Pyro-gas analysis of fixed bed reactor end of life tyres (ELTs) pyrolysis: A comparative study.

Pyrolysis of end of life tyres (ELTs) present a promising alternative to their incineration or classical product recovery using mechanical means. It can produce light hydrocarbons (HCs) and other valuable chemicals as part of the pyro-gas stream it generates. In this work, two grades of tyres namely a fresh (virgin) one and a waste disposed ELTs, were used as a feedstock to analyse their pyro-gas constituents. There wasn't much difference in the maximum conversion rate between both tyre grades where the fresh tyres had an estimated 15.17% conversion and the ELTs was 13.45% conversion (both at 800 °C). The difference herein was attributed to release of free radicals prior to subjecting the samples to pyrolysis due to their history. The analysis of the pyro-gas samples showed a large make of light hydrocarbon (HC) products, namely methane (CH4/C1), ethane (C2H6/C2), ethylene (C2H4), propane (C3H8/C3), propylene (C3H6), n-butane (C4H10), butadiene compounds, carbon mono and dioxide (CO,CO2). Light HCs mimciking natural gas were more abundant in the case of ELTs were C1 was estimated as 14.53% at 500 °C and 16.73% at 800 °C. C2 was also estimated higher than the fresh tyres where a 11.78% at 500 °C was noted and 7.67% at 800 °C. It can be recommended that future integration plans in oil and gas ventures, namely refinery and petrochemical complexes, are to start taking responsible measures towards the environment by substituting part of their operations with sustainable feedstock such as ELTs.

Ability of Three Lactic Acid Bacteria to Grow in Sessile Mode and to Inhibit Biofilm Formation of Pathogenic Bacteria.

In this study, we explored the effect of three lactic acid bacteria (LAB), i.e. Enterococcus sp CM9, Enterococcus sp CM18 and Enterococcus faecium H3, and their supernatants, on seven biofilm-forming pathogenic strains isolated from human urinary tract or nose infections. By quantitative biofilm production assay, a strong adherence ability of Enterococcus sp CM9 and Enterococcus sp CM18 was revealed while E. faecium H3 resulted to be moderately adherent. Inhibition tests demonstrated an antimicrobial activity of LAB against pathogens.The presence of cell free supernatant (CFS) of CM9 and CM18 strains significantly decreased the adhesion of S. aureus 10,850, S. epidermidis 4,296 and E. coli FSL24. The CFS of H3 strain was effective against S. epidermidis 4,296 and P. aeruginosa PA1FSL biofilms only. Biofilm formation of K. pneumoniae Kp20FSL, A. baumannii AB8FSL and ESBL+ E. coli FS101570 have not been affected by any CSF while P. aeruginosa PA1FSL biofilm increase in presence of CM9 and CM18 CFS.Confocal Laser Scanning Microscopy revealed that K. pneumoniae Kp20FSL biofilm was inhibited by Enterococcus sp CM9, when grown together.Our results suggest that the LAB strains and/or their bacteriocins can be considered as potential tools to control biofilm formation of some bacterial pathogens.

Insights into the evaluation of the abiotic and biotic degradation rate of commercial pro-oxidant filled polyethylene (PE) thin films.

In this study, commercial products formulated from polyethylene (PE) with pro-oxidant additives, were subjected to abiotic and biotic environments. The materials were presumed to be oxo-biodegradable plastics with thicknesses varying between 30 and 70 µm, and calcium carbonate (CaCO3) filler content reaching up to 11 wt%. Accelerated (aging) weathering tests conducted revealed that UV radiation triggered the biodegradation mechanism. Weight loss reached 50% after exposure to weathering which was attributed to triggering the fragmentation of the plastic films. Furthermore, some 83% of weight loss was estimated after 12 months of soil burial. Fluctuation of weight in mid exposure time spans was related to the cross-linking reaction within the polymeric matrix. The mechanical properties investigated along with the thermal stability profile determined for the materials showed that weathering was more severe than soil burial. Thermogravimetry revealed that onset temperature (Tos) was lower than conventional PO products by 25 °C. This could be attributed to the thermal response of the materials due to presence of ion salts and sterates within their composition. The claims by the manufacturing companies which provided the original specimens under an environmentally friendly pretence is disputed due to the fact that none of the products actually showed evidence of major fragmentation or deterioration after exposure to harsh environments. The work also paves the way in standardising assessment methodology for examining biodegradable plastics.

On the Kinetics of Degradation Reaction Determined Post Accelerated Weathering of Polyolefin Plastic Waste Blends.

Polyolefin (PO) polymers constitute the majority of consumer plastic commodities. The reliance on such materials make it near imposable to avoid touching one in any given day. Therefore, the accumulation of plastic solid waste (PSW) in developed and developing societies alike requires immediate attention to manage and valorize this type of waste. In this work, PSW originating from real life sources and virgin linear low-density polyethylene (LLDPE) films were compounded in a mechanical recycling effort. The recycled blends constituted up to 100% (by weight) of the waste material. Accelerated weathering (aging) was conducted on the blends, reaching threshold limit of exposure to study the major changes occurring on the recycled blends. Thermogravimetry and differential scanning calorimetry (DSC) were used to determine their characteristics and applicability for future recycling using thermo-chemical treatment (TCT) methods. Analytical solution methods following the international committee of thermal analysis and calorimetry (ICTAC) were followed in conducting the measurements and kinetic calculations alike. A novel analytical mathematical solution model is also introduced to determine both the pre-exponential factor (Ao) and apparent activation energy (Ea) of the degradation reaction. The model proved to be a more accurate analysis tool, and the work in whole enabled the determination of future plans for using such waste components as a feedstock to thermal units.

Contrasting effects of selective T- and L-type calcium channel blockade on glomerular damage in DOCA hypertensive rats.

Mibefradil and amlodipine are calcium antagonists with different channel selectivities. Mibefradil blocks both L- and T-type calcium channels; although in the usual pharmacological doses, it predominantly blocks the T-type channels. In contrast, amlodipine selectively blocks L-type channels. The goal of the present study was to assess whether this differential selectivity would result in different effects on end-organ damage in experimental hypertension. For this purpose, deoxycorticosterone acetate (DOCA)-salt hypertensive rats were treated either with equipotent doses of mibefradil or amlodipine (30 mg. kg(-1). d(-1) as food admix). Despite the fact that both drugs decreased systolic arterial pressure to the same extent (140+/-5 mm Hg in the mibefradil group and 144+/-3 mm Hg in the amlodipine group versus 225+/-5 mm Hg in the untreated-DOCA group), only mibefradil decreased proteinuria (35. 5+/-6.5 versus 103.3+/-14.1 mg/24 h in untreated DOCA-salt animals) and prevented glomerular lesions. Both drugs, however, prevented the occurrence of vascular renal lesions. To elucidate the mechanism responsible for this difference, we evaluated in an additional series of experiments the effects of mibefradil and amlodipine on plasma and renal renin concentrations, as well as the effects of the addition of enalapril, an ACE inhibitor, given on top of both drugs on proteinuria. Amlodipine, in contrast to mibefradil, markedly stimulated the plasma (17.8+/-2.6 ng Ang I. mL(-1). h(-1) in the amlodipine group versus 3.9+/-0.4 ng Ang I. mL(-1). h(-1) in the mibefradil group and 3.2+/-0.3 ng Ang I. mL(-1). h(-1) in the untreated-DOCA group) and renal (2.42+/-0.37 ng Ang I. mL(-1). h(-1) in the amlodipine group versus 0.36+/-0.04 ng Ang I. mL(-1). h(-1) in the mibefradil group and 0.26+/-0.08 ng Ang I. mL(-1). h(-1) in the untreated-DOCA group) renin concentrations. Stimulation of the renin-angiotensin system could explain the absence of a renal protective effect of amlodipine. This was also suggested by the fact that enalapril given in addition to amlodipine could decrease proteinuria. In conclusion, T-type channel blockade by mibefradil decreases blood pressure without stimulation of the renin-angiotensin system and therefore prevents most of the glomerular damage in DOCA hypertensive rats.

The endothelin system in human and monkey ovaries: in situ gene expression of the different components.

The endothelin system is composed of three endothelin isoforms (ET-1, ET-2, and ET-3), the endothelin receptors ETA and ETB, and the endothelin-converting enzyme (ECE). Besides having a major vasoactive role, endothelins have roles in different cell types at a local level. We investigated the presence of the different components of the endothelin system in primate ovaries. Human ovaries and gonadotropin-stimulated monkey ovaries were studied using immunohistochemistry for endothelin, and in situ hybridization with probes for ET-1, ET-2, ET-3, ETA and ETB receptors, and ECE. ET-1 and ETA receptors were detected in endothelial cells and vascular smooth muscle cells, respectively, in stromal vessels adjacent to follicles and corpora lutea. ETB receptors and ET-1 were found in the endothelial cells of capillaries of corpora lutea. ECE was present in internal theca cells of secondary, de Graaf, atretic follicles, and in luteinized granulosa cells of the corpora lutea. The endothelin system components are present in or around the follicles of human and monkey ovaries. Although the components are not expressed in the same cell types, they are synthesized, mainly in follicles, by cells that are in close proximity. Thus, the endothelin system could act in a paracrine manner. ECE expression in steroid-producing cells changes its compartmentalization during follicle maturation.

Antioxidant activity in alveolar epithelial type 2 cells of rats during the development of bleomycin injury.

Bleomycin (BLM) induces lung inflammation and subsequent fibrosis in human and in animal models. Alveolar epithelial type 2 cells (T2 cells) are known to play a crucial role in the repair process after BLM injury. We hypothesized that resistance of T2 cells to BLM-damage was associated with an increase in their antioxidant system activity. We developed an animal model of lung lesions preceding fibrosis, using daily intraperitoneal administration of BLM (1.5 mg/day over 7 and 14 days). We observed a body weight stabilization in BLM-treated rats from the third day. After 14 days of BLM treatment, the number of cells recovered by bronchoalveolar lavage was significantly increased (p < 0.05), with a dramatic increase (p < 0.01) in the percentage of neutrophils associated with a decrease in macrophage percentage (p < 0.01) No evidence of fibrosis was seen by microscopic studies at this time. However, T2 cells in 14-day-treated rats were swollen with enlarged lamellar inclusion bodies. Biochemical study of freshly isolated T2 cells displayed a significant decrease of lactate dehydrogenase (LDH) released by these cells when isolated from 14-day-treated rats as compared with 7-day. By contrast, BLM induced an increase in superoxide dismutase (SOD) and glutathione peroxidase activities. Cell content of glutathione was decreased and gamma-glutamyl transpeptidase activity was markedly increased. These results show that BLM induces changes in the antioxidant system of T2 cells, particularly in the glutathione system.

Respective role of humoral factors and blood pressure in aortic remodeling of DOCA hypertensive rats.

Hypertension results in increased thickness and stiffness of large artery walls. The goal of our study was to assess the respective roles of humoral factors such as Ang II, endothelin and blood pressure in these aortic modifications. For this purpose, uninephrectomized rats received DOCA and high salt diet, and when hypertension was installed, they were treated for 5 weeks with either a long-acting calcium antagonist, mibefradil (30 mg/kg/day), an ACE inhibitor, enalapril (3 mg/kg/day), or a mixed ETA and ETB endothelin receptor antagonist, bosentan (100 mg/kg/day). A group of hypertensive rats was left untreated and a sham-operated group of normotensive rats was used for control. At the end of treatment, aortic medial thickness and elastin as well as collagen were evaluated by quantitative morphometry. DOCA-salt hypertensive rats exhibited a marked increase in medial thickness associated with no change in absolute content in extracellular matrix. Elastin relative density decreased in DOCA rats. Enalapril had no effect on arterial pressure. Bosentan decreased slightly (by 12 mm Hg), but not significantly, blood pressure. None of these drugs had an effect on medial thickness suggesting that in DOCA hypertensive rats neither Ang II nor endothelin play a significant role in the remodeling of the aorta. In contrast, mibefradil almost normalized arterial pressure, prevented medial hypertrophy and increased elastin density. Further studies are required in order to assess if this effect is directly linked to the blood pressure decrease or to another mechanism related to the calcium antagonistic property of mibefradil.

Endothelin antagonism in end-organ damage of spontaneously hypertensive rats. Comparison with angiotensin-converting enzyme inhibition and calcium antagonism.

High blood pressure results in cardiac hypertrophy and fibrosis, increased thickness and stiffness of large artery walls, and decreased renal function. The objective of our study was to assess the role of endothelin, angiotensin II, and high blood pressure in the end-organ damage observed in spontaneously hypertensive rats (SHR). For this purpose, SHR were treated for 10 weeks with either a mixed endothelin-A and endothelin-B receptor antagonist, bosentan (100 mg/kg per day), an angiotensin-converting enzyme inhibitor, enalapril (10 mg/kg per day), or a long-acting calcium antagonist, mibefradil (20 mg/kg per day). A group of SHR was left untreated, and a group of normotensive Wistar rats was used as control. At the end of treatment, maximal coronary blood flow was measured in isolated perfused hearts. Cardiac hypertrophy and fibrosis, aortic medial thickness, and extracellular matrix content were evaluated by quantitative morphometry. Proteinuria and urea and creatinine clearances were measured, and renal histopathology was assessed. SHR exhibited cardiac hypertrophy, perivascular fibrosis, and decreased maximal coronary blood flow. Aortic medial thickness was increased, whereas elastin density was decreased. Finally, SHR showed decreased urinary excretion and decreased urea and creatinine clearances. No renal histological lesions were observed. Although bosentan did not affect blood pressure, it normalized renal function and slightly decreased left ventricular hypertrophy and fibrosis. Enalapril and mibefradil were both effective in significantly decreasing blood pressure, left ventricular hypertrophy, and aortic medial thickness and improving coronary blood flow, but in contrast to bosentan, they did not improve creatinine clearance. We conclude that in SHR, high blood pressure plays a major role in end-organ damage and that endothelin may partly mediate renal dysfunction and cardiac remodeling independently of a direct hemodynamic effect.

Respective role of humoral factors and blood pressure in cardiac remodeling of DOCA hypertensive rats.

OBJECTIVES: Recent studies have shown that beside elevated arterial blood pressure, humoral factors such as angiotensin II, aldosterone, endothelin or bradykinin might play a role in the cardiac hypertrophy and fibrosis secondary to hypertension. In addition, it seems that perivascular fibrosis and interstitial fibrosis are controlled by independent mechanisms. Therefore, the goal of our study was to evaluate the respective role of the increased arterial pressure and of humoral factors on cardiac remodeling in an experimental hypertension model. METHODS: Uninephrectomized rats received DOCA, a high salt diet, and when hypertension was installed, they were treated for 6 weeks with either a long-acting calcium antagonist, mibefradil (30 mg/kg day-1), an ACE inhibitor, enalapril (3 mg/kg day-1), or a mixed ETA-ETB endothelin receptor antagonist, bosentan (100 mg/kg day-1). A group of hypertensive rats was left untreated and a sham-operated group of normotensive rats was used for control. At the end of treatment, maximal coronary blood flow was measured in isolated perfused hearts. Cardiac hypertrophy and interstitial as well as perivascular fibrosis were evaluated by quantitative morphometry. RESULTS: DOCA-salt hypertensive rats exhibited a marked cardiac hypertrophy associated with a decrease of maximal coronary blood flow and interstitial and perivascular fibrosis. The calcium antagonist nearly normalized arterial pressure and suppressed all these changes. Enalapril had no effect on arterial pressure and perivascular fibrosis but decreased subendocardial fibrosis. Bosentan had a very small effect on arterial pressure but decreased cardiac hypertrophy and both perivascular and subendocardial fibrosis. CONCLUSIONS: We conclude that in DOCA salt hypertension, humoral factors such as endothelin may play a role beside high blood pressure in cardiac remodeling. In addition, the different components of this remodeling (decrease of vascular reserve, cardiac hypertrophy and cardiac fibrosis) are controlled independently.

Role of endothelin in acute renal failure due to rhabdomyolysis in rats.

Rhabdomyolysis and other causes of massive myoglobin release are often complicated by an acute ischemic renal failure. We tested the hypothesis that endothelin-1, the most potent renal vasoconstrictor known, plays a role in the renal toxicity of myoglobin. For this purpose, we induced rhabdomyolysis (8 ml/kg i.m. of a 50% glycerol solution) in rats pretreated or not pretreated with bosentan, a novel potent nonpeptide endothelin receptor antagonist. Glycerol decreased renal function dramatically, increased proteinuria and induced a massive tubular necrosis. This effect was associated with a 22% increase in plasma endothelin concentration. Bosentan prevented the decrease in creatinine clearance (1.12 +/- 0.07 ml/min vs. 0.83 +/- 0.05 ml/min, P < .01), the increase in proteinuria (19.9 mg/24 hr vs. 31.8 mg/24 hr, P < .001) and the tubular necrosis induced by glycerol (as assessed by histopathological evaluation), without affecting myoglobinuria. Involvement of endothelin was further suggested by the observation that myoglobin could markedly increase endothelin-1 release by rat mesangial cells in culture. We conclude that endothelin is, at least in part, responsible for the massive tubular necrosis observed in myoglobinuric nephropathy.

Direct toxic effect of bleomycin on alveolar type 2 cells.

We studied the in vitro toxicity of bleomycin (BLM) on primary cultures of rat alveolar type 2 cells (T2 cells). It was shown that BLM was directly toxic for T2 cells in a dose- and time-dependent manner. Lung fibroblasts (LF) appear to be more resistant than T2 cells. Modulation of intracellular glutathione concentration was associated with changes in cytotoxicity. Furthermore, the addition of O-phenanthroline to the cellular medium reduced significantly BLM toxicity, suggesting the involvement of intra-cellular ferric ion. We also found that BLM toxicity was associated with a decreased release of phosphatidylcholine by T2 cells, the main component of surfactant. Protective effect of O-phenanthroline and the involvement of glutathione may be an alternative approach to the protection of BLM-induced damage.

Assessing the relationship between environmental lead concentrations and adult blood lead levels.

This paper presents a model for predicting blood lead levels in adults who are exposed to elevated environmental levels of lead. The model assumes a baseline blood lead level based on average blood lead levels for adults described in two recent U.S. studies. The baseline blood level in adults arises primarily from exposure to lead in diet. Media-specific ingestion and absorption parameters are assessed for the adult population, and a biokinetic slope factor that relates uptake of lead into the body to blood lead levels is estimated. These parameters are applied to predict blood lead levels for adults exposed to a hypothetical site with elevated lead levels in soil, dust and air. Blood lead levels ranging from approximately 3-57 micrograms/dl are predicted, depending on the exposure scenarios and assumptions.

Toxic effects of oxygen on cultured alveolar epithelial cells, lung fibroblasts and alveolar macrophages.

Exposure to hyperoxia results in endothelial necrosis followed by type II cell proliferation. This suggests that type II cells are resistant to hyperoxia. Oxygen-induced lung injury may result from an overproduction of oxygen metabolites normally scavenged by antioxidants such as superoxide dismutase (SOD), glutathione peroxidase, catalase and reduced glutathione (GSH). Therefore, resistance of type II cells to hyperoxia may be linked to high antioxidant activities. To test this hypothesis we compared in vitro the effects of a 24 h exposure period to 95% O2 on cultured type II cells, lung fibroblasts and alveolar macrophages isolated from rats. We show that type II cells, when compared with other cell types, are highly sensitive to hyperoxia as shown by increased lactate dehydrogenase (LDH) release, decreased deoxyribose nucleic acid (DNA) and protein content of Petri dishes and decreased thymidine incorporation into DNA. Synthesis of dipalmitoylphosphatidylcholine was also significantly reduced. Antioxidant enzyme activities as well as glutathione content were not higher in type II cells than in other cell types. However, hyperoxia results in a decreased SOD activity and glutathione content in type II cells which was not observed in fibroblasts. We conclude that adaptative changes in SOD and glutathione metabolism could be important defence mechanisms in cells exposed to hyperoxia.

In vitro penetration of pesticides through human newborn foreskin.

The in vitro dermal penetration of 14C-labelled parathion, fenvalerate, carbofuran, and lindane through fresh full-thickness human newborn foreskin was determined at 1, 6, 24, and 48 h. The pesticides were applied to a constant dosing area (0.031 cm2), and a fixed dose (1.18 microgram), for each of the compounds studied. 90%, or greater, of the labelled pesticides were recovered in all cases. Carbofuran showed the greatest mean penetration of 82% followed by parathion and lindane with mean penetrations of 79 and 66%, respectively. Fenvalerate exhibited a mean penetration of 9% which is significantly lower than that of the other three compounds. No difference was noted in the penetration of pesticides through human skin from blacks and whites.

Pseudocholinesterase activity and atracurium v. suxamethonium block.

Serum pseudocholinesterase activity in pregnant women was assayed spectrophotometrically using either propionylthiocholine or suxamethonium as substrate. All patients had a normal phenotype as indicated by normal dibucaine and fluoride numbers. However, the mean cholinesterase activity was lower than in the general population. There was a negative correlation between cholinesterase activity and the duration of neuromuscular blockade following suxamethonium, but no correlation was observed between the cholinesterase activity and the duration of block following atracurium.