| 971. |
- Schmitz, Birger
(författare)
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How a world came to be
- 2012
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Ingår i: Nature. - : Springer Science and Business Media LLC. - 0028-0836 .- 1476-4687. ; 485:7396, s. 39-39
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Recension (övrigt vetenskapligt/konstnärligt)
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| 972. |
- Schmitz, Birger
(författare)
-
The cosmological you
- 2013
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Ingår i: Nature. - : Springer Science and Business Media LLC. - 0028-0836 .- 1476-4687. ; 493:7430, s. 25-25
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Recension (övrigt vetenskapligt/konstnärligt)
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| 973. |
- Schnadt, Joachim, et al.
(författare)
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Experimental evidence for sub-3-fs charge transfer from an aromatic adsorbate to a semiconductor
- 2002
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Ingår i: Nature. - : Springer Science and Business Media LLC. - 0028-0836 .- 1476-4687. ; 418:6898, s. 620-623
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Tidskriftsartikel (refereegranskat)abstract
- The ultrafast timescale of electron transfer processes is crucial to their role in many biological systems and technological devices. In dye-sensitized solar cells(1-4), the electron transfer from photoexcited dye molecules to nanostructured semiconductor substrates needs to be sufficiently fast to compete effectively against loss processes and thus achieve high solar energy conversion efficiencies(4). Time-resolved laser techniques indicate an upper limit of 20 to 100 femtoseconds(5-9) for the time needed to inject an electron from a dye into a semiconductor, which corresponds to the timescale on which competing processes such as charge redistribution(10,11) and intramolecular thermalization of excited states(12-14) occur. Here we use resonant photoemission spectroscopy, which has previously been used to monitor electron transfer in simple systems with an order-of-magnitude improvement in time resolution(15,16), to show that electron transfer from an aromatic adsorbate to a TiO2 semiconductor surface can occur in less than 3 fs. These results directly confirm that electronic coupling of the aromatic molecule to its substrate is sufficiently strong to suppress competing processes(17).
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| 974. |
- Schneider, Florian H, et al.
(författare)
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Financial incentives for vaccination do not have negative unintended consequences
- 2023
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Ingår i: Nature. - : Springer Science and Business Media LLC. - 0028-0836 .- 1476-4687. ; 613:7944, s. 526-533
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Tidskriftsartikel (refereegranskat)abstract
- Financial incentives to encourage healthy and prosocial behaviours often trigger initial behavioural change, but a large academic literature warns against using them. Critics warn that financial incentives can crowd out prosocial motivations and reduce perceived safety and trust, thereby reducing healthy behaviours when no payments are offered and eroding morals more generally. Here we report findings from a large-scale, pre-registered study in Sweden that causally measures the unintended consequences of offering financial incentives for taking the first dose of a COVID-19 vaccine. We use a unique combination of random exposure to financial incentives, population-wide administrative vaccination records and rich survey data. We find no negative consequences of financial incentives; we can reject even small negative impacts of offering financial incentives on future vaccination uptake, morals, trust and perceived safety. In a complementary study, we find that informing US residents about the existence of state incentive programmes also has no negative consequences. Our findings inform not only the academic debate on financial incentives for behaviour change but also policy-makers who consider using financial incentives to change behaviour.
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| 975. |
- Schoebel, Stefan, et al.
(författare)
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Cryo-EM structure of the protein-conducting ERAD channel Hrd1 in complex with Hrd3
- 2017
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Ingår i: Nature. - : Springer Science and Business Media LLC. - 0028-0836 .- 1476-4687. ; 548:7667, s. 352-
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Tidskriftsartikel (refereegranskat)abstract
- Misfolded endoplasmic reticulum proteins are retro-translocated through the membrane into the cytosol, where they are poly-ubiquitinated, extracted from the membrane, and degraded by the proteasome(1-4)-a pathway termed endoplasmic reticulum-associated protein degradation (ERAD). Proteins with misfolded domains in the endoplasmic reticulum lumen or membrane are discarded through the ERAD-L and ERAD-M pathways, respectively. In Saccharomyces cerevisiae, both pathways require the ubiquitin ligase Hrd1, a multi-spanning membrane protein with a cytosolic RING finger domain(5,6). Hrd1 is the crucial membrane component for retro-translocation(7,8), but it is unclear whether it forms a protein-conducting channel. Here we present a cryo-electron microscopy structure of S. cerevisiae Hrd1 in complex with its endoplasmic reticulum luminal binding partner, Hrd3. Hrd1 forms a dimer within the membrane with one or two Hrd3 molecules associated at its luminal side. Each Hrd1 molecule has eight transmembrane segments, five of which form an aqueous cavity extending from the cytosol almost to the endoplasmic reticulum lumen, while a segment of the neighbouring Hrd1 molecule forms a lateral seal. The aqueous cavity and lateral gate are reminiscent of features of protein-conducting conduits that facilitate polypeptide movement in the opposite direction-from the cytosol into or across membranes(9-11). Our results suggest that Hrd1 forms a retro-translocation channel for the movement of misfolded polypeptides through the endoplasmic reticulum membrane.
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| 976. |
|
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| 977. |
|
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| 978. |
- Schramke, V, et al.
(författare)
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RNA-interference-directed chromatin modification coupled to RNA polymerase II transcription
- 2005
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Ingår i: Nature. - : Springer Science and Business Media LLC. - 0028-0836 .- 1476-4687. ; 435:7046, s. 1275-1279
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Tidskriftsartikel (refereegranskat)abstract
- RNA interference (RNAi) acts on long double-stranded RNAs (dsRNAs) in a variety of eukaryotes to generate small interfering RNAs that target homologous messenger RNA, resulting in their destruction. This process is widely used to 'knock-down' the expression of genes of interest to explore phenotypes(1-3). In plants(3-5), fission yeast(6-8), ciliates(9,10), flies(11) and mammalian cells(12,13), short interfering RNAs (siRNAs) also induce DNA or chromatin modifications at the homologous genomic locus, which can result in transcriptional silencing or sequence elimination(14). siRNAs may direct DNA or chromatin modification by siRNA - DNA interactions at the homologous locus(4,5). Alternatively, they may act by interactions between siRNA and nascent transcript(15,16). Here we show that in fission yeast ( Schizosaccharomyces pombe), chromatin modifications are only directed by RNAi if the homologous DNA sequences are transcribed. Furthermore, transcription by exogenous T7 polymerase is not sufficient. Ago1, a component of the RNAi effector RISC/RITS complex, associates with target transcripts and RNA polymerase II. Truncation of the regulatory carboxy-terminal domain (CTD) of RNApol II disrupts transcriptional silencing, indicating that, like other RNA processing events(17-19), RNAi-directed chromatin modification is coupled to transcription.
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| 979. |
- Schröder, Björn, et al.
(författare)
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Reduction of disulphide bonds unmasks potent antimicrobial activity of human β-defensin 1
- 2011
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Ingår i: Nature. - : Macmillan Publishers Ltd.. - 0028-0836 .- 1476-4687. ; 469:7330, s. 419-423
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Tidskriftsartikel (refereegranskat)abstract
- Human epithelia are permanently challenged by bacteria and fungi, including commensal and pathogenic microbiota. In the gut, the fraction of strict anaerobes increases from proximal to distal, reaching 99% of bacterial species in the colon. At colonic mucosa, oxygen partial pressure is below 25% of airborne oxygen content, moreover microbial metabolism causes reduction to a low redox potential of -200 mV to -300 mV in the colon. Defensins, characterized by three intramolecular disulphide-bridges, are key effector molecules of innate immunity that protect the host from infectious microbes and shape the composition of microbiota at mucosal surfaces. Human β-defensin 1 (hBD-1) is one of the most prominent peptides of its class but despite ubiquitous expression by all human epithelia, comparison with other defensins suggested only minor antibiotic killing activity. Whereas much is known about the activity of antimicrobial peptides in aerobic environments, data about reducing environments are limited. Herein we show that after reduction of disulphide-bridges hBD-1 becomes a potent antimicrobial peptide against the opportunistic pathogenic fungus Candida albicans and against anaerobic, Gram-positive commensals of Bifidobacterium and Lactobacillus species. Reduced hBD-1 differs structurally from oxidized hBD-1 and free cysteines in the carboxy terminus seem important for the bactericidal effect. In vitro, the thioredoxin (TRX) system is able to reduce hBD-1 and TRX co-localizes with reduced hBD-1 in human epithelia. Hence our study indicates that reduced hBD-1 shields the healthy epithelium against colonisation by commensal bacteria and opportunistic fungi. Accordingly, an intimate interplay between redox-regulation and innate immune defence seems crucial for an effective barrier protecting human epithelia.
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| 980. |
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