| 1. |
- Klionsky, Daniel J., et al.
(författare)
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Guidelines for the use and interpretation of assays for monitoring autophagy
- 2012
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Ingår i: Autophagy. - : Informa UK Limited. - 1554-8635 .- 1554-8627. ; 8:4, s. 445-544
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Forskningsöversikt (refereegranskat)abstract
- In 2008 we published the first set of guidelines for standardizing research in autophagy. Since then, research on this topic has continued to accelerate, and many new scientists have entered the field. Our knowledge base and relevant new technologies have also been expanding. Accordingly, it is important to update these guidelines for monitoring autophagy in different organisms. Various reviews have described the range of assays that have been used for this purpose. Nevertheless, there continues to be confusion regarding acceptable methods to measure autophagy, especially in multicellular eukaryotes. A key point that needs to be emphasized is that there is a difference between measurements that monitor the numbers or volume of autophagic elements (e.g., autophagosomes or autolysosomes) at any stage of the autophagic process vs. those that measure flux through the autophagy pathway (i.e., the complete process); thus, a block in macroautophagy that results in autophagosome accumulation needs to be differentiated from stimuli that result in increased autophagic activity, defined as increased autophagy induction coupled with increased delivery to, and degradation within, lysosomes (in most higher eukaryotes and some protists such as Dictyostelium) or the vacuole (in plants and fungi). In other words, it is especially important that investigators new to the field understand that the appearance of more autophagosomes does not necessarily equate with more autophagy. In fact, in many cases, autophagosomes accumulate because of a block in trafficking to lysosomes without a concomitant change in autophagosome biogenesis, whereas an increase in autolysosomes may reflect a reduction in degradative activity. Here, we present a set of guidelines for the selection and interpretation of methods for use by investigators who aim to examine macroautophagy and related processes, as well as for reviewers who need to provide realistic and reasonable critiques of papers that are focused on these processes. These guidelines are not meant to be a formulaic set of rules, because the appropriate assays depend in part on the question being asked and the system being used. In addition, we emphasize that no individual assay is guaranteed to be the most appropriate one in every situation, and we strongly recommend the use of multiple assays to monitor autophagy. In these guidelines, we consider these various methods of assessing autophagy and what information can, or cannot, be obtained from them. Finally, by discussing the merits and limits of particular autophagy assays, we hope to encourage technical innovation in the field.
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| 2. |
- Xue-Jian, Xu, et al.
(författare)
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Enhanced Performance and Stability in Polymer Photovoltaic Cells Using Ultraviolet-Treated PEDOT:PSS
- 2013
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Ingår i: Chinese Physics Letters. - : Institute of Physics. - 0256-307X .- 1741-3540. ; 30:7
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Tidskriftsartikel (refereegranskat)abstract
- We investigate the effects of ultraviolet (UV) irradiation treatment with varying irradiation intensities for different treatment times of poly(3, 4-ethylenedioxythiophene):poly(styrenesulfonate) (PEDOT:PSS) film on the performance and stability of polymer solar cells (PSCs) based on regioregular poly(3-hexylthiophene) (P3HT) and methanofullerene [6,6]-phenyl C-61-butyric acid methyl ester (PCBM) blend. Ultraviolet-visible transmission spectra, x-ray photoelectron spectroscopy, contact angle measurement, atomic force microscopy and the Kelvin probe method are conducted to characterize the UV-treated PEDOT:PSS film. The results demonstrate that UV treatment can improve the power conversion efficiency (PCE) and stability of PSCs effectively. The best performance is achieved under 1200 mu W/cm(2) UV treatment for 50 min. Compared to the control device, the optimized device exhibits enhanced performance with a V-OC of 0.59 V, J(SC) of 12.3 mA/cm(2), fill factor of 51%, and PCE of 3.64%, increased by 3.5%, 33%, 8.7% and 50%, respectively. The stability of the PSCs is enhanced by 2.5 times simply through the UV treatment on the PEDOT:PSS buffer layer. The improvement in the device performance and stability is attributed to the improvement in the wettability property and the increase in the work function of the PEDOT:PSS film by UV treatment, while the impact of UV treatment on the transparency of the PEDOT:PSS film is negligible. The strategy of using UV treatment to improve device performance and stability is attractive due to its simplicity, cost-effectiveness, and because it is suitable for large-scale commercial production.
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| 3. |
- Zhang, Wei, et al.
(författare)
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Activation of nuclear factor-kappa B pathway is responsible for tumor necrosis factor-a-induced up-regulation of endothelin B2 receptor expression in vascular smooth muscle cells in vitro
- 2012
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Ingår i: Toxicology Letters. - : Elsevier BV. - 1879-3169 .- 0378-4274. ; 209:2, s. 107-112
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Tidskriftsartikel (refereegranskat)abstract
- The endothelin B2 (ETB2) receptors are induced in vascular smooth muscle cells (VSMCs) in cardiovascular diseases. We tested if in vitro short-term exposure to the pro-inflammatory cytokine tumor necrosis factor-alpha (TNF-alpha) could up-regulate ETB2 receptors in rat mesenteric arteries, and if this effect is through activation of intracellular nuclear factor-kappa B (NF-kappa B) pathway. The mesenteric arteries were dissected from male Sprague-Dawley rats and the endothelium was removed. The arteries were co-incubated with TNF-alpha in serum-free Dulbecco's modified Eagle's medium. Real-time reverse transcription-PCR, Western blot and immunohistochemical staining were employed to assess the mRNA/protein expression of ETB2 receptors and activation of NF-kappa B pathway. The results showed that, during organ culture. TNF-alpha concentration-dependently enhanced ET52 receptors expression at both mRNA and protein levels, paralleled with activation of NF-kappa B pathway in VSMC. The up-regulated ETB2 receptor expression and NF-kappa B activation could be effectively suppressed by general transcriptional inhibitor actinomycin D, or either of the selective I kappa B kinase inhibitors wedelolactone and IMD-0354. Conclusively, the activation of intracellular NF-kappa B pathway is responsible for the up-regulation of ETB2 receptors induced by short-term exposure to TNF-alpha. This could partly explain the toxic effects of TNF-alpha on VSMCs that account for cardiovascular diseases. (C) 2011 Elsevier Ireland Ltd. All rights reserved.
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