Critical test of multi-{\it j} supersymmetries from magnetic moment measurements

Magnetic moment measurements in odd nuclei directly probe the distribution of fermion states and hence provide one of the most critical tests for multi-$j$ supersymmetries in collective nuclei. Due to complexity of calculations and lack of data, such tests have not been performed in the past. Using the Mathematica software, we derive analytic expressions for magnetic moments in the $SO^{(BF)}(6) \times SU^{(F)}(2)$ limit of the $U(6/12)$ supersymmetry and compare the results with recent measurements in $^{195}$Pt.Comment: 10 pages with 1 figur

Effect of die surface on the onset of stick-slip flow in polymer processing

International audienceIn this paper, we investigate the relationships between stick-slip defect and molecular slip at the wall for linear polymers. By considering Brochard-de Gennes slip model and molecular chain dynamics at the wall, we propose an expression for the critical shear stress at the onset of stick-slip as a function of the wettability of the polymer on the die surface or, more precisely, as a function of the apparent contact angle between polymer and die surface

Description des noyaux de A impair en termes de bosons et de fermions en interaction

École thématiqu

Étude des isotones N = 81 : 139Ce, 141Nd, 143Sm, au moyen des réactions (d, t ) et (3He, α)

Les niveaux excités des isotones N = 81 : 139Ce, 141Nd, 143Sm, ont été étudiés au Tandem MP d'Orsay jusqu'à plus de 3 MeV d'énergie d'excitation, essentiellement au moyen d'un spectromètre magnétique split pole, en utilisant les réactions (d, t) à 26,21 MeV (resolution :14 keV) et (3He, α) à 25 MeV (résolution : 23 keV). Les distributions angulaires correspondant à un grand nombre de niveaux finaux (~ 90 pour les 3 isotones) ont été analysées en approximation de Born avec ondes distordues (DWBA). Beaucoup des niveaux analysés (plus de 30) n'avaient pas été observés ou séparés dans les expériences (p, d) ou (d, t) antérieures. La force à une particule est généralement répartie sur plusieurs niveaux, la fragmentation étant particulièrement importante pour les sous-couches 2d 5/2 et 1g 7/2. Des calculs tenant compte du couplage des états à un trou avec les états collectifs du cœur, effectués par Heyde et Brussaard, reproduisent convenablement la partie de basse énergie d'excitation des spectres expérimentaux, mais ne reproduisent pas la fragmentation observée à énergie d'excitation plus élevée

Section of the corpus callosum in kainic acid induced seizures in rats: behavioral, electroencephalographic and neuropathological study.

Clinical and experimental data suggest that the role of corpus callosum in epilepsy includes synchronization, spread, excitation and inhibition. Section of the corpus callosum (SCC) is known to be a useful therapy in selected types of generalized epilepsy, i.e., tonic, atonic and generalized convulsive seizures, but not partial seizures which may be exacerbated by this procedure. The goal of this study was to determine the effect of SCC in the kainic acid (KA) model of limbic seizures in rats. Using several doses of KA (2.5, 5 and 10 mg/kg) injected systemically, we found a potentiation of the behavioral, electrographic and histological effects of KA in the SCC group of animals compared to the sham-operated control rats. A low dose of kainic acid (2.5 and 5 mg/kg) induced status epilepticus in the SCC animals, but not in the sham-operated control rats. These data demonstrate that in the KA model of temporal lobe seizures, SCC not only fails to protect, but actually intensifies seizures. This finding is compatible with the hypothesis that there is an inhibitory influence, via the corpus callosum, of the non epileptic neocortex on its contralateral homologue in the kainic acid model

PON2 Deficiency Leads to Increased Susceptibility to Diet-Induced Obesity.

(1) Background: Paraoxonase 2 (PON2) is a ubiquitously expressed protein localized to endoplasmic reticulum and mitochondria. Previous studies have shown that PON2 exhibits anti-oxidant and anti-inflammatory functions, and PON2-deficient (PON2-def) mice are more susceptible to atherosclerosis. Furthermore, PON2 deficiency leads to impaired mitochondrial function. (2) Methods: In this study, we examined the susceptibility of PON2-def mice to diet-induced obesity. (3) Results: After feeding of an obesifying diet, the PON2-def mice exhibited significantly increased body weight due to increased fat mass weight as compared to the wild-type (WT) mice. The increased adiposity was due, in part, to increased adipocyte hypertrophy. PON2-def mice had increased fasting insulin levels and impaired glucose tolerance after diet-induced obesity. PON2-def mice had decreased oxygen consumption and energy expenditure. Furthermore, the oxygen consumption rate of subcutaneous fat pads from PON2-def mice was lower compared to WT mice. Gene expression analysis of the subcutaneous fat pads revealed decreased expression levels of markers for beige adipocytes in PON2-def mice. (4) Conclusions: We concluded that altered systemic energy balance, perhaps due to decreased beige adipocytes and mitochondrial dysfunction in white adipose tissue of PON2-def mice, leads to increased obesity in these mice

Noggin depletion in adipocytes promotes obesity in mice.

ObjectiveObesity has increased to pandemic levels and enhanced understanding of adipose regulation is required for new treatment strategies. Although bone morphogenetic proteins (BMPs) influence adipogenesis, the effect of BMP antagonists such as Noggin is largely unknown. The aim of the study was to define the role of Noggin, an extracellular BMP inhibitor, in adipogenesis.MethodsWe generated adipose-derived progenitor cells and a mouse model with adipocyte-specific Noggin deletion using the AdiponectinCre transgenic mouse, and determined the adipose phenotype of Noggin-deficiency.ResultsOur studies showed that Noggin is expressed in progenitor cells but declines in adipocytes, possibly allowing for lipid accumulation. Correspondingly, adipocyte-specific Noggin deletion in vivo promoted age-related obesity in both genders with no change in food intake. Although the loss of Noggin caused white adipose tissue hypertrophy, and whitening and impaired function in brown adipose tissue in both genders, there were clear gender differences with the females being most affected. The females had suppressed expression of brown adipose markers and thermogenic genes including peroxisome proliferator activated receptor gamma coactivator 1 alpha (PGC1alpha) and uncoupling protein 1 (UCP1) as well as genes associated with adipogenesis and lipid metabolism. The males, on the other hand, had early changes in a few BAT markers and thermogenic genes, but the main changes were in the genes associated with adipogenesis and lipid metabolism. Further characterization revealed that both genders had reductions in VO2, VCO2, and RER, whereas females also had reduced heat production. Noggin was also reduced in diet-induced obesity in inbred mice consistent with the obesity phenotype of the Noggin-deficient mice.ConclusionsBMP signaling regulates female and male adipogenesis through different metabolic pathways. Modulation of adipose tissue metabolism by select BMP antagonists may be a strategy for long-term regulation of age-related weight gain and obesity