411 research outputs found

    Oviposition-site shift in phytophagous mites reflects a trade-off between predator avoidance and rainstorm resistance

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    捕食者と風雨に対する害虫のジレンマを発見 --捕食者は捕食するより大きな抑止力を及ぼす--. 京都大学プレスリリース. 2021-03-04.Predators can reduce prey population densities by driving them to undertake costly defences. Here, we report on a remarkable example of induced antipredator defence in spider mites that enhances the risk to rainstorms. Spider mites live on the undersides of host plant leaves and usually oviposit on the leaf undersurface. When they are threatened by predatory mites, they oviposit on three-dimensional webs to avoid egg predation, although the cost of ovipositing on webs has not yet been clearly determined. We prepared bean plants harbouring spider mite (Tetranychus kanzawai) eggs on either leaf surfaces or webs and exposed them to rainstorms outdoors. We found that fewer eggs remained on webs than on leaf surfaces. We then examined the synergistic effect of wind and rain by simulating both in the laboratory. We conclude that ovipositing on webs comes at a cost, as eggs are washed off the host plants by wind and rain. This may explain why spider mite populations decrease drastically in the rainy season, although they inhibit leaf undersides where they are not directly exposed to rainfall

    Age-Related Differences in Stepping Response When Stepping onto a Known Soft Surface under Dual Task Conditions

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    The purpose of this study was to investigate whether age-related differences in stepping response influence postural control when stepping onto a known soft surface under dual task conditions. Nine young and eleven older female adults participated. First, they stepped on a flat surface while grasping an empty cup (single task), and then they repeated the task while grasping a cup filled with water (dual task). For the second experiment, they stepped on a soft surface placed in front of them while performing the above tasks. The main result was that %DIP (initiation phase as a percentage of the total stepping task time) was significantly higher for older than for young adults during the dual task on the soft surface. In conclusion, caution due to previous experience may increase attentional demand during dual tasks and lengthen the time required for central nervous processing in order to avoid losing postural stability in older adults, resulting in reductions in step velocity and step length compared to those in young adults

    Expression of vascular endothelial growth factor in patients with acute myocardial infarction

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    AbstractOBJECTIVEThe purpose of this study was to investigate the clinical significance of vascular endothelial growth factor (VEGF) in acute myocardial infarction (AMI). We also examined the involvement of peripheral blood mononuclear cells (PBMCs), which are a possible source of VEGF in AMI.BACKGROUNDVEGF is a potent endothelial cell–specific mitogen and could affect the outcome of AMI.METHODSThirty patients with AMI were used for this study. Serum and PBMCs were isolated from peripheral blood on days 1, 7, 14 and 21 after the onset of AMI. PBMCs were cultured at a density of 5 × 106cells/ml for 24 h. VEGF levels in serum and the culture media were measured by enzyme-linked immunosorbent assay using a specific anti-human VEGF antibody.RESULTSSerum VEGF levels elevated gradually after the onset of AMI and reached a peak on day 14. VEGF levels in the culture medium of PBMCs after incubation for 24 h (PBMC-VEGF) were maximally elevated 7 days after the onset. Maximum serum VEGF levels showed significant positive correlations with maximum creatine phosphokinase (CPK) levels (r = +0.70, p < 0.001), but maximum PBMC-VEGF levels did not correlate with maximum CPK levels. Patients showing improvement in left ventricular systolic function during the course of AMI showed significantly higher PBMC-VEGF levels than patients without improvement.CONCLUSIONSThe extent of myocardial damage contributes to the elevation of serum VEGF levels in AMI. VEGF produced by PBMCs may play an important role in the improvement of left ventricular function by promoting angiogenesis and reendothelialization after AMI

    Fyn phosphorylates AMPK to inhibit AMPK activity and AMP-dependent activation of autophagy

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    We previously demonstrated that proto-oncogene Fyn decreased energy expenditure and increased metabolic phenotypes. Also Fyn decreased autophagy-mediated muscle mass by directly inhibiting LKB1 and stimulating STAT3 activities, respectively. AMPK, a downstream target of LKB1, was recently identified as a key molecule controlling autophagy. Here we identified that Fyn phosphorylates the α subunit of AMPK on Y436 and inhibits AMPK enzymatic activity without altering the assembly state of the AMPK heterotrimeric complex. As pro-inflammatory mediators are reported modulators of the autophagy processes, treatment with the pro-inflammatory cytokine TNFα resulted in 1) increased Fyn activity 2) stimulated Fyn-dependent AMPKα tyrosine phosphorylation and 3) decreased AICAR-dependent AMPK activation. Importantly, TNFα induced inhibition of autophagy was not observed when AMPKα was mutated on Y436. 4) These data demonstrate that Fyn plays an important role in relaying the effects of TNFα on autophagy and apoptosis via phosphorylation and inhibition of AMPK

    Akt2 phosphorylates Synip to regulate docking and fusion of GLUT4-containing vesicles

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    We have identified an unusual potential dual Akt/protein kinase B consensus phosphorylation motif in the protein Synip (RxKxRS97xS99). Surprisingly, serine 97 is not appreciably phosphorylated, whereas serine 99 is only a specific substrate for Akt2 but not Akt1 or Akt3. Although wild-type Synip (WT-Synip) undergoes an insulin-stimulated dissociation from Syntaxin4, the Synip serine 99 to phenylalanine mutant (S99F-Synip) is resistant to Akt2 phosphorylation and fails to display insulin-stimulated Syntaxin4 dissociation. Furthermore, overexpression of WT-Synip in 3T3L1 adipocytes had no effect on insulin-stimulated recruitment of glucose transporter 4 (GLUT4) to the plasma membrane, whereas overexpression of S99F-Synip functioned in a dominant-interfering manner by preventing insulin-stimulated GLUT4 recruitment and plasma membrane fusion. These data demonstrate that insulin activation of Akt2 specifically regulates the docking/fusion step of GLUT4-containing vesicles at the plasma membrane through the regulation of Synip phosphorylation and Synip–Syntaxin4 interaction

    Structural analysis of three novel trisaccharides isolated from the fermented beverage of plant extracts

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    <p>Abstract</p> <p>Background</p> <p>A fermented beverage of plant extracts was prepared from about fifty kinds of vegetables and fruits. Natural fermentation was carried out mainly by lactic acid bacteria (<it>Leuconostoc </it>spp.) and yeast (<it>Zygosaccharomyces </it>spp. and <it>Pichia </it>spp.). We have previously examined the preparation of novel four trisaccharides from the beverage: <it>O</it>-β-D-fructopyranosyl-(2->6)-<it>O</it>-β-D-glucopyranosyl-(1->3)-D-glucopyranose, <it>O</it>-β-D-fructopyranosyl-(2->6)-<it>O</it>-[β-D-glucopyranosyl-(1->3)]-D-glucopyranose, <it>O</it>-β-D-glucopyranosyl-(1->1)-<it>O</it>-β-D-fructofuranosyl-(2<->1)-α-D-glucopyranoside and <it>O</it>-β-D-galactopyranosyl-(1->1)-<it>O</it>-β-D-fructofuranosyl-(2<->1)- α-D-glucopyranoside.</p> <p>Results</p> <p>Three further novel oligosaccharides have been found from this beverage and isolated from the beverage using carbon-Celite column chromatography and preparative high performance liquid chromatography. Structural confirmation of the saccharides was provided by methylation analysis, MALDI-TOF-MS and NMR measurements.</p> <p>Conclusion</p> <p>The following novel trisaccharides were identified: <it>O</it>-β-D-fructofuranosyl-(2->1)-<it>O</it>-[β-D-glucopyranosyl-(1->3)]-β-D-glucopyranoside (named "3<sup>G</sup>-β-D-glucopyranosyl β, β-isosucrose"), <it>O</it>-β-D-glucopyranosyl-(1->2)-<it>O</it>-[β-D-glucopyranosyl-(1->4)]-D-glucopyranose (4<sup>1</sup>-β-D-glucopyranosyl sophorose) and <it>O</it>-β-D-fructofuranosyl-(2->6)-<it>O</it>-β-D-glucopyranosyl-(1->3)-D-glucopyranose (6<sup>2</sup>-β-D-fructofuranosyl laminaribiose).</p
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