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Sö,derströ,m, P.-A.,Walker, P.M.,Wu, J.,Liu, H.L.,Regan, P.H.,Watanabe, H.,Doornenbal, P.,Korkulu, Z.,Lee, P.,Liu, J.J.,Lorusso, G.,Nishimura, S.,Phong, V.H.,Sumikama, T.,Xu, F.R.,Yagi, A.,Zha North-Holland Pub. Co 2016 Physics letters. Section B Vol.762 No.-
<P><B>Abstract</B></P> <P>A detailed study of the structure of the doubly mid-shell nucleus Dy 104 1 66 170 has been carried out, following isomeric and <I>β</I> decay. We have measured the yrast band up to the spin-parity <SUP> J π </SUP> = <SUP> 6 + </SUP> state, the K = 2 <I>γ</I>-vibration band up to the <SUP> 5 + </SUP> state, a low-lying negative-parity band based on a <SUP> 2 − </SUP> state that could be a candidate for the lowest energy octupole vibration state within this nucleus, and a candidate for the <SUP> K π </SUP> = <SUP> 6 + </SUP> two quasi-particle isomer. This state was determined to have an excitation energy of 1643.91(23) keV and a half life of 0.99(4) μs, with a reduced hindrance for its decay to the ground-state band an order of magnitude lower than predicted by <SUB> N p </SUB> <SUB> N n </SUB> systematics. This is interpreted as being due to <I>γ</I>-vibrational mixing from a near degeneracy of the isomer and the <SUP> 6 + </SUP> state of the <I>γ</I> band. Furthermore, the parent nucleus <SUP>170</SUP>Tb has been determined to have a half-life of 0.91 ( − 13 + 18 ) s with a possible spin-parity of <SUP> 2 − </SUP> .</P>
Calderón–Zygmund estimates in generalized Orlicz spaces
Hä,stö,, Peter,Ok, Jihoon Academic Press 2019 Journal of differential equations Vol.267 No.5
<P><B>Abstract</B></P> <P>We establish the <SUP> W 2 , φ ( ⋅ ) </SUP> -solvability of the linear elliptic equations in non-divergence form under a suitable, essentially minimal, condition of the generalized Orlicz function φ ( ⋅ ) = φ ( x , t ) , by deriving Calderón–Zygmund type estimates. The class of generalized Orlicz spaces we consider here contains as special cases classical Lebesgue and Orlicz spaces, as well as non-standard growth cases like variable exponent and double phase growth.</P>
Two-hole structure outsideNi78: Existence of aμsisomer ofCo76andβdecay intoNi76
Sö,derströ,m, P.-A.,Nishimura, S.,Xu, Z. Y.,Sieja, K.,Werner, V.,Doornenbal, P.,Lorusso, G.,Browne, F.,Gey, G.,Jung, H. S.,Sumikama, T.,Taprogge, J.,Vajta, Zs.,Watanabe, H.,Wu, J.,Baba, H.,Dom American Physical Society 2015 PHYSICAL REVIEW C - Vol.92 No.5
Sarikaya Bayram, Ö,zlem,Bayram, Ö,zgü,r,Valerius, Oliver,Park, Hee Soo,Irniger, Stefan,Gerke, Jennifer,Ni, Min,Han, Kap-Hoon,Yu, Jae-Hyuk,Braus, Gerhard H. Public Library of Science 2010 PLoS genetics Vol.6 No.12
<▼1><P>VeA is the founding member of the velvet superfamily of fungal regulatory proteins. This protein is involved in light response and coordinates sexual reproduction and secondary metabolism in <I>Aspergillus nidulans</I>. In the dark, VeA bridges VelB and LaeA to form the VelB-VeA-LaeA (velvet) complex. The VeA-like protein VelB is another developmental regulator, and LaeA has been known as global regulator of secondary metabolism. In this study, we show that VelB forms a second light-regulated developmental complex together with VosA, another member of the velvet family, which represses asexual development. LaeA plays a key role, not only in secondary metabolism, but also in directing formation of the VelB-VosA and VelB-VeA-LaeA complexes. LaeA controls VeA modification and protein levels and possesses additional developmental functions. The <I>laeA</I> null mutant results in constitutive sexual differentiation, indicating that LaeA plays a pivotal role in inhibiting sexual development in response to light. Moreover, the absence of LaeA results in the formation of significantly smaller fruiting bodies. This is due to the lack of a specific globose cell type (Hülle cells), which nurse the young fruiting body during development. This suggests that LaeA controls Hülle cells. In summary, LaeA plays a dynamic role in fungal morphological and chemical development, and it controls expression, interactions, and modification of the velvet regulators.</P></▼1><▼2><P><B>Author Summary</B></P><P>Numerous fungi have the potential to infect immunocompromised patients or to contaminate and spoil our nutrients. They represent an increasing danger that threatens public health and agriculture. This requires improved understanding of fungal growth, development, dissemination of spores, and mycotoxin production. We have discovered two related fungal specific protein complexes that provide a molecular link among spore formation, fungal development, and secondary metabolite production. The subunit allocation of both complexes depends on each other, and they share a common subunit. These complexes comprise three related and in fungi conserved proteins of the velvet family that function in concert with a known regulator of secondary metabolism, LaeA. This protein controls the formation of both complexes but is only a part of the trimeric complex. We found that this regulator of secondary metabolism also possesses several developmental control functions in gene expression. These protein complexes discovered in the fungal model system <I>Aspergillus nidulans</I> are conserved in fungal pathogens where they might provide novel insights for understanding growth, development, and interaction with their respective hosts.</P></▼2>
Hybridization gap and Fano resonance in SmB<sub>6</sub>
Rö,ßler, Sahana,Jang, Tae-Hwan,Kim, Dae-Jeong,Tjeng, L. H.,Fisk, Zachary,Steglich, Frank,Wirth, Steffen National Academy of Sciences 2014 PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF Vol.111 No.13
<P>Hybridization between conduction electrons and the strongly interacting <I>f</I>-electrons in rare earth or actinide compounds may result in new states of matter. Depending on the exact location of the concomitant hybridization gap with respect to the Fermi energy, a heavy fermion or an insulating ground state ensues. To study this entanglement locally, we conducted scanning tunneling microscopy and spectroscopy (STS) measurements on the “Kondo insulator” SmB<SUB>6</SUB>. The vast majority of surface areas investigated were reconstructed, but infrequently, patches of varying sizes of nonreconstructed Sm- or B-terminated surfaces also were found. On the smallest patches, clear indications for the hybridization gap with logarithmic temperature dependence (as expected for a Kondo system) and for intermultiplet transitions were observed. On nonreconstructed surface areas large enough for coherent cotunneling, we were able to observe clear-cut Fano resonances. Our locally resolved STS indicated considerable finite conductance on all surfaces independent of their structure, not proving but leaving open the possibility of the existence of a topologically protected surface state.</P>
Search for a standard-model-like Higgs boson with a mass in the range 145 to 1000 GeV at the LHC
Chatrchyan, S.,Khachatryan, V.,Sirunyan, A. M.,Tumasyan, A.,Adam, W.,Bergauer, T.,Dragicevic, M.,Erö,, J.,Fabjan, C.,Friedl, M.,Frü,hwirth, R.,Ghete, V. M.,Hö,rmann, N.,Hrubec, J.,Jeitler, Springer Berlin Heidelberg 2013 The European physical journal. C, Particles and fi Vol.73 No.6
<P>A search for a standard-model-like Higgs boson in the H→WW and H→ZZ decay channels is reported, for Higgs boson masses in the range 145<<I>m</I><SUB>H</SUB><1000 GeV. The search is based upon proton–proton collision data samples corresponding to an integrated luminosity of up to 5.1 fb<SUP>−1</SUP> at [FORMULA OMISSION] and up to 5.3 fb<SUP>−1</SUP> at [FORMULA OMISSION], recorded by the CMS experiment at the LHC. The combined upper limits at 95 % confidence level on products of the cross section and branching fractions exclude a standard-model-like Higgs boson in the range 145<<I>m</I><SUB>H</SUB><710 GeV, thus extending the mass region excluded by CMS from 127–600 GeV up to 710 GeV.</P>
Paik, Yong‐,Han,Iwaisako, Keiko,Seki, Ekihiro,Inokuchi, Sayaka,Schnabl, Bernd,Ö,sterreicher, Christoph H.,Kisseleva, Tatiana,Brenner, David A. Wiley Subscription Services, Inc., A Wiley Company 2011 Hepatology Vol.53 No.5
<P><B>Abstract</B></P><P>Nicotinamide adenine dinucleotide phosphate oxidase (NOX) is a multicomponent enzyme that mediates electron transfer from nicotinamide adenine dinucleotide phosphate to molecular oxygen, which leads to the production of superoxide. NOX2/gp91<SUP>phox</SUP> is a catalytic subunit of NOX expressed in phagocytic cells. Several homologues of NOX2, including NOX1, have been identified in nonphagocytic cells. We investigated the contributory role of NOX1 and NOX2 in hepatic fibrosis. Hepatic fibrosis was induced in wild‐type (WT) mice, NOX1 knockout (NOX1KO) mice, and NOX2 knockout (NOX2KO) mice by way of either carbon tetrachloride (CCl<SUB>4</SUB>) injection or bile duct ligation (BDL). The functional contribution of NOX1 and NOX2 in endogenous liver cells, including hepatic stellate cells (HSCs), and bone marrow (BM)‐derived cells, including Kupffer cells (KCs), to hepatic reactive oxygen species (ROS) generation and hepatic fibrosis was assessed <I>in vitro</I> and <I>in vivo</I> using NOX1 or NOX2 BM chimeric mice. Hepatic NOX1 and NOX2 messenger RNA expression was increased in the two experimental mouse models of hepatic fibrosis. Whereas NOX1 was expressed in HSCs but not in KCs, NOX2 was expressed in both HSCs and KCs. Hepatic fibrosis and ROS generation were attenuated in both NOX1KO and NOX2KO mice after CCl<SUB>4</SUB> or BDL. Liver fibrosis in chimeric mice indicated that NOX1 mediates the profibrogenic effects in endogenous liver cells, whereas NOX2 mediates the profibrogenic effects in both endogenous liver cells and BM‐derived cells. Multiple NOX1 and NOX2 components were up‐regulated in activated HSCs. Both NOX1‐ and NOX2‐deficient HSCs had decreased ROS generation and failed to up‐regulate collagen α1(I) and transforming growth factor β in response to angiotensin II. <I>Conclusion:</I> Both NOX1 and NOX2 have an important role in hepatic fibrosis in endogenous liver cells, including HSCs, whereas NOX2 has a lesser role in BM‐derived cells. (H<SMALL>EPATOLOGY</SMALL> 2011;)</P>
Plasma zinc's alter ego is a low-molecular-weight humoral factor
Ou, Ou,Allen-Redpath, Keith,Urgast, Dagmar,Gordon, Margaret-Jane,Campbell, Gill,Feldmann, Jö,rg,Nixon, Graeme F.,Mayer, Claus-Dieter,Kwun, In-Sook,Beattie, John H. The Federation of American Societies for Experimen 2013 The FASEB Journal Vol.27 No.9
<P>Mild dietary zinc deprivation in humans and rodents has little effect on blood plasma zinc levels, and yet cellular consequences of zinc depletion can be detected in vascular and other tissues. We proposed that a zinc-regulated humoral factor might mediate the effects of zinc deprivation. Using a novel approach, primary rat vascular smooth muscle cells (VSMCs) were treated with plasma from zinc-deficient (<1 mg Zn/kg) or zinc-adequate (35 mg Zn/kg, pair-fed) adult male rats, and zinc levels were manipulated to distinguish direct and indirect effects of plasma zinc. Gene expression changes were analyzed by microarray and qPCR, and incubation of VSMCs with blood plasma from zinc-deficient rats strongly changed the expression of >2500 genes, compared to incubation of cells with zinc-adequate rat plasma. We demonstrated that this effect was caused by a low-molecular-weight (∼2-kDa) zinc-regulated humoral factor but that changes in gene expression were mostly reversed by adding zinc back to zinc-deficient plasma. Strongly regulated genes were overrepresented in pathways associated with immune function and development. We conclude that zinc deficiency induces the production of a low-molecular-weight humoral factor whose influence on VSMC gene expression is blocked by plasma zinc. This factor is therefore under dual control by zinc.—Ou, O., Allen-Redpath, K., Urgast, D., Gordon, M.-J., Campbell, G., Feldmann, J., Nixon, G. F., Mayer, C.-D., Kwun, I.-S., and Beattie, J. H. Plasma zinc's alter ego is a low-molecular-weight humoral factor.</P>
Watanabe, H.,Wang, H.K.,Lorusso, G.,Nishimura, S.,Xu, Z.Y.,Sumikama, T.,Sö,derströ,m, P.-A.,Doornenbal, P.,Browne, F.,Gey, G.,Jung, H.S.,Taprogge, J.,Vajta, Zs.,Wu, J.,Yagi, A.,Baba, H.,Benzon Elsevier 2019 Physics letters: B Vol.792 No.-
<P><B>Abstract</B></P> <P>The neutron-rich isotopes of palladium have attracted considerable interest in terms of the evolution of the N = 82 neutron shell closure and its influence on the <I>r</I>-process nucleosynthesis. In this Letter, we present the first spectroscopic information on the excited states in <SUP>125</SUP>Pd<SUB>79</SUB> and <SUP>127</SUP>Pd<SUB>81</SUB> studied using the EURICA <I>γ</I>-ray spectrometer, following production via in-flight fission of a high-intensity <SUP>238</SUP>U beam at the RIBF facility. New isomeric states with half-lives of 144(4) ns and 39(6) μs have been assigned spins and parities of ( 23 / <SUP> 2 + </SUP> ) and ( 19 / <SUP> 2 + </SUP> ) in <SUP>125</SUP>Pd and <SUP>127</SUP>Pd, respectively. The observed level properties are compared to a shell-model calculation, suggesting the competition between proton excitations and neutron excitations in the proton-hole and neutron-hole systems in the vicinity of the doubly magic nucleus <SUP>132</SUP>Sn.</P>
Watanabe, H.,Lorusso, G.,Nishimura, S.,Otsuka, T.,Ogawa, K.,Xu, Z. Y.,Sumikama, T.,Sö,derströ,m, P.-A.,Doornenbal, P.,Li, Z.,Browne, F.,Gey, G.,Jung, H. S.,Taprogge, J.,Vajta, Zs.,Wu, J.,Yagi, American Physical Society 2014 Physical Review Letters Vol.113 No.4
<P>A new isomer with a half-life of 23.0(8) ms has been identified at 2406 keV in (126)Pd and is proposed to have a spin and parity of 10(+) with a maximally aligned configuration comprising two neutron holes in the 1h(11/2) orbit. In addition to an internal-decay branch through a hindered electric octupole transition, β decay from the long-lived isomer was observed to populate excited states at high spins in (126)Ag. The smaller energy difference between the 10(+) and 7(-) isomers in (126)Pd than in the heavier N=80 isotones can be interpreted as being ascribed to the monopole shift of the 1h(11/2) neutron orbit. The effects of the monopole interaction on the evolution of single-neutron energies below (132)Sn are discussed in terms of the central and tensor forces.</P>