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6,818 results for “inhibition”
Raw data for Kierdorf et al, "Muscle function and homeostasis require cytokine inhibition of AKT activity in Drosophila"
<p>This upload contains the raw data corresponding to the publication "Muscle function and homeostasis require cytokine inhibition of AKT activity in Drosophila" by Katrin Kierdorf et al., eLife 2020.</p>
Molecular docking: Hydroxychloroquine alternative to inhibit the COVID-19 main protease (MPro)
<p>Docking study shows best binding affinity against the main protease of COVID-19. As per the docking results top twelve compounds as a MPro inhibitor, Coumermycin A1 (-10.2), Irinotecan (-9.4), Suramin (-9.4), Trovafloxacin (-9.3), Aclarubicin (-9.0), Dactinomycin (-9.0), TG-100801 (-9.0), Raltegravir (-8.9), Digoxin (-8.9), Etoposide (-8.9), Doxorubicin (-8.8), and Venetoclax (-8.8) from the tested compounds.</p> <p>ARULANANDAM, CHARLI DEEPAK (2020): Molecular docking: Hydroxychloroquine alternative to inhibit the COVID-19 main protease (MPro). figshare. Dataset. https://doi.org/10.6084/m9.figshare.12032745.v26</p>
Pterostilbene Protects Cochlea from Ototoxicity in Streptozotocin-Induced Diabetic Rats by Inhibiting Apoptosis
<p>Diabetes mellitus (DM) causes ototoxicity by inducing oxidative stress, microangiopathy, and apoptosis in the cochlear sensory hair cells. The natural anti-oxidant pterostilbene (PTS) (trans-3,5-dimethoxy-4-hydroxystylbene) has been reported to relieve oxidative stress and apoptosis in DM, but its role in diabetic-induced ototoxicity is unclear. This study aimed to investigate the effects of dose-dependent PTS on the cochlear cells of streptozotocin (STZ)-induced diabetic rats. The study included 30 albino male Wistar rats that were randomized into five groups: non-diabetic control (Control), diabetic control (DM), and diabetic rats treated with intraperitoneal PTS at 10, 20, or 40 mg/kg/day during the four-week experimental period (DM + PTS10, DM + PTS20, and DM + PTS40). Distortion product otoacoustic emission (DPOAE) tests were performed at the beginning and end of the study. At the end of the experimental period, apoptosis in the rat cochlea was investigated using caspase-8, cytochrome-c, and terminal deoxyribonucleotidyl transferase-mediated dUTP-biotin end labeling (TUNEL). Quantitative real-time polymerase chain reaction was used to assess the mRNA expression levels of the following genes: CASP-3, BCL-associated X protein (BAX), and BCL-2. Body weight, blood glucose, serum insulin, and malondialdehyde (MDA) levels in the rat groups were evaluated. The mean DPOAE amplitude in the DM group was significantly lower than the means of the other groups (0.9–8 kHz; P < 0.001 for all). A dose-dependent increase of the mean DPOAE amplitudes was observed with PTS treatment (P < 0.05 for all). The Caspase-8 and Cytochrome-c protein expressions and the number of TUNEL-positive cells in the hair cells of the Corti organs of the DM rat group were significantly higher than those of the PTS treatment and control groups (DM > DM + PTS10 > DM + PTS20 > DM + PTS40 > Control; P < 0.05 for all). PTS treatment also reduced cell apoptosis in a dose-dependent manner by increasing the mRNA expression of the anti-apoptosis BCL2 gene and by decreasing the mRNA expressions of both the pro-apoptosis BAX gene and its effector CASP-3 and the ratio of BAX/BCL-2 in a dose-dependent manner (P < 0.05 compared to DM for all). PTS treatment significantly improved the metabolic parameters of the diabetic rats, such as body weight, blood glucose, serum insulin, and MDA levels, consistent with our other findings (P < 0.05 compared to DM for all). PTS decreased the cochlear damage caused by diabetes, as confirmed by DPOAE, biochemical, histopathological, immunohistochemical, and molecular findings. This study reports the first in vivo findings to suggest that PTS may be a protective therapeutic agent against diabetes-induced ototoxicity.</p>
Inhibition of Parkinson's Disease-related LRRK2 by type-I and type-II kinase inhibitors: activity and structures
<p>Mutations in Leucine Rich Repeat Kinase 2 (LRRK2) are a common cause of familial Parkinson’s Disease (PD), and a risk factor for the sporadic form. Increased kinase activity has been shown in both familial and sporadic PD patients. This has made LRRK2 kinase inhibitors a major focus of drug development efforts in PD. Although significant progress has been made in understanding the structural biology of LRRK2, there are no available structures of LRRK2 inhibitor complexes. To this end, we solved cryo-EM structures of LRRK2, wild-type and PD-linked mutants, bound to the LRRK2-specific type-I inhibitor MLi-2 and the broad-spectrum type-II inhibitor GZD-824. Our structures revealed LRRK2’s kinase in the active-like state, stabilized by type-I inhibitor interactions, and an inactive DYG-out type-II inhibitor complex. The structures also showed how inhibitor-induced conformational changes are affected by the N-terminal half of LRRK2. The structural models provide a template for the rational development of LRRK2 kinase inhibitors covering both canonical inhibitor binding modes.</p>
Acetylcholine receptor based chemogenetics engineered for neuronal inhibition and seizure control assessed in mice
<p>Analysis scripts and underlying data used to produce the figures in our study entitled "Acetylcholine receptor based chemogenetics engineered for neuronal inhibition and seizure control assessed in mice", in Nature Communications. The listed project leaders can be contacted with any questions.</p>
Data from: High temperatures and low soil moisture synergistically reduce switchgrass yields from marginal field sites and inhibit fermentation
<p>'Marginal lands' are low productivity sites abandoned from agriculture for reasons such as low or high soil water content, challenging topography, or nutrient deficiency. To avoid competition with crop production, cellulosic bioenergy crops have been proposed for cultivation on marginal lands, however on these sites they may be more strongly affected by environmental stresses such as low soil water content. In this study we used rainout shelters to induce low soil moisture on marginal lands and determine the effect of soil water stress on switchgrass growth and the subsequent production of bioethanol. Five marginal land sites that span a latitudinal gradient in Michigan and Wisconsin were planted to switchgrass in 2013 and during the 2018-2021 growing seasons were exposed to reduced precipitation under rainout shelters in comparison to ambient precipitation. The effect of reduced precipitation was related to the environmental conditions at each site and biofuel production metrics (switchgrass biomass yields and composition and ethanol production). During the first year (2018), the rainout shelters were designed with 60% rain exclusion, which did not affect biomass yields compared to ambient conditions at any of the field sites, but decreased switchgrass fermentability at the Wisconsin Central - Hancock site. In subsequent years, the shelters were redesigned to fully exclude rainfall, which led to reduced biomass yields and inhibited fermentation for three sites. When switchgrass was grown in soils with large reductions in moisture and increases in temperature, the potential for biofuel production was significantly reduced, exposing some of the challenges associated with producing biofuels from lignocellulosic biomass grown under drought conditions.</p>
Identifying Unexpected Neurotoxicity Drivers with Acetylcholinesterase Inhibition by Virtual Effect-Directed Analysis in Nationwide Estuarine Waters
<p><span>Neurotoxicity is frequently observed in the global aquatic environment, </span><span>threatening aquatic ecosystems and human health</span><span>. </span><span>However, </span><span>a very limited proportion of neurotoxic effects (~1%) has been explained by known chemicals of concern. Here, we integrated</span><span> machine learning, nontargeted analysis, and <em>in vitro</em> biotesting</span><span> to identify neurotoxic drivers of acetylcholinesterase (AChE) inhibition in estuarine waters along the coastline of China. Machine learning was used as a virtual fractionation tool to reduce the complexity of chemical mixtures, thus guiding nontargeted screening of AChE inhibitors. Ultimately, sixty chemicals with diverse </span><span>known and presently unknown</span><span> structures were identified, explaining 82.1% of the observed AChE inhibition </span><span>in estuarine water samples</span><span>. Polyunsaturated fatty acids were unexpectedly found to be neurotoxic drivers, accounting for 80.5% of the overall effect. This proof-of-concept study demonstrates that our approach enables rapid and comprehensive screening of </span><span>causative organic pollutants</span><span> </span><span>associated with various <em>in vitro</em> endpoints </span><span>for large-scale monitoring of water quality</span><span>.</span></p>
Dataset for "Exploring Mechanism of Corrosion Inhibition of WE43 and AZ31 Alloys by Aqueous Molybdate in Hank's Solution by Multisine Impedimetric Monitoring"
<p>This dataset contains raw data of the publication “Exploring Mechanism of Corrosion Inhibition of WE43 and AZ31 Alloys by Aqueous Molybdate in Hank’s Solution by Multisine Impedimetric Monitoring”. Corrosion Science, Volume 231, 2024, 111979, ISSN 0010-938X, <a href="https://doi.org/10.1016/j.corsci.2024.111979">https://doi.org/10.1016/j.corsci.2024.111979</a>. The data was collected at Jerzy Haber Institute of Catalysis and Surface Chemistry, Polish Academy of Sciences (Poland) and Gdansk University of Technology (Poland). All data are provided under CC0 license. The dataset includes Scanning electron and optical microscopy images (.tiff and ,jpg format); X-ray photoelectron spectroscopy spectra (.vms format); Electrochemical impedance spectra (.txt format). Dzmitry Kharytonau gratefully acknowledges the financial support of this study by the National Science Centre (Poland) under research Grant Sonatina no. 2021/40/C/ST5/00266. This work was also supported by Gdansk University of Technology under the Aurum Supporting International Research Team Building – ‘Excellence Initiative – Research University’ [grant number: 2/2021/IDUB/II.1.3].<br><br></p>
Data from: Do genetic loci that cause reproductive isolation in the lab inhibit gene flow in nature?
<p>The genetic dissection of reproductive barriers between diverging lineages provides enticing clues into the origin of species. One strategy uses linkage analysis in experimental crosses to identify genomic locations involved in phenotypes that mediate reproductive isolation. A second framework searches for genomic regions that show reduced rates of exchange across natural hybrid zones. It is often assumed that these approaches will point to the same loci, but this assumption is rarely tested. In this perspective, we discuss the factors that determine whether loci connected to postzygotic reproductive barriers in the laboratory are inferred to reduce gene flow in nature. We synthesize data on the genetics of postzygotic isolation in house mice, one of the most intensively studied systems in speciation genetics. In a rare empirical comparison, we measure the correspondence of loci tied to postzygotic barriers via genetic mapping in the laboratory and loci at which gene flow is inhibited across a natural hybrid zone. We find no evidence that the two sets of loci overlap beyond what is expected by chance. In light of these results, we recommend avenues for empirical and theoretical research to resolve the potential incongruence between the two predominant strategies for understanding the genetics of speciation.</p>
PI3Kg inhibition circumvents inflammation and mortality in SARS-CoV-2 and other infections
<p>Virulent infectious agents such as SARS-CoV-2 and Methicillin Resistant <em>Staphylococcus Aureus</em> (MRSA) induce tissue damage that recruits neutrophils and monocyte/macrophages that promote T cell exhaustion, fibrosis, vascular leak, epithelial cell depletion, and fatal organ damage. Neutrophils and macrophages recruited to pathogen infected lungs, including SARS-CoV-2 infected lungs, express phosphatidylinositol 3-kinase gamma (PI3Kg), a signaling protein that coordinately controls granulocyte and monocyte trafficking to diseased tissues and immune suppressive, pro-fibrotic transcription in myeloid cells. PI3Kg deletion and inhibition with the clinical PI3Kg inhibitor eganelisib promoted survival in models of infectious diseases, including SARS-CoV-2 and MRSA, by suppressing inflammation, vascular leak, organ damage and cytokine storm. These results demonstrate essential roles for PI3Kg in inflammatory lung disease and support the potential use of PI3Kg inhibitors to suppress inflammation in severe infectious diseases.</p>
Phenoxytacrine derivatives: Low-toxicity neuroprotectants exerting affinity to ifenprodil-binding site and cholinesterase inhibition
<p><a title="Learn more about Tacrine from ScienceDirect's AI-generated Topic Pages" href="https://www.sciencedirect.com/topics/chemistry/tacrine">Tacrine</a> (THA), a long withdrawn drug, is still a popular scaffold used in medicinal <a title="Learn more about chemistry from ScienceDirect's AI-generated Topic Pages" href="https://www.sciencedirect.com/topics/chemistry/chemistry">chemistry</a>, mainly for its good reactivity and multi-targeted effect. However, THA-associated hepatotoxicity is still an issue and must be considered in <a title="Learn more about drug discovery from ScienceDirect's AI-generated Topic Pages" href="https://www.sciencedirect.com/topics/pharmacology-toxicology-and-pharmaceutical-science/drug-discovery">drug discovery</a> based on the THA scaffold. Following our previously identified hit compound 7-phenoxytacrine (7-PhO-THA), we systematically explored the chemical space with 30 novel derivatives, with a focus on low hepatotoxicity, <a title="Learn more about anticholinesterase from ScienceDirect's AI-generated Topic Pages" href="https://www.sciencedirect.com/topics/pharmacology-toxicology-and-pharmaceutical-science/cholinesterase-inhibitor">anticholinesterase</a> action, and antagonism at the GluN1/GluN2B subtype of the <a title="Learn more about NMDA receptor from ScienceDirect's AI-generated Topic Pages" href="https://www.sciencedirect.com/topics/pharmacology-toxicology-and-pharmaceutical-science/n-methyl-dextro-aspartic-acid-receptor">NMDA receptor</a>. Applying the down-selection process based on <em>in vitro</em> and <em>in vivo</em> <a title="Learn more about pharmacokinetic from ScienceDirect's AI-generated Topic Pages" href="https://www.sciencedirect.com/topics/pharmacology-toxicology-and-pharmaceutical-science/pharmacokinetics">pharmacokinetic</a> data, two candidates, <strong>I-52</strong> and <strong>II-52,</strong> selective GluN1/GluN2B inhibitors thanks to the interaction with the ifenprodil-binding site, have entered <em>in vivo</em> <a title="Learn more about pharmacodynamic from ScienceDirect's AI-generated Topic Pages" href="https://www.sciencedirect.com/topics/biochemistry-genetics-and-molecular-biology/pharmacodynamics">pharmacodynamic</a> studies. Finally, compound <strong>I-52,</strong> showing only minor affinity to <a title="Learn more about AChE from ScienceDirect's AI-generated Topic Pages" href="https://www.sciencedirect.com/topics/pharmacology-toxicology-and-pharmaceutical-science/acetylcholinesterase">AChE</a>, was identified as a lead candidate with favorable behavioral and <a title="Learn more about neuroprotective from ScienceDirect's AI-generated Topic Pages" href="https://www.sciencedirect.com/topics/pharmacology-toxicology-and-pharmaceutical-science/neuroprotective-agent">neuroprotective</a> effects using open-field and <a title="Learn more about prepulse inhibition from ScienceDirect's AI-generated Topic Pages" href="https://www.sciencedirect.com/topics/biochemistry-genetics-and-molecular-biology/prepulse-inhibition">prepulse inhibition</a> tests, along with scopolamine-based behavioral and NMDA-induced hippocampal lesion models. Our data show that compound <strong>I-52</strong> exhibits low toxicity often associated with <a title="Learn more about NMDA receptor from ScienceDirect's AI-generated Topic Pages" href="https://www.sciencedirect.com/topics/biochemistry-genetics-and-molecular-biology/nmda-receptor">NMDA receptor</a> ligands, and low hepatotoxicity, often related to THA-based compounds.</p>
Spike-induced cytoarchitectonic changes in epileptic human cortex are reduced via MAP2K inhibition
<p>Interictal spikes are electroencephalographic discharges that occur at or near brain regions that produce epileptic seizures. While their role in generating seizures is not well understood, spikes have profound effects on cognition and behavior, depending on where and when they occur. We previously demonstrated that spiking areas of the human neocortex show sustained MAPK activation in superficial cortical layers I-III and are associated with microlesions in deeper cortical areas characterized by reduced neuronal nuclear protein (NeuN) staining and increased microglial infiltration. Based on these findings, we chose to investigate additional neuronal populations within microlesions, specifically inhibitory interneurons. Additionally, we hypothesized that spiking would be sufficient to induce similar cytoarchitectonic changes within the rat cortex and that inhibition of MAPK signaling, using a MAP2K inhibitor, would not only inhibit spike formation but also reduce these cytoarchitectonic changes and improve behavioral outcomes. To test these hypotheses, we analyzed tissue samples from 16 patients with intractable epilepsy who required cortical resections. We also utilized a tetanus toxin-induced animal model of interictal spiking, designed to produce spikes without seizures in male Sprague-Dawley rats. Rats were fitted with epidural electrodes, to permit EEG recording for the duration of the study, and automated algorithms were implemented to quantify spikes. After 6 months, animals were sacrificed to assess the effects of chronic spiking on cortical cytoarchitecture. Here, we show that microlesions may promote excitability due to a significant reduction of inhibitory neurons that could be responsible for promoting interictal spikes in superficial layers. Similarly, we found that the induction of epileptic spikes in the rat model produced analogous changes, including reduced NeuN, calbindin, and parvalbumin-positive neurons and increased microglia, suggesting that spikes are sufficient for inducing these cytoarchitectonic changes in humans. Finally, we implicated MAPK signaling as a driving force producing these pathological changes. Using CI-1040 to inhibit MAP2K, both acutely and after spikes developed, resulted in fewer interictal spikes, reduced microglial activation, and less inhibitory neuron loss. Treated animals had significantly fewer high-amplitude, short-duration spikes, which correlated with improved spatial memory performance on the Barnes maze. Together, our results provide evidence for a cytoarchitectonic pathogenesis underlying the epileptic cortex, which can be ameliorated through both early and delayed MAP2K inhibition. These findings highlight the potential role of CI-1040 as a pharmacological treatment that could prevent the development of epileptic activity and reduce cognitive impairment in both patients with epilepsy and those with non-epileptic spike-associated neurobehavioral disorders.</p>
Saxagliptin: a doping agent? Inhibition of NPY1-36 cleavage improves cycling performance
<p><strong>Introduction -</strong> Neuropeptides Y (NPYs) contribute to the adreno-sympathetic stimulation, NPY1-36 potentiates catecholamines (CATs) effects whilst NPY3-36 inhibits CATs’ release.</p> <p><strong>Objectives -</strong> Investigate whether inhibiting dipeptidyl-peptidase-4 (DPP4), the main enzyme cleaving NPY1-36 into NPY3-36 increases NPY1-36 potentiating effects and reduces NPY3-36 inhibiting effects on CATs; thereby leading to performance improvement.</p> <p><strong>Methods -</strong> Seven participants performed a time-to-exhaustion cycling exercise at 95% of peak power output under either placebo (pcb) or saxagliptin (gpt), a DPP4 inhibitor, <em>per os</em>. Oxygen consumption (V̇O<sub>2</sub>), heart rate variability, NPY1-36, NPY3-36, catecholamines and lactate were measured at several time points before, during, and after exercise.</p> <p><strong>Results -</strong> DPP4 activity (12.7 ± 1.6 vs. 0.2 ± 0.3 U/L) and NPY3-36 (1.94 ± 0.88 vs. 0.73 ± 0.22 pM) decreased at rest in gpt whilst NPY1-36 increased (2.64 ± 2.22 vs. 4.59 ± 2.98 pM) and CATs was unchanged. Time-to-exhaustion was 32% higher in gpt, and pcb-to-gpt increase in time-to-exhaustion was correlated to NPY1-36 changes (R=0.78, p<0.05). Peak V̇O<sub>2</sub> values were not different whilst there was a tendency for peak lactate to be higher and peak NPYs concentrations were higher in gpt. Exercise and post-exercise kinetics in all parameters were not different.</p> <p><strong>Discussion -</strong> DPP4 blockade increased NPY1-36 and decreased NPY3-36 concentrations which resulted in an increased potentiating effect on CATs and was likely responsible for performance improvement. Future studies need to determine the specific effects of NPYs and incretins on skeletal and myocardial muscles and establish whether DPP4 inhibitors could be a new class of doping agents.</p>
FSS7B - Inhibiting human aversive memory by transcranial theta-burst stimulation to primary sensory cortex: Supplementary fMRI data
<p>Functional magnetic resonance imaging (fMRI) data supplementing a publication on inhibiting somatosensory fear memory in humans with transcranial magnetic stimulation (TMS). Contains 1) individual regions-of-interest (ROIs) masks in the bilateral primary somatosensory cortex (S1) to target with TMS, 2) S1 masks for left and right hemisphere used in restricting the ROIs to a priori expected area, 3) sum and probability maps of the ROIs over participants, and 4) summary group level fMRI NIFTI images including beta images and T-maps. Individual SPMs/beta images can be requested from the authors for academic research purposes (k.ojala@uke.de). Details on the methods are found in the Supplement of the publication (see linked DOI). </p>
Fangxi-Xu/Succinate_Periodontitis: Targeting Succinate Receptor Effectively Inhibits Periodontitis
<p>Periodontal disease (PD) is one of the most common inflammatory diseases in humans and is initiated by an oral microbial dysbiosis that stimulates inflammation and bone loss. Here, we report an abnormal elevation of succinate in the subgingival plaque of subjects with severe PD. Succinate activates the succinate receptor-1 (SUCNR1) and stimulates inflammation. We detected SUCNR1 expression in the human and mouse periodontium and hypothesize that succinate activates SUCNR1 to accelerate periodontitis through the inflammatory response. Administration of exogenous succinate enhanced periodontal disease, whereas SUCNR1 knockout mice were protected from inflammation, oral dysbiosis, and subsequent periodontal bone loss in two different models of periodontitis. Therapeutic studies demonstrated that a novel SUCNR1 antagonist inhibited inflammatory events and osteoclastogenesis in vitro and reduced periodontal bone loss in vivo. Our study reveals a previously unknown action of succinate in promoting periodontitis and provides a novel topical treatment for this disease.</p> <p>Any microbiome data and r code used for downstream analysis in the manuscript were deposited to this repository.</p> <p><strong>Full Changelog</strong>: <a href="https://github.com/Fangxi-Xu/Succinate_Periodontitis/commits/microbiome">https://github.com/Fangxi-Xu/Succinate_Periodontitis/commits/microbiome</a></p>
The structural basis for the self-inhibition of DNA binding by apo-σ70 - smFRET raw data and analyses pipeline
<p>This dataset includes all raw data of nsALEX smFRET measurements of doubly-labeled sigma70 reported in Joron et al. ("The structural basis for the self-inhibition of DNA binding by apo-σ70"), as well as Jupyter Notebooks documenting the analysis pipeline that takes us from the raw data to dual channel burst search and filtered bursts, and to the analyses of within-burst dynamics in the system</p>
Sclerostin blockade inhibits bone resorption through PDGF receptor signaling in osteoblast lineage cells
<p>While sclerostin-neutralizing antibodies (Scl-Ab) transiently stimulate bone formation by activating Wnt signaling in osteoblast lineage cells, they exert sustained inhibition of bone resorption, suggesting an alternate signaling pathway by which Scl-Ab control osteoclast activity. Since sclerostin can activate platelet-derived growth factor receptors (PDGFRs) in osteoblast lineage cells in vitro and PDGFR signaling in these cells induces bone resorption through M-CSF secretion, we hypothesized that the prolonged anti-catabolic effect of Scl-Ab could result from PDGFR inhibition. We show here that inhibition of PDGFR signaling in osteoblast lineage cells is sufficient and necessary to mediate prolonged Scl-Ab effect on M-CSF secretion and osteoclast activity in mice. Indeed, sclerostin co-activates PDGFRs independently of Wnt/β-catenin signaling inhibition, by forming a ternary complex with LRP6 and PDGFRs in pre-osteoblasts. In turn, Scl-Ab prevents sclerostin-mediated co-activation of PDGFR signaling and consequent M-CSF up-regulation in pre-osteoblast cultures, thereby inhibiting osteoclast activity in pre-osteoblast/osteoclast co-culture assays. These results provide a new potential mechanism explaining the dissociation between anabolic and anti-resorptive effects of long-term Scl-Ab.</p>
Figure 6 in Blue and red light photoemitters as approach to inhibit Staphylococcus aureus and Pseudomonas aeruginosa growth
Figure 6. Percentage of growth inhibition induced by blue light on bacteria inoculated on saline solution or nutrient rich BHI broth. *Statistically significant difference using Mann-Whitney U test (p <0.05) between blue light exposed S. aureus in saline solution and BHI broth.
Figure 5 in Blue and red light photoemitters as approach to inhibit Staphylococcus aureus and Pseudomonas aeruginosa growth
Figure 5. Effect of blue and red light on S. aureus e P. aeruginosa diluted in BHI nutrient rich medium applied for a period of 3 hours. *Statistically significant difference using Mann-Whitney U test (p <0.05) between blue light exposed and control groups.
Figure 3 in Blue and red light photoemitters as approach to inhibit Staphylococcus aureus and Pseudomonas aeruginosa growth
Figure 3. Determination of the influence of glass or polystyrene plate on the antimicrobial effect of red or blue light in S. aureus and P. aeruginosa cultures. *Statistically significant difference using Mann-Whitney U test (p <0.05) between blue light exposed group and control groups.
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Allen Brain Atlas
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Annotated Behaviour and Observability Dataset (ABODe)
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