Neuroprotective Effect of Insulin-like Growth Factor-II on 1- Methyl-4-Phenyl Pyridinium-Induced Oxidative Damage in Cortical Neuronal Cells

Purpose: To evaluate the receptor-mediated neuroprotective effect of insulin-like growth factor-II (IGFII) on 1-methyl-4-phenyl pyridinium (MPP) induced oxidative damage in adult cortical neuronal cultures.Methods: Adult rats were randomly divided into 5 groups. Cortical neurons were prepared from rats. The cells were exposed to 10 μM of MPP (group 1, G1); MPP + 100 ng/mL of IGF-II (group 2, G2); MPP + IGF in the presence of 20 ng/μL IGF-I analogue (group 3; G3); 5 ng/μL anti-IGF-IIR (group 4; G4); or MPP + IGF II + IGF inhibitor (group 5; G5). The level of reactive oxygen species (ROS), levels of oxidative stress markers, antioxidant enzymes, mitochondrial functional markers were analyzed in the MPP-treated neuronal cells (with or without treatment with IGF-II).Results: The results demonstrate that IGF-II treatment protects MPP-induced toxicity by decreasing ROS production (58.33 %; p ˂ 0.001), AChE levels (50 %), and maintaining the innate antioxidants to near normal levels. The study on oxidative functional markers showed that IGF-II significantly decreased the MPP-induced elevated levels and mitochondrial markers (TBARS, 40 %, LOOH-39.28 %) to near normal levels. Further analysis using inhibitors of IGF-IR (IGF-I analogue) and IGF-IIR (anti- IGF-IIR) showed that involvement of IGF-IIR might have greatly contributed to the neuroprotective effect of IGF-II.Conclusion: IGF-II receptors play a significant role in the neuroprotective mechanism of IGF-II by acting as an antioxidant, thereby reducing the neuro-degeneration induced by oxidative insults. This indicates that IGF-II receptors are a potential target for the treatment of diseases related to imbalance in redox homeostasis.Keywords: Insulin-like Growth Factor-II, Neuronal Cells, 1-Methyl-4-phenyl Pyridinium, Mitochondrial Markers, Oxidative Stress, Neuroprotection, Antioxidan

Management of Extracranial Carotid Artery Aneurysms:17 Years» Experience

AbstractObjectives:a retrospective review of seventeen-year (1980–1996) experience of the management of extracranial carotid artery aneurysms.Patients and methods:sixty-six aneurysms of extracranial carotid artery were seen in 63 patients. The diagnosis was confirmed by angiography in 51 patients and duplex ultrasonography in twelve. Twenty-eight (42%) patients had an atherosclerotic aneurysm, twenty-two (33%) had false aneurysms secondary to trauma, nine were congenital and seven were mycotic. All underwent aneurysm resection with saphenous-vein-graft interposition as the most common means of reconstruction.Results:one death occurred due to septicaemia in a diabetic patient with a mycotic aneurysm, giving an operative mortality of 1.5%. One patient had an immediate hemiparesis after carotid artery ligation, and three had a hemiparesis within 48 hours of operation (6.1%). After a change in technique to avoid a residual carotid stump, no further neurological problems were encountered in the following 28 patients.Conclusion:extracranial carotid aneurysms may be successfully managed with resection and reconstruction with autogenous saphenous vein. End-to-side anastomosis avoids a blind-ending stump which may be the source of emboli

Localized-Surface-Plasmon Enhanced the 357 nm Forward Emission from ZnMgO Films Capped by Pt Nanoparticles

The Pt nanoparticles (NPs), which posses the wider tunable localized-surface-plasmon (LSP) energy varying from deep ultraviolet to visible region depending on their morphology, were prepared by annealing Pt thin films with different initial mass-thicknesses. A sixfold enhancement of the 357 nm forward emission of ZnMgO was observed after capping with Pt NPs, which is due to the resonance coupling between the LSP of Pt NPs and the band-gap emission of ZnMgO. The other factors affecting the ultraviolet emission of ZnMgO, such as emission from Pt itself and light multi-scattering at the interface, were also discussed. These results indicate that Pt NPs can be used to enhance the ultraviolet emission through the LSP coupling for various wide band-gap semiconductors

Long-term deformation monitoring of metro-tunnel airshaft excavation during construction stage

Version of RecordPublishe

Discriminating Astragali Radix from its adulterants using HPLC coupled with chemometric clustering techniques

Author name used in this publication: Da-Jian YangVersion of RecordPublishe

Transcriptional and Post-Transcriptional Mechanisms for Oncogenic Overexpression of Ether À Go-Go K+ Channel

The human ether-à-go-go-1 (h-eag1) K+ channel is expressed in a variety of cell lines derived from human malignant tumors and in clinical samples of several different cancers, but is otherwise absent in normal tissues. It was found to be necessary for cell cycle progression and tumorigenesis. Specific inhibition of h-eag1 expression leads to inhibition of tumor cell proliferation. We report here that h-eag1 expression is controlled by the p53−miR-34−E2F1 pathway through a negative feed-forward mechanism. We first established E2F1 as a transactivator of h-eag1 gene through characterizing its promoter region. We then revealed that miR-34, a known transcriptional target of p53, is an important negative regulator of h-eag1 through dual mechanisms by directly repressing h-eag1 at the post-transcriptional level and indirectly silencing h-eag1 at the transcriptional level via repressing E2F1. There is a strong inverse relationship between the expression levels of miR-34 and h-eag1 protein. H-eag1antisense antagonized the growth-stimulating effects and the upregulation of h-eag1 expression in SHSY5Y cells, induced by knockdown of miR-34, E2F1 overexpression, or inhibition of p53 activity. Therefore, p53 negatively regulates h-eag1 expression by a negative feed-forward mechanism through the p53−miR-34−E2F1 pathway. Inactivation of p53 activity, as is the case in many cancers, can thus cause oncogenic overexpression of h-eag1 by relieving the negative feed-forward regulation. These findings not only help us understand the molecular mechanisms for oncogenic overexpression of h-eag1 in tumorigenesis but also uncover the cell-cycle regulation through the p53−miR-34−E2F1−h-eag1 pathway. Moreover, these findings place h-eag1 in the p53−miR-34−E2F1−h-eag1 pathway with h-eag as a terminal effecter component and with miR-34 (and E2F1) as a linker between p53 and h-eag1. Our study therefore fills the gap between p53 pathway and its cellular function mediated by h-eag1

Nanoscale phase separation of antiferromagnetic order and superconductivity in K0.75_{0.75}Fe1.75_{1.75}Se2_2

We report an in-plane optical spectroscopy study on the iron-selenide superconductor K$_{0.75}$Fe$_{1.75}$Se$_2$. The measurement revealed the development of a sharp reflectance edge below T$_c$ at frequency much smaller than the superconducting energy gap on a relatively incoherent electronic background, a phenomenon which was not seen in any other Fe-based superconductors so far investigated. Furthermore, the feature could be noticeably suppressed and shifted to lower frequency by a moderate magnetic field. Our analysis indicates that this edge structure arises from the development of a Josephson-coupling plasmon in the superconducting condensate. Together with the transmission electron microscopy analysis, our study yields compelling evidence for the presence of nanoscale phase separation between superconductivity and magnetism. The results also enable us to understand various seemingly controversial experimental data probed from different techniques.Comment: 6 figures, published versio

Observation of a ppb mass threshoud enhancement in \psi^\prime\to\pi^+\pi^-J/\psi(J/\psi\to\gamma p\bar{p}) decay

The decay channel $\psi^\prime\to\pi^+\pi^-J/\psi(J/\psi\to\gamma p\bar{p})$ is studied using a sample of $1.06\times 10^8$ $\psi^\prime$ events collected by the BESIII experiment at BEPCII. A strong enhancement at threshold is observed in the $p\bar{p}$ invariant mass spectrum. The enhancement can be fit with an $S$-wave Breit-Wigner resonance function with a resulting peak mass of $M=1861^{+6}_{-13} {\rm (stat)}^{+7}_{-26} {\rm (syst)} {\rm MeV/}c^2$ and a narrow width that is $\Gamma<38 {\rm MeV/}c^2$ at the 90% confidence level. These results are consistent with published BESII results. These mass and width values do not match with those of any known meson resonance.Comment: 5 pages, 3 figures, submitted to Chinese Physics