Microstructural study in heteroepitaxial YBa/sub 2/Cu/sub 3/O/sub 7//Nd/sub 2/CuO/sub 4/ multi-layers by using electron microscopy

Neodymium copper oxide Nd/sub 2/CuO/sub 4/ (NCO) has been applied as a buffer material to improve the epitaxy of YBa/sub 2/Cu/sub 3/O/sub 7/ (YBCO) thin films on reactive substrates and as a potential barrier to construct multi-layer junctions. The microstructures and interfaces in heteroepitaxial Nd/sub 2/CuO/sub 4//YBCO multi-layer have been characterized by using an electron microscopy. Cross-sectional images obtained on a transmission electron microscopy (TEM) revealed an atomically sharp boundary between layers, underlining the excellent compatibility of NCO with YBCO. No chemical reaction occurred between film and substrate. It was found that all layers grow highly epitaxially with their c-axis perpendicular to the substrate surface. On the other hand, various defects such as mis-oriented grains and stacking faults were found near the interfaces.published_or_final_versio

Lithium chloride reinforces the regeneration-promoting effect of chondroitinase ABC on rubrospinal neurons after spinal cord injury

After spinal cord injury, enzymatic digestion of chondroitin sulfate proteoglycans promotes axonal regeneration of central nervous system neurons across the lesion scar. We examined whether chondroitinase ABC (ChABC) promotes the axonal regeneration of rubrospinal tract (RST) neurons following injury to the spinal cord. The effect of a GSK-3β inhibitor, lithium chloride (LiCl), on the regeneration of axotomized RST neurons was also assessed. Adult rats received a unilateral hemisection at the seventh cervical spinal cord segment (C7). Four weeks after different treatments, regeneration of RST axons across the lesion scar was examined by injection of Fluoro-Gold at spinal segment T2, and locomotor recovery was studied by a test of forelimb usage. Injured RST axons did not regenerate spontaneously after spinal cord injury, and intraperitoneal injection of LiCl alone did not promote the regeneration of RST axons. Administration of ChABC at the lesion site enhanced the regeneration of RST axons by 20%. Combined treatment of LiCl together with ChABC significantly increased the regeneration of RST axons to 42%. Animals receiving combined treatment used both forelimbs together more often than animals that received sham or single treatment. Immunoblotting and immunohistochemical analysis revealed that LiCl induced the expression of inactive GSK-3β as well as the upregulation of Bcl-2 in injured RST neurons. These results indicate that in vivo, LiCl inhibits GSK-3β and reinforces the regeneration-promoting function of ChABC through a Bcl-2-dependent mechanism. Combined use of LiCl together with ChABC could be a novel treatment for spinal cord injury.published_or_final_versio

Using the Higgs boson to probe the littlest Higgs model with T-parity through ZHWHZ_H W_H production at the LHC

In the littlest Higgs model with T-parity, the production cross section of the T-odd heavy gauge boson pair $Z_H W_H$ is quite sizable at the LHC. In addition, both the $W_H$ and $Z_H$ bosons have almost exclusively one decay channel into $W A_H$ and $H A_H$ respectively, where the dark matter candidate $A_H$ yields a large missing energy signal. Upon the discovery of the Higgs boson at 125 GeV, we study the discovery sensitivity of the final state $pp \to b\bar{b} l+\rlap{\,/}{E}_T$ to probe the model at the LHC. We find that the standard model backgrounds are manageable by applying suitable kinematic cuts. The LHC running at $\sqrt{s}=14$ TeV with a 100/fb total luminosity is sensitive to the model if the symmetry breaking scale $f$ is below about 850 GeV.Comment: references added: 12 pages, 2 figures, 1 tabl

Copy number gain of granulin-epithelin precursor (GEP) at chromosome 17q21 associates with overexpression in human liver cancer

Background: Granulin-epithelin precursor (GEP), a secretory growth factor, demonstrated overexpression in various human cancers, however, mechanism remain elusive. Primary liver cancer, hepatocellular carcinoma (HCC), ranks the second in cancer-related death globally. GEP controlled growth, invasion, metastasis and chemo-resistance in liver cancer. Noted that GEP gene locates at 17q21 and the region has been frequently reported to be amplified in subset of HCC. The study aims to investigate if copy number gain would associate with GEP overexpression. Methods: Quantitative Microsatellite Analysis (QuMA) was used to quantify the GEP DNA copy number, and fluorescent in situ hybridization (FISH) was performed to consolidate the amplification status. GEP gene copy number, mRNA expression level and clinico-pathological features were analyzed. Results: GEP DNA copy number determined by QuMA corroborated well with the FISH data, and the gene copy number correlated with the expression levels (n = 60, r = 0.331, P = 0.010). Gain of GEP copy number was observed in 20% (12/60) HCC and associated with hepatitis B virus infection status (P = 0.015). In HCC with increased GEP copy number, tight association between GEP DNA and mRNA levels were observed (n = 12, r = 0.664, P = 0.019). Conclusions: Gain of the GEP gene copy number was observed in 20% HCC and the frequency comparable to literatures reported on the chromosome region 17q. Increased gene copy number contributed to GEP overexpression in subset of HCC. © Yung et al; licensee BioMed Central.published_or_final_versio

Configurable Architectures For Multi-mode Floating Point Adders

published_or_final_versio