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1
Linden, Jennifer, Kiel Telesford, Samantha Shetty, Paige Winokour, Sylvia Haigh, Ellen Cahir-McFarland, Giovanna Antognetti, et al. "A Novel Panel of Rabbit Monoclonal Antibodies and Their Diverse Applications Including Inhibition of Clostridium perfringens Epsilon Toxin Oligomerization." Antibodies 7, no. 4 (October 25, 2018): 37. http://dx.doi.org/10.3390/antib7040037.
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The pore-forming epsilon toxin (ETX) produced by Clostridium perfringens is among the most lethal bacterial toxins known. Sensitive antibody-based reagents are needed to detect toxin, distinguish mechanisms of cell death, and prevent ETX toxicity. Using B-cell immuno-panning and cloning techniques, seven ETX-specific monoclonal antibodies were generated from immunized rabbits. ETX specificity and sensitivity were evaluated via western blot, ELISA, immunocytochemistry (ICC), and flow cytometry. ETX-neutralizing function was evaluated both in vitro and in vivo. All antibodies recognized both purified ETX and epsilon protoxin via western blot with two capable of detecting the ETX-oligomer complex. Four antibodies detected ETX via ELISA and three detected ETX bound to cells via ICC or flow cytometry. Several antibodies prevented ETX-induced cell death by either preventing ETX binding or by blocking ETX oligomerization. Antibodies that blocked ETX oligomerization inhibited ETX endocytosis and cellular vacuolation. Importantly, one of the oligomerization-blocking antibodies was able to protect against ETX-induced death post-ETX exposure in vitro and in vivo. Here we describe the production of a panel of rabbit monoclonal anti-ETX antibodies and their use in various biological assays. Antibodies possessing differential specificity to ETX in particular conformations will aid in the mechanistic studies of ETX cytotoxicity, while those with ETX-neutralizing function may be useful in preventing ETX-mediated mortality.
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Li, Jihong, John C. Freedman, and Bruce A. McClane. "NanI Sialidase, CcpA, and CodY Work Together To Regulate Epsilon Toxin Production by Clostridium perfringens Type D Strain CN3718." Journal of Bacteriology 197, no. 20 (August 10, 2015): 3339–53. http://dx.doi.org/10.1128/jb.00349-15.
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ABSTRACTClostridium perfringenstype D strains are usually associated with diseases of livestock, and their virulence requires the production of epsilon toxin (ETX). We previously showed (J. Li, S. Sayeed, S. Robertson, J. Chen, and B. A. McClane, PLoS Pathog 7:e1002429, 2011,http://dx.doi.org/10.1371/journal.ppat.1002429) that BMC202, ananInull mutant of type D strain CN3718, produces less ETX than wild-type CN3718 does. The current study proved that the lower ETX production by strain BMC202 is due tonanIgene disruption, since both genetic and physical (NanI or sialic acid) complementation increased ETX production by BMC202. Furthermore, a sialidase inhibitor that interfered with NanI activity also reduced ETX production by wild-type CN3718. The NanI effect on ETX production was shown to involve reductions incodYandccpAgene transcription levels in BMC202 versus wild-type CN3718. Similar to CodY, CcpA was found to positively control ETX production. A doublecodYccpAnull mutant produced even less ETX than acodYorccpAsingle null mutant. CcpA bound directly to sequences upstream of theetxorcodYstart codon, and bioinformatics identified putative CcpA-bindingcresites immediately upstream of both thecodYandetxstart codons, suggesting possible direct CcpA regulatory effects. AccpAmutation also decreasedcodYtranscription, suggesting that CcpA effects on ETX production can be both direct and indirect, including effects oncodYtranscription. Collectively, these results suggest that NanI, CcpA, and CodY work together to regulate ETX production, with NanI-generated sialic acid from the intestines possibly signaling type D strains to upregulate their ETX production and induce disease.IMPORTANCEClostridium perfringensNanI was previously shown to increase ETX binding to, and cytotoxicity for, MDCK host cells. The current study demonstrates that NanI also regulates ETX production via increased transcription of genes encoding the CodY and CcpA global regulators. Results obtained using singleccpAorcodYnull mutants and accpAcodYdouble null mutant showed thatcodYandccpAregulate ETX production independently of one another but thatccpAalso affectscodYtranscription. Electrophoretic mobility shift assays and bioinformatic analyses suggest that both CodY and CcpA may directly regulateetxtranscription. Collectively, results of this study suggest that sialic acid generated by NanI from intestinal sources signals ETX-producingC. perfringensstrains, via CcpA and CodY, to upregulate ETX production and cause disease.
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Marshall, Skye, Beth McGill, Helen Morcrette, C. Peter Winlove, Catalin Chimerel, Peter G. Petrov, and Monika Bokori-Brown. "Interaction of Clostridium perfringens Epsilon Toxin with the Plasma Membrane: The Role of Amino Acids Y42, Y43 and H162." Toxins 14, no. 11 (November 3, 2022): 757. http://dx.doi.org/10.3390/toxins14110757.
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Clostridium perfringens epsilon toxin (Etx) is a pore forming toxin that causes enterotoxaemia in ruminants and may be a cause of multiple sclerosis in humans. To date, most in vitro studies of Etx have used the Madin-Darby canine kidney (MDCK) cell line. However, studies using Chinese hamster ovary (CHO) cells engineered to express the putative Etx receptor, myelin and lymphocyte protein (MAL), suggest that amino acids important for Etx activity differ between species. In this study, we investigated the role of amino acids Y42, Y43 and H162, previously identified as important in Etx activity towards MDCK cells, in Etx activity towards CHO-human MAL (CHO-hMAL) cells, human red blood cells (hRBCs) and synthetic bilayers using site-directed mutants of Etx. We show that in CHO-hMAL cells Y42 is critical for Etx binding and not Y43 as in MDCK cells, indicating that surface exposed tyrosine residues in the receptor binding domain of Etx impact efficiency of cell binding to MAL-expressing cells in a species-specific manner. We also show that Etx mutant H162A was unable to lyse CHO-hMAL cells, lysed hRBCs, whilst it was able to form pores in synthetic bilayers, providing evidence of the complexity of Etx pore formation in different lipid environments.
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Bossu, Jean Louis, Laetitia Wioland, Frédéric Doussau, Philippe Isope, Michel R. Popoff, and Bernard Poulain. "Epsilon Toxin from Clostridium perfringens Causes Inhibition of Potassium inward Rectifier (Kir) Channels in Oligodendrocytes." Toxins 12, no. 1 (January 6, 2020): 36. http://dx.doi.org/10.3390/toxins12010036.
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Epsilon toxin (ETX), produced by Clostridium perfringens types B and D, causes serious neurological disorders in animals. ETX can bind to the white matter of the brain and the oligodendrocytes, which are the cells forming the myelin sheath around neuron axons in the white matter of the central nervous system. After binding to oligodendrocytes, ETX causes demyelination in rat cerebellar slices. We further investigated the effects of ETX on cerebellar oligodendrocytes and found that ETX induced small transmembrane depolarization (by ~ +6.4 mV) in rat oligodendrocytes primary cultures. This was due to partial inhibition of the transmembrane inward rectifier potassium current (Kir). Of the two distinct types of Kir channel conductances (~25 pS and ~8.5 pS) recorded in rat oligodendrocytes, we found that ETX inhibited the large-conductance one. This inhibition did not require direct binding of ETX to a Kir channel. Most likely, the binding of ETX to its membrane receptor activates intracellular pathways that block the large conductance Kir channel activity in oligodendrocyte. Altogether, these findings and previous observations pinpoint oligodendrocytes as a major target for ETX. This supports the proposal that ETX might be a cause for Multiple Sclerosis, a disease characterized by myelin damage.
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Mandell, Erica, Kyle N. Powers, Julie W. Harral, Gregory J. Seedorf, Kendall S. Hunter, Steven H. Abman, and R. Blair Dodson. "Intrauterine endotoxin-induced impairs pulmonary vascular function and right ventricular performance in infant rats and improvement with early vitamin D therapy." American Journal of Physiology-Lung Cellular and Molecular Physiology 309, no. 12 (December 15, 2015): L1438—L1446. http://dx.doi.org/10.1152/ajplung.00302.2015.
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High pulmonary vascular resistance (PVR), proximal pulmonary artery (PA) impedance, and right ventricular (RV) afterload due to remodeling contribute to the pathogenesis and severity of pulmonary hypertension (PH). Intra-amniotic exposure to endotoxin (ETX) causes sustained PH and high mortality in rat pups at birth, which are associated with impaired vascular growth and RV hypertrophy in survivors. Treatment of ETX-exposed pups with antenatal vitamin D (vit D) improves survival and lung growth, but the effects of ETX exposure on RV-PA coupling in the neonatal lung are unknown. We hypothesized that intrauterine ETX impairs RV-PA coupling through sustained abnormalities of PA stiffening and RV performance that are attenuated with vit D therapy. Fetal rats were exposed to intra-amniotic injections of ETX, ETX+vit D, or saline at 20 days gestation (term = 22 days). At postnatal day 14, pups had pressure-volume measurements of the RV and isolated proximal PA, respectively. Lung homogenates were assayed for extracellular matrix (ECM) composition by Western blot. We found that ETX lungs contain decreased α-elastin, lysyl oxidase, collagen I, and collagen III proteins ( P < 0.05) compared control and ETX+vit D lungs. ETX-exposed animals have increased RV mechanical stroke work ( P < 0.05 vs. control and ETX+vit D) and elastic potential energy ( P < 0.05 vs. control and ETX+vit D). Mechanical stiffness and ECM remodeling are increased in the PA ( P < 0.05 vs. control and ETX+vit D). We conclude that intrauterine exposure of fetal rats to ETX during late gestation causes persistent impairment of RV-PA coupling throughout infancy that can be prevented with early vit D treatment.
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Miyamoto, Kazuaki, Jihong Li, Sameera Sayeed, Shigeru Akimoto, and Bruce A. McClane. "Sequencing and Diversity Analyses Reveal Extensive Similarities between Some Epsilon-Toxin-Encoding Plasmids and the pCPF5603 Clostridium perfringens Enterotoxin Plasmid." Journal of Bacteriology 190, no. 21 (September 5, 2008): 7178–88. http://dx.doi.org/10.1128/jb.00939-08.
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ABSTRACT Clostridium perfringens type B and D isolates produce epsilon-toxin, the third most potent clostridial toxin. The epsilon-toxin gene (etx) is plasmid borne in type D isolates, but etx genetics have been poorly studied in type B isolates. This study reports the first sequencing of any etx plasmid, i.e., pCP8533etx, from type B strain NCTC8533. This etx plasmid is 64.7 kb, carries tcp conjugative transfer genes, and encodes additional potential virulence factors including beta2-toxin, sortase, and collagen adhesin but not beta-toxin. Interestingly, nearly 80% of pCP8533etx open reading frames (ORFs) are also present on pCPF5603, an enterotoxin-encoding plasmid from type A isolate F5603. Pulsed-field gel electrophoresis and overlapping PCR indicated that a pCP8533etx-like etx plasmid is also present in most, if not all, other type B isolates and some beta2-toxin-positive, cpe-negative type D isolates, while other type D isolates carry different etx plasmids. Sequences upstream of the etx gene vary between type B isolates and some type D isolates that do not carry a pCP8533etx-like etx plasmid. However, nearly all type B and D isolates have an etx locus with an upstream IS1151, and those etx loci typically reside near a dcm ORF. These results suggest that pCPF5603 and pCP8533etx evolved from insertion of mobile genetic elements carrying enterotoxin or etx genes, respectively, onto a common progenitor plasmid.
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Dorca-Arévalo, Jonatan, Inmaculada Gómez de Aranda, and Juan Blasi. "New Mutants of Epsilon Toxin from Clostridium perfringens with an Altered Receptor-Binding Site and Cell-Type Specificity." Toxins 14, no. 4 (April 16, 2022): 288. http://dx.doi.org/10.3390/toxins14040288.
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Epsilon toxin (Etx) from Clostridium perfringens is the third most potent toxin after the botulinum and tetanus toxins. Etx is the main agent of enterotoxemia in ruminants and is produced by Clostridium perfringens toxinotypes B and D, causing great economic losses. Etx selectively binds to target cells, oligomerizes and inserts into the plasma membrane, and forms pores. A series of mutants have been previously generated to understand the cellular and molecular mechanisms of the toxin and to obtain valid molecular tools for effective vaccination protocols. Here, two new non-toxic Etx mutants were generated by selective deletions in the binding (Etx-ΔS188-F196) or insertion (Etx-ΔV108-F135) domains of the toxin. As expected, our results showed that Etx-ΔS188-F196 did not exhibit the usual Etx binding pattern but surprisingly recognized specifically an O-glycoprotein present in the proximal tubules of the kidneys in a wide range of animals, including ruminants. Although diminished, Etx-ΔV108-F135 maintained the capacity for binding and even oligomerization, indicating that the mutation particularly affected the pore-forming ability of the toxin.
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Tang, Jen-Ruey, Gregory J. Seedorf, Vincent Muehlethaler, Deandra L. Walker, Neil E. Markham, Vivek Balasubramaniam, and Steven H. Abman. "Moderate postnatal hyperoxia accelerates lung growth and attenuates pulmonary hypertension in infant rats after exposure to intra-amniotic endotoxin." American Journal of Physiology-Lung Cellular and Molecular Physiology 299, no. 6 (December 2010): L735—L748. http://dx.doi.org/10.1152/ajplung.00153.2010.
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To determine the separate and interactive effects of fetal inflammation and neonatal hyperoxia on the developing lung, we hypothesized that: 1) antenatal endotoxin (ETX) causes sustained abnormalities of infant lung structure; and 2) postnatal hyperoxia augments the adverse effects of antenatal ETX on infant lung growth. Escherichia coli ETX or saline (SA) was injected into amniotic sacs in pregnant Sprague-Dawley rats at 20 days of gestation. Pups were delivered 2 days later and raised in room air (RA) or moderate hyperoxia (O2, 80% O2 at Denver's altitude, ∼65% O2 at sea level) from birth through 14 days of age. Heart and lung tissues were harvested for measurements. Intra-amniotic ETX caused right ventricular hypertrophy (RVH) and decreased lung vascular endothelial growth factor (VEGF) and VEGF receptor-2 (VEGFR-2) protein contents at birth. In ETX-exposed rats (ETX-RA), alveolarization and vessel density were decreased, pulmonary vascular wall thickness percentage was increased, and RVH was persistent throughout the study period compared with controls (SA-RA). After antenatal ETX, moderate hyperoxia increased lung VEGF and VEGFR-2 protein contents in ETX-O2 rats and improved their alveolar and vascular structure and RVH compared with ETX-RA rats. In contrast, severe hyperoxia (≥95% O2 at Denver's altitude) further reduced lung vessel density after intra-amniotic ETX exposure. We conclude that intra-amniotic ETX induces fetal pulmonary hypertension and causes persistent abnormalities of lung structure with sustained pulmonary hypertension in infant rats. Moreover, moderate postnatal hyperoxia after antenatal ETX restores lung growth and prevents pulmonary hypertension during infancy.
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Schuster, Daniel P., James K. Kozlowski, Tim McCarthy, Jason Morrow, and Alan Stephenson. "Effect of endotoxin on oleic acid lung injury does not depend on priming." Journal of Applied Physiology 91, no. 5 (November 1, 2001): 2047–54. http://dx.doi.org/10.1152/jappl.2001.91.5.2047.
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Recent studies have demonstrated significant synergistic physiological and biochemical effects between low-dose endotoxin (Etx) administration and oleic acid (OA)-induced canine lung injury. To evaluate whether this interaction depends on Etx priming of some key cell population, we compared the effects of giving low-dose Etx both after as well as before inducing lung injury with OA. In addition to hemodynamic and blood-gas measurements, positron emission tomographic imaging was used to measure edema accumulation and intrapulmonary blood flow distribution. Biochemical measurements of the stable metabolites of prostacyclin and thromboxane were obtained as well as measurements of isoprostanes and reactive sulfhydryls as evidence for possible concomitant oxidant production. We found that the physiological and biochemical effects of low-dose Etx developed 30–45 min after its administration, regardless of whether Etx was administered before or after OA. No increase in either isoprostane or reactive sulfhydryl production after Etx and/or OA was detected. These data suggest that the synergistic effect of low-dose Etx and OA-induced lung injury is not due to a priming effect of Etx.
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Purnomo, A., Widyawan, W. Najib, R. Hartono, and Hartatik. "Performance Comparison of Modified AODV-ETX with AODV and AODV-ETX Routing Protocol in an MANET." IOP Conference Series: Materials Science and Engineering 578 (October 4, 2019): 012082. http://dx.doi.org/10.1088/1757-899x/578/1/012082.
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Fernandez Miyakawa, Mariano E., Osvaldo Zabal, and Claudia Silberstein. "Clostridium perfringens epsilon toxin is cytotoxic for human renal tubular epithelial cells." Human & Experimental Toxicology 30, no. 4 (May 20, 2010): 275–82. http://dx.doi.org/10.1177/0960327110371700.
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Clostridium perfringens epsilon toxin (ETX) is responsible for a fatal enterotoxemia in different animal species, producing extensive renal damage, neurological disturbance and edema of lungs, heart and kidneys. However, there is no information about the susceptibility of humans to ETX. Here, we report that primary cultures of human renal tubular epithelial cells (HRTEC) exposed to ETX showed a marked swelling with subsequent large blebs surrounding most cells. The incubation of HRTEC with ETX produced a reduction of cell viability in a dose- and time-dependent manner. The CD50 after 1-hour and 24-hour incubation were 3 µg/mL and 0.5 µg/mL, respectively. The pulse with ETX for 3 min was enough to produce a significant cytotoxic effect on HRTEC after 1-hour incubation. ETX binds to HRTEC forming a large complex of about 160 kDa similar to what was found in the Madin-Darby canine kidney (MDCK) cell line. The HRTEC could be a useful cell model to improve the understanding of the mechanisms involved on the cell damage mediated by ETX.
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Mandell, Erica, Gregory Seedorf, Jason Gien, and Steven H. Abman. "Vitamin D treatment improves survival and infant lung structure after intra-amniotic endotoxin exposure in rats: potential role for the prevention of bronchopulmonary dysplasia." American Journal of Physiology-Lung Cellular and Molecular Physiology 306, no. 5 (March 1, 2014): L420—L428. http://dx.doi.org/10.1152/ajplung.00344.2013.
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Vitamin D (vit D) has anti-inflammatory properties and modulates lung growth, but whether vit D can prevent lung injury after exposure to antenatal inflammation is unknown. We hypothesized that early and sustained vit D treatment could improve survival and preserve lung growth in an experimental model of bronchopulmonary dysplasia induced by antenatal exposure to endotoxin (ETX). Fetal rats (E20) were exposed to ETX (10 μg), ETX + Vit D (1 ng/ml), or saline (control) via intra-amniotic (IA) injections and delivered 2 days later. Newborn pups exposed to IA ETX received daily intraperitoneal injections of vit D (1 ng/g) or saline for 14 days. Vit D treatment improved oxygen saturations (78 vs. 87%; P < 0.001) and postnatal survival (84% vs. 57%; P < 0.001) after exposure to IA ETX compared with IA ETX alone. Postnatal vit D treatment improved alveolar and vascular growth at 14 days by 45% and 25%, respectively ( P < 0.05). Vit D increased fetal sheep pulmonary artery endothelial cell (PAEC) growth and tube formation by 64% and 44%, respectively ( P < 0.001), and prevented ETX-induced reductions of PAEC growth and tube formation. Vit D directly increased fetal alveolar type II cell (ATIIC) growth by 26% ( P < 0.001) and enhanced ATIIC growth in the presence of ETX-induced growth suppression by 73% ( P < 0.001). We conclude that antenatal vit D therapy improved oxygenation and survival in newborn rat pups and enhanced late lung structure after exposure to IA ETX in vivo, which may partly be due to direct effects on vascular and alveolar growth.
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Pulido, Edward J., Brian D. Shames, Craig H. Selzman, Hazel A. Barton, Anirban Banerjee, Denis D. Bensard, and Robert C. McIntyre. "Inhibition of PARS attenuates endotoxin-induced dysfunction of pulmonary vasorelaxation." American Journal of Physiology-Lung Cellular and Molecular Physiology 277, no. 4 (October 1, 1999): L769—L776. http://dx.doi.org/10.1152/ajplung.1999.277.4.l769.
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Endotoxin (Etx) causes excessive activation of the nuclear repair enzyme poly(ADP-ribose) synthase (PARS), which depletes cellular energy stores and leads to vascular dysfunction. We hypothesized that PARS inhibition would attenuate injury to mechanisms of pulmonary vasorelaxation in acute lung injury. The purpose of this study was to determine the effect of in vivo PARS inhibition on Etx-induced dysfunction of pulmonary vasorelaxation. Rats received intraperitoneal saline or Etx ( Salmonella typhimurium; 20 mg/kg) and one of the PARS inhibitors, 3-aminobenzamide (3-AB; 10 mg/kg) or nicotinamide (Nic; 200 mg/kg), 90 min later. After 6 h, concentration-response curves were determined in isolated pulmonary arterial rings. Etx impaired endothelium-dependent (response to ACh and calcium ionophore) and -independent (sodium nitroprusside) cGMP-mediated vasorelaxation. 3-AB and Nic attenuated Etx-induced impairment of endothelium-dependent and -independent pulmonary vasorelaxation. 3-AB and Nic had no effect on Etx-induced increases in lung myeloperoxidase activity and edema. Lung ATP decreased after Etx but was maintained by 3-AB and Nic. Pulmonary arterial PARS activity increased fivefold after Etx, which 3-AB and Nic prevented. The beneficial effects were not observed with benzoic acid, a structural analog of 3-AB that does not inhibit PARS. Our results suggest that PARS inhibition with 3-AB or Nic improves pulmonary vasorelaxation and preserves lung ATP levels in acute lung injury.
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Siddesh, G. K., C. P. Mallikarjuna Gowda, H. R. Shashidhara, K. Sathish Shet, K. Shashi Raj, V. Arunarashmi, S. Chaithanya, B. N. Latha, and Dawit Mamiru Teressa. "Optimization in the Ad Hoc On-Demand Distance Vector Routing Protocol." Wireless Communications and Mobile Computing 2022 (July 26, 2022): 1–11. http://dx.doi.org/10.1155/2022/7322291.
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The main challenge of the MANET network is the continuous management of information, each device, to ensure the correct direction of traffic. MANET consists of a peer-to-peer connection; the network is self-repairing and at the same time self-formed. The network can be used in the field of road safety, in sensors in the home, healthcare, robotics, etc. The aim of this work was to study the MANET network and its protocols and especially the AODV protocol, the choice of peer in the AODV protocol, and the subsequent improvement of this mechanism. The work deals with ETX metrics and its subsequent implementation in the AODV protocol. The work includes simulations of the AODV protocol and subsequently also simulations of the AODV-ETX protocol. The implementation of the proposed result simulation takes place in Network Simulator 3 tool. The work contains a comparison of the AODV and AODV-ETX protocols. The simulation results are shown in tables and plotted. The AODV-ETX has better properties compared to the AODV protocol, but with a larger number of nodes over 20, these properties approach the AODV protocol. The packet loss, packet delay, and permeability are considered for performance evaluations.
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Zhou, Zhaohui, James Kozlowski, Andrea L. Goodrich, Nathaniel Markman, Delphine L. Chen, and Daniel P. Schuster. "Molecular imaging of lung glucose uptake after endotoxin in mice." American Journal of Physiology-Lung Cellular and Molecular Physiology 289, no. 5 (November 2005): L760—L768. http://dx.doi.org/10.1152/ajplung.00146.2005.
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Positron emission tomographic imaging after administration of the glucose analog fluorine-18 fluorodeoxyglucose ([18F]FDG) may be useful to study neutrophilic inflammation of the lungs. In this study, we sought to determine the specificity of the increase in lung [18F]FDG uptake after intraperitoneal endotoxin (Etx) for neutrophil influx into mouse lungs and to determine the regulation of glucose uptake after Etx by Toll-like receptors (TLRs) and TNF-α. Lung tissue radioactivity measurements by imaging were validated against counts in a gamma well counter. Glucose uptake was quantified as the [18F]FDG tissue-to-blood radioactivity ratio (TBR) after validating this measure against the “gold standard” measure of glucose uptake, the “net influx rate constant.” TBR measurements were made in a control group (no intervention), a group administered Etx, and a group administered Etx plus an additional agent (e.g., vinblastine) or Etx administered to a mutant mouse strain. The glucose uptake measurements were compared with measurements of myeloperoxidase. Increases in TBR after Etx were significantly but not completely eliminated by neutrophil depletion with vinblastine. Increases in TBR after Etx were consistent with signaling via either TLR-4 or TLR-2 (the latter probably secondary to peptidoglycan contaminants in Etx preparation) and were decreased by drug inhibition of TLR-4 but not by inhibition of TNF-α. Thus molecular imaging can be used to noninvasively monitor biological effects of Etx on lungs in mice, and changes in lung glucose uptake can be used to monitor effects of anti-inflammatory agents. Such imaging capacity provides a powerful new paradigm for translational “mouse-to-human” pulmonary research.
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Mandell, Erica, Gregory J. Seedorf, Sharon Ryan, Jason Gien, Scott D. Cramer, and Steven H. Abman. "Antenatal endotoxin disrupts lung vitamin D receptor and 25-hydroxyvitamin D 1α-hydroxylase expression in the developing rat." American Journal of Physiology-Lung Cellular and Molecular Physiology 309, no. 9 (November 1, 2015): L1018—L1026. http://dx.doi.org/10.1152/ajplung.00253.2015.
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Vitamin D [vit D; 1,25-(OH)2D] treatment improves survival and lung alveolar and vascular growth in an experimental model of bronchopulmonary dysplasia (BPD) after antenatal exposure to endotoxin (ETX). However, little is known about lung-specific 1,25-(OH)2D3 regulation during development, especially regarding maturational changes in lung-specific expression of the vitamin D receptor (VDR), 1α-hydroxylase (1α-OHase), and CYP24A1 during late gestation and the effects of antenatal ETX exposure on 1,25-(OH)2D3 metabolism in the lung. We hypothesized that vit D regulatory proteins undergo maturation regulation in the late fetal and early neonatal lung and that prenatal exposure to ETX impairs lung growth partly through abnormal endogenous vit D metabolism. Normal fetal rat lungs were harvested between embryonic day 15 and postnatal day 14. Lung homogenates were assayed for VDR, 1α-OHase, and CYP24A1 protein contents by Western blot analysis. Fetal rats were injected on embryonic day 20 with intra-amniotic ETX, ETX + 1,25-(OH)2D3, or saline and delivered 2 days later. Pulmonary artery endothelial cells (PAECs) from fetal sheep were assessed for VDR, 1α-OHase, and CYP24A1 expression after treatment with 25-(OH)D3, 1,25-(OH)2D3, ETX, ETX + 25-(OH)D3, or ETX + 1,25-(OH)2D3. We found that lung VDR, 1α-OHase, and CYP2741 protein expression dramatically increase immediately before birth ( P < 0.01 vs. early fetal values). Antenatal ETX increases CYP24A1 expression ( P < 0.05) and decreases VDR and 1α-OHase expression at birth ( P < 0.001), but these changes are prevented with concurrent vit D treatment ( P < 0.001). ETX-induced reduction of fetal PAEC growth and tube formation and lung 1α-OHase expression are prevented by vit D treatment ( P < 0.001). We conclude that lung VDR, 1α-OHase, and CYP24A1 protein content markedly increase before birth and that antenatal ETX disrupts lung vit D metabolism through downregulation of VDR and increased vit D catabolic enzyme expression, including changes in developing endothelium. We speculate that endogenous vitamin D metabolism modulates normal fetal lung development and that prenatal disruption of vit D signaling may contribute to impaired postnatal lung growth at least partly through altered angiogenic signaling.
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Suffredini, Dante A., Yan Li, Wanying Xu, Mahtab Moayeri, Stephen Leppla, Yvonne Fitz, Xizhong Cui, and Peter Q. Eichacker. "Shock and lethality with anthrax edema toxin in rats are associated with reduced arterial responsiveness to phenylephrine and are reversed with adefovir." American Journal of Physiology-Heart and Circulatory Physiology 313, no. 5 (November 1, 2017): H946—H958. http://dx.doi.org/10.1152/ajpheart.00285.2017.
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Although edema toxin (ETx) and lethal toxin (LTx) contribute to Bacillus anthracis shock and lethality, the mechanisms underlying their cardiovascular effects are unclear. We have previously shown that ETx but not LTx inhibited phenylephrine-stimulated contraction of aortic rings prepared from healthy rats and that adefovir, a selective inhibitor of ETx cAMP production, blocked this effect. Here, we examined arterial function in rats that received 24-h ETx or LTx infusions. Compared with control rats, ETx reduced mean arterial pressure (MAP) and survival over 48 h ( P ≤ 0.0003) and increased plasma cAMP at 4, 24, and 48 h ( P < 0.0001) and nitric oxide (NO) at 24 and 48 h ( P ≤ 0.01). Compared with control animals, at 24- and 48-h phenylephrine stimulation of aortic rings from ETx animals produced decreased maximal contractile force (MCF; P = 0.05 and 0.006) and in vivo phenylephrine infusion in ETx animals produced decreased proportional increases in MAP ( P < 0.0001 and P = 0.05). In ETx-treated animals, compared with placebo-treated animals, adefovir treatment prevented all lethality ( P = 0.01), increased MAP ( P ≤ 0.0001), decreased plasma and aortic tissue cAMP at 24 and 48 h, respectively ( P ≤ 0.03), and plasma NO at both times ( P ≤ 0.004), and increased phenylephrine-stimulated increases in MCF in aortic rings and MAP in vivo at 48 h ( P = 0.02). LTx decreased MAP and survival also, but it did not alter the response to phenylephrine of MCF in aortic rings prepared from LTx animals or of MAP in vivo. In conclusion, in rats, hypotension and lethality are associated with reduced arterial contractile function with ETx but not LTx and adefovir improves ETx-induced hypotension and lethality. NEW & NOTEWORTHY The most important aspects of the present study are the findings that 1) in vivo challenge with anthrax edema but not lethal toxin depresses arterial contractile function measured both ex vivo and in vivo and 2) adefovir inhibits the effects of edema toxin on arterial hypotension and improves survival with lethal dose of edema toxin challenge.
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Inaba, H., and J. P. Filkins. "Augmentation of endotoxic lethality and glucose dyshomeostasis by phorbol ester." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 260, no. 3 (March 1, 1991): R494—R502. http://dx.doi.org/10.1152/ajpregu.1991.260.3.r494.
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To investigate the role of protein kinase C (PKC) activation in the pathogenesis of endotoxin (ETX) shock, the in vivo effects of phorbol 12-myristate 13-acetate (PMA) on ETX-induced lethality and glucose dyshomeostasis were determined. Fed rats (300-400 g) were treated intravenously with incremental doses of Salmonella enteritidis ETX and either the vehicle, 110 mg/kg ip dimethyl sulfoxide (DMSO), or 0.5 mg/kg ip PMA dissolved in DMSO. PMA significantly increased ETX-induced lethality to doses of 1.0-20 mg/kg. PMA augmented the initial hyperglycemia, late hypoglycemia, and hyperlactacidemia after 1 mg/kg iv ETX to rats anesthetized with pentobarbital sodium. In contrast, 4 alpha-phorbol, a phorbol derivative that does not activate PKC, had no effect on either lethality or the glucose and lactate responses. Hyperinsulinemia after 1 mg/kg iv ETX was prolonged by PMA but not by 4 alpha-phorbol. Insulin tolerance testing (0.5 U/kg iv) produced an exaggerated hypoglycemic response in PMA-treated endotoxic (0.33 mg/kg) rats. Glucose tolerance to 1.2 g/kg iv was increased by ETX and PMA attenuated the increased tolerance. Thus PKC activation may be involved in the pathogenesis of lethal endotoxicosis and associated glucose dyshomeostasis.
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Finnie, John W., and Francisco A. Uzal. "Pathology and Pathogenesis of Brain Lesions Produced by Clostridium perfringens Type D Epsilon Toxin." International Journal of Molecular Sciences 23, no. 16 (August 12, 2022): 9050. http://dx.doi.org/10.3390/ijms23169050.
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Clostridium perfringens type D epsilon toxin (ETX) produces severe, and frequently fatal, neurologic disease in ruminant livestock. The disorder is of worldwide distribution and, although vaccination has reduced its prevalence, ETX still causes substantial economic loss in livestock enterprises. The toxin is produced in the intestine as a relatively inactive prototoxin, which is subsequently fully enzymatically activated to ETX. When changed conditions in the intestinal milieu, particularly starch overload, favor rapid proliferation of this clostridial bacterium, large amounts of ETX can be elaborated. When sufficient toxin is absorbed from the intestine into the systemic circulation and reaches the brain, two neurologic syndromes can develop from this enterotoxemia. If the brain is exposed to large amounts of ETX, the lesions are fundamentally vasculocentric. The neurotoxin binds to microvascular endothelial receptors and other brain cells, the resulting damage causing increased vascular permeability and extravasation of plasma protein and abundant fluid into the brain parenchyma. While plasma protein, particularly albumin, pools largely perivascularly, the vasogenic edema becomes widely distributed in the brain, leading to a marked rise in intracranial pressure, coma, sometimes cerebellar herniation, and, eventually, often death. When smaller quantities of ETX are absorbed into the bloodstream, or livestock are partially immune, a more protracted clinical course ensues. The resulting brain injury is characterized by bilaterally symmetrical necrotic foci in certain selectively vulnerable neuroanatomic sites, termed focal symmetrical encephalomalacia. ETX has also been internationally listed as a potential bioterrorism agent. Although there are no confirmed human cases of ETX intoxication, the relatively wide species susceptibility to this toxin and its high toxicity mean it is likely that human populations would also be vulnerable to its neurotoxic actions. While the pathogenesis of ETX toxicity in the brain is incompletely understood, the putative mechanisms involved in neural lesion development are discussed.
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Cookson, Michael, Sharon Ryan, Gregory Seedorf, R. Dodson, Steve Abman, and Erica Mandell. "Antenatal Vitamin D Preserves Placental Vascular and Fetal Growth in Experimental Chorioamnionitis Due to Intra-amniotic Endotoxin Exposure." American Journal of Perinatology 35, no. 13 (May 1, 2018): 1260–70. http://dx.doi.org/10.1055/s-0038-1642033.
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Background Chorioamnionitis (CA) is associated with a high risk for the development of bronchopulmonary dysplasia (BPD) after preterm birth, but mechanisms that increase susceptibility for BPD and strategies to prevent BPD are uncertain. As a model of CA, antenatal intra-amniotic (IA) endotoxin (ETX) exposure alters placental structure, causes fetal growth restriction, increases perinatal mortality, and causes sustained cardiorespiratory abnormalities throughout infancy. Vitamin D (Vit D) has been shown to have both anti-inflammatory and proangiogenic properties. Antenatal IA treatment with Vit D (1,25-(OH)2D3) during IA ETX exposure improves survival and increases vascular and alveolar growth in infant rats. Whether IA ETX causes decreased placental vascular development and if the protective effects of prenatal Vit D treatment are due to direct effects on the fetus or to improved placental vascular development remain unknown. Objective The objective of this study was to determine if IA ETX impairs placental vascular development and Vit D metabolism, and whether 1,25-(OH)2D3 treatment improves placental vascularity after IA ETX exposure during late gestation in pregnant rats. Design/Methods Fetal rats were exposed to ETX (10 mg), ETX + 1,25-(OH)2D3 (1 ng/mL), 1,25-(OH)2D3 (1 ng/mL), or saline (control) via IA injection at E20 and delivered 2 days later. To assess placental vascular development, histologic sections from the placenta were stained for CD31 and vessel density per high power field (HPF) was determined and analyzed using Matlab software. To determine the effects of ETX on placental Vit D metabolism, Vit D receptor (VDR) and activity of the Vit D conversion enzyme, CYP27B1, were assayed from placental homogenates. Angiogenic mediators were measured by reverse transcription polymerase chain reaction by RNA extracted from placental tissue. Results IA ETX reduced placenta and newborn birth weights by 22 and 20%, respectively, when compared with controls (placental weight: 0.60 vs. 0.47 g; p < 0.0001; birth weight: 4.68 vs. 5.88 g; p < 0.0001). IA 1,25-(OH)2D3 treatment increased birth weight by 12% in ETX-exposed pups (5.25 vs. 4.68 g; p < 0.001). IA ETX decreased placental vessel density by 24% in comparison with controls (1,114 vs. 848 vessels per HPF; p < 0.05). Treatment with IA 1,25-(OH)2D3 increased placenta vessel density twofold after ETX exposure (1,739 vs. 848); p < 0.0001), and increased vessel density compared with saline controls by 56% (1,739 vs. 1,114; p < 0.0001). IA ETX decreased both VDR and CYP27B1 expression by 83 and 35%, respectively (p < 0.01). Conclusion IA ETX decreases placental growth and vessel density and decreases placental VDR and CYP27B1 protein expression, and that antenatal 1,25-(OH)2D3 restores placental weight and vessel density, as well as birth weight. We speculate that 1,25-(OH)2D3 treatment preserves placental function in experimental CA and that these effects may be mediated by increased vascular growth.
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Ono, S., J. Y. Westcott, S. W. Chang, and N. F. Voelkel. "Endotoxin priming followed by high altitude causes pulmonary edema in rats." Journal of Applied Physiology 74, no. 4 (April 1, 1993): 1534–42. http://dx.doi.org/10.1152/jappl.1993.74.4.1534.
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Rapid ascent to high altitude may be associated with the development of high-altitude pulmonary edema (HAPE) in susceptible individuals. Because lung lavage fluid obtained from such patients can be rich in protein and neutrophils, we considered that an element of lung injury and inflammation contributed to the pathogenesis of some forms of HAPE. On the basis of such a likely contribution of inflammatory mechanisms, we induced pulmonary lung injury and inflammation by priming rats with Salmonella enteritidis endotoxin (ETX) (0.1 or 0.5 mg/kg body wt ip) and examined the influence of added exposure to simulated hypobaric hypoxia (24 h, 4,300 m). The animals that were primed with ETX and exposed to hypoxia, but not those that received either ETX or hypoxia alone, developed lung vascular damage. This vascular damage manifested itself histologically and by increases in the lung vascular permeability-surface area product and the lung bloodless wet weight-to-dry weight ratio. The bronchoalveolar lavage fluid of ETX-primed hypoxia-exposed rats contained a greater number of white blood cells and a higher concentration of protein compared with that of the ETX-primed rats. Hearts of ETX + hypoxia-treated rats showed an increased ratio of right ventricular weight divided by body weight (RV/BW). Neutropenia prevented the development of pulmonary edema and the increase in ETX + hypoxia rats with a Ca2+ entry blocker inhibited lung injury and RV hypertrophy, these results indicate that ETX priming causes pulmonary edema at high altitude and suggest a role for neutrophils and Ca2+ in this rat model of lung injury.
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Osiecka, Natalia, Ewa Juszyńska-Gałązka, Zbigniew Galewski, Teresa Jaworska-Gołąb, Aleksandra Deptuch, and Maria Massalska-Arodź. "Insight into polymorphism of the ethosuximide (ETX)." Journal of Thermal Analysis and Calorimetry 133, no. 2 (March 8, 2018): 961–67. http://dx.doi.org/10.1007/s10973-018-7142-x.
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Mander, Kimberley A., Francisco A. Uzal, Ruth Williams, and John W. Finnie. "Clostridium perfringens type D epsilon toxin produces a rapid and dose-dependent cytotoxic effect on cerebral microvascular endothelial cells in vitro." Journal of Veterinary Diagnostic Investigation 32, no. 2 (October 14, 2019): 277–81. http://dx.doi.org/10.1177/1040638719882745.
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Clostridium perfringens type D epsilon toxin (ETX) is responsible for a severe and frequently fatal neurologic disorder in ruminant livestock. Light microscopic, immunohistochemical, and ultrastructural studies have suggested that ETX injury to the cerebral microvasculature, with subsequent severe, generalized vasogenic edema and increased intracranial pressure, is critically important in producing neurologic dysfunction. However, the effect of ETX on brain capillary endothelial cells in vitro has not been examined previously, to our knowledge. We exposed a well-characterized human blood–brain barrier cell line to increasing concentrations of ETX, and demonstrated a direct and dose-dependent endotheliotoxic effect. Our findings are concordant with the primacy of vasculocentric brain lesions in the diagnosis of acute epsilon toxin enterotoxemia in ruminant livestock.
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Pitcher, Jeffrey M., Meijing Wang, Ben M. Tsai, Ajay Kher, Nicholas T. Nelson, and Daniel R. Meldrum. "Endogenous estrogen mediates a higher threshold for endotoxin-induced myocardial protection in females." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 290, no. 1 (January 2006): R27—R33. http://dx.doi.org/10.1152/ajpregu.00452.2005.
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Myocardial endotoxin tolerance may be induced in both males and females; however, it remains unknown whether there are mechanistic and threshold differences between the sexes. We hypothesized that endogenous estrogen mediates a higher threshold for endotoxin (ETX)-induced protection in females. Adult proestrus and ovariectomized (OVX) female rats were preconditioned (PC) with intraperitoneal injections of 125 (PC+125) or 500 (PC+500) μg/kg Salmonella typhimurium LPS (ETX) or normal saline (PC−). Twenty-four hours later, injury dose ETX (500 μg/kg) was injected. After 6 h, myocardial function was measured via Langendorff. p38 MAPK and JNK activation and TNF-α, IL-1, and IL-6 expression were evaluated. ETX injury significantly decreased left ventricular developed pressure in PC− groups vs. controls. PC+500 regimen protected against ETX injury, resulting in normal cardiac function. PC+125 regimen protected OVX but not proestrus females, which had diminished myocardial function. Activated JNK and TNF-α increased in PC− but were diminished in PC+500 animals. Importantly, activated JNK and TNF increased in PC+125 proestrus females, whereas PC+125 OVX females displayed decreases in these molecules. There were no differences in p38 MAPK activation or expression of IL-1 or IL-6. These results demonstrate that proestrus females require a higher stimulus (PC+500) to achieve myocardial protection against ETX injury. Removal of endogenous estrogen (OVX) lowered the preconditioning threshold (PC+125), resulting in protection after lesser injury. Additionally, myocardial JNK and TNF expression was decreased in OVX PC+125 females, which correlated with myocardial function differences. Therefore, we conclude that endogenous estrogen mediates a higher threshold for ETX tolerance in female myocardium.
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Sayeed, Sameera, Jihong Li, and Bruce A. McClane. "Virulence Plasmid Diversity in Clostridium perfringens Type D Isolates." Infection and Immunity 75, no. 5 (March 5, 2007): 2391–98. http://dx.doi.org/10.1128/iai.02014-06.
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ABSTRACT Clostridium perfringens type D isolates are important in biodefense and also cause natural enterotoxemias in sheep, goats, and occasionally cattle. In these isolates, the gene (etx) encoding ε-toxin is thought to reside on poorly characterized large plasmids. Type D isolates sometimes also produce other potentially plasmid-encoded toxins, including C. perfringens enterotoxin and beta2 toxin, encoded by the cpe and cbp2 genes, respectively. In the current study we demonstrated that the etx, cpe, and cpb2 genes are carried on plasmids in type D isolates and characterized the toxin-encoding plasmids to obtain insight into their genetic organization, potential transferability, and diversity. Southern blotting of pulsed-field gels showed that the etx gene of type D isolates can be present on at least five different plasmids, whose sizes range from 48 to 110 kb. The etx plasmids also typically carried IS1151 and tcp open reading frames (ORFs) known to mediate conjugative transfer of C. perfringens plasmid pCW3. PCR studies revealed that other than their tcp ORFs, etx plasmids of type D isolates do not carry substantial portions of the conserved or variable regions in the cpe plasmids of type A isolates. Southern blotting also demonstrated that in type D isolates the cpe and cpb2 genes are sometimes present on the etx plasmid. Collectively, these findings confirmed that the virulence of type D isolates is heavily plasmid dependent and indicated that (i) a single type D isolate can carry multiple virulence plasmids, (ii) a single type D virulence plasmid can carry up to three different toxin genes, and (iii) many etx plasmids should be capable of conjugative transfer.
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Chen, Delphine L., and Daniel P. Schuster. "Positron emission tomography with [18F]fluorodeoxyglucose to evaluate neutrophil kinetics during acute lung injury." American Journal of Physiology-Lung Cellular and Molecular Physiology 286, no. 4 (April 2004): L834—L840. http://dx.doi.org/10.1152/ajplung.00339.2003.
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We measured neutrophil glucose uptake with positron emission tomographic imaging and [18F]fluorodeoxyglucose ([18F]FDG-PET) in anesthetized dogs after intravenous oleic acid-induced acute lung injury (ALI; OA group, n = 6) or after low-dose intravenous endotoxin (known to activate neutrophils without causing lung injury) followed by OA (Etx + OA group, n = 7). The following two other groups were studied as controls: one that received no intervention ( n = 5) and a group treated with Etx only ( n = 6). PET imaging was performed ∼1.5 h after initiating experimental interventions. The rate of [3H]deoxyglucose ([3H]DG) uptake was also measured in vitro in cells recovered from bronchoalveolar lavage (BAL) performed after PET imaging. Circulating neutrophil counts fell significantly in animals treated with Etx but not in the other two groups. The rate of [18F]FDG uptake, measured by the influx constant Ki, was significantly elevated ( P < 0.05) in both Etx-treated groups (7.9 ± 2.6 × 10-3ml blood·ml lung-1·min-1in the Etx group, 9.3 ± 4.8 × 10-3ml blood·ml lung-1·min-1in the Etx + OA group) but not in the group treated only with OA (3.4 ± 0.8 × 10-3ml blood·ml lung-1·min-1) when compared with the normal control (1.6 ± 0.4 × 10-3ml blood·ml lung-1·min-1). [3H]DG uptake was increased (73 ± 7%) in BAL neutrophils recovered from the Etx + OA group ( P < 0.05) but not in the OA group. Kiand [3H]DG uptake rates were linearly correlated ( R2= 0.65). We conclude that the rate of [18F]FDG uptake in the lungs during ALI reflects the state of neutrophil activation. [18F]FDG-PET imaging can detect pulmonary sequestration of activated neutrophils, despite the absence of alveolar neutrophilia. Thus [18F]FDG-PET imaging may be a useful tool to study neutrophil kinetics during ALI.
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Sanmartin, Paul, Daladier Jabba, Randy Sierra, and Elker Martinez. "Objective Function BF-ETX for RPL Routing Protocol." IEEE Latin America Transactions 16, no. 8 (August 2018): 2275–81. http://dx.doi.org/10.1109/tla.2018.8528246.
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Abele, Alison N., Elizabeth S. Taglauer, Maricar Almeda, Noah Wilson, Abigail Abikoye, Gregory J. Seedorf, S. Alex Mitsialis, Stella Kourembanas, and Steven H. Abman. "Antenatal mesenchymal stromal cell extracellular vesicle treatment preserves lung development in a model of bronchopulmonary dysplasia due to chorioamnionitis." American Journal of Physiology-Lung Cellular and Molecular Physiology 322, no. 2 (February 1, 2022): L179—L190. http://dx.doi.org/10.1152/ajplung.00329.2021.
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Antenatal stressors such as chorioamnionitis (CA) increase the risk for bronchopulmonary dysplasia (BPD). Studies have shown that experimental BPD can be ameliorated by postnatal treatment with mesenchymal stromal cell-derived extracellular vesicles (MEx). However, the antenatal efficacy of MEx to prevent BPD is unknown. To determine whether antenatal MEx therapy attenuates intrauterine inflammation and preserves lung growth in a rat model of CA-induced BPD. At embryonic day ( E) 20, rat litters were treated with intra-amniotic injections of saline, endotoxin (ETX) to model chorioamnionitis, MEx, or ETX plus MEx followed by cesarean section delivery with placental harvest at E22. Placental and lung evaluations were conducted at day 0 and day 14, respectively. To assess the effects of ETX and MEx on lung growth in vitro, E15 lung explants were imaged for distal branching. Placental tissues from ETX-exposed pregnancies showed increased expression of inflammatory markers NLRP-3 and IL-1ß and altered spiral artery morphology. In addition, infant rats exposed to intrauterine ETX had reduced alveolarization and pulmonary vessel density (PVD), increased right ventricular hypertrophy (RVH), and decreased lung mechanics. Intrauterine MEx therapy of ETX-exposed pups reduced inflammatory cytokines, normalized spiral artery architecture, and preserved distal lung growth and mechanics. In vitro studies showed that MEx treatment enhanced distal lung branching and increased VEGF and SPC gene expression. Antenatal MEx treatment preserved distal lung growth and reduced intrauterine inflammation in a model of CA-induced BPD. We speculate that MEx may provide a novel therapeutic strategy to prevent BPD due to antenatal inflammation.
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Meldrum, D. R., J. C. Cleveland, R. T. Rowland, A. Banerjee, A. H. Harken, and X. Meng. "Early and delayed preconditioning: differential mechanisms and additive protection." American Journal of Physiology-Heart and Circulatory Physiology 273, no. 2 (August 1, 1997): H725—H733. http://dx.doi.org/10.1152/ajpheart.1997.273.2.h725.
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The purposes of this study were to determine whether 1) 24-h endotoxin (ETX) pretreatment induces delayed ("second window") myocardial protection against ischemia-reperfusion (I/R), 2) acute adenosine (Ado) or phenylephrine (PE) pretreatment confers similar protection, 3) the mechanisms of Ado- and PE-induced early protection remain intact after endotoxemia, 4) Ado- and PE-induced protection may combine with ETX-induced delayed protection to optimize cardiac protection, and 5) these strategies of early and/or delayed myocardial protection require de novo protein synthesis. Rats (n = 6-8/group) were treated with ETX (0.5 mg/kg i.p.) or vehicle, with or without prior inhibition of protein synthesis. Twenty-four hours later, the hearts were isolated, perfused, and acutely pretreated with Ado or PE before I/R (20-min ischemia and 40-min reperfusion). Developed pressure, coronary flow, compliance (end-diastolic pressure), and reperfusion creatine kinase leak were measured. Results indicated that 1) Ado, PE, and ETX independently induced myocardial functional protection; 2) either Ado or PE acutely enhanced ETX induced protection; and 3) cycloheximide abolished delayed, but not acute, protection. We conclude that early and delayed forms of protection 1) may be combined to optimize protection and 2) differentially rely on de novo protein synthesis.
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Wagley, Sariqa, Monika Bokori-Brown, Helen Morcrette, Andrea Malaspina, Caroline D’Arcy, Sharmilee Gnanapavan, Nicholas Lewis, et al. "Evidence of Clostridium perfringens epsilon toxin associated with multiple sclerosis." Multiple Sclerosis Journal 25, no. 5 (April 21, 2018): 653–60. http://dx.doi.org/10.1177/1352458518767327.
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Background: It was recently reported that, using Western blotting, some multiple sclerosis (MS) patients in the United States had antibodies against epsilon toxin (Etx) from Clostridium perfringens, suggesting that the toxin may play a role in the disease. Objective: We investigated for serum antibodies against Etx in UK patients with clinically definite multiple sclerosis (CDMS) or presenting with clinically isolated syndrome (CIS) or optic neuritis (ON) and in age- and gender-matched controls. Methods: We tested sera from CDMS, CIS or ON patients or controls by Western blotting. We also tested CDMS sera for reactivity with linear overlapping peptides spanning the amino acid sequence (Pepscan) of Etx. Results: Using Western blotting, 24% of sera in the combined CDMS, CIS and ON groups ( n = 125) reacted with Etx. In the control group ( n = 125), 10% of the samples reacted. Using Pepscan, 33% of sera tested reacted with at least one peptide, whereas in the control group only 16% of sera reacted. Out of 61 samples, 21 (43%) were positive to one or other testing methodology. Three samples were positive by Western blotting and Pepscan. Conclusion: Our results broadly support the previous findings and the role of Etx in the aetiology of MS warrants further investigation.
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Huang, Jinze, Fengbiao Zan, Xin Liu, and Da Chen. "Wireless Communications and Mobile Computing UAV Routing Protocol Based on Link Stability and Selectivity of Neighbor Nodes in ETX Metrics." Wireless Communications and Mobile Computing 2022 (May 14, 2022): 1–12. http://dx.doi.org/10.1155/2022/5428280.
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With the extensive application of UAVs in various fields, it becomes more important to design a routing protocol that ensures stable transmit between UAV groups. This is because UAV groups are densely packed, move fast, and communication links are fragile. Aiming at the intensive and highly maneuverable UAV group, the AODV-NLS-ETX—a routing protocol based on the link stability of neighbor nodes—is proposed on the basis of the ETX metric based AODV protocol. The protocol is simulated and compared with other protocols. The simulation results show that AODV-NLS-ETX is superior to other protocols in packet delivery rate and throughput under high shift speed, dense nodes, and high routing overhead. It can effectively reduce the high delay brought by the ETX mechanism. The delay is the most stable and is not easy to cause network congestion. It can be better applied to dense and highly mobile unmanned aerial vehicles.
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Ab. Rahim, Rosminazuin, Abdallah Awad, Aisha Hassan Abdalla Hashim, and ALIZA AINI MD RALIB. "EVALUATION OF THE ROUTING METIRC W-METRIC USED WITH RPL PRTOCOL IN LLNS." IIUM Engineering Journal 19, no. 2 (December 1, 2018): 80–89. http://dx.doi.org/10.31436/iiumej.v19i2.840.
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ABSTRACT: The current de-facto routing protocol over Low Power and Lossy Networks (LLN) developed by the IETF Working Group (6LOWPAN), is named as Routing Protocol for Low Power and Lossy networks (RPL). RPL in the network layer faces throughput challenges due to the potential large networks, number of nodes, and that multiple coexisting applications will be running in the same physical layer. In this study, a node metric for RPL protocol based on the node’s Queue Backlogs is introduced, which leads to a better throughput performance while maintaining the delay and the ability to use with different network applications. This metric depends on the length of Packet Queue of the nodes with the consideration of other link and node metrics, like ETX or energy usage, leading to better load balancing in the network. To implement and evaluate the proposed metric compared to other RPL metrics, ContikiOS and COOJA simulator are used. Extensive simulations have been carried out in a systematic way resulting in a detailed analysis of the introduced metric namely W-metric, expected transmission count (ETX) and objective function zero (OF0) that uses hop-count as a routing metric. The analysis and comparison are based on five performance parameters, which are throughput, packet delivery ratio (PDR), latency, average queue length, and power consumption. Simulation results show that the introduced W-metric has a good performance compared to other RPL metrics with regards to performance parameters mentioned above. At the same time, the results show that its latency performance is comparable with other RPL routing metrics. In a sample simulation of 500 seconds with 25 nodes and with nodes sending packets periodically to the network root at a rate of 1 packet per 4 seconds, W-metric showed a very efficient throughput of 5.16 kbps, an increase of 8.2% compared to ETX. Results showed that it has a packet delivery ratio of 93.3%, which is higher compared to 83.3% for ETX and 74.2% for OF0. Average queue length of 0.48 packet shows improvement of 15.8% better than ETX. In addition, it exhibits an energy consumption of 5.16 mW which is 2.1% less than ETX. Overall, W-metric appears to be a promising alternative to ETX and OF0 as it selects routes that are more efficient by working on load balancing of the network and by considering the link characteristics.
ABSTRAK: Protokol penghalaan de-facto semasa ke atas Rangkaian Kekuatan Rendah dan Lossy yang dibangunkan oleh Kumpulan Kerja IETF (6LOWPAN), dinamakan Protokol Penghalaan untuk Kekuatan Rendah dan Rugi (RPL). RPL dalam lapisan rangkaian menghadapi cabaran throughput berikutan jangkaan rangkaian besar, bilangan nod dan aplikasi berganda bersama akan diproses dalam lapisan fizikal yang sama. Dalam kajian ini, satu metrik nod untuk protokol RPL berdasarkan pada Backend Queue node diperkenalkan, yang membawa kepada prestasi yang lebih baik sambil mengekalkan kelewatan dan keupayaan untuk digunakan dengan aplikasi rangkaian yang berbeza. Metrik ini bergantung pada panjang Packet Queue dari node dengan pertimbangan metrik lain dan nodus lain, seperti ETX atau penggunaan tenaga, yang mengarah kepada keseimbangan beban yang lebih baik dalam rangkaian. Untuk melaksanakan dan menilai metrik yang dicadangkan berbanding metrik RPL lain, ContikiOS dan COOJA simulator telah digunakan. Simulasi meluas telah dijalankan dengan cara yang sistematik yang menghasilkan analisis terperinci mengenai metrik yang diperkenalkan iaitu W-metrik, kiraan penghantaran dijangkakan (ETX) dan fungsi objektif sifar (OF0) yang menggunakan kiraan hop sebagai metrik penghalaan. Analisis dan perbandingan adalah berdasarkan lima parameter prestasi, iaitu throughput, nisbah penghantaran paket (PDR), latency, panjang panjang antrian, dan penggunaan kuasa. Hasil simulasi menunjukkan bahawa W-metrik yang diperkenalkan mempunyai prestasi yang lebih baik berbanding dengan metrik RPL lain berkaitan dengan parameter prestasi yang dinyatakan di atas. Pada masa yang sama, hasil menunjukkan bahawa prestasi latency W-metrik adalah setanding dengan metrik penghalaan RPL yang lain. Dalam simulasi sampel 500 saat dengan 25 nod dan dengan nod yang menghantar paket secara berkala ke akar rangkaian pada kadar 1 paket setiap 4 saat, W-metrik menunjukkan keluaran yang sangat efisien iaitu 5.16 kbps, peningkatan sebanyak 8.2% berbanding ETX. Keputusan menunjukkan bahawa ia mempunyai nisbah penghantaran paket 93.3%, yang lebih tinggi berbanding 83.3% untuk ETX dan 74.2% untuk OF0. Purata panjang giliran 0.48 packet menunjukkan peningkatan 15.8% lebih baik daripada ETX. Di samping itu, ia mempamerkan penggunaan tenaga sebanyak 5.16 mW iaitu 2.1% kurang daripada ETX. Secara keseluruhan, W-metrik nampaknya menjadi alternatif yang berpotensi menggantikan ETX dan OF0 kerana ia memilih laluan yang lebih cekap dengan bekerja pada keseimbangan beban rangkaian dan dengan mempertimbangkan ciri-ciri pautan.
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Zhang, Qi, Xin Gao, Jixiong Wu, and Min Chen. "The Correlation between Endotoxin, D-Lactate, and Diamine Oxidase with Endoscopic Activity in Inflammatory Bowel Disease." Disease Markers 2022 (September 16, 2022): 1–11. http://dx.doi.org/10.1155/2022/9171436.
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Background and Objective. The disease activity monitoring of inflammatory bowel disease (IBD) plays a crucial role for making therapeutic strategies. Endoscopy has been recognized as a gold standard for evaluating disease activity of IBD. However, this method is invasive. Currently, a noninvasive biomarker that could replace endoscope is needed in clinical practice. In this study, we examined whether the diamine oxidase (DAO), D-lactate, and endotoxin (ETX) could monitor the disease activity and predict endoscopic remission in patient with IBD. Methods. A total of 149 eligible IBD patients including 82 Crohn disease (CD) and 67 Ulcerative colitis (UC) who had received both endoscopic examination and intestinal barrier function detection in our hospital were enrolled in this study. Endoscopic activity was estimated by the Simple Endoscopic Score (SES-CD) for Crohn’s Disease and the ulcerative colitis endoscopic index of severity (UCEIS) for ulcerative colitis. The predictive value and optimal predictive thresholds for those biomarkers were determined by receiver operating characteristic analysis. Results. For UC patients, DAO, D-lactate, and ETX showed better correlation with UCEIS than erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) and exhibited satisfactory predictive value in predicting remission. Among patients with CD, DAO and ETX not only showed a better correlation than WBC, ESR, and CRP with SES-CD but also capable to identify more severe patients. Conclusion. DAO and ETX could be used to distinguish different endoscopic activity of CD. DAO, D-lactate, and ETX could predict UC endoscopic remission.
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Nguyen, Melissa L., Jimmy D. Ballard, Judith A. James, and Darise Farris. "Cross-reactive humoral epitopes of EF and LF are identified but do not constitute major anthrax toxin neutralization responses following EF and LF vaccination (132.20)." Journal of Immunology 182, no. 1_Supplement (April 1, 2009): 132.20. http://dx.doi.org/10.4049/jimmunol.182.supp.132.20.
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Abstract BACKGROUND: Anthrax Lethal and Edema Toxins (LTx and ETx) are formed by binding of Lethal Factor (LF) or Edema Factor (EF) to the pore-forming moiety, Protective Antigen (PA). Immunity to LF and EF neutralize anthrax toxins. AIM: LF and EF immune sera were used to identify cross-reactive B cell epitopes in their conserved PA-binding domains and to determine the relative contribution of such antibodies to LTx and ETx neutralization. METHODS: A/J mice were immunized with recombinant (r) LF or EF. EF-binding antibodies were purified from LF immune sera, and LF-binding antibodies from EF immune sera by column absorption. Whole immune sera and purified cross-reactive antibodies were tested for IgG to rLF or rEF by ELISA, in vitro neutralization of LTx and ETx, and binding to solid phase, overlapping LF and EF decapeptides. RESULTS: Cross-reactive epitopes were identified as EF aa 98-257 and 257-268 and LF aa 265-274. Whole LF and EF immune sera neutralized LTx and ETx, respectively. However, LF sera did not neutralize ETx nor did EF sera neutralize LTx. Purified cross-reactive IgG also failed to cross-neutralize. CONCLUSIONS: Cross-reactive B cell epitopes in the PA-binding domains of whole rLF and rEF occur and have been identified; however, the major anthrax toxin-neutralizing humoral responses to these antigens are constituted by non-cross-reactive epitopes that likely lie outside of their PA-binding sites.
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Tissot Van Patot, M. C., S. MacKenzie, A. Tucker, and N. F. Voelkel. "Endotoxin-induced adhesion of red blood cells to pulmonary artery endothelial cells." American Journal of Physiology-Lung Cellular and Molecular Physiology 270, no. 1 (January 1, 1996): L28—L36. http://dx.doi.org/10.1152/ajplung.1996.270.1.l28.
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Cell-cell interactions are important in intravascular inflammation. Neutrophils and monocytes adhere to the vascular endothelium and release mediators, such as tumor necrosis factor-alpha (TNF-alpha), interleukin (IL)-1 beta, and reactive oxygen species. Red blood cells (RBC) from patients with malaria, sickle cell anemia, and diabetes also adhere to endothelial cells. The objectives of this investigation were to develop a bovine system of RBC adhesion to endothelial cells and to begin to investigate the mechanisms involved in the RBC adhesion. We show that 51Cr-RBC adhere to bovine pulmonary artery endothelial cells (BPAEC) after stimulation of both cell types with endotoxin (ETX; 50 micrograms/ml). RBC adhesion to BPAEC depended on the ETX concentration and the presence of divalent cations. TNF-alpha, IL-1 beta, and antioxidants (superoxide dismutase; catalase; and dimethyl sulfoxide) all induced RBC adhesion to BPAEC. Phosphatidylserine, which has been implicated in adhesion of sickle cells and aged RBC to endothelium, reduced RBC adhesion to BPAEC, whether ETX-treated or not. In conclusion, ETX, proinflammatory cytokines and, surprisingly, antioxidants increase RBC adherence to BPAEC monolayers. RBC adhesion to endothelium is decreased by phosphatidylserine.
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Sayeed, Sameera, M. E. Fernandez-Miyakawa, Derek J. Fisher, Vicki Adams, Rachael Poon, Julian I. Rood, Francisco A. Uzal, and Bruce A. McClane. "Epsilon-Toxin Is Required for Most Clostridium perfringens Type D Vegetative Culture Supernatants To Cause Lethality in the Mouse Intravenous Injection Model." Infection and Immunity 73, no. 11 (November 2005): 7413–21. http://dx.doi.org/10.1128/iai.73.11.7413-7421.2005.
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ABSTRACT Clostridium perfringens type D enterotoxemias have significant economic impact by causing rapid death of several domestic animal species. Consequently, domestic animals are commonly vaccinated, at varying efficacy, with inactivated type D vegetative supernatants. Improved type D vaccines might become possible if the lethal toxins produced by type D isolates were characterized and the contributions of those toxins to supernatant-induced lethality were established. Therefore, the current study evaluated the presence of lethal toxins in supernatants prepared from late-log-phase vegetative cultures of a large collection of genotype D isolates. Under this growth condition, most genotype D isolates produced variable levels of at least three different lethal toxins, including epsilon-toxin (ETX). To model the rapid lethality of type D enterotoxemias, studies were conducted involving intravenous (i.v.) injection of genotype D vegetative supernatants into mice, which were then observed for neurotoxic distress. Those experiments demonstrated a correlation between ETX (but not alpha-toxin or perfringolysin O) levels in late-log-phase genotype D supernatants and lethality. Consistent with the known proteolytic activation requirement for ETX toxicity, trypsin pretreatment was required for, or substantially increased, the lethality of nearly all of the tested genotype D vegetative supernatants. Finally, the lethality of these trypsin-pretreated genotype D supernatants could be completely neutralized by an ETX-specific monoclonal antibody but not by an alpha-toxin-specific monoclonal antibody. Collectively, these results indicate that, under the experimental conditions used in the present study, ETX is necessary for the lethal properties of most genotype D vegetative supernatants in the mouse i.v. injection model.
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Świąder, Mariusz J., Katarzyna Świąder, Izabela Zakrocka, Maciej Krzyżanowski, Andrzej Wróbel, Jarogniew J. Łuszczki, and Stanisław J. Czuczwar. "Long-term vigabatrin treatment modifies pentylenetetrazole-induced seizures in mice: focused on GABA brain concentration." Pharmacological Reports 72, no. 2 (December 20, 2019): 322–30. http://dx.doi.org/10.1007/s43440-019-00037-6.
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Abstract Background The goal of our study was to examine the long-term effect of vigabatrin (VGB), a γ-aminobutyric acid aminotransferase (GABA-AT) inhibitor on clonazepam (CLO), ethosuximide (ETX) and valproate (VPA) anticonvulsive activity against pentylenetetrazole (PTZ)-induced seizures in mice. Methods VGB was administered for 3 and 7 days. Convulsions were evoked by PTZ at its CD97 (99 mg/kg). The influence of CLO, ETX and VPA alone or in combination with VGB on motor performance and long-term memory was analyzed. γ-aminobutyric acid (GABA) concentration in mice brain and plasma as well as glutamate decarboxylase (GAD) activity was measured. Results After 3 days of treatment, VGB in doses up to 500 mg/kg increased PTZ-induced seizure threshold, whereas after 7 days VGB (at the dose of 125 mg/kg) inhibited clonic seizures in experimental mice. 7 days of VGB administration did not change the protective effect of CLO, ETX and VPA against PTZ-induced seizures. 7 days of VGB treatment at a subthreshold dose of 75 mg/kg decreased TD50 of ETX and CLO in the chimney test, but did not affect TD50 value for VPA. 7 days of VGB administration in combination with AEDs did not affect long-term memory in mice. VGB after 3 days or 7 days of administration increased brain GABA concentration. GAD activity was decreased after 3 and 7 days of VGB administration. Conclusions The presented results confirm anticonvulsive activity of VGB through GABA metabolism alteration and suggest care when combining VGB with ETX or CLO in the therapy.
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Lam, John, Stephen Robinson, Daniel Gregson, Ranjani Somayaji, John Conly, Lisa Welikovitch, and Michael Parkins. "1079. When Does a Trans-Esophageal Echocardiogram (TEE) Change Management of Staphylococcus aureus Bacteremia (SAB)?" Open Forum Infectious Diseases 5, suppl_1 (November 2018): S322—S323. http://dx.doi.org/10.1093/ofid/ofy210.915.
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Abstract Background The recognition of infective endocarditis (IE) as a serious complication of SAB has led to a low threshold for echocardiography, extended treatment (eTx) with anti-staphylococcal agents (anti-SA), and even surgery. However, indications for eTx outside of IE are numerous. We sought to determine the frequency in which findings from a TEE changed clinical SAB management. Methods Adults with SAB within the Calgary Health Zone between 2012 and 2014 were included if both a transthoracic echocardiogram (TTE) and TEE were performed within 7 days of each other. Patients potentially benefiting from eTx courses were a priori defined as having ≥1 of; (1) metastatic phenomena, (2) complicated SAB (defined as community acquired (CA), persistent fever/bacteremia at ≥48 hours), (3) intracardiac devices, and/or (4) Duke criteria defined IE (separately evaluated using TTE or TEE). Patient demographics, treatment (including changes to anti-SA duration and surgical indications), and clinical outcomes were extracted and evaluated. Results Of 961 SAB episodes, 179 (18% MRSA) met inclusion criteria (median 3.0 days, IQR 1.9–5.1 between TTE and TEE). Within the cohort 29% (n = 51) had metastatic phenomena (intracranial; 9% [n = 16], vertebral; 8% [n = 14]; empyema; 6% [n = 11]). Complicated bacteremia was present in 89% (n = 159), while 13% (n = 23) had intravascular hardware (39% pacemakers, 65% valve prostheses). IE was diagnosed in 22% (n = 40) of SAB episodes, with TTE identifying 58% of vegetations (n = 23) and TEE identifying an additional 30% (n = 15). Of the cohort, 89% (n = 160), 37% (n = 67), 4% (n = 7) of SAB had ≥1, 2, and 3 nonechocardiographic indications for eTx, respectively. Only one patient met criteria for eTx solely based on IE diagnosed from concordant TTE and TEE. Actual duration of therapy did not differ in SAB episodes that had ≥1 a priori eTx criteria but had a negative TEE relative to those who had a positive TEE (36.7 days, IQR 23.4–48.6 vs. 43.8 days, IQR 33.3–49.5, P = 0.17). Of the 15 episodes of TEE-only evident IE, 14 were CA, 12 had prolonged BSI, and nine embolic phenomena. Only 11 patients in the cohort required cardiac surgery, none were identified exclusively by TEE. Conclusion Routine performance of TEE may not be required in all SAB as many patients have alternate indications for eTx with anti-SA regardless of TEE findings. Disclosures All authors: No reported disclosures.
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Law, W. R., and J. L. Ferguson. "Effect of naloxone on regional cerebral blood flow during endotoxin shock in conscious rats." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 253, no. 3 (September 1, 1987): R425—R433. http://dx.doi.org/10.1152/ajpregu.1987.253.3.r425.
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Maintenance of cerebral blood flow (CBF) is vital during cardiovascular shock. Since opioids have been implicated in the pathophysiology of endotoxin shock and have been shown to alter cerebral perfusion patterns, we determined whether opioids were responsible for any of the changes in regional CBF observed during endotoxin shock and whether the use of naloxone might impair or aid in the maintenance of CBF. When blood flow (BF) is studied with microspheres in rats, the left ventricle of the heart is often cannulated via the right carotid artery. Questions have arisen concerning the potential adverse effects of this method on CBF in the hemisphere ipsilateral to the ligated artery. We measured right and left regional CBF by use of this route of cannulation. Twenty-four hours after cannulations were performed, flow measurements were made using radiolabeled microspheres in conscious unrestrained male Sprague-Dawley rats (300-400 g) before and 10, 30 and 60 min after challenging with 10 mg/kg Escherichia coli endotoxin (etx) or saline. Naloxone (2 mg/kg) or saline was given as a treatment 25 min post-etx. We found no significant differences between right and left cortical, midbrain, or cerebellar BF at any time in any treatment group. After etx, the whole brain received a large share of the depressed cardiac output. Thus global CBF was not significantly reduced below its pre-etx value, an effect unaltered by naloxone. Regionally, BF was reduced to cerebellum and midbrain by 30 min post-etx. Naloxone prevented this depression. No region was affected to a greater or lesser degree than others.(ABSTRACT TRUNCATED AT 250 WORDS)
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Sun, Weifeng, Haotian Wang, Xianglan Piao, and Tie Qiu. "An Opportunistic Routing Mechanism Combined with Long-Term and Short-Term Metrics for WMN." Scientific World Journal 2014 (2014): 1–11. http://dx.doi.org/10.1155/2014/432123.
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WMN (wireless mesh network) is a useful wireless multihop network with tremendous research value. The routing strategy decides the performance of network and the quality of transmission. A good routing algorithm will use the whole bandwidth of network and assure the quality of service of traffic. Since the routing metric ETX (expected transmission count) does not assure good quality of wireless links, to improve the routing performance, an opportunistic routing mechanism combined with long-term and short-term metrics for WMN based on OLSR (optimized link state routing) and ETX is proposed in this paper. This mechanism always chooses the highest throughput links to improve the performance of routing over WMN and then reduces the energy consumption of mesh routers. The simulations and analyses show that the opportunistic routing mechanism is better than the mechanism with the metric of ETX.
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Rocha O., Leonardo, Carolina Torres G., María Corena-McLeod, Iván D. Vélez B., and Sara M. Robledo R. "Effect of carbonic anhydrase inhibitors on Anopheles albimanus larvae (Diptera: Culicidae)." Revista Colombiana de Entomología 39, no. 2 (December 31, 2013): 226–28. http://dx.doi.org/10.25100/socolen.v39i2.8240.
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Carbonic anhydrase (CA) catalyzes the reversible conversion of CO2 to bicarbonate and participates in mechanisms of alkalinization in the intestine of mosquitoes. The toxicity of four CA inhibitors (CAI ): acetazolamide (AZ M), methazolamide (MZM), ethoxolamide (ETX) and dorzolamide (DZA ) were evaluated in larvae of Anopheles albimanus by monitoring mortality 24, 48 and 72 hours post application, at a concentration of 50 ug/ml diluted in dimethyl sulfoxide previously. All IA C reduced the population of larvae in variable proportions. ETX showed the highest toxicity, achieving more than 80% mortality after 24 hours and 98% after 72 hours of application. The CAI , AZ M, MZM and DZA showed less toxicity (<50% mortality). Our results indicate that the CAI , including ETX in particular, is a worthy candidate as an alternative for the control of An. albimanus, which is considered a primary vector of malaria in Colombia.
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MIYAKITA, Kazuyuki, Keisuke NAKANO, Yusuke MORIOKA, Masakazu SENGOKU, and Shoji SHINODA. "Characterization of Minimum Route ETX in Multi-Hop Wireless Networks." IEICE Transactions on Communications E92-B, no. 3 (2009): 745–54. http://dx.doi.org/10.1587/transcom.e92.b.745.
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Bindel, Sébastien, Serge Chaumette, and Benoît Hilt. "F-ETX: a predictive link state estimator for mobile networks." ICST Transactions on Mobile Communications and Applications 2, no. 7 (June 20, 2016): 151517. http://dx.doi.org/10.4108/eai.20-6-2016.151517.
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Garcia, J. P., V. Adams, J. Beingesser, M. L. Hughes, R. Poon, D. Lyras, A. Hill, B. A. McClane, J. I. Rood, and F. A. Uzal. "Epsilon Toxin Is Essential for the Virulence of Clostridium perfringens Type D Infection in Sheep, Goats, and Mice." Infection and Immunity 81, no. 7 (April 29, 2013): 2405–14. http://dx.doi.org/10.1128/iai.00238-13.
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ABSTRACTClostridium perfringenstype D causes disease in sheep, goats, and other ruminants. Type D isolates produce, at minimum, alpha and epsilon (ETX) toxins, but some express up to five different toxins, raising questions about which toxins are necessary for the virulence of these bacteria. We evaluated the contribution of ETX toC. perfringenstype D pathogenicity in an intraduodenal challenge model in sheep, goats, and mice using a virulentC. perfringenstype D wild-type strain (WT), an isogenic ETX null mutant (etxmutant), and a strain where theetxmutation has been reversed (etxcomplemented). All sheep and goats, and most mice, challenged with the WT isolate developed acute clinical disease followed by death in most cases. Sheep developed various gross and/or histological changes that included edema of brain, lungs, and heart as well as hydropericardium. Goats developed various effects, including necrotizing colitis, pulmonary edema, and hydropericardium. No significant gross or histological abnormalities were observed in any mice infected with the WT strain. All sheep, goats, and mice challenged with the isogenicetxmutant remained clinically healthy for ≥24 h, and no gross or histological abnormalities were observed in those animals. Complementation ofetxknockout restored virulence; most goats, sheep, and mice receiving this complemented mutant developed clinical and pathological changes similar to those observed in WT-infected animals. These results indicate that ETX is necessary for type D isolates to induce disease, supporting a key role for this toxin in type D disease pathogenesis.
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Fernandez-Miyakawa, Mariano E., Derek J. Fisher, Rachael Poon, Sameera Sayeed, Vicki Adams, Julian I. Rood, Bruce A. McClane, and Francisco A. Uzal. "Both Epsilon-Toxin and Beta-Toxin Are Important for the Lethal Properties of Clostridium perfringens Type B Isolates in the Mouse Intravenous Injection Model." Infection and Immunity 75, no. 3 (January 8, 2007): 1443–52. http://dx.doi.org/10.1128/iai.01672-06.
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ABSTRACT Clostridium perfringens is capable of producing up to 15 toxins, including alpha-toxin (CPA), beta-toxin (CPB), epsilon-toxin (ETX), enterotoxin, beta2-toxin (CPB2), and perfringolysin O. Type B isolates, which must produce CPA, CPB, and ETX, are associated with animal illnesses characterized by sudden death or acute neurological signs, with or without intestinal damage. Type B pathogenesis in ruminants is poorly understood, with some animals showing lesions and clinical signs similar to those caused by either type C or type D infections. It is unknown whether host or environmental conditions are dominant for determining the outcome of type B disease or if disease outcomes are determined by variable characteristics of type B isolates. To help clarify this issue, 19 type B isolates were evaluated for toxin production during late-log-phase growth via quantitative Western blotting and by biological activity assays. Most type B isolates produced CPB levels similar to those produced by type C isolates in vitro and have the potential to produce genotype C-like disease. The lethality of type B isolate supernatants administered intravenously to mice was evaluated with or without prior trypsin treatment, and monoclonal antibody neutralization studies also were performed. Correlation analyses comparing toxin levels in type B supernatants versus lethality and neutralization studies both found that the main contributor to lethality without pretreatment with trypsin was CPB, whereas neutralization studies indicated that CPB and ETX were both important after trypsin pretreatment. At least part of the CPB produced by type B isolates remained active after trypsin treatment. However, the overall lethalities of most supernatants were lower after trypsin pretreatment. Also, there was a significant association between ETX, CPB2, and CPA production in vitro among type B isolates. However, our results suggest that both CPB and ETX are likely the most important contributors to the pathogenesis of C. perfringens type B infections in domestic animals.
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Mohiuddin, Mudassar, Zahid Iqbal, Abubakar Siddique, Shenquan Liao, Muhammad Khalid Farooq Salamat, Nanshan Qi, Ayesha Mohiud Din, and Mingfei Sun. "Prevalence, Genotypic and Phenotypic Characterization and Antibiotic Resistance Profile of Clostridium perfringens Type A and D Isolated from Feces of Sheep (Ovis aries) and Goats (Capra hircus) in Punjab, Pakistan." Toxins 12, no. 10 (October 14, 2020): 657. http://dx.doi.org/10.3390/toxins12100657.
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Clostridium perfringens poses a serious threat to small ruminants by causing moderate to severe enterotoxaemia. Due to its ability to produce a wide arsenal of toxins, it is ranked among the most prevalent and important pathogens in livestock. This study focused on the molecular characterization of different Clostridium perfringens types along with their antimicrobial resistance profile. An overall higher prevalence of C. perfringens (46.1%) was detected based on mPCR among sheep and goats (healthy and diseased) in the Punjab province, Pakistan. The majority of the isolates were characterized as type A (82%), followed by type D (18%). Among the isolates from diseased sheep and goats, 27% were positive for cpa, 49% for cpa and cpb2, 9% for cpa and etx, 15% for cpa, cpb2 and etx. In the case of isolates from healthy sheep and goats, 59% were positive for cpa, 34% for cpb2 and cpa, 4% for cpa and etx, and 3% for cpa, cpb2 and etx. The prevalence of the beta2 toxin gene in the diseased sheep and goat population was 64% as compared to 37% in healthy animals. All 184 isolates (100%) were sensitive to rifampin and ceftiofur; the majority (57%) was sensitive to teicoplanin, chloramphenicol, amoxicillin, linezolid and enrofloxacin. A lower proportion of isolates (43%) were sensitive to ciprofloxacin and only 14% were susceptible to erythromycin. The findings of this study highlight the higher prevalence of C. perfringens in small ruminants and indicate that detailed pathogenesis studies are necessary to understand the explicit role of various toxins in causing enteric infections in sheep and goats including how they might be exploited to develop vaccines against these diseases.
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Roberts, J. C., H. L. Mathews, M. Weber, and S. B. Jones. "A Role for Endotoxin (ETX) in a Lymphoid-Adrenal Medullary Axis." Shock 3, no. 6 (June 1995): 37. http://dx.doi.org/10.1097/00024382-199506000-00129.
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Roberts, J. C., H. L. Mathews, M. Weber, and S. B. Jones. "A Role for Endotoxin (ETX) in a Lymphoid-Adrenal Medullary Axis." Shock 3 (June 1995): 37. http://dx.doi.org/10.1097/00024382-199506002-00128.
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Ji, Bin, Ahmad Kenaan, Shan Gao, Jin Cheng, Daxiang Cui, Hao Yang, Jinglin Wang, and Jie Song. "Label-free detection of biotoxins via a photo-induced force infrared spectrum at the single-molecular level." Analyst 144, no. 20 (2019): 6108–17. http://dx.doi.org/10.1039/c9an01338e.
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Moro, L. "ETX-2514. Broad-spectrum beta-lactamase inhibitor, Treatment of multidrug-resistant infections." Drugs of the Future 43, no. 8 (2018): 555. http://dx.doi.org/10.1358/dof.2018.043.08.2824713.
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