Comparación de los niveles sonoros generados por ruido de tránsito continuo e interrumpido

En este trabajo se realiza un estudio que permite proponer un modelo para la distribución de nilvel sonoro en el tiempo, que produce el flujo vehicular, para dos condiciones de circulación: flujo libre y flujo interrumpido. Los resultados obtenidos muestran que no hay evidencias para rechazar un modelo normal en ambos casos y que los valores medios de las distribuciones de nivel sonoro para la condición flujo libre, son significativamente distintos de los obtenidos para la condición de flujo interrumpido. Para flujos libres con velocidades comprendidas entre 50 y 70 km/hr, el nivel sonoro medio es mayor para la condición de flujo libre respecto de la condición de flujo interrumpido

Medio ambiente acústico en el metro de Santiago

En este trabajo se analizan los niveles de ruido existentes en el metro de Santiago, tanto en banda ancha como en banda angosta. Se utilizan como cuantificadores L 1 0 , L5 0 , L 9 0, L 9 5, Leq y PSIL. Los valores encontrados en Leq, para un viaje típico en la línea 1, es de 86.2 dB (A) y en la linea 2 de 86.7 dB (A). Para L 5 0 se obtuvo un valor de 80.3 dB (A) para ambas líneas; el ruido de fondo que se puede asociar a L 9 5 es levemente superior a 70 dB (A). Los climas de ruido obtenidos para un viaje típico en línea 1 y 2 resulta ser 20 dB (A) y 20.5 dB (A), respectivamente. Los niveles encontrados para los distintos cuantificadores analizados, sobrepasan todos los límites recomendados

Peroxynitrite activates ERK via Raf-1 and MEK, independently from EGF receptor and p21Ras in H9C2 cardiomyocytes

Peroxynitrite is a potent oxidant and nitrating species proposed as a direct effector of myocardial damage in a wide range of cardiac diseases. Whether peroxynitrite also acts indirectly, by modulating cell signal transduction pathways in the myocardium, has not been investigated. Here, we examined the ability of peroxynitrite to activate extracellular signal-related kinase (ERK), a MAP kinase which has been linked with hypertrophic and anti-apoptotic responses in the heart, in cultured H9C2 cardiomyocytes. Peroxynitrite elicited a concentration- and time-dependent activation of ERK, secondary to the upstream activation of MEK 1 (ERK kinase). Activation of MEK-ERK by peroxynitrite was related to the upstream activation of Raf-1 kinase, as ERK and MEK phosphorylation were prevented by the Raf-1 inhibitor BAY43-9006. These effects of peroxynitrite were not associated with the activation of p21(Ras), known as a common signaling target of cellular oxidative stress. In contrast to ERK activation mediated by the epidermal growth factor (EGF), ERK activation by peroxynitrite was not prevented by AG1478 (EGF receptor inhibitor). Peroxynitrite acted through oxidative, but not nitrative chemistry, as ERK remained activated while nitration was prevented by the flavanol epicatechin. In addition to ERK, peroxynitrite also potently activated two additional members of the MAP kinase family of signaling proteins, JNK and p38. Thus, peroxynitrite activates ERK in cardiomyocytes through an unusual signaling cascade involving Raf-1 and MEK 1, independently from EGFR and P21(Ras), and also acts as a potent activator of JNK and p38. These results provide the novel concept that peroxynitrite may represent a previously unrecognized signaling molecule in various cardiac pathologies

Peroxynitrite is a potent inhibitor of NF-{kappa}B activation triggered by inflammatory stimuli in cardiac and endothelial cell lines.

Peroxynitrite is a potent oxidant and nitrating species proposed as a direct effector of myocardial damage in numerous cardiac pathologies. Whether peroxynitrite also acts indirectly, by modulating cell signal transduction in the myocardium, has not been investigated. Therefore, we examined a possible role for peroxynitrite on the activation of NF-kappaB, a crucial pro-inflammatory transcription factor, in cultured H9C2 cardiomyocytes. H9C2 cells were stimulated with tumor necrosis factor-alpha or lipopolysaccharide following a brief (20-min) exposure to peroxynitrite. NF-kappaB activation (phosphorylation and degradation of its inhibitor IkappaBalpha, nuclear translocation of NF-kappaB p65, and NF-kappaB DNA binding) triggered by lipopolysaccharide or tumor necrosis factor-alpha was abrogated by peroxynitrite. Peroxynitrite also inhibited NF-kappaB in two human endothelial cell lines activated with tumor necrosis factor-alpha or interleukin-1beta. These effects were related to oxidative but not nitrative chemistry and were still being observed while nitration was suppressed by epicatechin. The mechanism of NF-kappaB inhibition by peroxynitrite was a complete blockade of phosphorylation and activation of the upstream kinase IkappaB kinase (IKK) beta, required for canonical, pro-inflammatory NF-kappaB activation. At the same time, peroxynitrite activated phosphorylation of NF-kappaB-inducing kinase and IKKalpha, considered as part of an alternative, noncanonical NF-kappaB activation pathway. Suppression of IKKbeta-dependent NF-kappaB activation translated into a marked inhibition of the transcription of NF-kappaB-dependent genes by peroxynitrite. Thus, peroxynitrite has a dual effect on NF-kappaB, inhibiting canonical IKKbeta-dependent NF-kappaB activation while activating NF-kappaB-inducing kinase and IKKalpha phosphorylation, which suggests its involvement in an alternative pathway of NF-kappaB activation. These findings offer new perspectives for the understanding of the relationships between redox stress and inflammation

Peroxynitrite is a major trigger of cardiomyocyte apoptosis in vitro and in vivo

Recent evidence indicates that peroxynitrite represents a major cytotoxic effector in heart diseases, but its mechanisms of action are still not known exactly. Notably, the ability of peroxynitrite to trigger cardiomyocyte apoptosis, a crucial mode of cell death in many cardiac conditions, remains poorly defined. We evaluated apoptotic and necrotic cell death in cultured H9C2 cardiomyocytes, following a brief (20 min) exposure to peroxynitrite (50-500 microM). Peroxynitrite-dependent myocardial toxicity was then investigated in a rat model of myocardial ischemia-reperfusion (MIR), where the effects of peroxynitrite were blocked by the superoxide dismutase mimetics and peroxynitrite scavenger Mn(III)-tetrakis(4-benzoic acid) porphyrin (MnTBAP). In vitro, peroxynitrite killed cardiomyocytes mostly through apoptosis (DNA fragmentation, apoptotic nuclear alterations, caspase-3 activation, and PARP cleavage), but not necrosis (propidium iodide staining and LDH release). In vivo, MIR triggered myocardial oxidative stress (malondialdehyde generation), nitrotyrosine formation, neutrophil accumulation, and the cleavage of caspase-3 and PARP, indicating ongoing myocardial apoptosis. MnTBAP suppressed these alterations, allowing a considerable reduction of myocardial injury. Thus, peroxynitrite triggers apoptosis in cardiomyocytes in vitro and in the myocardium in vivo, through a pathway involving caspase-3 activation and the cleavage of PARP. These results provide important novel information on the mechanisms of myocardial toxicity of peroxynitrite

Homocysteine induces cell death in H9C2 cardiomyocytes through the generation of peroxynitrite

Homocysteine (HCY) is toxic on blood vessels, but a potential direct toxicity of HCY on the heart is unknown. We addressed this issue by exposing H9C2 cardiomyocytes to HCY (0.1-5 mM) for up to 6h. At these concentrations, HCY reduced cell viability, induced necrosis and apoptosis and triggered the cleavage of caspase-3 and poly(ADP-ribose) polymerase (PARP). This was associated with the intracellular generation of the potent oxidant peroxynitrite. Removing peroxynitrite by the decomposition catalyst FeTPPS considerably reduced LDH release, DNA fragmentation, cleavage of caspase-3 and PARP, and restored normal cell morphology. In additional experiments performed in primary rat ventricular cardiomyocytes, HCY (1 mM, 6h) activated the phosphorylation of the MAP kinases ERK and JNK, two essential stress signaling kinases regulating myocardial apoptosis, hypertrophy and remodeling. These results provide the first demonstration that HCY kills cardiomyocytes through the generation of peroxynitrite and can activate key signaling cascades in the myocardium

VOLATILITÉ DU TAUX DE CHANGE ET LES INVESTISSEMENTS DIRECTS ETRANGERS EN RÉPUBLIQUE DÉMOCRATIQUE DU CONGO DE 1985 À 2020

This research aimed to assess the existence of a link between exchange rate volatility and FDI (Foreign Direct Investment) in the Democratic Republic of Congo. To do this, it used the Autoregressive Distributed Lag model, using annual data from 1985 to 2020, a period of 36 years. The results reveal that in the short term, exchange rate volatility has a positive and statistically insignificant effect on FDI. However, in the long term, the effect of exchange rate volatility becomes negative and statistically insignificant on FDI in the DRC during the period under review

Chanson Fleurie

https://digitalcommons.library.umaine.edu/mmb-ps/3341/thumbnail.jp

POLITIQUE FISCALE, INSTITUTIONS ET INVESTISSEMENTS DIRECTS ETRANGERS EN REPUBLIQUE DEMOCRATIQUE DU CONGO

This article, which discusses "fiscal policy, institutions, and FDI in the DRC," aimed to explain how the effects of fiscal policy, interacting with the quality of institutions, have impacted FDI in the DRC from 1990 to 2022.It is important to note that debates exist regarding the link between fiscal policy and foreign direct investment, the multiplicity or proliferation of taxes and low FDI rates in the DRC. These debates motivated the realization of this study, the results of which reveal that fiscal pressure is one of the key factors in the attractiveness of FDI in the Democratic Republic of Congo. Hence, the need to solidify its fiscal policy through an improvement in indicators of institutional quality, including business freedom, trade freedom, fiscal freedom, and regulatory quality