Pre-concentration and determination of trace uranium (VI) in environments using ion-imprinted chitosan resin via solid phase extraction

The uranyl-ion-imprinted and non-imprinted cross-linked chitosan resins possessing quinoline-8-ol moiety have been prepared. In all the cases, a significant imprinting effect was noticed on comparing percent extraction of uranium (VI). The resulting ion-imprinted resin was used for solid phase extractive preconcentration of uranium (VI) prior to its determination by spectrophotometry. Experimental variables that influence the quantitative extraction of uranium (VI) were optimized by both static and column methods. The retention capacity found for uranium (VI) was 218 mg g-1 of resin which is higher than the corresponding non-imprinted resins and other solid phase extraction sorbents possessing quinoline-8-ol moiety. The optimum pH range was 4.5-7.0. Uranium adsorbed was easily and quantitatively eluted with 1 mol L-1 HCl (10 mL) at a flow rate of 2 mL min-1. Interference studies showed a high tolerance of diverse ions and electrolyte species. The limit of detection was 2 µg L-1 and the dynamic linear range was 5-100 µg L-1. The accuracy of the developed method was tested with one uranium ore standard reference material. Furthermore, the proposed method was successfully applied for the determination of uranium in contaminated soil and sediment samples

Screening and evaluating of long noncoding RNAs in the puberty of goats

GO analysis of predicted targets of lncRNAs in trans. (XLS 1551 kb

High resolution mapping and positional cloning of ENU-induced mutations in the Rw region of mouse chromosome 5

<p>Abstract</p> <p>Background</p> <p>Forward genetic screens in mice provide an unbiased means to identify genes and other functional genetic elements in the genome. Previously, a large scale ENU mutagenesis screen was conducted to query the functional content of a ~50 Mb region of the mouse genome on proximal Chr 5. The majority of phenotypic mutants recovered were embryonic lethals.</p> <p>Results</p> <p>We report the high resolution genetic mapping, complementation analyses, and positional cloning of mutations in the target region. The collection of identified alleles include several with known or presumed functions for which no mutant models have been reported (<it>Tbc1d14</it>, <it>Nol14</it>, <it>Tyms</it>, <it>Cad</it>, <it>Fbxl5</it>, <it>Haus3</it>), and mutations in genes we or others previously reported (<it>Tapt1</it>, <it>Rest</it>, <it>Ugdh</it>, <it>Paxip1</it>, <it>Hmx1, Otoe, Nsun7</it>). We also confirmed the causative nature of a homeotic mutation with a targeted allele, mapped a lethal mutation to a large gene desert, and localized a spermiogenesis mutation to a region in which no annotated genes have coding mutations. The mutation in <it>Tbc1d14 </it>provides the first implication of a critical developmental role for RAB-GAP-mediated protein transport in early embryogenesis.</p> <p>Conclusion</p> <p>This collection of alleles contributes to the goal of assigning biological functions to all known genes, as well as identifying novel functional elements that would be missed by reverse genetic approaches.</p

Global change effects on plant communities are magnified by time and the number of global change factors imposed

Global change drivers (GCDs) are expected to alter community structure and consequently, the services that ecosystems provide. Yet, few experimental investigations have examined effects of GCDs on plant community structure across multiple ecosystem types, and those that do exist present conflicting patterns. In an unprecedented global synthesis of over 100 experiments that manipulated factors linked to GCDs, we show that herbaceous plant community responses depend on experimental manipulation length and number of factors manipulated. We found that plant communities are fairly resistant to experimentally manipulated GCDs in the short term (<10 y). In contrast, long-term (≥10 y) experiments show increasing community divergence of treatments from control conditions. Surprisingly, these community responses occurred with similar frequency across the GCD types manipulated in our database. However, community responses were more common when 3 or more GCDs were simultaneously manipulated, suggesting the emergence of additive or synergistic effects of multiple drivers, particularly over long time periods. In half of the cases, GCD manipulations caused a difference in community composition without a corresponding species richness difference, indicating that species reordering or replacement is an important mechanism of community responses to GCDs and should be given greater consideration when examining consequences of GCDs for the biodiversity–ecosystem function relationship. Human activities are currently driving unparalleled global changes worldwide. Our analyses provide the most comprehensive evidence to date that these human activities may have widespread impacts on plant community composition globally, which will increase in frequency over time and be greater in areas where communities face multiple GCDs simultaneously

Genetic Dissection Of Checkpoint Signaling In Mouse Primordial Germ Cells

Although mutations are the force of evolution, most mutations are deleterious. Faithful inheritance of genetic information is the key to evolutionary success. The only cell lineage that is capable of transferring genetic information is the germ line. Therefore, refined control of mutation frequency in germ cells is of great importance. The control mechanism mainly involves the DNA damage response (DDR), since DNA damage is the major source of mutations. In mammals, most studies on germ line mutation and DDR focus on meiosis. In contrast, little is known about these processes in primordial germ cells (PGCs). In particular, checkpoint signaling has not been characterized in PGCs. Multiple analysis showed that the mutation rate in germ cells is consistently lower than that in somatic cells. Therefore, it has been proposed that there is a fundamental difference in DDR between germ cells and somatic cells. Indeed, a few DDR mutants have revealed a hypersensitivity of PGCs to DNA damage. In this dissertation, I characterized two such genes in mouse model: FancmC4/C4 and Mcm9XG/XG. Deficiency of either Fancm or Mcm9 causes genome instability as well as PGC depletion. PGC depletion in both mutants is largely due to reduced PGC proliferation between E11.5 and E13.5. In order to understand the correlation between genome instability and reduced PGC proliferation, I conducted genetic studies using 5 checkpoint mutants, including Hus1, Atm, Chk2, p53 and p21. My studies indicated that ATM-p53-p21 signaling is partially responsible for the germ cell deficiency in FancmC4/C4 males. None of the 5 genes is required for the germ cell depletion in FancmC4/C4 females or either sex of Mcm9XG/XG. Additionally, there is an additive germ cell depletion in FancmC4/C4 and Mcm9XG/XG compound mutants, suggesting FancmC4 and Mcm9XG alleles have independent impacts on DDR. Together, my results imply that there are at least 3 checkpoint pathways responsible for DDR in PGCs

On the Innovation of Marketing Channel Modes of China’s Seed Industry

In China, the seed industry has fierce competition. The situation of homogeneous management and homogeneous products is serious. A key problem is simple and outmoded marketing channel of seed. It threatens sustainable development of seed enterprises. At present, the two-level distribution channel of seed industry has problems of similarity, low access threshold, and unfair benefit distribution, and thus urgently needs innovation. The innovation of distribution channel is inevitable requirement for promoting reorganization of China’s seed industry and building of new order, is necessary weapon for dealing with trans-national seed industry competition, is essential measure for lifting the overall service level of seed industry, and is also essential means for conforming to stage development of China’s agriculture. The innovation of seed marketing channel should consider changes of future agricultural development, deep-level demand of industrial market and services, sci-tech development level, fair distribution of industrial profit, and differentiated competition. It is recommended that channel innovation should follow the flat principle, have new and unique conception, give full play connection advantage of marginal industry, realize complementary advantages and mutual promotion, strengthen service awareness, combine with agricultural development trend, and seek sci-tech innovation of channel carrier – variety

Comprehensive analysis of circular RNA profiling in AZD9291‐resistant non‐small cell lung cancer cell lines

Background Osimertinib (AZD9291), a third‐generation EGFR‐tyrosine kinase inhibitor, can effectively prolong survival in non‐small cell lung cancer (NSCLC) patients with EGFR mutations, particularly T790M mutations; however, acquired resistance to AZD9291 is inevitable, thus exploration of the targets of resistance is urgent. Methods Considering the important role of circular RNAs (circRNAs) in cancers, we established AZD9291‐resistant NSCLC cell lines (H1975/AZDR and HCC827/AZDR) and used microarray analysis to determine the circRNA expression profiles of the cells. The H1975/AZDR and HCC827/AZDR cell lines were induced by gradually increasing the drug concentration. CircRNA microarray expression profiles were obtained from H1975, HCC827, H1975/AZDR, and HCC827/AZDR cells and validated by quantitative reverse transcription PCR. Expression data were analyzed bioinformatically. Results The H1975/AZDR and HCC827/AZDR cell lines were successfully established. The half‐maximal inhibitory concentration and the invasion ability of H1975/AZDR and HCC827/AZDR cells were significantly enhanced. The proliferation rates of H1975/AZDR and HCC827/AZDR were much lower than H1975 and HCC827. Microarray analysis identified 15 504 circRNAs differentially expressed in H1975, HCC827, H1975/AZDR, and HCC827/AZDR cells. Among them, 7966 were upregulated and 7538 were downregulated more than two‐fold. We predicted the possible miRNAs of the top dysregulated circRNAs. Furthermore, Kyoto Encyclopedia of Genes and Genomes pathway analysis showed that the most modulated circRNAs regulate several cancers and cancer‐related pathways. Conclusion Our results reveal that circRNAs may play a role in NSCLC AZD9291 resistance and might be a promising molecular target candidate for gene therapy

PPM1G regulates hepatic ischemia/reperfusion injury through STING‐mediated inflammatory pathways in macrophages

Abstract Background Ischemia/reperfusion injury (IRI) is generally unavoidable following liver transplantation. Here, we investigated the role of protein phosphatase, Mg2+/Mn2+ dependent 1G (PPM1G) in hepatic IRI. Methods Hepatic IRI was mimicked by employing a hypoxia/reperfusion (H/R) model in RAW 264.7 cells and a 70% warm ischemia model in C57BL/6 mice, respectively. In vitro, expression changes of tumor necrosis factor‐α and interleukin were detected by quantitative real‐time polymerase chain reaction (qRT‐PCR), western blot analysis, and enzyme‐linked immunosorbent assay. The protein expressions of PPM1G and the stimulator of interferon genes (STING) pathway components were analyzed by western blot. Interaction between PPM1G and STING was verified by coimmunoprecipitation (CO‐IP). Immunofluorescence was applied for detection of p‐IRF3. Flow cytometry, qRT‐PCR and western blot were utilized to analyze markers of macrophage polarization. In vivo, histological analyses of mice liver were carried out by TUNEL and H&E staining. Changes in serum aminotransferases were also detected. Results Following H/R intervention, a steady decline in PPM1G along with an increase in inflammatory cytokines in vitro was observed. Addition of plasmid with PPM1G sequence limited the release of inflammatory cytokines and downregulated phosphorylation of STING. CO‐IP validated the interaction between PPM1G and STING. Furthermore, inhibition of PPM1G with lentivirus enhanced phosphorylation of STING and its downstream components; meanwhile, p65, p38, and Jnk were also surged to phosphorylation. Expression of INOS and CD86 was surged, while CD206, Arg‐1, and IL‐10 were inhibited. In vivo, PPM1G inhibition further promoted liver damage, hepatocyte apoptosis, and transaminases release. Selective inhibition of STING with C‐176 partially reversed the activation of STING pathway and inflammatory cytokines in vitro. M1 markers were also suppressed by C‐176. In vivo, C‐176 rescued liver damage and transaminase release caused by PPM1G inhibition. Conclusion PPM1G suppresses hepatic IRI and macrophage M1 phenotype by repressing STING‐mediated inflammatory pathways

Phylogenetic analysis and molecular characteristics of seven variant Chinese field isolates of PRRSV

BACKGROUND: Porcine reproductive and respiratory syndrome (PRRS) has now been widely recognized as an economically important disease. The objective of this study was to compare the molecular and biological characteristics of porcine reproductive and respiratory syndrome virus (PRRSV) field isolates in China to those of the modified live virus (MLV) PRRS vaccine and its parent strain (ATCC VR2332). RESULTS: Five genes (GP2, GP3, GP4, GP5 and NSP2) of seven isolates of PRRSV from China, designated LS-4, HM-1, HQ-5, HQ-6, GC-2, GCH-3 and ST-7/2008, were sequenced and analyzed. Phylogenetic analyses based on the nucleotide sequence of the ORF2-5 and NSP2 showed that the seven Chinese isolates belonged to the same genetic subgroup and were related to the North American PRRSV genotype. Comparative analysis with the relevant sequences of another Chinese isolate (BJ-4) and North American (VR2332 and MLV) viruses revealed that these isolates have 80.8-92.9% homology with VR-2332, and 81.3-98.8% identity with MLV and 80.7-92.9% with BJ-4. All Nsp2 nonstructural protein of these seven isolates exhibited variations (a 29 amino acids deletion) in comparison with other North American PRRSV isolates. Therefore, these isolates were novel strain with unique amino acid composition. However, they all share more than 97% identity with other highly pathogenic Chinese PRRSV strains. Additionally, there are extensive amino acid (aa) mutations in the GP5 protein and the Nsp2 protein when compared with the previous isolates. CONCLUSIONS: These results might be useful to study the genetic diversity of PRRSV in China and to track the infection sources as well as for vaccines development