Treatment technology for leachate from faecal sludge drying beds

The use of planted drying beds for faecal sludge treatment is effective for solid-liquid separation, but the leachate produced requires further treatment prior to discharge or reuse. This study investigates the potential of a new and low-cost solution for leachate treatment

Whole-thorax irradiation induces hypoxic respiratory failure, pleural effusions and cardiac remodeling

To study the mechanisms of death following a single lethal dose of thoracic radiation, WAG/RijCmcr (Wistar) rats were treated with 15 Gy to the whole thorax and followed until they were morbid or sacrificed for invasive assays at 6 weeks. Lung function was assessed by breathing rate and arterial oxygen saturation. Lung structure was evaluated histologically. Cardiac structure and function were examined by echocardiography. The frequency and characteristics of pleural effusions were determined. Morbidity from 15 Gy radiation occurred in all rats 5 to 8 weeks after exposure, coincident with histological pneumonitis. Increases in breathing frequencies peaked at 6 weeks, when profound arterial hypoxia was also recorded. Echocardiography analysis at 6 weeks showed pulmonary hypertension and severe right ventricular enlargement with impaired left ventricular function and cardiac output. Histologic sections of the heart revealed only rare foci of lymphocytic infiltration. Total lung weight more than doubled. Pleural effusions were present in the majority of the irradiated rats and contained elevated protein, but low lactate dehydrogenase, when compared with serum from the same animal. Pleural effusions had a higher percentage of macrophages and large monocytes than neutrophils and contained mast cells that are rarely present in other pathological states. Lethal irradiation to rat lungs leads to hypoxia with infiltration of immune cells, edema and pleural effusion. These changes may contribute to pulmonary vascular and parenchymal injury that result in secondary changes in heart structure and function. We report that conditions resembling congestive heart failure contribute to death during radiation pneumonitis, which indicates new targets for therapy

Thrombin increases inflammatory cytokine and angiogenic growth factor secretion in human adipose cells in vitro

<p>Abstract</p> <p>Background</p> <p>Abdominal obesity is associated with pro-thrombotic and inflammatory states. Therefore, the purpose of this study was to examine the expression of thrombin receptors (PAR1 and PAR4) human adipose tissue and whether thrombin stimulates an inflammatory cytokine and growth factor profile in human adipose tissue.</p> <p>Methods</p> <p>Human adipose tissue, isolated preadipocytes and differentiated adipocytes were used in this study. PAR1 and PAR4 mRNA and protein were detected by RT-PCR and immunoblot analysis in both adipose tissue and adipose microvessels. In separate studies, IL-1β, IL-6, MCP-1, TNF-α, IL-10, FGF-2, VEGF, and PDGF production were measured from adipose tissue (n = 5), adipocytes (n = 5), and preadipocytes (n = 3) supernatants with and without thrombin (1 or 10 U/ml; 24 hrs) treatment.</p> <p>Results</p> <p>Thrombin increased cytokine secretion of IL-1β, IL-6, MCP-1 and TNF-α and growth factor secretion of VEGF from adipocytes along with MCP-1 and VEGF from preadipocytes. The direct thrombin inhibitor lepirudin given in conjunction with thrombin prevented the thrombin-mediated increase in cytokine and growth factor secretion.</p> <p>Conclusion</p> <p>Here we show that thrombin PAR1 and PAR4 receptors are present and that thrombin stimulates inflammatory cytokine generation and growth factor release in human adipose tissue and cells <it>in vitro</it>. These data suggest that thrombin may represent a molecular link between obesity and associated inflammation.</p

Algal diversity and distribution in Waste Stabilization Ponds treating faecal sludge leachate from drying vegetated beds

Waste Stabilization Ponds (WSP) were tested at pilot scale for the polishing of faecal sludge leachate from planted drying beds in Yaoundé, Cameroon. Water was sampled at three different depths (10, 30, 45 cm) and three different hydraulic retention times (HRT) (4, 7 and 10 days) in two  maturation basins in series for physico-chemical and biological analyses. As a removal mechanism, algae diversity, density and biomass were assessed and correlated to the physical parameters within the ponds. Results showed the presence of nine algal species belonging to three divisions, four classes, six orders, eight families and eight genera. Among these species found in WSPs, Chlamydomonas globosa, Monoraphidium convolutum and pseudanabaena catena were the most abundant whatever the basin, the hydraulic retention time (HRT) and depth. PO4P, NH4N andthe total chlorophyll showed strong correlation with the algal biomass (0.582, 0.731 and 0.895 respectively) at the surface (0-15 cm) followed by TSS, temperature and COD (0.556, 0.509 and 0.533 respectively) at HRT 4days. These correlations were not observed at HRT 7 and 10 days.Keywords: Algal dynamic, Waste Stabilization Pond, faecal sludge leachate, depth, hydraulic retention time

Gadolinium decreases inflammation related to myocardial ischemia and reperfusion injury

<p>Abstract</p> <p>Background</p> <p>The lanthanide cation, gadolinium (GdCl₃) protects the myocardium against infarction following ischemia and reperfusion. Neutrophils and macrophages are the main leukocytes responsible for infarct expansion after reperfusion. GdCl₃interferes with macrophage and neutrophil function in the liver by decreasing macrophage secretion of inflammatory cytokines and neutrophil infiltration. We hypothesized that GdCl₃protects against ischemia and reperfusion injury by decreasing inflammation. We determined the impact of GdCl₃treatment for reperfusion injury on 1) circulating monoctye and neutrophil counts, 2) secretion of inflammatory cytokines, and 3) influx of monocytes and neutrophils into the myocardium.</p> <p>Methods</p> <p>Rats (n = 3-6/gp) were treated with saline or GdCl₃(20 μmol/kg) 15 min prior to a 30 min period of regional ischemia and 120 min reperfusion. Sham rats were not subject to ischemia. Blood was collected either after 30 min ischemia or 120 min reperfusion and hearts were harvested at 120 min reperfusion for tissue analysis. Blood was analyzed for leukocytes counts and cytokines. Tissue was analyzed for cytokines and markers of neutrophil and monocyte infiltration by measuring myeloperoxidase (MPO) and α-naphthyl acetate esterase (ANAE).</p> <p>Results</p> <p>GdCl₃did not affect the number of circulating neutrophils prior to ischemia. Two hours reperfusion resulted in a 2- and 3- fold increase in circulating monocytes and neutrophils, respectively. GdCl₃decreased the number of circulating monocytes and neutrophils during reperfusion to levels below those present prior to ischemia. Furthermore, after 120 min of reperfusion, GdCl₃decreased ANAE and MPO activity in the myocardium by 1.9-fold and 6.5-fold respectively. GdCl₃decreased MPO activity to levels below those measured in the Sham group. Serum levels of the major neutrophil chemoattractant cytokine, IL-8 were increased from pre-ischemic levels during ischemia and reperfusion in both control and GdCl₃treated rats. Likewise, IL-8 levels increased throughout the 3 hour time period in the Sham group. There was no difference in IL-8 detected in the myocardium after 120 min reperfusion between groups. In contrast, after 120 min reperfusion GdCl₃decreased the myocardial tissue levels of macrophage secreted cytokines, GM-CSF and IL-1.</p> <p>Conclusion</p> <p>GdCl₃treatment prior to ischemia and reperfusion injury decreased circulating monocytes and neutrophils, macrophage secreted cytokines, and leukocyte infiltration into injured myocardium. These results suggest GdCl₃decreased monoctye and neutrophil migration and activation and may be a novel treatment for inflammation during ischemia and reperfusion.</p

Characterization of faecal sludge during dry and rainy seasons in Ouagadougou, Burkina Faso

Faecal sludge (FS) management is a challenging problem in low-income countries where large parts of the urban population rely on onsite sanitation systems. The design of treatment plants relies on accurate knowledge of FS characteristics, but this information is lacking. The goal of this study, conducted between December 2010 and September 2011, was to determine physical and chemical characteristics of raw FS from collection and transport trucks in 5 discharge sites in Ouagadougou. Over 100 samples directly collected during truck discharge were analysed. Analyses included suspended solids, volatile suspended solids, total solids, total volatile solids, sludge volume index, chemical oxygen demand, biological oxygen demand, and heavy metals. The FS characteristics were highly variable, but had similar characteristics for FS collected during the dry and rainy seasons and at different discharge sites. The type of onsite system had an influence on FS characteristics

β1-Adrenergic Receptor Contains Multiple IA\u3csup\u3ek\u3c/sup\u3e and IE\u3csup\u3ek\u3c/sup\u3e Binding Epitopes That Induce T Cell Responses with Varying Degrees of Autoimmune Myocarditis in A/J Mice

Myocarditis/dilated cardiomyopathy (DCM) patients can develop autoantibodies to various cardiac antigens and one major antigen is β1-adrenergic receptor (β1AR). Previous reports indicate that animals immunized with a β1AR fragment encompassing, 197–222 amino acids for a prolonged period can develop DCM by producing autoantibodies, but existence of T cell epitopes, if any, were unknown. Using A/J mice that are highly susceptible to lymphocytic myocarditis, we have identified β1AR 171–190, β1AR 181–200, and β1AR 211–230 as the major T cell epitopes that bind major histocompatibility complex class II/IAk or IEk alleles, and by creating IAk and IEk dextramers, we demonstrate that the CD4 T cell responses to be antigen-specific. Of note, all the three epitopes were found also to stimulate CD8 T cells suggesting that they can act as common epitopes for both CD4 and CD8 T cells. While, all epitopes induced only mild myocarditis, the disease- incidence was enhanced in animals immunized with all the three peptides together as a cocktail. Although, antigen-sensitized T cells produced mainly interleukin-17A, their transfer into naive animals yielded no disease. But, steering for T helper 1 response led the T cells reacting to one epitope, β1AR 181–200 to induce severe myocarditis in naive mice. Finally, we demonstrate that all three β1AR epitopes to be unique for T cells as none of them induced antibody responses. Conversely, animals immunized with a non-T cell activator, β1AR 201–220, an equivalent of β1AR 197–222, had antibodies comprising of all IgG isotypes and IgM except, IgA and IgE. Thus, identification of T cell and B cell epitopes of β1AR may be helpful to determine β1AR-reactive autoimmune responses in various experimental settings in A/J mice

Branched chain α-ketoacid dehydrogenase kinase 111–130, a T cell epitope that induces both autoimmune myocarditis and hepatitis in A/J mice

Introduction: Organ-specific autoimmune diseases are believed to result from immune responses generated against self-antigens specific to each organ. However, when such responses target antigens expressed promiscuously in multiple tissues, then the immune-mediated damage may be wide spread. Methods: In this report, we describe a mitochondrial protein, branched chain α-ketoacid dehydrogenase kinase (BCKDk) that can act as a target autoantigen in the development of autoimmune inflammatory reactions in both heart and liver. Results: We demonstrate that BCKDk protein contains at least nine immunodominant epitopes, three of which, BCKDk 71–90, BCKDk 111–130 and BCKDk 141–160, were found to induce varying degrees of myocarditis in immunized mice. One of these, BCKDk 111–130, could also induce hepatitis without affecting lungs, kidneys, skeletal muscles, and brain. In immunogenicity testing, all three peptides induced antigen-specific T cell responses, as verified by proliferation assay and/or major histocompatibility complex class II/IAk dextramer staining. Finally, the disease-inducing abilities of BCKDk peptides were correlated with the production of interferon-γ, and the activated T cells could transfer disease to naive recipients. Conclusions: The disease induced by BCKDk peptides could serve as a useful model to study the autoimmune events of inflammatory heart and liver diseases