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1.
The morphology and infraciliature of a new ciliate, Metopus yantaiensis n. sp., discovered in coastal soil of northern China, were investigated. It is distinguished from its congeners by a combination of the following features: nuclear apparatus situated in the preoral dome; 18–21 somatic ciliary rows, of which three extend onto the preoral dome (dome kineties); three to five distinctly elongated caudal cilia, and 21–29 adoral polykinetids. The 18S rRNA genes of this new species and two congeners, Metopus contortus and Metopus hasei, were sequenced and phylogenetically analyzed. The new species is more closely related to M. hasei and the clevelandellids than to other congeners; both the genus Metopus and the order Metopida are not monophyletic. In addition, the digestion‐resistant bacteria in the cytoplasm of M. yantaiensis were identified, using a 16S rRNA gene clone library, sequencing, and fluorescence in situ hybridization. The detected intracellular bacteria are affiliated with Sphingomonadales, Rhizobiales, Rickettsiales (Alphaproteobacteria), Pseudomonas (Gammaproteobacteria), Rhodocyclales (Betaproteobacteria), Clostridiales (Firmicutes), and Flavobacteriales (Bacteroidetes).  相似文献   
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It was found that S-adenosylmethionine (SAM) could effectively improve avermectin titer with 30–60 μg/mL addition to FH medium. To clearly elucidate the mechanism of SAM on intracellular metabolites of Streptomyces avermitilis, a GC–MS-based comparative metabolomics approach was carried out. First, 230 intracellular metabolites were identified and 14 of them remarkably influenced avermectin biosynthesis were discriminative biomarkers between non-SAM groups and SAM-treated groups by principal components analysis (PCA) and partial least squares (PLS). Based on further key metabolic pathway analyses, these biomarkers, such as glucose, oxaloacetic acid, fatty acids (in soybean oil), threonine, valine, and leucine, were identified as potentially beneficial precursors and added in medium. Compared with single-precursor feeding, the combined feeding of the precursors and SAM markedly increased the avermectin titer. The co-feeding approach not only directly verified our hypothesis on the mechanism of SAM by comparative metabolomics, but also provided a novel strategy to increase avermectin production.  相似文献   
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Dissecting the genetic basis for the traits of northern-style Chinese steamed bread (NCSB) is of great significance for wheat quality breeding. Quantitative trait loci (QTLs) for the processing quality of NCSB were studied using a recombinant inbred line (RIL) consisting of 173 lines derived from a “Shannong01–35 × Gaocheng9411” cross. Twenty-four putative additive QTLs were detected on chromosomes 1A, 1B, 1D, 3A, 3B, 4A, 4B, 5B, 6B, and 7B. Of these QTLs, QTex1A.1-27, QHei5B.5-488, and QGum4B.4-17 had the highest contribution and accounted for 9.33, 10.9, and 12.0% of the phenotypic variations, respectively. Several co-located QTLs with additive effects were detected on chromosomes 1A, 1D, 4B, and 5B. Two clusters (RFL_CONTIG2160_524-WSNP_CAP12_C2438_1180601 and EX_C101685_705-RAC875_C27536_611) for height, total score, and texture and for chewiness, gumminess, and hardness were detected on chromosomes 1A and 4B, respectively. Two QTLs for chewiness and hardness (QCh1D-4, QHa1D-4) with additive effects were detected; these alleles could be good targets for improving the processing quality of steamed bread from common wheat (Triticum aestivum L.). In addition, QTLs for wheat flour quality and the associated correlations with NCSB were simultaneously analyzed. Negative correlations were detected between chewiness and the wet/dry gluten content (WGC/DGC) or protein content. Two QTLs (QCh4B.4-17 and QPr4B.4-17) and three QTLs (QCh4B.4-13, QWG4B.4-13, and QDG4B.4-13) clustered in the same chromosomal region. The detected QTL clusters should be further investigated during wheat breeding and could be used by breeders to improve wheat quality and especially the processing quality of NCSB.  相似文献   
4.
Kernel size and kernel weight are important factors possibly involved in the determination of grain yield in maize, so identifying the genetic basis of kernel-related traits provides insights into the breeding of high-yield maize varieties. Kernel length (KL), kernel width (KW) and hundred kernel weight (HKW) were evaluated in three various planting conditions for the 240 field-grown double haploid (DH) lines derived from the single-cross hybrid Xianyu335. Variations in KL, KW and HKW were observed among DH lines, and all three traits showed a broad sense heritability of 76%. A total of 964 single nucleotide polymorphisms (SNPs) from the MaizeSNP3072 chip was utilised to create a high-density genetic map of 1546.4 cM and to identify quantitative trait loci (QTLs). Using composite interval mapping, a total of five, seven and five QTLs have been mapped for KL, KW and HKW, respectively. qkl1-2 and qkl4-1 explained 17.8% and 14.2% of the phenotypic variation in KL, respectively, and the other three QTLs contributed 3.2–4.0%. The phenotypic variation explained (PVE) of seven QTLs responsible for KW ranged from 3.3 to 9.5%. Three QTLs for HKW, qhkw1, qhkw5 and qhkw10 each explained more than 10% of the phenotypic variation, and qhkw4 and qhkw9 accounted for 3.0% and 6.0%, respectively. Due to their detection in multiple planting environments, the loci mapped here appear to be potential targets for the improvement of maize grain yield.  相似文献   
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α1‐adrenoceptors (α1‐ARs) stimulation has been found to enhance excitatory processes in many brain regions. A recent study in our laboratory showed that α1‐ARs stimulation enhances glutamatergic transmission via both pre‐ and post‐synaptic mechanisms in layer V/VI pyramidal cells of the rat medial prefrontal cortex (mPFC). However, a number of pre‐synaptic mechanisms may contribute to α1‐ARs‐induced enhancement of glutamate release. In this study, we blocked the possible post‐synaptic action mediated by α1‐ARs to investigate how α1‐ARs activation regulates pre‐synaptic glutamate release in layer V/VI pyramidal neurons of mPFC. We found that the α1‐ARs agonist phenylephrine (Phe) induced a significant enhancement of glutamatergic transmission. The Phe‐induced potentiation was mediated by enhancing pre‐synaptic glutamate release probability and increasing the number of release vesicles via a protein kinase C‐dependent pathway. The mechanisms of Phe‐induced potentiation included interaction with both glutamate release machinery and N‐type Ca2+ channels, probably via a pre‐synaptic Gq/phospholipase C/protein kinase C pathway. Our results may provide a cellular and molecular mechanism that helps explain α1‐ARs‐mediated influence on PFC cognitive functions.

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8.
Drug delivery to the brain for the treatment of pathologies with a CNS component is a significant clinical challenge. P‐glycoprotein (PgP), a drug efflux pump in the endothelial cell membrane, is a major factor in preventing therapeutics from crossing the blood‐brain barrier (BBB). Identifying PgP regulatory mechanisms is key to developing agents to modulate PgP activity. Previously, we found that PgP trafficking was altered concomitant with increased PgP activity and disassembly of high molecular weight PgP‐containing complexes during acute peripheral inflammatory pain. These data suggest that PgP activity is post‐translationally regulated at the BBB. The goal of the current study was to identify proteins that co‐localize with PgP in rat brain microvessel endothelial cell membrane microdomains and use the data to suggest potential regulatory mechanisms. Using new density gradients of microvessel homogenates, we identified two unique pools (1,2) of PgP in membrane fractions. Caveolar constituents, caveolin1, cavin1, and cavin2, co‐localized with PgP in these fractions indicating the two pools contained caveolae. A chaperone (Hsc71), protein disulfide isomerase and endosomal/lysosomal sorting proteins (Rab5, Rab11a) also co‐fractionated with PgP in the gradients. These data suggest signaling pathways with a potential role in post‐translational regulation of PgP activity at the BBB.

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Transforming growth factor-β (TGF-β) signaling has been prominently implicated in the pathogenesis of vascular remodeling, especially the initiation and progression of flow-induced vascular remodeling. Smooth muscle cells (SMCs) are the principal resident cells in arterial wall and are critical for arterial remodeling. However, the role of TGF-β signaling in SMC for flow-induced vascular remodeling remains unknown. Therefore, the goal of our study was to determine the effect of TGF-β pathway in SMC for vascular remodeling, by using a genetical smooth muscle-specific (SM-specific) TGF-β type II receptor (Tgfbr2) deletion mice model. Mice deficient in the expression of Tgfbr2 (MyhCre.Tgfbr2f/f) and their corresponding wild-type background mice (MyhCre.Tgfbr2WT/WT) underwent partial ligation of left common carotid artery for 1, 2, or 4 weeks. Then the carotid arteries were harvested and indicated that the disruption of Tgfbr2 in SMC provided prominent inhibition of vascular remodeling. And the thickening of carotid media, proliferation of SMC, infiltration of macrophage, and expression of matrix metalloproteinase (MMP) were all significantly attenuated in Tgfbr2 disruption mice. Our study demonstrated, for the first time, that the TGF-β signaling in SMC plays an essential role in flow-induced vascular remodeling and disruption can prevent this process.  相似文献   
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