Emissions and economic costs of cycling compact fluorescent lamps with integrated ballasts

This paper proposes a way to quantify the emissions of mercury (Hg) and CO2 associated with the manufacture and operation of compact fluorescent lamps with integrated ballasts (CFLis), as well as the economic cost of using them under different operating cycles. The main purpose of this paper is to find simple criteria for reducing the polluting emissions under consideration and the economic cost of CFLi to a minimum. A lifetime model is proposed that allows the emissions and costs to be described as a function of degradation from turning CFLi on and their continuous operation. An idealized model of a CFLi is defined that combines characteristics stated by different manufacturers. In addition, two CFLi models representing poor-quality products are analyzed. It was found that the emissions and costs per unit of time of operation of the CFLi depend linearly on the number of times per unit of time it is turned on and the time of continuous operation. The optimal conditions (lowest emissions and costs) depend on the place of manufacture, the place of operation and the quality of the components of the lamp/ballast. Finally, it was also found that for each lamp, there are intervals when it is turned off during which emissions of pollutants and costs are identical regardless of how often the lamp is turned on or the time it remains on. For CO2 emissions, the lamp must be off up to 5 minutes; for the cost, up to 7 minutes and for Hg emissions, up to 43 minutes. It is advisable not to turn on a CFLi sooner than 43 minutes from the last time it was turned off

Control of Cell Migration and Inflammatory Mediators Production by CORM-2 in Osteoarthritic Synoviocytes

BackgroundOsteoarthritis (OA) is the most widespread degenerative joint disease. Inflamed synovial cells contribute to the release of inflammatory and catabolic mediators during OA leading to destruction of articular tissues. We have shown previously that CO-releasing molecules exert anti-inflammatory effects in animal models and OA chondrocytes. We have studied the ability of CORM-2 to modify the migration of human OA synoviocytes and the production of chemokines and other mediators sustaining inflammatory and catabolic processes in the OA joint.Methodology/Principal FindingsOA synoviocytes were stimulated with interleukin(IL)-1β in the absence or presence of CORM-2. Migration assay was performed using transwell chambers. Gene expression was analyzed by quantitative PCR and protein expression by Western Blot and ELISA. CORM-2 reduced the proliferation and migration of OA synoviocytes, the expression of IL-8, CCL2, CCL20, matrix metalloproteinase(MMP)-1 and MMP-3, and the production of oxidative stress. We found that CORM-2 reduced the phosphorylation of extracellular signal-regulated kinase1/2, c-Jun N-terminal kinase1/2 and to a lesser extent p38. Our results also showed that CORM-2 significantly decreased the activation of nuclear factor-κB and activator protein-1 regulating the transcription of chemokines and MMPs in OA synoviocytes.Conclusion/SignificanceA number of synoviocyte functions relevant in OA synovitis and articular degradation can be down-regulated by CORM-2. These results support the interest of this class of agents for the development of novel therapeutic strategies in inflammatory and degenerative conditions

Extracellular Vesicles from Adipose-Derived Mesenchymal Stem Cells Downregulate Senescence Features in Osteoarthritic Osteoblasts

Osteoarthritis (OA) affects all articular tissues leading to pain and disability. The dysregulation of bone metabolism may contribute to the progression of this condition. Adipose-derived mesenchymal stem cells (ASC) are attractive candidates in the search of novel strategies for OA treatment and exert anti-inflammatory and cytoprotective effects on cartilage. Chronic inflammation in OA is a relevant factor in the development of cellular senescence and joint degradation. In this study, we extend our previous observations of ASC paracrine effects to study the influence of conditioned medium and extracellular vesicles from ASC on senescence induced by inflammatory stress in OA osteoblasts. Our results in cells stimulated with interleukin- (IL-) 1β indicate that conditioned medium, microvesicles, and exosomes from ASC downregulate senescence-associated β-galactosidase activity and the accumulation of γH2AX foci. In addition, they reduced the production of inflammatory mediators, with the highest effect on IL-6 and prostaglandin E2. The control of mitochondrial membrane alterations and oxidative stress may provide a mechanism for the protective effects of ASC in OA osteoblasts. We have also shown that microvesicles and exosomes mediate the paracrine effects of ASC. Our study suggests that correction of abnormal osteoblast metabolism by ASC products may contribute to their protective effects

Effect of CORM-2 on NF-κB and AP-1 activation in OA synoviocytes.

<p>(A) NF-κB binding to DNA, (B) NF-κB p65 translocation (left panels: p65, right panels: DAPI), (C) IκBα phosphorylation and (D) AP-1 binding to DNA. Cells were stimulated with IL-1β (10 ng/ml) for 30 min (C) or 1 h (A, B, D) with IL-1β (10 ng/ml) in the presence or absence of CORM-2 (100, 200 µM). IκBα phosphorylation and NF-κB/AP-1 binding to DNA were determined by ELISA in cytosolic and nuclear fractions respectively, whereas p65 translocation was analyzed by immunofluorescence. Original magnification x400. Data are expressed as mean±S.E.M. of independent cultures with cells from 3 different donors. AU = arbitrary units. +<i>P</i><0.05, ++<i>P</i><0.01 with respect to nonstimulated cells. *<i>P</i><0.05, **<i>P</i><0.01 with respect to IL-1β.</p

Effect of CORM-2 on MMP activity and MMP levels released into the culture medium in OA synoviocytes.

<p>(A) MMP activity, (B) MMP-1 protein, (C) MMP-3 protein levels in the culture medium. Cells were stimulated with IL-1β (10 ng/ml) for 24 h in the presence or absence of CORM-2 (50, 100, 200 µM) or RuCl₃ (200 µM). MMP activity was analyzed by fluorometric procedures in cell supernatants (A) and protein levels were determined by ELISA in cell supernatants (B–C), Data are expressed as mean±S.E.M. Duplicate samples from 6 patients were used. ++<i>P</i><0.01 with respect to nonstimulated cells. *<i>P</i><0.05 with respect to IL-1β.</p

Effect of CORM-2 on HO-1 protein (A) and mRNA expression (B) in OA synoviocytes.

<p>Cells were stimulated with IL-1β (10 ng/ml) for 24 h (A) and 16 h (B) in the presence or absence of CORM-2 (50, 100, 200 µM) or RuCl₃ (200 µM). Protein expression was determined in cell lysates by Western blotting and mRNA levels were determined by real-time PCR. Relative expression of HO-1 and β-actin protein bands was calculated after densitometric analysis. Data are expressed as mean±S.E.M. Samples from 4 patients were used. ++<i>P</i><0.01 with respect to nonstimulated cells. **<i>P</i><0.01 with respect to IL-1β.</p

Effect of CORM-2 on MMP mRNA levels in OA synoviocytes.

<p>(A) MMP-1, (B) MMP-3 mRNA levels. Cells were stimulated with IL-1β (10 ng/ml) for 16 h in the presence or absence of CORM-2 (100, 200 µM) or RuCl₃ (200 µM). mRNA expression was measured by real-time PCR. Data are expressed as mean±S.E.M. Duplicate samples from 6 patients were used. ++<i>P</i><0.01 with respect to nonstimulated cells. *<i>P</i><0.05, **<i>P</i><0.01 with respect to IL-1β.</p

Effect of CORM-2 on synoviocyte proliferation and migration rate.

<p>Cells were stimulated with IL-1β (10 ng/ml) for 24 h in the presence or absence of CORM-2 (50, 100, 200 µM) or RuCl₃ (200 µM). (A) Cell proliferation was determined by the MTT assay. (B) Transwell chambers were kept in culture for 24 h. Upper compartment was detached and cells migrated to the lower side were counted in 6–8 microscopic power fields. Data (A) are expressed as mean±S.E.M. of % proliferating cells, considering 100% the proliferation induced in basal conditions whereas data (B) are expressed as % of cells migrated to the lower compartment, considering 100% the migration induced by IL-1β. Duplicate samples from 6 (A) and 4 (B) patients were used. +<i>P</i><0.05, ++<i>P</i><0.01 with respect to nonstimulated cells. **<i>P</i><0.01 with respect to IL-1β.</p

Effect of CORM-2 on chemokine mRNA levels in OA synoviocytes.

<p>(A) IL-8, (B) CCL2 and (C) CCL20 mRNA levels. Cells were stimulated with IL-1β (10 ng/ml) for 16 h in the presence or absence of CORM-2 (100, 200 µM) or RuCl₃ (200 µM). mRNA expression was determined by real-time PCR. Data are expressed as mean±S.E.M. Duplicate samples from 3 patients were used. ++<i>P</i><0.01 with respect to nonstimulated cells. *<i>P</i><0.05, **<i>P</i><0.01 with respect to IL-1β.</p