3,285 research outputs found

    Bee venom attenuates neuroinflammatory events and extends survival in amyotrophic lateral sclerosis models

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    <p>Abstract</p> <p>Background</p> <p>Amyotrophic lateral sclerosis (ALS) is a disease affecting the central nervous system that is either sporadic or familial origin and causing the death of motor neurons. One of the genetic factors contributing to the etiology of ALS is mutant SOD1 (mtSOD1), which induces vulnerability of motor neurons through protein misfolding, mitochondrial dysfunction, oxidative damage, cytoskeletal abnormalities, defective axonal transport, glutamate excitotoxicity, inadequate growth factor signaling, and neuroinflammation. Bee venom has been used in the practice of Oriental medicine and evidence from the literature indicates that BV plays an anti-inflammatory or anti-nociceptive role against inflammatory reactions associated with arthritis and other inflammatory diseases. The purpose of the present study was to determine whether bee venom suppresses motor neuron loss and microglial cell activation in hSOD1<sup>G93A </sup>mutant mice.</p> <p>Methods</p> <p>Bee venom (BV) was bilaterally injected (subcutaneously) into a 14-week-old (98 day old) male hSOD1<sup>G93A </sup>animal model at the Zusanli (ST36) acupoint, which is known to mediate an anti-inflammatory effect. For measurement of motor activity, rotarod test was performed and survival statistics were analyzed by Kaplan-Meier survival curves. The effects of BV treatment on anti-neuroinflammation of hSOD1<sup>G93A </sup>mice were assessed via immunoreactions using Iba 1 as a microglia marker and TNF-α antibody. Activation of ERK, Akt, p38 MAP Kinase (MAPK), and caspase 3 proteins was evaluated by western blotting.</p> <p>Results</p> <p>BV-treated mutant hSOD1 transgenic mice showed a decrease in the expression levels of microglia marker and phospho-p38 MAPK in the spinal cord and brainstem. Interestingly, treatment of BV in symptomatic ALS animals improved motor activity and the median survival of the BV-treated group (139 ± 3.5 days) was 18% greater than control group (117 ± 3.1 days). Furthermore, we found that BV suppressed caspase-3 activity and blocked the defects of mitochondrial structure and cristae morphology in the lumbar spinal cord of hSOD1<sup>G93A </sup>mice at the symptomatic stage.</p> <p>Conclusion</p> <p>From these findings, our research suggests BV could be a potential therapeutic agent for anti-neuroinflammatory effects in an animal model of ALS.</p

    FuelCell2009-85133 THE APPLICATION OF A PORTABLE DMFCS STACK WITH FRACTAL CURRENT COLLECTORS USING HILBERT GEOMETRY FOR A CHARGER SYSTEM

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    ABSTRACT The study develops a portable charger platform that contains a direct methanol fuel cell (DMFC) consisting of a set of planar DMFCs with current collectors, Fractal Hilbert Geometry and a power balance plant (BOP). The third order Hilbert geometry is used for the 35×35 mm2 current collectors. The system output design is set at 5V controlled by a power balance plant applied to 3C low power products. This paper discusses the Methanol feed rate, air flow rate, bipolar plate thickness and power balance plant layout for DMFC performance. To evaluate the reliability and efficiency of the DMFC power source, a data acquisition (DAQ) system connected to a real time monitor is used to assess the current and voltage output from the DMFC system while running different parameters. The results show the current of the charger system obtain 84 mA and 103 mA under 2V and 3V input voltage converters respectively. The transform efficiency for power balance plant is up to about 84% for 3V input voltage converter

    Synthesis of large-area multilayer hexagonal boron nitride for high material performance

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    Although hexagonal boron nitride (h-BN) is a good candidate for gate-insulating materials by minimizing interaction from substrate, further applications to electronic devices with available two-dimensional semiconductors continue to be limited by flake size. While monolayer h-BN has been synthesized on Pt and Cu foil using chemical vapour deposition (CVD), multilayer h-BN is still absent. Here we use Fe foil and synthesize large-area multilayer h-BN film by CVD with a borazine precursor. These films reveal strong cathodoluminescence and high mechanical strength (Young’s modulus: 1.16±0.1 TPa), reminiscent of formation of high-quality h-BN. The CVD-grown graphene on multilayer h-BN film yields a high carrier mobility of ~24,000 cm[superscript 2] V[superscript −1] s[superscript −1] at room temperature, higher than that (~13,000 [superscript 2] V[superscript −1] s[superscript −1]) with exfoliated h-BN. By placing additional h-BN on a SiO[subscript 2]/Si substrate for a MoS[subscript 2] (WSe[subscript 2]) field-effect transistor, the doping effect from gate oxide is minimized and furthermore the mobility is improved by four (150) times.Korea Institute of Science and Technology. Institutional ProgramNational Science Foundation (U.S.) (STC Center for Integrated Quantum Materials Grant DMR-1231319)Massachusetts Institute of Technology. Institute for Soldier Nanotechnologie

    Effects of Bee Venom on Glutamate-Induced Toxicity in Neuronal and Glial Cells

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    Bee venom (BV), which is extracted from honeybees, is used in traditional Korean medical therapy. Several groups have demonstrated the anti-inflammatory effects of BV in osteoarthritis both in vivo and in vitro. Glutamate is the predominant excitatory neurotransmitter in the central nervous system (CNS). Changes in glutamate release and uptake due to alterations in the activity of glutamate transporters have been reported in many neurodegenerative diseases, including Parkinson's disease, Alzheimer's disease, and amyotrophic lateral sclerosis. To assess if BV can prevent glutamate-mediated neurotoxicity, we examined cell viability and signal transduction in glutamate-treated neuronal and microglial cells in the presence and absence of BV. We induced glutamatergic toxicity in neuronal cells and microglial cells and found that BV protected against cell death. Furthermore, BV significantly inhibited the cellular toxicity of glutamate, and pretreatment with BV altered MAP kinase activation (e.g., JNK, ERK, and p38) following exposure to glutamate. These findings suggest that treatment with BV may be helpful in reducing glutamatergic cell toxicity in neurodegenerative diseases

    Methylphenidate Use and Infectious Diseases in Children With Attention Deficit and Hyperactivity Disorder:A Population-Based Study

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    Objective: Children with attention deficit hyperactivity disorder (ADHD) have more visits to the emergency department (ED) due to injuries than those without ADHD. However, no study has investigated whether children with ADHD have more ED visits or hospitalizations due to infectious diseases (IDs) and whether methylphenidate (MPH) treatment may reduce the risk. Method: The incidence of ID-related ED visits or hospitalizations was defined as the main outcome. The Cox regression and conditional Poisson regression models were calculated to estimate hazard ratios (HRs) in the population level and relative risks for the self-controlled case series design, respectively. Results: Children with ADHD had higher rates of emergency visits (HR = 1.25, 95% CI: 1.23~1.27) and hospitalizations (HR = 1.28, 95% CI: 1.26~1.31) due to IDs than those without ADHD. In the ADHD subgroup, those who received MPH treatment have a reduced risk of emergency visits (HR = 0.10, 95% CI: 0.09~0.10) and hospitalizations (HR = 0.73, 95% CI: 0.71~0.75), compared to those without treatment. The risk of ID-related emergency visits decreased to 0.21 (95% CI: 0.21~0.22); and hospitalizations decreased to 0.71 (95% CI: 0.69~0.73). Within self-controlled analysis, it is demonstrated that compared with non-MPH exposed period, children with ADHD had significantly decreased risks for infection-related emergency visits (RR = 0.73, 95% CI: 0.68~0.78) or hospitalizations (RR = 0.19, 95% CI: 0.17~0.21) during MPH-exposed periods. Conclusions and Relevance: This is the first study that reported an increased risk of ID-related healthcare utilizations in children with ADHD compared to those without, and that such risks may be significantly reduced in ADHD children that received MPH treatment.</p

    Tetraarsenic Hexoxide Induces Beclin-1-Induced Autophagic Cell Death as well as Caspase-Dependent Apoptosis in U937 Human Leukemic Cells

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    Tetraarsenic hexaoxide (As4O6) has been used in Korean folk remedy for the treatment of cancer since the late 1980s, and arsenic trioxide (As2O3) is currently used as a chemotherapeutic agent. However, evidence suggests that As4O6-induced cell death pathway was different from that of As2O3. Besides, the anticancer effects and mechanisms of As4O6 are not fully understood. Therefore, we investigated the anticancer activities of As4O6 on apoptosis and autophagy in U937 human leukemic cells. The growth of U937 cells was inhibited by As4O6 treatment in a dose- and a time-dependent manner, and IC50 for As4O6 was less than 2 μM. As4O6 induced caspase-dependent apoptosis and Beclin-1-induced autophagy, both of which were significantly attenuated by Bcl-2 augmentation and N-acetylcysteine (NAC) treatment. This study suggests that As4O6 should induce Beclin-1-induced autophagic cell death as well as caspase-dependent apoptosis and that it might be a promising agent for the treatment of leukemia
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