Axial Crushing Theory and Optimization of Lattice-Filled Multicellular Square Tubes.

A lattice-filled multicellular square tube features a regular cross-sectional shape, good energy consumption, and good crashworthiness, which is suitable for the design of energy absorbers in various protection fields such as automobiles, aerospace, bridges, etc. Based on the super folding theory, two reference planes are set to refine the energy consumption zone of the super folding element in this study. The energy consumption calculation of convex panel stretching is involved, and the critical crushing force formula is introduced in this study. Meanwhile, the calculation method from a single-cell square tube to a multicellular thin-walled square tube is extended and the structural optimization is investigated, in which the NSGAII algorithm is used to obtain the Pareto front (PF) of the crashworthiness performance index of the square multicellular tubes, the Normal Boundary Intersection (NBI) method is adopted to select knee points, and the influence of different cross-sectional widths on the number, as well as the thickness, of cells are discussed. This study's results indicate that the theoretical value is consistent with that obtained from the numerical simulation, meaning that the improved theoretical model can be applied to predict the crashworthiness of multicellular square cross-sectional tubes. Also, the optimization method and study results proposed in this study can provide a reference for the design of square lattice multicellular tubes.

1,2-Dichloroethane induces testicular pyroptosis by activating piR-mmu-1019957/IRF7 pathway and the protective effects of melatonin.

1,2-Dichloroethane (1,2-DCE) is a prevalent environmental contaminant, and our study revealed its induction of testicular toxicity in mice upon subacute exposure. Melatonin, a prominent secretory product of the pineal gland, has been shown to offer protection against pyroptosis in male reproductive toxicity. However, the exact mechanism underlying 1,2-DCE-induced testicular toxicity and the comprehensive extent of melatonin's protective effects in this regard remain largely unexplored. Therefore, we sequenced testis piRNAs in mice exposed to environmentally relevant concentrations of 1,2-DCE by 28-day dynamic inhalation, and investigated the role of key piRNAs using GC-2 spd cells. Our results showed that 1,2-DCE induced mouse testicular damage and GC-2 spd cell pyroptosis. 1,2-DCE upregulated the expression of pyroptosis-correlated proteins in both mouse testes and GC-2 spd cells. 1,2-DCE exposure caused pore formation on cellular membranes and lactate dehydrogenase leakage in GC-2 spd cells. Additionally, we identified three upregulated piRNAs in 1,2-DCE-exposed mouse testes, among which piR-mmu-1019957 induced pyroptosis in GC-2 spd cells, and its inhibition alleviated 1,2-DCE-induced pyroptosis. PiR-mmu-1019957 mimic and 1,2-DCE treatment activated the expression of interferon regulatory factor 7 (IRF7) in GC-2 spd cells. IRF7 knockdown reversed 1,2-DCE-induced cellular pyroptosis, and overexpression of piR-mmu-1019957 did not promote pyroptosis when IRF7 was inhibited. Notably, melatonin reversed 1,2-DCE-caused testicular toxicity, cellular pyroptosis, and upregulated piR-mmu-1019957 and IRF7. Collectively, our findings indicated that melatonin mitigates this effect, suggesting its potential as a therapeutic intervention against 1,2-DCE-induced male reproductive toxicity in clinical practice.

Preferential formation of stereocomplex crystals in poly(L-lactic acid)/poly(D-lactic acid) blends by a fullerene nucleator.

Selective formation of stereocomplex (sc) crystallization in enantiomeric poly(L-lactic acid)/poly(D-lactic acid) (PLLA/PDLA) blends is considered as one of the most effective and promising way to improve the mechanical and thermal properties of polylactide (PLA) materials. However, homocrystallization (hc) prevails over sc crystallization in high-molecular-weight (HMW) PLLA/PDLA blends. Herein, we propose a simple and straightforward approach for fabricating sc crystallization and suppress hc crystallization for HMW PLLA/PDLA blends through the addition of C70 as a nucleator. Non-isothermal crystallization and wide-angel X-ray diffraction studies demonstrate that, the incorporation of 1 wt% C70 overwhelmingly leads to the formation of sc crystallites, while preventing the formation of hc crystallites. Isothermal crystallization experiments at 140 °C reveal a significant reduction in the half-crystallization period of the PLLA/PDLA blend upon the addition of C70. Fourier-transformed infrared spectroscopy suggests that, the improved intermolecular interactions between PLLA and PDLA chains, as well as the inhibition of molecular chain diffusion and mobility, contribute to the accelerated formation of sc facilitated by C70. The enhanced sc crystallization results in a 15.5 °C higher thermal stability in the as-prepared PLLA/PDLA blend with 1 wt% C70 compared to the neat counterpart.

CircBCL11B acts as a ceRNA to facilitate 1,2-dichloroethane-induced astrocyte swelling via miR-29b-3p/AQP4 axis in SVG p12 cells.

1,2-Dichloroethane (1,2-DCE) is a pervasive environmental pollutant found in ambient and residential air, as well as ground and drinking water. Brain edema is the primary pathological consequence of 1,2-DCE overexposure. We found that microRNA (miRNA)-29b dysregulation after 1,2-DCE exposure can aggravate brain edema by suppressing aquaporin 4 (AQP4). Moreover, circular RNAs (circRNAs) can regulate the expression of downstream target genes through miRNA, and affect protein function. However, circRNAs' role in 1,2-DCE-induced brain edema via miR-29b-3p/AQP4 axis remains unclear. To address the mechanism's bottleneck, we explored the circRNA-miRNA-mRNA network underlying 1,2-DCE-driven astrocyte swelling in SVG p12 cells by circRNA sequencing, electron microscopy and isotope 3H labeling combined with the 3-O-methylglucose uptake method. The results showed that 25 and 50 mM 1,2-DCE motivated astrocyte swelling, characterized by increased water content, enlarged cell vacuoles, and mitochondrial swelling. This was accompanied by miR-29b-3p downregulation and AQP4 upregulation. We verified that AQP4 were negatively regulated by miR-29b-3p in 1,2-DCE-induced astrocyte swelling. Also, circRNA sequencing highlighted that circBCL11B was upregulated by 1,2-DCE. This was manifested as circBCL11B overexpression playing an endogenous competitive role via upregulating AQP4 by binding to miR-29b-3p, thus leading to astrocyte swelling. Conversely, circBCL11B knockdown reversed the 1,2-DCE-motivated AQP4 upregulation and alleviated the cell swelling. Finally, we demonstrated that the circBCL11B was targeted to miR-29b-3p by fluorescence in situ hybridization and dual-luciferase reporter assay. In conclusion, our findings indicate that circBCL11B acts as a competing endogenous RNA to facilitate 1,2-DCE-caused astrocyte swelling via miR-29b-3p/AQP4 axis. These observations provide new insight into the epigenetic mechanisms underlying 1,2-DCE-induced brain edema.

Applications of Antioxidants in Dental Procedures.

As people are paying more and more attention to dental health, various dental treatment procedures have emerged, such as tooth bleaching, dental implants, and dental restorations. However, a large number of free radicals are typically produced during the dental procedures. When the imbalance in distribution of reactive oxygen species (ROS) is induced, oxidative stress coupled with oxidative damage occurs. Oral inflammations such as those in periodontitis and pulpitis are also unavoidable. Therefore, the applications of exogenous antioxidants in oral environment have been proposed. In this article, the origin of ROS during dental procedures, the types of antioxidants, and their working mechanisms are reviewed. Additionally, antioxidants delivery in the complicated dental procedures and their feasibility for clinical applications are also covered. Finally, the importance of safety assessment of these materials and future work to take the challenge in antioxidants development are proposed for perspective.

ZIF-90 with biomimetic Zn-N coordination structures as an effective nanozyme to mimic natural hydrolase.

Inspired by the structures of enzymes, a fast and robust strategy for generating ZIF-90 metallo-nanozymes is presented. The Zn-N coordination structure in ZIF-90 can closely imitate the catalytic center of a natural zinc-based hydrolase. As expected, ZIF-90 possesses potent hydrolase-mimicking activity, high stability and excellent recyclability.

1,2-Dichloroethane induces cortex demyelination by depressing myelin basic protein via inhibiting aquaporin 4 in mice.

1,2-Dichloroethane (1,2-DCE) is a pervasive environmental pollutant, and overexposure to this hazardous material causes brain edema and demyelination in humans. We found that 1,2-DCE inhibits aquaporin 4 (AQP4) and is a primary pathogenic effector of 1,2-DCE-induced brain edema in animals. However, AQP4 down-regulation's link with cortex demyelination after 1,2-DCE exposure remains unclear. Thus, we exposed wild-type (WT) CD-1 mice and AQP4 knockout (AQP4-KO) mice to 0, 100, 350 and 700 mg/m3 1,2-DCE by inhalation for 28 days. We applied label-free proteomics and a cell co-culture system to elucidate the role of AQP4 inhibition in 1,2-DCE-induced demyelination. The results showed that 1,2-DCE down-regulated AQP4 in the WT mouse cortexes. Both 1,2-DCE exposure and AQP4 deletion induced neurotoxicity in mice, including increased brain water content, abnormal pathological vacuolations, and neurobehavioral damage. Tests for interaction of multiple regression analysis highlighted different effects of 1,2-DCE exposure level depending on the genotype, indicating the core role of AQP4 in regulation on 1,2-DCE-caused neurotoxicity. We used label-free quantitative proteomics to detect differentially expressed proteins associated with 1,2-DCE exposure and AQP4 inhibition, and identified down-regulation in myelin basic protein (MBP) and tyrosine-protein kinase Fyn (FYN) in a dose-dependent manner in WT mice but not in AQP4-KO mice. 1,2-DCE and AQP4 deletion separately resulted in demyelination, as detected by Luxol fast blue staining, and manifested as disordered nerve fibers and cavitation in the cortexes. Western blot and immunofluorescence confirmed the decreased AQP4 in the astrocytes and the down-regulated MBP in the oligodendrocytes by 1,2-DCE exposure and AQP4 inhibition, respectively. Finally, the co-culture results of SVG p12 and MO3.13 cells showed that 1,2-DCE-induced AQP4 down-regulation in the astrocytes was responsible for demyelination, by decreasing MBP in the oligodendrocytes. In conclusion, 1,2-DCE induced cortex demyelination by depressing MBP via AQP4 inhibition in the mice.

1,2-Dichloroethane induces apoptosis in the cerebral cortexes of NIH Swiss mice through microRNA-182-5p targeting phospholipase D1 via a mitochondria-dependent pathway.

1,2-Dichloroethane (1,2-DCE) is a pervasive environmental pollutant found in ambient and residential air, as well as ground and drinking water. Overexposure to it results in cortex edema, in both animals and humans. 1,2-DCE induces apoptosis in the cerebellum, liver and testes. This promotes the hypothesis that 1,2-DCE may induce apoptosis in the cortex as brain edema progresses. To validate our hypothesis, 40 NIH male mice were exposed to 0, 100, 350, 700 mg/m3 1,2-DCE by whole-body dynamic inhalation for 28 consecutive days. MicroRNA (miRNA) and mRNA microarray combined with TdT-mediated dUTP nick-end labeling, flow cytometry, and mitochondrial membrane potential (mtΔΨ) measurement were applied to identify the cortex apoptosis pathways' specific responses to 1,2-DCE, in vitro and in vivo. The results showed that 1,2-DCE caused brain edema and increased apoptosis in the mouse cortexes. We confirmed that 1,2-DCE induced increased apoptosis via mitochondrial pathway, both in vitro and in vivo, as evidenced by increased Caspase-3, cleaved Caspase-3, Cytochrome c and Bax expression, and decreased Bcl-2 expression. Additionally, mtΔΨ decreased after 1,2-DCE treatment in vitro. 1,2-DCE exposure increased miR-182-5p and decreased phospholipase D1 (PLD1) in the cerebral cortex of mice. MiR-182-5p overexpression and PLD1 inhibition reduced mtΔΨ and increased astrocyte apoptosis, yet miR-182-5p inhibition alleviated the 1,2-DCE-induced PLD1 down-regulation and the increased apoptosis. Finally, PLD1 was confirmed to be a target of miR-182-5p by luciferase assay. Taken together, our findings indicate that 1,2-DCE exposure induces apoptosis in the cortex via a mitochondria-dependent pathway. This pathway is regulated by a miR-182-5p⊣PLD1 axie.

Size-Dependent Activity and Selectivity of Atomic-Level Copper Nanoclusters during CO/CO2 Electroreduction.

As a favorite descriptor, the size effect of Cu-based catalysts has been regularly utilized for activity and selectivity regulation toward CO2 /CO electroreduction reactions (CO2 /CORR). However, little progress has been made in regulating the size of Cu nanoclusters at the atomic level. Herein, the size-gradient Cu catalysts from single atoms (SAs) to subnanometric clusters (SCs, 0.5-1 nm) to nanoclusters (NCs, 1-1.5 nm) on graphdiyne matrix are readily prepared via an acetylenic-bond-directed site-trapping approach. Electrocatalytic measurements show a significant size effect in both the activity and selectivity toward CO2 /CORR. Increasing the size of Cu nanoclusters will improve catalytic activity and selectivity toward C2+ productions in CORR. A high C2+ conversion rate of 312 mA cm-2 with the Faradaic efficiency of 91.2 % are achieved at -1.0 V versus reversible hydrogen electrode (RHE) over Cu NCs. The activity/selectivity-size relations provide a clear understanding of mechanisms in the CO2 /CORR at the atomic level.

Regulating kinetics and thermodynamics of electrochemical nitrogen reduction with metal single-atom catalysts in a pressurized electrolyser.

Using renewable electricity to synthesize ammonia from nitrogen paves a sustainable route to making value-added chemicals but yet requires further advances in electrocatalyst development and device integration. By engineering both electrocatalyst and electrolyzer to simultaneously regulate chemical kinetics and thermodynamic driving forces of the electrocatalytic nitrogen reduction reaction (ENRR), we report herein stereoconfinement-induced densely populated metal single atoms (Rh, Ru, Co) on graphdiyne (GDY) matrix (formulated as M SA/GDY) and realized a boosted ENRR activity in a pressurized reaction system. Remarkably, under the pressurized environment, the hydrogen evolution reaction of M SA/GDY was effectively suppressed and the desired ENRR activity was strongly amplificated. As a result, the pressurized ENRR activity of Rh SA/GDY at 55 atm exhibited a record-high NH3 formation rate of 74.15 µg h-1⋅cm-2, a Faraday efficiency of 20.36%, and a NH3 partial current of 0.35 mA cm-2 at -0.20 V versus reversible hydrogen electrode, which, respectively, displayed 7.3-, 4.9-, and 9.2-fold enhancements compared with those obtained under ambient conditions. Furthermore, a time-independent ammonia yield rate using purified 15N2 confirmed the concrete ammonia electroproduction. Theoretical calculations reveal that the driving force for the formation of end-on N2* on Rh SA/GDY increased by 9.62 kJ/mol under the pressurized conditions, facilitating the ENRR process. We envisage that the cooperative regulations of catalysts and electrochemical devices open up the possibilities for industrially viable electrochemical ammonia production.

1,2-Dichloroethane induces cerebellum granular cell apoptosis via mitochondrial pathway in vitro and in vivo.

1,2-Dichloroethane (1,2-DCE) is a widely used chlorinated organic toxicant, but little is known about the cerebellar dysfunction induced by excessive exposure to it. To uncover 1,2-DCE-induced neurotoxicity in cerebellar granular cells (CGCs), and to investigate the underlying mechanisms, we explored this, both in vitro and in vivo. Our findings showed significant cell viability inhibition in human CGCs (HCGCs) treated with 1,2-DCE. Flow cytometry and mitochondrial membrane potential analyses discovered an increase in apoptotic-mediated cell death in HCGCs after 1,2-DCE treatment. This HCGC apoptosis was involved in the increases of protein expression in Cytochrome c, Caspase-3, Bad, Bim, transformation related protein 53, Caspase-8, tumor necrosis factor-α, and Survivin. Quantitative real-time PCR (qPCR) and western blot confirmed the increases in Cytochrome c, Caspase-3, cleaved Caspase-3, and Bad in HCGCs after 1,2-DCE treatment. Bax inhibitor peptide V5 rescued 1,2-DCE-induced HCGC apoptosis. Furthermore, 80 CD-1 male mice were exposed to 1,2-DCE by inhalation at 0, 100, 350, and 700 mg/m3 for 6 h/day for 4 weeks. An open field test found abnormal neurobehavioral changes in the mice exposed to 1,2-DCE. Histopathological examination showed significantly shrunken and hypereosinophilic cytoplasm with nuclear pyknosis in mouse CGCs from the 700 mg/m3 1,2-DCE group. TdT-mediated dUTP nick-end labeling assay verified significant increases in apoptotic positive cells in the mouse CGCs after 1,2-DCE exposure. We confirmed the increases in the expressions of Cytochrome c, Caspase-3, cleaved Caspase-3 and Bad in the mice exposed to 1,2-DCE. These findings suggest that 1,2-DCE exposure can induce CGC apoptosis and cerebellar dysfunction, at least in part, through mitochondrial pathway.

MicroRNA-29b-3p aggravates 1,2-dichloroethane-induced brain edema by targeting aquaporin 4 in Sprague-Dawley rats and CD-1 mice.

Overexposure to 1,2-dichloroethane (1,2-DCE) can induce brain edema, but the underlying mechanisms remain largely unknown. Aquaporin 4 (AQP4) is the most prevalent water channel in the brain, and the pool of AQP4 facilitates brain edema by controlling the inflow and clearance of brain water. MicroRNAs play an important role in the regulation of brain edema via RNA silencing and post-transcriptional regulation of gene expression. To explore the regulation role of AQP4 and microRNA in 1,2-DCE-induced brain edema, Sprague-Dawley (SD) rats and AQP4 knockout CD-1 mice were exposed to 1,2-DCE by inhalation for 7 days (0, 600, 1,800 mg/m3) and 28 days (0, 100, 350, 700 mg/m3), respectively. The results showed that 1,2-DCE induces brain edema, in both rats and mice, characterized by an increase in brain water content and vacuolations in the brain parenchyma and around the vessels of the cerebral cortex. Notably, 1,2-DCE exposure can down-regulate AQP4 expression, in both rats and mice. Also, deleting AQP4 intensifies 1,2-DCE-induced brain edema in mice. Meanwhile, microRNA-29b-3p (miR-29b) expression increases with 1,2-DCE exposure, in both rats and mice. A negative correlation was found between the expression of miR-29b and AQP4 in vivo. Moreover, the negative regulation of miR-29b by direct targeting to AQP4 was confirmed by dual luciferase reporter assay in vitro. Taken together, our findings indicate that AQP4 plays an important role in balancing water content in 1,2-DCE-induced brain edema. The dysregulation of miR-29b after 1,2-DCE exposure can aggravate brain edema by directly suppressing the expression of AQP4.

Aberrant expression of miR-451a contributes to 1,2-dichloroethane-induced hepatic glycerol gluconeogenesis disorder by inhibiting glycerol kinase expression in NIH Swiss mice.

The identification of aberrant microRNA (miRNA) expression during chemical-induced hepatic dysfunction will lead to a better understanding of the substantial role of miRNAs in liver diseases. 1,2-Dichloroethane (1,2-DCE), a chlorinated organic toxicant, can lead to hepatic abnormalities in occupationally exposed populations. To explore whether aberrant miRNA expression is involved in liver abnormalities mediated by 1,2-DCE exposure, we examined alterations in miRNA expression patterns in the livers of NIH Swiss mice after dynamic inhalation exposure to 350 or 700 mg m-3 1,2-DCE for 28 days. Using a microarray chip, we discovered that only mmumiR-451a was significantly upregulated in the liver tissue of mice exposed to 700 mg m-3 1,2-DCE; this finding was validated by quantitative real-time polymerase chain reaction. In vitro study revealed that it was metabolite 2-chloroacetic acid, not 1,2-DCE that resulted in the upregulation of mmu-miR-451a in the mouse AML12 cell line. Furthermore, our data showed that the upregulation of mmu-miR-451a induced by 2-chloroacetic acid could suppress the expression of glycerol kinase and lead to the inhibition of glycerol gluconeogenesis in mouse liver tissue and AML12 cells. These observations provide evidence that hepatic mmu-miR-451a responds to 1,2-DCE exposure and might induce glucose metabolism disorders by suppressing the glycerol gluconeogenesis process.

1,2-Dichloroethane Induces Reproductive Toxicity Mediated by the CREM/CREB Signaling Pathway in Male NIH Swiss Mice.

1,2-Dichloroethane (1,2-DCE) is a widely used chlorinated organic toxicant but little is known about the reproductive disorders induced by its excessive exposure. To reveal 1,2-DCE-induced male reproductive toxicity and to elucidate the underlying mechanisms, we exposed male National Institutes of Health Swiss mice to 1,2-DCE by inhalation at 0, 100, 350, and 700 mg/m3 for 6 h/day, for 1 and 4 weeks. Our findings showed a significant decrease in body weight with increased testis/body weight ratio, reduced sperm concentration and induced malformation of spermatozoa, and vacuolar degeneration of germ cells in the seminiferous tubules of testes in mice exposed to 1,2-DCE. Cyclic adenosine monophosphate (cAMP)-response element binding protein (CREB) and cAMP-response element modulator (CREM) were significantly inhibited by 1,2-DCE. This is consistent with the declines in the transducer of regulated CREB activity 1 and activator of CREM in testis, which results in the decrease in lactate dehydrogenase C and testis-specific kinase 1 in the testes. Moreover, the activation of p53 and Bax with the inhibition of Bcl-2 might be the reason for the upregulation of caspase-3 in the apoptosis, as detected by TdT-mediated dUTP nick-end labeling assay in the testes induced by 1,2-DCE. Finally, elevated testosterone levels were found along with increased levels of gonadotropin-releasing hormone, cAMP, luteinizing hormone (LH), and LH receptors in the testes. These findings suggest that 1,2-DCE inhibits CREM/CREB signaling cascade and subsequently induces apoptosis associated with p53 activation and mitochondrial dysfunction. This also results in induced malformation of spermatozoa, reduced sperm concentration, and pathological impairment of the testes.

1,2-Dichloroethane impairs glucose and lipid homeostasis in the livers of NIH Swiss mice.

Excessive exposure to 1,2-Dichloroethane (1,2-DCE), a chlorinated organic toxicant, can lead to liver dysfunction. To fully explore the mechanism of 1,2-DCE-induced hepatic abnormalities, 30 male National Institutes of Health (NIH) Swiss mice were exposed to 0, 350, or 700mg/m3 of 1,2-DCE, via inhalation, 6h/day for 28days. Increased liver/body weight ratios, as well as serum AST and serum ALT activity were observed in the 350 and 700mg/m3 1,2-DCE exposure group mice, compared with the control group mice. In addition, decreased body weights were observed in mice exposed to 700mg/m3 1,2-DCE, compared with control mice. Exposure to 350 and 700mg/m3 1,2-DCE also led to significant accumulation of hepatic glycogen, free fatty acids (FFA) and triglycerides, elevation of blood triglyceride and FFA levels, and decreases in blood glucose levels. Results from microarray analysis indicated that the decreases in glucose-6-phosphatase catalytic subunit (G6PC) and liver glycogen phosphorylase (PYGL) expression, mediated by the activation of AKT serine/threonine kinase 1 (Akt1), might be responsible for the hepatic glycogen accumulation and steatosis. Further in vitro study demonstrated that 2-chloroacetic acid (1,2-DCE metabolite), rather than 1,2-DCE, up-regulated Akt1 phosphorylation and suppressed G6PC and PYGL expression, resulting in hepatocellular glycogen accumulation. These results suggest that hepatic glucose and lipid homeostasis are impaired by 1,2-DCE exposure via down-regulation of PYGL and G6PC expression, which may be primarily mediated by the 2-chloroacetic acid-activated Akt1 pathway.

Mesoporous silica nanoparticles with lactose-mediated targeting effect to deliver platinum(iv) prodrug for liver cancer therapy.

Chemotherapy is the most common therapeutic strategy for the treatment of unresectable hepatocellular carcinoma. However, the therapeutic efficacy is limited by the low delivery efficiency of chemotherapeutics and severe toxicity towards healthy tissues. To address these challenges, active-targeting mesoporous silica nanoparticles conjugating a platinum(iv) prodrug were developed as a therapy for liver cancer for the first time. Taking advantage of liver-targeting lactobionic acid (LA), the smart nano-carriers not only enhanced the circulation time, but also effectively concentrated at the liver tumor site. Moreover, the conjugated platinum(iv) could be reduced in the reductive tumor environment for the fast release of active platinum(ii). The novel targeting and self-responsive drug-loading system offers new prospects for liver cancer chemotherapy.

Lanthanum complexes containing a bis(phenolate) ligand with a ferrocene-1,1'-diyldithio backbone: synthesis, characterization, and ring-opening polymerization of rac-lactide.

Lanthanum complexes [(L)LaX] (X = N(SiMe3)2, O(i)Pr , BH4) supported by a ferrocene-based (OSSO)-type ligand LH2 were synthesized and characterized by elemental analysis, NMR spectroscopy and cyclic voltammetry. The structure of was confirmed by single crystal X-ray diffraction. These complexes were highly active initiators for the ring-opening polymerization of rac-lactide (rac-LA). The activity depended on the initiating group in the order of ≈ > . The activities of and during polymerization were controlled in situ with external redox reagents by reversibly switching the oxidation state of the iron center.

Neutral binuclear rare-earth metal complexes with four µ2-bridging hydrides.

The first neutral rare-earth metal dinuclear dihydrido complexes [(NPNPN)LnH2]2 (2-Ln; Ln = Y, Lu; NPNPN: N[Ph2PNC6H3((i)Pr)2]2) bearing µ2-bridging hydride ligands have been synthesized. In the presence of THF, 2-Y undergoes intramolecular activation of the sp(2) C-H bond to form dinuclear aryl-hydride complex 3-Y containing three µ2-bridging hydride ligands.

Intramolecular C-H bond activation induced by a scandium terminal imido complex.

A CpPN-based scandium terminal imido complex was isolated, which could induce the intramolecular C-H bond activation of a phenyl group even at room temperature.