186 research outputs found
Host-vector system for integration of recombinant DNA into chromosomes of transformable and nontransformable streptococci
No full textWe describe a genetic system in which transformation of Streptococcus pneumoniae and Streptococcus sanguis was used to insert recombinant DNA into the conjugative chromosomal element omega (cat tetM) 6001 (omega 6001). The element containing the recombinant DNA was then transferred by conjugation to the chromosome of transformable and nontransformable streptococci. When Escherichia coli plasmid pDP36 was used as donor in transformation, it was capable of inserting 5.9 kilobases of heterologous DNA into the chromosome of competent streptococcal strains carrying omega 6001; the transformants were scored for erythromycin resistance. Genetic analysis showed that in a fraction of the erythromycin-resistant transformants the integration via flanking homology of the heterologous DNA caused inactivation of the tetM gene of omega 6001. By analyzing the stability of the resistance markers, we found that stable integration of heterologous DNA was achieved only in the erythromycin-resistant, tetracycline-sensitive transformants. It was possible to detect conjugal transfer of the heterologous sequences from stable transformants to strains of S. pneumoniae, S. sanguis, Streptococcus pyogenes, and Streptococcus faecalis. The omega 6001-pDP36 host-vector system opens new possibilities for gene transfer in streptococci. By this method cloned streptococcal DNA (possibly mutagenized in vitro) can be returned to the original host, greatly facilitating complementation tests and fine physiological studies
RECOGNITION OF TOSCANA VIRUS NSs REGIONS INVOLVED IN RIG-I DEGRADATION AND IFN-b INHIBITION
No full textToscana Virus NSs protein inhibits the induction of type I interferon by interacting with RIG-I.
No full textToscana virus (TOSV) is a phlebovirus, of the Bunyaviridae family, that is responsible for central nervous system (CNS) injury in humans. Previous data have shown that the TOSV NSs protein is a gamma interferon (IFN-ß) antagonist when transiently overexpressed in mammalian cells, inhibiting IRF-3 induction (G. Gori Savellini, F. Weber, C. Terrosi, M. Habjan, B. Martorelli, and M. G. Cusi, J. Gen. Virol. 92:71-79, 2011). In this study, we investigated whether an upstream sensor, which has a role in the signaling cascade leading to the production of type I IFN, was involved. We found a significant decrease in RIG-I protein levels in cells overexpressing TOSV NSs, suggesting that the nonstructural protein interacts with RIG-I and targets it for proteasomal degradation. In fact, the MG-132 proteasome inhibitor was able to restore IFN-ß promoter activation in cells expressing NSs, demonstrating the existence of an evasion mechanism based on inhibition of the RIG-I sensor. Furthermore, a C-terminal truncated NSs protein (ΔNSs), although able to interact with RIG-I, did not affect the RIG-I-mediated IFN-ß promoter activation, suggesting that the NSs domains responsible for RIG-I-mediated signaling and interaction with RIG-I are mapped on different regions. These results contribute to identify a novel mechanism for bunyaviruses by which TOSV NSs counteracts the early IFN response
(Ca+Mg)ATPase and calcium influx in eruthrocytes of patients with idiopathic hypercalciuria
No full textIncreased erythrocyte (Ca+Mg)ATPase activity was previously observed in idiopathic hypercalciuria. In order to verify if this alteration is a primary or a secondary event, we studied Sr influx in erythrocytes from subjects with idiopathic hypercalciuria. (Ca+Mg)ATPase activity was significantly higher in hypercalciuric than in hypercalciuric than in normocalciuric subjects whereas no difference in Sr influx was found between the two groups. (Ca+Mg)ATPase activity positively correlated with the erythrocyte Sr content found after 5 min of incubation and with urine Ca excretion. The normal Sr permeability suggests that (Ca+Mg)ATPase is primarily altered in idiopathic hypercalciuria. The primary increase of (Ca+Mg)ATPase activity may enhance passive Ca influx by reduction of cellular Ca concentration. It may induce a defect in cellular Ca metabolism that may cause idiopathic hypercalciuria by stimulating bone Ca turn-over and enteral Ca absorption
Analisi retrospettiva su infezioni invasive e non invasive da batteri Gram negativi non fermentanti in pazienti ospedalizzati
No full textProprietμa di legame di anticorpi monoclonali contro il virus della Rab- bia ottenuti per mezzo di immunizzazione con un peptide sintetico.
No full textAB INITIO STUDY OF THE LOWEST ENERGY STATES OF CUSI USING MULTICONFIGURATION VALENCE BOND METHOD
No full textAuthor Institution: National Institute of Standards and Technology, GaithersburgAn all electron ab-initio multiconfiguration valence bond method is applied to study the lowest energy states of CuSi. This detailed gas phase study of copper-silicon molecule should allow us to better understand the bonding occuring at the copper-silicon interface in bulk material used in the construction of electronic devices. The molecular basis consists of Hartree-Fock wavefunctions and includes occupied and unoccupied virtual orbitals for both Cu and Si atoms. By increasing the number of excited virtual states in the basis set we have converged the electronic energies of the first , and states. These results are used to determine the spectroscopic molecular constants of CuSi
Development of a vaccine against hRSV and hPIV3 using a replication deficient Sendai virus vector.
No full textExercise-induced improvement in vasodilatory function accompanies increased insulin sensitivity in obesity and type 2 diabetes mellitus.
No full textExercise-induced improvement in vasodilatory function accompanies increased insulin sensitivity in obesity and type 2 diabetes mellitus.
De Filippis E, Cusi K, Ocampo G, Berria R, Buck S, Consoli A, Mandarino LJ.
Center for Metabolic Biology, Arizona State University, 350 East Orange Street, P.O. Box 873704, Tempe, Arizona 85287-3704, USA.
OBJECTIVE:
The present study was undertaken to determine whether improved vasodilatory function accompanies increased insulin sensitivity in overweight, insulin-resistant subjects (OW) and type 2 diabetic patients (T2DM) who participated in an 8-wk exercise training regimen.
DESIGN:
Before and after training, subjects had euglycemic clamps to determine insulin sensitivity. Brachial artery catheterization was done on another occasion for measurement of vasodilatory function. A lean, healthy, untrained group was studied as nonexercised controls.
RESULTS:
Training increased oxygen consumption (VO2) peak [OW, 29 +/- 1 to 37 +/- 4 ml/kg fat-free mass (FFM).min; T2DM, 33 +/- 2 to 43 +/- 3 ml/kg FFM.min; P < 0.05] and improved insulin-stimulated glucose disposal (OW, 6.5 +/- 0.5 to 7.2 +/- 0.4 mg/kg FFM.min; T2DM, 3.8 +/- 0.3 to 4.2 +/- 0.3 mg/kg FFM.min; P < 0.05) in insulin resistance. OW and T2DM, before training, had decreased acetylcholine chloride (ACh)- and sodium nitroprusside-mediated vasodilation and decreased reactive hyperemia compared with lean controls. Training increased the vasodilatory response to ACh [OW (30 microg ACh/min), 12.2 +/- 3.4 to 19 +/- 4.2 ml/100 g.min; T2DM (30 microg ACh/min), 10.1 +/- 1.5 to 14.2 +/- 2.1 ml/100 g.min; P < 0.05] in both groups without affecting nitroprusside response.
CONCLUSION:
Because vasodilatory dysfunction has been postulated to contribute to insulin resistance, the exercise-induced improvement in vasodilatory function may signify changes in the endothelium that could contribute to the improvement in insulin sensitivity observed after aerobic exercise training
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