150 research outputs found

    Root Herbivory has More Influence on Arabidopsis thaliana Survival Rates than Leaf Herbivory

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    Hypothesis: We hypothesize that the hypocotyl length, leaves number and survival rate will be greater in plants with cut leaves than cut roots. Background: Plants rely on root absorption and leaf photosynthesis to grow. Roots not only absorb nutrition from soil but also function in nutrient storage and reproduction. We exposed Arabidopsis thaliana to three different treatments: cutting leaves, cutting roots and a control group. We observed their growth, morphology and the survival rate

    Development of A 3D Log Sawing Optimization System for Small Sawmills in Central Appalachia, US

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    A 3D log sawing optimization system was developed to perform log generation, opening face determination, sawing simulation, and lumber grading using 3D modeling techniques. Heuristic and dynamic programming algorithms were used to determine opening face and grade sawing optimization. Positions and shapes of internal log defects were predicted using a model developed by the USDA Forest Service. Lumber grading procedures were based on National Hardwood Lumber Association rules. The system was validated through comparisons with sawmill lumber values. External characteristics of logs, including length, large-end and small-end diameters, diameters at each foot, and defects were collected from five local sawmills in central Appalachia. Results indicated that hardwood sawmills have the potential to increase lumber value through optimal opening face and sawing optimizations. With these optimizations, average lumber value recovery could be increased by 10.01% using the heuristic algorithm or 14.21% using the dynamic programming algorithm. Lumber grade was improved significantly by using the optimal algorithms. For example, recovery of select or higher grade lumber increased 16-30%. This optimization system would help small sawmill operators improve their processing performance and improve industry competitiveness

    Effects of dietary oxidized fish oil on the growth performance, intestinal health, and antioxidant capacity of zebrafish

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    This study aimed to investigate the effects of oxidized fish oil (OFO) on growth performance, intestinal health, and antioxidant function and to determine the minimum concentration of oxidized fish oil to cause irreversible damage to the intestinal tissue structure of zebrafish. A 30-day feeding trial on zebrafish (average weight 0.054 g) was conducted in triplicate groups of fish fed four test diets containing different concentrations of OFO: 0% OFO (OFF, blank control), 2% OFO (OF1), 4% OFO (OF2), and 6% OFO (OF3). The body weight gain (WG), specific growth rates (SGR), feed conversion ratio (FCR), survival rate (SR), and antioxidant function {glutathione peroxidase (GSH-PX), total superoxide dismutase (T-SOD), catalase (CAT), and malondialdehyde (MDA)} were recorded. The intestinal structure was observed at the end of the trial. After the 14-day experimental period, Final body weight (FBW), WG, and SGR decreased significantly with the increase in the concentration of feed OFO (P < 0.05), while FCR showed a downward trend. The activity of T-SOD decreased significantly, the activities of GSH-PX and CAT, and the MDA content increased significantly with the increase in the concentration of feed OFO (P < 0.05). The intestinal morphological damage score showed an upward trend with the increase in the concentration of OFO, and it was significantly higher in group OF2 and OF3 than in group OF1 (P < 0.05). After the 28-day test period, the experimental indexes and intestinal antioxidant function trends were the same as those on 14 days. The increased OFO concentration significantly increased the intestinal morphological injury score (P < 0.05). These results demonstrated that adding 4% OFO to the feed for 14 days could induce irreversible damage to the intestinal tissue structure, weaken the antioxidant function, and decrease the growth performance of zebrafish

    Small interference RNA targeting tissue factor inhibits human lung adenocarcinoma growth in vitro and in vivo

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    <p>Abstract</p> <p>Background</p> <p>The human coagulation trigger tissue factor (TF) is overexpressed in several types of cancer and involved in tumor growth, vascularization, and metastasis. To explore the role of TF in biological processes of lung adenocarcinoma, we used RNA interference (RNAi) technology to silence TF in a lung adenocarcinoma cell line A549 with high-level expression of TF and evaluate its antitumor effects in vitro and in vivo.</p> <p>Methods</p> <p>The specific small interfering RNA (siRNA) designed for targeting human TF was transfected into A549 cells. The expression of TF was detected by reverse transcription-PCR and Western blot. Cell proliferation was measured by MTT and clonogenic assays. Cell apoptosis was assessed by flow cytometry. The metastatic potential of A549 cells was determined by wound healing, the mobility and Matrigel invasion assays. Expressions of PI3K/Akt, Erk1/2, VEGF and MMP-2/-9 in transfected cells were detected by Western blot. In vivo, the effect of TF-siRNA on the growth of A549 lung adenocarcinoma xenografts in nude mice was investigated.</p> <p>Results</p> <p>TF -siRNA significantly reduced the expression of TF in the mRNA and protein levels. The down-regulation of TF in A549 cells resulted in the suppression of cell proliferation, invasion and metastasis and induced cell apoptosis in dose-dependent manner. Erk MAPK, PI3K/Akt pathways as well as VEGF and MMP-2/-9 expressions were inhibited in TF-siRNA transfected cells. Moreover, intratumoral injection of siRNA targeting TF suppressed the tumor growth of A549 cells in vivo model of lung adenocarcinoma.</p> <p>Conclusions</p> <p>Down-regulation of TF using siRNA could provide a potential approach for gene therapy against lung adenocarcinoma, and the antitumor effects may be associated with inhibition of Erk MAPK, PI3K/Akt pathways.</p

    Small RNA zippers lock miRNA molecules and block miRNA function in mammalian cells.

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    MicroRNAs (miRNAs) loss-of-function phenotypes are mainly induced by chemically modified antisense oligonucleotides. Here we develop an alternative inhibitor for miRNAs, termed \u27small RNA zipper\u27. It is designed to connect miRNA molecules end to end, forming a DNA-RNA duplex through a complementary interaction with high affinity, high specificity and high stability. Two miRNAs, miR-221 and miR-17, are tested in human breast cancer cell lines, demonstrating the 70∼90% knockdown of miRNA levels by 30-50 nM small RNA zippers. The miR-221 zipper shows capability in rescuing the expression of target genes of miR-221 and reversing the oncogenic function of miR-221 in breast cancer cells. In addition, we demonstrate that the miR-221 zipper attenuates doxorubicin resistance with higher efficiency than anti-miR-221 in human breast cancer cells. Taken together, small RNA zippers are a miRNA inhibitor, which can be used to induce miRNA loss-of-function phenotypes and validate miRNA target genes

    First in-depth analysis of the novel Th2-type cytokines in salmonid fish reveals distinct patterns of expression and modulation but overlapping bioactivities

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    ACKNOWLEDGMENTS The VHSV-infected samples were generated within the Scottish Government funded research project FC1996 and kindly provided by Marine Scotland staff. Thanks to ELANCO for providing the A. davidanieli (Renogen). FINANCIAL SUPPORT T. W. received funding from the MASTS pooling initiative (The Marine Alliance for Science and Technology for Scotland). MASTS is funded by the Scottish Funding Council (grant reference HR09011) and contributing institutions. Y.J., W.H. and Q.X. were supported financially by the National Scholarship Council of China. Z.Q. was supported by grants from the National Natural Science Foundation of China (31302221) and the overseas training plan for young and middle-aged teachers and principals of colleges and universities in Jiangsu Province, China. M.M.C. was funded by an Ángeles Alvariño postdoctoral contract from the Consejo Superior de Investigaciones Científicas and the Xunta de Galicia. P.D.-R. was funded by a European Commission (EC) Marie Curie Intra European Fellowship (FP7). J.W.H. was funded by the Biotechnology and Biological Sciences Research Council (BB/K009125/1). This work was also supported financially by the EC, under contract Nos. 222719 (LIFECYCLE) and 311993 (TargetFish), and by the European Research Council Starting Grant 2011 (contract No. 280469).Peer reviewedPublisher PD

    MUC1 Contributes to BPDE-Induced Human Bronchial Epithelial Cell Transformation through Facilitating EGFR Activation

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    Although it is well known that epidermal growth factor receptor (EGFR) is involved in lung cancer progression, whether EGFR contributes to lung epithelial cell transformation is less clear. Mucin 1 (MUC1 in human and Muc1 in animals), a glycoprotein component of airway mucus, is overexpressed in lung tumors; however, its role and underlying mechanisms in early stage lung carcinogenesis is still elusive. This study provides strong evidence demonstrating that EGFR and MUC1 are involved in bronchial epithelial cell transformation. Knockdown of MUC1 expression significantly reduced transformation of immortalized human bronchial epithelial cells induced by benzo[a]pyrene diol epoxide (BPDE), the active form of the cigarette smoke (CS) carcinogen benzo(a)pyrene (BaP)s. BPDE exposure robustly activated a pathway consisting of EGFR, Akt and ERK, and blocking this pathway significantly increased BPDE-induced cell death and inhibited cell transformation. Suppression of MUC1 expression resulted in EGFR destabilization and inhibition of the BPDE-induced activation of Akt and ERK and increase of cytotoxicity. These results strongly suggest an important role for EGFR in BPDE-induced transformation, and substantiate that MUC1 is involved in lung cancer development, at least partly through mediating carcinogen-induced activation of the EGFR-mediated cell survival pathway that facilitates cell transformation
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