The geometrical structure of small nickel clusters is probed via molecular adsorption of nitrogen on their surfaces. Nitrogen uptake patterns can be rationalized with the proposed structures if it is assumed that N2 binds to every exposed nickel atom, that the binding energies decrease with increasing metal—metal coordination, and that atoms that are four or less coordinate can bind two nitrogen molecules. In some cases nitrogen adsorption causes a change in cluster structure, usually to one that can accommodate more nitrogen molecules. Cluster structures are proposed for all clusters (bare and nitrogenated) in the 3–15-atom size range except Ni4 and Ni11. The nitrogen uptake for Ni4 is consistent with virtually any structure, and the data for Ni11 could not be interpreted in terms of a specific structure. In general, nickel cluster structures are different from those found for rare gas clusters as well as those derived from bulk packing. A comparison of the experimental results with existing theoretical calculations is presented.

No abstract

Prolonged or overdose glucocorticoids (GCs) usage is the common cause of osteoporosis. In the present study, we studied the cellular mechanism of dexamethasone (Dex)-induce osteoblast cell death by focusing on the role of mitochondrial permeability transition pore (mPTP). In cultured osteoblastic MC3T3-E1 cells, Dex-induced mPTP opening, which was demonstrated by mitochondrial membrane potential (MPP) decrease, cyclophilin-D (CyPD)-adenine nucleotide translocator 1 (ANT-1) mitochondrial complexation and cytochrome C (cyto-C) release. The mPTP inhibitor sanglifehrin A (SfA) dramatically inhibited Dex-induced MPP loss, cyto-C release and MC3T3-E1 cell death. Dex-induced cell death requires mPTP composing protein CyPD, as CyPD inhibitor cyclosporin A (CsA) and CyPD siRNA knockdown inhibited Dex-induced MC3T3-E1 cell death, while CyPD overexpression aggravated Dex's cytotoxic effect. We found that Dex induced P53 phosphorylation and translocation to mitochondria, where it formed a complex with CyPD. Glucocorticoid receptor (GR) siRNA knockdown, or P53 inhibition (by its inhibitor pifithrin-α or shRNA silencing) suppressed Dex-induced CyPD-P53 mitochondrial association and subsequent MC3T3-E1 cell death. Finally, in primary cultured osteoblasts, Dex-induced cell death was inhibited by CsA, SfA or pifithrin-α. Together, our data suggest that Dex-induced osteoblast cell death is associated with GR-P53-regulated mPTP opening.

Activation of AMP-activated protein kinase (AMPK) could potently protect osteoblasts/osteoblastic cells from dexamethasone (Dex). We aim to induce AMPK activation via microRNA (“miRNA”) downregulation of its phosphatase Ppm1e. We discovered that microRNA-135b (“miR-135b”) targets the 3' untranslated regions (UTRs) of Ppm1e. In human osteoblasticOB-6 cells and hFOB1.19 cells, forced-expression of miR-135b downregulated Ppm1e and activated AMPK signaling. miR-135b also protected osteoblastic cells from Dex. shRNA-induced knockdown of Ppm1e similarly activated AMPK and inhibited Dex-induced damages. Intriguingly, in the Ppm1e-silenced osteoblastic cells, miR-135b expression failed to offer further cytoprotection against Dex. Notably, AMPK knockdown (via shRNA) or dominant negative mutation abolished miR-135b-induced AMPK activation and cytoprotection against Dex. Molecularly, miR-135b, via activating AMPK, increased nicotinamide adenine dinucleotide phosphate (NADPH) activity and inhibited Dex-induced oxidative stress. At last, we found that miR-135b level was increased in human necrotic femoral head tissues, which was correlated with Ppm1e downregulation and AMPK activation. There results suggest that miR-135b expression downregulates Ppm1e to activate AMPK signaling, which protects osteoblastic cells from Dex.

Methane activation by nickel cluster cations, Ni n + (n=2-16): Reaction mechanisms and thermochemistry of cluster-CH x (x=0-3) complexesThe molecular adsorption of nitrogen on nickel clusters is used to probe the clusters' geometrical structures. The application of nitrogen binding rules derived from earlier studies of both larger and smaller nickel clusters allows a determination of structure from nitrogen uptake patterns. In the 16and 28-atom size region cluster structure is dominated by local pentagonal symmetry, a consequence of a preference for close packing of atoms on clusters with curved surfaces. In most cases, the structures that result can be derived from the 13-atom icosahedron, the polyicosahedral 19-, 23-, and 26-atom clusters, and the 55-atom icosahedron, by adding or removing atoms. Icosahedral and polyicosahedral clusters often have substantial surface strain, which in some cases is relieved by deviations from the ideal geometry. Structures are proposed for all clusters in the Ni 16 to Ni 28 size range, with the exception of Ni 27 . Generally, there is no evidence for structural changes as a consequence of nitrogen binding, so that the proposed structures are those of the bare as well as the nitrogenated clusters. Where possible, comparison with existing theoretical calculations of nickel cluster structure is made.