Active MnOx Electrocatalysts Prepared by Atomic Layer Deposition for Oxygen Evolution and Oxygen Reduction Reactions

The ability to deposit conformal catalytic thin films enables opportunities to achieve complex nanostructured designs for catalysis. Atomic layer deposition (ALD) is capable of creating conformal thin films over complex substrates. Here, ALD‐MnO_x on glassy carbon is investigated as a catalyst for the oxygen evolution reaction (OER) and the oxygen reduction reaction (ORR), two reactions that are of growing interest due to their many applications in alternative energy technologies. The films are characterized by X‐ray photoelectron spectroscopy, X‐ray diffraction, scanning electron microscopy, ellipsometry, and cyclic voltammetry. The as‐deposited films consist of Mn(II)O, which is shown to be a poor catalyst for the ORR, but highly active for the OER. By controllably annealing the samples, Mn₂O₃ catalysts with good activity for both the ORR and OER are synthesized. Hypotheses are presented to explain the large difference in the activity between the MnO and Mn₂O₃ catalysts for the ORR, but similar activity for the OER, including the effects of surface oxidation under experimental conditions. These catalysts synthesized though ALD compare favorably to the best MnO_x catalysts in the literature, demonstrating a viable way to produce highly active, conformal thin films from earth‐abundant materials for the ORR and the OER.     

Integrin alphaVbeta3 Binds to the RGD motif of glycoprotein B of Kaposi's sarcoma-associated herpesvirus and functions as an RGD-dependent entry receptor

Kaposi's sarcoma-associated herpesvirus (KSHV) envelope-associated glycoprotein B (gB) is involved in the initial steps of binding to host cells during KSHV infection. gB contains an RGD motif reported to bind the integrin α₃β₁ during virus entry. Although the ligand specificity of α₃β₁ has been controversial, current literature indicates that α₃β₁ ligand recognition is independent of RGD. We compared α₃β₁ to the RGD-binding integrin, α_Vβ₃, for binding to envelope-associated gB and a gB(RGD) peptide. Adhesion assays demonstrated that β₃-CHO cells overexpressing α_Vβ₃ specifically bound gB(RGD), whereas α₃-CHO cells overexpressing α₃β₁ did not. Function-blocking antibodies to α_Vβ₃ inhibited the adhesion of HT1080 fibrosarcoma cells to gB(RGD), while antibodies to α₃β₁ did not. Using affinity-purified integrins and confocal microscopy, α_Vβ₃ bound to gB(RGD) and KSHV virions, demonstrating direct receptor-ligand interactions. Specific α_Vβ₃ antagonists, including cyclic and dicyclic RGD peptides and α_Vβ₃ function-blocking antibodies, inhibited KSHV infection by 70 to 80%. Keratinocytes from α₃-null mice lacking α₃β₁ were fully competent for infection by KSHV, and reconstitution of α₃β₁ function by transfection with α₃ cDNA reduced KSHV infectivity from 74% to 55%. Additional inhibitory effects of α₃β₁ on the cell surface expression of α_Vβ₃ and on α_Vβ₃-mediated adhesion of α₃-CHO cells overexpressing α₃β₁ were detected, consistent with previous reports of transdominant inhibition of α_Vβ₃ function by α₃β₁. These observations may explain previous reports of an inhibition of KSHV infection by soluble α₃β₁. Our studies demonstrate that α_Vβ₃ is a cellular receptor mediating both the cell adhesion and entry of KSHV into target cells through binding the virion-associated gB(RGD).     

Silicon nanotechnologies of pigmented heterokonts

Many pigmented heterokonts are able to synthesize elements of their cell walls (the frustules) of dense biogenic silica. These include diatom algae, which occupy a significant place in the biosphere. The siliceous frustules of diatoms have species-specific patterns of surface structures between 10 and a few hundred nanometers. The present review considers possible mechanisms of uptake of silicic acid from the aquatic environment, its transport across the plasmalemma, and intracellular transport and deposition of silica inside the specialized Silica Deposition Vesicle (SDV) where elements of the new frustule are formed. It is proposed that a complex of silicic acid with positively charged proteins silaffins and polypropylamines remains a homogeneous solution during the intracellular transport to SDV, where biogenic silica precipitates. The high density of the deposited biogenic silica may be due to removal of water from the SDV by aquaporins followed by syneresis--a process during which pore water is expelled from the network of the contracting gel. The pattern of aquaporins in the silicalemma, the membrane embracing the SDV, can determine the pattern of species-specific siliceous nanostructures.     

G0 function of BCL2 and BCL-xL requires BAX, BAK, and p27 phosphorylation by Mirk, revealing a novel role of BAX and BAK in quiescence regulation

BCL2 and BCL-x(L) facilitate G(0) quiescence by decreasing RNA content and cell size and up-regulating p27 protein, but the precise mechanism is not understood. We investigated the relationship between cell cycle regulation and the anti-apoptosis function of BCL2 and BCL-x(L). Neither caspase inhibition nor abrogation of mitochondria-dependent apoptosis by BAX and BAK deletion fully recapitulated the G(0) effects of BCL2 or BCL-x(L), suggesting that mechanisms in addition to anti-apoptosis are involved in the cell cycle arrest function of BCL2 or BCL-x(L). We found that BCL2 and BCL-x(L) expression in bax(-/-) bak(-/-) cells did not confer cell cycle effects, consistent with the G(0) function of BCL2 and BCL-x(L) being mediated through BAX or BAK. Stabilization of p27 in G(0) in BCL2 or BCL-x(L) cells was due to phosphorylation of p27 at Ser(10) by the kinase Mirk. In bax(-/-) bak(-/-) cells, total p27 and p27 phosphorylated at Ser(10) were elevated. Re-expression of BAX in bax(-/-) bak(-/-) cells and silencing of BAX and BAK in wild type cells confirmed that endogenous BAX and BAK modulated p27. These data revealed a novel role for BAX and BAK in the regulation of G(0) quiescence.     

QTL analysis for capsaicinoid content in Capsicum

Pungency or “heat” found in Capsicum fruit results from the biosynthesis and accumulation of alkaloid compounds known as capsaicinoids in the dissepiment, placental tissue adjacent to the seeds. Pepper cultivars differ with respect to their level of pungency because of quantitative and qualitative variation in capsaicinoid content. We analyzed the segregation of three capsaicinoids: capsaicin, dihydrocapsaicin and nordihydrocapsaicin in an inter-specific cross between a mildly pungent Capsicum annuum ‘NuMex RNaky’ and the wild, highly pungent C. frutescens accession BG2814-6. F₃ families were analyzed in three trials in California and in Israel and a dense molecular map was constructed comprised mostly of loci defined by simple sequence repeat (SSR) markers. Six QTL controlling capsaicinoid content were detected on three chromosomes. One gene from the capsaicinoid biosynthetic pathway, BCAT, and one random fruit EST, 3A2, co-localized with QTL detected in this study on chromosomes 3 and 4. Because one confounding factor in quantitative determination of capsaicinoid is fruit size, fruit weight measurements were taken in two trials. Two QTL controlling fruit weight were detected, however, they did not co-localize with QTL detected for capsaicinoid content. The major contribution to the phenotypic variation of capsaicinoid content (24–42% of the total variation) was attributed to a digenic interaction between a main-effect QTL, cap7.1, and a marker located on chromosome 2 that did not have a main effect on the trait. A second QTL, cap7.2 is likely to correspond to the QTL, cap, identified in a previous study as having pronounced influence on capsaicinoid content.     

Molecular characterization of Streptococcus pneumoniae,particularly serotype19A/ST320, which emerged in Krasnoyarsk,Russia

Streptococcus pneumoniae , a common human pathogen, colonizes the nasopharynx and causes diseases including acute otitis media (AOM). Herein, pneumococcal serotype distributions in children before and after PCV7 vaccination and in patients with pneumococcal disease in Siberian Russia (Krasnoyarsk) are reported. Analyses included antimicrobial susceptibility testing, sequence typing (ST), pulsed field gel electrophoresis, virulence‐related surface protein gene (VSG) typing with novel primers and structural analysis by scanning electron microscopy. In healthy children (HC) prior to administration of PCV7, drug‐susceptible serotype23F/ST1500 was a major pneumococcal genotype. In the PCV7 trial, multidrug‐resistant serotype19A/ST320 emerged in vaccinees after PCV7, exhibiting a PCV7‐induced serotype replacement. Multidrug‐resistant serotype19A/ST320 was evident in patients with AOM. Community‐acquired pneumonia (CAP) isolates showed genetic similarities to the AOM (ST320) genotype, constituting a common non‐invasive AOM–CAP group. In contrast, meningitis isolates were more divergent. Overall, 25 ST types were identified; five (20%) of which were Krasnoyarsk‐native. Regarding VSGs, PI‐1 (rlrA /rrgB ), PI‐2 (pitA /B ), psrP and cbpA were present at 54.3%, 38.6%, 48.6%, and 95.7%, respectively, with two major VSG content types, PI‐1^?/PI‐2^?/psrP ⁺/cbpA ⁺ and PI‐1⁺/PI‐2⁺/psrP ^‐/cbpA ⁺, being found for HC and non‐invasive diseases, respectively. A major clone of serotype19A/ST320 (PI‐1⁺/PI‐2⁺) produced the longest pneumococcal wire (pilus) structures in colonies. ST1016 (PI‐1^?/PI‐2^?) in HC had HEp‐2 cell‐adherent pili. These results suggest that serotype19A/ST320 and related genotypes, with the VSG content type PI‐1⁺/PI‐2⁺/psrP ^?/cbpA ⁺, emerged in vaccinees after PCV7 in Siberia, accompanying diseases in non‐vaccinated children, and that some genotypes (serotypes19A/ST320 and 18/ST1016) produced novel pneumococcal structures, predicting their roles in colony formation and adherence.

     

The C terminus of the Vps34p phosphoinositide 3-kinase is necessary and sufficient for the interaction with the Vps15p protein kinase.

Vps34p is a phosphatidylinositol 3-kinase that is part of a membrane-associated complex with the Vps15p protein kinase. This kinase complex is required for the delivery of soluble proteins to the lysosomal/vacuolar compartment of eukaryotic cells. This study examined the Vps34p-Vps15p association and identified the domains within each protein that were important for this interaction. Using several different approaches, the interaction domain within Vps34p was mapped to a 28-amino acid element near its C terminus. This Vps34p motif was both necessary and sufficient for the interaction with Vps15p. Two-hybrid mapping experiments indicated that two separate regions of Vps15p were required for the association with Vps34p; they are the N-terminal protein kinase domain and a set of three tandem repeats of about 39 amino acids each. Neither domain alone was sufficient for the interaction. These Vps15p repeat elements are similar in sequence to the HEAT motifs that have been implicated in protein interactions in other proteins, including the Huntingtin protein. Finally, these studies identified a novel motif at the very C terminus of Vps34p that was required for phosphatidylinositol 3-kinase activity. This domain is highly conserved specifically in all Vps34p-like phosphatidylinositol 3-kinases but is not required for the interaction with Vps15p. This study thus represents a first step toward a better understanding of how this Vps15p.Vps34p kinase complex is assembled and regulated in vivo.     

Basic fibroblast growth factor: a potential inhibitor of glutamine synthetase expression in injured neural tissue

Basic fibroblast growth factor (bFGF) was recently shown to promote the survival of neural cells and tissues, raising hopes for its therapeutic potential in degenerative disorders of the CNS. Here we examine the effect of bFGF on the expression of glutamine synthetase, a key enzyme in the detoxification of the neurotransmitter glutamate. Expression of this enzyme is regulated by systemic glucocorticoids and, in chick neural retina tissue, is restricted to Müller glial cells. We report that exogenous supply of bFGF to retinal explants inhibits hormonal induction of glutamine synthetase expression. This inhibition appears to be mediated by the c-Jun protein which accumulated, in response to bFGF, exclusively in Müller glial cells. Ischemic conditions, which reportedly stimulate the release of endogenous bFGF, also led to an increase in c-Jun protein and a decline in glutamine synthetase expression. This decline could be competitively prevented by a soluble fibroblast growth factor receptor but not by a soluble epidermal growth factor receptor. The finding that endogenous release of bFGF or its exogenous supply down-regulates glutamine synthetase expression suggests that in addition to its reported neuroprotective effect, bFGF may exacerbate glutamate mediated neurotoxicity through direct down-regulation of glutamine synthetase.