A copy of this work was available on the public web and has been preserved in the Wayback Machine. The capture dates from 2020; you can also visit the original URL.
The file type is
Introduction There's near shore aquiculture area in coastal sea areas surrounding the Taishan Nuclear Power Plant of China Guangdong Nuclear Power Company, which is characteristic of small water depth ... The cold-source water point is set at the Dajin Island at 10km out of the Taishan Nuclear Power Plant and an about 2.8km long open water channel was built along the west side of Dajin Island. ...doi:10.1051/e3sconf/202019401033 fatcat:keifsx7cyrgezn55uqtnx5gwmi
Taishan Pinus massoniana pollen polysaccharide (TPPPS), a pleiotropic polysaccharide extracted from Taishan P. massoniana pollen, has been studied in our laboratory since 2003. ... Western blot analysis was performed using mouse anti-omp polyclonal antibody [prepared in accordance with our previous method (Hu et al., 2007) ], anti-His tag antibody (Cwbio, China), and rabbit anti-chicken ... Copyright © 2016 Dong, Zhang, Huang, Zhou, Hu, Lian, Zhu, Ma, Yang, Wei and Zhu. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). ...doi:10.3389/fmicb.2016.01708 pmid:27847501 pmcid:PMC5088198 fatcat:z5wy2vhf2vcw5pj23fxmvs76de
Dataset Dataset Size before Compressed Dataset Size Compression Ratio CR Name Compression (Bit) (Bit) (%) Line temper-ature 8920 7874 88.27 Ambient hu-midity 8712 6681 76.69 Rainfall 8836 7441 84.21 Wind ... ˆ Transmission Line Temperature Ambient Relative Humidity Leakage Current Ambient Wind Speed Conductor Wind Speed Rainfa Transmission line temperature 1 0.137 0.913 0.102 0.155 0.015 Ambient relative hu-midity ...doi:10.3390/en14248275 fatcat:otw3p3zhcjcanjyoosz2tveoaa
In this study, we demonstrated that Taishan Pinus massoniana pollen polysaccharide (TPPPS), a natural polysaccharide extracted from Taishan Pinus massoniana pollen, can significantly inhibit ALV-J replication ... In our previous studies, we have extracted Taishan Pinus massoniana pollen polysaccharide (TPPPS) and found that TPPPS exerts remarkable immune enhancement effects on animals 16, 17 . ...doi:10.1038/srep44353 pmid:28287165 pmcid:PMC5347021 fatcat:rvzqkiu6brc27fzmypjh6axhdq
In this paper, by employing comparison technique and invariance properties of a positively limited set, we investigate the convergence of precompact orbits of a class of discrete-time semiflows. In particular, we consider the convergence of precompact orbits of discrete-time semiflows generated by some monotone mapping. We then apply these abstract results to a class of difference systems to obtain the large-time behavior of solutions. Our results improve and extend some existing ones.doi:10.1016/j.aml.2004.08.009 fatcat:nwkxtn2flzgqrhhwyvro5svudu
iNKT cells derive from CD4 + CD8 + DP thymocytes, and are selected by thymocyte-thymocyte interactions through signals from their invariant Va14-Ja18 TCR and from the costimulatory molecules SLAMF1 and SLAMF6. Genetic studies have demonstrated the contribution of different signaling pathways to this process. Surprisingly, current models imply that the Ras/MAPK pathway, one of the critical mediators of conventional ab T cell positive selection, is not necessary for iNKT cell development. Usingdoi:10.1371/journal.pone.0019890 pmid:21572967 pmcid:PMC3091886 fatcat:6kokvsjczjhqtd6jj35qjy2f6a
more »... ce defective at different levels of this pathway our results refute this paradigm, and demonstrate that Ras, and its downstream effectors Egr-1 and Egr-2 are required for positive selection of iNKT cells. Interestingly our results also show that there are differences in the contributions of several of these molecules to the development of iNKT and conventional ab T cells.
AbstractSummaryA number of methods have been devised to address the need for targeted genomic resequencing. One of these methods, Region-specific extraction (RSE) of DNA is characterized by the capture of long DNA fragments (15-20 kb) by magnetic beads, after enzymatic extension of oligonucleotides hybridized to selected genomic regions. Facilitating the selection of the most optimal capture oligos targeting a region of interest, satisfying the properties of temperature (Tm) and entropy (ΔG),doi:10.1101/2019.12.12.873497 fatcat:nczdd5mq55bxrofvig6rj27kgq
more »... ile minimizing the formation of primer dimers in a pooled experiment is therefore necessary. Manual design and selection of oligos becomes an extremely arduous task complicated by factors such as length of the target region and number of targeted regions. Here we describe, AnthOligo, a web-based application developed to optimally automate the process of generation of oligo sequences to be used for the targeting and capturing the continuum of large and complex genomic regions. Apart from generating oligos for RSE, this program may have wider applications in the design of customizable internal oligos to be used as baits for gene panel analysis or even probes for large-scale comparative genomic hybridization (CGH) array processes.Implementation and AvailabilityThe application written in Java8 and run on Tomcat9 is a lightweight Java Spring MVC framework that provides the user with a simple interface to upload an input file in BED format and customize parameters for each task. A Redis-like MapReduce framework is implemented to run sub-tasks in parallel to optimize time and system resources alongside a 'task-queuing' system that runs submitted jobs as a server-side background daemon. The task of probe design in AnthOligo commences when a user uploads an input file and concludes with the generation of a result-set containing an optimal set of region-specific oligos.AnthOligo is currently available as a public web application with URL: http://antholigo.chop.edu.
doi:10.1038/ncomms8770 pmid:26183159 pmcid:PMC4507293 fatcat:ie43jfpv4rbq5pg3usojgdzd5y
Hu and J. Alberola-Ila, unpublished observations). Therefore, we decided to test whether TCR stimulation could upregulate GATA-3 in c-Myb f/f cd4Cre thymocytes. ...doi:10.4049/jimmunol.1003505 pmid:21357543 pmcid:PMC3074202 fatcat:bedg7snyd5abnd3u2opfqbdxqe
Two independent chimera experiments (BMQ-1 and Hu et al. Page 18Nat Immunol. Author manuscript; available in PMC 2010 November 01. ... Contribution of wild-type and c-MybKO bone marrow cells to iNKT populations in thymus, spleen and liver of the bone marrow chimeras Hu et al. Page 15Nat Immunol. ...doi:10.1038/ni.1865 pmid:20383148 pmcid:PMC2857587 fatcat:475dacvzz5aizkxt3kmvnsxkzu
The Fas-associated death domain-containing protein (FADD) is an adaptor for relaying apoptotic signals initiated by death receptors such as Fas. Whereas a lack of death receptors has no effect on mouse development, FADD deficiency results in early embryonic lethality, indicating that FADD has additional functions independent of death receptors. We have previously shown that conditional deletion of FADD not only impairs apoptosis but also leads to defective lymphocyte proliferation. Thedoi:10.1074/jbc.m900249200 pmid:19203997 pmcid:PMC2665115 fatcat:ay36jhfkgfbdxiscuuzcbhjnvq
more »... otic signaling mediated by FADD remains poorly understood. Earlier studies have suggested that FADD carboxyl terminal serine phosphorylation likely plays a role in FADDmediated proliferation signaling in T cells. The FADD death domain is presumably only required for apoptotic signaling, as it interacts with death receptors which are dispensable during embryonic development and lymphocyte proliferation. To test this hypothesis, we have performed mutational analyses of the FADD death domain and identified a mutant, R117Q, which lacks binding to Fas and, thus, is incapable of apoptotic signaling in cell lines. Unexpectedly, this death domain point mutation disrupted mouse embryonic development as shown by in vivo functional reconstitution analyses. Interestingly, a second FADD death domain mutant, V121N, retained normal Fas binding and apoptotic signaling ability but also failed to support mouse development. Furthermore, lymphocyte proliferation responses were impaired by V121N. This reverse genetic study has revealed a previously unappreciated role of the FADD death domain, which likely functions as a molecular switch regulating two distinct signals leading to apoptosis and cell proliferation and is critical for embryogenesis, lymphocyte development, and proliferation. The death domain (DD) 3 was initially identified during mutational studies of the pro-apoptotic receptors Fas and TNF-R1, also known as death receptors (DRs) (1, 2). Amino acid replacements targeted at the DD, a stretch of about 80 amino acids within the intracellular sequences of Fas and TNF-R1, abrogate cell death signaling induced by these two DRs. Sequence homology searches led to the identification of additional members of the DR family, including DR3, DR4 (TRAIL-R1), DR5 (TRAIL-R2), and DR6, which also contain an intracellular DD. The physiological function of DRs has been investigated by analyses of humans and animals carrying mutations in the DR genes. Mutations in the DD of Fas lead to lymphoproliferation (lpr) and autoimmune diseases (3, 4) and also result in predisposition to skin and lymphoid malignancy (5-7). TNF-R1-deficient mice are resistant to endotoxic shock but are highly susceptible to pathogens (8, 9) . DR3 Ϫ/Ϫ mice have no obvious abnormalities except compromised thymic negative selection (10). DR4/5 Ϫ/Ϫ mice have a normal lymphoid system but show enhanced innate immune responses to viral infection (11). Blocking the binding of TRAIL in mice with soluble DR5 enhances autoimmune inflammation and cell cycle progression in lymphocytes (12). TRAIL Ϫ/Ϫ mice are susceptible to induced and spontaneous tumors as well as metastasis of engrafted tumors (13-15). FADD (or Mort1) was initially identified as an adaptor for Fas-induced apoptosis (16 -18) and was later shown to be involved in apoptotic pathways initiated by TNF-R1, DR3, and TRAIL-Rs (19 -28). The adaptor protein, TRADD, is involved in the TNF-R1 signaling pathway and has been shown to associate with FADD (29). There is a DD-like sequence at the carboxyl proximal region of FADD that interacts with the DDs of DRs and TRADD. FADD contains a second protein interaction structure at the NH 2 terminus, called the death effector domain (DED), that binds to the DED present in the pro-domain of caspase 8 (FLICE or MACH) (30, 31). Gene-targeting studies have revealed a novel function of FADD essential for embryonic development (25, 32, 33) . FADD Ϫ/Ϫ and caspase 8 Ϫ/Ϫ mice die midgestation, whereas mice lacking individual DRs have no obvious defects regarding embryonic development. Analyses of conditional mutant mice demonstrated that lymphocytes lacking either FADD or caspase 8 are not only defective in apoptosis induced by Fas but also impaired in proliferative responses induced by the T cell antigen receptor and Toll-like receptors (TLRs) (34 -38). Overexpression of a fragment of FADD that contains the DD but lacks the DED blocks both apoptosis and proliferation in T cells (16, 18, 39 -41). During development cell death is required for proper organogenesis and generation of complex multicellular tissues (42, 43) . In adults, homeostasis in the lymphoid system and other
Aims/hypothesis-More than 90% of Chinese familial early-onset type 2 diabetes mellitus is genetically unexplained. To investigate the molecular aetiology, we identified and characterised whether mutations in the KCNJ11 gene are responsible for these families. Methods-KCNJ11 mutations were screened for 96 familial early-onset type 2 diabetic probands and their families. Functional significance of the identified mutations was confirmed by physiological analysis, molecular modelling and populationdoi:10.1007/s00125-013-3031-9 pmid:24018988 pmcid:PMC5333983 fatcat:hoyljoj76nbufbgoznozevfdk4
more »... survey. Results-Three novel KCNJ11 mutations, R27H, R192H and S116F117del, were identified in three families with early-onset type 2 diabetes mellitus. Mutated KCNJ11 with R27H or R192H markedly reduced ATP sensitivity (E23K>R27H>C42R>R192H>R201H), but no ATP-sensitive potassium channel currents were detected in the loss-of-function S116F117del channel in vitro. Molecular modelling indicated that R192H had a larger effect on the channel ATP-binding pocket than R27H, which may qualitatively explain why the ATP sensitivity of the R192H mutation is seven times less than R27H. The shape of the S116F117del channel may be compressed, which may explain why the mutated channel had no currents. Discontinuation of insulin and implementation of sulfonylureas for R27H or R192H carriers and continuation/switch to insulin therapy for S116F117del carriers resulted in good glycaemic control. Conclusions/interpretation Our results suggest that genetic diagnosis for the KCNJ11 mutations in familial early-onset type 2 diabetes mellitus may help in understanding the molecular aetiology and in providing more personalised treatment for these specific forms of diabetes in Chinese and other Asian patients. Keywords Familial early-onset type 2 diabetes mellitus; KCNJ11; Kir6.2; Mutation neonatal diabetes (PNDM) [2, 5] but also MODY and adult-onset diabetes in a number of Liu et al.
Reactive oxygen species production via NADPH oxidase mediates TGF-␤-induced cytoskeletal alterations in endothelial cells. Am J Physiol Renal Physiol 289: F816 -F825, 2005; doi:10.1152 doi:10. /ajprenal.00024.2005 alterations in endothelial cells have been linked to nitric oxide generation and cell-cell interactions. Transforming growth factor (TGF)-␤ has been described to affect cytoskeletal rearrangement in numerous cell types; however, the underlying pathway is unclear. In the present study,doi:10.1152/ajprenal.00024.2005 pmid:16159901 pmcid:PMC1460011 fatcat:kpqzqqgrk5fbpbv7jmkvqo73qe
more »... we found that human umbilical vein endothelial cells (HUVEC) have marked cytoskeletal alterations with short-term TGF-␤ treatment resulting in filipodia formation and F-actin assembly. The cytoskeletal alterations were blocked by the novel TGF-␤ type I receptor/ALK5 kinase inhibitor (SB-505124) but not by the p38 kinase inhibitor (SB-203580). TGF-␤ also induced marked stimulation of reactive oxygen species (ROS) within 5 min of TGF-␤ exposure. TGF-␤ stimulation of ROS was mediated by the NAPDH oxidase homolog Nox4 as DPI, an inhibitor of NADPH oxidase, and dominant-negative Nox4 adenovirus blocked ROS production. Finally, inhibition of ROS with ROS scavengers or dominant-negative Nox4 blocked the TGF-␤ effect on cytoskeleton changes in endothelial cells. In conclusion, our studies show for the first time that TGF-␤-induced ROS production in human endothelial cells is via Nox4 and that TGF-␤ alteration of cytoskeleton in HUVEC is mediated via a Nox4-dependent pathway. human umbilical vein endothelial cells; cell-cell interactions; cytoskeletal rearrangement; transforming growth factor-␤
Molecular ferroelectrics combine electromechanical coupling and electric polarizabilities, offering immense promise in stimuli-dependent metamaterials. Despite such promise, current physical realizations of mechanical metamaterials remain hindered by the lack of rapid-prototyping ferroelectric metamaterial structures. Here, we present a continuous rapid printing strategy for the volumetric deposition of water-soluble molecular ferroelectric metamaterials with precise spatial control indoi:10.1073/pnas.2013934117 pmid:33077582 fatcat:laub5r5szrg53mycigfzksb77u
more »... any three-dimensional (3D) geometry by means of an electric-field–assisted additive manufacturing. We demonstrate a scaffold-supported ferroelectric crystalline lattice that enables self-healing and a reprogrammable stiffness for dynamic tuning of mechanical metamaterials with a long lifetime and sustainability. A molecular ferroelectric architecture with resonant inclusions then exhibits adaptive mitigation of incident vibroacoustic dynamic loads via an electrically tunable subwavelength-frequency band gap. The findings shown here pave the way for the versatile additive manufacturing of molecular ferroelectric metamaterials.
Involvement of transforming growth factor-␤ in regulation of calcium transients in diabetic vascular smooth muscle cells.doi:10.1152/ajprenal.00145.2003 pmid:12876066 fatcat:qlt3rl5qbjd3jcomrtagto6ic4
« Previous Showing results 1 — 15 out of 712 results