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814 results for “LPS”
Linked collectors and determiners for: Fungario (LPS Tipos) - División Micología "Instituto Spegazzini".
Natural history specimen data linked to collectors and determiners held within, "Fungario (LPS Tipos) - División Micología "Instituto Spegazzini"". Claims or attributions were made on Bionomia by volunteer Scribes, <a href="https://bionomia.net/dataset/6b84f3b4-5824-41fb-b8f8-b41a7494873a">https://bionomia.net/dataset/6b84f3b4-5824-41fb-b8f8-b41a7494873a</a> using specimen data from the dataset aggregated by the Global Biodiversity Information Facility, <a href="https://gbif.org/dataset/6b84f3b4-5824-41fb-b8f8-b41a7494873a">https://gbif.org/dataset/6b84f3b4-5824-41fb-b8f8-b41a7494873a</a>. Formatted as a Frictionless Data package.
Data from: A synthetic cationic antimicrobial peptide inhibits inflammatory response and the NLRP3 inflammasome by neutralizing LPS and ATP
Antimicrobial peptides (AMPs) are one of the most important defense mechanisms against bacterial infections in insects, plants, non-mammalian vertebrates, and mammals. In the present study, a class of synthetic AMPs was evaluated for anti-inflammatory activity. One cationic AMP, GW-A2, demonstrated the ability to inhibit the expression levels of nitric oxide (NO), inducible NO synthase (iNOS), cyclooxygenase-2 (COX-2), tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) in lipopolysaccharide (LPS)-activated macrophages. GW-A2 reduced LPS-induced increases in the phosphorylation of mitogen-activated protein kinase and protein kinase C-α/δ and the activation of NF-κB. GW-A2 also inhibited NLRP3 inflammasome activation induced by LPS and ATP. Furthermore, in the mice injected with LPS, GW-A2 reduced (1) the concentration of IL-1β, IL-6 and TNF-α in the serum; (2) the concentration of TNF-α in the peritoneal lavage; (3) the expression levels of iNOS, COX-2 and NLRP3 in the liver and lung; (4) the infiltration of polymorphonuclear neutrophils in the liver and lung. The underlying mechanisms for the anti-inflammatory activity of GW-A2 were found to be partially due to LPS and ATP neutralization. These results provide insights into how GW-A2 inhibits inflammation and the NLRP3 inflammasome and provide a foundation for the design of rational therapeutics for inflammation-related diseases.
Body size and circulating levels of different molecules from tree swallows (Tachycineta bicolor) exposed to different doses of lipopolysaccharide (LPS)
<p class="CxSpFirst">The purpose of mounting an immune response is to destroy pathogens, but this response comes at a physiological cost, including the generation of oxidative damage. However, many studies on the effects of immune challenges employ a single high dose, meaning that the consequences of more mild immune challenges are poorly resolved. We tested whether the degree of immunological challenge in tree swallows (<i>Tachycineta bicolor</i>) affects oxidative physiology and body mass, and whether these metrics correlate with parasitic nest mite load. We injected 14-day-old nestlings with either 0, 0.01, 0.1, or 1 mg lipopolysaccharide (LPS) per kg body mass, then collected a blood sample 24-h later to quantify multiple physiological metrics, including oxidative damage (i.e., d-ROMs), circulating amounts of triglyceride and glycerol, and levels of the acute phase protein haptoglobin. After fledging, we identified and counted parasitic nest mites (<i>Dermanyssus</i> spp. and <i>Ornithonyssus</i> spp.). We found that only nestlings injected with 1 mg LPS/kg body mass, which is a common dosage in ecoimmunological studies, lost more body mass than individuals from other treatment groups. However, every dose of LPS resulted in a commensurate increase in oxidative damage. Parasitic mite abundance had no effect on oxidative damage across treatments. Amount of oxidative damage correlated with haptoglobin levels, suggesting compensatory mechanisms to limit self-damage during an immune response. We conclude that while only the highest-intensity immune challenges resulted in costs related to body mass, even low-intensity immune challenges result in detectable increases of oxidative damage.</p>
Fig. 6 in Ochrathinols A and B, two pairs of sulfur-containing racemates from an Antarctic fungus Aspergillus ochraceopetaliformis SCSIO 05702 inhibit LPS-induced pro-inflammatory cytokines and NO production
Fig. 6. Chiral HPLC analyses of ochrathinol B (±)-2.
Fig. 4 in Ochrathinols A and B, two pairs of sulfur-containing racemates from an Antarctic fungus Aspergillus ochraceopetaliformis SCSIO 05702 inhibit LPS-induced pro-inflammatory cytokines and NO production
Fig. 4. Experimental and calculated ECD spectra of (±)-1, (±)-2, and 4.
Fig. 3. X in Ochrathinols A and B, two pairs of sulfur-containing racemates from an Antarctic fungus Aspergillus ochraceopetaliformis SCSIO 05702 inhibit LPS-induced pro-inflammatory cytokines and NO production
Fig. 3. X-ray crystallographic structures of compounds 1–3.
Fig. 2 in Ochrathinols A and B, two pairs of sulfur-containing racemates from an Antarctic fungus Aspergillus ochraceopetaliformis SCSIO 05702 inhibit LPS-induced pro-inflammatory cytokines and NO production
Fig. 2. Key COSY (bold) and HMBC (arrows) correlations of 1 4.
Fig. 5 in Ochrathinols A and B, two pairs of sulfur-containing racemates from an Antarctic fungus Aspergillus ochraceopetaliformis SCSIO 05702 inhibit LPS-induced pro-inflammatory cytokines and NO production
Fig. 5. Chiral HPLC analyses of ochrathinol A (±)-1.
Fig. 1 in Ochrathinols A and B, two pairs of sulfur-containing racemates from an Antarctic fungus Aspergillus ochraceopetaliformis SCSIO 05702 inhibit LPS-induced pro-inflammatory cytokines and NO production
Fig. 1. Structures of compounds 1–4.
Fig. 2. Key 2D NMR correlations for 1–6 in Undescribed ecdysteroids and phenolic glycosides from the roots of Cyathula officinalis Kuan and their anti-inflammatory activity in LPS-induced RAW 264.7 macrophages in vitro
Fig. 2. Key 2D NMR correlations for 1–6.
Fig. 1 in Undescribed ecdysteroids and phenolic glycosides from the roots of Cyathula officinalis Kuan and their anti-inflammatory activity in LPS-induced RAW 264.7 macrophages in vitro
Fig. 1. Chemical structures of 1–6.
Fig. 5 in Chlorine-containing guaianolide sesquiterpenoids from Achillea millefolium L. with inhibitory effects against LPS-induced NO release in BV-2 microglial cells
Fig. 5. ORTEP diagrams of compounds 1, 4, 6 and 8.
Fig. 3. Key 1 H– 1 H in Chlorine-containing guaianolide sesquiterpenoids from Achillea millefolium L. with inhibitory effects against LPS-induced NO release in BV-2 microglial cells
Fig. 3. Key 1 H– 1 H COSY, HMBC, and NOESY correlations of compound 6.
Fig. 1 in Chlorine-containing guaianolide sesquiterpenoids from Achillea millefolium L. with inhibitory effects against LPS-induced NO release in BV-2 microglial cells
Fig. 1. Structures of Millefolactons B1–B9 (1–9) isolated from A. millefolium L.
Fig. 4 in Chlorine-containing guaianolide sesquiterpenoids from Achillea millefolium L. with inhibitory effects against LPS-induced NO release in BV-2 microglial cells
Fig. 4. Experimental ECD spectra of compounds 1–9.
Fig. 2. Key 1H–1H in Chlorine-containing guaianolide sesquiterpenoids from Achillea millefolium L. with inhibitory effects against LPS-induced NO release in BV-2 microglial cells
Fig. 2. Key 1H–1H COSY, HMBC, and NOESY correlations of compound 1.
Fig. 5 in Lanostane-type triterpenoids from Ganoderma applanatum and their inhibitory activities on NO production in LPS-induced BV-2 cells
Fig. 5. Putative biosynthetic pathway of 1 and 2.
Fig. 2. Key 1H–1H in Lanostane-type triterpenoids from Ganoderma applanatum and their inhibitory activities on NO production in LPS-induced BV-2 cells
Fig. 2. Key 1H–1H COSY, HMBC, and NOESY correlations of 1.
Fig. 1 in Lanostane-type triterpenoids from Ganoderma applanatum and their inhibitory activities on NO production in LPS-induced BV-2 cells
Fig. 1. Structures of the compounds from G. applanatum.
Prospective Multicenter Post Approval Study of the LPS-Flex Mobile Bearing Knee
ClinicalTrials.gov study NCT00854295. IPD Sharing: Not stated. Countries: 1. Publications: 0.
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