Selection rules for Raman-active electronic excitations in carbon nanotubes

Raman measurements in carbon allotropes are generally associated with the exploration of the vibrational modes. Here, we present a theory of the non-resonant inelastic light scattering accompanied by the excitations of intersubband electron-hole pairs in carbon nanotubes and predict the selection rules and polarization properties of the dominant intersubband Raman active modes.Comment: 4 pages, 3 figure

Signature of electronic excitations in the Raman spectrum of graphene

Inelastic light scattering from Dirac-type electrons in graphene is shown to be dominated by the generation of the inter-band electronic modes which are odd in terms of time-inversion symmetry and belong to the irreducible representation A$_2$ of the point group C$_{6v}$ of the honeycomb crystal. At high magnetic fields, these electron-hole excitations appear as peculiar $n^- \to n^+$ inter-Landau-level modes with energies $\omega_n=2\sqrt{2n} \hbar v/\lambda_B$ and characteristically crossed polarisation of in/out photons.Comment: 4 pages, 2 figures, revised and improve

The three graces in the Tits--Kantor--Koecher category

A metaphor of Jean-Louis Loday describes Lie, associative, and commutative associative algebras as ``the three graces'' of the operad theory. In this article, we study the three graces in the category of $\mathfrak{sl}_2$-modules that are sums of copies of the trivial and the adjoint representation. That category is not symmetric monoidal, and so one cannot apply the wealth of results available for algebras over operads. Motivated by a recent conjecture of the second author and Mathieu, we embark on the exploration of the extent to which that category ``pretends'' to be symmetric monoidal. To that end, we examine various homological properties of free associative algebras and free associative commutative algebras, and study the Lie subalgebra generated by the generators of the free associative algebra.Comment: 17 pages, comments are welcom

Epstein-Barr virus encoded nuclear protein EBNA-3 binds a novel human uridine kinase/uracil phosphoribosyltransferase

BACKGROUND: Epstein-Barr virus (EBV) infects resting B-lymphocytes and transforms them into immortal proliferating lymphoblastoid cell lines (LCLs) in vitro. The transformed immunoblasts may grow up as immunoblastic lymphomas in immuno-suppressed hosts. RESULTS: In order to identify cellular protein targets that may be involved in Epstein-Barr virus mediated B-cell transformation, human LCL cDNA library was screened with one of the transformation associated nuclear antigens, EBNA-3 (also called EBNA-3A), using the yeast two-hybrid system. A clone encoding a fragment of a novel human protein was isolated (clone 538). The interaction was confirmed using in vitro binding assays. A full-length cDNA clone (F538) was isolated. Sequence alignment with known proteins and 3D structure predictions suggest that F538 is a novel human uridine kinase/uracil phosphoribosyltransferase. The GFP-F538 fluorescent fusion protein showed a preferentially cytoplasmic distribution but translocated to the nucleus upon co-expression of EBNA-3. A naturally occurring splice variant of F538, that lacks the C-terminal uracil phosphoribosyltransferase part but maintain uridine kinase domain, did not translocate to the nucleus in the presence of EBNA3. Antibody that was raised against the bacterially produced GST-538 protein showed cytoplasmic staining in EBV negative Burkitt lymphomas but gave a predominantly nuclear staining in EBV positive LCL-s and stable transfected cells expressing EBNA-3. CONCLUSION: We suggest that EBNA-3 by direct protein-potein interaction induces the nuclear accumulation of a novel enzyme, that is part of the ribonucleotide salvage pathway. Increased intranuclear levels of UK/UPRT may contribute to the metabolic build-up that is needed for blast transformation and rapid proliferation

Spectral features due to inter-Landau-level transitions in the Raman spectrum of bilayer graphene

We investigate the contribution of the low-energy electronic excitations towards the Raman spectrum of bilayer graphene for the incoming photon energy Omega >> 1eV. Starting with the four-band tight-binding model, we derive an effective scattering amplitude that can be incorporated into the commonly used two-band approximation. Due to the influence of the high-energy bands, this effective scattering amplitude is different from the contact interaction amplitude obtained within the two-band model alone. We then calculate the spectral density of the inelastic light scattering accompanied by the excitation of electron-hole pairs in bilayer graphene. In the absence of a magnetic field, due to the parabolic dispersion of the low-energy bands in a bilayer crystal, this contribution is constant and in doped structures has a threshold at twice the Fermi energy. In an external magnetic field, the dominant Raman-active modes are the n_{-} to n_{+} inter-Landau-level transitions with crossed polarisation of in/out photons. We estimate the quantum efficiency of a single n_{-} to n_{+} transition in the magnetic field of 10T as I_{n_{-} to n_{+}}~10^{-12}.Comment: 7 pages, 3 figures, expanded version published in PR

Administration of Insurance Rate Regulatory Laws

microRNAs (miRNAs) are key posttranscriptional regulators of gene expression. In the present study, regulation of tumor-suppressor gene D-glucuronyl C5-epimerase (GLCE) by miRNA-218 was investigated. Significant downregulation of miRNA-218 expression was shown in primary breast tumors. Exogenous miRNA-218/anti-miRNA-218 did not affect GLCE mRNA but regulated GLCE protein level in MCF7 breast carcinoma cells in vitro. Comparative analysis showed a positive correlation between miRNA-218 and GLCE mRNA, and negative correlation between miRNA-218 and GLCE protein levels in breast tissues and primary tumors in vivo, supporting a direct involvement of miRNA-218 in posttranscriptional regulation of GLCE in human breast tissue. A common scheme for the regulation of GLCE expression in normal and tumor breast tissues is suggested.Funding Agencies|Russian Foundation for Basic Research|11-04-90400-Ukr_f_a|Ukranian State Foundation of Fundamental Research|F40/146-2011F46/457-2011|Swedish Institute|2011/00888|UICC International Cancer Technology Transfer Fellowship|ICRETT-09-069|FEBS Short-term Fellowship||Karolinska Institute||Swedish Cancer Society||Swedish Research Council||</p

Influence of impurity spin dynamics on quantum transport in epitaxial graphene

Experimental evidence from both spin-valve and quantum transport measurements points towards unexpectedly fast spin relaxation in graphene. We report magnetotransport studies of epitaxial graphene on SiC in a vector magnetic field showing that spin relaxation, detected using weak-localisation analysis, is suppressed by an in-plane magnetic field, $B_{\parallel}$, and thereby proving that it is caused at least in part by spinful scatterers. A non-monotonic dependence of effective decoherence rate on $B_{\parallel}$ reveals the intricate role of scatterers' spin dynamics in forming the interference correction to conductivity, an effect that has gone unnoticed in earlier weak localisation studie

Antiproliferative effect of D-glucuronyl C5-epimerase in human breast cancer cells

<p>Abstract</p> <p>Background</p> <p>D-glucuronyl C5-epimerase (GLCE) is one of the key enzymes in the biosynthesis of heparansulfate proteoglycans. Down-regulation of <it>GLCE </it>expression in human breast tumours suggests a possible involvement of the gene in carcinogenesis. In this study, an effect of <it>GLCE </it>ectopic expression on cell proliferation and viability of breast carcinoma cells MCF7 <it>in vitro </it>and its potential molecular mechanisms were investigated.</p> <p>Results</p> <p><it>D-glucuronyl C5-epimerase </it>expression was significantly decreased in MCF7 cells compared to normal human breast tissue. Re-expression of <it>GLCE </it>inhibited proliferative activity of MCF7 cells according to CyQUANT NF Cell Proliferation Assay, while it did not affect their viability in Colony Formation Test. According to Cancer PathFinder RT Profiler PCR Array, antiproliferative effect of <it>GLCE </it>in <it>vitro </it>could be related to the enhanced expression of tumour suppressor genes р53 (+3.3 fold), E2F1 (+3.00 fold), BRCA1 (+3.5 fold), SYK (+8.1 fold) and apoptosis-related genes BCL2 (+4.2 fold) and NFKB1 (+2.6 fold). Also, <it>GLCE </it>re-expression in MCF7 cells considerably changed the expression of some genes involved in angiogenesis (IL8, +4.6 fold; IFNB1, +3.9 fold; TNF, +4.6 fold and TGFB1, -5.7 fold) and invasion/metastasis (SYK, +8.1 fold; NME1, +3.96 fold; S100A4, -4.6 fold).</p> <p>Conclusions</p> <p>The ability of <it>D-glucuronyl С5-epimerase </it>to suppress proliferation of breast cancer cells MCF7 through the attenuated expression of different key genes involved in cell cycle regulation, angiogenesis and metastasis molecular pathways supports the idea on the involvement of the gene in regulation of breast cancer cell proliferation.</p

Simultaneous down-regulation of tumor suppressor genes RBSP3/CTDSPL, NPRL2/G21 and RASSF1A in primary non-small cell lung cancer

<p>Abstract</p> <p>Background</p> <p>The short arm of human chromosome 3 is involved in the development of many cancers including lung cancer. Three bona fide lung cancer tumor suppressor genes namely <it>RBSP3 </it>(AP20 region),<it>NPRL2 </it>and <it>RASSF1A </it>(LUCA region) were identified in the 3p21.3 region. We have shown previously that homozygous deletions in AP20 and LUCA sub-regions often occurred in the same tumor (P < 10^-6).</p> <p>Methods</p> <p>We estimated the quantity of <it>RBSP3, NPRL2, RASSF1A, GAPDH, RPN1 </it>mRNA and <it>RBSP3 </it>DNA copy number in 59 primary non-small cell lung cancers, including 41 squamous cell and 18 adenocarcinomas by real-time reverse transcription-polymerase chain reaction based on TaqMan technology and relative quantification.</p> <p>Results</p> <p>We evaluated the relationship between mRNA level and clinicopathologic characteristics in non-small cell lung cancer. A significant expression decrease (≥2) was found for all three genes early in tumor development: in 85% of cases for <it>RBSP3</it>; 73% for <it>NPRL2 </it>and 67% for <it>RASSF1A </it>(P < 0.001), more strongly pronounced in squamous cell than in adenocarcinomas. Strong suppression of both, <it>NPRL2 </it>and <it>RBSP3 </it>was seen in 100% of cases already at Stage I of squamous cell carcinomas. Deregulation of <it>RASSF1A </it>correlated with tumor progression of squamous cell (P = 0.196) and adenocarcinomas (P < 0.05). Most likely, genetic and epigenetic mechanisms might be responsible for transcriptional inactivation of <it>RBSP3 </it>in non-small cell lung cancers as promoter methylation of <it>RBSP3 </it>according to NotI microarrays data was detected in 80% of squamous cell and in 38% of adenocarcinomas. With NotI microarrays we tested how often LUCA (<it>NPRL2, RASSF1A</it>) and AP20 (<it>RBSP3</it>) regions were deleted or methylated in the same tumor sample and found that this occured in 39% of all studied samples (P < 0.05).</p> <p>Conclusion</p> <p>Our data support the hypothesis that these TSG are involved in tumorigenesis of NSCLC. Both genetic and epigenetic mechanisms contribute to down-regulation of these three genes representing two tumor suppressor clusters in 3p21.3. Most importantly expression of <it>RBSP3, NPRL2 </it>and <it>RASSF1A </it>was simultaneously decreased in the same sample of primary NSCLC: in 39% of cases all these three genes showed reduced expression (P < 0.05).</p