Absorption spectra and chirality of single-walled 4 Å carbon nanotubes

Absorption spectrum of recently discovered single-walled 4 Å carbon nanotubes is measured. The semiempirical PM3 localized-density-matrix method is employed to evaluate the absorption spectra of three possible 4 Å single-walled carbon nanotubes, (3,3), (4,2), and (5,0). Both experimental and calculated results reveal that these nanotubes have finite optical gaps and strong anisotropic optical responses. When the electric field is perpendicular to the nanotubes, they are transparent to visible lights; and this is confirmed and explained by the calculations. Compared to the measured absorption spectrum, calculated absorption spectra are used to determine the chirality of the nanotubes synthesized in the channels of porous zeolites. © 2002 American Institute of Physics.published_or_final_versio

Effect of dc bias on the Curie-Weiss exponent in 0.76Pb(Mg[sub ⅓]Nb[sub ⅔]) O₃-0.24PbTiO₃ ferroelectric single crystal

2004-2005 > Academic research: refereed > Publication in refereed journalVersion of RecordPublishe

Physical mapping of a powdery mildew resistance related gene Hv-S/TPK by FISH with a TAC clone in wheat

Dissertação de mestrado integrado em Medicina (Hematologia), apresentado á Faculdade de Medicina da Universidade de Coimbra.A Policitemia Vera (PV) é uma doença clonal de etiologia desconhecida, na maior parte dos casos, que envolve a célula estaminal progenitora hematopoiética multipotencial. É uma neoplasia mieloproliferativa crónica (NMP) que se caracteriza pela expansão das três linhas celulares hematopoiéticas: eritróide, granulocítica e megacariocítica, com predomínio da primeira, de modo independente dos mecanismos normais de regulação da eritropoiese. Além disso, as células têm aspecto morfológico normal, a fibrose medular é pouco significativa e os níveis de eritropoietina (Epo) são habitualmente normais a baixos. Além da hipercelularidade medular com sobreprodução de uma ou de todas as linhas celulares, a doença cursa com hematopoiese extramedular, hiperviscosidade, propensão para complicações como trombose ou hemorragia e risco de desenvolvimento de mielofibrose ou transformação em leucemia aguda. A descrição relativamente recente da associação de uma mutação no gene JAK2, localizado no cromosoma 9p24, com as doenças mieloproliferativas clássicas negativas para BCR-ABL, como a PV, veio permitir avanços significativos na compreensão da patofisiologia deste grupo de doenças hematológicas. A mutação provoca uma alteração do aminoácido V (valina) para F (fenilalanina) na posição 617 (JAK2V617F). De acordo com os dados publicados, a frequência da detecção da mutação JAK2V617F em doentes com PV é de cerca de 95%. A proteína JAK2 é uma tirosina cinase citoplasmática, que se encontra associada ao domínio intracelular dos receptores de citocinas (como a Epo e trombopoietina - Tpo), e de factores de crescimento, essenciais para a função destes receptores. A mutação da JAK2 conduz à activação constitutiva dos receptores, independente da ligação à respectiva citocina e/ou hipersensibilidade a factores de crescimento, com consequente activação de múltiplas vias de sinalização intracelulares como a JAK/STAT (Janus Kinase/Signal Transductor and activator of transcription), a PI3K (fosfatidilinositol 3 cinase) e a MAPK (proteína cinase activadora de mitose), envolvidas na transformação e proliferação dos progenitores hematopoiéticos. Por outro lado, as células evidenciam alteração na diferenciação terminal e resistência à apoptose in vitro que poderá estar relacionada com o aumento da expressão da proteína anti-apoptótica Bcl-XL. Além dos avanços no diagnóstico, a detecção da mutação JAK2V617F tem contribuido para melhorar a classificação e a terapêutica dos doentes com PV. Deste modo, o conhecimento dos mecanismos moleculares envolvidos na PV tem levado os investigadores à descoberta de novos fármacos dirigidos ao defeito molecular, permitindo novas abordagem terapêuticas mais eficazes e provavelmente de menor toxicidade. Este trabalho procura fazer uma revisão sobre o actual conhecimento da caracterização molecular e clínica da PV e quais as suas implicações no diagnóstico e abordagem terapêutica desta NMP.Polycythemia Vera (PV) is a clonal disease of unknown etiology, which often involves the pluripotential hematopoietic stem cell. This disease integrates the family of chronic myeloproliferative neoplasm (MPN) and is characterized by the growth of the three hematopoietic celular lineages: granulocytic, megakaryocytic and erythroid, with predominance of the last one and regardless the normal mechanisms of erythropoiesis regulation. Moreover, cells have normal morphological aspect, bone marrow shows slight fibrosis and the levels of erythropoietin (Epo) usually vary from normal to low. Besides marrow hypercellularity with overproduction of one or all the celular lineages, the disease courses with extramedullary hematopoiesis, hyperviscosity, leading to complications such as thrombosis or bleeding and risk of transformation to myelofibrosis or acute leukemia. Recently it has been described the association between the mutation in the JAK2 gene, located on chromosome 9p24, with the classic myeloproliferative disorders BCR-ABL negative, such as PV, which has brought significant advances in the understanding of the pathophysiology of this group of hematologic malignancies. The mutation causes a change of amino acid V (valine) to F (phenylalanine) at position 617 (JAK2V617F). According to published data, the frequency of JAK2V617F mutation detected in patients with PV is about 95%. JAK2 protein is a cytoplasmic tyrosine kinase, which is associated to the intracelular domain of cytokine receptors, such as Epo and thrombopoietin (Tpo), and growth factors which are essential to the function of these receptors. JAK2 mutation leads to the constitutive receptors activation, independent of connection to their cytokine and / or hypersensitivity to growth factors, with consequent activation of multiple intracellular signaling pathways such as JAK / STAT (Janus Kinase / Signal transducer and transcription activator), the PI3K (phosphatidylinositol 3 kinase) and MAPK (Mitogen-activated protein), involved in the transformation and proliferation of hematopoietic progenitors. Moreover, the cells show changes in terminal differentiation and resistance to in vitro apoptosis which is possibly related to the increasing expression of anti-apoptotic protein Bcl-XL. In addition to the advances in diagnosis, detection of JAK2V617F mutation has contributed to the improvement of classification and treatment in patients with PV. Thus, knowledge of the molecular mechanisms involved in PV has led investigators to the discovery of new drugs targeting molecular defects, allowing new therapeutic approach more efficient and probably less toxic. The aim of this article is to review the current knowledge of clinical and molecular characterization of PV, and its implications on the diagnosis and therapeutic approach of this myeloproliferative disorder

A new accuracy measure based on bounded relative error for time series forecasting

Many accuracy measures have been proposed in the past for time series forecasting comparisons. However, many of these measures suffer from one or more issues such as poor resistance to outliers and scale dependence. In this paper, while summarising commonly used accuracy measures, a special review is made on the symmetric mean absolute percentage error. Moreover, a new accuracy measure called the Unscaled Mean Bounded Relative Absolute Error (UMBRAE), which combines the best features of various alternative measures, is proposed to address the common issues of existing measures. A comparative evaluation on the proposed and related measures has been made with both synthetic and real-world data. The results indicate that the proposed measure, with user selectable benchmark, performs as well as or better than other measures on selected criteria. Though it has been commonly accepted that there is no single best accuracy measure, we suggest that UMBRAE could be a good choice to evaluate forecasting methods, especially for cases where measures based on geometric mean of relative errors, such as the geometric mean relative absolute error, are preferred

Effect of nickel on the microstructure and mechanical property of die-cast Al–Mg–Si–Mn alloy

The effect of nickel on the microstructure and mechanical properties of a die-cast Al–Mg–Si–Mn alloy has been investigated. The results show that the presence of Ni in the alloy promotes the formation of Ni-rich intermetallics. These occur consistently during solidification in the die-cast Al–Mg–Si–Mn alloy across different levels of Ni content. The Ni-rich intermetallics exhibit dendritic morphology during the primary solidification and lamellar morphology during the eutectic solidification stage. Ni was found to be always associated with iron forming AlFeMnSiNi intermetallics, and no Al3Ni intermetallic was observed when Ni concentrations were up to 2.06 wt% in the alloy. Although with different morphologies, the Ni-rich intermetallics were identified as the same AlFeMnSiNi phase bearing a typical composition of Al[100–140](Fe,Mn)[2–7]SiNi[4–9]. With increasing Ni content, the spacing of the α-Al–Mg2Si eutectic phase was enlarged in the Al–Mg–Si–Mn alloy. The addition of Ni to the alloy resulted in a slight increase in the yield strength, but a significant decrease in the elongation. The ultimate tensile strength (UTS) increased slightly from 300 to 320 MPa when a small amount (e.g. 0.16 wt%) of Ni was added to the alloy, but further increase of the Ni content resulted in a decrease of the UTS.The Engineering and Physical Sciences Research Council (EPSRC), Technology Strategy Board (TSB) and Jaguar Land Rover (JLR) in the United Kingdom

Time-resolved photoluminescence of barium titanate ultrafine powders

Author name used in this publication: C. L. MakAuthor name used in this publication: K. H. Wong2005-2006 > Academic research: refereed > Publication in refereed journalVersion of RecordPublishe

Viral integration drives multifocal HCC during the occult HBV infection

© 2019 The Author(s). Background & Aims: Although the prognosis of patients with occult hepatitis B virus (HBV) infection (OBI) is usually benign, a small portion may undergo cirrhosis and subsequently hepatocellular carcinoma (HCC). We studied the mechanism of life-long Integration of virus DNA into OBI host's genome, of which may induce hepatocyte transformation. Methods: We applied HBV capture sequencing on single cells from an OBI patient who, developed multiple HCC tumors and underwent liver resection in May 2013 at Tongji Hospital in China. Despite with the undetectable virus DNA in serum, we determined the pattern of viral integration in tumor cells and adjacent non-tumor cells and obtained the details of the viral arrangement in host genome, and furthermore the HBV integrated region in cancer genome. Results: HBV captured sequencing of tissues and individual cells revealed that samples from multiple tumors shared two viral integration sites that could affect three host genes, including CSMD2 on chr1 and MED30/EXT1 on chr8. Whole genome sequencing further indicated one hybrid chromosome formed by HBV integrations between chr1 and chr8 that was shared by multiple tumors. Additional 50 poorly differentiated liver tumors and the paired adjacent non-tumors were evaluated and functional studies suggested up-regulated EXT1 expression promoted HCC growth. We further observed that the most somatic mutations within the tumor cell genome were common among the multiple tumors, suggesting that HBV associated, multifocal HCC is monoclonal in origin. Conclusion: Through analyzing the HBV integration sites in multifocal HCC, our data suggested that the tumor cells were monoclonal in origin and formed in the absence of active viral replication, whereas the affected host genes may subsequently contribute to carcinogenesis

GdxSi grown with mass-analyzed low energy dual ion beam epitaxy technique

Semiconducting gadolinium silicide GdxSi samples were prepared by mass-analyzed low-energy dual ion beam epitaxy technique. Auger electron spectroscopy depth profiles indicate that the gadolinium ions are implanted into the single-crystal silicon substrate and formed 20 nm thick GdxSi film. X-ray double-crystal diffraction measurement shows that there is no new phase formed. The XPS spectra show that one type of silicon peaks whose binding energy is between that of silicide and silicon dioxide, and the gadolinium peak of binding energy is between that of metal Gd and Gd2O3. All of these results indicate that an amorphous semiconductor is formed. (C) 2002 Elsevier Science B.V. All rights reserved