The carbon coated Permalloy (CPy) nanorods array films with a thickness of 0.5 and 1.5 μm were grown in anodic aluminum oxide porous templates with a diameter of about 15 nm. To verify the ...electromagnetic characteristics of CPy nanorods array in the GHz frequency region, the CPy nanorods were measured by the coplanar waveguide (CPW) method up to 10 GHz. The signal attenuations of the CPy nanorods exhibited about 1 dB/cm at 1 GHz (in pass-band frequency) and about 17–18 dB/cm at 10 GHz (in stop-band frequency), respectively. The wavelengths of the CPy nanorods were shortened about 50 % at 1 GHz in comparison with that of the CPW.
ARD1 is an acetyltransferase with several variants derived from alternative splicing. Among ARD1 variants, mouse ARD1(225) (mARD1(225)), mouse ARD1(235) (mARD1(235)), and human ARD1(235) (hARD1(235)) ...have been the most extensively characterized and are known to have different biological functions. In the present study, we demonstrated that mARD1(225), mARD1(235), and hARD1(235) have conserved autoacetylation activities, and that they selectively regulate distinct roles of ARD1 variants in tumorigenesis. Using purified recombinants for ARD1 variants, we found that mARD1(225), mARD1(235), and hARD1(235) undergo similar autoacetylation with the target site conserved at the Lys136 residue. Moreover, functional investigations revealed that the role of mARD1(225) autoacetylation is completely distinguishable from that of mARD1(235) and hARD1(235). Under hypoxic conditions, mARD1(225) autoacetylation inhibited tumor angiogenesis by decreasing the stability of hypoxia-inducible factor-1α (HIF-1α). Autoacetylation stimulated the catalytic activity of mARD1(225) to acetylate Lys532 of the oxygen-dependent degradation (ODD) domain of HIF-1α, leading to the proteosomal degradation of HIF-1α. In contrast, autoacetylation of mARD1(235) and hARD1(235) contributed to cellular growth under normoxic conditions by increasing the expression of cyclin D1. Taken together, these data suggest that autoacetylation of ARD1 variants differentially regulates angiogenesis and cell proliferation in an isoform-specific manner.
The complex permeabilities of the permalloy nanorods and their composite in nonmagnetic matrix were calculated by the semi-empirical method. The mixture of nanorods with different aspect ratios ...exhibited the broadband frequency behaviors of the permeability. For the near-field conduction noise suppression applications, the electromagnetic wave absorption of the magnetic composite was evaluated by coplanar waveguide method. The permeability and the power loss effects of composite with the aspect ratios of nanorods were evaluated with the change of composite thickness.
Magnetic nanoparticles with a core/shell structure were fabricated by a sol-gel method and following hydrogen reduction process. The reduction process changed the crystal structure of synthesized ...nanoparticles from iron-oxide single phase to iron phase covered with an iron-aluminum oxide shell layer. These nanoparticles were dispersed by homogenizing and ultrasonication in order to form ferromagnetic ink. Using synthesized ink, patterns with soft magnetic properties were successfully printed on Si substrates by a direct printing method.
The purpose of our study is to show the usefulness and safety of sonography transmission gel as an endorectal contrast agent in preoperative rectal MRI for tumor visualization in rectal cancer.
...Sonography transmission gel is an effective and safe endorectal contrast agent for rectal MRI.
Pyramidal neurons in region I of hippocampus proper (CA1) are particularly vulnerable to excitotoxic processes following transient forebrain ischemia. Kynurenic acid (KYNA) is a small molecule ...derived from tryptophan when this amino acid is metabolized through the kynurenine pathway. In the present study, we examined the effects of ischemic preconditioning (IPC) on the immunoreactivity and protein levels of KYNA following 5 min of transient forebrain ischemia in gerbils. The animals were randomly assigned to 4 groups (sham-operated group, ischemia-operated group, IPC + sham-operated group and IPC + ischemia-operated group). IPC was induced by subjecting the gerbils to 2 min of ischemia followed by 1 day of recovery. In the ischemia-operated group, we observed a significant loss of pyramidal neurons in the CA1 stratum pyramidale (SP) at 5 days post-ischemia; however, in the IPC + ischemia-operated group, the pyramidal neurons were well protected. KYNA immunoreactivity in the SP of the ischemia-operated group was significantly altered following ischemia-reperfusion and was very low 5 days following ischemia-reperfusion. In the IPC + ischemia-operated group, however, KYNA immunoreactivity was constitutively detected in the SP of the CA1 region after the ischemic insult. We also found that the alteration pattern of the KYNA protein level in the CA1 region following ischemia was generally similar to the immunohistochemical changes observed. In brief, our findings demonstrated that IPC maintained and even increased KYNA immunoreactivity in the SP of the CA1 region following ischemia-reperfusion. The data from the present study thus indicate that the enhancement of KYNA expression by IPC may be necessary for neuronal survival following transient ischemic injury.
Abstract Young gerbils are much more resistant to transient cerebral ischemia than the adult. In the present study, we observed that about 90% of CA1 pyramidal cells in the adult hippocampus died 4 ...days post-ischemia; however, about 56% of them in the young hippocampus died at 7 days post-ischemia. To compare excitotoxicity between them, we carried out immunoreactivities of NMDA receptor 1 (NMDAR1) and NMDAR2A/B in the hippocampal CA1 region (CA1) induced by 5 min of transient cerebral ischemia in the young and adult gerbils. Their immunoreactivities and protein levels in the young sham-group were much lower than those in the adult sham-group. Four days after ischemia–reperfusion, they were significantly decreased in the adult ischemia-group; however, in the young ischemia-group, they were much higher than those in the adult. Seven days after ischemia–reperfusion, NMDAR1 immunoreactivity and its level in the young were much higher than those in the adult; NMDAR2A/B immunoreactivity and its level in the young were lower than in the adult. In brief, the immunoreactivities of NMDARs were not decreased in the ischemic CA1 region of the young 4 days after transient cerebral ischemia. This finding indicates that longer maintenance of NMDARs may contribute to less and more delayed neuronal death/damage in the young CA1.
Lacosamide, which is a novel antiepileptic drug, has been reported to exert various additional therapeutic effects. The present study investigated the neuroprotective effects of lacosamide against ...transient cerebral ischemia-induced neuronal cell damage in the hippocampal cornu ammonis (CA)-1 region of a gerbil model. Neuronal Nuclei immunohistochemistry demonstrated that pre- and post-surgical treatment (5 min ischemia) with 25 mg/kg lacosamide protected CA1 pyramidal neurons in the lacosamide-treated-ischemia-operated group from ischemic injury 5 days post-ischemia, as compared with gerbils in the vehicle-treated-ischemia-operated group. Furthermore, treatment with 25 mg/kg lacosamide markedly attenuated the activation of astrocytes and microglia in the ischemic CA1 region at 5 days post-ischemia. The results of the present study suggested that pre- and post-surgical treatment of the gerbils with lacosamide was able to protect against transient cerebral ischemic injury-induced CA1 pyramidal neuronal cell death in the hippocampus. In addition, the neuroprotective effects of lacosamide may be associated with decreased activation of glial cells in the ischemic CA1 region.
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