Sílabo de Finanzas I

El curso de Finanzas I es de naturaleza aplicativa y se propone desarrollar en los estudiantes la competencia para explicar y aplicar los principios y los modelos de la Teoría Financiera en la gestión financiera de una empresa con el objetivo de maximizar el valor de la empresa. El curso sirve de base para los cursos de Finanzas II ,Presupuestos, Contabilidad Gerencial y Formulación y Evaluación de Proyectos

Additional file 4: of Identification of new loci involved in the host susceptibility to Salmonella Typhimurium in collaborative cross mice

Figure S3. Founder contributions and haplotype around Stsl4 QTL on Chr 6. (A) Genome scan magnification for Stsl4 QTL region (60–100 Mb on Chr 6). The mouse genome location is on the X-axis and significance (−log10(P)) values on the Y-axis, with genome-wide thresholds of association at E < 0.5, E < 0.1 and E < 0.05 levels indicated respectively by the gray, orange and red lines. Peak location (maximum value of –log10(P)) is marked by a star. (B) Founder contributions in the same magnified region. The peak location is marked by a star. Each of the 8 founders is in a different color. The mouse genome location is on the X-axis and Y-axis shows the founder estimated effect on splenic bacterial load after S. Typhimurium infection. (C) Founder contributions at Stsl4 QTL peak (81.2 Mb). X-axis shows the different founder strains. Y-axis shows the estimated founder effect. No obvious contributions explain Stsl4 QTL, but B6 has the lowest estimated impact while NZO/HILtJ and PWK/PhJ have the highest estimates. (PDF 160 kb

Additional file 7: of Identification of new loci involved in the host susceptibility to Salmonella Typhimurium in collaborative cross mice

Table S3. Genes remaining in Stls2 interval post merge analysis. Gene symbol, start and end positions, name, high merged SNPs, expression in immune cell, cell-type major expression and Gene Ontology (GO) terms are given. Gene positions (build mm9), names as well as GO terms were collected from UCSC, MGI and ENSEMBL, while expression data were collected from Male/Female RNAseq of ImmGen. (XLSX 492 kb

Additional file 3: of Identification of new loci involved in the host susceptibility to Salmonella Typhimurium in collaborative cross mice

Figure S2. Founder contributions and haplotype around Stsl3 QTL on Chr 1. (A) Genome scan magnification for Stsl3 QTL region (70–100 Mb on Chr 1). The mouse genome location is on the X-axis and significance (−log10(P)) values on the Y-axis, with genome-wide thresholds of association at E < 0.5, E < 0.1 and E < 0.05 levels indicated respectively by the gray, orange and red lines. Peak locations Stsl3a and Stsl3b (maximum value of –log10(P)) are marked by stars. (B) Founder contributions in the same magnified region. The peak location of Stsl3a is marked by a star. Each of the 8 founders is in a different color. The mouse genome location is on the X-axis and Y-axis shows the founder estimated effect on splenic bacterial load after S. Typhimurium infection. (C) Founder contributions at Stsl3a QTL peak (83.9 Mb). X-axis shows the different founder strains. Y-axis shows the estimated founder effect. No obvious contributions explain Stsl3a QTL, but B6 (grey) has the highest estimated impact of the 8 founders. (D) Founder contributions at Stsl3b QTL peak (79.2 Mb). There is no obvious founder contribution for Stsl3b QTL peak region. 129 (pink) has the highest estimated impact of the 8 founders while PWK (red) has the lowest estimate. (PDF 215 kb

Additional file 6: of Identification of new loci involved in the host susceptibility to Salmonella Typhimurium in collaborative cross mice

Table S2. Genes remaining in Stls1 interval post merge analysis. Gene symbol, start and end positions, name, high merged SNPs, expression in immune cell, cell-type major expression and Gene Ontology (GO) terms are given. Gene positions (build mm9), names as well as GO terms were collected from UCSC, MGI and ENSEMBL, while expression data were collected from Male/Female RNAseq of ImmGen. (XLSX 496 kb

Schematic representation of the cloning strategy.

<p>The flavivirus genome is represented approximately to scale. Unique or rare restriction sites used for cloning and their location (numbering based on the sequence from Genbank no. AF481864) are shown at the top. Four cDNA fragments represented by thick lines were synthesized from IS-98-ST1 viral genomic RNA by RT-PCR to cover the complete coding WNV genome. The cDNA fragments were first cloned into the pCR2.1 plasmid, and then digested using unique restrictions sites and subcloned into the destination plasmid. The full length infectious clone was obtained by the extraction of fragment 2+3+4 from plasmid B after an enzymatic digestion with <i>XmaI</i> and <i>BamHI</i> followed by its insertion into plasmid A downstream of fragment 1+2. One silent mutation (shown in lower case) was engineered in the pCR2.1+ fragment 3 plasmid to create a <i>SnaBI</i> site.</p

Viral load in different organs of chicken embryo infected with IS-98-ST1 WNV.

<p>Groups of 6 ten-day-old pathogen-free chicken eggs were infected with 1 PFU of IS-98-ST1 parental virus via the intra-vascular route. Viral load in different organs was quantified by quantitative RT-PCR. PBS controls were negative for all organs.</p

<i>in vivo</i> validation of the biological properties of the IC virus in susceptible mice, histology.

<p>Histology performed on mouse brain 7 days p.i revealed inflammatory lesions in the meninges characterized by diffuse lymphocytic or lymphoplasmocytic infiltrates, characteristic of lymphocytic meningitis (right panel, arrows). Lymphocytic perivascular cuffs were also visible in the brain parenchyma, indicative of encephalitis (left panel, arrows). These lesions were observed in two of four animals or in one mouse for the infectious clone and the Israeli strain, respectively. Tissue sections were stained with hematoxylin, eosin and saffron.</p

<i>in vivo</i> validation of the biological properties of the IC virus in susceptible mice, viral load.

<p>Viral RNA copy number in brains of BALB/c outbred female mice (n = 5) injected i.p with 1, 10, 100, 1000 PFU of parental (P) or recombinant (IC) IS-98-ST1 virus. Quantification was performed in duplicate.</p

<i>Lago1</i> gene targeting by HR at the <i>Dct</i> locus.

<p>(A) Insertion of <i>Lago1</i> gene at the <i>Dct</i> locus. The <i>Dct^I-SceI</i> allele, the HR1 repair vector and the <i>Dct^Lago1</i>^-<i>Neo</i> targeted allele are represented from top to bottom. A lightning denotes I-<i>Sce</i>I expression from pCMV-I-<i>Sce</i>I or pCAG-I-<i>Sce</i>I plasmid. The 1.4 and 4.5 kb of <i>Dct</i> isogenic DNA are depicted by grey rectangles. (B) Southern blot analysis of <i>Dct^+/+</i>, <i>Dct^I-SceI/+</i> and <i>Dct^Lago1</i>^{-<i>Neo/+</i>} ES cells. Genomic DNAs were digested with <i>Bam</i>HI. The probe used for the hybridization is the external 5′ probe depicted by a black bar. The 11.7, 4.5, and 10.1 kb fragments are distinctive of the <i>Dct⁺</i>, <i>Dct^I-SceI</i>, and <i>Dct^Lago1</i>^-<i>Neo</i> alleles, respectively. (C) Diagram of DSB-induced homologous recombination with no insertion of the <i>Lago1</i> gene. The <i>Dct^I-SceI</i> allele, and the HR1 repair vector are represented from top to bottom. The short regions of homology, 58 bp and 125 bp in length, between the HR1 repair vector and the genomic DNA at the <i>Dct</i> locus in <i>Dct^I-SceI/+</i> cells, are depicted by grey rectangles. An HR between these two short regions of homology would lead to loss of the I-<i>Sce</i>I site with no integration of the Neo^R cassette. The resulting cells would die in the presence of G418.</p