The finite-temperature magnetism of Ni and permalloy in body-centered-cubic ͑bcc͒ and face-centered-cubic ͑fcc͒ phases is studied theoretically using ab initio supercell calculations and Green's function methods. The results confirm and explain the general experimental trend that the fcc phases have higher Curie temperatures than the bcc counterparts. In addition, the spin-wave stiffness constants of bcc-Ni and bcc-permalloy are predicted.

The Japanese eel (Anguilla japonica) and Nile tilapia (Oreochromis niloticus) 11 -hydroxysteroid dehydrogenase type 2 (11 -HSD2) cDNAs were isolated from their respective testes cDNA libraries. The cDNAs predict two peptides of 436 and 406 amino acid residues that share about 42% homology with mammalian 11 -HSD type 2 proteins. Analysis of the tissue distribution pattern by RT-PCR reveals that 11 -HSD2 is expressed in a wide variety of tissues in tilapia, with higher expression in kidney and gill of both sexes, and with the highest expression in testis. 11 -Dehydrogenase activity of the eel 11 -HSD2 was confirmed by demonstrating the conversion of cortisol to cortisone by the recombinant protein after transient expression of this cDNA clone in COS-1 cells. Bands of ∼2·7 and ∼3·8 Kb were detected in Northern blot of eel and tilapia testes respectively, which is consistent with the cloned cDNA sizes of the two species. Northern blot analysis also revealed that the expression of the eel testis 11 -HSD2 gene could be induced by human chorionic gonadotropin (hCG) injection, implying a role of 11 -HSD2 in hCG-induced 11-ketotestosterone production and spermatogenesis in the Japanese eel.

No abstract

1 found that the risk of death was not significantly higher with tranexamic acid than with placebo among patients undergoing cardiac surgery. This drug has a class IA indication for bleeding prophylaxis, decreasing the use of blood products and the risk of reintervention. Doses that are less than 50 mg per kilogram of body weight are effective in preventing bleeding as well as in decreasing the inflammatory response that is associated with cardiopulmonary bypass. 2Patients with the 5G/G genotype had a greater blood-sparing benefit with the use of tranexamic acid than those with the 4G genotype of the plasminogen-activator inhibitor type 1 polymorphism.3 It will be important for future studies to take into account the pharmacogenomics of tranexamic acid in order to adjust dosing appropriately and to decrease the risk of dose-related adverse effects.

No abstract

Abnormal proliferation of vascular smooth muscle cells (VSMCs) is known to be a key event in the development of atherosclerosis and restenosis. The present study examined the effect of a novel synthetic natriuretic peptide, vasonatrin peptide (VNP), on norepinephrine (NE)-induced proliferation of VSMCs from coronary bypass vessels. Human VSMCs were isolated from an internal mammary artery (IMA) and saphenous vein (SV) by explant culture and stimulated with NE. MTT assay and [3H] thymidine-incorporation were undertaken to analyze cell proliferation and radioimmunoassay was used to determine the level of intracellular cyclic 3’,5’-guanosine monophosphate (cyclic GMP). NE (10-8 - 10-7 mol/l) had a mitogenic effect in human VSMCs from both SV and IMA. However, NE-stimulated proliferation of VSMCs from SV was greater than that from IMA. Furthermore, low concentration of NE (10-10 mol/l) promoted cell growth in SV-derived cells but not in IMA-derived cells. VNP (10-8 - 10-6 mol/l) reduced NE-induced cell proliferation and increased intracellular cyclic GMP, which were abrogated by HS-142-1. In addition, the growth inhibition of VNP was mimicked by 8-bromo-cGMP. These results indicate that VNP has a significant inhibitory effect on NE-stimulated proliferation of human VSMCs from both IMA and SV, which is mediated by guanylate cyclase-linked receptors by increasing cyclic GMP.

No abstract

Age-related cognitive decline, a common component of the brain aging process, is associated with significant impairment in daily functioning and quality of life among geriatric adults. While the complexity of mechanisms underlying cognitive aging are still being elucidated, microbial exposure and the multifactorial inflammatory cascades associated with systemic infections is emerging as a potential driver of neurological senescence. The negative cognitive and neurobiological consequences of a single pathogen-associated inflammatory experience, such as that modeled through treatment with lipopolysaccharide (LPS), are well documented. Yet, the brain aging impacts of repeated, intermittent inflammatory challenges are less well studied. To extend the emerging literature assessing the impact of infection burden on cognitive function among normally aging mice, here, we repeatedly exposed adult mice to intermittent LPS challenges during the aging period. Male 10-month-old C57BL6 mice were systemically administered escalating doses of LPS once every two weeks for 2.5 months. We evaluated cognitive consequences using the non-spatial step-through inhibitory avoidance task and both spatial working and reference memory versions of the Morris water maze. We also probed several potential mechanisms, including cortical and hippocampal cytokine/chemokine gene expression as well as hippocampal neuronal function via extracellular field potential recordings. Though there was limited evidence for an ongoing inflammatory state in cortex and hippocampus, we observed impaired learning and memory and a disruption of hippocampal long-term potentiation. These data suggest that a history of intermittent exposure to LPS-induced inflammation is associated with a subtle but significantly accelerated trajectory of cognitive decline. The broader impact of these findings may have important implications for standard of care involving infections in aging individuals or populations at-risk for dementia.