Summary Obesity-induced inflammation mediated by immune cells in adipose tissue appears to participate in the pathogenesis of insulin resistance. We show that natural killer (NK) cells in adipose tissue play an important role. High fat diet (HFD) increases NK cell numbers and the production of pro-inflammatory cytokines, notably TNFα, in epididymal, but not subcutaneous, fat depots. When NK cells were depleted either with neutralizing antibodies or genetic ablation in E4bp4+/− mice, obesity-induced insulin resistance improved in parallel with decreases in both adipose tissue macrophage (ATM) numbers and ATMs and adipose tissue inflammation. Conversely, expansion of NK cells following IL-15 administration or reconstitution of NK cells into E4bp4−/−mice increased both ATM numbers and adipose tissue inflammation and exacerbated HFD-induced insulin resistance. These results indicate that adipose NK cells control ATMs as an upstream regulator potentially by producing pro-inflammatory mediators including TNFα and thereby contribute to the development of obesity-induced insulin resistance.

Here we show that the B-site cation (Fe/Mo) ordering in the double-perovskite magnetoresistor, Sr 2 FeMoO 6 , is controlled by either kinetics or thermal equilibrium depending on the temperature range. In order to enhance the ordering, long synthesis periods at moderate temperatures are thus required. Employment of a special oxygen-getter-controlled low-O 2 -pressure encapsulation technique for the sample synthesis enabled us to use long heating periods without evident evaporation of Mo, and thereby reach the thermal equilibrium state and a high degree of B-site cation order. For samples fired at 1150 o C for long periods (≥ 36 hours), record-high M S values of 3.7 ∼ 3.9 µ B were obtained.

We describe the first determination of thiol compounds with gold nanocomposites composed of gold nanoparticles and thermoresponsive copolymers having polyamino groups. The gold nanocomposites, which are used as a chromatic sensor, reveal chromatic change from blue to red with thermal stimuli, heating followed by cooling the solution. The blue-to-red chromatic change results from disassembly of the gold nanocomposites, which arises from shrinkage of the thermoresponsive copolymers bound to the gold nanoparticle surfaces due to the phase transition induced by thermal stimuli. The disassembly is inhibited by addition of thiol compounds through displacement of the adhered thermoresponsive copolymers. The detached copolymers no longer influence morphological change of the gold nanocomposites. Corresponding with increase of concentration of the thiol compounds, a solution of the gold nanocomposites after the thermal stimuli shows chromatic change, which was quantified with the a* value in L*a*b* chromatic coordinates. A linear relationship between the a* value and concentration of cysteine, examined as a bio-important thiol, is obtained below 7x10(-6) mol dm(-3), estimating a detection limit defined as 3sigma of the blank to be 2.8x10(-7) mol dm(-3). The chromatic sensor of the gold nanocomposites is applied to the determination of cysteine in commercial supplements containing ascorbic acid, which seriously interferes with redox-based determination of cysteine. Analytical results obtained with the chromatic sensor are identical to those obtained with HPLC.

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Psychostimulants, including amphetamine, act as antihyperkinetic agents in humans with hyperkinetic disorder such as attention-deficit hyperactivity disorder and are known to be effective in enhancing attention-related processes; however, the underlying mechanisms have not been adequately addressed. Mice lacking the Adcyap1 gene encoding the neuropeptide pituitary adenylate cyclase-activating polypeptide (Adcyap1 Ϫ / Ϫ ) display psychomotor abnormalities, including increased novelty-seeking behavior and hyperactivity. In this study, Adcyap1Ϫ / Ϫ mice showed sensory-motor gating deficits, measured as deficits in prepulse inhibition (PPI), and showed normal PPI in response to amphetamine. Amphetamine also significantly decreased hyperlocomotion in Adcyap1 Ϫ / Ϫ mice, and this paradoxical antihyperkinetic effect depended on serotonin 1A (5-HT 1A ) receptor signaling. c-Fos-positive neurons were increased in the prefrontal cortex in amphetamine-treated Adcyap1 Ϫ / Ϫ mice, suggesting increased inhibitory control by prefrontal neurons. Additionally, amphetamine produced an antihyperkinetic effect in wild-type mice that received the 5-HT 1A agonist 8-hydroxy-2-(di-n-propylamino)tetralin. These results indicate that Adcyap1Ϫ / Ϫ mice act as a model of hyperlocomotion and PPI deficits and suggest that 5-HT 1A -mediated pathways are important determinants of the psychostimulant-elicited, rate-dependent effects that are in a negative function of the baseline rate of activity.

Only persistent hyperglycemia and diabetes increased retinal VEGF expression. Some markers of inflammation and oxidative stress were elevated in the retina and systemic circulation of obese and insulin resistant rodents with and without diabetes. Induction of VEGF and its associated retinal pathologies by diabetes requires chronic hyperglycemia and factors in addition to inflammation and oxidative stress.

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