Metformin induces tolerogenicity of dendritic cells by promoting metabolic reprogramming.

Dendritic cells (DCs) can mediate immune responses or immune tolerance depending on their immunophenotype and functional status. Remodeling of DCs' immune functions can develop proper therapeutic regimens for different immune-mediated diseases. In the immunopathology of autoimmune diseases (ADs), activated DCs notably promote effector T-cell polarization and exacerbate the disease. Recent evidence indicates that metformin can attenuate the clinical symptoms of ADs due to its anti-inflammatory properties. Whether and how the therapeutic effects of metformin on ADs are associated with DCs remain unknown. In this study, metformin was added to a culture system of LPS-induced DC maturation. The results revealed that metformin shifted DC into a tolerant phenotype, resulting in reduced surface expression of MHC-II, costimulatory molecules and CCR7, decreased levels of proinflammatory cytokines (TNF-α and IFN-γ), increased level of IL-10, upregulated immunomodulatory molecules (ICOSL and PD-L) and an enhanced capacity to promote regulatory T-cell (Treg) differentiation. Further results demonstrated that the anti-inflammatory effects of metformin in vivo were closely related to remodeling the immunophenotype of DCs. Mechanistically, metformin could mediate the metabolic reprogramming of DCs through FoxO3a signaling pathways, including disturbing the balance of fatty acid synthesis (FAS) and fatty acid oxidation (FAO), increasing glycolysis but inhibiting the tricarboxylic acid cycle (TAC) and pentose phosphate pathway (PPP), which resulted in the accumulation of fatty acids (FAs) and lactic acid, as well as low anabolism in DCs. Our findings indicated that metformin could induce tolerance in DCs by reprogramming their metabolic patterns and play anti-inflammatory roles in vitro and in vivo.

Determination of nitrate sources in a karst plateau reservoir based on nitrogen and oxygen isotopes.

Investigating the sources, migration and proportional contribution of nitrate is essential to effectively protect water quality. δ15N-NO3-, δ18O-NO3- and Stable Isotope Analysis in R (SIAR) were used to qualitatively and quantitatively analyse nitrate sources in the Pingzhai Reservoir water body. The values of δ15N-NO3- and δ18O-NO3- in water vary with season. Soil organic nitrogen and chemical fertilisers are the main sources of nitrate in autumn, while domestic sewage and livestock manure are the primary sources of nitrate in winter and spring. The SIAR results showed that chemical fertilisers, livestock manure, sewage, and soil organic nitrogen had the highest proportional contribution. In autumn, the proportional contribution of chemical fertilisers to river and reservoir were 47 and 51 %. During winter, the proportional contributions of livestock manure and sewage to river and reservoir were 53 and 68 %, respectively, and in spring 49 and 68 %, respectively. Considering the fragility of karst ecosystems, strict measures should be formulated for the use of chemical fertilisers and standards for sewage discharge should be raised. Control nitrogen input from agricultural activities and prevent water quality deterioration.

Exploring key sectors of CO2 emissions and driving factors to spatiotemporal evolution in China from multiple perspectives.

Identifying CO2 emission from different perspectives is necessary for developing the effective mitigation policies for China. Previous studies mainly focus on exploring important sectors from production and consumption sides, while the perspective of betweenness has been neglected. For narrowing the gap, a new perspective for accounting the critical transmission sectors is discussed. In this study, we calculated and compared the CO2 emissions of production-based, consumption-based, and betweenness-based from 2012 to 2017 based on the multi-regional input-output (MRIO) model. A structural decomposition analysis (SDA) is conducted to uncover the driving forces of CO2 emissions change from three accounting principles. The Findings are as follows: (1) the heavy industry sector (559.26 Mt) in Shandong and Jiangsu (471.97 Mt), Power in Guangdong (83.77 Mt) and Beijing (199.24 Mt), Equipment in Jiangsu (213.88 Mt) are identified as the key transmission sectors; (2) the emission intensity effect and the final demand product structure effect contribute to CO2 emission decrease in China, which are largely offset by the structure effect of final demand source and the final demand scale effect. Based on this, we propose some typical policy implications, such as paying close attention to the production efficiency of the key transmission sectors, optimizing the intermediate product input structure and increasing investment in the technology level, and then reducing the intensity of carbon emission.

Technological roadmap towards optimal decarbonization development of China's iron and steel industry.

China's iron and steel (IS) industry contributes approximately 16 % of the nation's total CO2 emissions. This study evaluates the environmental impact of each step in the production process based on the life cycle assessment method. It then explores potential deep decarbonisation pathways, developing an integrated dynamic model to meet the carbon neutrality target. The results reveal three primary findings. (1) In 2020, the blast furnace-basic oxygen furnace contributed significantly to the global warming potential -1.77 E-8 kg CO2 equivalents per year (eq/yr) higher than the electric arc furnace-and the blast furnace process makes the largest contribution in ironmaking (8.9E-9 kg CO2 eq/yr). (2) Converter negative energy steelmaking technology has the highest energy savings at 39.07 million tons of coal equivalent (Mtce) and an emissions-reduction potential of 72.01 Mt. Its mitigation cost is 69 CNY/t CO2, followed by thick-layer sintering (30.21 Mtce, 61.21 Mt. and 70 CNY/t CO2) and the application of dry vacuum system for molten steel degassing circulation (26.17 Mtce, 56.03 Mt. and 102 CNY/t CO2). (3) Technological improvement could significantly impact the IS industry, reducing CO2 emissions through production structure improvement, technological development and ultra-low emissions technology, from 789 Mt. in a business-as-usual scenario to 516 Mt., 261 Mt. and 157 Mt. in 2060, respectively.

Impacts of international trade on global inequality of energy and water use.

We are not on track to meet the SDGs by 2030 despite considerable efforts. Sino-US trade war and the COVID-19 pandemic raise the tide of trade protection that may also go against SDGs. To explore how international trade affects SDGs, this study quantifies the impacts of international trade on global energy and water inequality by constructing resource-Gini-coefficients in terms of reserve, production, and consumption. We find that international trade alleviates global inequality in energy use, in which direct energy trade reduces the inequality significantly while nonenergy commodity trade aggravates it slightly. However, international trade has a pretty minor impact on improving global water inequality. The developing economies suffer a large amount of embodied energy and water outflows. For example, BRICS exported 712.3 Mtoe of embodied energy and 130.5 billion m3 of virtual water to the rest of the world, exceeding the sum of energy/water use in Germany and France. The developed economies, especially the USA and EU, outsource energy- and water-intensive commodities to reduce domestic energy shortage and water stress, roughly corresponding to India's energy use and two times of water use of South Africa.

Selenium can regulate the differentiation and immune function of human dendritic cells.

Selenium is an essential trace element that can regulate the function of immnue cells via selenoproteins. However, the effects of selenium on human dendritic cell (DCs) remain unclear. Thus, selenoprotein levels in monocytes, immature DCs (imDCs) and mature DCs (mDCs) treated with or without Na2SeO3 were evaluated using RT-PCR, and then the immune function of imDCs and mDCs was detected by flow cytometry, cell counting and the CCK8 assay. In addition, the effects of Se on cytokine and surface marker expression were investigated by RT-PCR. The results revealed different expression levels of selenoprotein in monocytes, imDCs and mDCs, and selenoproeins could be regulated by Se. Moreover, it was indicated that anti-phagocytic activity was improved by 0.1 µM Se, whereas it was suppressed by 0.2 µM Se in imDCs; The migration of imDCs and mDCs was improved by 0.1 µM Se, whereas their migration was inhibited by treatment with 0.05 or 0.2 µM Se; The mixed lymphocyte reaction of mDCs was improved by 0.1 µM Se, and it was inhibited by 0.05 and 0.2 µM Se. In addition, 0.1 µM Se improved the immune function of DCs through the regulation of CD80, CD86, IL12-p35 and IL12-p40. Wheres 0.05 and 0.2 µM Se impaired immune function of DCs by up-regulation of interleukin (IL-10) in imDCs and down-regulation of CD80, CD86, IL12-p35 and IL12-p40 in mDCs. In conclusion, 0.1 µM Se might improve the immune function of human DCs through selenoproteins.

Effect of Selenium and Peroxynitrite on Immune Function of Immature Dendritic Cells in Humans.

BACKGROUND Selenium and peroxynitrite are known to support the growth and activity of immune cells, including T cells, B cells and macrophages. However, the role of these factors in the immune function of human immature dendritic cells (imDCs) is not clear. MATERIAL AND METHODS Monocytes from a mixture of blood samples were isolated using Ficoll density gradient centrifugation and purified with immunomagnetic beads before being induced into imDCs. Cells then either received no treatment (control group), or treatment with sodium selenite (Na2SeO3, Se), 3-morpholinosydnonimine (SIN1, which decomposes into peroxynitrite), or Se+SIN1. Cell viability, migration, and antiphagocytic abilities, oxidative stress, and protein expression of extracellular signal-regulated kinases (ERK) and MMP2 were assessed using a CCK8 assay, cell counter and flow cytometry, microplate spectrophotometer, and Western blot analysis, respectively. RESULTS Viability of imDCs was unaffected by 0.1 µmol/L of Na2SeO3, although 1 mmol/L of SIN1 decreased it significantly (P<0.05). Chemotactic migration and antiphagocytic abilities were inhibited and enhanced, respectively, by treatment with Na2SeO3 and SIN1 (P<0.05). Activities of superoxide dismutase and glutathione peroxidase were increased by Na2SeO3 and Se+SIN1 (P<0.001). Glutathione content decreased with exposure to Na2SeO3 and SIN1 (P<0.05), but increased after treatment with Se+SIN1 (P<0.05). Levels of reactive oxygen species only increased with SIN1 treatment (P<0.05). Treatment with Na2SeO3, SIN1 and Se+SIN1 increased ERK phosphorylation and decreased MMP2 protein expression (P<0.05). CONCLUSIONS Selenium and peroxynitrite can influence immune function in imDCs by regulating levels of reactive oxygen species or glutathione to activate ERK and promote antigen phagocytosis, as well as by decreasing MMP2 expression to inhibit chemotactic migration.

Driving forces of temporal-spatial differences in CO2 emissions at the city level for China's transport sector.

The paper aims to investigate the influencing factors that drive the temporal and spatial differences of CO2 emissions for the transportation sector in China. For this purpose, this study adopts a Logistic Mean Division Index (LMDI) model to explore the driving forces of the changes for the transport sector's CO2 emissions from a temporal perspective during 2000-2017 and identifies the key factors of differences in the transport sector's CO2 emissions of China's 15 cities in four key years (i.e., 2000, 2005, 2010, and 2017) using a multi-regional spatial decomposition model (M-R). Based on the empirical results, it was found that the main forces for affecting CO2 emissions of the transport sector are not the same as those from temporal and spatial perspectives. Temporal decomposition results show that the income effect is the dominant factor inducing the increase of CO2 emissions in the transport sector, while the transportation intensity effect is the main factor for curbing the CO2 emissions. Spatial decomposition results demonstrate that income effect, energy intensity effect, transportation intensity effect, and transportation structure effect are important factors which result in enlarging the differences in city-level CO2 emissions. In addition, the less-developed cities and lower energy efficiency cities have greater potential to reduce CO2 emissions of the transport sector. Understanding the feature of CO2 emissions and the influencing factors of cities is critical for formulating city-level mitigation strategies of the transport sector in China. Overall, it is expected that the level of economic development is the main factor leading to the differences in CO2 emissions from a spatial-temporal perspective.

Selenium Regulation of the Immune Function of Dendritic Cells in Mice Through the ERK, Akt and RhoA/ROCK Pathways.

Selenium levels can regulate the function of T cells, macrophages, B cells, natural killer cells and other immune cells. However, the effect of selenium on the immune function of dendritic cells (DCs) isolated from selenium-supplemented mice is unknown. In this study, C57BL/6J mice were randomly divided into three groups and fed diets containing low (0.08 ppm), medium (0.25 ppm) or high (1 ppm) selenium levels for 8 weeks. Immature (imDCs) and mature (mDCs) dendritic cells were then isolated from the bone marrow. Next, the migration, phagocytic capacity and mixed lymphocyte reaction (MLR) for imDCs and mDCs were detected by transwell and flow cytometry. The levels of C-C chemokine receptor type 7 (CCR7), major histocompatibility complex II (MHCII) and reactive oxygen species (ROS) were assayed by flow cytometry. F-actin and superoxide dismutase (SOD) activity was detected by fluorescence microscopy and SOD assay kit, respectively. In addition, the extracellular signal-regulated kinase (ERK), Akt, Ras homolog gene family member A/Rho-associated protein kinase (RhoA/ROCK) signalling, selenoprotein K (SELENOK) and glutathione peroxidase 1 (GPX1) levels were measured by western blot analysis. The results indicated that selenium deficiency enhanced the migration of imDCs by ROS and SELENOK-mediated ERK, Akt and RhoA/ROCK pathways but impaired the antigen uptake of imDCs. Although a high selenium level inhibited the migration of imDCs, it had no effect on phagocytic capacity. For mDCs, low selenium levels impaired free migration, and high levels inhibited the chemotactic migration involved in F-actin and CCR7, respectively. Low and high selenium levels impaired the MLR by inhibiting MHCII surface localisation, which might be related to ROS- and SELENOK-mediated ERK, Akt and RhoA/ROCK signalling pathways. In summary, selenium may regulate the immune function of mouse DCs through the ROS- and SELENOK-mediated ERK, Akt and RhoA/ROCK signalling.

Tropomodulin1 Expression Increases Upon Maturation in Dendritic Cells and Promotes Their Maturation and Immune Functions.

Dendritic cells (DCs) are the most potent antigen-presenting cells. Upon maturation, DCs express costimulatory molecules and migrate to the lymph nodes to present antigens to T cells. The actin cytoskeleton plays key roles in multiple aspects of DC functions. However, little is known about the mechanisms and identities of actin-binding proteins that control DC maturation and maturation-associated functional changes. Tropomodulin1 (Tmod1), an actin-capping protein, controls actin depolymerization and nucleation. We found that Tmod1 was expressed in bone marrow-derived immature DCs and was significantly upregulated upon lipopolysaccharide (LPS)-induced DC maturation. By characterizing LPS-induced mature DCs (mDCs) from Tmod1 knockout mice, we found that compared with Tmod1+/+ mDCs, Tmod1-deficient mDCs exhibited lower surface expression of costimulatory molecules and chemokine receptors and reduced secretion of inflammatory cytokines, suggesting that Tmod1 deficiency retarded DC maturation. Tmod1-deficient mDCs also showed impaired random and chemotactic migration, deteriorated T-cell stimulatory ability, and reduced F-actin content and cell stiffness. Furthermore, Tmod1-deficient mDCs secreted high levels of IFN-ß and IL-10 and induced immune tolerance in an experimental autoimmune encephalomyelitis (EAE) mouse model. Mechanistically, Tmod1 deficiency affected TLR4 signaling transduction, resulting in the decreased activity of MyD88-dependent NFκB and MAPK pathways but the increased activity of the TRIF/IRF3 pathway. Rescue with exogenous Tmod1 reversed the effect of Tmod1 deficiency on TLR4 signaling. Therefore, Tmod1 is critical in regulating DC maturation and immune functions by regulating TLR4 signaling and the actin cytoskeleton. Tmod1 may be a potential target for modulating DC functions, a strategy that would be beneficial for immunotherapy for several diseases.

Identifying the driving forces of CO2 emissions of China's transport sector from temporal and spatial decomposition perspectives.

The transport sector is the fourth largest industrial CO2 emitter in China, next to power sector, iron and steel industries, and nonmetallic mineral product industry, and plays an important role in reducing China's CO2 emissions. In this study, a temporal decomposition analysis model, i.e., Logistic Mean Division Index (LMDI), is developed to analyze the influencing factors of CO2 emissions in China's transport sector during 2000-2015. Then, a multi-regional spatial decomposition model is employed to identify the key factors to induce the differences in CO2 emissions of China's 30 regional transport sectors in 2000, 2005, 2010, and 2015. Based on the empirical results, we find that both in the temporal and spatial perspectives, the main factors that affect CO2 emissions in the transport sector are the same ones. From the temporal perspective, the income effect is the dominant factor increasing CO2 emissions of transport sector, while energy intensity effect and transportation structure effect are the key influencing factors that curb the CO2 emissions of China's transport sector, during the whole study period. From the spatial perspective, the income effect, energy intensity effect, and transportation structure effect are the key influencing factors that enlarge the gap of CO2 emissions of various transport sectors in the key study years. More importantly, the less-developed regions and high energy intensity regions (i.e., the lower energy efficiency regions) are identified to have the great potential to reduce CO2 emissions of transport sector. Therefore, differentiated mitigation measures and interregional collaborations are encouraged to reduce transport sector's CO2 emissions in China.

Interleukin-10 reorganizes the cytoskeleton of mature dendritic cells leading to their impaired biophysical properties and motilities.

Interlukin-10 (IL-10) is an immunomodulatory cytokine which predominantly induces immune-tolerance. It has been also identified as a major cytokine in the tumor microenvironment that markedly mediates tumor immune escape. Previous studies on the roles of IL-10 in tumor immunosuppression mainly focus on its biochemical effects. But the effects of IL-10 on the biophysical characteristics of immune cells are ill-defined. Dendritic cells (DCs) are the most potent antigen-presenting cells and play a key role in the anti-tumor immune response. IL-10 can affect the immune regulatory functions of DCs in various ways. In this study, we aim to explore the effects of IL-10 on the biophysical functions of mature DCs (mDCs). mDCs were treated with different concentrations of IL-10 and their biophysical characteristics were identified. The results showed that the biophysical properties of mDCs, including electrophoresis mobility, osmotic fragility and deformability, as well as their motilities, were impaired by IL-10. Meanwhile, the cytoskeleton (F-actin) of mDCs was reorganized by IL-10. IL-10 caused the alternations in the expressions of fasin1 and profilin1 as well as the phosphorylation of cofilin1 in a concentration-dependent fashion. Moreover, Fourier transformed infrared resonance data showed that IL-10 made the status of gene transcription and metabolic turnover of mDCs more active. These results demonstrate a new aspect of IL-10's actions on the immune system and represent one of the mechanisms for immune escape of tumors. It may provide a valuable clue to optimize and improve the efficiency of DC-based immunotherapy against cancer.

[The effect of miR-124 on homocysteine-induced atherosclerosis via promoter region DNA methylation in ApoE(-/-) mice].

The aim of the present study is to explore the role of miR-124 and its promoter region DNA methylation in homocysteine (Hcy)-induced atherosclerosis. ApoE(-/-) mice were fed with hypermethionine diet for 16 weeks to duplicate hyperhomocysteinemia model. Meanwhile, a normal control group (C57BL/6J mice fed with normal diet, N-control) and a model control group (ApoE(-/-) mice fed with normal diet, A-control) were set. The degree of atherosclerosis was observed by HE and oil red O staining. Automatic biochemical analyzer was used to detect the serum levels of Hcy. Foam cell model was duplicated and oil red O staining was used to confirm whether the model was successfully established. And foam cells were stimulated with 0, 50, 100, 200, 500 µmol/L Hcy and 50 µmol/L Hcy + 10 µmol/L AZC respectively. Real-time quantitative PCR (RT-qPCR) was used to detect the expressions of miR-124 in mice aorta and foam cells; Nested landing methylation specific PCR (nMS-PCR) was used to detect the levels of miR-124 promoter DNA methylation in mice aorta and foam cells. Meanwhile, the effects of DNA methylation inhibitor AZC on miR-124 expression were observed at the cellular level. The effect of miR-124 promoter DNA methylation status on lipid accumulation in foam cells was observed by oil red O staining. The results showed that compared with model control group, the serum levels of Hcy in high methionine group were significantly increased (P < 0.01) and developed aortic atherosclerotic plaque, the expression of miR-124 was markedly decreased (P < 0.01), while the levels of miR-124 promoter DNA methylation were significantly increased (P < 0.01). Given different levels of Hcy, the expression of miR-124 in foam cells was decreased, while the levels of miR-124 promoter DNA methylation were increased in a dose-dependent manner (P < 0.05, P < 0.01). AZC reversed the results of mentioned indices as above markedly (P < 0.05). Downregulation of miR-124 may play a role in Hcy-induced atherosclerosis and its promoter DNA methylation status may be an important mechanism in this process.

Mononuclear and binuclear manganese carbonyl hydrides: the preference for bridging hydrogens over bridging carbonyls.

The structures of the mononuclear derivatives HMn(CO)n (n=4 and 3) are shown by density functional theory (B3LYP and PB86) to derive from octahedral HMn(CO)5 by losses of various combinations of carbonyl groups with relatively little change in the C-Mn-C angles involving the remaining carbonyl groups. The binuclear H2Mn2(CO)n structures are predicted to have bridging hydrogen atoms in preference to bridging carbonyl groups. Thus, two structures are found for the binuclear H2Mn2(CO)9, isoelectronic with Fe2(CO)9, in which all nine of the carbonyl groups are terminal carbonyl groups. The lowest lying H2Mn2(CO)9 structure is the dihydrogen complex (OC)5Mn-Mn(CO)4(eta2-H2), in which one of the equatorial CO groups of Mn2(CO)10 is replaced by a dihydrogen ligand. A slightly higher energy H2Mn2(CO)9 structure by approximately 6 kcal mol(-1) has an Mn-Mn bond bridged by a single hydrogen and all terminal carbonyl groups as well as a single terminal hydrogen. The H2Mn2(CO)8 molecule is predicted to have a structure with a central Mn(micro-H)2Mn core related to diborane. In this structure the manganese-manganese bond of length 2.703 A (BP86) can be considered the diprotonated formal double bond required to give both manganese atoms the favoured 18-electron configuration. The more highly unsaturated H2Mn2(CO)n (n=7, 6) derivatives have similar structures derived from the H2Mn2(CO)8 structure by loss of one or two carbonyl groups. In many cases the Mn[triple bond, length as m-dash]Mn distance in the central Mn(micro-H)2Mn unit shortens to approximately 2.4 A suggesting a diprotonated triple bond.

The diversity of difluoroacetylene coordination modes obtained by coupling fluorocarbyne ligands on binuclear manganese carbonyl sites.

Recent work has shown that the fluorocarbyne ligand CF, isoelectronic with the NO ligand, can be generated by the defluorination of CF(3) metal complexes, as illustrated by the 2006 synthesis by Hughes et al. of [C(5)H(5)Mo(CF)(CO)(2)] in good yield by the defluorination of [C(5)H(5)Mo(CF(3))(CO)(3)]. The fluorocarbyne ligand has now been investigated as a ligand in the manganese carbonyl complexes [Mn(CF)(CO)(n)] (n = 3, 4) and [Mn(2)(CF)(2)(CO)(n)] (n = 4-7) by using density functional theory. In mononuclear complexes, such as [Mn(CF)(CO)(4)], the CF ligand behaves very much like the NO ligand in terms of pi-acceptor strength. However, in the binuclear complexes the two CF ligands couple in many of the low-energy structures to form a bridging C(2)F(2) ligand derived, at least formally, from difluoroacetylene, FC[triple bond]CF. The geometries of such [Mn(2)(C(2)F(2))(CO)(n)] complexes suggest several different bonding modes of the bridging C(2)F(2) unit. These include bonding through the orthogonal pi bonds of FC[triple bond]CF, similar to the well-known [R(2)C(2)Co(2)(CO)(6)] complexes, or bonding of the C(2)F(2) unit as a symmetrical or unsymmetrical biscarbene. This research suggests that fluorocarbyne metal chemistry can serve as a means for obtaining a variety of difluoroacetylene metal complexes, thereby avoiding the need for synthesizing and handling the very unstable difluoroacetylene.

Effect of hydrogen atoms on the structures of trinuclear metal carbonyl clusters: trinuclear manganese carbonyl hydrides.

The structures of the trinuclear manganese carbonyl hydrides H(3)Mn(3)(CO)(n) (n = 12, 11, 10, 9) have been investigated by density functional theory (DFT). Optimization of H(3)Mn(3)(CO)(12) gives the experimentally known structure in which all carbonyl groups are terminal and each edge of a central Mn(3) equilateral triangle is bridged by a single hydrogen atom. This structure establishes the canonical distance 3.11 A for the Mn-Mn single bond satisfying the 18-electron rule. The central triangular (mu-H)(3)Mn(3) unit is retained in the lowest energy structure of H(3)Mn(3)(CO)(11), which may thus be derived from the H(3)Mn(3)(CO)(12) structure by removal of a carbonyl group with concurrent conversion of one of the remaining carbonyl groups into a semibridging carbonyl group to fill the resulting hole. The potential energy surface of H(3)Mn(3)(CO)(10) is relatively complicated with six singlet and five triplet structures. One of the lower energy H(3)Mn(3)(CO)(10) structures has one of the hydrogen atoms bridging the entire Mn(3) triangle and the other two hydrogen atoms bridging Mn-Mn edges. This H(3)Mn(3)(CO)(10) structure achieves the favored 18-electron configuration with a very short MnMn triple bond of 2.36 A. The other low energy H(3)Mn(3)(CO)(10) structure retains the (mu-H)(3)Mn(3) core of H(3)Mn(3)(CO)(12) but has a unique six-electron donor eta(2)-mu(3) carbonyl group bridging the entire Mn(3) triangle similar to the unique carbonyl group in the known compound Cp(3)Nb(3)(CO)(6)(eta(2)-mu(3)-CO). For H(3)Mn(3)(CO)(9) a structure with a central (mu(3)-H)(2)Mn(3) trigonal bipyramid lies >20 kcal/mol below any of the other structures. Triplet structures were found for the unsaturated H(3)Mn(3)(CO)(n) (n = 11, 10, 9) systems but at significantly higher energies than the lowest lying singlet structures.