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Journal articles on the topic 'Immunolesione'

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Author: Grafiati

Published: 11 March 2023

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1

Gu, Zezong, Juan Yu, Karin Werrbach‐Perez, and J. Regino Perez‐Polo. "Repeated immunolesions display diminished stress response signal." International Journal of Developmental Neuroscience 18, no. 2-3 (March 9, 2000): 177–83. http://dx.doi.org/10.1016/s0736-5748(99)00086-6.

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2

Gu, Zezong, Juan Yu, and J. Regino Perez-Polo. "Responses in the aged rat brain after total immunolesion." Journal of Neuroscience Research 54, no. 1 (October 1, 1998): 7–16. http://dx.doi.org/10.1002/(sici)1097-4547(19981001)54:1<7::aid-jnr2>3.0.co;2-m.

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3

Yu, J., R. G. Wiley, and R. J. Perez-Polo. "Altered NGF protein levels in different brain areas after immunolesion." Journal of Neuroscience Research 43, no. 2 (January 15, 1996): 213–23. http://dx.doi.org/10.1002/(sici)1097-4547(19960115)43:2<213::aid-jnr9>3.0.co;2-j.

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4

Ferreira, G., M. Meurisse, R. Gervais, N. Ravel, and F. Lévy. "Extensive immunolesions of basal forebrain cholinergic system impair offspring recognition in sheep." Neuroscience 106, no. 1 (September 2001): 103–16. http://dx.doi.org/10.1016/s0306-4522(01)00265-2.

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5

McMahan, Robert W., Thomas J. Sobel, and Mark G. Baxter. "Selective immunolesions of hippocampal cholinergic input fail to impair spatial working memory." Hippocampus 7, no. 2 (1997): 130–36. http://dx.doi.org/10.1002/(sici)1098-1063(1997)7:2<130::aid-hipo2>3.0.co;2-r.

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6

Guo, Yi, Yuanbin Dai, Junyu Lai, and Ying Fan. "Study about correlation of anti-neutrophil cytoplasmic antibodies and anticardiolipin antibodies with thromboangiitis obliterans." Vascular 21, no. 6 (May 13, 2013): 363–68. http://dx.doi.org/10.1177/1708538113478742.

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Doctors often have difficulties in clinical diagnosis and clinical stage of thromboangiitis obliterans (TAO). Immunolesion was important in the initiation and progression of various kinds of vasculitis diseases, including TAO. Several kinds of immune complexes were developed by immunolesion, including anti-neutrophil cytoplasmic antibodies (ANCA) and anticardiolipin antibodies (ACA). Our aim was to determine if it is an effective way for clinical diagnosis and clinical stage of TAO by detection of the presence of ANCA and ACA in blood serum of patients with TAO and the relationship among the presence of ANCA, ACA and patients with different grades of TAO. Blood samples and clinical characteristics were collected from 38 patients with Rutherford grade I TAO, 30 patients with Rutherford grade II–III TAO, 75 patients with arteriosclerosis obliterans (ASO) and 65 healthy volunteers. Their serum samples were investigated for ANCA by indirect immunofluorescent (IIF), and for ACA and ANCA specificity antigens including reactivity to proteinase 3(PR3), myeloperoxidase (MPO), cathepsin G (CG), bactericidal/permesbility-increasing protein (BPI), elastase (HLE) and lactoferrin (LF) by enzyme linked immunosorbent assay (ELISA). (1) ANCA positive rate and titre were much higher in cases with Rutherford grade I TAO (52.6%, 20/38, 0.386 ± 0.458) and Rutherford grade II–III TAO (73.3%, 22/30, 0.847 ± 0.658) than those in cases with ASO (4%, 3/75, 0.011 ± 0.002) and healthy volunteers (0%,0/65, 0.010 ± 0.002) ( P < 0.01). ANCA positive rate and titre were higher in cases with Rutherford grade II–III TAO (73.3%, 22/30, 0.847 ± 0.658) than those in cases with Rutherford grade I TAO (52.6%, 20/38, 0.386 ± 0.458) ( P < 0.05). (2) ACA concentration was much higher in cases with Rutherford grade I TAO (270.13 ± 13.05 IU/mL) and Rutherford grade II–III TAO (279.33 ± 19.98 IU/mL) than that in cases with ASO (236.85 ± 17.32 IU/mL) and healthy volunteers (229.16 ± 15.55 IU/mL) ( P < 0.05) respectively. (3) In 42 cases of ANCA-positive samples, there were 20 cases reacted with MPO, 14 cases reacted with LF, five cases reacted with HLE, five cases reacted with BPI and no one reacted with PR3 and CG. All cases were Rutherford grade II–III TAO. Our results indicate that ANCA, ANCA specificity antigens and ACA were detected susceptibly and availably in patients with TAO. Thus, detection of ANCA, ANCA specificity antigens and ACA was helpful for clinical diagnosis of TAO and detection of ANCA and ANCA specificity antigens was helpful for clinical staging of TAO. They are important assistance for clinical diagnosis and stage of TAO.

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7

Galani, Rodrigue, Olivia Lehmann, Tristan Bolmont, Elizabeth Aloy, Fabrice Bertrand, Christine Lazarus, Hélène Jeltsch, and Jean-Christophe Cassel. "Selective immunolesions of CH4 cholinergic neurons do not disrupt spatial memory in rats." Physiology & Behavior 76, no. 1 (May 2002): 75–90. http://dx.doi.org/10.1016/s0031-9384(02)00674-1.

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8

Berger-Sweeney, Joanne, Nancy A. Stearns, Stephanie L. Murg, Laura R. Floerke-Nashner, Douglas A. Lappi, and Mark G. Baxter. "Selective Immunolesions of Cholinergic Neurons in Mice: Effects on Neuroanatomy, Neurochemistry, and Behavior." Journal of Neuroscience 21, no. 20 (October 15, 2001): 8164–73. http://dx.doi.org/10.1523/jneurosci.21-20-08164.2001.

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9

Nilsson, O. G., G. Leanza, C. Rosenblad, D. A. Lappi, R. G. Wiley, and A. Björklund. "Spatial learning impairments in rats with selective immunolesion of the forebrain cholinergic system." NeuroReport 3, no. 11 (November 1992): 1005–8. http://dx.doi.org/10.1097/00001756-199211000-00015.

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10

Potter, H., E. Alenciks, K. Frazier, A. Porter, and G. S. Fraley. "Immunolesion of melanopsin neurons causes gonadal regression in Pekin drakes (Anas platyrhynchos domesticus)." General and Comparative Endocrinology 256 (January 2018): 16–22. http://dx.doi.org/10.1016/j.ygcen.2017.08.006.

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11

W�rtwein, Gitta, Juan Yu, Tracy Toliver-Kinsky, and J. R. Perez-Polo. "Responses of young and aged rat CNS to partial cholinergic immunolesions and NGF treatment." Journal of Neuroscience Research 52, no. 3 (May 1, 1998): 322–33. http://dx.doi.org/10.1002/(sici)1097-4547(19980501)52:3<322::aid-jnr8>3.0.co;2-f.

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12

Bassant, Marie-hélène, Anne Jouvenceau, Emmanuelle Apartis, Frederique Poindessous-jazat, Patrick Dutar, and Jean-marie Billard. "Immunolesion of the cholinergic basal forebrain :effects on functional properties of hippocampal and septalneurons." International Journal of Developmental Neuroscience 16, no. 7-8 (November 1998): 613–32. http://dx.doi.org/10.1016/s0736-5748(98)00073-2.

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13

Silveira, Diosely C., Gregory L. Holmes, Steven C. Schachter, Changiz Geula, and Donald L. Schomer. "Increased susceptibility to generalized seizures after immunolesions of the basal forebrain cholinergic neurons in rats." Brain Research 878, no. 1-2 (September 2000): 223–27. http://dx.doi.org/10.1016/s0006-8993(00)02703-7.

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14

Roßner, Steffen. "Cholinergic immunolesions by 192IgG‐saporin—a useful tool to simulate pathogenic aspects of alzheimer's disease." International Journal of Developmental Neuroscience 15, no. 7 (November 1997): 835–50. http://dx.doi.org/10.1016/s0736-5748(97)00035-x.

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15

Gu, Zezong, Juan Yu, and J. Regino Perez-Polo. "Long term changes in brain cholinergic markers and nerve growth factor levels after partial immunolesion." Brain Research 801, no. 1-2 (August 1998): 190–97. http://dx.doi.org/10.1016/s0006-8993(98)00579-4.

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16

Gil-Bea, Francisco J., Reinhard Schliebs, Ludmil Kirazov, Joaquı́n Del Rio, and Marı́a J. Ramı́rez. "P1-078: Basal forebrain cholinergic immunolesion in Tg2576 mice affects beta-amyloidogenesis and cognitive function." Alzheimer's & Dementia 2 (July 2006): S117—S118. http://dx.doi.org/10.1016/j.jalz.2006.05.453.

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17

Perry, TracyAnn, Helen Hodges, and Jeffrey A. Gray. "Behavioural, histological and immunocytochemical consequences following 192 IgG-saporin immunolesions of the basal forebrain cholinergic system." Brain Research Bulletin 54, no. 1 (January 2001): 29–48. http://dx.doi.org/10.1016/s0361-9230(00)00413-5.

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18

Kapás, Levente, Ferenc Obál, Adam A. Book, John B. Schweitzer, Ronald G. Wiley, and James M. Krueger. "The effects of immunolesions of nerve growth factor-receptive neurons by 192 IgG-saporin on sleep." Brain Research 712, no. 1 (March 1996): 53–59. http://dx.doi.org/10.1016/0006-8993(95)01431-4.

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19

Ro�ner, S., J. Yu, D. Pizzo, K. Werrbach-Perez, R. Schliebs, V. Bigl, and J. R. Perez-Polo. "Effects of intraventricular transplantation of NGF-secreting cells on cholinergic basal forebrain neurons after partial immunolesion." Journal of Neuroscience Research 45, no. 1 (July 1, 1996): 40–56. http://dx.doi.org/10.1002/(sici)1097-4547(19960701)45:1<40::aid-jnr4>3.0.co;2-h.

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20

Torres, E. M., T. A. Perry, A. Blokland, L. S. Wilkinson, R. G. Wiley, D. A. Lappi, and S. B. Dunnett. "Behavioural, histochemical and biochemical consequences of selective immunolesions in discrete regions of the basal forebrain cholinergic system." Neuroscience 63, no. 1 (November 1994): 95–122. http://dx.doi.org/10.1016/0306-4522(94)90010-8.

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21

Bassant, Marie-H., Frédérique Poindessous-Jazat, and Bernard H. Schmidt. "Sustained effect of metrifonate on cerebral glucose metabolism after immunolesion of basal forebrain cholinergic neurons in rats." European Journal of Pharmacology 387, no. 2 (January 2000): 151–62. http://dx.doi.org/10.1016/s0014-2999(99)00742-6.

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22

Gu, Zezong, Tracy Toliver‐Kinsky, Joel Glasgow, Karin Werrbach‐Perez, and J. Regino Perez‐Polo. "NGF‐mediated alteration of NF‐ κ B binding activity after partial immunolesions to rat cholinergic basal forebrain neurons." International Journal of Developmental Neuroscience 18, no. 4-5 (May 15, 2000): 455–68. http://dx.doi.org/10.1016/s0736-5748(00)00004-6.

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23

Fraley, G. S. "Immunolesion of Hindbrain Catecholaminergic Projections to the Medial Hypothalamus Attenuates Penile Reflexive Erections and Alters Hypothalamic Peptide mRNA." Journal of Neuroendocrinology 14, no. 5 (May 2002): 345–48. http://dx.doi.org/10.1046/j.0007-1331.2002.00782.x.

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24

Sorger, Dietlind, Reinhard Schliebs, Ingrid Kämpfer, Steffen Rossner, Jochen Heinicke, Claudia Dannenberg, and Peter Georgi. "In vivo [125I]-iodobenzovesamicol binding reflects cortical cholinergic deficiency induced by specific immunolesion of rat basal forebrain cholinergic system." Nuclear Medicine and Biology 27, no. 1 (January 2000): 23–31. http://dx.doi.org/10.1016/s0969-8051(99)00087-6.

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25

Calza, L., A. Giuliani, M. Fernandez, S. Pirondi, G. D'Intino, L. Aloe, and L. Giardino. "Neural stem cells and cholinergic neurons: Regulation by immunolesion and treatment with mitogens, retinoic acid, and nerve growth factor." Proceedings of the National Academy of Sciences 100, no. 12 (May 30, 2003): 7325–30. http://dx.doi.org/10.1073/pnas.1132092100.

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26

Bassant, Marie H., Emmanuelle Apartis, Frédérique R. Jazat-Poindessous, Ronald G. Wiley, Yvon A. Lamour, and Yvon A. Lamour. "Selective Immunolesion of the Basal Forebrain Cholinergic Neurons: Effects on Hippocampal Activity During Sleep and Wakefulness in the Rat." Neurodegeneration 4, no. 1 (March 1995): 61–70. http://dx.doi.org/10.1006/neur.1995.0007.

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27

Roßner, S., Reinhard Schliebs, J. R. Perez-Polo, R. G. Wiley, and V. Bigl. "Differential changes in cholinergic markers from selected brain regions after specific immunolesion of the rat cholinergic basal forebrain system." Journal of Neuroscience Research 40, no. 1 (January 1, 1995): 31–43. http://dx.doi.org/10.1002/jnr.490400105.

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28

Burjanadze, M., T. Naneishvili, M. Dashniani, N. Chkhikvishvili, and M. Chighladze. "P.1.h.004 Spatial long-term memory and modulation of NMDA receptor subunit expression in medial septal immunolesioned rats." European Neuropsychopharmacology 24 (October 2014): S272—S273. http://dx.doi.org/10.1016/s0924-977x(14)70428-6.

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29

Severino, Maurizio, Anja F. Pedersen, Viktorija Trajkovska, Ellen Christensen, Rasmus Lohals, Lone M. Veng, Gitte M. Knudsen, and Susana Aznar. "Selective immunolesion of cholinergic neurons leads to long-term changes in 5-HT2A receptor levels in hippocampus and frontal cortex." Neuroscience Letters 428, no. 1 (November 2007): 47–51. http://dx.doi.org/10.1016/j.neulet.2007.09.026.

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30

Härtig, W., A. Saul, J. Kacza, J. Grosche, S. Goldhammer, D. Michalski, and O. Wirths. "Immunolesion-induced loss of cholinergic projection neurones promotes β-amyloidosis and tau hyperphosphorylation in the hippocampus of triple-transgenic mice." Neuropathology and Applied Neurobiology 40, no. 2 (January 21, 2014): 106–20. http://dx.doi.org/10.1111/nan.12050.

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31

Naneishvili, T., K. Rusadze, and R. Sakandelidze. "Chronic memantine treatment prevents short-term memory impairment caused by conjoint immunolesions of GABAergic and cholinergic medial septal neurons in rats." European Neuropsychopharmacology 26 (October 2016): S274—S275. http://dx.doi.org/10.1016/s0924-977x(16)31161-0.

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32

Chambon, C., V. Paban, C. Manrique, and B. Alescio-Lautier. "Behavioral and immunohistological effects of cholinergic damage in immunolesioned rats: Alteration of c-Fos and polysialylated neural cell adhesion molecule expression." Neuroscience 147, no. 4 (July 2007): 893–905. http://dx.doi.org/10.1016/j.neuroscience.2007.05.022.

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33

Apelt, J., R. Schliebs, M. Beck, S. Roβner, and V. Bigl Paul. "119 developmental expression of splicing variants of the amyloid precursor protein in rat brain regions and the effect of cholinergic immunolesion." International Journal of Developmental Neuroscience 14 (July 1996): 79. http://dx.doi.org/10.1016/0736-5748(96)80309-1.

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34

Roßner, S., J. R. Perez-Polo, R. G. Wiley, R. Schliebs, and V. Bigl. "Differential expression of immediate early genes in distinct layers of rat cerebral cortex after selective immunolesion of the forebrain cholinergic system." Journal of Neuroscience Research 38, no. 3 (June 15, 1994): 282–93. http://dx.doi.org/10.1002/jnr.490380306.

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35

Barefoot, H. C., H. F. Baker, and R. M. Ridley. "Synergistic effects of unilateral immunolesions of the cholinergic projections from the basal forebrain and contralateral ablations of the inferotemporal cortex and hippocampus in monkeys." Neuroscience 98, no. 2 (June 2000): 243–51. http://dx.doi.org/10.1016/s0306-4522(00)00131-7.

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36

Szigeti, Csaba, Norbert Bencsik, Aurel Janos Simonka, Adam Legradi, Peter Kasa, and Karoly Gulya. "Long-term effects of selective immunolesions of cholinergic neurons of the nucleus basalis magnocellularis on the ascending cholinergic pathways in the rat: A model for Alzheimer's disease." Brain Research Bulletin 94 (May 2013): 9–16. http://dx.doi.org/10.1016/j.brainresbull.2013.01.007.

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37

Fraley, Gregory S. "Immunolesions of Glucoresponsive Projections to the Arcuate Nucleus Alter Glucoprivic-Induced Alterations in Food Intake, Luteinizing Hormone Secretion, and GALP mRNA, but Not Sex Behavior in Adult Male Rats." Neuroendocrinology 83, no. 2 (2006): 97–105. http://dx.doi.org/10.1159/000094375.

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38

Fraley, G. S., and S. Ritter. "Immunolesion of Norepinephrine and Epinephrine Afferents to Medial Hypothalamus Alters Basal and 2-Deoxy-d-Glucose-Induced Neuropeptide Y and Agouti Gene-Related Protein Messenger Ribonucleic Acid Expression in the Arcuate Nucleus." Endocrinology 144, no. 1 (January 1, 2003): 75–83. http://dx.doi.org/10.1210/en.2002-220659.

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Abstract:

Abstract Neuropeptide Y (NPY) and agouti gene-related protein (AGRP) are orexigenic peptides of special importance for control of food intake. In situ hybridization studies have shown that NPY and AGRP mRNAs are increased in the arcuate nucleus of the hypothalamus (ARC) by glucoprivation. Other work has shown that glucoprivation stimulates food intake by activation of hindbrain glucoreceptor cells and requires the participation of rostrally projecting norepinephrine (NE) or epinephrine (E) neurons. Here we determine the role of hindbrain catecholamine afferents in glucoprivation-induced increase in ARC NPY and AGRP gene expression. The selective NE/E immunotoxin saporin-conjugated antidopamineβ-hydroxylase (anti-dβh) was microinjected into the medial hypothalamus and expression of AGRP and NPY mRNA was analyzed subsequently in the ARC under basal and glucoprivic conditions using 33P-labeled in situ hybridization. Saporin-conjugated anti-dβh virtually eliminated dβh-immunoreactive terminals in the ARC without causing nonspecific damage. These lesions significantly increased basal but eliminated 2-deoxy-d-glucose-induced increases in AGRP and NPY mRNA expression. Results indicate that hindbrain catecholaminergic neurons contribute to basal NPY and AGRP gene expression and mediate the responsiveness of NPY and AGRP neurons to glucose deficit. Our results also suggest that catecholamine neurons couple potent orexigenic neural circuitry within the hypothalamus with hindbrain glucose sensors that monitor brain glucose supply.

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39

DASHNIANI, M. G., M. A. BURJANADZE, T. L. NANEISHVILI, N. C. CHKHIKVISHVILI, G. V. BESELIA, L. B. KRUASHVILI, N. O. POCHKHIDZE, and M. R. CHIGHLADZE. "Exploratory Behavior and Recognition Memory in Medial Septal Electrolytic, Neuro- and Immunotoxic Lesioned Rats." Physiological Research, October 16, 2015, 755–67. http://dx.doi.org/10.33549/physiolres.932809.

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In the present study, the effect of the medial septal (MS) lesions on exploratory activity in the open field and the spatial and object recognition memory has been investigated. This experiment compares three types of MS lesions: electrolytic lesions that destroy cells and fibers of passage, neurotoxic – ibotenic acid lesions that spare fibers of passage but predominantly affect the septal noncholinergic neurons, and immunotoxin – 192 IgG-saporin infusions that only eliminate cholinergic neurons. The main results are: the MS electrolytic lesioned rats were impaired in habituating to the environment in the repeated spatial environment, but rats with immuno- or neurotoxic lesions of the MS did not differ from control ones; the MS electrolytic and ibotenic acid lesioned rats showed an increase in their exploratory activity to the objects and were impaired in habituating to the objects in the repeated spatial environment; rats with immunolesions of the MS did not differ from control rats; electrolytic lesions of the MS disrupt spatial recognition memory; rats with immuno- or neurotoxic lesions of the MS were normal in detecting spatial novelty; all of the MS-lesioned and control rats clearly reacted to the object novelty by exploring the new object more than familiar ones. Results observed across lesion techniques indicate that: (i) the deficits after nonselective damage of MS are limited to a subset of cognitive processes dependent on the hippocampus, (ii) MS is substantial for spatial, but not for object recognition memory – the object recognition memory can be supported outside the septohippocampal system; (iii) the selective loss of septohippocampal cholinergic or noncholinergic projections does not disrupt the function of the hippocampus to a sufficient extent to impair spatial recognition memory; (iv) there is dissociation between the two major components (cholinergic and noncholinergic) of the septohippocampal pathway in exploratory behavior assessed in the open field – the memory exhibited by decrements in exploration of repeated object presentations is affected by either electrolytic or ibotenic lesions, but not saporin.

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