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Tissues derive ATP from two pathways-glycolysis and the tricarboxylic acid (TCA) cycle coupled to the electrontransport chain. Most energy in mammals is produced via TCA metabolism1. In tumours, however, the absolute rates of these pathways remain unclear. Here we optimize tracer infusion approaches to measure the rates of glycolysis and the TCA cycle in healthy mouse tissues, Kras-mutant solid tumours, metastases and leukaemia. Then,given the rates of these two pathways, we calculate total ATP synthesis rates. We find that TCA cycle flux is suppressed in all five primary solid tumour models examined and is increased in lung metastases of breast cancer relative to primary orthotopic tumours. As expected, glycolysis flux is increased in tumours compared with healthy tissues (the Warburg effect2,3), but this increase is insufficient to compensate for low TCA flux in terms of ATP production. Thus, instead of being hypermetabolic, as commonly assumed, solid tumours generally produce ATP at a slower than normal rate. In mouse pancreatic cancer, this is accommodated by the downregulation of protein synthesis, one of this tissue's major energy costs. We propose that, as solid tumours develop, cancer cells shed energetically expensive tissue-specific functions, enabling uncontrolled growth despite a limited ability to produce ATP.

Blockchain technology is valuable due to the renowned characteristics, such as immutability, security, and transparency. Although blockchain’s effectiveness and efficiency are yet to be proven, its potential for resolving social issues is attracting the attention of public administrations, private entities, and individuals to adopt or develop this technology. In this paper, some of the most high-profile blockchain-enabled smart city applications in South Korea, the United States and China are sampled and reviewed. The goal is to explore blockchain-related regulations or legislation in each country, which is the underlying basis to allow the blockchain pilots to proceed. Then, each country’s key blockchain initiatives are explored using a top-down framework (i.e., central/federal government – provincial/state governments – city governments). Lastly, by summarizing those blockchain-based smart city projects, the challenges and observations are discussed.

Autophagy defects are a risk factor for inflammatory bowel diseases (IBDs) through unknown mechanisms. Whole-body conditional deletion of autophagy-related gene (Atg) Atg7 in adult mice (Atg7Δ/Δ) causes tissue damage and death within 3 mo due to neurodegeneration without substantial effect on intestine. In contrast, we report here that whole-body conditional deletion of other essential Atg genes Atg5 or Fip200/Atg17 in adult mice (Atg5Δ/Δ or Fip200Δ/Δ) caused death within 5 d due to rapid autophagy inhibition, elimination of ileum stem cells, and loss of barrier function. Atg5Δ/Δ mice lost PDGFRα+ mesenchymal cells (PMCs) and Wnt signaling essential for stem cell renewal, which were partially rescued by exogenous Wnt. Matrix-assisted laser desorption ionization coupled to mass spectrometry imaging (MALDI-MSI) of Atg5Δ/Δ ileum revealed depletion of aspartate and nucleotides, consistent with metabolic insufficiency underlying PMC loss. The difference in the autophagy gene knockout phenotypes is likely due to distinct kinetics of autophagy loss, as deletion of Atg5 more gradually extended lifespan phenocopying deletion of Atg7 or Atg12. Thus, autophagy is required for PMC metabolism and ileum stem cell and mammalian survival. Failure to maintain PMCs through autophagy may therefore contribute to IBD.

An easily recyclable nanocomposite ascorbic acid-modified Fe3O4 (VC@Fe3O4) was synthesized, characterized, and evaluated as a green heterogeneous catalyst for activation of peroxymonosulfate (PMS). The structures of fresh and used VC@Fe3O4 were well characterized by TEM, XRD, FTIR, and XPS. The catalytic activity comparison between Fe3O4 and VC@Fe3O4 was performed under different parameters for depletion of sulfadiazine (SD). Additionally, scavenging tests and in-situ electron paramagnetic resonance (EPR) tests were applied to discern the primary radicals generated in the VC@Fe3O4/PMS system. The results indicate that the VC@Fe3O4 possesses a higher catalytic activity towards PMS compared with Fe3O4 for SD removal, and the observed pseudo first rate constant (kobs) were 7.24 × 10−2 min−1 for the VC@Fe3O4/PMS system and 1.05 × 10−2 min−1 for the Fe3O4/PMS system, correspondingly. 56.6% SD removal efficiency was obtained with 0.3 mM PMS and 0.8 g/L VC@Fe3O4 under pH 7.0. A large amount of hydroxyl radicals (OH ) and a few number of sulfate radicals (SO4− ) were discerned by the hyperfine splitting constant values and scavenging results. Mechanisms on the peroxymonosulfate activation and radical generation in the VC@Fe3O4/PMS system were supposed. Results indicate that VC would obviously boost the cycle of Fe2+-Fe3+ on surface of VC@Fe3O4 nanoparticles and newly generated Fe2+ can continuously be consumed to activate PMS, which is answer for the rapid generation of reactive radicals (OH , SO4− ). At last, mineralization and degradation pathway were also investigated. The findings of this study suggest that VC@Fe3O4 is a novel effective catalyst in activation of peroxymonosulfate under neutral pHs.

Microplastics have received growing attention as carriers of organic pollutants in the water environment. To better understand the contribution of hydrophobic interaction, hydrogen-bonding interaction, π-π interaction and electrostatic interaction on the adsorption of hydrophilic compounds on microplastics and their adsorption behavior in natural waters, polyethylene terephthalate (PET,150 μm) was used as an adsorbent and 4-chlorophenol (MCP), 2,4-dichlorophenol (DCP) and 2,4,6-trichlorophenol (TCP) were used as adsorbates. The results of batch adsorption experiments showed that chlorophenols (CPs) reached adsorption sites of PET through film diffusion and intra-particle diffusion. pH greatly affected the adsorption capacity. Hydrophobic interaction was the main adsorption mechanism of undissociated CPs on PET. Hydrogen-bonding interaction was also an adsorption mechanism between undissociated CPs and PET, and the contribution of hydrogen-bonding interaction to adsorption decreased with the increase of chlorine content. Meanwhile, the increase of chlorine content was favorable to the hydrophobic interaction between undissociated CPs and PET. However, higher chlorine content CPs with lower pK

NADH provides electrons for aerobic ATP production. In cells deprived of oxygen or with impaired electron transport chain activity, NADH accumulation can be toxic. To minimize such toxicity, elevated NADH inhibits the classical NADH producing pathways: glucose, glutamine, and fat oxidation. Here, through deuterium tracing studies in cultured cells and mice, we show that folate-dependent serine catabolism also produces substantial NADH. Strikingly, when respiration is impaired, serine catabolism through methylene tetrahydrofolate dehydrogenase (MTHFD2) becomes a major NADH source. In cells whose respiration is slowed by hypoxia, metformin, or genetic lesions, mitochondrial serine catabolism inhibition partially normalizes NADH levels and facilitates cell growth. In mice with engineered mitochondrial complex I deficiency (NDUSF4-/-), serine’s contribution to NADH is elevated and progression of spasticity is modestly slowed by pharmacological blockade of serine degradation. Thus, when respiration is impaired, serine catabolism contributes to toxic NADH accumulation.

Collaborative object transportation has become a popular study trend with its remarkable application foreground. In previous relevant studies, localization of the transported object has always been accomplished by additional devices rather than robot onboard equipments. This paper presents a generalized multi-robot leader-follower system for collaborative object transportation and an onboard object localization algorithm for trajectory tracking of the target object. In this system, the mobile robots can directly push a cubic object without extra gripping devices, when tracking the reference trajectory. During the control process, the object is regarded as an virtual leader, whose localization information is utilized as the feedback, while the mobile robots are considered as the followers. In absence of external localization systems, the proposed onboard localization algorithm provides the real-time position information of the object using scan data from lidars equipped on the robots. A performed measurement accuracy test shows high precision of this algorithm. Finally, a lane-changing experiment of object transportation is conducted, and it verifies this multi-robot leader-follower system.

Protein synthesis inhibition is an immediate response during stress to switch the composition of protein pool in order to adapt to the new environment. It was reported that this response could be either protective or deleterious. However, how cells choose to live or die upon protein synthesis inhibition is largely unknown. Previously, we have shown that elongation factor-2 kinase (eEF2K), a protein kinase that suppresses protein synthesis during elongation phase, is a positive regulator of apoptosis both in vivo and in vitro Consistently, here we report that knock-out of eEF2K protects mice from a lethal dose of whole-body ionizing radiation at 8 Gy by reducing apoptosis levels in both bone marrow and gastrointestinal tracts. Surprisingly, similar to the loss of p53, eEF2K deficiency results in more severe damage to the gastrointestinal tract at 20 Gy with the increased mitotic cell death in small intestinal stem cells. Furthermore, using epithelial cell lines, we showed that eEF2K is required for G2/M arrest induced by radiation to prevent mitotic catastrophe in a p53-independent manner. Specifically, we observed the elevation of Akt/ERK activity as well as the reduction of p21 expression in Eef2k(-/-) cells. Therefore, eEF2K also provides a protective strategy to maintain genomic integrity by arresting cell cycle in response to stress. Our results suggest that protective versus pro-apoptotic roles of eEF2K depend on the type of cells: eEF2K is protective in highly proliferative cells, such as small intestinal stem cells and cancer cells, which are more susceptible to mitotic catastrophe.

Tumor suppressor liver kinase B1 (LKB1) activates 5'-adenosine monophosphate protein kinase (AMPK) and plays an essential role in maintaining energy homeostasis. LKB1 mutations are the third most frequent mutation detected in non-small cell lung cancer (NSCLC). Compared to p53 mutation, co-mutations in LKB1 with KRAS cause aggressive tumor growth, metastases and resistance to chemotherapy as well as immunotherapy. Thus, identifying a novel target to improve LKB1-deficient Kras-driven NSCLC treatment is urgently needed. Our previous work demonstrates that autophagy inhibition is synthetically lethal in KrasG12D/+;Lkb1−/− (KL) mediated tumorigenesis; in contrast to intact autophagy KL lung tumors, loss of an autophagy-essential gene Atg7 dramatically impaired tumor initiation and tumor growth. This is in sharp contrast to wild-type (WT) Lkb1 (KrasG12D/+;p53−/− (KP)) tumors that are less sensitive to autophagy gene ablation. These observations indicate that LKB1 mutations predispose KRAS NSCLC to autophagy inhibition and that LKB1 mutations could be explored as a predictive biomarker for precision lung cancer therapy. To further value our discoveries in clinical translational ability, we treated mouse lung tumor-derived cell lines (TDCLs) with FDA approved autophagy inhibitor hydroxychloroquine (HCQ) and found that KL TDCLs were much sensitive to HCQ-induced cell death compared with Lkb1-WT KP TDCLs. Furthermore, a combination treatment of HCQ with mitogen-activated protein kinase kinase (MAPKK or MEK) inhibitor Trametinib showed synergistic anti-proliferative effects in KL TDCLs, but not in KP TDCLs. To elucidate the underlying mechanism of increased sensitivity of KL TDCLs to Trametinib by autophagy ablation, we performed metabolomic profiling of KL TDCLs with Trametinib, HCQ alone or in combination treatment. We found that the levels of several glycolytic and TCA cycle intermediates, as well as amino acids, were significantly upregulated upon treatment with Trametinib, which were significantly reduced by the combined treatment with HCQ and trametinib. Moreover, Trametinib treatment led to an increased level of ATP, which was decreased by the combination treatment. Similarly, we observed anti-tumor synergistic effects of the combination treatment in KL allograft tumor growth. In addition, metastases of KL TDCLs to the lung was reduced by the combination treatment compared to the single agents. We further found that in KRAS-mutant human lung cancer cell lines, LKB1-mutant cells were much sensitive to the combination treatment than LKB1-WT cells. Our observations suggest that KL TDCLs and KL human lung cancer cells resist to Trametinib treatment by upregulating autophagy to maintain energy homeostasis for survival. Therefore, combination therapy of autophagy and MEK inhibition could be a novel therapeutic strategy to specifically treat LKB1-deficient NSCLC. Citation Format: Vrushank Dharmesh Bhatt, Khoosheh Khayati, Jerry Kong, Akash Raju, Zhixian Hu, Xiaoyang Su, Jessie Yanxiang Guo. Autophagy inhibition sensitizes Liver Kinase B1 (LKB1) - deficient Kras-driven lung tumors to MEK inhibitor Trametinib [abstract]. In: Proceedings of the Annual Meeting of the American Association for Cancer Research 2020; 2020 Apr 27-28 and Jun 22-24. Philadelphia (PA): AACR; Cancer Res 2020;80(16 Suppl):Abstract nr 5710.

Tumor suppressor liver kinase B1 (LKB1) activates 5’-adenosine monophosphate protein kinase (AMPK) to maintain energy homeostasis. LKB1 mutations are the third most frequent mutation detected in non-small cell lung cancer (NSCLC). Compared to p53 mutation, mutations in LKB1 causes more aggressive tumor growth and resistance to chemotherapy as well as immunotherapy. Thus, identifying a novel target to improve LKB1-deficient NSCLC treatment is urgently needed. Autophagy degrades and recycles macromolecules for cells to survive starvation. Using genetically engineered mouse models for NSCLC with Kras activation and LKB1 loss (KL), we found that autophagy (Atg7) deficiency prevents tumor initiation, reduced tumor growth and extended the mouse lifespan compared to mice bearing Atg7 wild-type (WT) tumors. Most importantly, tumor growth inhibition by Atg7 deficiency was much more dramatic in KL than Kras/p53 (KP) lung tumors. Furthermore, we generated mouse tumor-derived cell lines (TDCLs) and found that Atg7 null TDCLs were more sensitive to starvation-induced cell death than Atg7 WT TDCLs, which can be rescued by palmitate supplementation, indicating that autophagy is required to maintain free fatty acid (FA) level for cells to survive starvation. We further performed 13C glucose tracing study and found that Atg7 deletion increased de novo FA synthesis and reduced FAs elongation. Fasnall, a selective FA synthase inhibitor, inhibited Atg7 null cell proliferation. Treatment with Orlistat, a lipase inhibitor, did not impact cell proliferation in nutrient-rich conditions but accelerated starvation-induced Atg7 null cell death, indicating that lipase-medicated lipid degradation compensates for autophagy loss to provide free FAs in starvation. A carnitine palmitoyltransferase I inhibitor, Etomoxir treatment, accelerated the starvation-induced Atg7 null cell death and reduced oxygen consumption rate (OCR) of Atg7 null cells in starvation, compared with Atg7 WT cells, indicating that autophagy-deficient cells rely more on FA oxidation for energy production in nutrient deprivation. To probe the significance of autophagy in human lung cancer cell lines with LKB1 mutation, we knocked down ATG7 using siRNA. ATG7 knockdown (KD) inhibited clonogenic survival of LKB1 mutant cells in starvation, but had no effect in LKB1 WT cells. Supplementation of glutamine or palmitate rescued the survival of LKB1 mutant cells with ATG7 KD in starvation and maintained OCR, demonstrating that KRAS-driven human lung cancer cells with mutant LKB1 rely on autophagy to maintain mitochondrial metabolism to survive energy crises. Taken together, our results demonstrate that autophagy modulates lipid metabolism for KL cells to survive metabolic stress. Thus, a combination of autophagy inhibition with interruption of lipid metabolism could be a novel therapeutic strategy to specifically treat LKB1-deficient NSCLC. Citation Format: Vrushank D. Bhatt, Khoosheh Khayati, Zhixian Hu, Xiaoyang Su, Jessie Yanxiang Guo. Autophagy modulates lipid metabolism in liver kinase B1 (LKB1)-deficient Kras-driven lung tumorigenesis [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2019; 2019 Mar 29-Apr 3; Atlanta, GA. Philadelphia (PA): AACR; Cancer Res 2019;79(13 Suppl):Abstract nr 2716.

Fe complexes ([Fe(Ox) 3 ] 3− and [Fe(Cit) 2 ] 3− ) have been heterogenized through preservation into MgAl-layered double hydroxides (LDHs). The SEM images and N 2 adsorption–desorption isotherm showed that the obtained products were mesoporous materials and the specific surface area of LDHs/Fe-complex composites were obviously greater than pristine LDHs, which is beneficial for the adsorption of organic pollutants. Measurement of adsorptive and heterogeneous photo-Fenton degradation of methylene blue (MB) suggested that the LDHs/Fe-complex composites had an excellent adsorption capacity at different pHs and the adsorption isotherm modeled well with the Langmuir equation. The enhancement of adsorption capacity may be attributed to the external hydroxyl groups of LDHs. MB was enriched on the surface of LDHs/Fe-complex composites, which favors MB degradation in situ. The obtained composites displayed an high photocatalytic activity in a pH range from 4.0 to 6.0 with dissolved Fe cation at a low concentration. Therefore, Fe complexes intercalated into LDHs can be an effective heterogeneous Fenton catalyst for oxidation of organic pollutants in a relatively wide pH range.

Magnesium ion (Mg(2+)) is the fourth most common cation in the human body, and has a crucial role in many physiological functions. Mg(2+) homeostasis is an important contributor to bone development, however, its roles in the development of dental mineralized tissues have not yet been well known. We identified that transient receptor potential cation channel, subfamily M, member 7 (TRPM7), was significantly upregulated in the mature ameloblasts as compared to other ameloblasts through our whole transcript microarray analyses of the ameloblasts. TRPM7, an ion channel for divalent metal cations with an intrinsic serine/threonine protein kinase activity, has been characterized as a key regulator of whole body Mg(2+) homeostasis. Semi-quantitative PCR and immunostaining for TRMP7 confirmed its upregulation during the maturation stage of enamel formation, at which ameloblasts direct rapid mineralization of the enamel matrix. The significantly hypomineralized craniofacial structures, including incisors, molars, and cranial bones were demonstrated by microCT analysis, von Kossa and trichrome staining in Trpm7 (Δkinase∕+) mice. A previously generated heterozygous mouse model with the deletion of the TRPM7 kinase domain. Interestingly, the skeletal phenotype of Trpm7 (Δkinase∕+) mice resembled those found in the tissue-nonspecific alkaline phosphatase (Alpl) KO mice, thus we further examined whether ALPL protein content and alkaline phosphatase (ALPase) activity in ameloblasts, odontoblasts and osteoblasts were affected in those mice. While ALPL protein in Trpm7 (Δkinase∕+) mice remained at the similar level as that in wt mice, ALPase activities in the Trpm7 (Δkinase∕+) mice were almost nonexistent. Supplemented magnesium successfully rescued the activities of ALPase in ameloblasts, odontoblasts and osteoblasts of Trpm7 (Δkinase∕+) mice. These results suggested that TRPM7 is essential for mineralization of enamel as well as dentin and bone by providing sufficient Mg(2+) for the ALPL activity, underlining the key importance of ALPL for biomineralization.

Autophagy degrades and recycles macromolecules for cells to survive starvation. In genetically engineered mouse models (GEMMs) for human non-small cell lung cancer (NSCLC), autophagy supports Kras-driven lung tumor growth with or without Trp53. Tumor suppressor liver kinase B1 (LKB1) activates 5'-adenosine monophosphate protein kinase (AMPK) to maintain energy homeostasis. LKB1 mutations are detected in 20-30% of NSCLC, causing aggressive tumor growth and resistance to chemotherapy. Identifying novel target to improve LKB1-deficient tumor treatment is urgently needed. Using GEMMs for NSCLC with oncogenic Kras and LKB1 loss (KL), we found that autophagy deficiency increased the survival of the mice bearing Atg7-/- tumors compared to mice bearing wild-type (WT) tumors. To determine the mechanism of autophagy in supporting LKB1-deficient Kras-driven lung tumor growth, tumor derived cell lines (TDCLs) were generated from the lung tumors of these mice. We found that Atg7 null TDCLs were more sensitive to glucose and glutamine deprivation-induced cell death compared to Atg7 WT TDCLs. Atg7 null TDCLs were also more sensitive to starvation-induced cell death than Atg7 WT TDCLs, which can be rescued by glucose, glutamine, pyruvate, lactate and nucleotide supplementation. Thus, autophagy is required for KL TDCLs to tolerate metabolic stress. Furthermore, we observed that palmitate supplementation successfully rescued starvation-induced Atg7 null TDCLs death, indicating that autophagy is required to maintain free fatty acid level for cells to survive starvation. We further performed metabolomics in TDCLs in normal and starvation conditions and found that level of amino acids and intermediates for glycolysis and TCA cycle metabolism were significantly lower in Atg7 null TDCLs compared to Atg7 WT TDCLs during HBSS starvation. Surprisingly, we observed a significant increase in the levels of biotin, a precursor for fatty acid synthesis, in Atg7 null TDCLs than that in WT TDCLs, indicating that accumulation of biotin in autophagy deficient cells might be due to defective fatty acid synthesis. In support of this, we found that the lipid droplets accumulation is significantly lower in Atg7 null KL TDCLs than that in Atg7 WT cells. To further evaluate the functional consequences of autophagy-mediated lipid metabolism in supporting KL tumor growth, we treated Atg7 null and WT cells with etomoxir, an irreversible inhibitor of carnitine palmitoyltransferase-1 (CPT-1) to inhibit fatty acid oxidation, in normal and starvation conditions. We found that Atg7 null TDCLs are much more sensitive to etomoxir treatment than WT cells. Taken together, autophagy plays a critical role in supporting lipid metabolism for cells to survive metabolic stress. Thus, a combination of autophagy inhibition with interruption of lipid metabolism could be a novel therapeutic strategy to treat LKB1-deficient lung tumor. Citation Format: Vrushank D. Bhatt, Zhixian Hu, Xiaoyang Su, Jessie Yanxiang Guo. Autophagy modulates lipid metabolism to support Liver Kinase B1 (LKB1) - deficient lung tumor growth [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2018; 2018 Apr 14-18; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2018;78(13 Suppl):Abstract nr 4969.

TRPM7 is an unusual bi-functional protein containing an ion channel covalently linked to a protein kinase domain. TRPM7 is implicated in regulating cellular and systemic magnesium homeostasis. While the biophysical properties of TRPM7 ion channel and its function are relatively well characterized, the function of the TRPM7 enzymatically active kinase domain is not understood yet. To investigate the physiological role of TRPM7 kinase activity, we constructed mice carrying an inactive TRPM7 kinase. We found that these mice were resistant to dietary magnesium deprivation, surviving three times longer than wild type mice; also they displayed decreased chemically induced allergic reaction. Interestingly, mutant mice have lower magnesium bone content compared to wild type mice when fed regular diet; unlike wild type mice, mutant mice placed on magnesium-depleted diet did not alter their bone magnesium content. Furthermore, mouse embryonic fibroblasts isolated from TRPM7 kinase-dead animals exhibited increased resistance to magnesium deprivation and oxidative stress. Finally, electrophysiological data revealed that the activity of the kinase-dead TRPM7 channel was not significantly altered. Together, our results suggest that TRPM7 kinase is a sensor of magnesium status and provides coordination of cellular and systemic responses to magnesium deprivation.

SummaryThe control of germline quality is critical to reproductive success and survival of a species; however, the mechanisms underlying this process remain unknown. Here, we demonstrate that elongation factor 2 kinase (eEF2K), an evolutionarily conserved regulator of protein synthesis, functions to maintain germline quality and eliminate defective oocytes. We show that disruption of eEF2K in mice reduces ovarian apoptosis and results in the accumulation of aberrant follicles and defective oocytes at advanced reproductive age. Furthermore, the loss of eEF2K in Caenorhabditis elegans results in a reduction of germ cell death and significant decline in oocyte quality and embryonic viability. Examination of the mechanisms by which eEF2K regulates apoptosis shows that eEF2K senses oxidative stress and quickly downregulates short-lived antiapoptotic proteins, XIAP and c-FLIPL by inhibiting global protein synthesis. These results suggest that eEF2K-mediated inhibition of protein synthesis renders cells susceptible to apoptosis and functions to eliminate suboptimal germ cells.

Ethylamine modified vermiculite (Ethyl-VER) with high specific surface area and excellent pore structure was prepared to remove cesium from aqueous solution. The physic-chemical properties of the pristine and modified vermiculite were analyzed by X-ray diffraction (XRD), Fourier-transform infrared (FTIR), specific surface area (BET) and scanning electron microscopy/energy disperse spectroscopy (SEM/EDS). The corroding effect of ethylamine increased the specific surface area of vermiculite from 4.35 to 15.59 m(2) g(-1), and the average pore diameter decreased from 6.8 to 5.34 nm. Batch adsorption experiments were conducted as a function of pH, initial Cs(+) concentration, contact time, coexisting cations (K(+), Na(+), Ca(2+)) and low-molecular-weight organic acids (acetic acid, oxalic acid, citric acid) to illustrate the adsorption behavior. The study found that the adsorption capacity of cesium in aqueous solution was improved from 56.92 to 78.17 mg g(-1) after modification. The formation of micropores and mesopores and the increased surface area played a critical role in the enhancement of cesium adsorption. Kinetic experiments indicated that the adsorption process can be simulated well with a pseudo-second-order model. The presence of cations or low-molecular-weight organic acids inhibited cesium adsorption in different degrees. On the basis of our results, Ethyl-VER with good surface characteristics and high adsorption capacity is a suitable adsorbent for cesium removal from aqueous solution.

It is an important guarantee of regaining aviation force effectiveness by implementing repair effectively on the battle-damaged plane. The study of the battle-damaged plane to repair has always been one of the most core issues focused on by the equipment support personnel. Aircraft battle repair system is a complex artificial system. Taking aircraft battle-damaged repair system as an object, this paper analyzed the concept and composition of the aircraft battle-damaged repair system. Then, adopting state space analysis method, the paper studied and established state-space model of the aircraft repair system. This model can be used as a framework for building repair demand analysis model, the repair system structure model, the repair process model, and effectiveness evaluation model.

Mg2+ is the second-most abundant cation in animal cells and is an essential cofactor in numerous enzymatic reactions. The molecular mechanisms controlling Mg2+ balance in the organism are not well understood. In this study, we report identification of TRPM7, a bifunctional protein containing a protein kinase fused to an ion channel, as a key regulator of whole body Mg2+ homeostasis in mammals. We generated TRPM7-deficient mice with the deletion of the kinase domain. Homozygous TRPM7Δkinase mice demonstrated early embryonic lethality, whereas heterozygous mice were viable, but developed signs of hypomagnesaemia and revealed a defect in intestinal Mg2+ absorption. Cells derived from heterozygous TRPM7Δkinase mice demonstrated reduced TRPM7 currents that had increased sensitivity to the inhibition by Mg2+. Embryonic stem cells lacking TRPM7 kinase domain displayed a proliferation arrest phenotype that can be rescued by Mg2+ supplementation. Our results demonstrate that TRPM7 is essential for the control of cellular and whole body Mg2+ homeostasis., Magnesium is an essential element of the diet and is a cofactor for many enzymes. In this study, the channel kinase TRPM7 is shown to be essential for magnesium homeostasis, and heterozygous mice lacking the kinase domain show a defect in absorption of magnesium from the diet.