T. Xu

Neuroprotection against ischemic brain injury by a small peptide inhibitor of c-Jun N-terminal kinase (JNK) via nuclear and non-nuclear pathways

Our previous studies and the others have strongly suggested that c-Jun N-terminal kinase (JNK) signaling pathway plays a critical role in ischemic brain injury. Here we reported that Tat-JNK binding domain (JBD) of JNK-interacting protein-1 (JIP-1), a smaller 11-mer peptide corresponding to residues 153-163 of murine JIP-1 conjugated to Tat peptide, perturbed the assembly of JIP-1-JNK3 complexes, thus inhibiting the activation of JNK3 induced by ischemia/reperfusion in the vulnerable hippocampal CA1 subregion. As a result, Tat-JBD diminished the increased phosphorylation of c-Jun (a nuclear substrate of JNK) and the increased expression of Fas ligand induced by ischemia/reperfusion in the vulnerable hippocampal CA1 subregion. At the same time, through inhibiting phosphorylation of Bcl-2 (a cytosolic target of JNK) and the release of Bax from Bcl-2/Bax dimers, Tat-JBD attenuated Bax translocation to mitochondria and the release of cytochrome c induced by ischemia/reperfusion. Furthermore, the activation of caspase3 and hydrolyzation of poly-ADP-ribose-polymerase induced by brain ischemia/reperfusion were also significantly suppressed by preinfusion of the peptide Tat-JBD. Importantly, Tat-JBD showed neuroprotective effects on ischemic brain damage in vivo, and administration of the peptide after ischemia also achieved the same effects as preinfusion of the peptide did. Thus, our findings imply that Tat-JBD induced neuroprotection against ischemia/reperfusion in rat hippocampal CA1 region via inhibiting nuclear and non-nuclear pathways of JNK signaling. Taken together, these results indicate that Tat-JBD peptide provides a promising therapeutic approach for ischemic brain injury.

Characterization of hydrogenated diamond-like carbon films electrochemically deposited on a silicon substrate

Diamond-like carbon (DLC) films were deposited on a Si substrate by electrolysis in a methanol solution at ambient pressure and low temperature. The morphology and microstructure of the resulting DLC films were analysed using atomic force microscopy, Raman spectroscopy, Fourier transformation infrared spectrometry, x-ray photoelectron spectroscopy (XPS), and x-ray excited Auger electron spectroscopy (XAES). The surface energy and mechanical properties of the DLC films were examined, and the growth mechanism of the DLC films in liquid phase electro-deposition is discussed as well. The results of the study show that the hydrogenated diamond-like carbon films are smooth and compact. The percentage of sp3 carbon in the DLC films is determined as 55?60%, based on the corresponding XPS and first-derivative XAES spectra of graphite, diamond, and the tested films. The DLC films show low surface free energy, good mechanical properties, excellent friction?reduction and wear-resistance. It is suggested that methanol dissociates to generate the active species of and C2H4 at high voltage applied to the electrode, followed by the generation of the alkyl chain [?CH2?CH2?]n whose C?C and C?H bond lengths and C?C?C and H?C?H bond angles are close to that of diamond. Subsequently, a diamond-like structure was formed by the ordered dehydrogenation of a short-chain [?CH2?CH2?]n in the electrolysis process.

Blue emission and Raman scattering spectrum from AlN nanocrystalline powders

Photoluminescence and Raman scattering spectra from AIN nanocrystalline powders are studied. A blue emission band centered at 420 nm (2.95 eV) is observed. This band may be ascribed to the transition from the shallow level of V-N to the ground state of the deep level of the V-Al(3-)-3 x O-N(+) defect complexes. A phonon structure resulting fi om the transition from the shallow level to the excited states of the deep level is also observed. The broadening of peaks and the low-wave-number-shift of the phonon frequency observed on the Raman scattering spectra are the result of nano-sized effects

Structure and Heat Capacity of Wurtzite GaN from 113 to 1073 K

High pure wurtzite structure GaN has been synthesized by gas reaction method. Its structure was determined by powder x-ray diffraction using the Rietveld technique. The heat capacity C-p was measured from 113 to 1073 K, which can be represented by C-p = 0.362 + 3.010 x 10(-4)T - 3.411 x 10(3)T(-2) - 7.791 x 10(-8)T(2). NO measurable phase transition was observed in this temperature range.

MECHANISMS OF MODULATION OF PREGNANOLONE ON GLYCINERGIC RESPONSE IN CULTURED SPINAL DORSAL HORN NEURONS OF RAT

The glycine receptors and neurosteroids in spinal cord are both implicated in nociceptive signal processing. However, the modulatory effects of neurosteroid pregnanolone (5beta-pregnan-3alpha-ol-20-one) on native glycine receptors remain unclear. In the present study, we examined the effects of pregnanolone and its three isomers on glycine receptors by using whole-cell patch-clamp technique. Our results showed that pregnanolone reversibly inhibited the amplitude of glycine-induced current mediated by native glycine receptors and recombinant alpha1-, alpha2-, alpha3- and alpha1beta-glycine receptors. In cultured spinal dorsal horn neurons of rats, pregnanolone inhibited the glycine-induced current in dose-dependent manner, with an antagonist concentration inducing half-maximal response of 1.0+/-0.3 microM. The inhibitory effect of pregnanolone on glycine-induced current was voltage-independent and pregnanolone shifted the concentration-response curve for glycine-induced current rightward in a parallel manner without altering the maximal value and Hill coefficient. The isomer of pregnanolone, allopregnanolone (5alpha-pregnan-3alpha-ol-20-one) slightly enhanced glycine-induced current, whereas iso-pregnanolone (5beta-pregnan-3beta-ol-20-one) and iso-allopregnanolone (5alpha-pregnan-3beta-ol-20-one) did not affect the glycine-induced current significantly in cultured spinal dorsal horn neurons. Thus, our results suggest that the inhibitory effect of pregnanolone on glycine-induced current is of a competitive type and depends on the stereo structure of pregnanolone. Furthermore, pregnanolone decreased the amplitude and frequency of the glycinergic miniature inhibitory postsynaptic currents. Through modulating the glycinergic inhibitory neurotransmission, pregnanolone may affect the nociceptive sensory processing under physiological and pathological conditions.

Synthesis and structure of nanocrystal-assembled bulk GaN

A new condensed form of GaN, nanocrystal-assembled bulk (NAB) GaN, was obtained directly from reactions of metal Ga and NH4Cl in liquid ammonia at 350-500 degrees C. High-resolution transmission electron microscopy observations reveal that the NAB GaN consists of well-crystallized nanocrystals with wurtzite structure. The synchronous densificated NAB GaN is transparent to visible light while the constituted nanocrystals have an average size of about 12 nm. A possible synthesis mechanism is discussed

Absence of GABA type A signaling in adult medial habenular neurons.

Neural inhibition in the brain is mainly mediated by ionotropic GABA type A receptors. Apart from the GABA type A receptors, both K(+)-Cl(-) cotransporter isoform 2 and the GABA-synthesizing enzyme, glutamic acid decarboxylase, are essential determinants for GABA type A receptor-mediated inhibition. By using immunofluorescent staining, we observed that K(+)-Cl(-) cotransporter isoform 2, GABA type A receptor beta2/3 subunits and a presynaptically localized glutamic acid decarboxylase isoform, glutamic acid decarboxylase 65, were all absent in adult Sprague-Dawley rat medial habenular nucleus, while immunopositive staining for glutamic acid decarboxylase 67, GABA and GABA type B receptor type 2 subunit were present in the medial habenular nucleus. Consistent with the lack of GABA type A signaling as detected by immunohistochemistry, GABA (100 muM) evoked no measurable currents in the medial habenular nucleus but induced bicuculline-sensitive currents in the lateral habenular nucleus and in the CA1 area of hippocampus. We also failed to record miniature inhibitory postsynaptic currents in medial habenular nucleus neurons. These results support the idea that GABAergic transmission in medial habenular nucleus is probably not mediated by any of the most common GABA type A receptor subtypes. Our data suggest that GABA type B receptor-mediated inhibition may play a role in balancing neuronal excitation in this special region. Further exploration for factors determining medial habenular nucleus neural inhibition will lead to a more complete understanding of control of synaptic balance in the CNS.

Ischemic preconditioning negatively regulates plenty of SH3s–mixed lineage kinase 3–Rac1 complex and c-Jun N-terminal kinase 3 signaling via activation of Akt

Activation of Akt/protein kinase B has been recently reported to play an important role in ischemic tolerance. We here demonstrate that the decreased protein expression and phosphorylation of phosphatase and tensin homolog deleted from chromosome 10 (PTEN) underlie the increased Akt-Ser-473 phosphorylation in the hippocampal CA1 subfield in ischemic preconditioning (IPC). Co-immunoprecipitation analysis reveals that Akt physically interacts with Rac1, a small Rho family GTPase required for mixed lineage kinase 3 (MLK3) autophosphorylation, and both this interaction and Rac1-Ser-71 phosphorylation induced by Akt are promoted in preconditioned rats. In addition, we show that Akt activation results in the disassembly of the plenty of SH3s (POSH)-MLK3-Rac1 signaling complex and down-regulation of the activation of MLK3/c-Jun N-terminal kinase (JNK) pathway. Akt activation results in decreased serine phosphorylation of 14-3-3, a cytoplasmic anchor of Bax, and prevents ischemia-induced mitochondrial translocation of Bax, release of cytochrome c, and activation of caspase-3. The expression of Fas ligand is also decreased in the CA1 region. Akt activation protects against apoptotic neuronal death as shown in TUNEL staining following IPC. Intracerebral infusion of LY294002 before IPC reverses the increase in Akt phosphorylation and the decrease in JNK signaling activation, as well as the neuroprotective action of IPC. Our results suggest that activation of pro-apoptotic MLK3/JNK3 cascade can be suppressed through activating anti-apoptotic phosphoinositide 3-kinase/Akt pathway induced by a sublethal ischemic insult, which provides a functional link between Akt and the JNK family of stress-activated kinases in ischemic tolerance.

Synthesis, Raman scattering, and infrared spectra of a new condensed form of GaN nanophase material

A new form of transparent condensed nanophase material of GaN was synthesized directly by ammono-thermal synthetic route. Nano-sized effects and thermal stability of that material were investigated through Raman scattering and infrared spectra. Compared with bulk GaN, we observed the Raman low-energy-shift of the phonon frequency of E-2(high) and the transverse optical mode [E-1(TO)], the infrared high-energy-shift of omega(T), and the variation of relative intensity I-E2/E1(TO). These characteristics can be attributed to the existence Of the interface effects and the vacancy of N in the GaN nanophase material. This material has a high thermal stability even at 900 degrees C as indicated through infrared and Raman spectral investigation of annealed samples of as-synthesized nanophase material.

Tribological behavior of gradient modified layer on 2024 aluminum alloy modified by plasma-based ion implantation

The N-pre-implanted 2024 aluminum alloy was implanted with Ti and N, or implanted with Ti, and then with Ti and N by plasma-based ion implantation (PBII) to form two gradient layers, respectively. The composition depth profiles of the gradient layers were characterized by X-ray photoelectron spectroscopy. A series of ball-on-disk wear experiments have been carried out in ambient air, to investigate the tribological behavior of the gradient layer against steel ball under dry and un-lubricated conditions, employing various applied loads and a constant sliding speed. The results revealed that tribological properties of the gradient layers were improved markedly in contrast with those of the unmodified sample, and strongly dependent on their composition depth profiles. The gradient layer implanted with Ti, and then with Ti and N was much thicker and contains higher N, thus it corresponded to higher hardness which slowly decrease from surface to substrate and the optimal tribological properties including higher load carrying capacity. As load was increasing, the tribological properties decreased, and the adhesive degree increased since the gradient layer became thinner rapidly. Of course, more proper gradient layers will be obtained as the qualified candidates in some particular engineering applications by optimizing PBII parameters.