Background: Interaction of advanced glycation end products (AGEs) with their receptor (RAGE) increases expression of inflammatory mediators (tumor necrosis factor alpha [TNF-α] and soluble vascular cell adhesion molecule-1 [sVCAM-1]) and induces oxygen radicals that are implicated in atherosclerosis. Balloon-injuryinduced atherosclerosis is associated with increased expression of AGEs and RAGE. The soluble receptor for AGE (sRAGE), which acts as a decoy for RAGE ligands (AGEs), prevents atherosclerosis in this model. Hypothesis: We evaluated: 1) whether post-percutaneous coronary intervention (PCI) restenosis is associated with low pre-PCI serum sRAGE, high serum AGEs, TNF-α, and sVCAM-1, and high AGE/sRAGE ratio; 2) whether pre-PCI and post-PCI levels of these markers are similar in patients with or without restenosis; and 3) whether sRAGE and AGE/sRAGE ratio have predictive value for post-PCI restenosis. Methods: Angiography was performed in 46 patients with non-ST-segment elevation myocardial infarction for assessment of restenosis. Serum sRAGE, AGEs, TNF-α, and sVCAM-1 were measured in these patients and 20 control subjects. Results: Nineteen of the 46 patients developed post-PCI restenosis, which was associated with lower sRAGE and higher TNF-α and sVCAM-1 levels, and higher AGE/sRAGE ratio compared with patients without restenosis. Pre-PCI and post-PCI levels of these biomarkers were similar in both groups, except in patients with restenosis, in whom the post-PCI level of sRAGE was lower and TNF-α was higher than the pre-PCI levels. The sensitivity and negative predictive value of sRAGE were 100%, and were higher than those of AGE/sRAGE ratio in identifying post-PCI restenosis. Conclusions: Both low serum sRAGE levels and high AGE/sRAGE ratio have predictive value for post-PCI restenosis.

A dvanced glycation end products (AGEs) are a heterogeneous group of irreversible adducts resulting from nonenzymatic glycation and oxidation of proteins, lipids and nucleic acids (1,2). AGEs act on cell receptors for AGEs (RAGEs). There are three forms of RAGEs (2-5) -full-length, N-truncated and C-truncated soluble RAGEs (sRAGE). The interaction of full-length RAGE with AGEs leads to increased expression of adhesion molecules, including soluble vascular cell adhesion molecule-1 (sVCAM-1) and the cytokine tumor necrosis factor-alpha (TNF-α) (2,6,7); activation of nuclear factor-kappa B (6), which in turn leads to increased expression of proinflammatory genes for adhesion molecules and cytokines (2); and generation of oxygen radicals (8,9). sRAGE circulates in the plasma (4) and acts as a decoy for RAGE ligands, competing with full-length RAGE for ligand binding (10). It has a protective role by preventing the activation of full-length RAGE.Adhesion molecules, cytokines and oxygen radicals are involved in atherosclerosis, progression of lesions and lesion instability (11)(12)(13)(14). The AGEs and RAGE axis has been implicated in the pathogenesis of atherosclerosis in diabetes (15)(16)(17). sRAGE in animal models reduces atherosclerotic lesions, aortic vascular cell adhesion molecule-1 and tissue factor (18)(19)(20). The proximate cause of acute coronary syndrome (ACS) is thrombosis and the principal underlying cause is atherosclerosis. Because the combination of AGEs, RAGEs and sRAGE determines the extent of vascular injury, the measurement of these factors is appropriate for determining vascular complications. However, it is not possible to measure RAGE in humans, which is on the cell surface of the artery.It is hypothesized that non-ST elevation myocardial infarction (NSTEMI) patients have lower levels of serum sRAGE and/or higher levels of AGEs, and a higher ratio of AGEs to sRAGE (AGEs/sRAGE) than healthy subjects. Because the interaction of RAGE with AGEs results in increased expression of cytokines and adhesion molecules, and because sRAGE neutralizes AGEs, low sRAGE levels would be associated with high levels of TNF-α and sVCAM-1. Therefore, the main objectives of the present study are to determine whether levels of serum sRAGE are lower, and whether levels of serum AGEs and AGEs/ sRAGE are higher in NSTEMI patients than in healthy subjects; whether low levels of serum sRAGE, and high levels of serum AGEs and AGEs/sRAGE are associated with high levels of serum TNF-α and sVCAM-1; whether the number of diseased , activation of nuclear factor-kappa B and induction of oxidative stress -all of which have been implicated in atherosclerosis. Soluble RAGE (sRAGE) acts as a decoy for the RAGE ligand and is protective against atherosclerosis. oBJECTIvES: To determine whether levels of serum sRAGE are lower, and whether levels of serum AGEs, TNF-α and sVCAM-1 are higher in non-ST elevation myocardial infarction (NSTEMI) patients than in healthy control subjects; and whether sRAGE or the ratio of AGEs to sRAGE (AGEs...

In this study, date-palm biochar MgAl-augmented double-layered hydroxide (biochar–MgAl–LDH) nanocomposite was synthesized, characterized, and used for enhancing the removal of phosphate and nitrate pollutants from wastewater. The biochar–MgAl–LDH had higher selectivity and adsorption affinity towards phosphate compared to nitrate. The adsorption kinetics of both anions were better explained by the pseudo-first-order model with a faster removal rate to attain equilibrium in a shorter time, especially at lower initial phosphate-nitrate concentration. The maximum monolayer adsorption capacities of phosphate and nitrate by the non-linear Langmuir model were 177.97 mg/g and 28.06 mg/g, respectively. The coexistence of anions (Cl−, SO42−, NO3−, CO32− and HCO3−) negligibly affected the removal of phosphate due to its stronger bond on the nano-composites, while the presence of Cl− and PO43− reduced the nitrate removal attributed to the ions’ participation in the active adsorption sites on the surface of biochar–MgAl–LDH. The excellent adsorptive performance is the main synergetic influence of the MgAl–LDH incorporation into the biochar. The regeneration tests confirmed that the biochar–MgAl composite can be restored effortlessly and has the prospective to be reused after several subsequent adsorption-desorption cycles. The biochar-LDH further demonstrated capabilities for higher removal of phosphate and nitrate from real wastewater.

This experimental work focused on the synthesis, characterization, and testing of a unique, magnetically separable, and eco-friendly adsorbent composite material for the advanced treatment and efficient removal of nitrate and phosphate pollutants from wastewater. The MgAl-augmented double-layered hydroxide (Mg-Fe/LDH) intercalated with sludge-based activated carbon (SBAC-MgFe) composites were characterized by FT-IR, XRD, BET, VSM, SEM, and TEM techniques, revealing homogeneous and efficient dispersion of MgFe/LDH within the activated carbon (AC) matrix, a highly mesoporous structure, and superparamagnetic characteristics. The initial solution pH, adsorbent dose, contact time, and temperature parameters were optimized in order to reach the best removal performance for both pollutants. The maximum adsorption capacities of phosphate and nitrate were found to be 110 and 54.5 mg/g, respectively. The competition between phosphate and coexisting ions (Cl−, CO32−, and SO42−) was studied and found to be remarkably lower in comparison with the nitrate adsorption. The adsorption mechanisms were elucidated by kinetic, isotherm, thermodynamic modeling, and post-adsorption characterizations of the composite. Modeling and mechanistic studies demonstrated that physisorption processes such as electrostatic attraction and ion exchange mainly governed the nitrate and phosphate adsorption. The composite indicated an outstanding regeneration performance even after five sequences of adsorption/desorption cycles. The fabricated composite with magnetically separable characteristics can be used as a promising adsorbent for the removal of phosphate and nitrate pollutants from wastewater.

The overproduction of reactive oxygen species (ROS) causes oxidative stress, such as Hydrogen peroxide (H 2 O 2 ). Acute oxidative stress is one of the main reasons for cell death. In this study, the antioxidant properties of vanillic acid- a polyphenolic compound was evaluated. Therefore, this study aims to check the effectiveness of vanillic acid in H 2 O 2 -induced oxidative stress in D. Mel-2 cell line. The efficacy was determined by biochemical tests to check the ROS production. The cytotoxicity of H 2 O 2 and vanillic acid was checked by MTT assay. The DNA fragmentation was visualized by gel electrophoresis. Protein biomarkers of oxidative stress were analyzed by western blotting. The results depict a promising antioxidant effect of vanillic acid. The IC 50 value of vanillic acid and H 2 O 2 was found 250 μg/ml and 125 μg/ml, respectively. The catalase activity, SOF, GPx, and PC was seen less in H 2 O 2 treated group compared with the control and vanillic acid treated group. However, the TBRAS activity was hight in H 2 O 2 treated group. The effect of H 2 O 2 on DNA fragmentation was high as compared with vanillic acid-treated cells. The protein expression of Hsp70, IL-6 and iNOS was seen significant in a vanillic acid-treated group as compared with H 2 O 2 treated group. These results reinforce that at low concentration, vanillic acid could be used as an antioxidant agent in the food and pharmaceutical industries.

Vitamin E suppresses the hypercholesterolemia-induced oxidative stress in the heart. The objectives were to investigate if: (a) hypercholesterolemia-induced oxidative stress is similar in heart, liver, and kidney, and is dependent upon duration of hypercholesterolemia; and (b) vitamin E slows the progression of oxidative stress in these organs. The rabbits were assigned to 4 groups: I, regular diet (2 months); II, 0.25 % cholesterol diet (2 months); III, 0.25 % cholesterol diet (4 months); and IV, 0.25 % cholesterol diet (2 months) followed by 0.25 % cholesterol diet plus vitamin E (2 months). Blood samples were collected before and at the end of protocol for the measurement of total cholesterol (TC). Hearts, livers, and kidneys were removed at the end of the protocol under anesthesia for the measurement of oxidative parameters, malondialdehyde (MDA), and chemiluminescence (CL). The basal MDA levels in the heart, liver, and kidney of rabbits in Group I were similar, but increased to 14.65-, 3.18-, and 10.35-fold, respectively, with hypercholesterolemia. The increases in MDA levels were dependent upon the duration of hypercholesterolemia. Vitamin E did not alter the TC levels, but reduced the MDA levels in all organs. Hypercholesterolemia and vitamin E had variable effects on CL activity. In conclusion, (i) hypercholesterolemia induces oxidative stress in heart, liver, and kidney, the heart being the most and the liver the least susceptible to oxidative stress; (ii) oxidative stress is positively associated with duration of hypercholesterolemia; and (iii) vitamin E slows the progression of oxidative stress in these organs.

High sensitivity C-reactive protein (hs-CRP) is synthesized mainly by hepatocytes in response to tumor necrosis factor-alpha (TNF-alpha), interleukin-1 (IL-1), and interleukin-6 (IL-6). The interaction of advanced glycation end products (AGEs) with the receptor for advanced glycation end products (RAGE) increases the expression of the cytokines TNF-alpha, IL-1, and IL-6. Soluble receptor for advanced glycation end products (sRAGE) competes with RAGE for binding with AGEs. Hence, low sRAGE levels may increase interaction of AGEs with RAGE resulting in the increased production of cytokines. It is hypothesized that serum levels of sRAGE modulate serum levels of hs-CRP. The objectives are to determine if (i) serum levels of sRAGE are lower and those of TNF-alpha and hs-CRP are higher in non-ST-segment elevation myocardial infarction (NSTEMI) patients compared to control subjects; (ii) serum levels of TNF-alpha and hs-CRP are positively correlated; and (iii) sRAGE is negatively correlated with hs-CRP and TNF-alpha. The study consisted of 36 patients with NSTEMI and 30 age-matched healthy male subjects. Serum levels of sRAGE and TNF-alpha were determined by enzyme-linked immunoassay and hs-CRP was measured using near infrared immunoassay. Serum levels of sRAGE were lower, while those of TNF-alpha and hs-CRP were higher in patients with NSTEMI compared to controls. The levels of sRAGE were negatively correlated with those of TNF-alpha and hs-CRP, while TNF-alpha was positively correlated with hs-CRP in both the control subjects and NSTEMI patients. The data suggest that sRAGE modulates the synthesis of hs-CRP through TNF-alpha.

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