Estudio de las propiedades físicas y químicas de recubrimientos de Tio2 elaborados mediante proyección térmica por combustión oxiacetilénica a partir de polvos nanométricos

RESUMEN: El presente estudio se enfoca en la elaboración de recubrimientos mediante proyección térmica por combustión, a partir de polvos de TiO2 usados como pigmento para aplicaciones cosméticas y pinturas. Los polvos empleados, dadas las aplicaciones para las cuales están desarrollados, poseen características físicas que impiden su uso en proyección térmica, por lo cual se requiere de su funcionalización mediante aglomeración para su posterior proyección. Previo a la elaboración de los recubrimientos se caracterizaron los polvos de TiO2 mediante pruebas de Difracción de Rayos X (DRX), Microscopía Electrónica de Barrido (MEB), Microscopía de Fuerza Atómica (MFA) y difracción láser, encontrando que a pesar de la imposibilidad de usarlo como materia prima en la elaboración de los recubrimientos mediante proyección térmica en las condiciones en las que es comercializado, su aglomeración permite cumplir tal cometido, obteniendo capas finamente estructuradas con un potencial de uso en procesos fotocatalíticos.ABSTRACT: This research is focused on manufacturing of coatings by oxyacetylene thermal spray from TiO2 particles usually used as pigment for cosmetic and paint applications. These powders are not usable in thermal spray processes because the particles’ size distribution exhibits very thin particles that block the torch. In order to manufacture the coatings it was necessary to carry out a functionalization by agglomeration of the particles. Before to the coatings’ manufacturing, the powders were characterized by X-Ray Diffraction, Scan Electron Microscopy, Atomic Force Microscopy and laser diffraction finding out that however the very thin particles the powder can be used in thermal spray processes after an agglomeration processes, getting coatings with bimodal microstructure conferring to the coatings potential applications in photo catalytic process

Metabolic Activation of Intrahepatic CD8+ T Cells and NKT Cells Causes Nonalcoholic Steatohepatitis and Liver Cancer via Cross-Talk with Hepatocytes

SummaryHepatocellular carcinoma (HCC), the fastest rising cancer in the United States and increasing in Europe, often occurs with nonalcoholic steatohepatitis (NASH). Mechanisms underlying NASH and NASH-induced HCC are largely unknown. We developed a mouse model recapitulating key features of human metabolic syndrome, NASH, and HCC by long-term feeding of a choline-deficient high-fat diet. This induced activated intrahepatic CD8+ T cells, NKT cells, and inflammatory cytokines, similar to NASH patients. CD8+ T cells and NKT cells but not myeloid cells promote NASH and HCC through interactions with hepatocytes. NKT cells primarily cause steatosis via secreted LIGHT, while CD8+ and NKT cells cooperatively induce liver damage. Hepatocellular LTβR and canonical NF-κB signaling facilitate NASH-to-HCC transition, demonstrating that distinct molecular mechanisms determine NASH and HCC development

CXC chemokine receptor 7 (CXCR7) regulates CXCR4 protein expression and capillary tuft development in mouse kidney

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CXCR7, CXCR4, and CXCL12 expression in mature glomeruli.

<p>(A–C) Brightfield micrographs of cresyl violet stained mature glomeruli (E16.5) after hybridization with ³⁵S- labeled probes for CXCR7, CXCR4, and CXCL12. (<b>A,B</b>) Signals for CXCR7 are restricted to the podocyte layer whereas CXCR4 is restricted to the center of the glomerulus. (<b>C</b>) CXCL12 is detected both in the podocytes and in the area of the vascular pole (vp, arrowhead). (D–E) Mature glomeruli after dual in situ hybridization with ³⁵S labeled probes for CXCR4 (D), CXCL12 (E), and a DIG-labeled probe for podocyte marker WT1 (D,E). (<b>D</b>) The darkfield micrograph reveals CXCR4 labeling (white signals) close to the vascular pole but not in WT1 stained podocytes of the visceral blade of Bowman's capsule. (<b>E</b>) The brightfield image shows labeling for CXCL12 mRNA (black grains) in the WT1 positive podocyte layer and in the WT1 negative area of the vascular pole (vp, arrowhead). (F–G) Confocal images of dual immunofluorescent stainings for GFP/CXCR4 (F) and GFP/podocin (G) in E16.5 BAC transgenic mice expressing EGFP under the control of the CXCR7 promoter. (<b>F</b>) CXCR4 immunoreactivity is present in the glomerular tuft (arrow), presumptive arterioles (arrowheads), and at the luminar membrane of tubular epithelial cells (asteriscs). Some tubules are co-positive for CXCR7-GFP and CXCR4 (filled asteristics), others display exclusively CXCR4 protein signals (open asteristics). In the glomerulus, signals for CXCR4 and CXCR7-GFP do not overlap. (<b>G</b>) Podocytes labeled by the selective marker podocin (red) are CXCR7-GFP positive. Scale bars represent 10 µm (C,G′″) and 20 µm (F).</p

Transmission electron microscopic analysis of the glomeruli.

<p>Glomerular capillaries at 3.300× magnification (<b>A</b>,<b>B</b>) and details of the filtration barrier at 21.600× magnification (<b>C</b>,<b>D</b>; framing in A,B). CXCR7^+/+ (C) and CXCR7^−/− (D) showed no differences in general morphology and glomerular basement membrane (gbm) attachment of podocytes (pod). However endothelial cells (en) seemed to be detached from the gbm (arrows). Scale bars correspond to 2 µm (A,B) and 0.3 µm (C,D).</p

Differential expression of CXCR7 and CXCR4 in nephrogenic mesenchyme, ureteric bud, and forming glomeruli.

<p>(A–D) A digoxigenin (DIG) labeled WT1 antisense probe was used as a marker for mesenchymal and mesenchyme derived nephrogenic structures at E14.5 and co-hybridized with ³⁵S labeled probes for CXCR7 or CXCR4. (<b>A</b>) Strong CXCR7 signals (black grains) are present in a T-shaped WT1 negative early ureteric bud tip (eub) which is associated with a CXCR7/WT1 co-positive pretubular aggregate (pa; black grains/brown staining). Weaker CXCR7 expression is found in a late ureteric bud tip (lub) which is associated with CXCR7/WT1 co-positive renal vesicles (rv). Note weak CXCR7 mRNA expression in the cap mesenchyme (cm) and strong CXCR7 gene activity above the cm (brown staining) at the renal capsule (rc). (<b>B,B′,C,C′</b>) Bright- and darkfield views of a comma-shaped body (cb in B) and S-shaped body (sb in C) after hybridization with a DIG labeled WT1 probe and a ³⁵S labeled CXCR7 riboprobe (black grains in B,C; white grains in B′,C′). Both WT1 positive structures exhibit clear CXCR7 antisense mRNA signals. (<b>D,D′</b>) Bright- and darkfield micrographs showing WT1-positive renal tissue (D) and radiosignals of CXCR4 riboprobe (D′). Strong CXCR4 gene expression is detected in a WT1 negative early ureteric bud tip (eub in D, dotted line in D′). Weak CXCR4 labeling is seen in a late ureteric bud tip (lub) which is associated with a WT1 positive/CXCR4 negative renal vesicle (rv). Note that CXCR4 mRNA is also present in WT1 positive cap mesenchyme (cm). WT1 positive epithelial cells of S-Shaped bodies display no CXCR4 mRNA expression. The vascular cleft of S-shaped bodies (arrows in D′) as well as putative arterioles (arrowhead in D′) are CXCR4 positive. (<b>E</b>,<b>F</b>) GFP immunostaining in sections from BAC transgenic mice expressing EGFP under the control of the CXCR7 promotor (G) or CXCR4 promotor (H). Calbindin was co-stained as an ureteric bud marker. (<b>G</b>) CXCR7-GFP is highly expressed in the renal capsule (rc) as well as in comma- and S-shaped bodies (cb, sb) associated with a calbindin positive late ureteric bud (lub). CXCR7-GFP is weak expressed in cap mesenchyme (cm) and not present in the late ureteric bud. (<b>H</b>) Strong CXCR4-GFP signals are detected only in cap mesenchyme (cm). All scale bars equal 20 µm.</p

Expression of CXCL12, CXCR7 and CXCR7 mRNA during nephrogenesis.

<p>Mapping of CXCL12, CXCR7, and CXCR4 expression was performed using the markers WT1 (dual in situ hybridization) and Podocin as well as VEGFR-2 (dual immunofluorescence). +, strong expression; (+) weak expression; (−) very weak expression; − no expression. ep, epithelial cells; mes, mesenchymal cells; mes→ep, mesenchymal-to-epithelial transition.</p

Patterns of CXCL12, CXCR7, and CXCR4 mRNAs in the early developing kidney.

<p>Adjacent kidney sections were hybridized with radiolabeled antisense riboprobes for CXCL12, CXCR7, and CXCR4 at E12.5 and E14.5. (<b>A</b>, <b>D</b>) CXCL12 expression pattern changed remarkably from E12.5 to E14.5 as no CXCL12 mRNA could be detected within the E12.5 kidney. At E14.5, CXCL12 signals are present in the kidney in stromal cells (asteristics in D), around the ureter (u) as well as in glomeruli (arrowheads in D). (<b>B</b>, <b>E</b>) CXCR7 mRNA is expressed in the region of the renal capsule (rc) and ureter at both indicated embryonic stages. The gene is also active in some ureteric buds (open arrows in B, E), immature glomeruli (closed arrows in E), and mature glomeruli (arrowheads in E). (<b>C</b>, <b>F</b>) CXCR4 mRNA is highly expressed in mesenchymal cells below the rc region at E12.5 (arrowheads in C) as well as in the cap mesenchyme at E14.5 (cm in F). CXCR4 is also expressed in some ureteric buds at E12.5 (open arrows in C). At E14.5, CXCR4 expression is found in presumptive blood vessels (closed arrows in F) and glomerular tufts (arrowheads in F). Allocation of detection signals to renal structures was performed using counterstaining with hematoxylin &amp; eosin. ag, adrenal gland; ov, ovarium; Scale bars correspond to 100 µm.</p