On observation of the downconversion mechanism in Er3+/Yb3+ co-doped tellurite glass using thermal and optical parameters

Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)

Constraints on the Higgs boson width from off-shell production and decay to Z-boson pairs

Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)

Search for top-squark pairs decaying into Higgs or Z bosons in pp collisions at root s=8 TeV

Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)

Combining Experimental Evidence and Molecular Dynamic Simulations To Understand the Mechanism of Action of the Antimicrobial Octapeptide Jelleine-I

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Searches for electroweak neutralino and chargino production in channels with Higgs, Z, and W bosons in pp collisions at 8 TeV

Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)

Search for invisible decays of Higgs bosons in the vector boson fusion and associated ZH production modes

Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)

Observation of the diphoton decay of the Higgs boson and measurement of its properties

Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)

Cytoxicity and Apoptotic Mechanism of Ruthenium(II) Amino Acid Complexes in Sarcoma-180 Tumor Cells

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Mechanical strain induces the production of spheroid mineralized microparticles in the aortic valve through a RhoA/ROCK-dependent mechanism

Calcific aortic valve disease (CAVD) is a chronic disorder characterized by an abnormal mineralization of the leaflets, which is accelerated in bicuspid aortic valve (BAV). It is suspected that mechanical strain may promote/enhance mineralization of the aortic valve. However, the effect of mechanical strain and the involved pathways during mineralization of the aortic valve remains largely unknown. Valve interstitial cells (VICs) were isolated and studied under strain conditions. Human bicuspid aortic valves were examined as a model relevant to increase mechanical strain. Cyclic strain increased mineralization of VICs by several-fold. Scanning electron microscope (SEM) and energy dispersive X-ray (EDX) analyses revealed that mechanical strain promoted the formation of mineralized spheroid microparticles, which coalesced into larger structure at the surface of apoptotic VICs. Apoptosis and mineralization were closely associated with expression of ENPP1. Inhibition of ENPP1 greatly reduced mineralization of VIC cultures. Through several lines of evidence we showed that mechanical strain promoted the export of ENPP1-containing vesicles to the plasma membrane through a RhoA/ROCK pathway. Studies conducted in human BAV revealed the presence of spheroid mineralized structures along with the expression of ENPP1 in areas of high mechanical strain. Mechanical strain promotes the production and accumulation of spheroid mineralized microparticles by VICs, which may represent one important underlying mechanism involved in aortic valve mineralization. RhoA/ROCK-mediated export of ENPP1 to the plasma membrane promotes strain-induced mineralization of VICs.

Diabetes reduces mesenchymal stem cells in fracture healing through a TNF alpha-mediated mechanism

Diabetes interferes with bone formation and impairs fracture healing, an important complication in humans and animal models. The aim of this study was to examine the impact of diabetes on mesenchymal stem cells (MSCs) during fracture repair.Fracture of the long bones was induced in a streptozotocin-induced type 1 diabetic mouse model with or without insulin or a specific TNF alpha inhibitor, pegsunercept. MSCs were detected with cluster designation-271 (also known as p75 neurotrophin receptor) or stem cell antigen-1 (Sca-1) antibodies in areas of new endochondral bone formation in the calluses. MSC apoptosis was measured by TUNEL assay and proliferation was measured by Ki67 antibody. In vitro apoptosis and proliferation were examined in C3H10T1/2 and human-bone-marrow-derived MSCs following transfection with FOXO1 small interfering (si)RNA.Diabetes significantly increased TNF alpha levels and reduced MSC numbers in new bone area. MSC numbers were restored to normal levels with insulin or pegsunercept treatment. Inhibition of TNF alpha significantly reduced MSC loss by increasing MSC proliferation and decreasing MSC apoptosis in diabetic animals, but had no effect on MSCs in normoglycaemic animals. In vitro experiments established that TNF alpha alone was sufficient to induce apoptosis and inhibit proliferation of MSCs. Furthermore, silencing forkhead box protein O1 (FOXO1) prevented TNF alpha-induced MSC apoptosis and reduced proliferation by regulating apoptotic and cell cycle genes.Diabetes-enhanced TNF alpha significantly reduced MSC numbers in new bone areas during fracture healing. Mechanistically, diabetes-enhanced TNF alpha reduced MSC proliferation and increased MSC apoptosis. Reducing the activity of TNF alpha in vivo may help to preserve endogenous MSCs and maximise regenerative potential in diabetic patients.

Down-regulation of SLC8A1 as a putative apoptosis evasion mechanism by modulation of calcium levels in penile carcinoma

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Dirac gaugions, R symmetry and the 125 GeV Higgs

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Search for a standard model-like Higgs boson in the mu(+)mu(-) and e(+)e(-) decay channels at the LHC

Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)

Colorless top partners, a 125 GeV Higgs boson, and the limits on naturalness

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Dynamics of classical particles in oval or elliptic billiards with a dispersing mechanism

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)