N, P and C removal simultaneously and microbial population numbers in a cyclic activated sludge system treating village and township domestic wastewater by altering the cycle times.

It was necessary to research an efficient treatment process suitable for township domestic wastewater. In this paper, the performance of the cyclic activated sludge system (CASS) system for simultaneous carbon (C), nitrogen (N) and phosphorus (P) removal was investigated by changing the operation cycle of the CASS reactor. Four operating conditions were set up, T1, T2, T3 and T4, with cycle times of 6, 8, 12 and 8 h (with carbon source), respectively. The results showed that the CASS system had good simultaneous removal of C, N and P. The highest removal rates of COD, TN, NH4+ -N and TP were 87.69, 72.99, 98.60 and 98.38%, respectively, at a cycle time of 8 h. The TN removal rate could be increased to 82.51% after the addition of carbon source. Microbial community analysis showed that Proteobacteria, Bacteroidetes and Candidatus Saccharibacteria were the main phylum-level bacteria. Their presence facilitated the effectiveness of the CASS process for nitrogen removal and phosphorus removal. Functional analysis of genes revealed that the abundance values of genes associated with C, N and P metabolism were higher when the treatment was effective.

PERK Regulates the Sensitivity of Hepatocellular Carcinoma Cells to High-LET Carbon Ions via either Apoptosis or Ferroptosis.

PERK is one of the transmembrane sensors of unfolded protein response (UPR) triggered by ER stress. In this study, we evaluated the role of PERK in the sensitivity of hepatocellular carcinoma (HCC) cells to high linear energy transfer (LET) carbon ions (CI). We found that CI irradiation could induce ER stress in HCC cells. On the one hand, PERK promoted autophagy via regulating ATF4 expression; on the other hand, PERK regulated p53 expression, and the latter either induced autophagy through up-regulating DRAM, or directly promoting apoptosis through the mitochondrial pathway or facilitating ferroptosis via down-regulating SLC7A11 (the extrinsic pathway), but independent of GPX4 (the intrinsic pathway). These factors jointly determined the sensitivity of HCC cells to high-LET CI radiation. Inhibiting TP53 directly increased cellular radioresistance definitely. Moreover, the death of HepG2 (TP53 wild type) cells induced by high-LET CI irradiation combined with sorafenib treatment might be caused by a mixed-type regulated cell death (RCD) including both apoptosis and ferroptosis, suggesting that apoptosis and ferroptosis are synergetic cell death modes regulated by TP53, which is one of the reasons why the sensitivity of HepG2 cells is higher than that of Hep3B (TP53 null type) and PLC/PRF5 (TP53 mutated type) cells. Therefore, our work might shed light on the potential therapeutic implication of CI radiotherapy combined with PERK targeted clinical drugs to implement personalized and precise treatment of HCCs.

CircZNF208 enhances the sensitivity to X-rays instead of carbon-ions through the miR-7-5p /SNCA signal axis in non-small-cell lung cancer cells.

BACKGROUND: Mounting evidence suggests that circular RNAs (circRNAs) are closely related to the regulation of gene expression during tumour development. However, the role of circRNAs in modulating the radiosensitivity of non-small cell lung cancer (NSCLC) cells has not been explored. METHODS: Transcriptome sequencing was used to explore the expression profiles of circRNAs in NSCLC. The expression level of circRNAs was changed by inducing instantaneous knockdown or overexpression. Changes in proliferation and radiosensitivity of NSCLC cells were investigated using CCK-8, EDU, and clonal survivals. RESULTS: By analysing the circRNA expression profile of NSCLC cells, we found that circRNA ZNF208 (circZNF208) was significantly upregulated in a radioresistant NSCLC cell line (A549-R11), which was acquired from the parental NSCLC cell line A549. Knockout experiments indicated that circZNF208 enhanced the radiosensitivity of A549 and A549-R11 cells to X-rays. Mechanistically, circZNF208 upregulated SNCA expression by acting as a sponge of miR-7-5p and subsequently promoted the resistance of NSCLC cells to low linear energy transfer (LET) X-rays. However, this effect was not observed in NSCLC cells exposed to high-LET carbon ions. CONCLUSIONS: Knockdown of circZNF208 altered the radiosensitivity of patients with NSCLC to X-rays but did not significantly change the sensitivity to carbon ions. Therefore, circZNF208 might serve as a potential biomarker and therapeutic target for NSCLC treatment with radiotherapy of different modalities.

Multiple functions of p21 in cancer radiotherapy.

BACKGROUND: Greater than half of cancer patients experience radiation therapy, for both radical and palliative objectives. It is well known that researches on radiation response mechanisms are conducive to improve the efficacy of cancer radiotherapy. p21 was initially identified as a widespread inhibitor of cyclin-dependent kinases, transcriptionally modulated by p53 and a marker of cellular senescence. It was once considered that p21 acts as a tumour suppressor mainly to restrain cell cycle progression, thereby resulting in growth suppression. With the deepening researches on p21, p21 has been found to regulate radiation responses via participating in multiple cellular processes, including cell cycle arrest, apoptosis, DNA repair, senescence and autophagy. Hence, a comprehensive summary of the p21's functions in radiation response will provide a new perspective for radiotherapy against cancer. METHODS: We summarize the recent pertinent literature from various electronic databases, including PubMed and analyzed several datasets from Gene Expression Omnibus database. This review discusses how p21 influences the effect of cancer radiotherapy via involving in multiple signaling pathways and expounds the feasibility, barrier and risks of using p21 as a biomarker as well as a therapeutic target of radiotherapy. CONCLUSION: p21's complicated and important functions in cancer radiotherapy make it a promising therapeutic target. Besides, more thorough insights of p21 are needed to make it a safe therapeutic target.

Genistein inhibits radiation-induced invasion and migration of glioblastoma cells by blocking the DNA-PKcs/Akt2/Rac1 signaling pathway.

BACKGROUND AND PURPOSE: Radiotherapy is the most important therapeutic measure against glioblastoma multiforme (GBM), which is regarded as the most common and highly lethal type of brain cancer. Nevertheless, most relapses originate in the close vicinity of the irradiated target volume. Genistein is a natural product that can suppress the invasive potential of cancer cells. In this study, DNA-dependent protein kinase catalytic subunit (DNA-PKcs)-proficient and -deficient GBM cells were selected for in vitro and in vivo studies to investigate the inhibiting effects of genistein on radiation-induced invasion and migration and the corresponding mechanism. MATERIALS AND METHODS: GBM cell lines with or without genistein pre-treatment were irradiated with X-rays. Cell survival was determined using colony formation assay and the rate of cellular proliferation was analyzed with a real-time cell electronic sensing system. For in vitro study, invasion and migration abilities were evaluated via wound-healing and transwell assays, while protein expression was determined with western blotting. Genistein interaction with DNA-PKcs was estimated with pull-down, recombinant and binding assays. For in vivo study, cells were stereotactically injected into NOD-SCID mice to establish tumors. Hematoxylin and eosin and immunohistochemistry were used to assess the invasive potential of GBM. RESULTS: X-ray irradiation enhanced the migration and invasion of DNA-PKcs-positive but not DNA-PKcs-negative GBM cells. It also activated the DNA-PKcs/Akt2/Rac1 signaling pathway, which contributed to GBM malignant progression by aggravating GBM cell invasive potential. The study successfully demonstrated that genistein can specifically bind to DNA-PKcs and block the DNA-PKcs/Akt2/Rac1 pathway, thereby effectively inhibiting radiation-induced invasion and migration of GBM cells in vitro and in vivo. The present study emphasized that radiation-induced invasive potential is initiated by DNA-PKcs, which is a well-known double strand breaks (DSB) repair protein, and determined the exact site for genistein binding to DNA-PKcs. CONCLUSION: DNA-PKcs is not only a potential target for cancer therapy, but also a reliable biomarker for predicting radiation-induced invasion and migration of GBM cells. Thus, genistein might serve as a novel therapeutic strategy for treating GBM.

Integrated analysis of circRNA-miRNA-mRNA network reveals potential prognostic biomarkers for radiotherapies with X-rays and carbon ions in non-small cell lung cancer.

BACKGROUND: This work was aimed at exploring the regulatory network of non-coding RNA (ncRNA) especially circular RNA (circRNA) and microRNA (miRNA), in the sensitivity of non-small cell lung cancer (NSCLC) cells to low linear energy transfer (LET) X-ray and high-LET carbon ion irradiations. METHODS: The radioresistant NSCLC cell line A549-R11 was obtained from its parental cell line A549 through irradiation with X-rays of 2.0 Gy per fraction for 30 times. The sensitivities of A549, A549-R11 and H1299 cells exposed to X-rays and carbon ions were verified using the colony formation assay. A comprehensive circRNA-miRNA-mRNA network was constructed through the sequencing data in parental A549, acquired radioresistant A549-R11 and intrinsic radioresistant H1299 cells, and the network was further optimized according to the prognostic results from the TCGA and GEO databases. RESULTS: Based on high-throughput sequencing of circRNAs, we found that 40 circRNAs were up-regulated while 184 circRNAs were down-regulated in the intersection of the sets of A549-R11 and H1299 cells. Subsequently, a circRNA- miRNA-mRNA network, including 14 interactive pairs and 8 circRNAs, 4 overall survival-associated miRNAs, and 4 mRNAs, was constructed through the high-throughput data screening and bioinformatics methods. CONCLUSIONS: Our results provide a complete understanding to the regulatory mechanism of the sensitivities to low-LET X-ray and high-LET carbon ion irradiations, and might be helpful to screen potential biomarkers for predicting the Carbon-ion radiotherapy (CIRT) and X-ray radiotherapy responses in NSCLC.

Radiosensitization of NSCLC cells to X-rays and carbon ions by the CHK1/CHK2 inhibitor AZD7762, Honokiol and Tunicamycin.

Although radiotherapy, especially carbon-ion radiotherapy, is an effective treatment modality against non-small-cell lung cancer (NSCLC), studies using radiation combined with sensitizer for improving the efficacy of radiotherapy are still needed. In this work, we aimed to investigate in NSCLC A549 and H1299 cell lines the effects of different linear energy transfer (LET) radiations combined with diverse sensitizing compounds. Cells pretreated with the CHK1/CHK2 inhibitor AZD7762, Honokiol or Tunicamycin were irradiated with low-LET X-rays and high-LET carbon ions. Cell survival was assessed using the clonogenic cell survival assay. Cell cycle distribution and apoptosis were measured with flow cytometry, and DNA double strand break (DSB) and repair were detected using γ-H2AX immunofluorescence staining. Our results revealed that AZD7762, Honokiol and Tunicamycin demonstrated low cytotoxicity to NSCLC cells and a pronounced radiosensitizing effect on NSCLC cells exposed to carbon ions than X-rays. Unrepaired DNA DSB damages, the abrogation of G2/M arrest induced by irradiation, and finally apoptotic cell death were the main causes of the radiosensitizing effect. Thus, our data suggest that high-LET carbon ion combined with these compounds may be a potentially effective therapeutic strategy for locally advanced NSCLC.

Enhanced performance of simultaneous carbon, nitrogen and phosphorus removal from municipal wastewater in an anaerobic-aerobic-anoxic sequencing batch reactor (AOA-SBR) system by alternating the cycle times.

The performance of simultaneous carbon (C), nitrogen (N) and phosphorus (P) removal was investigated by altering the cycle times in an anaerobic-aerobic-anoxic sequencing batch reactor (AOA-SBR) system. Results showed that the AOA-SBR system achieved high simultaneous C, N and P removal efficiency with a cycle time of 6 h, with average removal efficiencies for COD, TN, and TP of 96.81%, 96.32% and 94.33%, respectively. The highest anoxic removal rate of NOX-N was 203.44 mg·g-1- MLVSS·d-1. Meanwhile, anaerobic release rate and aerobic, anoxic removal rate of TP reached peak values of 104.31 and 85.81 mg·g-1- MLVSS·d-1, respectively. Microbial community analysis demonstrated that Proteobacteria, Bacteroidetes and Candidatus Saccharibacteria at phylum level and Betaproteobacteria, Gammaproteobacteria, Sphingobacteriia, Deltaproteobacteria and Alphaproteobacteria at the class level benefited AOA-SBR performance. Functional analysis of genes indicated that the metabolic potential related to C, N and P metabolism increased under the optimal cycle time condition.

Bioaccumulation investigation of bisphenol A in HepG2 cells and zebrafishes enabled by cobalt magnetic polystyrene microsphere derived carbon based magnetic solid-phase extraction.

A magnetic solid-phase extraction (MSPE) technique coupled with high performance liquid chromatography (HPLC) was developed and used for bioaccumulation investigation of bisphenol A (BPA) in HepG2 cells and zebrafishes. Cobalt magnetic polystyrene microsphere derived carbon (C-Co@PST) as an adsorbent was prepared by in situ polymerization reaction and further annealing treatment. Scanning electron microscopy, energy-dispersive X-ray spectroscopy, Fourier transform infrared spectrometry, X-ray photoelectron spectroscopy and X-ray diffraction were employed to confirm successful synthesis of C-Co@PST. A series of extraction parameters including the amount of the sorbent, the type of elute, extraction time and elution time were investigated to achieve high extraction efficiency. C-Co@PST based MSPE combined with HPLC was successfully established for bioaccumulation research of BPA in living creatures. It was found that the bioconcentration values of BPA in HepG2 cells underwent an increase, then a decrease, and finally reached an equilibrium level of 11.60 µg kg-1 at 8 h. The concentration of BPA in zebrafishes increased ranging from 6.05 µg kg-1 to 31.84 µg kg-1 over a culture time from 1 h to 12 h. Furthermore, linear and exponential models were employed to analyse the bioconcentration variation of BPA in organisms over the exposure time. Mathematical models have been developed to predict the transfer characteristics of BPA.

Inhibition of endoplasmic reticulum stress-induced autophagy promotes the killing effect of X-rays on sarcoma in mice.

Endoplasmic reticulum (ER) stress is a conserved cellular process for cells to clear unfolded or misfolded proteins and maintain cell homeostasis under stress conditions. Autophagy may act as a pro-survival strategy to cope with multiple stress conditions in tumor progression and distant metastasis. Although many studies have demonstrated that there is a close correlation between radiation-induced ER stress and autophagy, the molecular mechanisms currently remain unclear. In the present study, we performed an in vivo study concerning the effect of autophagy induced by ER stress on the radiosensitivity of mouse sarcoma using X-rays. Our results documented that X-rays could induce ER stress in sarcoma and then autophagy was activated by unfolded protein response (UPR) through the IRE1-JNK-pBcl2-Beclin1 signaling axis. The induction of autophagy caused a decline in cell apoptosis while inhibiting the autophagy resulted in increased apoptosis and inhibition of tumor progression. Combined treatment of X-ray exposure and chloroquine increased ER stress-related apoptosis and enhanced the radiosensitivity of mouse sarcoma that was not sensitive to X-ray irradiation alone. Thus, our study indicates that inhibition of ER stress-induced autophagy might be a novel strategy to improve the efficacy of radiotherapy against radioresistant sarcoma.

CircRNA CBL.11 suppresses cell proliferation by sponging miR-6778-5p in colorectal cancer.

BACKGROUND: Radiotherapy (RT) is considered an important therapeutic strategy in the fight against colorectal cancer (CRC). However, the existence of some radioresistance factors becomes the main challenge for the RT. Recently, non-coding RNAs (ncRNAs) have shown an important role in modulating cancer cell responses to ionizing radiation (IR). It is therefore of great significance to elucidate the exact mechanisms of ncRNAs in IR-mediated responses to CRC. METHODS: Microarrays were used to identify specific miRNAs that may be altered in response to IR. Bioinformatics, luciferase reporter analyses were used to explore the targets of miR-6778-5p. CircRNA CBL.11 was identified to bind with miR-6778-5p by bioinformatic analysis, AGO2 immunoprecipitation and biotinylated RNA pull-down assay. Functional experiments, including CCK-8 assay, cell colony formation assay and EdU incorporation were conducted to investigate the biological roles of miR-6778-5p and circular RNA CBL.11. RESULTS: MiR-6778-5p was suppressed in CRC cells after irradiation. Results of functional experiments indicated that miR-6778-5p promoted the proliferation of CRC cells. Luciferase reporter analyses showed that YWHAE was a target of miR-6778-5p, which mediated the function of miR-6778-5p in the proliferation of CRC cells via the p53 pathway. Furthermore, we have noticed that after carbon ion irradiation, circRNA CBL.11 was increased in CRC cells and could function as a competing endogenous RNA (ceRNA) to regulate YWHAE expression by sponging miR-6778-5p, resulting in regulation the proliferation of CRC cells. CONCLUSION: CircRNA CBL.11 may play an important role in improving the efficacy of carbon ion RT against CRC.

Predict MiRNA-Disease Association with Collaborative Filtering.

The era of human brain science research is dawning. Researchers utilize the various multi-disciplinary knowledge to explore the human brain,such as physiology and bioinformatics. The emerging disease association prediction technology can speed up the study of diseases, so as to better understanding the structure and function of human body. There are increasing evidences that miRNA plays a significant role in nervous system development, adult function, plasticity, and vulnerability to neurological disease states. In this paper ,we proposed the novel improved collaborative filtering-based miRNA-disease association prediction (ICFMDA) approach. Known miRNA-disease associations can be viewed as a bipartite network between diseases and miRNAs. ICFMDA defined significance SIG between pairs of diseases or miRNAs to model the preference on the choices of other entities. The collaborative filtering algorithm is further improved by incorporating similarity matrices to enable the prediction for new miRNA or disease without known associations. Potential miRNA-disease associations are scored with the addition of bidirectional recommendation results with low computational cost. ICFMDA achieved a 0.9076 AUC of ROC curve in global leave-one-out cross validation, which outperformed the state-of-the-art models. ICFMDA is a compact and accurate tool for potential miRNA-disease association prediction. We hope that ICFMDA would be useful in future miRNA and brain researches,and achieve better understanding of the nervous system in molecular level, cellular level, cell change process, and thus can support the research of human brain.

Different mitochondrial fragmentation after irradiation with X-rays and carbon ions in HeLa cells and its influence on cellular apoptosis.

Although mitochondria are known to play an important role in radiation-induced cellular damage, the mechanisms by which ionizing radiation modulates mitochondrial dynamics are largely unknown. In this study, human cervical carcinoma cell line HeLa was used to demonstrate the different modes of mitochondrial network in response to different quality radiations such as low linear energy transfer (LET) X-rays and high-LET carbon ions. Mitochondria fragmented into punctate and clustered ones upon carbon ion irradiation in a dose- and LET-dependent manner, which was associated with apoptotic cell death. In contrast, low-dose X-ray irradiation promoted mitochondrial fusion while mitochondrial fission was detected until the radiation dose was more than 1 Gy. This fission was driven by ERK1/2-mediated phosphorylation of Drp1 on Serine 616. Inhibition of mitochondrial fragmentation suppressed the radiation-induced apoptosis and thus enhanced the resistance of cells to carbon ions and high-dose X-rays, but not for cells irradiated with X-rays at the low dose. Our results suggest that radiations of different qualities cause diverse changes of mitochondrial dynamics in cancer cells, which play an important role in determining the cell fate.

Genistein sensitizes glioblastoma cells to carbon ions via inhibiting DNA-PKcs phosphorylation and subsequently repressing NHEJ and delaying HR repair pathways.

BACKGROUND AND PURPOSE: Previously, we found genistein could sensitize cancer cells to low linear energy transfer (LET) X-rays via inhibiting DNA-PKcs activities. Especially, high-LET heavy ion produces more DNA double strand breaks (DSBs) than low-LET radiation. Thus, the study was designed to investigate the detailed molecular mechanisms of genistein on sensitizing cancer cells to heavy ions. MATERIALS AND METHODS: Human glioblastoma (GBM) cell lines with or without genistein pre-treatment were irradiated with high-LET carbon ions. Cell survival was determined with colony formation assay. DNA DSBs were evaluated by means of detecting γ-H2AX foci and immuno-blotting DSB repair proteins, cell apoptosis was detected using Annexin V and PI staining. The interaction of genistein with DNA-PKcs activation site was estimated by molecular docking in the autodock software. RESULTS: Genistein sensitized DNA-PKcs proficient GBM cells to high-LET carbon ions via delaying the clearance of γ-H2AX foci. Genistein was physically bound to DNA-PKcs and functionally inhibited the phosphorylation of DNA-PKcs. Consequently, the non-homologous end joining (NHEJ) repair of DSBs was inhibited and the homologous recombination (HR) repair was delayed by genistein, thereby leading to an increase in apoptosis in DNA-PKcs proficient GBM cells after irradiation. CONCLUSION: Our study demonstrated that genistein holds promise as a radiosensitizer for enhancing the efficacy of carbon ion radiotherapy against DNA-PKcs proficient GBM via inhibiting DNA-PKcs phosphorylation and subsequently repressing NHEJ and delaying HR repair pathways.

SACMDA: MiRNA-Disease Association Prediction with Short Acyclic Connections in Heterogeneous Graph.

MiRNA-disease association is important to disease diagnosis and treatment. Prediction of miRNA-disease associations is receiving increasing attention. Using the huge number of known databases to predict potential associations between miRNAs and diseases is an important topic in the field of biology and medicine. In this paper, we propose a novel computational method of with Short Acyclic Connections in Heterogeneous Graph (SACMDA). SACMDA obtains AUCs of 0.8770 and 0.8368 during global and local leave-one-out cross validation, respectively. Furthermore, SACMDA has been applied to three important human cancers for performance evaluation. As a result, 92% (Colon Neoplasms), 96% (Carcinoma Hepatocellular) and 94% (Esophageal Neoplasms) of top 50 predicted miRNAs are confirmed by recent experimental reports. What's more, SACMDA could be effectively applied to new diseases and new miRNAs without any known associations, which overcomes the limitations of many previous methods.

Fragmentation level determines mitochondrial damage response and subsequently the fate of cancer cells exposed to carbon ions.

OBJECTIVES: Although mitochondria are known to play an important role in radiation-induced cellular damage response, the mechanisms of how radiation elicits mitochondrial responses are largely unknown. MATERIALS AND METHODS: Human cervical cancer cell line HeLa and human breast cancer cell lines MCF-7 and MDA-MB-231 were irradiated with high LET carbon ions at low (0.5 Gy) and high (3 Gy) doses. Mitochondrial functions, dynamics, mitophagy, intrinsic apoptosis and total apoptosis, and survival fraction were investigated after irradiation. RESULTS: We found that carbon ions irradiation induced two different mitochondrial morphological changes and corresponding responses in cancer cells. Cells exposed to carbon ions of 0.5 Gy exhibited only modestly truncated mitochondria, and subsequently damaged mitochondria could be eliminated through mitophagy. In contrast, mitochondria within cells insulted by 3 Gy radiation split into punctate and clustered ones, which were associated with apoptotic cell death afterward. Inhibition of mitochondrial fission by Drp1 or FIS1 knockdown or with the Drp1 inhibitor mdivi-1 suppressed mitophagy and potentiated apoptosis after irradiation at 0.5 Gy. However, inhibiting fission led to mitophagy and increased cell survival when cells were irradiated with carbon ions at 3 Gy. CONCLUSION: We proposed a stress response model to provide a mechanistic explanation for the mitochondrial damage response to high-LET carbon ions.

Genistein mediates the selective radiosensitizing effect in NSCLC A549 cells via inhibiting methylation of the keap1 gene promoter region.

Non-small cell lung cancer (NSCLC) cells often possess a hypermethylated Keap1 promoter, which decreases Keap1 mRNA and protein expression levels, thus impairing the Nrf2-Keap1 pathway and thereby leading to chemo- or radio-resistance. In this study, we showed that genistein selectively exhibited a radiosensitizing effect on NSCLC A549 cells but not on normal lung fibroblast MRC-5 cells. Genistein caused oxidative stress in A549 cells rather than MRC-5 cells, as determined by the oxidation of the ROS-sensitive probe DCFH-DA and oxidative damage marked by MDA, PCO or 8-OHdG content. In A549 instead of MRC-5 cells, genistein reduced the level of methylation in the Keap1 promoter region, leading to an increased mRNA expression, thus effectively inhibited the transcription of Nrf2 to the nucleus, which suppressed the Nrf2-dependent antioxidant and resulted in the upregulation of ROS. Importantly, when combined with radiation, genistein further increased the ROS levels in A549 cells whereas decreasing the radiation-induced oxidative stress in MRC-5 cells, possibly via increasing the expression levels of Nrf2, GSH and HO-1. Moreover, radiation combined with genistein significantly increased cell apoptosis in A549 but not MRC-5 cells. Together, the results herein show that the intrinsic difference in the redox status of A549 and MRC-5 cells could be the target for genistein to selectively sensitize A549 cells to radiation, thereby leading to an increase in radiosensitivity for A549 cells.

Bridging gold in electron-deficient Al2Au(n)(0/-) and BAlAu(n)(0/-) (n = 1-3) clusters.

The geometrical and electronic structures of the electron-deficient dialuminum aurides Al2Aun(0/-) and hybrid boron-aluminum aurides BAlAun(0/-) (n = 1-3) are systematically investigated based on the density and wave function theories. Ab initio theoretical evidence strongly suggests that bridging gold atoms exist in the ground states of C2v Al2Au(-) ((3)B1), C2v Al2Au ((2)B1), C2v Al2Au2(-) ((2)A1), C2v Al2Au2 ((1)A1), Cs Al2Au3(-) ((1)A'), and D3h Al2Au3 ((2)A1), which prove to possess an Al-Au-Al τ bond. For BAlAun(0/-) (n = 1-3) mixed clusters, bridging B-Au-Al units only exist in Cs BAlAu3(-) ((1)A') and Cs BAlAu3 ((2)A'), whereas Cs BAlAu(-) ((3)A''), Cs BAlAu ((2)A''), Cs BAlAu2(-) ((2)A'), and Cs BAlAu2 ((1)A') do not possess a bridging gold, as demonstrated by the fact that B-Al and B-Au exhibit significantly stronger electronic interaction than Al-Au in the same clusters. Orbital analyses indicate that Au 6s contributes approximately 98%-99% to the Au-based orbital in these Al-Au-Al/B-Au-Al interactions, whereas Au 5d contributes 1%-2%. The adiabatic and vertical detachment energies of Al2Aun(-) (n = 1-3) are calculated to facilitate future experimental characterizations. The results obtained in this work establish an interesting τ bonding model (Al-Au-Al/B-Au-Al) for electron-deficient systems in which Au 6s plays a major factor.

Diaqua-bis-{1-[(1H-benzimidazol-2-yl)meth-yl]-1H-1,2,4-triazole-κN}bis-(2,4,5-tricarb-oxy-benzoato-κO)cadmium dihydrate.

In the title complex, [Cd(C(10)H(5)O(8))(2)(C(10)H(9)N(5))(2)(H(2)O)(2)]·2H(2)O, the Cd(II) ion lies on an inversion center and is coordinated by two N atoms from two symmetry-related 1-[(1H-benzimidazol-2-yl)meth-yl]-1H-1,2,4-triazole ligands and two O atoms from two monodeprotonated 2,4,5-tricarb-oxy-benzoate anions in equatorial positions and by two water O atoms in axial positions, leading to a distorted octa-hedral environment. In the crystal, complex mol-ecules and solvent water mol-ecules are linked through inter-molecular O-H⋯O, O-H⋯N and N-H⋯O hydrogen bonds into a three-dimensional network. Intra-molecular O-H⋯O hydrogen bonds are also present.

Bis{1-[(1H-benzimidazol-2-yl)meth-yl]-1H-imidazole-κN}-bis-(3,5-dicarb-oxy-benzoato-κO)zinc octa-hydrate.

In the title complex, [Zn(C(9)H(5)O(6))(2)(C(11)H(10)N(4))(2)]·8H(2)O, the Zn(II) ion exhibits site symmetry 2. It shows a distorted tetra-hedral coordination defined by two N atoms from two symmetry-related 1-[(1H-benzimidazol-2-yl)meth-yl]-1H-imid-azole ligands and by two O atoms from two symmetry-related monodeprotonated 3,5-dicarb-oxy-benzoate anions. In the crystal, complex mol-ecules and solvent water mol-ecules are linked through inter-molecular O-H⋯O, O-H⋯N, and N-H⋯O hydrogen bonds into a three-dimensional network.