Modelo de decaimiento de cloro libre en la red de distribución de agua potable en la ciudad de Azogues, Ecuador

Universidad Nacional Agraria La Molina. Escuela de Posgrado. Doctorado en Ingeniería y Ciencias AmbientalesLas redes de distribución de agua potable (RDAP) deben mantener concentraciones mínimas de cloro (0,3mg/L) para asegurar la desinfección. Niveles elevados de cloro podrían ocasionar corrosión en las tuberías de cobre que son usadas a nivel domiciliario. Los modelos de decaimiento de cloro permiten predecir concentraciones del desinfectante y optimizar la dosificación del desinfectante en RDAP. Este estudio tuvo como objetivo evaluar un modelo de decaimiento de cloro residual en una RDAP usando EPANET y la relación del cloro libre en la corrosión. Para la modelación del cloro libre fue necesario elaborar un modelo hidráulico perfectamente calibrado y validado, así como determinar la constante de reacción del cloro con el agua kb, mediante el test de botella; mientras la constante de reacción con la pared del tubo kw fue calculada a partir de mediciones de campo. Para estimar la corrosión de las tuberías de cobre se utilizaron cupones extraíbles construidos con material de la misma tubería usada por la EMAPAL. Estos cupones fueron instalados en agua a diferentes concentraciones de cloro durante 30, 60, 90 y 180 días, luego de lo cual se determinó la tasa de corrosion por pérdida de peso. Las concentraciones de cloro residual simuladas por el modelo fueron muy cercanas a las concentraciones reales medidas en diferentes puntos de la RDAP. Los resultados demostraron que se puede lograr un mayor nivel de precisión usando coeficientes kb y kw calculados experimentalmente en cada RDAP en estudio. Se determinó que el cloro influye en la corrosión de tuberías de cobre. La simulación permitió determinar las concentraciones de cloro que debe mantenerse en el tanque de distribución, para mantener la mínima concentración en la RDAP de la ciudad de Azogues. Los modelos predicen la calidad del agua, pudiéndose usar como una herramienta de gestión para optimizar la calidad del servicio proporcionada por las empresas operadoras.Drinking water distribution networks (WDN) must maintain minimum chlorine concentrations (0.3mg / L) to ensure disinfection. High levels of chlorine could cause corrosion in copper pipes that are used at the home level. Chlorine decay models allow to predict concentrations of the disinfectant and optimize the dosage of the disinfectant in WDN. The objective of this study was to evaluate a model of residual chlorine decay in a WDN using EPANET and the relation of free chlorine in corrosion. For the modeling of free chlorine it was necessary to elaborate a perfectly calibrated and validated hydraulic model, as well as to determine the reaction constant of chlorine with water kb, by means of the bottle test; while the reaction constant with the tube wall kw was calculated from field measurements. To estimate the corrosion of the copper pipes, extractable coupons constructed with material from the same pipeline used by EMAPAL were used. These coupons were installed in water at different concentrations of chlorine for 30, 60, 90 and 180 days, after which the corrosion rate for weight loss was determined. The residual chlorine concentrations simulated by the model were very close to the actual concentrations measured at different points of the WDN. The results showed that a higher level of precision can be achieved using kb and kw coefficients experimentally calculated in each WDN under study. It was determined that chlorine influences the corrosion of copper pipes. The simulation allowed to determine the chlorine concentrations that must be maintained in the distribution tank, in order to maintain the minimum concentration in the WDN of the Azogues city. The models predict water quality, and can be used as a management tool to optimize the quality of service provided by the operating companies.Tesi

La irradiación del estado social de derecho en el contrato de seguro en Colombia

La asunción del estado social de derecho como nuevo modelo en el ordenamiento jurídico colombiano, ello en respuesta a un modelo clásico de derecho, sin lugar a dudas esta modificación tuvo unas importantes repercusiones en todo el sistema jurídico, de allí que entre las principales características que posea este modelo social sea la garantía de algunos derechos económicos, sociales y culturales por conexidad con los derechos fundamentales, de allí que el contrato de seguro que en un inicio se encontrara regido por normas eminentemente de origen legal, con la misma constitucionalización ese ostente un nuevo alcance, de allí que deba estudiarse cuales han sido las implicaciones directas que ha tenido el contrato de seguro dentro de la noción del estado social de derecho. de tal manera en un inicio se abordará la noción de estado social de derecho, junto con algunas características entre ellas la consecución del mínimo vital como derecho fundamental. así mismo se estudiarán los principales elementos del contrato de seguro, para finalmente determinar que efectos y cuales han sido las implicaciones que ha tenido el estado social de derecho en el contrato de seguro, ello teniendo en cuenta el abuso de la posición dominante y la protección del derecho al mínimo vital, que terminara desembocando en la procedencia de la acción de tutela en algunas disputas aseguraticias1. La noción del estado social de derecho y su delimitación en el estado colombiano. -- 1.2. La naturaleza del estado social de derecho y su implantación en colombia.-- 1.3.El derecho al mínimo vital como derecho fundamental. -- 2.El contrato de seguro. -- 2.1. Antecedentes históricos. -- 2.2. Definición del contrato de seguro. -- 2.3. Características del contrato de seguros. -- 2.3.1. Consensualidad. -- 2.3.2. Bilateralidad. -- 2.3.3. Oneroso. -- 2.3.4. Aleatorio. -- 2.3.5. Ejecución sucesiva. -- 2.3.6. Principal. -- 2.3.7. Adhesión. -- 2.3.8. Buena fe. -- 2.4. Partes y elementos esenciales. -- 2.4.1. Partes del contrato de seguro. -- 2.4.2. Elementos. -- 2.4.2.1. Interés asegurable. -- 2.4.2.2. Riesgo asegurable. -- 2.4.2.3. La prima. -- 2.4.2.4. La obligación condicional a cargo del asegurador. -- 2.5. Recapitulación. -- 3. La irradiación del estado social de derecho en el contrato de seguro. -- 3.1. La constitucionalización del derecho privado. -- 3.2. Jurisprudencia constitucional y la irradiación del estado social de derecho en los contratos de seguro. -- 4. Conclusiones. -- 5. Bibliografia

Methylthioadenosine

5'-Methylthioadenosine (MTA) is a naturally occurring sulfur-containing nucleoside present in all mammalian tissues. MTA is produced from S-adenosylmethionine mainly through the polyamine biosynthetic pathway, where it behaves as a powerful inhibitory product. This compound is metabolized solely by MTA-phosphorylase, to yield 5-methylthioribose-1-phosphate and adenine, a crucial step in the methionine and purine salvage pathways, respectively. Abundant evidence has accumulated over time suggesting that MTA can affect cellular processes in many ways. MTA has been shown to influence numerous critical responses of the cell including regulation of gene expression, proliferation, differentiation and apoptosis. Although most of these responses have been observed at the pharmacological level, their specificity makes it tempting to speculate that endogenous MTA could play a regulatory role in the cell. Finally, observations carried out in models of liver damage and cancer demonstrate a therapeutic potential for MTA that deserves further consideration

Inhibition of liver methionine adenosyltransferase gene expression by 3-methylcolanthrene: protective effect of S-adenosylmethionine

Methionine adenosyltransferase (MAT) is an essential enzyme that catalyzes the synthesis of S-adenosylmethionine (AdoMet), the most important biological methyl donor. Liver MAT I/III is the product of the MAT1A gene. Hepatic MAT I/III activity and MAT1A expression are compromised under pathological conditions such as alcoholic liver disease and hepatic cirrhosis, and this gene is silenced upon neoplastic transformation of the liver. In the present work, we evaluated whether MAT1A expression could be targeted by the polycyclic arylhydrocarbon (PAH) 3-methylcholanthrene (3-MC) in rat liver and cultured hepatocytes. MAT1A mRNA levels were reduced by 50% following in vivo administration of 3-MC to adult male rats (100 mg/kg, p.o., 4 days' treatment). This effect was reproduced in a time- and dose-dependent fashion in cultured rat hepatocytes, and was accompanied by the induction of cytochrome P450 1A1 gene expression. This action of 3-MC was mimicked by other PAHs such as benzo[a]pyrene and benzo[e]pyrene, but not by the model arylhydrocarbon receptor (AhR) activator 2,3,7,8-tetrachlorodibenzo-p-dioxin. 3-MC inhibited transcription driven by a MAT1A promoter-reporter construct transfected into rat hepatocytes, but MAT1A mRNA stability was not affected. We recently showed that liver MAT1A expression is induced by AdoMet in cultured hepatocytes. Here, we observed that exogenously added AdoMet prevented the negative effects of 3-MC on MAT1A expression. Taken together, our data demonstrate that liver MAT1A gene expression is targeted by PAHs, independently of AhR activation. The effect of AdoMet may be part of the protective action of this molecule in liver damage

Modeling of Chemical Oxygen Demand and Total Suspended Solids Removal Using the Fenton Process

Predictive mathematical models were developed for removing Chemical Oxygen Demand (COD) and Total Suspended Solids (TSS) and optimizing the main operating parameters of the Fenton process, applied to effluents from a fish canning industry. The maximum removals obtained for COD and TSS were 89.2 % and 76.1 %, respectively. The optimum doses for COD removal were: 200 mg/L FeSO4 7H2O and 1,000 mg/L H2O2 at pH 2.5. While for TSS removal the optimum parameters were 1 200 mg/L H2O2, 300 mg/L FeSO4 7H2O, and pH 3. The adjusted R2 values of the COD and TSS removal models were 70.64 % and 98.01 %, respectively, indicating that the models obtained are acceptable in the prediction of both parameters

Hyperhomocysteinemia in liver cirrhosis: mechanisms and role in vascular and hepatic fibrosis

Numerous clinical and epidemiological studies have identified elevated homocysteine levels in plasma as a risk factor for atherosclerotic vascular disease and thromboembolism. Hyperhomocysteinemia may develop as a consequence of defects in homocysteine-metabolizing genes; nutritional conditions leading to vitamin B(6), B(12), or folate deficiencies; or chronic alcohol consumption. Homocysteine is an intermediate in methionine metabolism, which takes place mainly in the liver. Impaired liver function leads to altered methionine and homocysteine metabolism; however, the molecular basis for such alterations is not completely understood. In addition, the mechanisms behind homocysteine-induced cellular toxicity are not fully defined. In the present work, we have examined the expression of the main enzymes involved in methionine and homocysteine metabolism, along with the plasma levels of methionine and homocysteine, in the liver of 26 cirrhotic patients and 10 control subjects. To gain more insight into the cellular effects of elevated homocysteine levels, we have searched for changes in gene expression induced by this amino acid in cultured human vascular smooth muscle cells. We have observed a marked reduction in the expression of the main genes involved in homocysteine metabolism in liver cirrhosis. In addition, we have identified the tissue inhibitor of metalloproteinases-1 and alpha1(I)procollagen to be upregulated in vascular smooth muscle cells and liver stellate cells exposed to pathological concentrations of homocysteine. Taken together, our observations suggest (1) impaired liver function could be a novel determinant in the development of hyperhomocysteinemia and (2) a role for elevated homocysteine levels in the development of liver fibrosis

Importance of a deficiency in S-adenosyl-L-methionine synthesis in the pathogenesis of liver injury

One of the features of liver cirrhosis is an abnormal metabolism of methionine--a characteristic that was described more than a half a century ago. Thus, after an oral load of methionine, the rate of clearance of this amino acid from the blood is markedly impaired in cirrhotic patients compared with that in control subjects. Almost 15 y ago we observed that the failure to metabolize methionine in cirrhosis was due to an abnormally low activity of the enzyme methionine adenosyltransferase (EC 2.5.1.6). This enzyme converts methionine, in the presence of ATP, to S-adenosyl-L-methionine (SAMe), the main biological methyl donor. Since then, it has been suspected that a deficiency in hepatic SAMe may contribute to the pathogenesis of the liver in cirrhosis. The studies reviewed here are consistent with this hypothesis

Methylthioadenosine phosphorylase gene expression is impaired in human liver cirrhosis and hepatocarcinoma

Methylthioadenosine phosphorylase (MTAP) is a key enzyme in the methionine and adenine salvage pathways. In mammals, the liver plays a central role in methionine metabolism, and this essential function is lost in the progression from liver cirrhosis to hepatocarcinoma. Deficient MTAP gene expression has been recognized in many transformed cell lines and tissues. In the present work, we have studied the expression of MTAP in human and experimental liver cirrhosis and hepatocarcinoma. We observe that MTAP gene expression is significantly reduced in human hepatocarcinoma tissues and cell lines. Interestingly, MTAP gene expression was also impaired in the liver of CCl4-cirrhotic rats and cirrhotic patients. We provide evidence indicating that epigenetic mechanisms, involving DNA methylation and histone deacetylation, may play a role in the silencing of MTAP gene expression in hepatocarcinoma. Given the recently proposed tumor suppressor activity of MTAP, our observations can be relevant to the elucidation of the molecular mechanisms of multistep hepatocarcinogenesis

Methylthioadenosine reverses brain autoimmune disease

OBJECTIVE: To assess the immunomodulatory activity of methylthioadenosine (MTA) in rodent experimental autoimmune encephalomyelitis (EAE) and in patients with multiple sclerosis. METHODS: We studied the effect of intraperitoneal MTA in the acute and chronic EAE model by quantifying clinical and histological scores and by performing immunohistochemistry stains of the brain. We studied the immunomodulatory effect of MTA in lymphocytes from EAE animals and in peripheral blood mononuclear cells from healthy control subjects and multiple sclerosis patients by assessing cell proliferation and cytokine gene expression, by real-time polymerase chain reaction, and by nuclear factor-kappaB modulation by Western blot. RESULTS: We found that MTA prevents acute EAE and, more importantly, reverses chronic-relapsing EAE. MTA treatment markedly inhibited brain inflammation and reduced brain damage. Administration of MTA suppressed T-cell activation in vivo and in vitro, likely through a blockade in T-cell signaling resulting in the prevention of inhibitor of kappa B (IkappaB-alpha) degradation and in the impaired activation transcription factor nuclear factor-kappaB. Indeed, MTA suppressed the production of proinflammatory genes and cytokines (interferon-gamma, tumor necrosis factor-alpha, and inducible nitric oxide synthase) and increased the production of antiinflammatory cytokines (interleukin-10). INTERPRETATION: MTA has a remarkable immunomodulatory activity and may be beneficial for multiple sclerosis and other autoimmune diseases

Impaired liver regeneration in mice lacking methionine adenosyltransferase 1A

Methionine adenosyltransferase (MAT) is an essential enzyme because it catalyzes the formation of S-adenosylmethionine (SAMe), the principal biological methyl donor. Of the two genes that encode MAT, MAT1A is mainly expressed in adult liver and MAT2A is expressed in all extrahepatic tissues. Mice lacking MAT1A have reduced hepatic SAMe content and spontaneously develop hepatocellular carcinoma. The current study examined the influence of chronic hepatic SAMe deficiency on liver regeneration. Despite having higher baseline hepatic staining for proliferating cell nuclear antigen, MAT1A knockout mice had impaired liver regeneration after partial hepatectomy (PH) as determined by bromodeoxyuridine incorporation. This can be explained by an inability to up-regulate cyclin D1 after PH in the knockout mice. Upstream signaling pathways involved in cyclin D1 activation include nuclear factor kappaB (NFkappaB), the c-Jun-N-terminal kinase (JNK), extracellular signal-regulated kinases (ERKs), and signal transducer and activator of transcription-3 (STAT-3). At baseline, JNK and ERK are more activated in the knockouts whereas NFkappaB and STAT-3 are similar to wild-type mice. Following PH, early activation of these pathways occurred, but although they remained increased in wild-type mice, c-jun and ERK phosphorylation fell progressively in the knockouts. Hepatic SAMe levels fell progressively following PH in wild-type mice but remained unchanged in the knockouts. In culture, MAT1A knockout hepatocytes have higher baseline DNA synthesis but failed to respond to the mitogenic effect of hepatocyte growth factor. Taken together, our findings define a critical role for SAMe in ERK signaling and cyclin D1 regulation during regeneration and suggest chronic hepatic SAMe depletion results in loss of responsiveness to mitogenic signals