| 1. |
- Alexander, Helen K., et al.
(författare)
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Selected technologies to control genes and their products for experimental and clinical purposes
- 2007
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Ingår i: Archivum Immunologiae et Therapiae Experimentalis. - : Springer Science and Business Media LLC. - 0004-069X .- 1661-4917. ; 55:3, s. 139-149
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Tidskriftsartikel (refereegranskat)abstract
- "On-demand" regulation of gene expression is a powerful tool to elucidate the functions of proteins and biologically-active RNAs. We describe here three different approaches to the regulation of expression or activity of genes or proteins. Promoter-based regulation of gene expression was among the most rapidly developing techniques in the 1980s and 1990s. Here we provide basic information and also some characteristics of the metallothionein-promoter-based system, the tet-off system, Muristerone-A-regulated expression through the ecdysone response element, RheoSwitch (R), coumermycin/novobiocin-regulated gene expression, chemical dimerizer-based promoter activation systems, the "Dual Drug Control" system, "constitutive androstane receptor"-based regulation of gene expression, and RU486/mifepristone-driven regulation of promoter activity. A large part of the review concentrates on the principles and usage of various RNA interference techniques (RNAi: siRNA, shRNA, and miRNA-based methods). Finally, the last part of the review deals with historically the oldest, but still widely used, methods of temperature-dependent regulation of enzymatic activity or protein stability (temperature-sensitive mutants). Due to space limitations we do not describe in detail but just mention the tet-regulated systems and also fusion-protein-based regulation of protein activity, such as estrogen-receptor fusion proteins. The information provided below is aimed to assist researchers in choosing the most appropriate method for the planned development of experimental systems with regulated expression or activity of studied proteins.
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| 2. |
- Fan, Qunping, 1989, et al.
(författare)
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High-performance all-polymer solar cells enabled by a novel low bandgap non-fully conjugated polymer acceptor
- 2021
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Ingår i: Science in China Series B. - : Springer Nature. - 1674-7291 .- 1869-1870. ; 64, s. 1380-1388
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Tidskriftsartikel (refereegranskat)abstract
- Anon-fully conjugated polymer as a new class of acceptor materials has shown some advantages over its small molecular counterpart when used in photoactive layers for all-polymer solar cells (all-PSCs), despite a low power conversion efficiency (PCE) caused by its narrow absorption spectra. Herein, a novel non-fully conjugated polymer acceptor PFY-2TS with a low bandgap of similar to 1.40 eV was developed, via polymerizing a large pi-fused small molecule acceptor (SMA) building block (namely YBO) with a non-conjugated thioalkyl linkage. Compared with its precursor YBO, PFY-2TS retains a similar low bandgap but a higher LUMO level. Moreover, compared with the structural analog of YBO-based fully conjugated polymer acceptor PFY-DTC, PFY-2TS shows similar absorption spectrum and electron mobility, but significantly different molecular crystallinity and aggregation properties, which results in optimal blend morphology with a polymer donor PBDB-T and better device physical processes in all-PSCs. As a result, PFY-2TS-based all-PSCs achieved a PCE of 12.31% with a small energy loss of 0.56 eV enabled by the reduced non-radiative energy loss (0.24 eV), which is better than that of 11.08% for the PFY-DTC-based ones. Our work clearly demonstrated that non-fully conjugated polymers as a new class of acceptor materials are very promising for the development of high-performance all-PSCs.
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| 3. |
- Fan, Qunping, 1989, et al.
(författare)
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Over 14% efficiency all-polymer solar cells enabled by a low bandgap polymer acceptor with low energy loss and efficient charge separation
- 2020
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Ingår i: Energy & Environmental Science. - : Royal Society of Chemistry. - 1754-5692 .- 1754-5706. ; 13:12, s. 5017-5027
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Tidskriftsartikel (refereegranskat)abstract
- Obtaining both high open-circuit voltage (V-oc) and short-circuit current density (J(sc)) has been a major challenge for efficient all-polymer solar cells (all-PSCs). Herein, we developed a polymer acceptor PF5-Y5 with excellent optical absorption capability (onset extending to similar to 880 nm and maximum absorption coefficient exceeding 105 cm(-1) in a film), high electron mobility (3.18 x 10(3) cm(2) V-1 s(-1)) and high LUMO level (-3.84 eV) to address such a challenge. As a result, the PBDB-T:PF5-Y5-based all-PSCs achieved a high power conversion efficiency of up to 14.45% with both a high Voc (0.946 V) and a high Jsc (20.65 mA cm(-2)), due to the high and broad absorption coverage, small energy loss (0.57 eV) and efficient charge separation and transport in the device, which are among the best values in the all-PSC field. In addition, the all-PSC shows a similar to 15% improvement in PCE compared to its counterpart small molecule acceptor (Y5)-based device. Our results suggest that PF5-Y5 is a very promising polymer acceptor candidate for applications in efficient all-PSCs.
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| 4. |
- Ghavami, Saeid, et al.
(författare)
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S100A8/9 induces cell death via a novel, RAGE-independent pathway that involves selective release of Smac/DIABLO and Omi/HtrA2
- 2008
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Ingår i: Biochimica et Biophysica Acta. Molecular Cell Research. - : Elsevier. - 0167-4889 .- 1879-2596. ; 1783:2, s. 297-311
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Tidskriftsartikel (refereegranskat)abstract
- A complex of two S100 EF-hand calcium-binding proteins S100A8/A9 induces apoptosis in various cells, especially tumor cells. Using several cell lines, we have shown that S100A8/A9-induced cell death is not mediated by the receptor for advanced glycation endproducts (RAGE), a receptor previously demonstrated to engage S100 proteins. Investigation of cell lines either deficient in, or over-expressing components of the death signaling machinery provided insight into the S100A8/A9-mediated cell death pathway. Treatment of cells with S100A8/A9 caused a rapid decrease in the mitochondrial membrane potential (ΔΨm) and activated Bak, but did not cause release of apoptosis-inducing factor (AIF), endonuclease G (Endo G) or cytochrome c. However, both Smac/DIABLO and Omi/HtrA2 were selectively released into the cytoplasm concomitantly with a decrease in Drp1 expression, which inhibits mitochondrial fission machinery. S100A8/A9 treatment also resulted in decreased expression of the anti-apoptotic proteins Bcl2 and Bcl-XL, whereas expression of the pro-apoptotic proteins Bax, Bad and BNIP3 was not altered. Over-expression of Bcl2 partially reversed the cytotoxicity of S100A8/A9. Together, these data indicate that S100A8/A9-induced cell death involves Bak, selective release of Smac/DIABLO and Omi/HtrA2 from mitochondria, and modulation of the balance between pro- and anti-apoptotic proteins.
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| 5. |
- Ma, Ruijie, et al.
(författare)
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All-polymer solar cells with over 16% efficiency and enhanced stability enabled by compatible solvent and polymer additives
- 2022
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Ingår i: Aggregate. - : Wiley. - 2692-4560 .- 2766-8541. ; 3:3
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Tidskriftsartikel (refereegranskat)abstract
- Considering the robust and stable nature of the active layers, advancing the power conversion efficiency (PCE) has long been the priority for all-polymer solar cells (all-PSCs). Despite the recent surge of PCE, the photovoltaic parameters of the state-of-the-art all-PSC still lag those of the polymer:small molecule-based devices. To compete with the counterparts, judicious modulation of the morphology and thus the device electrical properties are needed. It is difficult to improve all the parameters concurrently for the all-PSCs with advanced efficiency, and one increase is typically accompanied by the drop of the other(s). In this work, with the aids of the solvent additive (1-chloronaphthalene) and the n-type polymer additive (N2200), we can fine-tune the morphology of the active layer and demonstrate a 16.04% efficient all-PSC based on the PM6:PY-IT active layer. The grazing incidence wide-angle X-ray scattering measurements show that the shape of the crystallites can be altered, and the reshaped crystallites lead to enhanced and more balanced charge transport, reduced recombination, and suppressed energy loss, which lead to concurrently improved and device efficiency and stability.
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| 6. |
- Mestre, Humberto, et al.
(författare)
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Aquaporin-4-dependent glymphatic solute transport in the rodent brain
- 2018
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Ingår i: eLife. - 2050-084X. ; 7
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Tidskriftsartikel (refereegranskat)abstract
- The glymphatic system is a brain-wide clearance pathway; its impairment contributes to the accumulation of amyloid-β. Influx of cerebrospinal fluid (CSF) depends upon the expression and perivascular localization of the astroglial water channel aquaporin-4 (AQP4). Prompted by a recent failure to find an effect of Aqp4 knock-out (KO) on CSF and interstitial fluid (ISF) tracer transport, five groups re-examined the importance of AQP4 in glymphatic transport. We concur that CSF influx is higher in wild-type mice than in four different Aqp4 KO lines and in one line that lacks perivascular AQP4 (Snta1 KO). Meta-analysis of all studies demonstrated a significant decrease in tracer transport in KO mice and rats compared to controls. Meta-regression indicated that anesthesia, age, and tracer delivery explain the opposing results. We also report that intrastriatal injections suppress glymphatic function. This validates the role of AQP4 and shows that glymphatic studies must avoid the use of invasive procedures.
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| 7. |
- Xiao, Manjun, et al.
(författare)
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Approaching 19% efficiency and stable binary polymer solar cells enabled by a solidification strategy of solvent additive
- 2023
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Ingår i: Science in China Series B. - : SCIENCE PRESS. - 1674-7291 .- 1869-1870. ; 66, s. 1500-1510
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Tidskriftsartikel (refereegranskat)abstract
- Additives play a crucial role in enhancing the photovoltaic performance of polymer solar cells (PSCs). However, the typical additives used to optimize blend morphology of PSCs are still high boiling-point solvents, while their trace residues may reduce device stability. Herein, an effective strategy of "solidification of solvent additive (SSA)" has been developed to convert additive from liquid to solid, by introducing a covalent bond into low-cost solvent diphenyl sulfide (DPS) to synthesize solid dibenzothiophene (DBT) in one-step, which achieves optimized morphology thus promoting efficiency and device stability. Owing to the fine planarity and volatilization of DBT, the DBT-processed films achieve ordered molecular crystallinity and suitable phase separation compared to the additive-free or DPS-treated ones. Importantly, the DBT-processed device also possesses improved light absorption, enhanced charge transport, and thus a champion efficiency of 11.9% is achieved in the PM6:Y6-based PSCs with an excellent additive component tolerance, reproducibility, and stability. Additionally, the DBT-processed PM6:L8-BO-based PSCs are further fabricated to study the universality of SSA strategy, offering an impressive efficiency approaching 19% as one of the highest values in binary PSCs. In conclusion, this article developed a promising strategy named SSA to boost efficiency and improve stability of PSCs.
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| 8. |
- Yi, Fan, et al.
(författare)
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Non-Fully Conjugated Dimerized Giant Acceptors with Different Alkyl-Linked Sites for Stable and 19.13 % Efficiency Organic Solar Cells
- 2024
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Ingår i: Angewandte Chemie International Edition. - : WILEY-V C H VERLAG GMBH. - 1433-7851 .- 1521-3773.
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Tidskriftsartikel (refereegranskat)abstract
- Achieving both high power conversion efficiency (PCE) and device stability is a major challenge for the practical development of organic solar cells (OSCs). Herein, three non-fully conjugated dimerized giant acceptors (named 2Y-sites, including wing-site-linked 2Y-wing, core-site-linked 2Y-core, and end-site-linked 2Y-end) are developed. They share the similar monomer precursors but have different alkyl-linked sites, offering the fine-tuned molecular absorption, packing, glass transition temperature, and carrier mobility. Among their binary active layers, D18/2Y-wing has better miscibility, leading to optimized morphology and more efficient charge transfer compared to D18/2Y-core and D18/2Y-end. Therefore, the D18/2Y-wing-based OSCs achieve a superior PCE of 17.73 %, attributed to enhanced photocurrent and fill factor. Furthermore, the D18/2Y-wing-based OSCs exhibit a balance of high PCE and improved stability, distinguishing them within the 2Y-sites. Building on the success of 2Y-wing in binary systems, we extend its application to ternary OSCs by pairing it with the near-infrared absorbing D18/BS3TSe-4F host. Thanks to the complementary absorption within 300-970 nm and further optimized morphology, ternary OSCs obtain a higher PCE of 19.13 %, setting a new efficiency benchmark for the dimer-derived OSCs. This approach of alkyl-linked site engineering for constructing dimerized giant acceptors presents a promising pathway to improve both PCE and stability of OSCs. Three new non-fully conjugated dimerized giant acceptors with different alkyl-linked sites are developed. Among them, wing-sited 2Y-wing has fine-tuned packing and better miscibility with donor, allowing to 19.13 % efficiency (which is the highest value among the devices with giant acceptors) and highly stable organic solar cells. image
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| 9. |
- Zhang, Yuehui, et al.
(författare)
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Hyperandrogenism and insulin resistance-induced fetal loss : evidence for placental mitochondrial abnormalities and elevated reactive oxygen species production in pregnant rats that mimic the clinical features of polycystic ovary syndrome
- 2019
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Ingår i: Journal of Physiology. - : WILEY. - 0022-3751 .- 1469-7793. ; 597:15, s. 3927-3950
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Tidskriftsartikel (refereegranskat)abstract
- Women with polycystic ovary syndrome (PCOS) commonly suffer from miscarriage, but the underlying mechanisms remain unknown. Herein, pregnant rats chronically treated with 5 alpha-dihydrotestosterone (DHT) and insulin exhibited hyperandrogenism and insulin resistance, as well as increased fetal loss, and these features are strikingly similar to those observed in pregnant PCOS patients. Fetal loss in our DHT+insulin-treated pregnant rats was associated with mitochondrial dysfunction, disturbed superoxide dismutase 1 and Keap1/Nrf2 antioxidant responses, over-production of reactive oxygen species (ROS) and impaired formation of the placenta. Chronic treatment of pregnant rats with DHT or insulin alone indicated that DHT triggered many of the molecular pathways leading to placental abnormalities and fetal loss, whereas insulin often exerted distinct effects on placental gene expression compared to co-treatment with DHT and insulin. Treatment of DHT+insulin-treated pregnant rats with the antioxidant N-acetylcysteine improved fetal survival but was deleterious in normal pregnant rats. Our results provide insight into the fetal loss associated with hyperandrogenism and insulin resistance in women and suggest that physiological levels of ROS are required for normal placental formation and fetal survival during pregnancy. Women with polycystic ovary syndrome (PCOS) commonly suffer from miscarriage, but the underlying mechanism of PCOS-induced fetal loss during pregnancy remains obscure and specific therapies are lacking. We used pregnant rats treated with 5 alpha-dihydrotestosterone (DHT) and insulin to investigate the impact of hyperandrogenism and insulin resistance on fetal survival and to determine the molecular link between PCOS conditions and placental dysfunction during pregnancy. Our study shows that pregnant rats chronically treated with a combination of DHT and insulin exhibited endocrine aberrations such as hyperandrogenism and insulin resistance that are strikingly similar to those in pregnant PCOS patients. Of pathophysiological significance, DHT+insulin-treated pregnant rats had greater fetal loss and subsequently decreased litter sizes compared to normal pregnant rats. This negative effect was accompanied by impaired trophoblast differentiation, increased glycogen accumulation, and decreased angiogenesis in the placenta. Mechanistically, we report that over-production of reactive oxygen species (ROS) in the placenta, mitochondrial dysfunction, and disturbed superoxide dismutase 1 (SOD1) and Keap1/Nrf2 antioxidant responses constitute important contributors to fetal loss in DHT+insulin-treated pregnant rats. Many of the molecular pathways leading to placental abnormalities and fetal loss in DHT+insulin treatment were also seen in pregnant rats treated with DHT alone, whereas pregnant rats treated with insulin alone often exerted distinct effects on placental gene expression compared to insulin treatment in combination with DHT. We also found that treatment with the antioxidant N-acetylcysteine (NAC) improved fetal survival in DHT+insulin-treated pregnant rats, an effect related to changes in Keap1/Nrf2 and nuclear factor-kappa B signalling. However, NAC administration resulted in fetal loss in normal pregnant rats, most likely due to PCOS-like endocrine abnormality induced by the treatment. Our results suggest that the deleterious effects of hyperandrogenism and insulin resistance on fetal survival are related to a constellation of mitochondria-ROS-SOD1/Nrf2 changes in the placenta. Our findings also suggest that physiological levels of ROS are required for normal placental formation and fetal survival during pregnancy.
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| 10. |
- Zhang, Yuehui, et al.
(författare)
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Hyperandrogenism and insulin resistance-induced fetal loss: evidence for placental mitochondrial abnormalities and elevated ROS production in pregnant rats that mimic the clinical features of PCOS. : PCOS-induced fetal loss is linked to placental defects
- 2019
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Ingår i: The Journal of physiology. - 1469-7793. ; 597:15, s. 3927-3950
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Tidskriftsartikel (refereegranskat)abstract
- Women with polycystic ovary syndrome (PCOS) commonly suffer from miscarriage, but the underlying mechanisms remain unknown. Herein, pregnant rats chronically treated with 5α-dihydrotestosterone (DHT) and insulin exhibited hyperandrogenism and insulin resistance, as well as increased fetal loss, and these features are strikingly similar to those observed in pregnant PCOS patients. Fetal loss in our DHT+insulin-treated pregnant rats was associated with mitochondrial dysfunction, disturbed SOD1 and Keap1/Nrf2 antioxidant responses, over-production of reactive oxygen species (ROS), and impaired formation of the placenta. Chronic treatment of pregnant rats with DHT or insulin alone indicated that DHT triggered many of the molecular pathways leading to placental abnormalities and fetal loss, whereas insulin often exerted distinct effects on placental gene expression compared to co-treatment with DHT and insulin. Treatment of DHT+insulin-treated pregnant rats with the antioxidant N-acetylcysteine improved fetal survival but was deleterious in normal pregnant rats. Our results provide insight into the fetal loss associated with hyperandrogenism and insulin resistance in women and suggest that physiological levels of ROS are required for normal placental formation and fetal survival during pregnancy.Women with polycystic ovary syndrome (PCOS) commonly suffer from miscarriage, but the underlying mechanism of PCOS-induced fetal loss during pregnancy remains obscure and specific therapies are lacking. We used pregnant rats treated with 5α-dihydrotestosterone (DHT) and insulin to investigate the impact of hyperandrogenism and insulin resistance on fetal survival and to determine the molecular link between PCOS conditions and placental dysfunction during pregnancy. Our study shows that pregnant rats chronically treated with a combination of DHT and insulin exhibited endocrine aberrations such as hyperandrogenism and insulin resistance that are strikingly similar to those in pregnant PCOS patients. Of pathophysiological significance, DHT+insulin-treated pregnant rats had greater fetal loss and subsequently decreased litter sizes compared to normal pregnant rats. This negative effect was accompanied by impaired trophoblast differentiation, increased glycogen accumulation, and decreased angiogenesis in the placenta. Mechanistically, we report that over-production of reactive oxygen species (ROS) in the placenta, mitochondrial dysfunction, and disturbed SOD1 and Keap1/Nrf2 antioxidant responses constitute important contributors to fetal loss in DHT+insulin-treated pregnant rats. Many of the molecular pathways leading to placental abnormalities and fetal loss in DHT+insulin treatment were also seen in pregnant rats treated with DHT alone, whereas pregnant rats treated with insulin alone often exerted distinct effects on placental gene expression compared to insulin treatment in combination with DHT. We also found that treatment with the antioxidant N-acetylcysteine (NAC) improved fetal survival in DHT+insulin-treated pregnant rats, an effect related to changes in Keap1/Nrf2 and NFκB signaling. However, NAC administration resulted in fetal loss in normal pregnant rats, most likely due to PCOS-like endocrine abnormality induced by the treatment. Our results suggest that the deleterious effects of hyperandrogenism and insulin resistance on fetal survival are related to a constellation of mitochondrial-ROS-SOD1/Nrf2 changes in the placenta. Our findings also suggest that physiological levels of ROS are required for normal placental formation and fetal survival during pregnancy. This article is protected by copyright. All rights reserved.
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