Isomeric states in 253^{253}No

6 pagesInternational audienceIsomeric states in 253No have been investigated by conversion-electron and gamma-ray spectroscopy with the GABRIELA detection system. The 31 micro second isomer reported more than 30 years ago is found to decay to the ground state of 253No by the emission of a 167 keV M2 transition. The spin and parity of this low-lying isomeric state are established to be 5/2+. The presence of another longer-lived isomeric state is also discussed

Medium-spin states in neutron-rich 83As and 81As

The 83,81 As nuclei have been produced as fission fragments in the fusion reaction 18O + 208Pb at 85 MeV bombarding energy and studied with the Euroball array. Medium-spin states of 83,81 As have been established up to ∼3.5 MeV excitation energy. From angular correlation analysis, spin values have been assigned to most of the 81 As excited states. The behaviors of the yrast structures identified in this work are discussed in comparison with the general features known in the mass region. Then they are compared to the results of two theoretical approaches: the "rotor + quasiparticle" for 81 As and the shell model using the effective interactions JUN45 for 83,81 As

New high-spin states of 58142^{142}_ {58}Ce and 56140^{140}_{56}Ba from fusion-fission reactions: Proton excitations in the N = 84 isotones

High-spin states in the $^{142}$Ce and $^{140}$Ba nuclei have been populated in the $^{12}$C + $^{238}$U and $^{18}$O + $^{208}$Pb fusion-fission reactions at 90 MeV and 85 MeV bombarding energy, respectively. The emitted $\gamma$-radiation was detected using the Euroball III and IV arrays. The high-spin yrast and near-to-yrast structures of $^{142}$Ce have been considerably extended. The level scheme of $^{140}$Ba has been extended by six new levels. The newly observed structures in these N = 84 isotones are discussed by analogy with the neighbouring nuclei

Nucleic Acids Res

Fragile X syndrome (FXS), the most common form of inherited intellectual disability, is caused by the silencing of the FMR1 gene encoding an RNA-binding protein (FMRP) mainly involved in translational control. We characterized the interaction between FMRP and the mRNA of GRK4, a member of the guanine nucleotide-binding protein (G protein)-coupled receptor kinase super-family, both in vitro and in vivo. While the mRNA level of GRK4 is unchanged in the absence or in the presence of FMRP in different regions of the brain, GRK4 protein level is increased in Fmr1-null cerebellum, suggesting that FMRP negatively modulates the expression of GRK4 at the translational level in this brain region. The C-terminal region of FMRP interacts with a domain of GRK4 mRNA, that we called G4RIF, that is folded in four stem loops. The SL1 stem loop of G4RIF is protected by FMRP and is part of the S1/S2 sub-domain that directs translation repression of a reporter mRNA by FMRP. These data confirm the role of the G4RIF/FMRP complex in translational regulation. Considering the role of GRK4 in GABAB receptors desensitization, our results suggest that an increased GRK4 levels in FXS might contribute to cerebellum-dependent phenotypes through a deregulated desensitization of GABAB receptors

Expression of uncoupling proteins-1,-2 and-3 mRNA is induced by an adenocarcinoma-derived lipid-mobilizing factor

The abnormalities of lipid metabolism observed in cancer cachexia may be induced by a lipid-mobilizing factor produced by adenocarcinomas. The specific molecules and metabolic pathways that mediate the actions of lipid-mobilizing factor are not known. The mitochondrial uncoupling proteins-1, -2 and -3 are suggested to play essential roles in energy dissipation and disposal of excess lipid. Here, we studied the effects of lipid-mobilizing factor on the expression of uncoupling proteins-1, -2 and -3 in normal mice. Lipid-mobilizing factor isolated from the urine of cancer patients was injected intravenously into mice over a 52-h period, while vehicle was similarly given to controls. Lipid-mobilizing factor caused significant reductions in body weight (-10%, P=0.03) and fat mass (-20%, P<0.01) accompanied by a marked decrease in plasma leptin (-59%, P<0.01) and heavy lipid deposition in the liver. In brown adipose tissue, uncoupling protein-1 mRNA levels were elevated in lipid-mobilizing factor-treated mice (+96%, P<0.01), as were uncoupling proteins-2 and -3 (+57% and +37%, both P<0.05). Lipid-mobilizing factor increased uncoupling protein-2 mRNA in both skeletal muscle (+146%, P<0.05) and liver (+142%, P=0.03). The protein levels of uncoupling protein-1 in brown adipose tissue and uncoupling protein-2 in liver were also increased with lipid-mobilizing factor administration (+49% and +67%, both P=0.02). Upregulation by lipid-mobilizing factor of uncoupling proteins-1, -2 and -3 in brown adipose tissue, and of uncoupling protein-2 in skeletal muscle and liver, suggests that these uncoupling proteins may serve to utilize excess lipid mobilized during fat catabolism in cancer cachexia

Direct targets of Klf5 transcription factor contribute to the maintenance of mouse embryonic stem cell undifferentiated state

<p>Abstract</p> <p>Background</p> <p>A growing body of evidence has shown that Krüppel-like transcription factors play a crucial role in maintaining embryonic stem cell (ESC) pluripotency and in governing ESC fate decisions. Krüppel-like factor 5 (Klf5) appears to play a critical role in these processes, but detailed knowledge of the molecular mechanisms of this function is still not completely addressed.</p> <p>Results</p> <p>By combining genome-wide chromatin immunoprecipitation and microarray analysis, we have identified 161 putative primary targets of Klf5 in ESCs. We address three main points: (1) the relevance of the pathways governed by Klf5, demonstrating that suppression or constitutive expression of single Klf5 targets robustly affect the ESC undifferentiated phenotype; (2) the specificity of Klf5 compared to factors belonging to the same family, demonstrating that many Klf5 targets are not regulated by Klf2 and Klf4; and (3) the specificity of Klf5 function in ESCs, demonstrated by the significant differences between Klf5 targets in ESCs compared to adult cells, such as keratinocytes.</p> <p>Conclusions</p> <p>Taken together, these results, through the definition of a detailed list of Klf5 transcriptional targets in mouse ESCs, support the important and specific functional role of Klf5 in the maintenance of the undifferentiated ESC phenotype.</p> <p>See: <url>http://www.biomedcental.com/1741-7007/8/125</url></p

Interaction entre les dislocations extrinsèques du joint de grains et l'impureté carbone dans le fer α et ses alliages cubiques centrés

La stabilisation des dislocations extrinsèques des joints de grains du fer, des alliages fer-4 % nickel et fer-9 % chrome a été étudiée par microscopie électronique par transmission en fonction :— de la géométrie du joint de grains (désorientation entre cristaux),— de la présence ou non d'une ségrégation intergranulaire de carbone. Le formalisme géométrique de Bollmann est opérant pour comprendre la présence de dislocations extrinsèques dans les joints spéciaux et leur élimination dans les joints généraux en l'absence d'impureté ségrégée. En revanche, si une ségrégation active intervient, la différence de comportement des deux types de joints disparaît, en particulier les joints généraux, nombreux dans les polycristaux réels, peuvent retenir des dislocations extrinsèques