CBSV and UCBSV quantitation in rootstocks and TME 7 scions.

<p>A. CBSV quantitation by qPCR in CBSV-infected cv. 60444 roostock plants and corresponding grafted scions from transgenic, wild-type and control TME 7 lines. B. UCBSV quantitation by qPCR in UCBSV-infected Ebwanateraka roostock plants and corresponding grafted scions from transgenic, wild-type and control TME 7 lines. Numbers following the cassava line identifiers indicate the biological replicates.</p

CBSV and UCBSV-associated symptoms in cassava leaves.

<p>A. Fully expanded leaf of wild-type TME 7 scion grafted on a CBSV-infected rootstock at 10 wpg. B. Fully expanded leaf of wild-type TME 7 scion grafted on an UCBSV-infected rootstock at 10 wpg. C. Fully expanded leaf of TME 7–Hp 9 scion grafted on a CBSV-infected rootstock at 10 wpg. D. Fully expanded leaf of TME 7 scion grafted on an UCBSV-infected rootstock at 10 wpg.</p

CBSV and UCBSV quantitation in rootstocks and cv. 60444 scions.

<p>A. CBSV quantitation by qPCR in CBSV-infected cv. 60444 roostock plants and corresponding grafted scions from transgenic, wild-type and control cv. 60444 lines. B. UCBSV quantitation by qPCR in UCBSV-infected Ebwanateraka roostock plants and corresponding grafted scions from transgenic, wild-type and control cv. 60444 lines. Numbers following the cassava line identifiers indicate the biological replicates.</p

Phenotypic and molecular data of the 60444-Hp scion-propagated plants.

<p>Stem cuttings from inoculated scions were propagated. Leaves and roots were evaluated 3 and 7 months after propagation, respectively.</p

CBSV-associated symptoms in cassava storage roots.

<p>A. Storage roots of CBSV-inoculated cv. 60444 cassava at 7 month after stem propagation. B. Storage roots of CBSV-inoculated 60444–Hp 9 cassava line at 7 month after stem propagation.</p

Biological activity of pyrazole and imidazole-dehydroepiandrosterone derivatives on the activity of 17<b>β</b>-hydroxysteroid dehydrogenase 5

<div><p></p><p>The enzyme type 5 17β-hydroxysteroid dehydrogenase 5 (17β-HSD5) catalyzes the transformation of androstenedione (4-dione) to testosterone (T) in the prostate. This metabolic pathway remains active in cancer patients receiving androgen deprivation therapy. Since physicians seek to develop advantageous and better new treatments to increase the average survival of these patients, we synthesized several different dehydroepiandrosterone derivatives. These compounds have a pyrazole or imidazole function at C-17 and an ester moiety at C-3 and were studied as inhibitors of 17β-HSD5. The kinetic parameters of this enzyme were determined for use in inhibition assays. Their pharmacological effect was also determined on gonadectomized hamsters treated with Δ⁴-androstenedione (4-dione) or testosterone (T) and/or the novel compounds. The results indicated that the incorporation of a heterocycle at C-17 induced strong 17β-HSD5 inhibition. These derivatives decreased flank organ diameter and prostate weight in castrated hamsters treated with T or 4-dione. Inhibition of 17β-HSD5 by these compounds could have therapeutic potential for the treatment of prostate cancer and benign prostatic hyperplasia.</p></div

Ingenuity network analysis constructed using significant down-regulated genes (BH<0.05) founded during hASC culture evolution.

<p>The top network functions were Hematopoietic cell lineage, Cell adhesion molecules, Leucocyte transendothelial migration and Complement and coagulation cascades. B2M = beta-2-microglobulin; BCR = breakpoint cluster region; CD14 = monocyte differentiation antigen CD14; CD3 = T-cell surface glycoprotein CD3 epsilon chain; EPOR = erythropoietin receptor; ERK1/2 = mitogen activated protein kinase; EZR = ezrin; F13A1 = coagulation factor XIII, A1 polypeptide; FCRLA = Fc receptor-like A; FXN = frataxin, nuclear gene encoding mitochondrial protein; FYN = tyrosine-protein kinase Fyn; GRM1 = glutamate receptor, metabotropic 1; GZMB = granzyme B (granzyme 2, cytotoxic T-lymphocyte-associated serine esterase 1); HBEGF = heparin-binding EGF-like growth factor; HLA-DRB1 = MHC class II antigen HLA-DRB1 beta 1; HLA-F = HLA class I histocompatibility antigen, alpha chain F; IFNGR1 = Interferon gamma receptor 1; IGF1 = insulin-like growth factor 1 (somatomedin C); IL10RA = interleukin 10 receptor, alpha; IL13 = interleukin 13; IL1R2 = interleukin 1 receptor, type I; Immunoglobulin = Immunoglobulin; Karyopherin beta = nucleo cytoplasmic transporter; lgG = inmunoglobulin G; lgm = immunoglobulin M; Mapk = Mitogen-activated protein kinase; NFKB = NF-kappa-beta; NFKB1 = nuclear factor NF-kappa-B p105 subunit; P38MAPK = map kinase p38; PI3K = phosphatidylinositol 4-phosphate 3-kinase; PIK3R3 = phosphatidylinositol 3-kinase regulatory subunit gamma; PLCG2 = 1-phosphatidylinositol 4,5-bisphosphate phosphodiesterase gamma-2; STAT5A = signal transducer and activator of transcription 5B; TCR = T cell antigen receptor; VEGF = vascular endothelial growth factor. The grey nodes are the genes classified as significant. The asterisk (*) indicates the degree of down-regulation.</p

General scheme of the procedure highlighting the modifications introduced.

<p>General scheme of the procedure highlighting the modifications introduced.</p

Up-regulated genes between passages involved in significant KEEG pathways.

<p>Up-regulated genes between passages involved in significant KEEG pathways.</p

Characterization and comparison of hASC HS/FBS maintained.

<p>(<b>A</b>) RT-PCR analysis of gene expression in hASCs cultured for 3 and 5 passages on either HS or FBS. Adipose tissue markers or human adipose stem cell markers (respectively). (<b>B</b>) Analysis of the morphology of the hASCs cultured under our protocol at passages 1, 3 and 5 respectively. For these structural studies semi-thin sections stained with toluidine blue were used. All the images were captured in a Zeiss Axiovert 200 M microscope. Magnification = 100 X.</p