Implementation and evaluation of different techniques to modify DRASTIC method for groundwater vulnerability assessment: a case study from Bouficha aquifer, Tunisia.

Groundwater vulnerability assessment has nowadays evolved into an essential tool towards proper groundwater protection and management, while the DRASTIC method is included among the most widely applied vulnerability assessment methods. However, the high uncertainty of the DRASTIC method mainly associated with the subjectivity in assigning parameters ratings and weights has driven many researchers to apply various methods for improving its efficiency. In this context, in the present study, different techniques were implemented with the aim of modifying the DRASTIC framework and thus enhancing its performance for groundwater vulnerability assessment in the Bouficha aquifer, Tunisia. In a first stage, the land use type (L) was incorporated as an additional parameter in the typical DRASTIC framework, thus taking into consideration the impact of anthropogenic activities on groundwater vulnerability. Subsequently, the rating and weighting systems of the developed DRASTIC-L framework were modified through the application of statistical methods (DRASTIC-L-SA) and genetic algorithms (GA) (DRASTIC-L-GA) in an attempt to investigate and compare both linear and nonlinear modifications. To evaluate the various vulnerability frameworks, correlation between vulnerability values and nitrate concentrations, expressed as Spearman's rank correlation coefficient (ρ) and Correlation Index (CI), was examined. The results revealed that the DRASTIC-L-GA framework developed by applying a fully GA-based optimization procedure provided the highest values in terms of the performance metrics used, making it the most suitable for the study area. In addition, the aquifer under study was found to be less vulnerable to pollution when employing the typical DRASTIC framework instead of the modified ones, leading to the conclusion that the former substantially underestimates pollution potential in the study area.

A methodological framework to assess the environmental and economic effects of injection barriers against seawater intrusion.

Seawater intrusion is responsible for the progressive deterioration of groundwater quality in numerous coastal aquifers worldwide. As a consequence, seawater intrusion may constitute a serious threat to local groundwater resources, as well as to the regional economy of coastal areas. To alleviate these negative effects, a number of well-designed protective measures could be implemented. The implementation of these measures is usually associated with significant benefits for the environment and the local economy. In this perspective, the present study investigates the particular case of constructing injection barriers for controlling seawater intrusion by developing a methodological framework that combines numerical modeling with spatial and cost-benefit analyses. To this task, we introduce a novel approach, which considers the socio-economic aspects of seawater intrusion in the modeling procedure, and at the same time focuses on the spatial and temporal relationships between water salinity and farmers' income. To test the proposed methodology two alternative artificial recharge scenarios - with different volumes of water used for injection - are assessed. According to the results of this analysis, both scenarios are likely to have a positive impact on groundwater quality, as well as, a net economic benefit to local society.

Reversible inhibition of vasoconstriction by thiazolidinediones related to PI3K/Akt inhibition in vascular smooth muscle cells.

Thiazolidinediones (also referred to as glitazones), agonists for Peroxisome Proliferator-Activated Receptor gamma (PPARγ), are used for treating type 2 diabetes mellitus, where they decrease insulin resistance and cardiovascular risk. Compounds bearing the thiazolidinedione structure have also been shown to inhibit phosphoinositide 3-kinase (PI3K). Here we tried to elucidate the poorly defined role of PI3K/Akt in the physiology of vascular smooth muscle cell contraction and tested the hypothesis that thiazolidinediones, by affecting the PI3K/Akt pathway, may influence vascular physiology. Isolated rat femoral arteries segments were mounted in a wire myograph and challenged with 100mM KCl or phenylephrine (PE), in the absence or presence of troglitazone, rosiglitazone, pioglitazone, LY294002 (PI3K inhibitor) and 10-DEBC (Akt inhibitor). All these compounds dose-dependently inhibited vasoconstriction to KCl or PE; their effect was reversible (after 60-120 min washout) and not affected by GW9662 (a PPARγ antagonist) or by N(G)-nitro-L-arginine (LNNA, an inhibitor of NO biosynthesis). Analysis of phospho-Akt (ser 473) in lysates from rat arteries (by immunoblot) revealed that thiazolidinediones, LY294002 and 10-DEBC, at the same concentration and kinetics inhibiting vasoconstriction, produced a similar decrease of Akt phosphorylation. PI3K/Akt pathway therefore appears to be an important, fast acting, modulator of contraction of vascular smooth muscle. Thiazolidinediones decrease vasoconstriction of isolated vessels possibly by inhibiting PI3K/Akt pathway. Such an effect of glitazones, if occurring in vivo, may impact cardiovascular syndromes related to vasospasm in diabetic patients.

Effect of silibinin on endothelial dysfunction and ADMA levels in obese diabetic mice.

BACKGROUND: Cardiovascular diseases (CVD) in diabetic patients have endothelial dysfunction as a key pathogenetic event. Asymmetric dimethylarginine (ADMA), an endogenous inhibitor of nitric oxide synthase (NOS), plays a pivotal role in endothelial dysfunction. Different natural polyphenols have been shown to preserve endothelial function and prevent CVD. In this study, we assessed the effect of silibinin, a widely used flavonolignan from milk thistle, on ADMA levels and endothelial dysfunction in db/db mice. METHODS: Eight-week-old db/db mice were administrated a 20 mg/Kg i.p. daily dose of silibinin (n = 6) or vehicle (n = 6) for four weeks. Heterozygous lean db/m mice served as control. Plasma, aorta and liver ADMA levels were determined by ELISA. Vascular reactivity to phenilephrine (PE), acetylcholine (ACh), sodium nitroprusside (SNP) and ADMA was assessed in isolated aortic segments, in wire myograph. RESULTS: Plasma and aorta ADMA levels were higher in db/db than in control lean mice. Silibinin administration markedly decreased plasma ADMA; consistently, aorta ADMA was reduced in silibinin-treated animals. Plasma and aorta ADMA levels exhibited a positive correlation, whereas liver ADMA was inversely correlated with both plasma and aorta ADMA concentrations. Endothelium-(NO)-dependent vasodilatation to ACh was impaired in db/db mice and was restored in the silibinin group, in accordance with the observed reduction of plasma and vascular levels of ADMA. Endothelium-independent vasodilatation to SNP was not modified by silibinin administration; contractile tone induced in isolated aorta from db/db mice by challenging with exogenous ADMA was not affected by the treatment. CONCLUSIONS: Silibinin markedly improves endothelial dysfunction in db/db mice by reducing circulating and vascular ADMA levels. Clinical studies are warranted to assess the efficacy of silibinin for cardiovascular protection.

Endothelium-dependent vasomotor effects of telmisartan in isolated rat femoral arteries.

AT(1) receptor antagonists (ARBs) are drugs widely used for preventing and/or treating major cardiovascular diseases. Some of these drugs also show AT(1) receptor-independent effects that may have patho-physiological significance, such as Peroxisome Proliferator-Activated Receptors gamma (PPARγ) stimulation. Here we investigated the effect of telmisartan (that also stimulates PPARγ) on vasomotor responses of femoral arteries isolated from rat, in comparison to losartan. Femoral artery segments were mounted in a wire myograph and challenged with cumulative concentrations of phenylephrine (PE) and acetylcholine (ACh) after 30-min incubation in the absence or presence of 30 µM telmisartan or 30 µM losartan. Vasomotor responses were not significantly changed by losartan, whereas telmisartan reduced vasoconstriction to PE and increased vasodilatation to ACh. Incubation with 0.1 mM N(G)-nitro-l-arginine abolished relaxation to ACh in untreated controls as well as in losartan-treated preparations, but did not in telmisartan-treated preparations (were 20% relaxation subsisted); this residual relaxing effect was abolished by indomethacin and by endothelium removal. Incubation with 30 µM GW9662 (PPARγ antagonist), 10 µM PD123319 (AT(2) antagonist) or 30 µM A779 (angiotensin(1-7)/Mas antagonist) did not change the effect of telmisartan on vasomotor responses in preparations with intact endothelium. We conclude that telmisartan modifies constriction and dilatation of isolated arteries in an endothelium-dependent manner, involving both nitric oxide and prostanoid production. The present effect of telmisartan, however, does not seem to involve PPARγ, AT(2) or angiotensin(1-7)/Mas.