A comprehensive review for removal of non-steroidal anti-inflammatory drugs attained from wastewater observations using carbon-based anodic oxidation process

Non-steroidal anti-inflammatory drugs (NSAIDs) (concentration <µg/L) are globally acknowledged as hazardous emerging pollutants that pass via various routes in the environment and ultimately enter aquatic food chains. In this context, the article reviews the occurrence, transport, fate, and electrochemical removal of some selected NSAIDs (diclofenac (DIC), ketoprofen (KTP), ibuprofen (IBU), and naproxen (NPX)) using carbon-based anodes in the aquatic environment. However, no specific protocol has been developed to date, and various approaches have been adopted for the sampling and elimination processes of NSAIDs from wastewater samples. The mean concentration of selected NSAIDs from different countries varies considerably, ranging between 3992–27,061 µg/L (influent wastewater) and 1208–7943 µg/L (effluent wastewater). An assessment of NSAIDs removal efficiency across different treatment stages in various wastewater treatment plants (WWTPs) has been performed. Overall, NSAIDs removal efficiency in wastewater treatment plants has been reported to be around 4–89%, 8–100%, 16–100%, and 17–98% for DIC, KTP, NPX, and IBU, respectively. A microbiological reactor (MBR) has been proclaimed to be the most reliable treatment technique for NSAIDs removal (complete removal). Chlorination (81–95%) followed by conventional mechanical biological treatment (CMBT) (94–98%) treatment has been demonstrated to be the most efficient in removing NSAIDs. Further, the present review explains that the electrochemical oxidation process is an alternative process for the treatment of NSAIDs using a carbon-based anode. Different carbon-based carbon anodes have been searched for electrochemical removal of selected NSAIDs. However, boron-doped diamond and graphite have presented reliable applications for the complete removal of NSAIDs from wastewater samples or their aqueous solution

Abnormal macrophage response to microbial stimulus in a 43-year-old man with a severe form of atherosclerosis: a case report

<p>Abstract</p> <p>Introduction</p> <p>New evidence indicates infections are emerging as risk factors for atherosclerosis although their specific role in the development and progression of atherosclerosis is still unclear.</p> <p>Case presentation</p> <p>A 43-year-old Caucasian man who had been treated for four years for multiple sclerosis progressively manifested systemic hypertension, polycythemia, peripheral arterial occlusion with intermittent claudication, and persistent headaches. In 2006, an instrumental analysis (magnetic resonance imaging) of our patient revealed widespread fibrocalcific atherosclerotic lesions which accounted for all his current symptoms, including those related to microbial stimulus. Two particular aspects were of interest, namely a lack of conventional cardiovascular risk factors and a negative family history for cardiovascular events. His chemical blood tests all yielded negative findings although a low positive hepatitis C virus-ribonucleic acid titer was detected. The titer had progressively increased and worsening atherosclerosis threatened the life of our patient. Interferon therapy was not appropriate for our patient due to the severe adverse effects observed shortly after its administration.</p> <p>Conclusions</p> <p>The reaction of individual cells to infections may provide an explanation as to why individuals with a similar microbial burden, corrected for the presence of other risk factors, display a different susceptibility to developing or worsening atherosclerosis. The identification of susceptible individuals and the treatment even of silent infections may provide an additional tool against atherosclerosis and its clinical complications. The evaluation of cell susceptibility before and after the correction of risk factors may contribute to the assessment of the efficacy of drug therapy.</p

Cochlear Implant: the complexity involved in the decision making process by the family

El objetivo de esta investigación es comprender los significados atribuidos por la familia a las etapas del proceso de la toma de decisiones para el implante coclear en el hijo

Human antimicrobial peptide LL-37 is present in atherosclerotic plaques and induces death of vascular smooth muscle cells: a laboratory study

BACKGROUND: Death of smooth muscle cells in the atherosclerotic plaques makes the plaques more prone to rupture, which can initiate an acute ischemic event. The development of atherosclerosis includes the migration of immune cells e.g. monocytes/macrophages and T lymphocytes into the lesions. Immune cells can release antimicrobial peptides. One of these, human cathelicidin antimicrobial peptide hCAP-18, is cleaved by proteinase 3 generating a 4.5 kDa C-terminal fragment named LL-37, which has been shown to be cytotoxic. The aim of the study was to explore a potential role of LL-37 in the pathophysiology of atherosclerosis. METHODS: We investigated the presence of LL-37 in human atherosclerotic lesions obtained at autopsy using immunohistochemistry. The direct effects of LL-37 on cultured vascular smooth muscle cells and isolated neutrophil granulocytes were investigated with morphological, biochemical and flow cytometry analysis. RESULTS: The neointima of atherosclerotic plaques was found to contain LL-37-like immunoreactivity, mainly in macrophages. In cultured smooth muscle cells, LL-37 at 30 μg/ml caused cell shrinkage, membrane blebbing, nuclear condensation, DNA fragmentation and an increase in caspase-3 activity as studied by microscopy, ELISA and enzyme activity assay, respectively. Flow cytometry demonstrated that LL-37 in a subset of the cells caused a small but rapidly developing increase in membrane permeability to propidium iodide, followed by a gradual development of FITC-annexin V binding. Another cell population stained heavily with both propidium iodide and FITC-annexin V. Neutrophil granulocytes were resistant to these effects of LL-37. CONCLUSION: This study shows that LL-37 is present in atherosclerotic lesions and that it induces death of vascular smooth muscle cells. In a subset of cells, the changes indicate the development of apoptosis triggered by an initial mild perturbation of plasma membrane integrity. The findings suggest a role for LL-37 as a mediator of immune cell-induced death of vascular smooth muscle cells in atherosclerosis