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Relevant bibliographies by topics / IgG-Saporin

Academic literature on the topic 'IgG-Saporin'

Author: Grafiati

Published: 4 June 2021

Last updated: 20 February 2023

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Journal articles on the topic "IgG-Saporin"

1

Book, Adam A., Ronald G. Wiley, and John B. Schweitzer. "192 IgG-saporin." Acta Neuropathologica 89, no. 6 (1995): 519–26. http://dx.doi.org/10.1007/bf00571506.

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Book, Adam A., Ronald G. Wiley, and John B. Schweitzer. "192 IgG-saporin." Acta Neuropathologica 89, no. 6 (May 1, 1995): 519–26. http://dx.doi.org/10.1007/s004010050283.

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Grindstaff, Ryan J., Regina R. Grindstaff, and J. Thomas Cunningham. "Baroreceptor sensitivity of rat supraoptic vasopressin neurons involves noncholinergic neurons in the DBB." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 279, no. 5 (November 1, 2000): R1934—R1943. http://dx.doi.org/10.1152/ajpregu.2000.279.5.r1934.

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Previous studies suggest that cholinergic neurons in the diagonal band of Broca (DBB) participate in the baroreceptor-mediated inhibition of phasic vasopressin neurons in the supraoptic nucleus (SON). To test this hypothesis, extracellular recordings were obtained from putative vasopressin SON neurons of anesthetized rats injected with the cholinergic immunotoxin 192 IgG-saporin (0.8 μg/μl) in the DBB. Baroreceptor sensitivity of neurons was tested with brief phenylephrine-induced (10 μg/10 μl iv) increases in blood pressure of at least 40 mmHg. In rats injected with vehicle or unconjugated saporin, 19 of 21 and 18 of 20 phasic neurons, respectively, were inhibited by increased blood pressure. In rats injected with 192 IgG-saporin, which significantly reduced the number of choline acetyltransferase (ChAT)-positive DBB neurons, 33 of 36 phasic neurons were inhibited. Normal rats and rats with DBB saporin injections received rhodamine bead injections into the perinuclear zone (PNZ) to retrogradely label DBB neurons, and their brains were stained for ChAT. ChAT-positive DBB neurons were not retrogradely labeled from the PNZ. Together, these results indicate that the pathway relaying baroreceptor information to the SON involves noncholinergic DBB neurons.

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Harrell, Lindy E., Dee Parsons, and Krystyna Kolasa. "Hippocampal sympathetic ingrowth occurs following 192-IgG–Saporin administration." Brain Research 911, no. 2 (August 2001): 158–62. http://dx.doi.org/10.1016/s0006-8993(01)02626-9.

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Markovitz, Rebecca C., John F. Healey, W. Hunter Baldwin, Ernest T. Parker, Shannon L. Meeks, and Pete Lollar. "Decreasing the Humoral Response to Factor VIII By Targeted Deletion of Factor VIII - Specific B Cells." Blood 124, no. 21 (December 6, 2014): 238. http://dx.doi.org/10.1182/blood.v124.21.238.238.

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Abstract The development of neutralizing anti-factor VIII (fVIII) antibodies (inhibitors) remains the most significant complication in the treatment of hemophilia A patients. Treatment of inhibitor patients consists of management of bleeding episodes using bypassing agents or porcine fVIII. Inhibitors can be eradicated by immune tolerance induction (ITI) using thrice-weekly administration of large doses of fVIII. However, ITI fails in approximately 30% of patients. Additionally, the median time to tolerance in successful cases is ~18 months, making ITI expensive and inconvenient. In the current study, we used a murine E16 hemophilia A model to test a novel approach to both prevent and eradicate fVIII inhibitors. We hypothesized that conjugation of fVIII to the toxin saporin, a Type I ribosome-inactivating protein, would target fVIII-specific cell surface immunoglobulin and selectively delete fVIII-specific naïve and memory B cells. Recombinant full-length fVIII was covalently linked to saporin using the heterobifunctional crosslinker N-succinimidyl-3-(2-pyridyldithio)propionate (SPDP). To test for eradication of existing fVIII inhibitors by fVIII-saporin, an adoptive transfer protocol was developed to measure fVIII-specific memory B cells. Hemophilia A donor mice were immunized with 2 μg of full-length fVIII by intravenous injection every other week for 8 weeks, followed by a final dose of 4 μg at ten weeks. Four weeks later, the mice were randomized into three treatment groups to receive equimolar doses of saporin, fVIII, or fVIII-saporin. Seven days after treatment, the mice were sacrificed and 4 x 106 plasma cell CD138+-depleted splenocytes were adoptively transferred as a source of fVIII-specific memory B cells into naïve recipient hemophilia A mice. At 24 hours, recipient mice were given a single injection of 0.5, 1.0 or 2.0 μg of recombinant full-length fVIII by tail vein injection. Anti-fVIII IgG antibodies in recipient mice were measured by ELISA 2 and 5 weeks following the fVIII injection. In the absence of fVIII-specific memory B cells from donor mice, naïve hemophilia A mice did not produce detectable anti-fVIII antibodies. Recipient hemophilia A mice receiving splenocytes from fVIII donor and saporin donor mice displayed a dose-dependent increase in anti-fVIII antibodies. In contrast, the slope of the anti-fVIII titer versus dose of fVIII was significantly decreased in recipient mice receiving splenocytes from fVIII-saporin donor mice. To test for prevention of fVIII inhibitor formation by fVIII-saporin, naïve hemophilia A mice were divided into three treatment groups to receive a single dose of saporin, fVIII, or fVIII-saporin by tail vein injection. Seven days after treatment, the mice were immunized by tail vein injection with 2 μg of full-length fVIII every other week for 10 weeks. Anti-fVIII IgG antibodies were measured 1 week after the fourth and sixth injections of fVIII. Anti-fVIII antibody titers were significantly lower in the fVIII-saporin group compared to the fVIII group (1,900 vs. 21,400 (p=0.027, n=4, Mann-Whitney test, see figure) after the fourth injection. After 6 injections, the average anti-fVIII titer of the fVIII group was 23,000 compared to 4,000 in the fVIII-saporin group (p=0.057, n=4, Mann-Whitney test, see figure). In conclusion, our results suggest that infusion of fVIII-saporin results in the depletion of both fVIII-specific naïve B cells and memory B cells. FVIII-saporin potentially could be used in the treatment of congenital hemophilia A patients with inhibitors and patients with acquired hemophilia A. In addition, fVIII-saporin potentially could be used in previously untreated patients with hemophilia A to prevent inhibitor development. Similar therapeutic strategies could be extended to other antigen-specific immune disorders. Figure 1 Figure 1. Disclosures No relevant conflicts of interest to declare.

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Blanco-Centurion, Carlos A., Anjelica Shiromani, Elizabeth Winston, and Priyattam J. Shiromani. "Effects of hypocretin-1 in 192-IgG-saporin-lesioned rats." European Journal of Neuroscience 24, no. 7 (October 2006): 2084–88. http://dx.doi.org/10.1111/j.1460-9568.2006.05074.x.

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Moga, Margaret M. "192 IgG-saporin abolishes p75 neurotrophin receptor immunoreactivity in rat SCN." NeuroReport 9, no. 14 (October 1998): 3197–200. http://dx.doi.org/10.1097/00001756-199810050-00012.

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Sachdev, Robert N. S., Shao-Ming Lu, Ron G. Wiley, and Ford F. Ebner. "Role of the Basal Forebrain Cholinergic Projection in Somatosensory Cortical Plasticity." Journal of Neurophysiology 79, no. 6 (June 1, 1998): 3216–28. http://dx.doi.org/10.1152/jn.1998.79.6.3216.

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Sachdev, Robert N. S., Shao-Ming Lu, Ron G. Wiley, and Ford F. Ebner. Role of the basal forebrain cholinergic projection in somatosensory cortical plasticity. J. Neurophysiol. 79: 3216–3228, 1998. Trimming all but two whiskers in adult rats produces a predictable change in cortical cell-evoked responses characterized by increased responsiveness to the two intact whiskers and decreased responsiveness to the trimmed whiskers. This type of synaptic plasticity in rat somatic sensory cortex, called “whisker pairing plasticity,” first appears in cells above and below the layer IV barrels. These are also the cortical layers that receive the densest cholinergic inputs from the nucleus basalis. The present study assesses whether the cholinergic inputs to cortex have a role in regulating whisker pairing plasticity. To do this, cholinergic basal forebrain fibers were eliminated using an immunotoxin specific for these fibers. A monoclonal antibody to the low-affinity nerve growth factor receptor 192 IgG, conjugated to the cytotoxin saporin, was injected into cortex to eliminate cholinergic fibers in the barrel field. The immunotoxin reduces acetylcholine esterase (AChE)-positive fibers in S1 cortex by >90% by 3 wk after injection. Sham-depleted animals in which either saporin alone or saporin unconjugated to 192 IgG is injected into the cortex produces no decrease in AChE-positive fibers in cortex. Sham-depleted animals show the expected plasticity in barrel column neurons. In contrast, no plasticity develops in the ACh-depleted, 7-day whisker-paired animals. These results support the conclusion that the basal forebrain cholinergic projection to cortex is an important facilitator of synaptic plasticity in mature cortex.

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Wrenn, Craige C., and Ronald G. Wiley. "The behavioral functions of the cholinergic basalforebrain : lessons from 192 IgG‐SAPORIN." International Journal of Developmental Neuroscience 16, no. 7-8 (November 1998): 595–602. http://dx.doi.org/10.1016/s0736-5748(98)00071-9.

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Burk, Joshua A., Matthew W. Lowder, and Kathleen E. Altemose. "Attentional demands for demonstrating deficits following intrabasalis infusions of 192 IgG-saporin." Behavioural Brain Research 195, no. 2 (December 2008): 231–38. http://dx.doi.org/10.1016/j.bbr.2008.09.006.

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Dissertations / Theses on the topic "IgG-Saporin"

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Peterson, William E. "Immunolesioning of identified motoneuron pools by the intramuscular injection of the immunotoxins, 192-IgG-saporin and OX7-saporin, in rats." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2002. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp05/MQ62820.pdf.

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Perry, Tracyann. "Behavioural, histological and immunocytochemical consequences following 192 IgG saporin immunolesions of the basal forebrain." Thesis, King's College London (University of London), 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.314079.

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Sherren, Nicole. "Neural and behavioral effects of intracranial 192 IgG-saporin in neonatal rats, sexually dimorphic effects?" Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1998. http://www.collectionscanada.ca/obj/s4/f2/dsk2/tape15/PQDD_0015/MQ36938.pdf.

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Cabrera, Sara Michelle. "192 IgG-Saporin lesions of the nucleus basalis magnocellularis impair serial reversal learning in rats." CSUSB ScholarWorks, 2005. https://scholarworks.lib.csusb.edu/etd-project/2778.

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In order to assess flexibility in acquiring and using conflicting response rules, rats with selective lesions of the NBM or sham-lesion controls were subjected to serial reversal training in a simple operant discrimination paradigm. The NBM lesion group did not differ from the control group in acquisition of the original rules; the NBM lesion group required more time to master the changes in rules in the first reversal, but not in subsequent reversals.

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Kitto, Michael Ryan. "Biconditional discrimination learning in rats with 192 IgG-saporin lesions of the nucleus basalis magnocellularis." CSUSB ScholarWorks, 2006. https://scholarworks.lib.csusb.edu/etd-project/3002.

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The experiment tested the hypothesis that 192 IgG-saporin lesions of the nucleus basalis magnocellularis (NBM) in rats would impair performance in a biconditional visual discrimination task, which requires configural association learning. Experiment used 22 male Long-Evan rats (Harlan Sprague-Dawley). Behavioral testing was conducted in two identical T-mazes. Rats were randomly assigned to either a bilateral 192 IgG-saporin lesion group (n = 10) or to a control group (n = 12). Results support the hypothesis that NBM is critically involved in configural but not simple association learning and suggest that NBM may be involved more generally in cognitive flexibility.

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Quinlivan, Mitchell Owen Jeffrey. "Functions of the Cholinergic System in the Morbidities Associated with Alzheimer’s Disease and the Further Evaluation of Tools for the Molecular Imaging of this System." Thesis, The University of Sydney, 2007. http://hdl.handle.net/2123/1933.

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The aims of this project were to contribute to the elucidation of the role of the cholinergic system in attention and memory, two cognitive processes severely compromised in Alzheimer’s disease (AD), and to evaluate and develop tools for the functional molecular imaging of this system with a view to improving knowledge of AD and other neurological disorders. Towards the first aim, the specific anti-cholinergic toxin 192 IgG-saporin (SAP) was administered to female Sprague-Dawley rats via either an intracerebroventricular (icv) or an intracortical route and animals were tested with a vibrissal-stimulation reaction-time task and an object recognition task to evaluate their attentional and mnemonic function, respectively. The second aim was approached in two ways. Firstly, relative neuronal densities from animals with icv lesions were assessed with both ex vivo and in vitro autoradiography with the specific cholinergic radiopharmaceuticals [123I]iodobenzovesamicol (123IBVM) and 125I-A-85380, ligands for the vesicular acetylcholine transporter and the nicotinic acetylcholine receptor, respectively. Secondly, a number of in vivo and in vitro studies were performed on a novel and unique molecular imaging system (TOHR), with which it had been hoped initially to image eventually SAP-lesioned animals, with a view to measuring and ameliorating its performance characteristics and assessing its in-principle suitability for small-animal molecular imaging. The behavioural studies support a critical role for the cholinergic system in normal attentional function. Additionally, in accord with literature evidence, no significant impairment was observed in mnemonic function. It is postulated however that the results observed in the intracortically-lesioned animals support the published hypothesis that cholinergic projections to the perirhinal cortex are critical for object-recognition memory. In autoradiographic studies, SAP-lesioned animals demonstrated reduced uptake of 123IBVM in multiple regions. A reduction of nicotinic receptors was also seen in SAP-lesioned animals, a novel finding supportive of the excellent characteristics of radioiodinated I-A-85380. Examination of the performance characteristics of the TOHR support in principle its utility for targeted small-animal molecular imaging studies.

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Quinlivan, Mitchell Owen Jeffrey. "Functions of the Cholinergic System in the Morbidities Associated with Alzheimer’s Disease and the Further Evaluation of Tools for the Molecular Imaging of this System." University of Sydney, 2007. http://hdl.handle.net/2123/1933.

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Doctor of Philosophy(PhD)
The aims of this project were to contribute to the elucidation of the role of the cholinergic system in attention and memory, two cognitive processes severely compromised in Alzheimer’s disease (AD), and to evaluate and develop tools for the functional molecular imaging of this system with a view to improving knowledge of AD and other neurological disorders. Towards the first aim, the specific anti-cholinergic toxin 192 IgG-saporin (SAP) was administered to female Sprague-Dawley rats via either an intracerebroventricular (icv) or an intracortical route and animals were tested with a vibrissal-stimulation reaction-time task and an object recognition task to evaluate their attentional and mnemonic function, respectively. The second aim was approached in two ways. Firstly, relative neuronal densities from animals with icv lesions were assessed with both ex vivo and in vitro autoradiography with the specific cholinergic radiopharmaceuticals [123I]iodobenzovesamicol (123IBVM) and 125I-A-85380, ligands for the vesicular acetylcholine transporter and the nicotinic acetylcholine receptor, respectively. Secondly, a number of in vivo and in vitro studies were performed on a novel and unique molecular imaging system (TOHR), with which it had been hoped initially to image eventually SAP-lesioned animals, with a view to measuring and ameliorating its performance characteristics and assessing its in-principle suitability for small-animal molecular imaging. The behavioural studies support a critical role for the cholinergic system in normal attentional function. Additionally, in accord with literature evidence, no significant impairment was observed in mnemonic function. It is postulated however that the results observed in the intracortically-lesioned animals support the published hypothesis that cholinergic projections to the perirhinal cortex are critical for object-recognition memory. In autoradiographic studies, SAP-lesioned animals demonstrated reduced uptake of 123IBVM in multiple regions. A reduction of nicotinic receptors was also seen in SAP-lesioned animals, a novel finding supportive of the excellent characteristics of radioiodinated I-A-85380. Examination of the performance characteristics of the TOHR support in principle its utility for targeted small-animal molecular imaging studies.

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Quinlivan, Mitchell. "Rôles du système cholinergique dans le disfonctionnement cognitif associé à la maladie Alzheimer et évaluation d'outils pour l'imagerie moléculaire." Tours, 2007. http://www.theses.fr/2007TOUR3324.

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La dégénérescence des neurones cholinergiques (NC) est une caractéristique importante de la maladie Alzheimer (MA). Afin d’imiter cet aspect de la MA, nous avons utilisé une toxine permettant la destruction, dans le prosencéphale basal chez le rat, des NC. Cette technique a été validée par immunohistochimie (IHC). Les études comportementales démontrent que le système cholinergique est nécessaire pour l’attention mais que celui-ci joue également un rôle relativement mineur dans le processus mnémonique, domaines cognitifs très touchés par la MA. Dans ce cadre, nos études, utilisant des radioligands spécifiques pour les récepteurs nicotiniques (nAChR) ou le transporteur acétylcholine vésiculaire, pouvaient démontrer, et pour la première fois sur les nAChR, la lésion validée par IHC. Nous avons donc développé et décrit un système d’imagerie moléculaire pour l’étude in vivo du petit animal. Toutefois ce système n’a pas pu être encore utilisé pour l’étude de radioligand
Cholinergic neuron degeneration is a prominent hallmark of Alzheimer’s disease (AD). Using a specific immunotoxin (SAP), basal forebrain cholinergic neurons in the rat were lesioned, as assessed by immunohistochemistry (IHC), to model this facet of AD. Behavioural testing, utilising models with two different routes of SAP administration, further demonstrated the necessity of this system for normal attentional function and its relatively minor role in mnemonic function, cognitive domains greatly affected by AD. Studies with radioligands specific for the nicotinic receptor (nAChR) or the Vesicular Acetylcholine Transporter were both able to demonstrate the lesion validated by IHC, the first time a nAChR radioligand has done this in a SAP model. Although eventually it was unable to be used for the in vivo continuation of this work, studies for the development of a small-animal molecular imaging system initially intended for such a continuation are also reported

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Book chapters on the topic "IgG-Saporin"

1

Petrosini, Laura, Paola De Bartolo, Debora Cutuli, and Francesca Gelfo. "Perinatal 192 IgG-Saporin as Neuroteratogen." In Neurotoxin Modeling of Brain Disorders—Life-long Outcomes in Behavioral Teratology, 111–23. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/7854_2015_418.

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Walsh, Thomas J. "Models of Cholinergic Degeneration: AF64A and 192-IgG-Saporin." In Advances in Behavioral Biology, 667–74. Boston, MA: Springer US, 1998. http://dx.doi.org/10.1007/978-1-4615-5337-3_94.

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Schliebs, Reinhard, Steffen Roßner, Mechthild Heider, and Volker Bigl. "Targeted Immunolesion of Cholinergic Neurons by 192 IgG-Saporin." In Neurochemistry, 829–35. Boston, MA: Springer US, 1997. http://dx.doi.org/10.1007/978-1-4615-5405-9_136.

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Petrosini, Laura, P. De Bartolo, and D. Cutuli. "Neurotoxic Effects, Mechanisms, and Outcome of 192-IgG Saporin." In Handbook of Neurotoxicity, 591–609. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4614-5836-4_79.

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Petrosini, L., P. De Bartolo, and D. Cutuli. "Neurotoxic Effects, Mechanisms, and Outcome of 192 IgG-Saporin Lesions." In Handbook of Neurotoxicity, 1–23. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-71519-9_79-1.

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Petrosini, L., P. De Bartolo, and D. Cutuli. "Neurotoxic Effects, Mechanisms, and Outcome of 192 IgG-Saporin Lesions." In Handbook of Neurotoxicity, 1251–72. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-031-15080-7_79.

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Chang, J. W., and Y. S. Park. "Use of 192 IgG-saporin as a model of dementia and its application." In Genetics, Neurology, Behavior, and Diet in Dementia, 849–63. Elsevier, 2020. http://dx.doi.org/10.1016/b978-0-12-815868-5.00053-0.

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