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           Search results for: 4-[(3R)-3-Amino-1-oxo-4-(phenylthio)butyl]morpholine C14H20N2O2S CAS: 870812-94-5   

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In-situ creating elastic lattice OO bonds over semicrystalline yellow TiO nanoparticles for significantly enhanced photocatalytic H production.

Atomic defects (e.g., Ti, oxygen vacancies) have been intenstively investigated for modifying TiO in order to reach visible light active photocatalytic H production. However, the atomic defects within TiO could easily act as photo-generated charge-carrier recombination centers, resulting in relatively low H conversion efficiency. In this paper, semicrystalline yellow TiO nanoparticles rich of superoxide ions are new synthesized by a simple aqueous solution method. Instead of introducing atomic defects, we show for the first time that catalytic performance can also be significantly improved via in-situ creating lattice OO bonds within metastable semicrystalline TiO. The synthesized semicrystalline yellow TiO exhibits significantly enhanced photocatalytic activity for H production after cycle tests. The formaldehyde in aqueous solution is used as target pollutant to simulate industrial wastewater. In-situ created elastic lattice OO bonds are proposed to improve catalytic performance through facilitating the breakage of CH bonds of HCHO. A series of internally consistent reaction equations is proposed that describes the role of in-situ created lattice OO bonds for improving the catalytic performance. This is strongly supported by that the H production rate at the end of the fourth cycle test is significantly more than that of the beginning of the first cycle test.

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PML nuclear bodies are recruited to persistent DNA damage lesions in an RNF168-53BP1 dependent manner and contribute to DNA repair.

The bulk of DNA damage caused by ionizing radiation (IR) is generally repaired within hours, yet a subset of DNA lesions may persist even for long periods of time. Such persisting IR-induced foci (pIRIF) co-associate with PML nuclear bodies (PML-NBs) and are among the characteristics of cellular senescence. Here we addressed some fundamental questions concerning the nature and determinants of this co-association, the role of PML-NBs at such sites, and the reason for the persistence of DNA damage in human primary cells. We show that the persistent DNA lesions are devoid of homologous recombination (HR) proteins BRCA1 and Rad51. Our super-resolution microscopy-based analysis showed that PML-NBs are juxtaposed to and partially overlap with the pIRIFs. Notably, depletion of 53BP1 resulted in decreased intersection between PML-NBs and pIRIFs implicating the RNF168-53BP1 pathway in their interaction. To test whether the formation and persistence of IRIFs is PML-dependent and to investigate the role of PML in the context of DNA repair and senescence, we genetically deleted PML in human hTERT-RPE-1 cells. Unexpectedly, upon high-dose IR treatment, cells displayed similar DNA damage signalling, repair dynamics and kinetics of cellular senescence regardless of the presence or absence of PML. In contrast, the PML knock-out cells showed increased sensitivity to low doses of IR and DNA-damaging agents mitomycin C, cisplatin and camptothecin that all cause DNA lesions requiring repair by HR. These results, along with enhanced sensitivity of the PML knock-out cells to DNA-PK and PARP inhibitors implicate PML as a factor contributing to HR-mediated DNA repair.

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Cerebral Hemodynamic Variations in the Early Stage after Carotid Artery Stenting in Patients with and without Near Occlusion.

To evaluate the unclear cerebral hemodynamic variations in patients with and without near occlusion (NO) in hours following carotid artery stenting (CAS) by transcranial Doppler (TCD).

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Perioperative and follow-up results of Carotid Artery Stenting and Carotid Endarterectomy in Patients with carotid near-occlusion.

Comparing perioperative and follow-up results of Carotid Artery Stenting (CAS) and Carotid Endarterectomy (CEA) in Patients with carotid near-occlusion (NO).

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CRISPR-Cas: more than ten years and still full of mysteries.


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Exon 2 Skipping Eliminates Gamma-Glutamyl Carboxylase Activity, Indicating a Partial Splicing Defect in a Patient with Vitamin K Clotting Factor Deficiency.

Mutations in the gamma-glutamyl carboxylase (GGCX), which is required for vitamin K-dependent (VKD) protein activation, can result in vitamin K clotting factor deficiency (VKCFD1). A recent report described a VKCFD1 patient with a homozygous carboxylase mutation that altered splicing and deleted exon 2 (Δ2GGCX). Only Δ2GGCX RNA was observed in the patient.

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BES1 regulated BEE1 controls photoperiodic flowering downstream of blue light signaling pathway in Arabidopsis.

BRI1-EMS-SUPPRESSOR 1 (BES1) functions as a key regulator in the brassinosteroid (BR) pathway that promotes plant growth. However, whether BES1 is involved in photoperiodic flowering is unknown. Here we report that BES1 acts as a positive regulator of photoperiodic flowering, but it cannot directly bind FLOWERING LOCUS T (FT) promoter. BR ENHANCED EXPRESSION 1 (BEE1) is the direct target of BES1 and acts downstream of BES1. BEE1 is also a positive regulator of photoperiodic flowering. BEE1 binds directly to the FT chromatin to activate the transcription of FT and promote flowering initiation. More importantly, BEE1 promotes flowering in a blue light photoreceptor Cryptochrome 2 (cry2) partially dependent manner, since it physically interacts with cry2 under the blue light. Furthermore, BEE1 is regulated by both BRs and blue light. The transcription of BEE1 is induced by BRs, and the BEE1 protein is stabilized under the blue light. Our findings indicate that BEE1 is the integrator of BES1 and cry2 mediating flowering, and BES1-BEE1-FT is a new signaling pathway in regulating photoperiodic flowering. This article is protected by copyright. All rights reserved.

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Arabinose biosynthesis is critical for salt stress tolerance in Arabidopsis.

The capability to maintain cell wall integrity is critical for plants to adapt to unfavorable conditions. L-arabinose (Ara) is a constituent of several cell wall polysaccharides and many cell wall-localized glycoproteins, but so far the contribution of Ara metabolism to abiotic stress tolerance is still poorly understood. Here, we report that mutations in the MUR4 (also known as HSR8) gene, which is required for the biosynthesis of UDP-Arap in Arabidopsis, lead to a reduced root elongation under high concentrations of NaCl, KCl, NaNO , or KNO . The short root phenotype of the mur4/hsr8 mutants under high salinity is rescued by exogenous Ara or gum arabic, a commercial product of arabinogalactan proteins (AGPs) from Acacia senegal. Mutation of MUR4 gene leads to abnormal cell-cell adhesion under salt stress. MUR4 forms either a homodimer or heterodimers with its isoforms. Analysis of the higher order mutants of MUR4 with its three paralogs, MURL, DUR, MEE25, reveals that the paralogs of MUR4 also contribute to the biosynthesis of UDP-Ara and are critical for root elongation. Taken together, our work reveals the importance of the Ara metabolism in salt stress tolerance and also provides new insights into the enzymes involved in the UDP-Ara biosynthesis in plants. This article is protected by copyright. All rights reserved.

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Thinning Can Reduce Losses in Carbon Use Efficiency and Carbon Stocks in Managed Forests Under Warmer Climate.

Forest carbon use efficiency (CUE, the ratio of net to gross primary productivity) represents the fraction of photosynthesis that is not used for plant respiration. Although important, it is often neglected in climate change impact analyses. Here we assess the potential impact of thinning on projected carbon cycle dynamics and implications for forest CUE and its components (i.e., gross and net primary productivity and plant respiration), as well as on forest biomass production. Using a detailed process-based forest ecosystem model forced by climate outputs of five Earth System Models under four representative climate scenarios, we investigate the sensitivity of the projected future changes in the autotrophic carbon budget of three representative European forests. We focus on changes in CUE and carbon stocks as a result of warming, rising atmospheric CO concentration, and forest thinning. Results show that autotrophic carbon sequestration decreases with forest development, and the decrease is faster with warming and in unthinned forests. This suggests that the combined impacts of climate change and changing CO concentrations lead the forests to grow faster, mature earlier, and also die younger. In addition, we show that under future climate conditions, forest thinning could mitigate the decrease in CUE, increase carbon allocation into more recalcitrant woody pools, and reduce physiological-climate-induced mortality risks. Altogether, our results show that thinning can improve the efficacy of forest-based mitigation strategies and should be carefully considered within a portfolio of mitigation options.

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Rare Complication of Carotid Stenting: New-Onset Refractory Status Epilepticus: A Study of Five Patients.

New-onset refractory status epilepticus (NORSE) is uncommon and almost 50% of cases are cryptogenic. We report the rare development of NORSE following carotid artery stenting (CAS), a procedure which is increasingly being used to treat the carotid stenosis.

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Non small cell lung carci Ofloxacin CAS Number [824 B-Phycoerythrin antibody 2-Amino Benzimidazole Su 2-Amino Benzimidazole Su EZH2 KMT6 Control Peptid EZH2 KMT6 antibody Isoty EXOC7 antibody Host Goat Uroguanylin (1-8) antibo Uroguanylin antibody Hos Interleukin-34 IL34 (N-t Interleukin-34 IL34 anti

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