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6,818 results for “inhibition”
FIGURE 2. Mitodiplosis graminis. a–f in Redescription of Mitodiplosis graminis (Diptera: Cecidomyiidae), a gall midge inhibiting the flowering of pyp grass Ehrharta villosa (Poaceae) in South Africa
FIGURE 2. Mitodiplosis graminis. a–f: male, g–n: female. (a) head, (b) terminalia in dorsal view, (c) gonostyle in ventral view, (d) hypoproct in dorsal view, (d) fifth flagellomere in dorsal view, (e) fifth flagellomere in dorsal view, (f) fifth flagellomere in ventral view, (g) fifth flagellomere in lateral view, (h) palpi of four separate specimens inside pupa, (i) wing, (j) tarsal claws with empodium and pulvilli in ventral view, (k) tarsal claw with empodium and pulvillus in lateral view of specimens inside pupa, (l) terminalia in ventral view (position of omitted setae indicated with arrows), (m) first tarsomere, (n) terminalia in lateral view.
FIGURE 1 in Redescription of Mitodiplosis graminis (Diptera: Cecidomyiidae), a gall midge inhibiting the flowering of pyp grass Ehrharta villosa (Poaceae) in South Africa
FIGURE 1. Gall of Mitodiplosis graminis on Ehrharta villosa. (a) plants bearing galls, (b) gall with partially removed superficial tissue to reveal pupae inside chambers, (c) galls with stems protruding variable lengths from the leaf sheaths, with attached pupal skins left behind by emerged adults, (d) terminal part of gall with attached pupal skins. Localities (both Western Cape Province): (a) Koude Vlakte Nature Conservancy (photo by Jan-Hendrik Keet), b–c: Sedgefield.
Supplementary material for "Molecular dynamics gives new insights into the glucose tolerance and inhibition mechanisms on β-glucosidases" (2 video files)
<p>Video S1: MD of the glucose exit in a glucose-tolerant GH1 β-Glucosidase</p> <p>Video S2: Interactions among glucose, D228, K257, and N312 in a glucose-tolerant GH1 β-glucosidase</p>
Lipidomic and fatty acid metabolism changes in pancreatic cancer upon ELOVL6 inhibition
<p>LC-MS data for the analysis of lipidomic and fatty acid metabolism changes in pancreatic cancer upon ELOVL6 inhibition and MYC deletion or overexpression</p>
Data and software for "A numerical study of inhibiting effect and mechanism of thermal front on sediment transport in a stratified continental sea"
<p>Data and software for "A numerical study of inhibiting effect and mechanism of thermal front on sediment transport in a stratified continental sea"</p>
Dataset and codes for 'Enhancing glymphatic fluid transport by pan-adrenergic inhibition suppresses epileptogenesis in male mice'
<p>This is the code and dataset repository for the publication entitled 'Enhancing glymphatic fluid transport by pan-adrenergic inhibition suppresses epileptogenesis in male mice' on Nature Communications, 2024. Author list: </p> <p>Qian Sun<sup>†</sup>, Sisi Peng<sup>†</sup>, Qiwu Xu, Pia Weikop, Rashad Hussain, Wei Song, Maiken Nedergaard§, Fengfei Ding§</p>
GSK-3ß inhibitor and Actinonin can eliminate HNF-1ß overexpression in Clear Cell Carcinoma through glycolysis inhibition and mitochondrial turnover.
Open the record for dataset details and reuse information.
Raw datas for "Bacillus xiamenensis inhibits the growth of Moraxella osloensis by producing indole-3-carboxaldehyde"
<p>Raw datas for the manuscript entitled "Bacillus xiamenensis inhibits the growth of Moraxella osloensis by producing indole-3-carboxaldehyde" by Watanabe, Masahiro; Sekino, Yuika; Kuramochi, Kouji; Furuyama, Yuuki</p>
Data from: Strain identification and quorum sensing inhibition characterization of marine-derived Rhizobium sp. NAO1
A novel strategy for combating pathogens is through the ongoing development and use of anti-quorum sensing (QS) treatments such as therapeutic bacteria or their anti-QS substances. Relatively little is known about the bacteria that inhabit the open ocean and of their potential anti-pathogenic attributes; thus, in an initiative to identify these types of therapeutic bacteria, planktonic microbes from the North Atlantic Ocean were collected, isolated, cultured and screened for anti-QS activity. Screening analysis identified one such strain, Rhizobium sp. NAO1. Extracts of Rhizobium sp. NAO1 were identified via ultra-performance liquid chromatography (UPLC) analysis. They were shown to contain N-acyl homoserine lactone (AHL)-based QS analogues (in particular, the N-butyryl homoserine lactone (C4-AHL) analogue) and could disrupt biofilm formation by Pseudomonas aeruginosa PAO1. QS inhibition was confirmed using confocal scanning laser microscopy and growth curves, and it was shown to occur in a dose-dependent manner without affecting bacterial growth. Secondary metabolites of Rhizobium sp. NAO1 inhibited PAO1 pathogenicity by downregulating AHL-mediated virulence factors such as elastase activity and siderophore production. Furthermore, as a result of biofilm structure damage, the secondary metabolite products of Rhizobium sp. NAO1 significantly increased the sensitivity of PAO1 to aminoglycoside antibiotics. Our results demonstrated that Rhizobium sp. strain NAO1 has the ability to disrupt P. aeruginosa PAO1 biofilm architecture, in addition to attenuating P. aeruginosa PAO1 virulence factor production and pathogenicity. Therefore, the newly identified ocean-derived Rhizobium sp. NAO1 has the potential to serve as a QS inhibitor and may be a new microbial resource for drug development.
Data from: Inhibition decorrelates visual feature representations in the inner retina
The retina extracts visual features for transmission to the brain. Different types of bipolar cell split the photoreceptor input into parallel channels and provide the excitatory drive for downstream visual circuits. Mouse bipolar cell types have been described at great anatomical and genetic detail, but a similarly deep understanding of their functional diversity is lacking. Here, by imaging light-driven glutamate release from more than 13,000 bipolar cell axon terminals in the intact retina, we show that bipolar cell functional diversity is generated by the interplay of dendritic excitatory inputs and axonal inhibitory inputs. The resulting centre and surround components of bipolar cell receptive fields interact to decorrelate bipolar cell output in the spatial and temporal domains. Our findings highlight the importance of inhibitory circuits in generating functionally diverse excitatory pathways and suggest that decorrelation of parallel visual pathways begins as early as the second synapse of the mouse visual system.
Supplementary Material for "Engineering of a β-galactosidase from Bacillus coagulans to relieve product inhibition and improve hydrolysis performance""
<p><a href="https://zenodo.org/record/5109535">Suppl. Information</a> Tab. S1<a href="https://zenodo.org/record/5109535">:</a> Primers of alanine scanning</p> <p><a href="https://zenodo.org/record/5109535">Suppl. Information</a> Tab. S2<a href="https://zenodo.org/record/5109535">:</a> Primers of N148 saturation mutation</p> <p><a href="https://zenodo.org/record/5109535">Suppl. Information</a> Fig. S1<a href="https://zenodo.org/record/5109535">:</a> Reaction mechanism of β-galactosidase.</p> <p> </p>
Supplementary Material Video S1 Method to show how the new grafting tool is used-A new grafting method for watermelon to inhibit rootstock regrowth and enhance scion growth
<p>Supplementary Material: A new grafting method for watermelon to inhibit rootstock regrowth and enhance scion growth</p>
Analysis of antibody signal loss for elongating RNA polymerase II upon transcription inhibition
<p>This data set assesses the loss of antibody signal for elongating RNA polymerase II in zebrafish embryos upon transcription inhibition with flavopiridol. Polymerase was labeled by immunofluorescence, microscopy images were acquired by instant-SIM micrscopy, and analyzed using MatLab scripts and the bioformats importer. This data set contains the raw image data as well as all further analysis scripts.</p>
Screening of anti-Acinetobacter baumannii plant-based compounds, based on potential inhibition of OmpA and OmpW functions
<p><span>Considering the adverse effect of antimicrobial resistance (AMR) crisis on human life, there is an immediate need for finding new alternatives for treatment of emerging infectious diseases. Therapeutic options, including last-line or combined antibiotic therapies for <i>Acinetobacter baumannii</i>, as an emergent multi-drug resistant (MDR) human pathogen responsible for severe nosocomial and several other infections, are apparently ineffective. The outer membrane protein A (OmpA) and outer membrane protein W (OmpW) are two porins known as virulence factors with different cellular functions. Identification of natural compounds with potentials to block these putative virulence factors can possibly attenuate the growth of the bacteria and control the relating diseases. The current work aimed to screen the therapeutic potential of a library of 371 phytochemicals, as multi-blockers of OmpA and OmpW in <em>A. baumannii</em>. Although the anti-virulence activities of these biomolecules are reported previously, no evaluation on <i>A. baumannii </i>has been performed so far. Moreover, there is no safety screening and early alerts of these compounds. In this study, hits were initially selected based on their physicochemical, absorption, distribution, metabolism, excretion, and toxicity (ADMET) drug-like properties. Afterwards, the selected ligands were subjected to standard docking calculations against predicted three-dimensional structure of OmpA and OmpW in <i>A. baumannii</i>. We identified five phytochemicals (Amorphigenin (PUBCHEM CID 92207), Bisdemethoxy-curcumin (PUBCHEM CID 5315472), Dalbinol (PUBCHEM CID 44257412), Epicatechin gallate (PUBCHEM CID 72276) and Nordihydroguaiaretic acid (PUBCHEM CID 4534)) bearing appreciable binding affinity towards the selected binding pocket of OmpA and OmpW. </span></p>
Data from: Parallel cognitive processing streams in human prefrontal cortex: parsing areal-level brain network for response inhibition
<p>Multiple cognitive processes are recruited to achieve adaptive behavior. However, it is poorly understood how such cognitive processes are implemented in temporal cascades of human cerebral cortical areas as processing streams to achieve behavior. In the present study, we identify cortical processing streams for response inhibition and examine relationships among the processing streams. Functional magnetic resonance imaging (MRI) and time-resolved single-pulse transcranial magnetic stimulation (TMS) reveal three distinct critical timings of transient disruption in the functionally essential cortical areas that belong to two distinct cerebrocortical networks. Furthermore, single-pulse TMS following suppression of the ventral posterior inferior frontal cortex (vpIFC) with repetitive TMS reveals information flow from the vpIFC to the presupplementary motor area (preSMA) within the same network but not to the dorsal posterior inferior frontal cortex (dpIFC) across different networks. These causal behavioral effects suggest two parallel processing streams (vpIFC-preSMA versus dpIFC-intraparietal sulcus) that act concurrently during response inhibition.</p>
The lncRNA TUG1 regulates Smac/DIABLO expression by competitively inhibiting miR-29b and modulates the apoptosis of lens epithelial cells in age-related cataracts
<p>As one of the first discovered lncRNAs, TUG1 has been reported to be widely expressed in a variety of tumours. It promotes cell proliferation, differentiation, apoptosis and migration. However, our understanding of its importance in cataracts is limited. This study aims to explore the mechanism by which TUG1 mediates the apoptosis of lens epithelial cells by regulating the miR-29b/Smac axis in age-related cataracts and to identify more strategies for the nonsurgical treatment of cataracts. In this experiment we found TUG1 and Smac were expressed at high levels in age-related cataract (ARC) samples and HLEB3 cells treated with H2O2, while miR-29b expression was decreased. In vitro cell-based experiments confirmed that the downregulation of TUG1 inhibits lens epithelial cell apoptosis. Mechanistically, Smac expression is negatively regulated by miR-29b. TUG1 competitively inhibits miR-29b expression and causes the release of more Smac. In addition, miR-29b reverses the effect of TUG1 on HLE-B3 cells. In conclusion, lncRNATUG1 increases Smac expression by competitively inhibiting miR-29b and promoting the apoptosis of lens epithelial cells in age-related cataracts. This mechanism is the cytological basis of ARC formation. Based on these results, the TUG1-miR29b-Smac axis may be a new molecular pathway to regulate the development of age-related cataracts.</p>
Single vesicle fusion experiments illustrating the inhibition of the calcium triggered release by the inhibitory peptide SP9
<p>Synaptic neurotransmitter release is mediated by an orchestra of presynaptic proteins that precisely control and trigger fusion between synaptic vesicles and the neuron terminal at the active zone upon an action potential. Critical to this process are the neuronal SNAREs (Soluble N-ethylmaleimide sensitive factor Attachment protein REceptor), the Ca2+-sensor synaptotagmin, the activator/regulator complexin, and other factors. Here we present the data for single vesicle fusion experiments with synaptic vesicles in absence and presence of the inhibitory peptide SP9 that illustrate the inhibition of calcium-triggered release. </p>
Identifying neprilysin-inhibiting FDA approved drugs as possible risk factors for Alzheimer's disease
<p>Although Alzheimer’s disease is the most common type of dementia, unfortunately, safe and effective treatments that could slow the progress of this progressive neurodegenerative disease are still lacking. This amplifies the importance of preventing this disease and, thus, identifying its risk factors. It has already been known that various drugs may increase the risk for Alzheimer’s disease. Here, we searched for approved drugs that may increase this risk through inhibiting neprilysin. Neprilysin is the rate-limiting enzyme in the amyloid beta clearance pathway and is even able to catalyze unphysiologically large amount of amyloid beta. Inhibitors of neprilysin may increase the risk of Alzheimer’s disease and exacerbate its progress via increasing the amounts of the accumulated amyloid beta and its secondary products.</p> <p>In this study, after predicting the blood-brain barrier (BBB) penetration of approved drugs and their metabolites, we used various computational tools to identify potential inhibitors of neprilysin among them. These tools included various structure-based approaches like docking with AutoDockZn, PLANTS, FlexX, Fitted, Molegro, and Flare and rescoring with these scoring functions: Convex-PL, GNINA, JamdaScorer, KORP-PL, RF-Score-VS, Rank Score, dG, VScore. The reliability of these methods was assessed by investigating the correlations of their predictions with experimental measurements. We also used these ligand-based approaches: 2D-QSAR modelling and similarity comparison based on feature trees.</p> <p>These <em>in silico</em> tools suggested that several drugs deserve to be further investigated beacuase of their considerable binding affinity to neprilysin and BBB penetration: aripiprazole, etoricoxib, nabumetone, fentiazac, clorotepine, pitolisant, and chloroquine. Other drugs whose BBB penetration were not predicted to be much high yet their chronic or common use may lead to consequential inhibition of neprilysin can be added to this list, like glyburide, lisinopril, cilazapril, fosinopril, prucalopride, ibersartan, valsartan, and montelukast. Further investigations, including <em>in vitro</em>, animal, and human investigations, can help mitigate the huge and rising societal and economic burden of Alzheimer’s disease globally.</p>
Epigenetic changes in inflammatory arthritis monocytes contribute to disease and can be targeted by JAK inhibition
<p><strong>Objectives</strong> How the local inflammatory environment regulates epigenetic changes in the context of inflammatory arthritis remains unclear. Here we assessed the transcriptional and active enhancer profile of monocytes derived from the inflamed joints of Juvenile Idiopathic Arthritis (JIA) patients, a model well-suited for studying inflammatory arthritis.<br> <strong>Methods </strong>RNA-sequencing and H3K27me3 chromatin immunoprecipitation sequencing (ChIP-seq) were used to analyze the transcriptional and epigenetic profile, respectively, of JIA synovial fluid-derived monocytes.<br> <strong>Results </strong>Synovial-derived monocytes display an activated phenotype, which is regulated on the epigenetic level. IFN signaling-associated genes are increased and epigenetically altered in synovial monocytes, indicating a driving role for IFN in establishing the local inflammatory phenotype. Treatment of synovial monocytes with the Janus-associated kinase (JAK) inhibitor ruxolitinib, which inhibits IFN signaling, transformed the activated enhancer landscape and reduced disease-associated gene expression, thereby inhibiting the inflammatory phenotype.<br> <strong>Conclusion </strong>This study provides novel insights into epigenetic regulation of inflammatory arthritis patient-derived monocytes and highlights the therapeutic potential of epigenetic modulation for the treatment of inflammatory rheumatic diseases.</p> <p><br> <strong>Data deposited</strong></p> <ul> <li>H3K27ac ChIP-seq peak coordinates of healthy control peripheral blood-derived monocytes and JIA peripheral blood- and synovial fluid-derived monocytes (Figure 2 in article).</li> <li>Individual and merged peak coordinates of H3K27ac and H3K4me1 ChIP-seq on JIA monocytes with and without Ruxolitinib and IFN gamma (Figure 4 in article).</li> <li>Gene expression data of JIA monocytes treated with and without JQ1 (Figure 2 in article).</li> <li>Gene expression data of Ruxolitinib- and IFN-stimulated JIA monocytes (Figure 5 in article).</li> </ul>
Data explanation for Manuscript "'An optimized hydroponic pipeline for large-scale identification of wheat genotypes with resilient biological nitrification inhibition (BNI) activity'"
<p>Data explanation for Manuscript "'An optimized hydroponic pipeline for large-scale identification of wheat genotypes with resilient biological nitrification inhibition (BNI) activity'"</p>
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Allen Brain Atlas
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Annotated Behaviour and Observability Dataset (ABODe)
ABODe is a University of Edinburgh DataShare dataset for behavior classification in group-housed mice using home-cage video, identities, bounding boxes, ground-plate positions, and annotator labels.
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The International Brain Laboratory public data releases expose standardized mouse decision-making experiments, including Neuropixels recordings, widefield calcium imaging, behavior, and session metadata accessed through the ONE API.
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