Inactivation of vesicular stomatitis virus through inhibition of membrane fusion by chemical modification of the viral glycoprotein

Membrane fusion is an essential step in the entry of enveloped viruses into their host cells triggered by conformational changes in viral glycoproteins. We have demonstrated previously that modification of vesicular stomatitis virus (VSV) with diethylpyrocarbonate (DEPC) abolished conformational changes on VSV glycoprotein and the fusion reaction catalyzed by the virus. In the present study, we evaluated whether treatment with DEPC was able to inactivate the virus. Infectivity and viral replication were abolished by viral treatment with 0.5 mM DEPC. Mortality profile and inflammatory response in the central nervous system indicated that G protein modification with DEPC eliminates the ability of the virus to cause disease. In addition, DEPC treatment did not alter the conformational integrity of surface proteins of inactivated VSV as demonstrated by transmission electron microscopy and competitive ELISA. Taken together, our results suggest a potential use of histidine (His) modification to the development of a new process of viral inactivation based on fusion inhibition. © 2006 Elsevier B.V. All rights reserved.

Modification of the industrialization model in Latin America

Esboza los trazos principales de interpretacion del proceso de industrializacion desde la decada de los anos 30 hasta el presente. Aborda el tema central de la transformacion del modelo hasta ahora predominante de industrializacion. Propone una estrategia industrial basada en el crecimiento hacia adentro, mediante la creacion de industrias de bienes de capital y de consumo masivo, la continuacion del proceso de sustitucion selectiva de importaciones, el establecimiento de criterios claros de division del trabajo dentro de la region, y la aplicacion de una politica selectiva y dinamica de insercion en los mercados de los paises centrales.

Interlacing of zeros of orthogonal polynomials under modification of the measure

We investigate the mutual location of the zeros of two families of orthogonal polynomials. One of the families is orthogonal with respect to the measure dμ (x), supported on the interval (a, b) and the other with respect to the measure |x -c|τ|x -d|γdμ (x), where c and d are outside (a, b) We prove that the zeros of these polynomials, if they are of equal or consecutive degrees, interlace when either 0 < τ, γ ≤ 1 or γ = 0 and 0 < τ ≤ 2. This result is inspired by an open question of Richard Askey and it generalizes recent results on some families of orthogonal polynomials. Moreover, we obtain further statements on interlacing of zeros of specific orthogonal polynomials, such as the Askey-Wilson ones. © 2013 Elsevier Inc.

Chemical modification of the surface of alumina with alkaline earth metal oxides using the polymeric precursor method for catalysis application

In this study, modifications of alumina surface with of alkaline earth metal oxides were studied, using the polymeric precursor method. The modified compounds were characterized by X-ray diffraction, nitrogen adsorption-desorption and scanning electron microscopy. The catalytical properties of these new catalysts were evaluated for the transesterification reaction of babassu oil. It is observed that the transesterification reaction of babassu oil with methanol was successfully carried out using the modified alumina samples.

Block Bone Graft Fixation ( Onlay): A Modification of the Surgical Technique

Several reconstructive methods of the alveolar ridge have been reported to make possible future rehabilitations with implants. Many of these methods come from studies done in animals, mainly rats. With this clinical practice based on scientific evidence, any experimental procedure that can be undertaken in real life is fundamental. Thus, any research that emulates as closely as possible those techniques used in humans are important. This study describes the modification of the technique for block bone graft fixation (onlay) in rats using the lag screw-type technique, normally used in clinical procedures for grafts in humans. The conclusion was that the execution of the described procedures minimizes interference of blood flow in the area because of the maintenance of the muscle insertion in the buckle aspect of the most anterior region of the mandible, providing better stability to the graft and better contact interface of the graft and receptor bed.

Modification of the B meson mass in a magnetic field from QCD sum rules

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

Hypusine Modification of the Ribosome-binding Protein eIF5A, a Target for New Anti-Inflammatory Drugs: Understanding the Action of the Inhibitor GC7 on a Murine Macrophage Cell Line

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

Modification of the brain proteome of Africanized honeybees (Apis mellifera) exposed to a subaEurolethal doses of the insecticide fipronil

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

Post-translational modification of the RhoGTPase activating protein 21, ARHGAP21, by SUMO2/3

ARHGAP21 is a 217 kDa RhoGAP protein shown to modulate cell migration through the control of Cdc42 and FAK activities. In the present work a 250 kDa-ARHGAP21 was identified by mass spectrometry. This modified form is differentially expressed among cell lines and human primary cells. Co-immunoprecipitations and in vitro SUMOylation confirmed ARHGAP21 specific modification by SUMO2/3 and mapped the SUMOylation site to ARHGAP21 lysine K1443. Immunofluorescence staining revealed that ARHGAP21 co-localizes with SUMO2/3 in the cytoplasm and membrane compartments. Interestingly, our results suggest that ARHGAP21 SUMOylation may be related to cell proliferation. Therefore, SUMOylation of ARHGAP21 may represent a way of guiding its function. (C) 2012 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.

ABCA4 and ROM1: Implications for modification of the PRPH2-associated macular dystrophy phenotype

To identify the causative mutation leading to autosomal dominant macular dystrophy, cone dystrophy, and cone-rod dystrophy in a five-generation family and to explain the high intrafamilial phenotypic variation by identifying possible modifier genes.

Modification of the magnetic properties of a heterometallic wheel by inclusion of a Jahn-Teller distorted Cu(II) ion

An investigation into the physical consequences of including a Jahn-Teller distorted Cu(II) ion within an antiferromagnetically coupled ring, [R(2)NH(2)][Cr(7)CuF(8)((O(2)C(t)Bu)(16))] is reported. Inelastic neutron scattering (INS) and electron paramagnetic resonance (EPR) spectroscopic data are simulated using a microscopic spin Hamiltonian, and show that the two Cr-Cu exchange interactions must be inequivalent. One Cr-Cu exchange is found to be antiferromagnetic and the other ferromagnetic. The geometry of the Jahn-Teller elongation is deduced from these results, and shows that a Jahn-Teller elongation axis must lie in the plane of the Cr(7)Cu wheel; the elongation is not observed by X-ray crystallography, due to positional disorder of the Cu site within the wheel. An electronic structure calculation confirms the structural distortion of the Cu site.

Posttranslational modification of the AU-rich element binding protein HuR by protein kinase Cdelta elicits angiotensin II-induced stabilization and nuclear export of cyclooxygenase 2 mRNA

The mRNA stabilizing factor HuR is involved in the posttranscriptional regulation of many genes, including that coding for cyclooxygenase 2 (COX-2). Employing RNA interference technology and actinomycin D experiments, we demonstrate that in human mesangial cells (hMC) the amplification of cytokine-induced COX-2 by angiotensin II (AngII) occurs via a HuR-mediated increase of mRNA stability. Using COX-2 promoter constructs with different portions of the 3' untranslated region of COX-2, we found that the increase in COX-2 mRNA stability is attributable to a distal class III type of AU-rich element (ARE). Likewise, the RNA immunoprecipitation assay showed AngII-induced binding of HuR to this ARE. Using the RNA pulldown assay, we demonstrate that the AngII-caused HuR assembly with COX-2 mRNA is found in free and cytoskeleton-bound polysomes indicative of an active RNP complex. Mechanistically, the increased HuR binding to COX-2-ARE by AngII is accompanied by increased nucleocytoplasmic HuR shuttling and depends on protein kinase Cdelta (PKCdelta), which physically interacts with nuclear HuR, thereby promoting its phosphorylation. Mapping of phosphorylation sites identified serines 221 and 318 as critical target sites for PKCdelta-triggered HuR phosphorylation and AngII-induced HuR export to the cytoplasm. Posttranslational modification of HuR by PKCdelta represents an important novel mode of HuR activation implied in renal COX-2 regulation.