Самоорганізовані метал-напівпровідникові мікро- та наноструктури Au-GaAs для застосування у плазмонній фотовольтаїці

Au-GaAs metal-semiconductor composite microstructures have been prepared by an anisotropic etching of n-GaAs (100) wafers doped with Te (1016 to 1017 cm-3) with subsequent photostimulated chemical deposition of noble metal (Au) on formed semiconductor quasigratings. The microrelief topology of GaAs surface is controlled by the anisotropic etching conditions. Au metal was deposited on the structured GaAs surface as randomly placed nanoparticles of various shape and size and/or nanowires on the top of the hills of formed semiconductor microstructure. As the number of Au nanoparticles increases, they tend to localize on the ledges of the GaAs microrelief forming a system of approximately parallel nanowires. Obtained periodic structures with submicron to microns periods without Au nanoparticles and with deposited nanoparticles have been studied by means of scanning electron microscopy, optical spectroscopy (photoluminescence spectroscopy at room temperature), and photoelectric measurements. The decrease of the relative intensity of main photoluminescence band for samples with Au nanostructures compared to ones without nanoparticles deposition and simultaniously changes of the shape of photocurrent spectra of Au-GaAs microstructures have been observed. Such correlation in behaviour of measured spectra make formed Au-GaA metal-semiconductor microstructures perspective for the application in plasmonic photovoltaics. Pages of the article in the issue: 139 - 142 Language of the article: EnglishМетал-напівпровідникові композитні мікроструктури Au-GaAs були отримані шляхом анізотропного травлення з подальшим фотостимульованим хімічним осадженням благородного металу (Au) на сформовані напівпровідникові квазігратки. Золото наносилося на структуровану поверхню GaAs у вигляді хаотично розміщених наночастинок металу та/або нанодротів на вершинах пагорбів напівпровідникової мікроструктури. Сформовані структури вивчаються за допомогою скануючої електронної мікроскопії, оптичної спектроскопії та фотоелектричних вимірювань. Створені метал-напівпровідникові мікроструктури Au-GaAs є перспективними для застосування в плазмонній фотовольтаїці, що підтверджується поведінкою спектрів фотолюмінесценції та змінами форми спектрів фотоструму

ERK2 alone drives inflammatory pain but cooperates with ERK1 in sensory neuron survival

Extracellular signal-regulated kinases 1 and 2 (ERK1/2) are highly homologous yet distinct components of signal transduction pathways known to regulate cell survival and function. Recent evidence indicates an isoform-specific role for ERK2 in pain processing and peripheral sensitization. However, the function of ERK2 in primary sensory neurons has not been directly tested. To dissect the isoform-specific function of ERK2 in sensory neurons, we used mice with Cre-loxP-mediated deletion of ERK2 in Na(v)1.8(+) sensory neurons that are predominantly nociceptors. We find that ERK2, unlike ERK1, is required for peripheral sensitization and cold sensation. We also demonstrate that ERK2, but not ERK1, is required to preserve epidermal innervation in a subset of peptidergic neurons. Additionally, deletion of both ERK isoforms in Na(v)1.8(+) sensory neurons leads to neuron loss not observed with deletion of either isoform alone, demonstrating functional redundancy in the maintenance of sensory neuron survival. Thus, ERK1 and ERK2 exhibit both functionally distinct and redundant roles in sensory neurons. SIGNIFICANCE STATEMENT ERK1/2 signaling affects sensory neuron function and survival. However, it was not clear whether ERK isoform-specific roles exist in these processes postnatally. Previous work from our laboratory suggested either functional redundancy of ERK isoforms or a predominant role for ERK2 in pain; however, the tools to discriminate between these possibilities were not available at the time. In the present study, we use new genetic knock-out lines to demonstrate that ERK2 in sensory neurons is necessary for development of inflammatory pain and for postnatal maintenance of peptidergic epidermal innervation. Interestingly, postnatal loss of both ERK isoforms leads to a profound loss of sensory neurons. Therefore, ERK1 and ERK2 display both functionally distinct and redundant roles in sensory neurons

ZAPS is a potent stimulator of signaling mediated by the RNA helicase RIG-I during antiviral responses

The poly(ADP-ribose) polymerases (PARPs) participate in various processes. Here, we report that the PARP-13/ZAP shorter isoform (hereafter called ZAPS), rather than the full length protein, is selectively induced by 3pRNA, and functions as a potent stimulator of retinoic acid-inducible gene-I (RIG-I)-mediated interferon (IFN) responses in human cells. ZAPS associates with RIG-I to promote the oligomerization and ATPase activity of RIG-I, leading to robust activation of IRF3 and NF-κB pathways. Disruption of the PARP-13/ZAP gene, ZC3HAV1, severely abrogated the induction of IFN-α, IFN-β and other cytokines upon viral infection. These results indicate that ZAPS is a key regulator of RIG-I signaling during the innate antiviral immune response, suggesting its possible use as a therapeutic target for viral control

Further Characterization of Galloyl Pedunculagin as an Effective Autophosphorylation Inhibitor of C-Kinase in Vitro

The inhibitory effect of galloyl pedunculagin (GP) isolated from Platycarya strobilacea on the activity and autophosphorylation of Ca2+- and phospholipid-dependent protein kinase (C-kinase) was examined in vitro. It was found that (i) GP inhibited the activity (phosphorylation of complement C3 from guinea pig) of C-kinaseα (rat brain) in a dose-dependent manner with an ID50 of approx. 0.12 μM; (ii) GP at lower doses (ID50=approx. 6 nM) inhibited autophosphorylation of C-kinaseα; and (iii) the GP-induced inhibition of autophosphorylation of C-kinaseα and its enzyme activity was a manner non-competitive to ATP. Similar inhibitory effect of GP on autophosphorylation of recombinant human C-kinaseη (rhC-kinaseη) and its phosphorylating activity was observed. These results suggest that GP is an effective autophosphorylation inhibitor of these two C-kinase isoforms (α and η) in vitro. In addition, the CD analysis suggests that the proline-containing six amino acid residues (PVLTPP) including a threonine residue (autophosphorylation site) at the C-terminal region (positions 635?640) of C-kinaseα may be one of the GP-binding sites