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Since the late 1990s, the trend of plastic waste shipment from developed to developing countries has been increasing. In 2017, China announced an unprecedented ban on its import of most plastic waste, resulting in a sharp decline in global plastic waste trade flow and changes in the treatment structure of countries, whose impacts on global environmental sustainability are enormous but yet unexamined. Here, through the life cycle assessment (LCA) method, we quantified the environmental impacts of changes in the flow patterns and treatment methods of 6 types of plastic waste in 18 countries subsequent to the ban. In the short term, the ban significantly improved four midpoint indicators of environmental impact, albeit contributed to global warming. An annual saving of about 2.35 billion euros of eco-cost was realized, which is equivalent to 56% of plastic waste global trade value in 2017. To achieve global environmental sustainability in the long run, countries should gradually realize the transition from export to domestic management, and from landfill to recycling, which would realize eco-costs savings of about 1.54–3.20 billion euros. China announced a ban on its import of most plastic waste in 2017, resulting in an impact on global environmental sustainability. Here the authors quantify the environmental impacts of changes in the flow patterns and treatment methods of 6 types of plastic waste in 18 countries subsequent to the ban.

In this study, quaternary-ammonium-functionalized metal–organic frameworks (MOFs) Et-N-Cu(BDC-NH2)(DMF), were prepared, characterized, and applied for the highly effective removal of metal cyanide complexes, including Pd(CN)42−, Co(CN)63−, and Fe(CN)63−. Batch studies were carried out, and the maximum adsorption capacities of Pd(II), Co(III), and Fe(III) reached 172.9, 101.0, and 102.6, respectively. Adsorption was rapid, and equilibrium was established within 30 min. Et-N-Cu(BDC-NH2)(DMF) exhibited high thermal and chemical stability. Furthermore, absorbed Pd(CN)42− was selectively recovered by two-step elution. First, Co(CN)63− and Fe(CN)63− were eluted with a 1.5 mol L−1 KCl solution. Elution rates of Co(CN)63− and Fe(CN)63− were greater than 98.0%, whereas the elution percentage of Pd(CN)42− was less than 2.0%. Second, >97.0% Pd(CN)42− on the loaded MOFs was eluted using a 2.0 mol L−1 KI solution. The recovery rate of Pd(CN)42− was greater than 91.0% after five testing cycles. Adsorption isotherms, kinetics models, and adsorption thermodynamics of Pd(CN)42− on Et-N-Cu(BDC-NH2) (DMF) were also systematically investigated. The Et-N-Cu(BDC-NH2) (DMF) absorbent exhibited a rapid, excellent ability for the adsorption of metal cyanide complexes.

Resistance of intracellular pathogens is a challenge in microbial therapy. Methicillin-resistant (MRSA), which is able to persist inside the cells of infected tissues, is protected from attack by the immune system and many antimicrobial agents. To overcome these limitations, nano-delivery systems can be used for targeted therapy of intracellular MRSA. Hyaluronic acid-modified azithromycin/quercetin micelles (HA-AZI/Qe-M) were synthesized by thin film hydration. The micelles were characterized by transmission electron microscopy (TEM), dynamic light scattering (DLS) and Fourier transform infrared spectroscopy (FTIR), and the drug loading (DL) and encapsulation efficiency (EE) were detected by high performance liquid chromatography (HPLC). The uptake ability of RAW264.7 cells was investigated, and its distribution in mice was evaluated by in vivo imaging. The inhibitory effect of the micelles against MRSA in vitro and its ability to eliminate intracellular bacteria were evaluated. Bacterial muscle-infected mice were constructed to evaluate the therapeutic effect of the micelles on bacterial infections in vivo and the biocompatibility of the micelles was investigated. HA-AZI/Qe-M had suitable physical and chemical properties and characterization. In vitro ntibacterial experiments showed that HA-AZI/Qe-M could effectively inhibit the growth of MRSA, inhibit and eliminate the biofilm formed by MRSA, and have an excellent therapeutic effect on intracellular bacterial infection. The results of RAW264.7 cells uptake and in vivo imaging showed that HA-AZI/Qe-M could increase the cellular uptake, target the infection site, and prolong the treatment time. The results of in vivo antibacterial infection experiments showed that HA-AZI/Qe-M was able to ameliorate the extent of thigh muscle infections in mice and reduce the expression of inflammatory factors. HA-AZI/Qe-M is a novel and effective nano-drug delivery system that can target intracellular bacterial infection, and it is expected to be safely used for the treatment of MRSA infection.

Ovarian cancer is a malignant tumor that arises in the female reproductive system and is associated with a very high mortality rate. This is primarily due to the highly invasive nature of metastasis and recurrence. Transforming the immune environment from an immunosuppressive state to an anti-tumor state through the phenotypic transformation of tumor-associated macrophages is crucial for inhibiting the growth, metastasis, and recurrence of ovarian cancer. A polymer micelle (RC-PH-Ms) containing paclitaxel (PTX) and honokiol (HNK) was designed based on high expression of reactive oxygen species in the tumor microenvironment. Once the micelles are actively targeted to the tumor microenvironment characterized by elevated levels of reactive oxygen species, the responsive bond is cleaved, thereby exposing the secondary targeting ligand C7R. The released PTX and HNK facilitate the transformation of relevant macrophages in the tumor microenvironment from an M2 phenotype to an M1 phenotype, which in turn inhibits tumor growth, invasion and metastasis, inhibit angiogenesis and reduce tumor recurrence. The effects of RC-PH-Ms on modulating the immune microenvironment and inhibiting tumor growth, invasion and metastasis, vascularization and recurrence were investigated both in vivo and in vitro. RC-PH-Ms can significantly inhibit the metastasis and recurrence of ovarian cancer, which provides a new perspective for clinical treatment.

A novel functional ion-exchange/adsorption metal organic resin (MOR), TEBAC-HKUST-1, was prepared and characterized. Ethanedithiol was used as the grafting agent to introduce thiol groups onto HKUST-1, and 4-vinylbenzyl chloride was then grafted onto SH-HKUST-1 using thiol groups. Finally, the quaternary ammonium functional group was immobilized onto the carrier by performing a quaternization reaction. The structure and property of TEBAC-HKUST-1 MOR were characterized by TGA, N2 adsorption–desorption, FTIR, SEM, and XRD. TEBAC-HKUST-1 MOR was used to remove metal cyanide complexes from wastewater. The adsorption was rapid, and the metal cyanide complexes including Pt(CN)42−, Co(CN)63−, Cu(CN)32−, and Fe(CN)63− were removed in 30 min. TEBAC-HKUST-1 MOR exhibited a high stability in neutral and weak basic aqueous solutions. Furthermore, Pt(II) could be efficiently recovered through two-step elution. The recovery rate of Pt(II) for five cycles were over 92.0% in the mixture solution containing Pt(CN)42−, Co(CN)63−, Cu(CN)32−, and Fe(CN)63−. The kinetic data were best fitted with the pseudo second-order model. Moreover, the isothermal data were best fitted with the Langmuir model. The thermodynamic results show that the adsorption is a spontaneous and exothermic process. TEBAC-HKUST-1 MOR not only exhibited excellent ability for the rapid removal of metal cyanide complexes, but also provided a new idea for the extraction of noble metals from cyanide-contaminated water.

Conventional separation methods are not suitable for recovering palladium present in low concentrations in ore leaching solutions. In this study, a novel isopentyl sulfide (S201)-impregnated α-MnO2 nanorod adsorbent (BISIN) was prepared, characterized, and applied for the selective adsorption and separation of palladium from the leaching liquor of ores. Batch studies were carried out, and the main adsorption parameters were systematically investigated, in addition to the relevant thermodynamic parameters, isotherms, and kinetic models. The thermodynamic parameters reflected the endothermic and spontaneous nature of the adsorption. Moreover, the experimental results indicated that the Langmuir isotherm model fits the palladium adsorption data well and the adsorption was well described by the pseudo-second-order kinetic model. The main adsorption mechanisms of palladium were elucidated at the molecular level by X-ray crystal structure analysis. Thiourea was found to be an excellent desorption agent, and the palladium-thiourea complex was also confirmed by X-ray crystal structure analysis. The results indicated that almost all of the Pd(II) (>99.0%) is adsorbed on BISIN, whereas less than 2% of the adsorbed Pt(IV), Fe3+, Cu2+, Ni2+, and Co2+ is observed under the optimum conditions. The proposed method can be used for the efficient adsorption and separation of palladium from the leaching liquor of ores.

Growth factor receptor levels are aberrantly high in diverse cancers, driving the proliferation and survival of tumor cells. Understanding the molecular basis for this aberrant elevation has profound clinical implications. Here we show that the pleckstrin homology domain leucine-rich repeat protein phosphatase (PHLPP) suppresses receptor tyrosine kinase (RTK) signaling output by a previously unidentified epigenetic mechanism unrelated to its previously described function as the hydrophobic motif phosphatase for the protein kinase AKT, protein kinase C, and S6 kinase. Specifically, we show that nuclear-localized PHLPP suppresses histone phosphorylation and acetylation, in turn suppressing the transcription of diverse growth factor receptors, including the EGF receptor. These data uncover a much broader role for PHLPP in regulation of growth factor signaling beyond its direct inactivation of AKT: By suppressing RTK levels, PHLPP dampens the downstream signaling output of two major oncogenic pathways, the PI3 kinase/AKT and the Rat sarcoma (RAS)/ERK pathways. Our data are consistent with a model in which PHLPP modifies the histone code to control the transcription of RTKs. Significance This work unveils a previously unidentified function of the tumor suppressor pleckstrin homology domain leucine-rich repeat protein phosphatase (PHLPP) in inhibiting oncogenic signaling by suppressing the steady-state levels of receptor tyrosine kinases such as the EGF receptor. Specifically, PHLPP modifies the histone code to control the transcription of receptor tyrosine kinases. This epigenetic function can account for the upregulation of receptor tyrosine kinases in the multiple cancer types where PHLPP function is compromised.

Amplification of 1q21 is the most frequent genetic alteration in hepatocellular carcinoma (HCC), which was detected in 58-78% of primary HCC cases by comparative genomic hybridization (CGH). Using chromosome microdissection/hybrid selection approach we recently isolated a candidate oncogene CHD1L from 1q21 region. Our previous study has demonstrated that CHD1L had strong oncogenic ability, which could be effectively suppressed by siRNA against CHD1L. The molecular mechanism of CHD1L in tumorigenesis has been associated with its role in promoting cell proliferation. To further investigate the in vivo oncogenic role of CHD1L, CHD1L ubiquitous-expression transgenic mouse model was generated. Spontaneous tumor formations were found in 10/41 (24.4%) transgenic mice, including 4 HCCs, but not in their 39 wild-type littermates. In addition, alcohol intoxication was used to induce hepatocyte pathological lesions and results found that overexpression of CHD1L in hepatocytes could promote tumor susceptibility in CHD1L-transgenic mice. To address the mechanism of CHD1L in promoting cell proliferation, DNA content between CHD1L-transgenic and wildtype mouse embryo fibroblasts (MEFs) was compared by flow cytometry. Flow cytometry results found that CHD1L could facilitate DNA synthesis and G1/S transition through the up-regulation of Cyclin A, Cyclin D1, Cyclin E, CDK2, and CDK4, and down-regulation of Rb, p27(Kip1), and p53. Taken together, our data strongly support that CHD1L is a novel oncogene and plays an important role in HCC pathogenesis.

In this paper, three imidazolium-based ionic liquids, viz., 1-butyl-3-undecyl imidazolium bromide ([BUIm]Br), 1-butyl-3-octyl imidazolium bromide ([BOIm]Br), and 1-butyl-3-hexadecyl imidazolium bromide ([BCIm]Br), were synthesized. Three novel microemulsions systems were constructed and then were used to recover Pd (II) from cyanide media. Key extraction parameters such as the concentration of ionic liquids (ILs), equilibration time, phase ratio (RA/O), and pH were evaluated. The [BUIm]Br/n-heptane/n-pentanol/sodium chloride microemulsion system exhibited a higher extraction percentage of Pd (II) than the [BOIm]Br/n-heptane/n-pentanol/sodium chloride and [BCIm]Br/n-heptane/n-pentanol/sodium chloride microemulsion systems. Under the optimal conditions (equilibrium time of 10 min and pH 10), the extraction percentages of these metals were all higher than 98.5% when using the [BUIm]Br/n-heptane/n-pentanol/sodium chloride microemulsion system. Pd(CN)42− was separated through a two-step stripping procedure, in which Fe (III) and Co (III) were first separated using KCl solution, then Pd(CN)42− was stripped using KSCN solution (separation factors of Pd from Fe and Co exceeded 103). After five extraction–recovery experiments, the recovery of Pd (II) through the microemulsion system remained over 90%. The Pd (II) extraction mechanism of the ionic liquid [BUIm]Br was determined to occur via anion exchange, as shown by spectral analysis (UV, FTIR), Job’s method, and DFT calculations. The proposed process has potential applications for the comprehensive treatment of cyanide metallurgical wastewater.

Background Amplification of 3q26 is one of the most frequent genetic alterations in many human malignancies. Recently, we isolated a novel oncogene eIF-5A2 within the 3q26 region. Functional study has demonstrated the oncogenic role of eIF-5A2 in the initiation and progression of human cancers. In the present study, we aim to investigate the physiological and pathological effect of eIF-5A2 in an eIF-5A2 transgenic mouse model. Methods An eIF-5A2 transgenic mouse model was generated using human eIF-5A2 cDNA. The eIF-5A2 transgenic mice were characterized by histological and immunohistochemistry analyses. The aging phenotypes were further characterized by wound healing, bone X-ray imaging and calcification analysis. Mouse embryo fibroblasts (MEF) were isolated to further investigate molecular mechanism of eIF-5A2 in aging. Results Instead of resulting in spontaneous tumor formation, overexpression of eIF-5A2 accelerated the aging process in adult transgenic mice. This included decreased growth rate and body weight, shortened life span, kyphosis, osteoporosis, delay of wound healing and ossification. Investigation of the correlation between cellular senescence and aging showed that cellular senescence is not required for the aging phenotypes in eIF-5A2 mice. Interestingly, we found that activation of eIF-5A2 repressed p19 level and therefore destabilized p53 in transgenic mouse embryo fibroblast (MEF) cells. This subsequently allowed for the accumulation of chromosomal instability, such as errors in cell dividing during metaphase and anaphase. Additionally, a significantly increase in number of aneuploidy cells ( p < 0.05) resulted from an increase in the incidences of misaligned and lagging chromosomal materials, anaphase bridges, and micronuclei in the transgenic mice. Conclusion These observations suggest that eIF-5A2 mouse models could accelerate organismal aging by increasing chromosome instability.