 months in this study). Therefore, this transformation system is feasible in producing stable transgenic lines for a wide range of L. minor genotypes.

TNFSF15 inhibits VEGF-stimulated vascular hyperpermeability by inducing VEGFR2 dephosphorylation.

Vascular hyperpermeability is critical in ischemic diseases, including stroke and myocardial infarction, as well as in inflammation and cancer. It is well known that the VEGF-VEGFR2 signaling pathways are pivotal in promoting vascular permeability; however, counterbalancing mechanisms that restrict vascular permeability to maintain the integrity of blood vessels are not yet fully understood. We report that TNF superfamily member 15 (TNFSF15), a cytokine largely produced by vascular endothelial cells and a specific inhibitor of the proliferation of these same cells, can inhibit VEGF-induced vascular permeability in vitro and in vivo, and that death receptor 3 (DR3), a cell surface receptor of TNFSF15, mediates TNFSF15-induced dephosphorylation of VEGFR2. Src homology region 2 domain-containing phosphatase-1 (SHP-1) becomes associated with DR3 upon TNFSF15 interaction with the latter. In addition, a protein complex consisting of VEGFR2, DR3, and SHP-1 is formed in response to the effects of TNFSF15 and VEGF on endothelial cells. It is plausible that this protein complex provides a structural basis for the molecular mechanism in which TNFSF15 induces the inhibition of VEGF-stimulated vascular hyperpermeability.-Yang, G.-L., Zhao, Z., Qin, T.-T., Wang, D., Chen, L., Xiang, R., Xi, Z., Jiang, R., Zhang, Z.-S., Zhang, J., Li. L.-Y. TNFSF15 inhibits VEGF-stimulated vascular hyperpermeability by inducing VEGFR2 dephosphorylation.

Tumour necrosis factor superfamily member 15 (Tnfsf15) facilitates lymphangiogenesis via up-regulation of Vegfr3 gene expression in lymphatic endothelial cells.

Lymphangiogenesis is essential in embryonic development but is rare in adults. It occurs, however, in many disease conditions including cancers. Vascular endothelial growth factor-C/D (VEGF-C/D) and VEGF receptor-3 (Vegfr3) play a critical role in the regulation of lymphangiogenesis. We investigated how the VEGF-C/Vegfr3 signalling system is regulated by tumour necrosis factor superfamily member 15 (Tnfsf15), an endothelium-derived cytokine. We report here that Tnfsf15, which is known to induce apoptosis in vascular endothelial cells, can promote lymphatic endothelial cell (LEC) growth and migration, stimulate lymphangiogenesis, and facilitate lymphatic circulation. Treatment of mouse LECs with Tnfsf15 results in up-regulation of Vegfr3 expression; this can be inhibited by gene silencing of death domain-containing receptor-3 (DR3; Tnfrsf25), a cell surface receptor for Tnfsf15, with siRNA, or by blocking Tnfsf15-DR3 interaction with a Tnfsf15 neutralizing antibody, 4-3H. Additionally, Tnfsf15/DR3 signalling pathways in LECs include activation of NF-κB. Tnfsf15-overexpressing transgenic mice exhibit a marked enhancement of lymph drainage; this is confirmed by treatment of wild-type mice with intraperitoneal injection of recombinant Tnfsf15. Moreover, systemic treatment of pregnant Tnfsf15 transgenic mice with 4-3H leads to inhibition of embryonic lymphangiogenesis. Our data indicate that Tnfsf15, a cytokine produced largely by endothelial cells, facilitates lymphangiogenesis by up-regulating Vegfr3 gene expression in LECs, contributing to the maintenance of the homeostasis of the circulatory system. This finding also suggests that Tnfsf15 may be of potential value as a therapeutic tool for the treatment of lymphoedema.

TNFSF15 inhibits vasculogenesis by regulating relative levels of membrane-bound and soluble isoforms of VEGF receptor 1.

Mouse bone marrow-derived Lin(-)-Sca-1(+) endothelial progenitor cell (EPC) has pluripotent abilities such as supporting neovascularization. Vascular endothelial growth factor (VEGF) receptor 1 (VEGFR1) (Flt1) recognizes various VEGF isoforms and is critically implicated in a wide range of physiological and pathological settings, including vasculogenesis. Mouse EPC expresses two isoforms of VEGFR1: mFlt1, which transmits ligand-induced signals; and sFlt1, which acts as a negative regulator by sequestering ligands of VEGF receptors. How the relative levels of mFlt1 and sFlt1 are regulated is not yet clear. We report here that tumor necrosis factor superfamily 15 (TNFSF15) (also known as VEGI or TL1A), an endothelial cell-secreted cytokine, simultaneously promotes mFlt1 degradation and up-regulates sFlt1 expression in EPC, giving rise to disruption of VEGF- or PlGF-induced activation of eNOS and MAPK p38 and effective inhibition of VEGF-driven, EPC-supported vasculogenesis in a murine Matrigel implant model. TNFSF15 treatment of EPC cultures facilitates Akt deactivation-dependent, ubiquitin-assisted degradation of mFlt1 and stimulates sFlt1 expression by activating the PKC, Src, and Erk1/2 signaling pathway. Additionally, TNFSF15 promotes alternative splicing of the Flt1 gene in favor of sFlt1 production by down-regulating nuclear protein Jumonji domain-containing protein 6 (Jmjd6), thus alleviating Jmjd6-inhibited sFlt1 expression. These findings indicate that TNFSF15 is a key component of a molecular mechanism that negatively modulates EPC-supported vasculogenesis through regulation of the relative levels of mFlt1 and sFlt1 in EPC.

Subcellular distribution, chemical forms of cadmium and rhizosphere microbial community in the process of cadmium hyperaccumulation in duckweed.

Duckweed is a newly reported Cd hyperaccumulator that grow rapidly; however, little is known about its tolerance and detoxification mechanisms. In this study, we investigated the tissue, subcellular, and chemical form distribution of the Cd in duckweed and studied the influences of Cd on duckweed growth, ultrastructure, and rhizosphere microbial community. The results showed that Cd could negatively affect the growth of duckweed and shorten the root length. More Cd accumulated in the roots than in the leaves, and Cd was transferred from the roots to the leaves with time. During 12-24 h, Cd mainly existed in the cell wall fraction (2.05 %-95.52 %) and the organelle fraction (5.03 %-97.80 %), followed the soluble fraction (0.14 %-16.98 %). Over time, the proportion of Cd in the organelles increased (46.64 %-92.83 %), exceeding that in the cell wall (6.79 %-66.23 %), which indicated that duckweed detoxification mechanism may be related to the retention of cell wall and vacuole. The main chemical form of Cd was the NaCl-extracted state (30.15 %-88.66 %), which was integrated with pectate and protein. With increasing stress concentration and time, the proportion of the HCl-extracted state and HAc-extracted state increased, and they were low-toxic Cd oxalate and Cd phosphate, respectively. Cd damaged the ultrastructure of cells such as chloroplasts and mitochondria and inhibited the diversity of microbial communities in the duckweed rhizosphere; however, the dominant populations that could tolerate heavy metals increased. It was speculated that duckweed distributed Cd in a less toxic chemical form in a less active location, mainly through retention in the root cell wall and sequestration in the leaf vacuoles, and is dynamically adjusted. The rhizosphere microbial communities tolerate heavy metals may also be one of the mechanisms by which duckweed can tolerate Cd. This study revealed the mechanism of duckweed tolerance and detoxification of Cd at the molecular level and provides a theoretical basis for further development of duckweed.

Physiological response, microbial diversity characterization, and endophytic bacteria isolation of duckweed under cadmium stress.

Duckweed is a cadmium (Cd) hyperaccumulator. However, its enrichment characteristics and physiological responses to Cd have not been systematically studied. The physiological responses, enrichment characteristics, diversity of endophytic bacterial communities, and isolation of Cd-resistant endophytes in duckweed (Lemna minor 0014) were studied for different durations and Cd concentrations. The results indicated that peroxidase (POD) and catalase (CAT) activities decreased while superoxide dismutase activity first increased and then decreased with increasing Cd stress duration. POD activities, CAT activities, and O2- increased as Cd concentrations increased. Malondialdehyde content and Cd accumulation in duckweed increased with increasing concentrations and time. This endophytic diversity study identified 488 operational taxonomic units, with the dominant groups being Proteobacteria, Firmicutes, and Actinobacteria. Paenibacillus sp. Y11, a strain tolerant to high concentrations of Cd and capable of significantly promoting duckweed growth, was isolated from the plant. Our study revealed the effects of heavy metals on aquatic plants, providing a theoretical basis for the application of duckweed in water pollution.

Effects of microplastics and cadmium on growth rate, photosynthetic pigment content and antioxidant enzymes of duckweed (Lemma minor).

Cadmium (Cd) and polyethylene (PE) seriously contaminate the aquatic environment and threaten human health. Many studies have reported the toxic effects of Cd and PE on plants, whereas few have reported the combined contamination of these two pollutants. In this study, duckweed (Lemma minor) was used as an indicator to explore the effect of PE microplastics (PE-MPs) at concentrations of 10, 50, 100, 200, and 500 mg/L on tolerance to 1 mg/L Cd. The results showed that different concentrations of PE-MPs inhibited the growth rate and chlorophyll content of duckweed to different degrees, both of which were minimal at 50 mg/L PE-MPs, 0.11 g/d, and 0.32 mg/g, respectively. The highest Cd enrichment (7.77 mg/kg) and bioaccumulation factors (94.22) of duckweed were detected when Cd was co-exposed with 50 mg/L of PE-MPs. Catalase and peroxidase activity first decreased and then increased with increasing PE-MPs concentrations, showing "hormesis effects", with minimum values of 11.47 U/g and 196.00 U/g, respectively. With increasing concentrations of PE-MPs, the effect on superoxide dismutase activity increased and then declined, peaking at 162.05 U/g, and displaying an "inverted V" trend. The amount of malondialdehyde rose with different PE-MPs concentrations. This research lay a foundation for using duckweed to purify water contaminated with MPs and heavy metals.

Maraviroc promotes recovery from traumatic brain injury in mice by suppression of neuroinflammation and activation of neurotoxic reactive astrocytes.

Neuroinflammation and the NACHT, LRR, and PYD domains-containing protein 3 inflammasome play crucial roles in secondary tissue damage following an initial insult in patients with traumatic brain injury (TBI). Maraviroc, a C-C chemokine receptor type 5 antagonist, has been viewed as a new therapeutic strategy for many neuroinflammatory diseases. We studied the effect of maraviroc on TBI-induced neuroinflammation. A moderate-TBI mouse model was subjected to a controlled cortical impact device. Maraviroc or vehicle was injected intraperitoneally 1 hour after TBI and then once per day for 3 consecutive days. Western blot, immunohistochemistry, and TUNEL (terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling) analyses were performed to evaluate the molecular mechanisms of maraviroc at 3 days post-TBI. Our results suggest that maraviroc administration reduced NACHT, LRR, and PYD domains-containing protein 3 inflammasome activation, modulated microglial polarization from M1 to M2, decreased neutrophil and macrophage infiltration, and inhibited the release of inflammatory factors after TBI. Moreover, maraviroc treatment decreased the activation of neurotoxic reactive astrocytes, which, in turn, exacerbated neuronal cell death. Additionally, we confirmed the neuroprotective effect of maraviroc using the modified neurological severity score, rotarod test, Morris water maze test, and lesion volume measurements. In summary, our findings indicate that maraviroc might be a desirable pharmacotherapeutic strategy for TBI, and C-C chemokine receptor type 5 might be a promising pharmacotherapeutic target to improve recovery after TBI.

[Effects of multi-walled carbon nano onions on platelet adhesion and experimental thrombogenesis in rats].

OBJECTIVE: To observe the effects of multi-walled carbon nano-onions (MWCNOs) on platelet adhesion and experimental thrombosis in rats. METHODS: Experimental rats were randomly divided into sham operation group, solvent group, and MWCNO group, each including 6 ∼ 9 rats. An inverted fluorescence microscope and a flow chamber were used to observe the effects of 20 g/ml MWCNOs on platelet adhesion at shear rates of 500 s(-1) and 1000 s(-1); the experiment was repeated at least three times in each group. A rat model of carotid artery thrombosis was induced by 25% FeCl3, and the effects of 2 mg/kg MWCNOs on the blood flow and wet weight of thrombus per millimeter in the model were observed. RESULTS: When the shear rate was 500 s(-1), the MWCNO group showed a significantly smaller number of adhering platelets than the solvent group (58.3 ± 16.1 platelets/0.01 mm(2) vs 190.1 ± 36.0 platelets/0.01 mm(2)), but the inhibitory effect of MWCNOs on platelet adhesion disappeared as the shear rate increased to 1000 s(-1). The wet weights of thrombus per millimeter at 0 h after injection of a solvent or MWCNOs via the caudal vein were 0.83 ± 0.12 mg/mm in the solvent group and 0.97 ± 0.11 mg/mm in the MWCNO group, and the wet weights of thrombus per millimeter at 12 h after injection were 0.89 ± 0.12 mg/mm in the solvent group and 1.01 ± 0.15 mg/mm in the MWCNO group, exhibiting no significant differences between the two groups (P > 0.05). There were also no significant differences between the two groups in terms of blood flow at 0 h and 12 h after injection (P > 0.05). CONCLUSION: MWCNOs have inhibitory effect on platelet adhesion in vitro, but the injection of MWCNOs via the caudal vein has no effects on the blood flow and wet weight of thrombus per millimeter in experimental thrombosis in rats.

[Oxidative damage of single-walled carbon nanotubes in striaturn and hippocampi of mice].

OBJECTIVE: To study the oxidative damage of SWCNTs in striaturn and hippocampi of mice. METHODS: Forty male ICR mice were divided into experiment group (12.5 mg/kg SWCNTs) and control group (saline containing 0.1% Tween80) randomly. Each group was subdivided into 1, 7, 14 and 28 days group, 5 mice in each subgroup, then treated with tail intravenous injection for 5 continuous days. The striatum and hippocampus were isolated on the ice bath and homogenized in saline. SOD, GSH-Px, and MDA in the supernatants were measured with xanthine oxidize, GSH consumption in enzymatic reaction and TBA methods. RESULTS: After exposure to 12.5 mg/kg SWCNTs for 5 d, SOD activity in striaturn and hippocampi decreased on 1st day and reached the minimum on 7th day, then increased gradually. The SOD activity in the SWCNTs treatment groups on 7th day were significantly decreased when compared to control (P < 0.05). Comparison with control group, GSH-Px activity in striaturn obviously decreased on 7th day then increased on 14th day, the difference between 7th day and 14th day was significantly (P < 0.05). GHS-Px activity in the hippocampi in SWCNTs group on 7th day and 14th day was significantly lower than that in control group (P < 0.05), then increased to the level of control group on 28th day. MDA contents of striaturn and hippocampi in SWCNTs group reduced on 1st day, then gradually increased on 7th day and 14th day, then reduced, MDA contents on7th day and 14th day n SWCNTs group were significantly higher than that in control group (P < 0.05). CONCLUSIONS: The results of present study indicated that SWCNTs could decrease antioxidase activity and increase the Lipid peroxide in striaturn and hippocampi of mice.

[Effects of multiwall carbon nano-onions on platelet aggregation and hemostatic function].

OBJECTIVE: To observe the effects of multiwall carbon nano-onions (MWCNOs) on platelet aggregation and hemostatic function. METHODS: The platelet aggregation was determined with Born's method at different concentration of MWCNOs (0, 0.2, 2.0, 20.0 microg/ml) in vitro. Twenty male SD rats were randomly divided into 4 groups which were exposed to 0, 2, 4 and 8 mg/kg MWCNOs, respectively. Then platelet count, platelet aggregation, activated partial thromboplastin time (APTT), prothrombin time (PT), thrombin time (TT), bleeding time (BT) and platelet count (PC) were measured at 12 h after receiving tail intravenous injection of MWCNOs. The effects of MWCNOs (4 mg/kg) on platelet aggregation and platelet count at different time points were observed. RESULTS: In vitro, MWCNOs exhibited the potent inhibitory effects on rat platelet aggregation caused by ADP in a concentration-dependent manner. The platelet aggregation in the highest dosage of 20.0 microg/ml group was 50.0% +/- 6.9% which was significantly lower than that (73.2% +/- 4.3%) in control group (P<0.01). In vivo, the highest inhibitory was up to 20.4%, but there was no significant difference, as compared with control group. MWCNOs did not affect the APTT, PT, TT, BT and PC. CONCLUSION: Under this experimental condition, MWCNOs might inhibit platelet aggregation but not affect hemostatic function.

The effect of chelating agents on iron plaques and arsenic accumulation in duckweed (Lemna minor).

Iron plaques have been found to limit the phytoremediation efficiency by reducing iron solubility, while chelating agents can increase the bioavailability of iron from Fe plaques to numerous terrestrial plants. However, the effects of chelating agents on Fe plaques along the As accumulation in aquatic plants remain unknown. In this study, the effects of five chelating agents (EDTA, DTPA, NTA, GLDA, and CA) on the As (As(III) or As(V)), phosphate, and iron uptake by iron plaques and duckweed (Lemna minor) were examined. The results showed that the chelating agents increased the As accumulation in L. minor plants by desorbing and mobilizing As from Fe plaques. The desorption rates of As(V) (As(III)) from the Fe plaques by the chelating agents were 5.26-8.77% (8.70-15.02%), and the plants/DCB extract ratios of As(V) (As(III)) increased from 2.63 ± 0.13 (1.97 ± 0.06) to the peak value of 3.38 ± 0.21 (2.70 ± 0.14) upon adding chelating agents. Besides, the addition of chelating agents increased the uptake of P and Fe by L. minor plants. This work provides a theoretical basis for the remediation of As-contaminated waters by duckweed with the help of chelating agents.

Joint effects of naphthalene and microcystin-LR on physiological responses and toxin bioaccumulation of Landoltia punctata.

The co-contamination of naphthalene (NAP) and microcystin-LR (MC-LR) commonly occurs in eutrophic waters. However, the joint effects of NAP and MC-LR on plants in aquatic environments remain unknown. Landoltia punctata is characterized by high starch yields and high biomass in polluted waters and has been proven to be a bioenergy crop and phytoremediation plant. In this study, L. punctata was cultured in a nutrient medium with environmentally relevant NAP (0.1, 1, 3, 5, and 10 µg/L) and MC-LR (5, 10, 25, 50, and 100 µg/L) to determine individual and joint toxic effects. The effects of NAP and MC-LR on physiological responses of L. punctata, including growth, starch accumulation, and antioxidant responses, were studied. Bioaccumulation of MC-LR in L. punctata, with or without NAP, was also examined. The results showed that growth and chlorophyll-a contents of L. punctata were reduced at high concentrations of MC-LR (≥ 25 µg/L), NAP (≥ 10 µg/L) and their mixture (≥ 10 + 1 µg/L) after exposure for 7 d. Starch accumulation in L. punctata did not decrease when exposed to NAP and MC-LR, and higher starch content of 29.8 % ± 2.7 % DW could be due to the destruction of starch-degrading enzymes. The antioxidant responses of L. punctata were stronger after exposure to MC-LR + NAP than when exposed to a single pollutant, although not enough to avoid oxidative damage. NAP enhanced the bioaccumulation of MC-LR in L. punctata when NAP concentration was higher than 5 µg/L, suggesting that higher potentials of MC-LR phytoremediation with L. punctata may be observed in NAP and MC-LR co-concomitant waters. This study provides theoretical support for the application of duckweed in eutrophic waters containing organic chemical pollutants.

Research Progress of a Potential Bioreactor: Duckweed.

Recently, plant bioreactors have flourished into an exciting area of synthetic biology because of their product safety, inexpensive production cost, and easy scale-up. Duckweed is the smallest and fastest-growing aquatic plant, and has advantages including simple processing and the ability to grow high biomass in smaller areas. Therefore, duckweed could be used as a new potential bioreactor for biological products such as vaccines, antibodies, pharmaceutical proteins, and industrial enzymes. Duckweed has made a breakthrough in biosynthesis as a chassis plant and is being utilized for the production of plenty of biological products or bio-derivatives with multiple uses and high values. This review summarizes the latest progress on genetic background, genetic transformation system, and bioreactor development of duckweed, and provides insights for further exploration and application of duckweed.

Research on the Mechanisms of Plant Enrichment and Detoxification of Cadmium.

The heavy metal cadmium (Cd), as one of the major environmentally toxic pollutants, has serious impacts on the growth, development, and physiological functions of plants and animals, leading to deterioration of environmental quality and threats to human health. Research on how plants absorb and transport Cd, as well as its enrichment and detoxification mechanisms, is of great significance to the development of phytoremediation technologies for ecological and environmental management. This article summarises the research progress on the enrichment of heavy metal cadmium in plants in recent years, including the uptake, transport, and accumulation of Cd in plants. The role of plant roots, compartmentalisation, chelation, antioxidation, stress, and osmotic adjustment in the process of plant Cd enrichment are discussed. Finally, problems are proposed to provide a more comprehensive theoretical basis for the further application of phytoremediation technology in the field of heavy metal pollution.

A Protective Role of Tumor Necrosis Factor Superfamily-15 in Intracerebral Hemorrhage-Induced Secondary Brain Injury.

Destabilization of blood vessels by the activities of vascular endothelial growth factor (VEGF) and matrix metalloproteinases (MMPs) following intracerebral hemorrhage (ICH) has been considered the main causes of aggravated secondary brain injury. Here, we show that tumor necrosis factor superfamily-15 (TNFSF15; also known as vascular endothelial growth inhibitor), an inhibitor of VEGF-induced vascular hyper-permeability, when overexpressed in transgenic mice, exhibits a neuroprotective function post-ICH. In this study, we set-up a collagenase-induced ICH model with TNFSF15-transgenic mice and their transgene-negative littermates. We observed less lesion volume and neural function perturbations, together with less severe secondary injuries in the acute phase that are associated with brain edema and inflammation, including vascular permeability, oxidative stress, microglia/macrophage activation and neutrophil infiltration, and neuron degeneration, in the TNFSF15 group compared with the littermate group. Additionally, we show that there is an inhibition of VEGF-induced elevation of MMP-9 in the perihematomal blood vessels of the TNFSF15 mice following ICH, concomitant with enhanced pericyte coverage of the perihematomal blood vessels. These findings are consistent with the view that TNFSF15 may have a potential as a therapeutic agent for the treatment of secondary injuries in the early phase of ICH.