Geometric biplane graphs I: maximal graphs

We study biplane graphs drawn on a finite planar point set in general position. This is the family of geometric graphs whose vertex set is and can be decomposed into two plane graphs. We show that two maximal biplane graphs-in the sense that no edge can be added while staying biplane-may differ in the number of edges, and we provide an efficient algorithm for adding edges to a biplane graph to make it maximal. We also study extremal properties of maximal biplane graphs such as the maximum number of edges and the largest maximum connectivity over -element point sets.Peer ReviewedPostprint (author's final draft

Geometric biplane graphs II: graph augmentation

We study biplane graphs drawn on a finite point set in the plane in general position. This is the family of geometric graphs whose vertex set is and which can be decomposed into two plane graphs. We show that every sufficiently large point set admits a 5-connected biplane graph and that there are arbitrarily large point sets that do not admit any 6-connected biplane graph. Furthermore, we show that every plane graph (other than a wheel or a fan) can be augmented into a 4-connected biplane graph. However, there are arbitrarily large plane graphs that cannot be augmented to a 5-connected biplane graph by adding pairwise noncrossing edges.Peer ReviewedPostprint (author's final draft

Geometric biplane graphs I: maximal graphs

Postprint (author’s final draft

Geometric Biplane Graphs II: Graph Augmentation

We study biplane graphs drawn on a nite point set S in the plane in general position. This is the family of geometric graphs whose vertex set is S and which can be decomposed into two plane graphs. We show that every su ciently large point set admits a 5-connected biplane graph and that there are arbitrarily large point sets that do not admit any 6- connected biplane graph. Furthermore, we show that every plane graph (other than a wheel or a fan) can be augmented into a 4-connected biplane graph. However, there are arbitrarily large plane graphs that cannot be augmented to a 5-connected biplane graph by adding pairwise noncrossing edges.Peer ReviewedPostprint (author’s final draft

ACE2-angiotensin-(1-7)-Mas axis in renal ischaemia/reperfusion injury in rats

AngII (angiotensin II), ACE (angiotensin I-converting enzyme) and the AT(1) receptor (AngII type I receptor) are associated with the inflammatory process and microvascular dysfunction of AKI (acute kidney injury) induced by renal I/R (ischaemia/reperfusion). However, Ang-(1-7) [angiotensin-(1-7)], ACE2 (angiotensin I-converting enzyme 2) and the Mas receptor also play a role in renal disease models. Therefore, in the present study, we have examined the renal profile of Ang-(1-7), ACE2 and the Mas receptor in renal I/R and compared them with that of AngII, ACE and the AT(1) receptor. Male Wistar rats were submitted to left nephrectomy and ischaemia (45 min) followed by reperfusion (2 or 4 h) in the right kidney. At 4 h of reperfusion, renal AngII was increased (P < 0.01) and renal Ang-(1-7) was decreased substantially (P < 0.05), although plasma levels of both angiotensins were unchanged. in addition, renal I/R decreased the renal mRNA expression of renin (P < 0.05), AT(1) receptors (P < 0.001) and ACE2 (P < 0.05). At 2 and 4 h of reperfusion, renal ACE activity was reduced (P < 0.05). On the other hand, renal expression of the Mas receptor was greatly increased at 4 h of reperfusion (P < 0.01), which was confirmed by immunohistochemical and Western blot analysis. in conclusion, increased renal expression of the Mas receptor associated with changes in the RAS (renin-angiotensin-system)-related peptidases support an important role for the ACE2 Ang-(1-7) Mas axis in AKI.Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)Fundação de Amparo à Pesquisa do Estado de Minas Gerais (FAPEMIG)Univ Fed Minas Gerais, Inst Biol Sci, Dept Physiol & Biophys, BR-31270901 Belo Horizonte, MG, BrazilUniversidade Federal de São Paulo, Escola Paulista Med, Dept Biophys, BR-04044020 São Paulo, SP, BrazilUniv Fed Minas Gerais, Dept Pathol, BR-31270901 Belo Horizonte, MG, BrazilUniv Fed Minas Gerais, Dept Microbiol, BR-31270901 Belo Horizonte, MG, BrazilUniv Fed Minas Gerais, Clin Pathol Unit COLTEC, BR-31270901 Belo Horizonte, MG, BrazilUniv Fed Minas Gerais, Dept Biochem, Inst Biol Sci, BR-31270901 Belo Horizonte, MG, BrazilUniv Fed Minas Gerais, Dept Pediat, Fac Med, BR-31270901 Belo Horizonte, MG, BrazilUniversidade Federal de São Paulo, Escola Paulista Med, Dept Biophys, BR-04044020 São Paulo, SP, BrazilCAPES: PRDEX2009CNPq: 8701480/1997-4FAPEMIG: CBS 2044/96Web of Scienc

Determination of rosmarinic acid in Cordia verbenacea by liquid chromatography : applicability in seasonal study

Neste estudo, uma técnica de cromatografia líquida de alta resolução em fase reversa (CLAE-FR) para a determinação de ácido rosmarínico em Cordia verbenacea foi desenvolvida e validada. A análise de regressão foi avaliada, com observação de uma boa linearidade (r = 0,9997). Os valores obtidos para a precisão e exatidão estão de acordo com as diretrizes do ICH e com a legislação brasileira. Os valores de repetibilidade e precisão intermediária foram 2,79% e 4,76%, respectivamente. Os limites de detecção e de quantificação de ácido rosmarínico foram de 1,92 µg/mL e 5,81 µg/mL, respectivamente. Os resultados mostraram que o método desenvolvido é uma técnica por CLAE-FR de confiança para a determinação de ácido rosmarínico em tintura de C. verbenacea. Além disso, essa metodologia foi aplicada em estudo sazonal, que revela uma correlação positiva relativamente forte entre o período de chuvas e o teor de ácido rosmarínico.In this study, a reverse phase-high performance liquid chromatography (RP-HPLC) technique for determination of rosmarinic acid in the Cordia verbenacea was developed and validated. A regression analysis was performed, with the observation of good linearity (r =0.999949). The values obtained for precision and accuracy determination are in agreement with ICH guidelines and the Brazilian legislation. The values of repeatability and intermediate precision were 2.79% and 4.76%, respectively. The detection and the quantitation limits of the rosmarinic acid were 1.92 µg/mL and 5.81 µg/mL, respectively. The results demonstrated that the developed method is a reliable RP-HPLC technique for the determination of rosmarinic acid in C. verbenacea tincture. In addition, this methodology was applied at a seasonal study indicating relatively strong positive correlation between the rain period and the rosmarinic acid content

A Model of DENV-3 Infection That Recapitulates Severe Disease and Highlights the Importance of IFN-γ in Host Resistance to Infection

There are few animal models of dengue infection, especially in immunocompetent mice. Here, we describe alterations found in adult immunocompetent mice inoculated with an adapted Dengue virus (DENV-3) strain. Infection of mice with the adapted DENV-3 caused inoculum-dependent lethality that was preceded by several hematological and biochemical changes and increased virus dissemination, features consistent with severe disease manifestation in humans. IFN-γ expression increased after DENV-3 infection of WT mice and this was preceded by increase in expression of IL-12 and IL-18. In DENV-3-inoculated IFN-γ−/− mice, there was enhanced lethality, which was preceded by severe disease manifestation and virus replication. Lack of IFN-γ production was associated with diminished NO-synthase 2 (NOS2) expression and higher susceptibility of NOS2−/− mice to DENV-3 infection. Therefore, mechanisms of protection to DENV-3 infection rely on IFN-γ-NOS2-NO-dependent control of viral replication and of disease severity, a pathway showed to be relevant for resistance to DENV infection in other experimental and clinical settings. Thus, the model of DENV-3 infection in immunocompetent mice described here represents a significant advance in animal models of severe dengue disease and may provide an important tool to the elucidation of immunopathogenesis of disease and of protective mechanisms associated with infection