New isomeric states in the neutron-rich nuclei near the $Z=28\mathrm{}$ and $N=40\mathrm{}$ shell closures have been identified among the reaction products of a $60.3A$ MeV ${}^{86}\mathrm{Kr}$ beam on a ${}^{\mathrm{nat}}\mathrm{Ni}$ target. From the measured isomeric decay properties information about the excited states and their nuclear structure has been obtained. The isomerism is related mostly to the occupation of the neutron $g_{9/2}$ orbital, an intruder level in the $N=3\mathrm{}$ $\mathrm{fp}$ shell. It is illustrated with the decay properties of ${}^{69}{\mathrm{Ni}}^m$, ${}^{70}{\mathrm{Ni}}^m$, and ${}^{71}{\mathrm{Cu}}^m$ interpreted within the nuclear shell model.

It has been recently shown that the Alzheimer9s disease (AD) pathogenic peptide amyloid β_1–42 (Aβ_1–42) binds to the α7 nicotinic acetylcholine receptor (α7nAChR) with high affinity and the α7nAChR and Aβ_1–42 are both found colocalized in neuritic plaques of human brains with AD. Moreover, the intraneuronal accumulation of Aβ_1–42 was shown to be facilitated by its high-affinity binding to the α7nAChR, and α7nAChR activation mediates Aβ-induced tau protein phosphorylation. To test the hypothesis that α7nAChRs are involved in AD pathogenesis, we used a transgenic mouse model of AD overexpressing a mutated form of the human amyloid precursor protein (APP) and lacking the α7nAChR gene (APPα7KO). We have shown that, despite the presence of high amounts of APP and amyloid deposits, deleting the α7nAChR subunit in the mouse model of AD leads to a protection from the dysfunction in synaptic integrity (pathology and plasticity) and learning and memory behavior. Specifically, APPα7KO mice express APP and Aβ at levels similar to APP mice, and yet they were able to solve a cognitive challenge such as the Morris water maze test significantly better than APP, with performances comparable to control groups. Moreover, deleting the α7nAChR subunit protected the brain from loss of the synaptic markers synaptophysin and MAP2, reduced the gliosis, and preserved the capacity to elicit long-term potentiation otherwise deficient in APP mice. These results are consistent with the hypothesis that the α7nAChR plays a role in AD and suggest that interrupting α7nAChR function could be beneficial in the treatment of AD.

This study assessed the potential therapeutic efficacy of adipose-derived stem cells (ASCs) on infarcted hearts. Myocardial infarction was induced in rat hearts by occlusion of the left anterior descending artery (LAD). One week after LAD occlusion, the rats were divided into three groups and subjected to transplantation of ASCs or transplantation of cell culture medium (CCM) or remained untreated. During a 1-mo recovery period, magnetic resonance imaging showed that the ASC-treated hearts had a significantly greater left ventricular (LV) ejection fraction and LV wall thickening than did the CCM-treated and untreated hearts. The capillary density in infarct border zone was significantly higher in the ASC-treated hearts than in the CCM-treated and untreated hearts. However, only 0.5% of the ASCs recovered from the ASC-treated hearts were stained positive for cardiac-specific fibril proteins. It was also found that ASCs under a normal culture condition secreted three cardiac protective growth factors: vascular endothelial growth factor, hepatocyte growth factor, and insulin-like growth factor-1. Results of this study suggest that ASCs were able to improve cardiac function of infarcted rat hearts. Paracrine effect may be the mechanism underlying the improved cardiac function and increased capillary density.