Remediation technologies for heavy metal contaminated groundwater.

The contamination of groundwater by heavy metal, originating either from natural soil sources or from anthropogenic sources is a matter of utmost concern to the public health. Remediation of contaminated groundwater is of highest priority since billions of people all over the world use it for drinking purpose. In this paper, thirty five approaches for groundwater treatment have been reviewed and classified under three large categories viz chemical, biochemical/biological/biosorption and physico-chemical treatment processes. Comparison tables have been provided at the end of each process for a better understanding of each category. Selection of a suitable technology for contamination remediation at a particular site is one of the most challenging job due to extremely complex soil chemistry and aquifer characteristics and no thumb-rule can be suggested regarding this issue. In the past decade, iron based technologies, microbial remediation, biological sulphate reduction and various adsorbents played versatile and efficient remediation roles. Keeping the sustainability issues and environmental ethics in mind, the technologies encompassing natural chemistry, bioremediation and biosorption are recommended to be adopted in appropriate cases. In many places, two or more techniques can work synergistically for better results. Processes such as chelate extraction and chemical soil washings are advisable only for recovery of valuable metals in highly contaminated industrial sites depending on economical feasibility.

Predicting QT prolongation in humans during early drug development using hERG inhibition and an anaesthetized guinea-pig model.

BACKGROUND AND PURPOSE: Drug-induced prolongation of the QT interval can lead to torsade de pointes, a life-threatening ventricular arrhythmia. Finding appropriate assays from among the plethora of options available to predict reliably this serious adverse effect in humans remains a challenging issue for the discovery and development of drugs. The purpose of the present study was to develop and verify a reliable and relatively simple approach for assessing, during preclinical development, the propensity of drugs to prolong the QT interval in humans. EXPERIMENTAL APPROACH: Sixteen marketed drugs from various pharmacological classes with a known incidence -- or lack thereof -- of QT prolongation in humans were examined in hERG (human ether a-go-go-related gene) patch-clamp assay and an anaesthetized guinea-pig assay for QT prolongation using specific protocols. Drug concentrations in perfusates from hERG assays and plasma samples from guinea-pigs were determined using liquid chromatography-mass spectrometry. KEY RESULTS: Various pharmacological agents that inhibit hERG currents prolong the QT interval in anaesthetized guinea-pigs in a manner similar to that seen in humans and at comparable drug exposures. Several compounds not associated with QT prolongation in humans failed to prolong the QT interval in this model. CONCLUSIONS AND IMPLICATIONS: Analysis of hERG inhibitory potency in conjunction with drug exposures and QT interval measurements in anaesthetized guinea-pigs can reliably predict, during preclinical drug development, the risk of human QT prolongation. A strategy is proposed for mitigating the risk of QT prolongation of new chemical entities during early lead optimization.

Sero-prevalence of peste des petits ruminants virus antibodies in sheep and goats from the Sudan, 2016-2017.

Recently, severe outbreaks of PPR among small ruminants were reported regularly in different parts of the country leading to significant economic losses. Between 2016 and 2017, a total of 320 sera were collected from sheep (258) and goats (62) from PPR suspected outbreaks from four different States in the Sudan. Screening of sera for the presence of PPRV antibodies by competitive ELISA revealed an overall antibodies sero-prevalence of 80.9% (259/320, 95% CI 20.5-28) among sheep and goats. On the species basis, sheep sera yielded the higher antibodies sero-prevalence of 84.5% (218/258, 95% CI 16.7-24.1) compared to a lower sero-prevalence of 66.1% (41/62, 95% CI 28.5-51.1) obtained from goats sera. Within Sudanese States where outbreaks occurred, the highest overall sero-prevalence of PPRV antibodies in sheep and goats was demonstrated in River Nile State 90.3% (159/176 sera, 95% CI 12.8-18.2) while the lowest incidence was present in Northern State 00.0% (0/2 sera, 95% CI 69.9-72.2). Of note, higher sero-prevalence values were achieved in this study than previously documented. Results of the present study indicated that PPR is currently circulating widely in the Sudan and still is a leading cause of disease outbreaks and higher fatalities in small ruminants. Therefore, the effective PPR vaccine is recommended to cover all parts of the Sudan to prevent the occurrence of disease outbreaks.

Copper biosorption on immobilized seaweed biomass: column breakthrough characteristics.

The biosorption of copper by the brown seaweed Sargassum baccularia, immobilized onto polyvinyl alcohol (PVA) gel beads, was investigated with fixed-bed experiments. Laboratory-scale column tests were performed to determine breakthrough curves with varying flow rates and feed concentrations. A theoretical fixed-bed model, known as the Bohart-Adams equation, was evaluated in simulating the experimental breakthrough curves. The Bohart-Adams model qualitatively predicted the breakthrough trends. PVA-immobilized seaweed biomass beads were amenable to efficient regeneration with aqueous solution containing the chelating agent ethylenediaminetetraacetic acid (EDTA). The biosorbent retained most of its original uptake capacity over three cycles of use. The excellent reusability of the biosorbent could lead to the development of a viable metal remediation technology.

A novel N-aryl tyrosine activator of peroxisome proliferator-activated receptor-gamma reverses the diabetic phenotype of the Zucker diabetic fatty rat.

The discovery that peroxisome proliferator-activated receptor (PPAR)-gamma was the molecular target of the thiazolidinedione class of antidiabetic agents suggested a key role for PPAR-gamma in the regulation of carbohydrate and lipid metabolism. Through the use of high-throughput biochemical assays, GW1929, a novel N-aryl tyrosine activator of human PPAR-gamma, was identified. Chronic oral administration of GW1929 or troglitazone to Zucker diabetic fatty (ZDF) rats resulted in dose-dependent decreases in daily glucose, free fatty acid, and triglyceride exposure compared with pretreatment values, as well as significant decreases in glycosylated hemoglobin. Whole body insulin sensitivity, as determined by the euglycemic-hyperinsulinemic clamp technique, was significantly increased in treated animals. Comparison of the magnitude of glucose lowering as a function of serum drug concentrations showed that GW1929 was 2 orders of magnitude more potent than troglitazone in vivo. These data were consistent with the relative in vitro potencies of GW1929 and troglitazone. Isolated perfused pancreas studies performed at the end of the study confirmed that pancreata from vehicle-treated rats showed no increase in insulin secretion in response to a step change in glucose from 3 to 10 mmol/l. In contrast, pancreata from animals treated with GW1929 showed a first- and second-phase insulin secretion pattern. Consistent with the functional data from the perfusion experiments, animals treated with the PPAR-gamma agonist had more normal islet architecture with preserved insulin staining compared with vehicle-treated ZDF rats. This is the first demonstration of in vivo efficacy of a novel nonthiazolidinedione identified as a high-affinity ligand for human PPAR-gamma. The increased potency of GW1929 compared with troglitazone both in vitro and in vivo may translate into improved clinical efficacy when used as monotherapy in type 2 diabetic patients. In addition, the significant improvement in daily meal tolerance may impact cardiovascular risk factor management in these patients.

Excitatory amino acid receptor-mediated activation of solitarial deglutitive loci.

The deglutitive actions of glutamate were investigated in urethane-anaesthetised rats in order to determine whether different excitatory amino acid receptors mediate activation of pattern generator elements contained within the nucleus tractus solitarii. When applied by micropneumophoresis (0.01-10 pmol) from multibarrelled glass micropipettes (tip diameter 2-5 microns), the excitatory amino acid-receptor agonists, N-methyl-D, L-aspartate (NMA), N-methyl-D-aspartate (NMDA), quisqualate and kainate displayed a rank order of potency at glutamate-responsive pharyngeal sites, in the subnuclei ventralis and intermedialis, where KA greater than NMA/NMDA greater than QA; however, the potency followed the order NMA/NMDA greater than KA greater than QA at oesophageal sites within the subnucleus centralis. The NMDA-receptor blockers, 2-amino-5-phosphonovaleric acid (APV) and 2-amino-7-phosphonoheptanoic acid (AP7), selectively and reversibly inhibited the glutamate-evoked oesophageal responses, but had no corresponding effect on rhythmic oesophageal responses elicited by muscarine. At loci in the nucleus tractus solitarius, where glutamate elicited a complete swallowing sequence, APV/AP7 spared the pharyngeal component but selectively blocked the oesophageal component. The nonselective glutamate-receptor antagonist, gamma-D-glutamylglycine suppressed both pharyngeal and oesophageal responses elicited by glutamate. It is concluded that different types of excitatory amino acid receptors are associated with the deglutitive premotor subnuclei of the nucleus tractus solitarii; kainate receptors predominate within the subnuclei ventralis and intermedialis and NMDA receptors within the subnucleus centralis. Both kainate- and NMDA-mediated mechanisms can operate under physiological conditions.

Modulation of solitarial deglutitive N-methyl-D-aspartate receptors by dihydropyridines.

The ability of the dihydropyridine calcium channel activators, (-)-S-BAY K 8644 and (+)-S-202-791 and the calcium channel inhibitor, (+)-R-BAY K 8644, to modify the differential deglutitive actions of glutamate and muscarine at premotor loci in the nucleus tractus solitarii was investigated in urethane-anaesthetised rats. At subnuclei ventralis and intermedialis loci, pneumophoretic application (20-100 pl) from multibarrelled glass micropipettes (tip diameter 2-5 microns) of glutamate (10-20 pmol) evoked aminophosphonovaleric acid (APV)-insensitive pharyngeal swallows; at sites in the subnucleus centralis of the nucleus tractus solitarii glutamate evoked an APV-sensitive single-wave oesophageal response, whereas muscarine (5-10 pmol) evoked rhythmic oesophageal contractions. Both (-)-S-BAY K 8644 and (+)-S-202-791, applied in prepulses of 10-20 fmol and 100-200 fmol, respectively, either had no effect or selectively and reversibly enhanced or inhibited the glutamate-evoked responses. Identical results were obtained by intravenous administration of (-)-S-BAY K 8644 (10-50 micrograms/kg). Micropneumophoretic (20-50 fmol) or intravenous (10-50 micrograms/kg) administration of (+)-R-BAY K 8644 suppressed the N-methyl-D-aspartate (NMDA)-mediated oesophageal responses in a reversible and selective manner. The dihydropyridine vehicle produced a transient depression of all types of deglutitive responses. It is concluded that, within the deglutitive subnuclei of the nucleus tractus solitarii, "L"-type voltage-operated calcium channels are associated with NMDA-receptor-mediated deglutitive mechanisms. The inhibition or a lack of effect produced by the dihydropyridine calcium channel activators is explained in part by their actions at other sites e.g. release of inhibitory transmitters.

N-(2-Benzoylphenyl)-L-tyrosine PPARgamma agonists. 1. Discovery of a novel series of potent antihyperglycemic and antihyperlipidemic agents.

We have identified a novel series of antidiabetic N-(2-benzoylphenyl)-L-tyrosine derivatives which are potent, selective PPARgamma agonists. Through the use of in vitro PPARgamma binding and functional assays (2S)-3-(4-(benzyloxy)phenyl)-2-((1-methyl-3-oxo-3-phenylpropenyl)+ ++amin o)propionic acid (2) was identified as a structurally novel PPARgamma agonist. Structure-activity relationships identified the 2-aminobenzophenone moiety as a suitable isostere for the chemically labile enaminone moiety in compound 2, affording 2-((2-benzoylphenyl)amino)-3-(4-(benzyloxy)phenyl)propionic acid (9). Replacement of the benzyl group in 9 with substituents known to confer in vivo potency in the thiazolidinedione (TZD) class of antidiabetic agents provided a dramatic increase in the in vitro functional potency and affinity at PPARgamma, affording a series of potent and selective PPARgamma agonists exemplified by (2S)-((2-benzoylphenyl)amino)-3-¿4-[2-(methylpyridin-2-ylamino+ ++)ethoxy ]phenyl¿propionic acid (18), 3-¿4-[2-(benzoxazol-2-ylmethylamino)ethoxy]phenyl¿-(2S)-((2- benzoylph enyl)amino)propanoic acid (19), and (2S)-((2-benzoylphenyl)amino)-3-¿4-[2-(5-methyl-2-phenyloxazol-4-y l)e thoxy]phenyl¿propanoic acid (20). Compounds 18 and 20 show potent antihyperglycemic and antihyperlipidemic activity when given orally in two rodent models of type 2 diabetes. In addition, these analogues are readily prepared in chiral nonracemic fashion from L-tyrosine and do not show a propensity to undergo racemization in vitro. The increased potency of these PPARgamma agonists relative to troglitazone may translate into superior clinical efficacy for the treatment of type 2 diabetes.

Hemodynamic profile of neuropeptide Y in dogs: effect of ganglionic blockade.

The hemodynamic effects of neuropeptide Y (NPY) were examined over a dose range of 0.03-30 nmol/kg, i.v., in anesthetized open-chest, ventilated dogs with and without ganglionic blockade. In normal (non-ganglion-blocked) animals, NPY produced significant, dose-dependent, and sustained (lasting 15-45 min) increases in mean arterial blood pressure and systemic vascular resistance (SVR) with a threshold dose of 0.3 nmol/kg and a maximum effective dose of 10 nmol/kg. Cardiac index (CI) decreased at doses > 1 nmol/kg, but stroke volume was not altered; heart rate (HR) decreased significantly at and above the 3 nmol/kg dose. No significant changes were observed in the left ventricular dP/dt (LVdP/dt) or the contractility index (LVdP/dt divided by systolic pressure). In ganglion-blocked animals, pressor and SVR responses to NPY were similar to those seen in normal animals but HR was not affected and a small but significant decrease in CI was seen only at the 30 nmol/kg. Furthermore, whereas LVdP/dt of ganglion-blocked dogs increased significantly at and above the 1 nmol/kg dose, the contractility index increased slightly only with the 10 and 30 nmol/kg doses. These data indicate that NPY produces sustained hypertension in dogs secondary to peripheral vasoconstriction, has a weak, direct positive inotropic action on the heart, and lacks chronotropic effects.

Cutaneous vasomotor effects of neuropeptide Y.

The effects of neuropeptide Y (NPY) were examined on the cutaneous microvascular blood flow (CMF) of the hindpaws in anesthetized rats. NPY (0.5-50 nmol/kg), infused intra-arterially into the hindpaw circulation, produced sustained dose-dependent increases in CMF (29 +/- 7% to 210 +/- 52%) indicating cutaneous vasodilation. Denervation of a hindpaw, ganglionic or alpha-adrenergic blockade significantly elevated the resting CMF indicating tonic vasoconstrictor sympathetic input to the cutaneous vasculature. In the denervated hindpaw or following ganglionic blockade, NPY produced sustained decreases in CMF (up to 51 +/- 8%) indicating vasoconstriction. Effects of the Y1 receptor agonist, (Leu31, Pro34) NPY were identical to those of NPY. The Y2 receptor agonist, NPY13-36 increased CMF of the intact hindpaw (24 +/- 10%-68 +/- 16% at 5-150 nmol/kg, i.a.) but did not affect CMF of the denervated hindpaw. NPY and (Leu31, Pro34)NPY, but not NPY13-36, produced significant pressor effects. These data suggest that: 1) NPY produces neurogenic cutaneous vasodilation via presynaptic Y2 receptor-mediated inhibition of sympathetic tone, 2) Y1 receptors may also exist presynaptically, however, it is likely that (Leu31, Pro34)NPY does not distinguish between Y1 and Y2 receptors, and 3) activation of postsynaptic Y1 receptors produces vasoconstriction which is unmasked only when the noradrenergic tone is eliminated.

Excitatory action of 5-HT on deglutitive substrates in the rat solitary complex.

The excitatory effect of serotonin (5-HT) on the pharyngeal stage of swallowing was investigated in urethane anaesthetised rats with respect to the involvement of neural substrates located in the central and intermediolateral regions of the nucleus tractus solitarii (NTS). Micropneumophoretic ejection of 5-HT 5-50 pmol either produced deglutitory responses or selectively facilitated the S-glutamate-evoked pharyngeal responses when applied in 1-10 pmol prepulses. The excitatory/facilitatory effect of 5-HT was enhanced by intravenous threshold doses of the 5-HT-mimetic, quipazine (0.3-1 mumol/kg) and reversibly blocked by the 5-HT2-receptor antagonists, methysergide, metergoline and ketanserin. 5-HT doses exceeding 10-60 pmol gave rise to a non-selective reversible inhibition of glutamate- and acetylcholine (ACh)-evoked pharyngeal or oesophageal responses which was not prevented or reversed by 5-HT2-receptor antagonists, but was readily overcome by increasing the amount of glutamate or ACh ejected. Non-selective deglutitive inhibition after high doses of 5-HT could, therefore, result from neuronal desensitization secondary to excessive stimulation or activation of a different type of 5-HT receptor. These results corroborate an excitatory role of 5-HT in both reflex and automatic swallowing and demonstrate that the NTS is a major site of serotoninergic facilitation of swallowing.

Mechanisms of central endothelin-induced hypotension.

The aims of the present study were i) to determine the type of endothelin receptor(s) mediating the hypotension produced by central administration of endothelin-1 (ET-1), ii) to delineate the hemodynamic factors contributing to this hypotension and iii) to differentiate between the neural and cerebrovascular actions of ET-1. Towards these objectives, we monitoreal blood flow from the choroid plexus of the IVth cerebral ventricle (4CV) as an index of local cerebral blood flow (CBF); also, aortic blood flow (ABF) and cutaneous microvascular blood flow (CMF) of the hindpaw were monitored. In anesthetized, ventilated rats, ET-1 (1, 3 and 10 pmol) applied to the 4CV produced significant decreases in mean arterial blood pressure (15 +/- 4%, 34 +/- 3% and 37 +/- 3% respectively); hypotension was sustained at the two higher doses. ET-1 also produced a profound and sustained reduction in CBF (36 +/- 10%, 54 +/- 10% and 57 +/- 11% respectively). Prior administration of a low dose (1 nmol) of the ETA receptor selective antagonist, BQ-123 [cyclo (D-Trp-D-Asp-L-Pro-D-Val-L-Leu)], abolished only the central ET-1-induced hypotension; the decreases in CBF were not altered (57 +/- 11% and 56 +/- 6% respectively after 3 and 10 pmol). Pretreatment with a high dose (20 nmol) of BQ-123 attenuated but did not abolish the CBF response to 10 pmol of ET-1 (-26 +/- 1% vs. -57 +/- 11%).(ABSTRACT TRUNCATED AT 250 WORDS)

Functional evidence for the presence of a phosphoramidon-sensitive enzyme in rat brain that converts big endothelin-1 to endothelin-1.

Endothelin-1 (ET-1) is produced from its precursor, big endothelin-1 (BigET-1), by a putative endothelin-converting enzyme (ECE), but it is not known whether the enzyme is present in the brain. This study was conducted to examine the central hemodynamic effects of BigET-1 and to indirectly determine the presence of an ECE in rat brain. Cardiovascular effects of centrally administered BigET-1 and ET-1 were examined in anesthetized, ventilated rats. BigET-1 (100 pmol) or ET-1 (10 pmol) applied to the IV ventricle produced similar prolonged decreases in mean arterial pressure (MAP) and renal blood flow (RBF). Thus, peak decreases with BigET-1 were (mean +/- S.E.): MAP = -35 +/- 4%; RBF = -27 +/- 5%, while those with ET-1 were: MAP = -36 +/- 5%; RBF = -29 +/- 9%. Pretreatment with phosphoramidon, a metalloprotease inhibitor (90 nmol), abolished the hemodynamic responses elicited by BigET-1 (MAP = -9 +/- 2%; RBF = -3 +/- 2%) but not those produced by ET-1. These data indicate that; i) conversion of BigET-1 to ET-1 in the brain is essential for the expression of hemodynamic actions and ii) a metalloprotease capable of converting BigET-1 to ET-1 is present in rat brain.

Effects of acepromazine, pethidine and atropine premedication on lower oesophageal sphincter pressure and barrier pressure in anaesthetised cats.

Combinations of acepromazine maleate, pethidine hydrochloride and atropine sulphate (0.05 mg/kg) or acepromazine maleate and pethidine hydrochloride and acepromazine maleate alone or atropine sulphate (0.1 mg/kg) alone were used to premedicate cats before they were anaesthetised with thiopentone, to investigate their effects on gastric pressure, lower oesophageal sphincter pressure and barrier pressure under anaesthesia. Manometric measurements were made by using a non-perfused manometric technique. The lower oesophageal sphincter pressure was lowest in the cats premedicated with atropine sulphate alone. The difference in barrier pressure between the atropine (0.1 mg/kg) and acepromazine treated cats was highly significant. The risk of gastro-oesophageal reflux appeared to be highest with atropine (0.1 mg/kg) if barrier pressure is used as an indicator of the likelihood of reflux.

Effects of thiopentone, propofol, alphaxalone-alphadolone, ketamine and xylazine-ketamine on lower oesophageal sphincter pressure and barrier pressure in cats.

The anaesthetic induction agents thiopentone, propofol and alphaxalone-alphadolone were administered to cats intravenously and ketamine and xylazine-ketamine-atropine were administered intramuscularly in order to determine their effects on gastric pressure, lower oesophageal sphincter pressure, and barrier pressure. Manometric measurements were made with a non-perfused catheter tip pressure transducer. All the anaesthetic induction agents decreased the tone of the lower oesophageal sphincter but the reduction was least with ketamine. Lower oesophageal sphincter tone was significantly higher in cats anaesthetised with either xylazine-ketamine-atropine or propofol than in cats anaesthetised with either thiopentone or alphaxalone-alphadolone. Despite a higher gastric pressure in the cats anaesthetised with ketamine rather than with the other drugs except propofol, the barrier pressure was also significantly higher in cats anaesthetised with ketamine than in cats anaesthetised with any of the other drugs except xylazine-ketamine-atropine. The risk of gastrooesophageal reflux seemed to be higher with alphaxalone-alphadolone than with thiopentone if the lower oesophageal sphincter pressure and gastric pressure are used as indicators of likely reflux.

Measurement of the length and position of the lower oesophageal sphincter by correlation of external measurements and radiographic estimations in dogs.

Fifty dogs were investigated in order to correlate the length and position of the lower oesophageal sphincter (LOS) with external measurements. Various external measurements were taken while the dogs were anaesthetised and positioned in lateral recumbency. An oesophageal tube was then introduced into the oesophagus and thoracic radiographs were taken. The 'real internal length of the oesophagus' was calculated as the length from the lower jaw incisor tooth to the position of the oesophageal tube at the costal border of the diaphragm. A highly significant linear correlation was found between this internal length and the external length from lower jaw incisor tooth to the anterior border of the head of the 10th rib. Using oesophageal manometry, the length and position of the LOS was also studied in 25 clinically normal bitches. The mean length of the LOS was found to be 4.6 +/- 0.92 cm. The position of the LOS was a mean of 4.4 +/- 1.69 cm cranial to the costal border of the diaphragm. The findings of this study indicate that the external measurements can be used to position catheters for accurate oesophageal manometry in the dog.

A comparison of the effects of halothane and isoflurane in combination with nitrous oxide on lower oesophageal sphincter pressure and barrier pressure in anaesthetised dogs.

The effects of surgery, and of halothane and isoflurane, on oesophageal pressures were examined in 30 dogs. The dogs were premedicated with a combination of acepromazine maleate (0.1 mg/kg) and pethidine hydrochloride (1 mg/kg), and anaesthesia was induced with thiopentone (10 mg/kg). Ten of the dogs underwent abdominal surgery with halothane, 10 underwent abdominal surgery with isoflurane and 10 underwent non-abdominal surgery with halothane. Gastric pressure, lower oesophageal sphincter pressure and oesophageal barrier pressures were measured at five to 10 minutes after induction, five to 10 minutes after the initial surgical incision, during the abdominal surgery and while the skin was being sutured. There were no significant differences in lower oesophageal sphincter pressure between the groups of dogs but the pressures were greater in all the dogs during the surgical manipulation than shortly after induction or while the skin was being sutured. During abdominal surgery with halothane the barrier pressure was significantly higher (P < 0.05) than during non-abdominal surgery with halothane. The barrier pressure was lower (P < 0.001) during skin suturing after abdominal surgery with isoflurane than after abdominal or non-abdominal surgery with halothane. The lower oesophageal sphincter appears to be more sensitive to isoflurane than halothane.

Effect of body position on oesophageal and gastric pressures in the anaesthetised dog.

The effect of body position on lower oesophageal sphincter pressure (LOSP), gastric pressure and barrier pressure (BrP) was investigated in 40 dogs anaesthetised for neutering procedures. The dogs were placed in lateral recumbency followed by dorsal recumbency (group 1) or vice versa (group 2). LOSP decreased significantly in the animals which were positioned initially in lateral recumbency, when they were then placed in dorsal recumbency, while those initially positioned in dorsal recumbency showed no significant change in their LOSP or BrP when their position was altered to lateral recumbency. When the data from both groups were pooled, LOSP and BrP were significantly lower when the dogs were in dorsal compared to lateral recumbency (P < 0.05).

Performance evaluation of supported ionic liquid membrane for removal of phenol.

This work evaluates the performance of ionic liquid in supported liquid membrane (SLM) for the removal of phenol from wastewater. Ionic liquids are organic salts entirely composed of organic cations and either organic or inorganic anions. Due to the fact that the vapor pressure of ionic liquid is not detectable and they are sparingly soluble in most conventional solvents, they can be applied in SLM as the organic phase. In this work, 1-n-alkyl-3-methylimidazolium salts, [C(n)MIM](+)[X](-) have been investigated so as to determine an optimal supported ionic liquid membrane. The effect of operational parameters such as pH, stirring speed and the concentration of stripping agent has been studied, and an evaluation of different membrane supports were also carried out. With a minimal amount of the ionic liquid 1-Butyl-3-methylimidazolium hydrogensulfate, 85% phenol removal could be achieved by using polytetrafluoroethylene hydrophobic membrane filter in the SLM.

Emulsion stabilization using ionic liquid [BMIM]+[NTf2]- and performance evaluation on the extraction of chromium.

This study focuses on the role of a hydrophobic ionic liquid 1-butyl-3-methylimidazolium bis(trifluoromethylsulfonyl)imide, [BMIM](+)[NTf(2)](-) in the preparation of emulsion liquid membrane (ELM) phase containing kerosene as solvent, Span 80 as surfactant, NaOH as internal phase and TOMAC (tri-n-octylmethylammonium chloride) a second ionic liquid as carrier. The first time used [BMIM](+)[NTf(2)](-) in ELM was found to play the role of a stabilizer. The emulsion prepared using [BMIM](+) [NTf(2)](-) has a long period of stability of about 7h (at 3% (w/w) of [BMIM](+)[NTf(2)](-)) which otherwise has a brief stability up to only 7 min. The stability of the emulsion increases with the increase in concentration of [BMIM](+)[NTf(2)](-) up to 3% (w/w). Nevertheless, with further increase in concentration of [BMIM](+)[NTf(2)](-), a reduction in the stability occurs. The extraction experiments were carried out after holding the ELM for 2h after the preparation and a removal efficiency of approximately 80% was obtained for Cr. The destabilization of the emulsion was studied by observing the change in the interface height. An empirical correlation for the stability of the emulsion has been proposed.