Atomic data and electron-impact broadening effect in DO white dwarf atmospheres: Si VI

Energy levels, electric dipole transition probabilities and oscillator strengths in five times ionized silicon have been calculated in intermediate coupling. The present calculations were carried out with the general purpose atomic-structure program SUPERSTRUCTURE. The relativistic corrections to the non-relativistic Hamiltonian are taken into account through the Breit-Pauli approximation. We have also introduced a semi-empirical correction (TEC) for the calculation of the energy-levels. These atomic data are used to provide semiclassical electron-, proton- and ionized helium- impact line widths and shifts for 15 Si VI muliplet. Calculated results have been used to consider the influence of Stark broadening for DO white dwarf atmospheric conditions.Comment: MNRAS, accepted, 14 page

Theoretical determination of lifetimes of metastable states in Sc III and Y III

Lifetimes of the first two metastable states in Sc^{2+} and Y^{2+} are determined using the relativistic coupled-cluster theory. There is a considerable interest in studying the electron correlation effects in these ions as though their electronic configurations are similar to the neutral alkali atoms, their structures are very different from the latter. We have made a comparative study of the correlation trends between the above doubly ionized systems with their corresponding neutral and singly ionized iso-electronic systems. The lifetimes of the excited states of these ions are very important in the field of astrophysics, especially for the study of post-main sequence evolution of the cool giant stars.Comment: 13 pages, 1 figure and 5 table

3D Coronal Density Reconstruction and Retrieving the Magnetic Field Structure during Solar Minimum

Measurement of the coronal magnetic field is a crucial ingredient in understanding the nature of solar coronal phenomena at all scales. We employed STEREO/COR1 data obtained during a deep minimum of solar activity in February 2008 (Carrington rotation CR 2066) to retrieve and analyze the three-dimensional (3D) coronal electron density in the range of heights from 1.5 to 4 Rsun using a tomography method. With this, we qualitatively deduced structures of the coronal magnetic field. The 3D electron density analysis is complemented by the 3D STEREO/EUVI emissivity in the 195 A band obtained by tomography for the same CR. A global 3D MHD model of the solar corona was used to relate the reconstructed 3D density and emissivity to open/closed magnetic field structures. We show that the density maximum locations can serve as an indicator of current sheet position, while the locations of the density gradient maximum can be a reliable indicator of coronal hole boundaries. We find that the magnetic field configuration during CR 2066 has a tendency to become radially open at heliocentric distances greater than 2.5 Rsun. We also find that the potential field model with a fixed source surface (PFSS) is inconsistent with the boundaries between the regions with open and closed magnetic field structures. This indicates that the assumption of the potential nature of the coronal global magnetic field is not satisfied even during the deep solar minimum. Results of our 3D density reconstruction will help to constrain solar coronal field models and test the accuracy of the magnetic field approximations for coronal modeling.Comment: Published in "Solar Physics

Flow cytometric quantification of tumour endothelial cells; an objective alternative for microvessel density assessment

Assessment of microvessel density by immunohistochemical staining is subject to a considerable inter-observer variation, and this has led to variability in correlation between microvessel density and clinical outcome in different studies. In order to improve the method of microvessel density measurement in tumour biopsies, we have developed a rapid, objective and quantitative method using flow cytometry on frozen tissues. Frozen tissue sections of archival tumour material were enzymatically digested. The single-cell suspension was stained for CD31 and CD34 for flow cytometry. The number of endothelial cells was quantified using light scatter- and fluorescence-characteristics. Tumour endothelial cells were detectable in a single cell suspension, and the percentage of endothelial cells detected in 32 colon carcinomas correlated highly (r=0.84, P<0.001) with the immunohistochemical assessment of microvessel density. Flow cytometric endothelial cells quantification was found to be more sensitive especially at lower levels of immunohistochemical microvessel density measurement. The current method was found to be applicable for various tumour types and has the major advantage that it provides a retrospective and quantitative approach to the angiogenic potential of tumours

The Reg3alpha (HIP/PAP) Lectin Suppresses Extracellular Oxidative Stress in a Murine Model of Acute Liver Failure

BACKGROUND AND AIMS: Acute liver failure (ALF) is a rapidly progressive heterogeneous illness with high mortality rate and no widely accessible cure. A promising drug candidate according to previous preclinical studies is the Reg3alpha (or HIP/PAP) lectin, which alleviates ALF through its free-radical scavenging activity. Here we study the therapeutic targets of Reg3alpha in order to gain information on the nature of the oxidative stress associated with ALF. METHODS: Primary hepatocytes stressed with the reactive oxygen species (ROS) inducers TNFalpha and H2O2 were incubated with a recombinant Reg3alpha protein. ALF was induced in C57BL/6J mice by an anti-CD95 antibody. Livers and primary hepatocytes were harvested for deoxycholate separation of cellular and extracellular fractions, immunostaining, immunoprecipitation and malondialdehyde assays. Fibrin deposition was studied by immunofluorescence in frozen liver explants from patients with ALF. RESULTS: Fibrin deposition occurs during experimental and clinical acute liver injuries. Reg3alpha bound the resulting transient fibrin network, accumulated in the inflammatory extracellular matrix (ECM), greatly reduced extracellular ROS levels, and improved cell viability. Hepatocyte treatment with ligands of death receptors, e.g. TNFalpha and Fas, resulted in a twofold increase of malondialdehyde (MDA) level in the deoxycholate-insoluble fractions. Reg3alpha treatment maintained MDA at a level similar to control cells and thereby increased hepatocyte survival by 35%. No antioxidant effect of Reg3alpha was noted in the deoxycholate-soluble fractions. Preventing fibrin network formation with heparin suppressed the prosurvival effect of Reg3alpha. CONCLUSIONS: Reg3alpha is an ECM-targeted ROS scavenger that binds the fibrin scaffold resulting from hepatocyte death during ALF. ECM alteration is an important pathogenic factor of ALF and a relevant target for pharmacotherapy

IQGAP1 Is Involved in Post-Ischemic Neovascularization by Regulating Angiogenesis and Macrophage Infiltration

Neovascularization is an important repair mechanism in response to ischemic injury and is dependent on inflammation, angiogenesis and reactive oxygen species (ROS). IQGAP1, an actin-binding scaffold protein, is a key regulator for actin cytoskeleton and motility. We previously demonstrated that IQGAP1 mediates vascular endothelial growth factor (VEGF)-induced ROS production and migration of cultured endothelial cells (ECs); however, its role in post-ischemic neovascularization is unknown.Ischemia was induced by left femoral artery ligation, which resulted in increased IQGAP1 expression in Mac3(+) macrophages and CD31(+) capillary-like ECs in ischemic legs. Mice lacking IQGAP1 exhibited a significant reduction in the post-ischemic neovascularization as evaluated by laser Doppler blood flow, capillary density and α-actin positive arterioles. Furthermore, IQGAP1(-/-) mice showed a decrease in macrophage infiltration and ROS production in ischemic muscles, leading to impaired muscle regeneration and increased necrosis and fibrosis. The numbers of bone marrow (BM)-derived cells in the peripheral blood were not affected in these knockout mice. BM transplantation revealed that IQGAP1 expressed in both BM-derived cells and tissue resident cells, such as ECs, is required for post-ischemic neovascularization. Moreover, thioglycollate-induced peritoneal macrophage recruitment and ROS production were inhibited in IQGAP1(-/-) mice. In vitro, IQGAP1(-/-) BM-derived macrophages showed inhibition of migration and adhesion capacity, which may explain the defective macrophage recruitment into the ischemic tissue in IQGAP1(-/-) mice.IQGAP1 plays a key role in post-ischemic neovascularization by regulating, not only, ECs-mediated angiogenesis but also macrophage infiltration as well as ROS production. Thus, IQGAP1 is a potential therapeutic target for inflammation- and angiogenesis-dependent ischemic cardiovascular diseases

Comparison of serum hepatitis B virus replication markers in patients with chronic hepatitis B: studies on HBeAg/Anti-HBe system, viral dna polymerase and HBV-DNA

The detection of HBV-DNA in serum by molecular hybridization is the most sensitive and specific marker of replication and infectivity of hepatitis B virus and currently is proposed as a routine diagnostic technique in the follow-up of HBV - related diseases. Comparing different techniques already described, we found that direct spotting of serum samples on nitrocellulose membranes under vacuum filtration, followed by denaturing and neutralizing washes is more practical, simple, sensible and reproducible. DNA polymerase assay using phosphonoformic acid as specific viral inhibitor has shown 86.8% of concordance with HBV-DNA detection, and so, it is an useful alternative in the follow-up of hepatitis B chronic patients. We found 19.2% HBeAg positive samples with no other markers of viral replication and no anti-HBe positive sample had detectable HBV-DNA. Discordance between the 2 systems have been extensively described, and we confirm this for the first time in our country. Molecular biological techniques are essential to determine the replication status of chronic hepatitis B patients.A detecção do genoma do HBV no soro por hibridização molecular é o mais sensível e específico marcador da replicação e infectividade do HBV, sendo sua utilização proposta como técnica rotineira no acompanhamento de doenças relacionadas a este vírus. Comparando diferentes técnicas descritas anteriormente, escolhemos a deposição direta das amostras séricas sobre a membrana de nitrocelulose sob filtração a vácuo, seguida de banhos desnaturantes e neutralisantes como mais prática e simples, com sensibilidade equivalente. O ensaio da DNA polimerase usando ácido fosfonofórmico como inibidor virai específico mostrou 86.8% de concordância com a detecção direta do DNA viral, sendo, portanto, uma alternativa viável no acompanhamento de pacientes com hepatite crônica B. Encontramos 19,2% das amostras AgHBe positivos sem outros marcadores de replicação viral. Por outro lado, nenhuma amostra anti-HBe positiva teve HBV-DNA detectável. Discordância entre estes dois sistemas foi extensamente descrita, e confirmamos pela primeira vez este fato em pacientes com hepatite crônica B em nosso país. Técnicas de biologia molecular são, portanto, fundamentais na determinação da replicação viral em cada paciente

A comparison of echocardiography to invasive measurement in the evaluation of pulmonary arterial hypertension in a rat model

Pulmonary arterial hypertension (PAH) is a life-threatening condition characterized by progressive elevation in pulmonary artery pressure (PAP) and total pulmonary vascular resistance (TPVR). Recent advances in imaging techniques have allowed the development of new echocardiographic parameters to evaluate disease progression. However, there are no reports comparing the diagnostic performance of these non-invasive parameters to each other and to invasive measurements. Therefore, we investigated the diagnostic yield of echocardiographically derived TPVR and Doppler parameters of PAP in screening and measuring the severity of PAH in a rat model. Serial echocardiographic and invasive measurements were performed at baseline, 21 and 35 days after monocrotaline-induction of PAH. The most challenging echocardiographic derived TPVR measurement had good correlation with the invasive measurement (r = 0.92, P < 0.001) but also more simple and novel parameters of TPVR were found to be useful although the non-invasive TPVR measurement was feasible in only 29% of the studies due to lack of sufficient tricuspid valve regurgitation. However, echocardiographic measures of PAP, pulmonary artery flow acceleration time (PAAT) and deceleration (PAD), were measurable in all animals, and correlated with invasive PAP (r = −0.74 and r = 0.75, P < 0.001 for both). Right ventricular thickness and area correlated with invasive PAP (r = 0.59 and r = 0.64, P < 0.001 for both). Observer variability of the invasive and non-invasive parameters was low except in tissue-Doppler derived isovolumetric relaxation time. These non-invasive parameters may be used to replace invasive measurements in detecting successful disease induction and to complement invasive data in the evaluation of PAH severity in a rat model

E2F-1 Directly Regulates Thrombospondin 1 Expression

Thrombospondin 1 (TSP1) has been shown to play a critical role in inhibiting angiogenesis, resulting in inhibition of tumor growth and metastases. To figure out TSP1's regulators will lead to reveal its biological function mechanistically. In this study, we show that E2F-1 could activate the transcription of TSP1 by both promoter assays and Northern blot. Analysis of various TSP1 promoter mutant constructs showed that a sequence located −144/−137 up-stream of the transcriptional initiation site, related to the consensus E2F-responsive sequence, is necessary for the activation. In consistence with up-regulation of TSP-1 activity by over-expression of E2F-1, the knockdown of endogenous E2F-1 inhibited TSP-1 promoter activity significantly, implying that E2F-1 mediated regulation of TSP-1 is relevant in vivo. In addition, E2F-1 could also directly bind to the TSP1 promoter region covering −144/−137 region as revealed by ChIP assays. Furthermore, the E2F-1-induced activation of TSP1 gene transcription is suppressed by pRB1 in a dose-dependent manner. Taken together, the results demonstrate that TSP1 is a novel target for E2F1, which might imply that E2F-1 can affect angiogenesis by modulating TSP1 expression