Fabrication of Mesoporous Materials Based on Supramolecular Self-Assembly of Guanosine Monophosphonate-Nickel Chloride (GMP-Ni) for High-Performance Hybrid Supercapacitors.

Supramolecular self-assembly of nickel chloride and guanosine mono-phosphonate (GMP) and nickel (Ni)-based GMP-Ni and their calcinated mesoporous electrode materials GMP-Ni-500 and GMP-Ni-700 at 500 and 700 °C, respectively, have been fabricated. GMP-Ni, GMP-Ni-500, and GMP-Ni-700 are examined for their supercapacitor performance in a three-electrode configuration. The electrochemical tests demonstrate the mesoporous battery-type nature of GMP-Ni-500 which exhibited a specific capacity (Cs) of about 289 C g-1 at 0.5 A g-1 current density. In addition, a cost-effective and simple asymmetric supercapacitor device has been fabricated with battery-type GMP-Ni-500 as a cathode material and capacitive-type activated carbon (AC) as an anodic material. In an operating voltage window of 0 to 1.5 V, hybrid supercapacitors (HSCs) based on GMP-Ni-500//AC exhibited a remarkable performance with a specific capacity (Cs) of 144 C g-1 at 0.5 A g-1. For the HSC device, the maximum of 66% capacity retention has been observed after 5000 charging/discharging cycles at 5 A g-1. Furthermore, the HSC device demonstrates a high energy density of 24 W h kg-1 at a power density of 297 W kg-1. The molecular transformation was established by employing theoretical calculations. These results suggest that our HSC has outstanding potential in technology development for next-generation commercial applications.

Fluoxetine Inhibits Natural Decay of Long-Term Memory via Akt/GSK-3ß Signaling.

Understanding the mechanisms underlying the natural decay of long-term memory can help us find means of extending the duration of long-term memory. However, the neurobiological processes involved in the decay of long-term memory are poorly understood. In the present study, we examined the effect of acute and chronic treatment of fluoxetine on natural decay of long-term memory and the possible mechanism. Late administration of fluoxetine prolonged the persistence of long-term memory in mice, as demonstrated by object location recognition and Barnes maze tests. Fluoxetine altered Akt/glycogen synthase kinase-3ß (GSK-3ß)/ß-catenin signaling in the hippocampus. Late short- and long-term pharmacological inhibition of GSK-3ß mimicked the effect of fluoxetine on memory persistence. Pharmacological inhibition of Akt blocked the effect of fluoxetine on memory persistence. Finally, late infusion of fluoxetine increased hippocampal long-term potentiation (LTP) and pharmacological inhibition of GSK-3ß blocked the natural decline in LTP. These results demonstrate that GSK-3ß might be a key molecule in memory decay process, and fluoxetine extends the period of long-term memory maintenance via Akt/GSK-3ß signaling.

Direct pharmacological Akt activation rescues Alzheimer's disease like memory impairments and aberrant synaptic plasticity.

Amyloid ß (Aß) is a key mediator for synaptic dysfunction and cognitive impairment implicated in Alzheimer's disease (AD). However, the precise mechanism of the toxic effect of Aß is still not completely understood. Moreover, there is currently no treatment for AD. Protein kinase B (PKB, also termed Akt) is known to be aberrantly regulated in the AD brain. However, its potential function as a therapeutic target for AD-associated memory impairment has not been studied. Here, we examined the role of a direct Akt activator, SC79, in hippocampus-dependent memory impairments using Aß-injected as well as 5XFAD AD model mice. Oligomeric Aß injections into the 3rd ventricle caused concentration-dependent and time-dependent impairments in learning/memory and synaptic plasticity. Moreover, Aß aberrantly regulated caspase-3, GSK-3ß, and Akt signaling, which interact with each other in the hippocampus. Caspase-3 and GSK-3ß inhibitor ameliorated memory impairments and synaptic deficits in Aß-injected AD model mice. We also found that pharmacological activation of Akt rescued memory impairments and aberrant synaptic plasticity in both Aß-treated and 5XFAD mice. These results suggest that Akt could be a therapeutic target for memory impairment observed in AD.

Mutational hotspots in the mitochondrial genome of lung cancer.

We determined the somatic mutations in the mitochondrial genomes of 70 lung cancer patients by pair-wise comparative analyses of the normal- and tumor-genome sequences acquired using Affymetrix Mitochondrial Resequencing Array 2.0. The overall mutation rates in lung cancers were Approximately 100 fold higher than those in normal cells, with significant statistical correlation with smoking (p=0.00088). Total of 532 somatic mutations were evenly distributed in 499 positions with very low overall frequency (1.07/bp), but the non-synonymous mutations causing amino acid substitution occurred more frequently (1.83/bp), particularly at two positions, 8701 and 10398 (10.5/bp) that code for ATPase6 and NADH dehydrogenase 3, respectively. Despite the randomness or even distribution of the mutations, these two mutations occurred together in 86% of the cases. The linkage between the two most frequent mutations suggests that they were selected together, possibly due to their cooperative role during cancer development. Indeed, the mutation at 10398 was shown by Canter, Pezzotti, and their colleagues in 2009, as a risk factor for breast cancer. In this study, we identified two potential biomarkers that might be functionally linked together during the development of cancer.

Compression of the trigeminal ganglion produces prolonged nociceptive behavior in rats.

The present study is the first demonstration of prolonged nociceptive behavior in the trigeminal region following compression of the trigeminal ganglion in rats. Experiments were carried out on male Sprague-Dawley rats mounted onto a stereotaxic frame under pentobarbital sodium anesthesia. For compression of the trigeminal ganglion, a 4% agar solution (8microl) was injected into the trigeminal ganglion through a stainless steel injector (24 gauge), which extended 2mm beyond the end of a guide cannula (21 gauge). Following agar injection, the injector and guide cannula were removed. In the control group, rats were sham operated without agar injection. Air-puff thresholds (mechanical allodynia), pin prick responses (mechanical hyperalgesia), and spontaneous scratching behavior were examined 3 days before surgery and at 3, 7, 10, 14, 17, 21, 24, 30, and 40 days after surgery. Data were analyzed using a repeated measures ANOVA followed by multiple group comparisons using the LSD post-hoc test. Air-puff thresholds significantly decreased after compression of the trigeminal ganglion. Mechanical allodynia was established within 3 days and lasted beyond postoperative day 24. Mechanical hyperalgesia was also evident 3 days after compression and persisted until the 40th postoperative day. Although mechanical allodynia and hyperalgesia appeared bilaterally, the ipsilateral side was significantly more sensitive. Intraperitoneal treatment with carbamazepine significantly blocked mechanical allodynia produced by compression of the trigeminal ganglion. These findings suggest that prolonged nociceptive behavior following compression of the trigeminal ganglion may mimic trigeminal neuralgia in this animal model.