First Step Towards a Devil's Staircase in Spin-Crossover Materials.

The unprecedented bimetallic 2D coordination polymer {Fe[(Hg(SCN)3 )2 ](4,4'-bipy)2 }n exhibits a thermal high-spin (HS)↔low-spin (LS) staircase-like conversion characterized by a multi-step dependence of the HS molar fraction γHS . Between the fully HS (γHS =1) and LS (γHS =0) phases, two steps associated with different ordering appear in terms of spin-state concentration waves (SSCW). On the γHS ≈0.5 step, a periodic SSCW forms with a HS-LS-HS-LS sequence. On the γHS ≈0.34 step, the 4D superspace crystallography structural refinement reveals an aperiodic SSCW, with a HS-LS sequence incommensurate with the molecular lattice. The formation of these different long-range spatially ordered structures of LS and HS states during the multi-step spin-crossover is discussed within the framework of "Devil's staircase"-type transitions. Spatially modulated phases are known in various types of materials but are uniquely related to molecular HS/LS bistability in this case.

Olfactory bulbectomy induced oxidative and cell damage in rat: protective effect of melatonin.

In this study we analyzed the effects of melatonin (Mel, 1 mg/kg ip) on behavioral changes as well as cell and oxidative damage prompted by bilaterally olfactory bulbectomy. Olfactory bulbectomy caused an increase in lipid peroxidation products and caspase-3, whereas it prompted a decrease of reduced glutathione (GSH) content and antioxidative enzymes activities. Additionally, olfactory bulbectomy induced behavioral changes characterized by the enhancement of immobility time in the forced swim test and hyperactivity in the open field test. All these changes were normalized by treatment of Mel (14 days). Our data show that Mel has a beneficial neuropsychiatric action against oxidative stress, cell damage and behavior alterations.

[Not Available]. / Dificultades frecuentes para la acreditación como Hospital Amigo de los Niños: nuestro abordaje.

A good way to promote breastfeeding is to implement the Ten Steps to Successful Breastfeeding of UNICEF. However, this is not an easy task and there are many difficulties prior to success. Based on our experience on the subject, supported by our recent accreditation as a Baby-friendly hospital, we have analyzed various doubts and problems that we think are important in order to enhance breastfeeding in a hospital setting: how to begin, how to train the health personnel and keep them updated, when and how to supplement breastfeeding, how to promote the activity of support groups, how to improve the support to the mother after discharge, how much time may be necessary, etc. Furthermore, we comment on factors that we consider important and that may be essential for success.

Effect of transcranial magnetic stimulation on oxidative stress induced by 3-nitropropionic acid in cortical synaptosomes.

This study evaluates the effect of transcranial magnetic stimulation (TMS; 60 Hz and 0.7 mT) treatment on 3-nitropropionic acid (20 mg/kg i.p./day for 4 days)-induced oxidative stress in cortical synaptosomes of Wistar rats. The oxidative derangement was confirmed by a high level of lipid peroxidation products and protein carbonyls, together with a decreased in reduced glutathione (GSH) content, catalase and GSH-peroxidase (GSH-Px) activities. Additionally, it was observed a reduction in succinate dehydrogenase (SDH) activity. All changes were partially prevented or reversed by administration of TMS. These results show that TMS reduces oxidative stress in cortical synaptosomes, and suggest that TMS may protect neuronal and maintain synaptic integrity.

Protective effect of melatonin on 3-nitropropionic acid-induced oxidative stress in synaptosomes in an animal model of Huntington's disease.

The effect of melatonin (1 mg/kg BW i.p./day) on the oxidative changes produced by 3-nitropropionic acid (20 mg/kg BW/day for 4 days) in rat striatal and cortical synaptosomes was investigated. The effects of 3-nitropropionic acid were evaluated as changes in the quantity of lipid peroxidation products, protein carbonyl groups and superoxide dismutase and succinate dehydrogenase activities. 3-Nitropropionic acid caused a rise in lipid peroxidation levels and protein carbonyls content whereas it induced a reduction in the activity of succinate dehydrogenase and triggered an enhancement in superoxide dismutase activity. These changes were prevented by previous administration of melatonin. Our results reveal: (i) 3-nitropropionic acid induces a status of oxidative stress in some brain regions of the Wistar rat; (ii) melatonin prevents the deleterious effects induced by the acid. In conclusion, the results show the ability of melatonin to modify the neural response to 3-nitropropionic acid with the protective mechanism likely involving the antioxidative processes of melatonin.

Thermal and light induced polymorphism in iron(II) spin crossover compounds.

The spin crossover complexes [Fe[H(2)B(pz)(2)](2)L]([H(2)B(pz)(2)](-)= dihydrobis(pyrazolyl)borate, L = 2,2[prime or minute]-bipyridine (1), bipy and 1,10-phenanthroline, phen (2)) undergo both thermal and light induced spin crossover, but the structure of the low spin and light induced high spin states for are different from that of the thermally induced high spin state and from those of.

Liver hyperplasia and paradoxical regulation of glycogen metabolism and glucose-sensitive gene expression in GLUT2-null hepatocytes. Further evidence for the existence of a membrane-based glucose release pathway.

We investigated the impact of GLUT2 gene inactivation on the regulation of hepatic glucose metabolism during the fed to fast transition. In control and GLUT2-null mice, fasting was accompanied by a approximately 10-fold increase in plasma glucagon to insulin ratio, a similar activation of liver glycogen phosphorylase and inhibition of glycogen synthase and the same elevation in phosphoenolpyruvate carboxykinase and glucose-6-phosphatase mRNAs. In GLUT2-null mice, mobilization of glycogen stores was, however, strongly impaired. This was correlated with glucose-6-phosphate (G6P) levels, which remained at the fed values, indicating an important allosteric stimulation of glycogen synthase by G6P. These G6P levels were also accompanied by a paradoxical elevation of the mRNAs for L-pyruvate kinase. Re-expression of GLUT2 in liver corrected the abnormal regulation of glycogen and L-pyruvate kinase gene expression. Interestingly, GLUT2-null livers were hyperplasic, as revealed by a 40% increase in liver mass and 30% increase in liver DNA content. Together, these data indicate that in the absence of GLUT2, the G6P levels cannot decrease during a fasting period. This may be due to neosynthesized glucose entering the cytosol, being unable to diffuse into the extracellular space, and being phosphorylated back to G6P. Because hepatic glucose production is nevertheless quantitatively normal, glucose produced in the endoplasmic reticulum may also be exported out of the cell through an alternative, membrane traffic-based pathway, as previously reported (Guillam, M.-T., Burcelin, R., and Thorens, B. (1998) Proc. Natl. Acad. Sci. U. S. A. 95, 12317-12321). Therefore, in fasting, GLUT2 is not required for quantitative normal glucose output but is necessary to equilibrate cytosolic glucose with the extracellular space. In the absence of this equilibration, the control of hepatic glucose metabolism by G6P is dominant over that by plasma hormone concentrations.