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| 14556941 | MOG | MOG | 1.9 | clinical features of MS-like disease in myelin oligodendrocyte glycoprotein (MOG)-induced MOG -induced EAE in mice | |  |
| 14556941 | MOG | MOG-induced | 1.9 | appearance of clinical symptoms dramatically reduced the clinical severity of MOG-induced EAE while all the MOG-immunized control mice developed significant clinical | | |
| 14556941 | MOG | MOG-immunized | 1.9 | reduced the clinical severity of MOG-induced EAE while all the MOG-immunized control mice developed significant clinical manifestations | | |
| 14556941 | MOG | MOG-treated | 1.9 | demonstrated only mild focal inflammation and less demyelination compared to MOG-treated mice using histological methods | | |
| 14556941 | MOG | MOG | 1.9 | in the immune system potency as T-cell proliferative responses to MOG were similar in both groups | | |
| 14556941 | MOG | MOG-induced | 1.9 | damage in the CNS and attenuate the clinical severity of MOG-induced EAE | | |
| 14556941 | MOG | MOG | 1.9 | insult to neurons and axons in myelin oligodendrocyte glycoprotein (MOG)-induced MOG -induced EAE in C3H.SW mice a chronic model which appears | | |
| 14556941 | MOG | MOG | 1.9 | with the peptide encompassing amino acids 35_amp_#x2013 55 of rat MOG | | |
| 14556941 | MOG | MOG | 1.9 | with a 200 _amp_#x3bc l emulsion containing 75 _amp_#x3bc g MOG peptide (300 300 _amp_#x3bc g in the case of C57/bl) | | |
| 14556941 | MOG | MOG | 1.9 | Spinal cords from riluzole-treated and MOG mice were dissected 28 days after immunization with pMOG 35_amp_#x2013 | | |
| 14556941 | MOG | MOG- | 1.9 | severity of EAE following pMOG 35_amp_#x2013 55 induction between the MOG- and riluzole-treated mice groups was evaluated using Student_amp_#x2019 s t | | |
| 14556941 | MOG | MOG | 1.9 | when it was administered together with the first injection of MOG was shown to be beneficial in reducing clinical symptoms ( | | |
| 14556941 | MOG | MOG | 1.9 | twice a day was given 14 days after the first MOG injection at the appearance of symptoms | | |
| 14556941 | MOG | MOG | 1.9 | riluzole-treated mice ( n =10 as measured 30 days after MOG injection was much lower than for the MOG-treated mice (1.18_amp_#xb1;0.47 | | |
| 14556941 | MOG | MOG-treated | 1.9 | days after MOG injection was much lower than for the MOG-treated mice (1.18_amp_#xb1;0.47 1.18_amp_#xb1 0.47 vs 2.31_amp_#xb1 0.23 P _amp_#x3c 0.03 | | |
| 14556941 | MOG | MOG | 1.9 | Twenty-seven days after MOG injection there were marked differences between the control (CC) CC | | |
| 14556941 | MOG | MOG-induced | 1.9 | of the 10 riluzole-treated (RR) RR mice remained resistant to MOG-induced EAE and remained disease free ( P =0.001 using _amp_#x3c7 | | |
| 14556941 | MOG | MOG | 1.9 | Representative H_amp_#x26 E staining of spinal cords from five immunized MOG mice 28 days after immunization revealed marked multifocal lymphohistiocytic inflammation | | |
| 14556941 | MOG | MOG-treated | 1.9 | in the number of lymphocytes in the spinal cord of MOG-treated mice compared to naive mice as indicated by arbitrary units | | |
| 14556941 | MOG | MOG-treated | 1.9 | was dramatically reduced in riluzole-treated mice as compared to the MOG-treated group (0.036_amp_#xb1;0.007 0.036_amp_#xb1 0.007 vs 0.072_amp_#xb1 0.01 P _amp_#x3c 0.01 | | |
| 14556941 | MOG | MOG-treated | 1.9 | Inflammation in the MOG-treated mice was associated with myelin loss as indicated by LFB | | |
| 14556941 | MOG | MOG-treated | 1.9 | Axonal staining of spinal cord sections from MOG-treated mice showed severe axonal damage using Bielshowesky_amp_#x2019 s method ( | | |
| 14556941 | MOG | MOG-treated | 1.9 | we found marked axonal loss in the spinal cords of MOG-treated mice compared to naive mice (0.44_amp_#xb1;0.03 0.44_amp_#xb1 0.03 vs 0.65_amp_#xb1 | | |
| 14556941 | MOG | MOG-treated | 1.9 | the riluzole-treated mice axonal integrity was preserved compared to the MOG-treated group (0.54_amp_#xb1;0.02 0.54_amp_#xb1 0.02 vs 0.44_amp_#xb1 0.03 P _amp_#x3c 0.02 | | |
| 14556941 | MOG | MOG-treated | 1.9 | Based on such testing the spinal cords of MOG-treated mice showed an increase of abnormal dephosphorylated NF-H ( Fig | | |
| 14556941 | MOG | MOG-treated | 1.9 | Pro Plus analysis we found massive axonal damage in the MOG-treated mice compared to naive mice (0.03_amp_#xb1;0.003 0.03_amp_#xb1 0.003 vs 0.0005_amp_#xb1 | | |
| 14556941 | MOG | MOG-treated | 1.9 | in the area stained by SMI-32 as compared to the MOG-treated group (0.0006_amp_#xb1;0.0001 0.0006_amp_#xb1 0.0001 vs 0.03_amp_#xb1 0.003 P _amp_#x3c 0.0001 | | |
| 14556941 | MOG | MOG-treated | 1.9 | We compared the T-cell response in the riluzole- and MOG-treated mice groups to rule out the possibility that the observed | | |
| 14556941 | MOG | MOG-treated | 1.9 | Riluzole-treated and MOG-treated mice (three three in each group were immunized with pMOG | | |
| 14556941 | MOG | MOG | 1.9 | Fig 4 the in vitro primary proliferative response of both MOG and riluzole-treated mice against pMOG 35_amp_#x2013 55 was similar | | |
| 14556941 | MOG | MOG-induced | 1.9 | study shows that riluzole-treated C3H.SW mice are highly resistant to MOG-induced chronic EAE | | |
| 14556941 | MOG | MOG-immunized | 1.9 | disruption indicating a large increase of abnormally dephosphorylated NF-H in MOG-immunized spinal cords in the riluzole-treated mice there was minimal abnormal | | |
| 14556941 | MOG | MOG-immunized | 1.9 | for pMOG 35_amp_#x2013 55 was similar in the riluzole-treated and MOG-immunized mice suggesting that the beneficial effect of riluzole is probably | | |
| 17569578 | MOG | MOG | 1.9 | demonstrated in the myelin oligodendrocyte glycoprotein peptide 35_amp_#x2013 55 (MOG MOG 35_amp_#x2013 55 induced EAE model that activation of PPAR_amp_#x3b3 limits | | |
| 17569578 | MOG | MOG | 1.9 | then the first to show that oral pioglitzone treatment of MOG 35_amp_#x2013 55 -immunized mice not only reduced brain inflammation and | | |
| 17569578 | MOG | MOG | 1.9 | as pioglitazone or GW7845 within the first two weeks of MOG 35_amp_#x2013 55 -induced EAE a phenomenon that may be explained | | |
| 17569578 | MOG | MOG | 1.9 | suppressed the IFN_amp_#x3b3 secretion of splenic T cells stimulated by MOG 35_amp_#x2013 55 in vitro 61 | | |
| 17569578 | MOG | MOG | 1.9 | levels for MIP1_amp_#x3b1 and RANTES both key chemokines in the MOG 35_amp_#x2013 55 induced EAE model has been observed 61 | | |
| 17569578 | MOG | MOG | 1.9 | an increase in T cell proliferation and Th1 response upon MOG peptide stimulation when compared to PPAR_amp_#x3b3 wild type littermate controls | | |
| 17569578 | MOG | MOG | 1.9 | PPAR_amp_#x3b2;/_amp_#x3b4; PPAR_amp_#x3b2 _amp_#x3b4 agonist GW0742 exerted beneficial effects in the MOG 35_amp_#x2013 55 induced EAE model 136 | | |
| 17569578 | MOG | MOG | 1.9 | PPAR_amp_#x3b1 agonist reduced the IgG response in mice immunized with MOG 35_amp_#x2013 55 and complete Freund_amp_#x2019 s adjuvant 43 | | |
| 17569578 | MOG | MOG | 1.9 | impaired generation of IFN_amp_#x3b3 TNF_amp_#x3b1 and IL-6 in response to MOG peptide in vitro restimulation | | |
| 14556941 | myelin oligodendrocyte glycoprotein | myelin oligodendrocyte glycoprotein | 1.0 | encephalomyelitis eae the conventional model of ms. therefore we examined whether riluzole an inhibitor of glutamate transmission affects the pathogenesis and clinical features of ms like disease in myelin oligodendrocyte glycoprotein mog induced eae in mice. | | |
| 14556941 | myelin oligodendrocyte glycoprotein | myelin oligodendrocyte glycoprotein | 1.0 | we therefore investigated the clinical effects of riluzole in reducing the insult to neurons and axons in myelin oligodendrocyte glycoprotein mog induced eae in c3h.sw mice a chronic model which appears to resemble the clinical course of progressive ms better than the other disorders induced by auto antigens [ 27 ]. | | |
| 17569578 | myelin oligodendrocyte glycoprotein | myelin oligodendrocyte glycoprotein | 1.0 | using the synthetic ppar_amp_#x3b3; ligand troglitazone niino et al. first demonstrated in the myelin oligodendrocyte glycoprotein peptide 35_amp_#x2013;55 mog 35_amp_#x2013;55 induced eae model that activation of ppar_amp_#x3b3; limits the development of clinical symptoms and infiltration of brain parenchyma by peripherial leuk | | |