paragraph_index int64 | sec string | p_has_citation int64 | cites string | citeids list | pmid int64 | cited_id string | sentences string | all_sent_cites list | sent_len int64 | sentence_batch_index int64 | sent_has_citation float64 | qc_fail bool | cited_sentence string | cites_in_sentence list | cln_sentence string | is_cap bool | is_alpha bool | ends_wp bool | cit_qc bool | lgtm bool | __index_level_0__ int64 |
|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|
10 | DISCUSSION | 1 | 11 | [
"R11"
] | 19,672,332 | pmid-18980509 | Regarding the relationship between subgingival deposits and the surrounding soft tissues, a recent endoscopical publication has interestingly described a pathological connection. | [
"11"
] | 178 | 38,716 | 0 | false | Regarding the relationship between subgingival deposits and the surrounding soft tissues, a recent endoscopical publication has interestingly described a pathological connection. | [] | Regarding the relationship between subgingival deposits and the surrounding soft tissues, a recent endoscopical publication has interestingly described a pathological connection. | true | true | true | true | true | 6,659 |
10 | DISCUSSION | 1 | 11 | [
"R11"
] | 19,672,332 | pmid-18980509 | In that study, both calculus and biofilm were in fact directly related to pocket wall inflammation as measured by increased redness of the pocket epithelium [11]. | [
"11"
] | 162 | 38,717 | 1 | false | In that study, both calculus and biofilm were in fact directly related to pocket wall inflammation as measured by increased redness of the pocket epithelium. | [
"11"
] | In that study, both calculus and biofilm were in fact directly related to pocket wall inflammation as measured by increased redness of the pocket epithelium. | true | true | true | true | true | 6,659 |
11 | DISCUSSION | 0 | null | null | 19,672,332 | null | Our findings disclose that a linear association between BOP and the presence of subgingival deposits is not particularly strong for each examined sites, anyway the data show how the amount of subgingival deposits rise with the incidence of BOP (Table 2). | null | 254 | 38,718 | 0 | false | null | null | Our findings disclose that a linear association between BOP and the presence of subgingival deposits is not particularly strong for each examined sites, anyway the data show how the amount of subgingival deposits rise with the incidence of BOP (Table 2). | true | true | true | true | true | 6,660 |
11 | DISCUSSION | 0 | null | null | 19,672,332 | null | Relative Risk analysis further demonstrates that the incidence of BOP could be up to 6 times with calculus and up to 8 times with plaque (Table 4). | null | 147 | 38,719 | 0 | false | null | null | Relative Risk analysis further demonstrates that the incidence of BOP could be up to 6 times with calculus and up to 8 times with plaque (Table 4). | true | true | true | true | true | 6,660 |
12 | DISCUSSION | 1 | 14 | [
"R14",
"R16"
] | 19,672,332 | pmid-3550036|pmid-7014822 | The present research shows a linear association between the increase in quantity of subgingival deposits and increase of PPD (Table 3), a result in accordance with previous findings [14-16]. | [
"14",
"16"
] | 190 | 38,720 | 0 | false | The present research shows a linear association between the increase in quantity of subgingival deposits and increase of PPD (Table 3), a result in accordance with previous findings. | [
"14-16"
] | The present research shows a linear association between the increase in quantity of subgingival deposits and increase of PPD (Table 3), a result in accordance with previous findings. | true | true | true | true | true | 6,661 |
12 | DISCUSSION | 1 | 14 | [
"R14",
"R16"
] | 19,672,332 | pmid-3550036|pmid-7014822 | The disto-vestibular site was the only area where it was not possible to observe a linear association between subgingival deposits and PPD. | [
"14",
"16"
] | 139 | 38,721 | 0 | false | The disto-vestibular site was the only area where it was not possible to observe a linear association between subgingival deposits and PPD. | [] | The disto-vestibular site was the only area where it was not possible to observe a linear association between subgingival deposits and PPD. | true | true | true | true | true | 6,661 |
12 | DISCUSSION | 1 | 14 | [
"R14",
"R16"
] | 19,672,332 | pmid-3550036|pmid-7014822 | The anatomical features of this area, that undeniably limit the endoscope handling, could be the reason of this finding. | [
"14",
"16"
] | 120 | 38,722 | 0 | false | The anatomical features of this area, that undeniably limit the endoscope handling, could be the reason of this finding. | [] | The anatomical features of this area, that undeniably limit the endoscope handling, could be the reason of this finding. | true | true | true | true | true | 6,661 |
12 | DISCUSSION | 1 | 14 | [
"R14",
"R16"
] | 19,672,332 | pmid-3550036|pmid-7014822 | In spite of its flexibility, the fiber of the endoscope finds few limitations in anatomical conditions like fairly small mouths and distal portion of the molar teeth. | [
"14",
"16"
] | 166 | 38,723 | 0 | false | In spite of its flexibility, the fiber of the endoscope finds few limitations in anatomical conditions like fairly small mouths and distal portion of the molar teeth. | [] | In spite of its flexibility, the fiber of the endoscope finds few limitations in anatomical conditions like fairly small mouths and distal portion of the molar teeth. | true | true | true | true | true | 6,661 |
12 | DISCUSSION | 1 | 14 | [
"R14",
"R16"
] | 19,672,332 | pmid-3550036|pmid-7014822 | This hypothesis is supported by the observation that among the other sites studied is the disto-lingual, the one with the lower significance (Table 3). | [
"14",
"16"
] | 151 | 38,724 | 0 | false | This hypothesis is supported by the observation that among the other sites studied is the disto-lingual, the one with the lower significance (Table 3). | [] | This hypothesis is supported by the observation that among the other sites studied is the disto-lingual, the one with the lower significance (Table 3). | true | true | true | true | true | 6,661 |
13 | DISCUSSION | 0 | null | null | 19,672,332 | null | Overall, it is possible to conclude that, when BOP is present especially in deep periodontal pockets after an adequate non-surgical therapy, a higher probability of residual deposits can be assumed. | null | 198 | 38,725 | 0 | false | null | null | Overall, it is possible to conclude that, when BOP is present especially in deep periodontal pockets after an adequate non-surgical therapy, a higher probability of residual deposits can be assumed. | true | true | true | true | true | 6,662 |
14 | DISCUSSION | 1 | 21 | [
"R21"
] | 19,672,332 | pmid-2179516 | Bleeding on probing was found to have high levels of specificity of residual deposits but low sensitivity values. | [
"21"
] | 113 | 38,726 | 0 | false | Bleeding on probing was found to have high levels of specificity of residual deposits but low sensitivity values. | [] | Bleeding on probing was found to have high levels of specificity of residual deposits but low sensitivity values. | true | true | true | true | true | 6,663 |
14 | DISCUSSION | 1 | 21 | [
"R21"
] | 19,672,332 | pmid-2179516 | These findings are in accordance with those reported by Sherman et al in 1990 on subgingival calculus [21]. | [
"21"
] | 107 | 38,727 | 1 | false | These findings are in accordance with those reported by Sherman et al in 1990 on subgingival calculus. | [
"21"
] | These findings are in accordance with those reported by Sherman et al in 1990 on subgingival calculus. | true | true | true | true | true | 6,663 |
15 | DISCUSSION | 1 | 22 | [
"R22",
"R23"
] | 19,672,332 | pmid-2179515|pmid-3283319 | The BOP’s sensitivity interestingly changes if the classes either of EBI or ECI are considered singularly. | [
"22",
"23"
] | 106 | 38,728 | 0 | false | The BOP’s sensitivity interestingly changes if the classes either of EBI or ECI are considered singularly. | [] | The BOP’s sensitivity interestingly changes if the classes either of EBI or ECI are considered singularly. | true | true | true | true | true | 6,664 |
15 | DISCUSSION | 1 | 22 | [
"R22",
"R23"
] | 19,672,332 | pmid-2179515|pmid-3283319 | As reported on Table 5, the sensitivity values increase with the index classes. | [
"22",
"23"
] | 79 | 38,729 | 0 | false | As reported on Table 5, the sensitivity values increase with the index classes. | [] | As reported on Table 5, the sensitivity values increase with the index classes. | true | true | true | true | true | 6,664 |
15 | DISCUSSION | 1 | 22 | [
"R22",
"R23"
] | 19,672,332 | pmid-2179515|pmid-3283319 | This observation confirms the previous statements of a possible level of periodontal soft tissues tolerance of subgingival calculus [22, 23]. | [
"22",
"23"
] | 141 | 38,730 | 0 | false | This observation confirms the previous statements of a possible level of periodontal soft tissues tolerance of subgingival calculus. | [
"22, 23"
] | This observation confirms the previous statements of a possible level of periodontal soft tissues tolerance of subgingival calculus. | true | true | true | true | true | 6,664 |
15 | DISCUSSION | 1 | 22 | [
"R22",
"R23"
] | 19,672,332 | pmid-2179515|pmid-3283319 | At the same time, it is possible to deduce that the presence of bleeding upon probing could be a quite good indicator of important amounts of residual deposits in the subgingival area. | [
"22",
"23"
] | 184 | 38,731 | 0 | false | At the same time, it is possible to deduce that the presence of bleeding upon probing could be a quite good indicator of important amounts of residual deposits in the subgingival area. | [] | At the same time, it is possible to deduce that the presence of bleeding upon probing could be a quite good indicator of important amounts of residual deposits in the subgingival area. | true | true | true | true | true | 6,664 |
16 | DISCUSSION | 0 | null | null | 19,672,332 | null | These results show that either soft or hard deposits are associated to the presence of BOP underlining their insight virulence. | null | 127 | 38,732 | 0 | false | null | null | These results show that either soft or hard deposits are associated to the presence of BOP underlining their insight virulence. | true | true | true | true | true | 6,665 |
17 | DISCUSSION | 1 | 24 | [
"R24",
"R25"
] | 19,672,332 | pmid-3476716|pmid-3263398 | However, further studies are recommended to determine if the present observations are true for a larger number of periodontal patients, since the sites within a mouth behave more alike than surfaces from different mouths [24, 25]. | [
"24",
"25"
] | 230 | 38,733 | 0 | false | However, further studies are recommended to determine if the present observations are true for a larger number of periodontal patients, since the sites within a mouth behave more alike than surfaces from different mouths. | [
"24, 25"
] | However, further studies are recommended to determine if the present observations are true for a larger number of periodontal patients, since the sites within a mouth behave more alike than surfaces from different mouths. | true | true | true | true | true | 6,666 |
18 | DISCUSSION | 0 | null | null | 19,672,332 | null | Finally, the results of this study suggest that the measurements obtained using the endoscope should be considered reliable in better predicting the disease establishment and progression, therefore, future studies investigating this hypothesis are required. | null | 257 | 38,734 | 0 | false | null | null | Finally, the results of this study suggest that the measurements obtained using the endoscope should be considered reliable in better predicting the disease establishment and progression, therefore, future studies investigating this hypothesis are required. | true | true | true | true | true | 6,667 |
0 | DISCUSSION | 0 | null | null | 18,852,291 | null | In this study, we used an adoptive transfer system to examine the capacity of IFN-γ–IFN-γR interactions to determine the sites of inflammation within the CNS. | null | 158 | 38,735 | 0 | false | null | null | In this study, we used an adoptive transfer system to examine the capacity of IFN-γ–IFN-γR interactions to determine the sites of inflammation within the CNS. | true | true | true | true | true | 6,668 |
0 | DISCUSSION | 0 | null | null | 18,852,291 | null | IFN-γ–expressing WT Th1 cells were found to initiate similar lesions in IFN-γR–null hosts as IFN-γ–null cells in WT hosts. | null | 122 | 38,736 | 0 | false | null | null | IFN-γ–expressing WT Th1 cells were found to initiate similar lesions in IFN-γR–null hosts as IFN-γ–null cells in WT hosts. | true | true | true | true | true | 6,668 |
0 | DISCUSSION | 0 | null | null | 18,852,291 | null | These data suggested that IFN-γ produced by the effector T cell population was selectively antiinflammatory in the cerebellum and brainstem. | null | 140 | 38,737 | 0 | false | null | null | These data suggested that IFN-γ produced by the effector T cell population was selectively antiinflammatory in the cerebellum and brainstem. | true | true | true | true | true | 6,668 |
0 | DISCUSSION | 0 | null | null | 18,852,291 | null | In the same mice, IFN-γ–IFN-γR interactions were necessary for inflammatory infiltration of the spinal cord. | null | 108 | 38,738 | 0 | false | null | null | In the same mice, IFN-γ–IFN-γR interactions were necessary for inflammatory infiltration of the spinal cord. | true | true | true | true | true | 6,668 |
0 | DISCUSSION | 0 | null | null | 18,852,291 | null | Together, these data demonstrate discrete regional responses to IFN-γ during neuroinflammation and suggest that these responses can shape the clinical manifestation of CNS autoimmunity. | null | 185 | 38,739 | 0 | false | null | null | Together, these data demonstrate discrete regional responses to IFN-γ during neuroinflammation and suggest that these responses can shape the clinical manifestation of CNS autoimmunity. | true | true | true | true | true | 6,668 |
1 | DISCUSSION | 0 | null | null | 18,852,291 | null | The experiments reported here reveal that the previously reported effects on EAE clinical outcome associated with IFN-γ deficiency are linked to two discrete functions of IFN-γ in EAE induction. | null | 194 | 38,740 | 0 | false | null | null | The experiments reported here reveal that the previously reported effects on EAE clinical outcome associated with IFN-γ deficiency are linked to two discrete functions of IFN-γ in EAE induction. | true | true | true | true | true | 6,669 |
1 | DISCUSSION | 0 | null | null | 18,852,291 | null | First, recognition of pathogenic T cell–produced IFN-γ is necessary to prevent inflammation of the cerebellum and brain stem. | null | 125 | 38,741 | 0 | false | null | null | First, recognition of pathogenic T cell–produced IFN-γ is necessary to prevent inflammation of the cerebellum and brain stem. | true | true | true | true | true | 6,669 |
1 | DISCUSSION | 0 | null | null | 18,852,291 | null | Adoptively transferred pathogenic Th1 cells appear to possess the necessary components for invasion of the cerebellum and brain stem as, in the absence of a host response to IFN-γ, these cells are fully capable of infiltrating and initiating cerebellar disease. | null | 261 | 38,742 | 0 | false | null | null | Adoptively transferred pathogenic Th1 cells appear to possess the necessary components for invasion of the cerebellum and brain stem as, in the absence of a host response to IFN-γ, these cells are fully capable of infiltrating and initiating cerebellar disease. | true | true | true | true | true | 6,669 |
1 | DISCUSSION | 0 | null | null | 18,852,291 | null | However, under ordinary circumstances the IFN-γ produced by the encephalitogenic cells is sufficient to prevent entry of the same cells into the cerebellum and brainstem. | null | 170 | 38,743 | 0 | false | null | null | However, under ordinary circumstances the IFN-γ produced by the encephalitogenic cells is sufficient to prevent entry of the same cells into the cerebellum and brainstem. | true | true | true | true | true | 6,669 |
1 | DISCUSSION | 0 | null | null | 18,852,291 | null | As such, IFN-γ–mediated protection of the cerebellum and brain stem represents an active process, acting under ordinary circumstances to prevent cerebellar inflammation. | null | 169 | 38,744 | 0 | false | null | null | As such, IFN-γ–mediated protection of the cerebellum and brain stem represents an active process, acting under ordinary circumstances to prevent cerebellar inflammation. | true | true | true | true | true | 6,669 |
1 | DISCUSSION | 0 | null | null | 18,852,291 | null | Second, recognition of encephalitogenic T cell–produced IFN-γ is required for the induction of inflammation within the spinal cord. | null | 131 | 38,745 | 0 | false | null | null | Second, recognition of encephalitogenic T cell–produced IFN-γ is required for the induction of inflammation within the spinal cord. | true | true | true | true | true | 6,669 |
1 | DISCUSSION | 0 | null | null | 18,852,291 | null | That is, in the absence of an IFN-γ signal, adoptively transferred cells are not capable of initiating spinal cord inflammation. | null | 128 | 38,746 | 0 | false | null | null | That is, in the absence of an IFN-γ signal, adoptively transferred cells are not capable of initiating spinal cord inflammation. | true | true | true | true | true | 6,669 |
1 | DISCUSSION | 0 | null | null | 18,852,291 | null | Interestingly, some mice showed symptoms of paralysis in the absence of measurable spinal cord infiltration. | null | 108 | 38,747 | 0 | false | null | null | Interestingly, some mice showed symptoms of paralysis in the absence of measurable spinal cord infiltration. | true | true | true | true | true | 6,669 |
1 | DISCUSSION | 0 | null | null | 18,852,291 | null | Unlike the ascending paralysis observed in classical EAE, the limb dysfunction that occurred in mice with the atypical clinical course was not necessarily caudal to rostral, as mice could demonstrate hind- and/or forelimb weakness and/or dystonia in the absence of tail involvement. | null | 282 | 38,748 | 0 | false | null | null | Unlike the ascending paralysis observed in classical EAE, the limb dysfunction that occurred in mice with the atypical clinical course was not necessarily caudal to rostral, as mice could demonstrate hind- and/or forelimb weakness and/or dystonia in the absence of tail involvement. | true | true | true | true | true | 6,669 |
1 | DISCUSSION | 0 | null | null | 18,852,291 | null | These findings suggest that the observed dystonia is induced by either inflammatory lesions within the spinal cord too small to be detected using standard histological techniques or, more likely, is induced by lesions within the cerebellum and/or brain stem. | null | 258 | 38,749 | 0 | false | null | null | These findings suggest that the observed dystonia is induced by either inflammatory lesions within the spinal cord too small to be detected using standard histological techniques or, more likely, is induced by lesions within the cerebellum and/or brain stem. | true | true | true | true | true | 6,669 |
1 | DISCUSSION | 0 | null | null | 18,852,291 | null | Together, these data reveal that encephalitogenic effector T cell cytokine production and concomitant host recognition of the cytokine plays a vital role in localizing the lesions associated with classical EAE. | null | 210 | 38,750 | 0 | false | null | null | Together, these data reveal that encephalitogenic effector T cell cytokine production and concomitant host recognition of the cytokine plays a vital role in localizing the lesions associated with classical EAE. | true | true | true | true | true | 6,669 |
2 | DISCUSSION | 1 | 6 | [
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] | Previous reports suggested that differences in cell localization followed from recognition of distinct antigens. | true | true | true | true | true | 6,670 |
2 | DISCUSSION | 1 | 6 | [
"bib6",
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"bib20",
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"20",
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] | 213 | 38,752 | 0 | false | Alternatively, it has been suggested that differences in cellular localization reflected anatomical differences in the capacity to support T cell invasion through breakdown of the blood–brain barrier. | [
"10, 20, 21"
] | Alternatively, it has been suggested that differences in cellular localization reflected anatomical differences in the capacity to support T cell invasion through breakdown of the blood–brain barrier. | true | true | true | true | true | 6,670 |
2 | DISCUSSION | 1 | 6 | [
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"bib10",
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] | 173 | 38,753 | 0 | false | Several groups previously demonstrated the induction of atypical axial-rotary disease in a variety of EAE models, and particularly within IFN-γ–deficient mice. | [
"6, 7, 22–24"
] | Several groups previously demonstrated the induction of atypical axial-rotary disease in a variety of EAE models, and particularly within IFN-γ–deficient mice. | true | true | true | true | true | 6,670 |
2 | DISCUSSION | 1 | 7 | [
"bib6",
"bib19",
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] | 296 | 38,754 | 1 | false | Reports suggested that the nature of the disease in IFN-γ–deficient systems reflected biased selection of the T cell repertoire, either through direct manipulation of the T cells themselves or by influencing the range of antigens presented to T cells during initiation of the immune response. | [
"7"
] | Reports suggested that the nature of the disease in IFN-γ–deficient systems reflected biased selection of the T cell repertoire, either through direct manipulation of the T cells themselves or by influencing the range of antigens presented to T cells during initiation of the immune response. | true | true | true | true | true | 6,670 |
2 | DISCUSSION | 1 | 12 | [
"bib6",
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"6",
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"12"
] | However, another group used a TCR transgenic mouse incapable of mediating T cell receptor recombination to demonstrate that T cells with identical specificities were capable of inducing either classical or atypical EAE depending on the conditions under which the cells were generated. | true | true | true | true | true | 6,670 |
2 | DISCUSSION | 1 | 6 | [
"bib6",
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3 | DISCUSSION | 0 | null | null | 18,852,291 | null | In this study we demonstrate, using adoptive transfer of WT Th1 cells into IFN-γR–deficient mice, that localization of T cells to specific regions of the brain relies on IFN-γ–IFN-γR interactions during the invasion process. | null | 224 | 38,757 | 0 | false | null | null | In this study we demonstrate, using adoptive transfer of WT Th1 cells into IFN-γR–deficient mice, that localization of T cells to specific regions of the brain relies on IFN-γ–IFN-γR interactions during the invasion process. | true | true | true | true | true | 6,671 |
3 | DISCUSSION | 0 | null | null | 18,852,291 | null | A single T cell preparation is able to induce atypical and/or classical disease depending on whether cells within the host are capable of recognizing IFN-γ. | null | 156 | 38,758 | 0 | false | null | null | A single T cell preparation is able to induce atypical and/or classical disease depending on whether cells within the host are capable of recognizing IFN-γ. | true | true | true | true | true | 6,671 |
3 | DISCUSSION | 0 | null | null | 18,852,291 | null | Thus, regional differences in T cell invasion represent regional differences in cytokine responsiveness rather than any intrinsic differences in the individual initiating T cells. | null | 179 | 38,759 | 0 | false | null | null | Thus, regional differences in T cell invasion represent regional differences in cytokine responsiveness rather than any intrinsic differences in the individual initiating T cells. | true | true | true | true | true | 6,671 |
4 | DISCUSSION | 0 | null | null | 18,852,291 | null | The mixing experiments demonstrate that the capacity for IFN-γ expression in only 50% of initiating T cells is sufficient to drive both protection of the cerebellum and infiltration of the spinal cord. | null | 201 | 38,760 | 0 | false | null | null | The mixing experiments demonstrate that the capacity for IFN-γ expression in only 50% of initiating T cells is sufficient to drive both protection of the cerebellum and infiltration of the spinal cord. | true | true | true | true | true | 6,672 |
4 | DISCUSSION | 0 | null | null | 18,852,291 | null | Further, protective IFN-γ production required antigenic stimulation of invading Th1 cells. | null | 90 | 38,761 | 0 | false | null | null | Further, protective IFN-γ production required antigenic stimulation of invading Th1 cells. | true | true | true | true | true | 6,672 |
4 | DISCUSSION | 0 | null | null | 18,852,291 | null | This suggests that both protection effects and infiltration are initiated by host cell recognition of an IFN-γ signal produced by a portion of CNS antigen-specific invading cells. | null | 179 | 38,762 | 0 | false | null | null | This suggests that both protection effects and infiltration are initiated by host cell recognition of an IFN-γ signal produced by a portion of CNS antigen-specific invading cells. | true | true | true | true | true | 6,672 |
4 | DISCUSSION | 0 | null | null | 18,852,291 | null | Invading cells are not necessarily discriminated on an individual basis, rather the overall group makeup determines tissue receptiveness to invasion. | null | 149 | 38,763 | 0 | false | null | null | Invading cells are not necessarily discriminated on an individual basis, rather the overall group makeup determines tissue receptiveness to invasion. | true | true | true | true | true | 6,672 |
5 | DISCUSSION | 1 | 17 | [
"bib17",
"bib17"
] | 18,852,291 | pmid-18278054|pmid-18278054 | This finding is particularly intriguing in light of a recent study that suggested that IL-17/IFN-γ–producing tissue invasive cell ratios determine the localization of T cell invasion and lesion formation (17). | [
"17",
"17"
] | 209 | 38,764 | 1 | false | This finding is particularly intriguing in light of a recent study that suggested that IL-17/IFN-γ–producing tissue invasive cell ratios determine the localization of T cell invasion and lesion formation. | [
"17"
] | This finding is particularly intriguing in light of a recent study that suggested that IL-17/IFN-γ–producing tissue invasive cell ratios determine the localization of T cell invasion and lesion formation. | true | true | true | true | true | 6,673 |
5 | DISCUSSION | 1 | 17 | [
"bib17",
"bib17"
] | 18,852,291 | pmid-18278054|pmid-18278054 | In contrast to the results demonstrated in the current study, Stromnes et al. | [
"17",
"17"
] | 77 | 38,765 | 0 | false | In contrast to the results demonstrated in the current study, Stromnes et al. | [] | In contrast to the results demonstrated in the current study, Stromnes et al. | true | true | true | true | true | 6,673 |
5 | DISCUSSION | 1 | 17 | [
"bib17",
"bib17"
] | 18,852,291 | pmid-18278054|pmid-18278054 | (17) found that IL-23–treated MOG35-55 cells were capable of inducing atypical EAE in WT mice. | [
"17",
"17"
] | 94 | 38,766 | 1 | false | found that IL-23–treated MOG35-55 cells were capable of inducing atypical EAE in WT mice. | [
"17"
] | found that IL-23–treated MOG35-55 cells were capable of inducing atypical EAE in WT mice. | false | true | true | true | false | 6,673 |
5 | DISCUSSION | 1 | 17 | [
"bib17",
"bib17"
] | 18,852,291 | pmid-18278054|pmid-18278054 | This capacity was linked to the change in the ratio of IL-17/IFN-γ T cell ratios as found in the CNS. | [
"17",
"17"
] | 101 | 38,767 | 0 | false | This capacity was linked to the change in the ratio of IL-17/IFN-γ T cell ratios as found in the CNS. | [] | This capacity was linked to the change in the ratio of IL-17/IFN-γ T cell ratios as found in the CNS. | true | true | true | true | true | 6,673 |
5 | DISCUSSION | 1 | 17 | [
"bib17",
"bib17"
] | 18,852,291 | pmid-18278054|pmid-18278054 | Given the large number of IFN-γ–producing cells still found in our IL-23–treated pathogenic T cells, it is perhaps not surprising that we found no capacity for IL-23–treated cells to induce atypical EAE. | [
"17",
"17"
] | 203 | 38,768 | 0 | false | Given the large number of IFN-γ–producing cells still found in our IL-23–treated pathogenic T cells, it is perhaps not surprising that we found no capacity for IL-23–treated cells to induce atypical EAE. | [] | Given the large number of IFN-γ–producing cells still found in our IL-23–treated pathogenic T cells, it is perhaps not surprising that we found no capacity for IL-23–treated cells to induce atypical EAE. | true | true | true | true | true | 6,673 |
6 | DISCUSSION | 1 | 17 | [
"bib17",
"bib17",
"bib17"
] | 18,852,291 | pmid-18278054|pmid-18278054|pmid-18278054 | The data presented here clearly demonstrate that interruption of IFN-γ/IFN-γR signaling resulted in redistribution of lesions from the classical pattern of spinal cord to the cerebellum and brain stem. | [
"17",
"17",
"17"
] | 201 | 38,769 | 0 | false | The data presented here clearly demonstrate that interruption of IFN-γ/IFN-γR signaling resulted in redistribution of lesions from the classical pattern of spinal cord to the cerebellum and brain stem. | [] | The data presented here clearly demonstrate that interruption of IFN-γ/IFN-γR signaling resulted in redistribution of lesions from the classical pattern of spinal cord to the cerebellum and brain stem. | true | true | true | true | true | 6,674 |
6 | DISCUSSION | 1 | 17 | [
"bib17",
"bib17",
"bib17"
] | 18,852,291 | pmid-18278054|pmid-18278054|pmid-18278054 | However, it remained possible that the disruption of IFN-γ/IFN-γR signaling lay upstream of a change in cytokine production capacity that resulted in the skewed IL-17/IFN-γ ratios reported by Stromnes et al. | [
"17",
"17",
"17"
] | 207 | 38,770 | 0 | false | However, it remained possible that the disruption of IFN-γ/IFN-γR signaling lay upstream of a change in cytokine production capacity that resulted in the skewed IL-17/IFN-γ ratios reported by Stromnes et al. | [] | However, it remained possible that the disruption of IFN-γ/IFN-γR signaling lay upstream of a change in cytokine production capacity that resulted in the skewed IL-17/IFN-γ ratios reported by Stromnes et al. | true | true | true | true | true | 6,674 |
6 | DISCUSSION | 1 | 17 | [
"bib17",
"bib17",
"bib17"
] | 18,852,291 | pmid-18278054|pmid-18278054|pmid-18278054 | (17) Examination of cytokine production in WT pathogenic T cells after transfer into IFN-γR revealed almost no change in IL-17/IFN-γ ratio, demonstrating that in our system an increased IL-17/IFN-γ ratio is not required to induce atypical disease. | [
"17",
"17",
"17"
] | 247 | 38,771 | 1 | false | Examination of cytokine production in WT pathogenic T cells after transfer into IFN-γR revealed almost no change in IL-17/IFN-γ ratio, demonstrating that in our system an increased IL-17/IFN-γ ratio is not required to induce atypical disease. | [
"17"
] | Examination of cytokine production in WT pathogenic T cells after transfer into IFN-γR revealed almost no change in IL-17/IFN-γ ratio, demonstrating that in our system an increased IL-17/IFN-γ ratio is not required to induce atypical disease. | true | true | true | true | true | 6,674 |
6 | DISCUSSION | 1 | 17 | [
"bib17",
"bib17",
"bib17"
] | 18,852,291 | pmid-18278054|pmid-18278054|pmid-18278054 | As such, although the demonstration that decreasing the fraction of IFN-γ–producing cells increases atypical disease is in accord with the recent observations of Stromnes et al. | [
"17",
"17",
"17"
] | 177 | 38,772 | 0 | false | As such, although the demonstration that decreasing the fraction of IFN-γ–producing cells increases atypical disease is in accord with the recent observations of Stromnes et al. | [] | As such, although the demonstration that decreasing the fraction of IFN-γ–producing cells increases atypical disease is in accord with the recent observations of Stromnes et al. | true | true | true | true | true | 6,674 |
6 | DISCUSSION | 1 | 17 | [
"bib17",
"bib17",
"bib17"
] | 18,852,291 | pmid-18278054|pmid-18278054|pmid-18278054 | (17), the induction of atypical disease in IFN-γR–deficient mice given WT cells indicates a very different mechanism active in our system. | [
"17",
"17",
"17"
] | 138 | 38,773 | 1 | false | , the induction of atypical disease in IFN-γR–deficient mice given WT cells indicates a very different mechanism active in our system. | [
"17"
] | , the induction of atypical disease in IFN-γR–deficient mice given WT cells indicates a very different mechanism active in our system. | false | false | true | true | false | 6,674 |
6 | DISCUSSION | 1 | 17 | [
"bib17",
"bib17",
"bib17"
] | 18,852,291 | pmid-18278054|pmid-18278054|pmid-18278054 | Although their results suggested that IL-17 was essential to the induction of atypical disease, the data shown by Stromnes et al. | [
"17",
"17",
"17"
] | 129 | 38,774 | 0 | false | Although their results suggested that IL-17 was essential to the induction of atypical disease, the data shown by Stromnes et al. | [] | Although their results suggested that IL-17 was essential to the induction of atypical disease, the data shown by Stromnes et al. | true | true | true | true | true | 6,674 |
6 | DISCUSSION | 1 | 17 | [
"bib17",
"bib17",
"bib17"
] | 18,852,291 | pmid-18278054|pmid-18278054|pmid-18278054 | (17) could also support the finding that dilution of IFN-γ–producing pathogenic T cells with pathogenic cells incapable of producing IFN-γ results in atypical disease, as reported in this paper. | [
"17",
"17",
"17"
] | 194 | 38,775 | 1 | false | could also support the finding that dilution of IFN-γ–producing pathogenic T cells with pathogenic cells incapable of producing IFN-γ results in atypical disease, as reported in this paper. | [
"17"
] | could also support the finding that dilution of IFN-γ–producing pathogenic T cells with pathogenic cells incapable of producing IFN-γ results in atypical disease, as reported in this paper. | false | true | true | true | false | 6,674 |
7 | DISCUSSION | 1 | 17 | [
"bib17",
"bib25",
"bib26"
] | 18,852,291 | pmid-18278054|pmid-17048276|pmid-16386239 | Interestingly, Stromnes et al. | [
"17",
"25",
"26"
] | 30 | 38,776 | 0 | false | Interestingly, Stromnes et al. | [] | Interestingly, Stromnes et al. | true | true | true | true | true | 6,675 |
7 | DISCUSSION | 1 | 17 | [
"bib17",
"bib25",
"bib26"
] | 18,852,291 | pmid-18278054|pmid-17048276|pmid-16386239 | (17) found that administration of IL-17RA–Fc protein preferentially blocked atypical disease induction. | [
"17",
"25",
"26"
] | 103 | 38,777 | 1 | false | found that administration of IL-17RA–Fc protein preferentially blocked atypical disease induction. | [
"17"
] | found that administration of IL-17RA–Fc protein preferentially blocked atypical disease induction. | false | true | true | true | false | 6,675 |
7 | DISCUSSION | 1 | 17 | [
"bib17",
"bib25",
"bib26"
] | 18,852,291 | pmid-18278054|pmid-17048276|pmid-16386239 | Combined with the cerebellar recruitment of host IL-17–producing cells seen in atypical disease, these data suggest that IL-17 plays a vital role in atypical EAE. | [
"17",
"25",
"26"
] | 162 | 38,778 | 0 | false | Combined with the cerebellar recruitment of host IL-17–producing cells seen in atypical disease, these data suggest that IL-17 plays a vital role in atypical EAE. | [] | Combined with the cerebellar recruitment of host IL-17–producing cells seen in atypical disease, these data suggest that IL-17 plays a vital role in atypical EAE. | true | true | true | true | true | 6,675 |
7 | DISCUSSION | 1 | 17 | [
"bib17",
"bib25",
"bib26"
] | 18,852,291 | pmid-18278054|pmid-17048276|pmid-16386239 | However, these data do not demonstrate that IL-17 is responsible for lesion localization to the cerebellum and brainstem but only that the atypical disease process requires IL-17 at some time during the pathogenesis process. | [
"17",
"25",
"26"
] | 224 | 38,779 | 0 | false | However, these data do not demonstrate that IL-17 is responsible for lesion localization to the cerebellum and brainstem but only that the atypical disease process requires IL-17 at some time during the pathogenesis process. | [] | However, these data do not demonstrate that IL-17 is responsible for lesion localization to the cerebellum and brainstem but only that the atypical disease process requires IL-17 at some time during the pathogenesis process. | true | true | true | true | true | 6,675 |
7 | DISCUSSION | 1 | 17 | [
"bib17",
"bib25",
"bib26"
] | 18,852,291 | pmid-18278054|pmid-17048276|pmid-16386239 | Indeed, it is perhaps more surprising that administration of the IL-17RA–Fc protein had so little effect on classical EAE incidence and symptoms in this model, a finding that contrasts with studies that reported a profound effect of IL-17 blockade on classical EAE induction (25, 26), than that IL-17 is required to driv... | [
"17",
"25",
"26"
] | 335 | 38,780 | 0 | false | Indeed, it is perhaps more surprising that administration of the IL-17RA–Fc protein had so little effect on classical EAE incidence and symptoms in this model, a finding that contrasts with studies that reported a profound effect of IL-17 blockade on classical EAE induction, than that IL-17 is required to drive atypica... | [
"25, 26"
] | Indeed, it is perhaps more surprising that administration of the IL-17RA–Fc protein had so little effect on classical EAE incidence and symptoms in this model, a finding that contrasts with studies that reported a profound effect of IL-17 blockade on classical EAE induction, than that IL-17 is required to drive atypica... | true | true | true | true | true | 6,675 |
7 | DISCUSSION | 1 | 17 | [
"bib17",
"bib25",
"bib26"
] | 18,852,291 | pmid-18278054|pmid-17048276|pmid-16386239 | Although it remains possible that IL-17 production is required for lesion localization to the brain after immunization with MOG97–114, it is equally possible that the necessary role for IL-17 in pathogenesis within the brain occurs after site selection. | [
"17",
"25",
"26"
] | 253 | 38,781 | 0 | false | Although it remains possible that IL-17 production is required for lesion localization to the brain after immunization with MOG97–114, it is equally possible that the necessary role for IL-17 in pathogenesis within the brain occurs after site selection. | [] | Although it remains possible that IL-17 production is required for lesion localization to the brain after immunization with MOG97–114, it is equally possible that the necessary role for IL-17 in pathogenesis within the brain occurs after site selection. | true | true | true | true | true | 6,675 |
8 | DISCUSSION | 0 | null | null | 18,852,291 | null | The differences in cell trafficking presented in the cell mixing experiments illustrate the discrete nature of the pro- and antiinflammatory (protective) aspects of IFN-γR signaling. | null | 182 | 38,782 | 0 | false | null | null | The differences in cell trafficking presented in the cell mixing experiments illustrate the discrete nature of the pro- and antiinflammatory (protective) aspects of IFN-γR signaling. | true | true | true | true | true | 6,676 |
8 | DISCUSSION | 0 | null | null | 18,852,291 | null | Although initial experiments left open the possibility that spinal cord invasion and cerebellar invasion were mutually exclusive, the histological and clinical data from the cell mixing experiments and BM chimeras clearly demonstrate the capacity for these two inflammatory pathways to occur simultaneously. | null | 307 | 38,783 | 0 | false | null | null | Although initial experiments left open the possibility that spinal cord invasion and cerebellar invasion were mutually exclusive, the histological and clinical data from the cell mixing experiments and BM chimeras clearly demonstrate the capacity for these two inflammatory pathways to occur simultaneously. | true | true | true | true | true | 6,676 |
8 | DISCUSSION | 0 | null | null | 18,852,291 | null | Thus, the IFN-γ–meditated protection of the cerebellum and brain stem and inflammation of the spinal cord are separable events. | null | 127 | 38,784 | 0 | false | null | null | Thus, the IFN-γ–meditated protection of the cerebellum and brain stem and inflammation of the spinal cord are separable events. | true | true | true | true | true | 6,676 |
9 | DISCUSSION | 1 | 27 | [
"bib27",
"bib28",
"bib27"
] | 18,852,291 | pmid-10337920|pmid-10076928|pmid-10337920 | The data presented here support previous studies that demonstrated differential responses to IFN-γ in discrete portions of the brain (27, 28). | [
"27",
"28",
"27"
] | 142 | 38,785 | 0 | false | The data presented here support previous studies that demonstrated differential responses to IFN-γ in discrete portions of the brain. | [
"27, 28"
] | The data presented here support previous studies that demonstrated differential responses to IFN-γ in discrete portions of the brain. | true | true | true | true | true | 6,677 |
9 | DISCUSSION | 1 | 27 | [
"bib27",
"bib28",
"bib27"
] | 18,852,291 | pmid-10337920|pmid-10076928|pmid-10337920 | These studies clearly demonstrated a differential capacity for IFN-γ responses within various sections of the brain after exogenous cytokine administration. | [
"27",
"28",
"27"
] | 156 | 38,786 | 0 | false | These studies clearly demonstrated a differential capacity for IFN-γ responses within various sections of the brain after exogenous cytokine administration. | [] | These studies clearly demonstrated a differential capacity for IFN-γ responses within various sections of the brain after exogenous cytokine administration. | true | true | true | true | true | 6,677 |
9 | DISCUSSION | 1 | 27 | [
"bib27",
"bib28",
"bib27"
] | 18,852,291 | pmid-10337920|pmid-10076928|pmid-10337920 | In contrast, the data presented here delineate differential responses to physiological levels of IFN-γ production. | [
"27",
"28",
"27"
] | 114 | 38,787 | 0 | false | In contrast, the data presented here delineate differential responses to physiological levels of IFN-γ production. | [] | In contrast, the data presented here delineate differential responses to physiological levels of IFN-γ production. | true | true | true | true | true | 6,677 |
9 | DISCUSSION | 1 | 27 | [
"bib27",
"bib28",
"bib27"
] | 18,852,291 | pmid-10337920|pmid-10076928|pmid-10337920 | This difference in methodology may explain the apparent discrepancies between IFN-γ–induced cell trafficking into the brainstem in the earlier study (27) and the IFN-γ–induced protection from cell trafficking observed in the brainstem in this study. | [
"27",
"28",
"27"
] | 249 | 38,788 | 1 | false | This difference in methodology may explain the apparent discrepancies between IFN-γ–induced cell trafficking into the brainstem in the earlier study and the IFN-γ–induced protection from cell trafficking observed in the brainstem in this study. | [
"27"
] | This difference in methodology may explain the apparent discrepancies between IFN-γ–induced cell trafficking into the brainstem in the earlier study and the IFN-γ–induced protection from cell trafficking observed in the brainstem in this study. | true | true | true | true | true | 6,677 |
10 | DISCUSSION | 1 | 29 | [
"bib29",
"bib33"
] | 18,852,291 | pmid-2461957|pmid-9628460 | The idea that regional CNS responses to cytokines are vital to the development of neuroinflammation also fits well with previous MS studies that demonstrated anti-myelin T cell responses in clinically silent individuals (29–33). | [
"29",
"33"
] | 228 | 38,789 | 0 | false | The idea that regional CNS responses to cytokines are vital to the development of neuroinflammation also fits well with previous MS studies that demonstrated anti-myelin T cell responses in clinically silent individuals. | [
"29–33"
] | The idea that regional CNS responses to cytokines are vital to the development of neuroinflammation also fits well with previous MS studies that demonstrated anti-myelin T cell responses in clinically silent individuals. | true | true | true | true | true | 6,678 |
10 | DISCUSSION | 1 | 29 | [
"bib29",
"bib33"
] | 18,852,291 | pmid-2461957|pmid-9628460 | The lack of clinical manifestation in individuals that are clearly capable of a vigorous antimyelin immune response could be explained by CNS responses that are either insufficient to allow inflammation or that are actively suppressive of inflammation. | [
"29",
"33"
] | 252 | 38,790 | 0 | false | The lack of clinical manifestation in individuals that are clearly capable of a vigorous antimyelin immune response could be explained by CNS responses that are either insufficient to allow inflammation or that are actively suppressive of inflammation. | [] | The lack of clinical manifestation in individuals that are clearly capable of a vigorous antimyelin immune response could be explained by CNS responses that are either insufficient to allow inflammation or that are actively suppressive of inflammation. | true | true | true | true | true | 6,678 |
10 | DISCUSSION | 1 | 29 | [
"bib29",
"bib33"
] | 18,852,291 | pmid-2461957|pmid-9628460 | Under this model, development of MS would rely on both induction of CNS specific autoimmune responses and the capacity of the CNS to respond to initial immune invasion. | [
"29",
"33"
] | 168 | 38,791 | 0 | false | Under this model, development of MS would rely on both induction of CNS specific autoimmune responses and the capacity of the CNS to respond to initial immune invasion. | [] | Under this model, development of MS would rely on both induction of CNS specific autoimmune responses and the capacity of the CNS to respond to initial immune invasion. | true | true | true | true | true | 6,678 |
11 | DISCUSSION | 0 | null | null | 18,852,291 | null | Interestingly, initial examination of IFN-γR1 within the cerebellum and spinal cord of both naive mice and mice with either typical or atypical EAE revealed little to no difference in expression between the two tissues. | null | 219 | 38,792 | 0 | false | null | null | Interestingly, initial examination of IFN-γR1 within the cerebellum and spinal cord of both naive mice and mice with either typical or atypical EAE revealed little to no difference in expression between the two tissues. | true | true | true | true | true | 6,679 |
11 | DISCUSSION | 0 | null | null | 18,852,291 | null | These data suggest that the capacity to bind IFN-γ is equivalent between the two tissues and that differential responses to IFN-γ within different regions reflect downstream components of the IFN-γ signaling pathway (unpublished data). | null | 235 | 38,793 | 0 | false | null | null | These data suggest that the capacity to bind IFN-γ is equivalent between the two tissues and that differential responses to IFN-γ within different regions reflect downstream components of the IFN-γ signaling pathway (unpublished data). | true | true | true | true | true | 6,679 |
12 | DISCUSSION | 1 | 34 | [
"bib34"
] | 18,852,291 | pmid-17709491 | The expression of both CXCL9 and CXCL10 were completely ablated in the CNS of mice that did not receive an IFN-γ signal from invading T cells. | [
"34"
] | 142 | 38,794 | 0 | false | The expression of both CXCL9 and CXCL10 were completely ablated in the CNS of mice that did not receive an IFN-γ signal from invading T cells. | [] | The expression of both CXCL9 and CXCL10 were completely ablated in the CNS of mice that did not receive an IFN-γ signal from invading T cells. | true | true | true | true | true | 6,680 |
12 | DISCUSSION | 1 | 34 | [
"bib34"
] | 18,852,291 | pmid-17709491 | These data demonstrate that in our model system, alternative inflammatory agents such as TNF-α are not sufficient to drive expression of CXCL9 and CXCL10. | [
"34"
] | 154 | 38,795 | 0 | false | These data demonstrate that in our model system, alternative inflammatory agents such as TNF-α are not sufficient to drive expression of CXCL9 and CXCL10. | [] | These data demonstrate that in our model system, alternative inflammatory agents such as TNF-α are not sufficient to drive expression of CXCL9 and CXCL10. | true | true | true | true | true | 6,680 |
12 | DISCUSSION | 1 | 34 | [
"bib34"
] | 18,852,291 | pmid-17709491 | The complete absence of these chemokines in the cerebellum of mice with atypical disease supports recent suggestions that these chemokines restrain T cells within the perivasculature of the cerebellum preventing development of atypical disease (34). | [
"34"
] | 249 | 38,796 | 1 | false | The complete absence of these chemokines in the cerebellum of mice with atypical disease supports recent suggestions that these chemokines restrain T cells within the perivasculature of the cerebellum preventing development of atypical disease. | [
"34"
] | The complete absence of these chemokines in the cerebellum of mice with atypical disease supports recent suggestions that these chemokines restrain T cells within the perivasculature of the cerebellum preventing development of atypical disease. | true | true | true | true | true | 6,680 |
13 | DISCUSSION | 1 | 35 | [
"bib35",
"bib36",
"bib37",
"bib38",
"bib41",
"bib42",
"bib43",
"bib44",
"bib45"
] | 18,852,291 | pmid-12690656|pmid-12451613|pmid-12140109|pmid-15262730|pmid-11959155|pmid-17657801|pmid-9670842|pmid-11784390|pmid-8905988 | The data presented here demonstrate the sufficiency and necessity for IFN-γ signaling during the invasion process to determine cellular localization within various anatomical components of the CNS. | [
"35",
"36",
"37",
"38",
"41",
"42",
"43",
"44",
"45"
] | 197 | 38,797 | 0 | false | The data presented here demonstrate the sufficiency and necessity for IFN-γ signaling during the invasion process to determine cellular localization within various anatomical components of the CNS. | [] | The data presented here demonstrate the sufficiency and necessity for IFN-γ signaling during the invasion process to determine cellular localization within various anatomical components of the CNS. | true | true | true | true | true | 6,681 |
13 | DISCUSSION | 1 | 35 | [
"bib35",
"bib36",
"bib37",
"bib38",
"bib41",
"bib42",
"bib43",
"bib44",
"bib45"
] | 18,852,291 | pmid-12690656|pmid-12451613|pmid-12140109|pmid-15262730|pmid-11959155|pmid-17657801|pmid-9670842|pmid-11784390|pmid-8905988 | The atypical EAE model may give useful information for cerebellar MS | [
"35",
"36",
"37",
"38",
"41",
"42",
"43",
"44",
"45"
] | 68 | 38,798 | 0 | false | The atypical EAE model may give useful information for cerebellar MS | [] | The atypical EAE model may give useful information for cerebellar MS | true | true | false | true | false | 6,681 |
13 | DISCUSSION | 1 | 35 | [
"bib35",
"bib36",
"bib37",
"bib38",
"bib41",
"bib42",
"bib43",
"bib44",
"bib45"
] | 18,852,291 | pmid-12690656|pmid-12451613|pmid-12140109|pmid-15262730|pmid-11959155|pmid-17657801|pmid-9670842|pmid-11784390|pmid-8905988 | but it may also tell us about other inflammatory diseases. | [
"35",
"36",
"37",
"38",
"41",
"42",
"43",
"44",
"45"
] | 58 | 38,799 | 0 | false | but it may also tell us about other inflammatory diseases. | [] | but it may also tell us about other inflammatory diseases. | false | true | true | true | false | 6,681 |
13 | DISCUSSION | 1 | 35 | [
"bib35",
"bib36",
"bib37",
"bib38",
"bib41",
"bib42",
"bib43",
"bib44",
"bib45"
] | 18,852,291 | pmid-12690656|pmid-12451613|pmid-12140109|pmid-15262730|pmid-11959155|pmid-17657801|pmid-9670842|pmid-11784390|pmid-8905988 | The atypical EAE findings described here may be a particularly good model of the human disease, Bickerstaff's brainstem encephalitis (BBE) (35). | [
"35",
"36",
"37",
"38",
"41",
"42",
"43",
"44",
"45"
] | 144 | 38,800 | 1 | false | The atypical EAE findings described here may be a particularly good model of the human disease, Bickerstaff's brainstem encephalitis (BBE). | [
"35"
] | The atypical EAE findings described here may be a particularly good model of the human disease, Bickerstaff's brainstem encephalitis (BBE). | true | true | true | true | true | 6,681 |
13 | DISCUSSION | 1 | 35 | [
"bib35",
"bib36",
"bib37",
"bib38",
"bib41",
"bib42",
"bib43",
"bib44",
"bib45"
] | 18,852,291 | pmid-12690656|pmid-12451613|pmid-12140109|pmid-15262730|pmid-11959155|pmid-17657801|pmid-9670842|pmid-11784390|pmid-8905988 | This is usually a monophasic inflammatory disease of the brainstem and cerebellum. | [
"35",
"36",
"37",
"38",
"41",
"42",
"43",
"44",
"45"
] | 82 | 38,801 | 0 | false | This is usually a monophasic inflammatory disease of the brainstem and cerebellum. | [] | This is usually a monophasic inflammatory disease of the brainstem and cerebellum. | true | true | true | true | true | 6,681 |
13 | DISCUSSION | 1 | 35 | [
"bib35",
"bib36",
"bib37",
"bib38",
"bib41",
"bib42",
"bib43",
"bib44",
"bib45"
] | 18,852,291 | pmid-12690656|pmid-12451613|pmid-12140109|pmid-15262730|pmid-11959155|pmid-17657801|pmid-9670842|pmid-11784390|pmid-8905988 | Patients have decreased consciousness, corticospinal tract abnormalities, multiple cranial nerve dysfunctions, and ataxia. | [
"35",
"36",
"37",
"38",
"41",
"42",
"43",
"44",
"45"
] | 122 | 38,802 | 0 | false | Patients have decreased consciousness, corticospinal tract abnormalities, multiple cranial nerve dysfunctions, and ataxia. | [] | Patients have decreased consciousness, corticospinal tract abnormalities, multiple cranial nerve dysfunctions, and ataxia. | true | true | true | true | true | 6,681 |
13 | DISCUSSION | 1 | 35 | [
"bib35",
"bib36",
"bib37",
"bib38",
"bib41",
"bib42",
"bib43",
"bib44",
"bib45"
] | 18,852,291 | pmid-12690656|pmid-12451613|pmid-12140109|pmid-15262730|pmid-11959155|pmid-17657801|pmid-9670842|pmid-11784390|pmid-8905988 | Its less severe form appears to be Miller Fisher syndrome (MFS), which has much less brainstem involvement and is defined by ophthalmoplegia, ataxia, and areflexia. | [
"35",
"36",
"37",
"38",
"41",
"42",
"43",
"44",
"45"
] | 164 | 38,803 | 0 | false | Its less severe form appears to be Miller Fisher syndrome (MFS), which has much less brainstem involvement and is defined by ophthalmoplegia, ataxia, and areflexia. | [] | Its less severe form appears to be Miller Fisher syndrome (MFS), which has much less brainstem involvement and is defined by ophthalmoplegia, ataxia, and areflexia. | true | true | true | true | true | 6,681 |
13 | DISCUSSION | 1 | 35 | [
"bib35",
"bib36",
"bib37",
"bib38",
"bib41",
"bib42",
"bib43",
"bib44",
"bib45"
] | 18,852,291 | pmid-12690656|pmid-12451613|pmid-12140109|pmid-15262730|pmid-11959155|pmid-17657801|pmid-9670842|pmid-11784390|pmid-8905988 | The differences between BBE and MFS, although controversial, may be a matter of the intensity of the immune response, given that both affect the same target areas of the brain (36, 37). | [
"35",
"36",
"37",
"38",
"41",
"42",
"43",
"44",
"45"
] | 185 | 38,804 | 0 | false | The differences between BBE and MFS, although controversial, may be a matter of the intensity of the immune response, given that both affect the same target areas of the brain. | [
"36, 37"
] | The differences between BBE and MFS, although controversial, may be a matter of the intensity of the immune response, given that both affect the same target areas of the brain. | true | true | true | true | true | 6,681 |
13 | DISCUSSION | 1 | 35 | [
"bib35",
"bib36",
"bib37",
"bib38",
"bib41",
"bib42",
"bib43",
"bib44",
"bib45"
] | 18,852,291 | pmid-12690656|pmid-12451613|pmid-12140109|pmid-15262730|pmid-11959155|pmid-17657801|pmid-9670842|pmid-11784390|pmid-8905988 | MFS in turn overlaps with Guillain Barre syndrome (GBS). | [
"35",
"36",
"37",
"38",
"41",
"42",
"43",
"44",
"45"
] | 56 | 38,805 | 0 | false | MFS in turn overlaps with Guillain Barre syndrome (GBS). | [] | MFS in turn overlaps with Guillain Barre syndrome (GBS). | true | true | true | true | true | 6,681 |
13 | DISCUSSION | 1 | 42 | [
"bib35",
"bib36",
"bib37",
"bib38",
"bib41",
"bib42",
"bib43",
"bib44",
"bib45"
] | 18,852,291 | pmid-12690656|pmid-12451613|pmid-12140109|pmid-15262730|pmid-11959155|pmid-17657801|pmid-9670842|pmid-11784390|pmid-8905988 | It is of interest that BBE, MFS, and a subset of GBS can have seemingly similar immune responses (all can have similar anti-GQ1B ganglioside antibodies) (38–41), yet have different inflammatory targeting (42). | [
"35",
"36",
"37",
"38",
"41",
"42",
"43",
"44",
"45"
] | 209 | 38,806 | 1 | false | It is of interest that BBE, MFS, and a subset of GBS can have seemingly similar immune responses (all can have similar anti-GQ1B ganglioside antibodies), yet have different inflammatory targeting. | [
"38–41",
"42"
] | It is of interest that BBE, MFS, and a subset of GBS can have seemingly similar immune responses (all can have similar anti-GQ1B ganglioside antibodies), yet have different inflammatory targeting. | true | true | true | true | true | 6,681 |
13 | DISCUSSION | 1 | 35 | [
"bib35",
"bib36",
"bib37",
"bib38",
"bib41",
"bib42",
"bib43",
"bib44",
"bib45"
] | 18,852,291 | pmid-12690656|pmid-12451613|pmid-12140109|pmid-15262730|pmid-11959155|pmid-17657801|pmid-9670842|pmid-11784390|pmid-8905988 | Differences in IFN-γ production in these diseases could account for these differences if they follow the same paradigm as described in our atypical EAE model. | [
"35",
"36",
"37",
"38",
"41",
"42",
"43",
"44",
"45"
] | 158 | 38,807 | 0 | false | Differences in IFN-γ production in these diseases could account for these differences if they follow the same paradigm as described in our atypical EAE model. | [] | Differences in IFN-γ production in these diseases could account for these differences if they follow the same paradigm as described in our atypical EAE model. | true | true | true | true | true | 6,681 |
13 | DISCUSSION | 1 | 43 | [
"bib35",
"bib36",
"bib37",
"bib38",
"bib41",
"bib42",
"bib43",
"bib44",
"bib45"
] | 18,852,291 | pmid-12690656|pmid-12451613|pmid-12140109|pmid-15262730|pmid-11959155|pmid-17657801|pmid-9670842|pmid-11784390|pmid-8905988 | As would be predicted by our disease paradigm, patients with MFS have lower IFN-γ production than patients with GBS (43). | [
"35",
"36",
"37",
"38",
"41",
"42",
"43",
"44",
"45"
] | 121 | 38,808 | 1 | false | As would be predicted by our disease paradigm, patients with MFS have lower IFN-γ production than patients with GBS. | [
"43"
] | As would be predicted by our disease paradigm, patients with MFS have lower IFN-γ production than patients with GBS. | true | true | true | true | true | 6,681 |
13 | DISCUSSION | 1 | 35 | [
"bib35",
"bib36",
"bib37",
"bib38",
"bib41",
"bib42",
"bib43",
"bib44",
"bib45"
] | 18,852,291 | pmid-12690656|pmid-12451613|pmid-12140109|pmid-15262730|pmid-11959155|pmid-17657801|pmid-9670842|pmid-11784390|pmid-8905988 | Also, cases have been described that started as one of these diseases that then changed or relapsed as a different disease (44, 45). | [
"35",
"36",
"37",
"38",
"41",
"42",
"43",
"44",
"45"
] | 132 | 38,809 | 0 | false | Also, cases have been described that started as one of these diseases that then changed or relapsed as a different disease. | [
"44, 45"
] | Also, cases have been described that started as one of these diseases that then changed or relapsed as a different disease. | true | true | true | true | true | 6,681 |
13 | DISCUSSION | 1 | 35 | [
"bib35",
"bib36",
"bib37",
"bib38",
"bib41",
"bib42",
"bib43",
"bib44",
"bib45"
] | 18,852,291 | pmid-12690656|pmid-12451613|pmid-12140109|pmid-15262730|pmid-11959155|pmid-17657801|pmid-9670842|pmid-11784390|pmid-8905988 | Fluctuations in IFN-γ production might be expected to produce exactly this scenario. | [
"35",
"36",
"37",
"38",
"41",
"42",
"43",
"44",
"45"
] | 84 | 38,810 | 0 | false | Fluctuations in IFN-γ production might be expected to produce exactly this scenario. | [] | Fluctuations in IFN-γ production might be expected to produce exactly this scenario. | true | true | true | true | true | 6,681 |
14 | DISCUSSION | 0 | null | null | 18,852,291 | null | The data presented here demonstrate the sufficiency and necessity for IFN-γ signaling during the invasion process to determine regional localization within various anatomical sites of the CNS. | null | 192 | 38,811 | 0 | false | null | null | The data presented here demonstrate the sufficiency and necessity for IFN-γ signaling during the invasion process to determine regional localization within various anatomical sites of the CNS. | true | true | true | true | true | 6,682 |
14 | DISCUSSION | 0 | null | null | 18,852,291 | null | An understanding of the exact mechanisms involved in cellular localization to the CNS and PNS may allow development of better methods for determining prognosis and modifying pathogenesis in many neurological diseases such as MS, BBE, MFS, and GBS. | null | 247 | 38,812 | 0 | false | null | null | An understanding of the exact mechanisms involved in cellular localization to the CNS and PNS may allow development of better methods for determining prognosis and modifying pathogenesis in many neurological diseases such as MS, BBE, MFS, and GBS. | true | true | true | true | true | 6,682 |
0 | INTRODUCTION | 1 | 1 | [
"B1",
"B2",
"B2",
"B1 B2 B3",
"B1",
"B3",
"B4",
"B5",
"B2"
] | 19,429,690 | pmid-10871379|pmid-18657049|pmid-18657049|pmid-10871379|pmid-18657049|pmid-16282471|pmid-10871379|pmid-16282471|pmid-16343488|pmid-15705566|pmid-18657049|pmid-10871379|pmid-16282471|pmid-18657049 | Small heterodimer partner interacting leucine zipper protein (SMILE) belongs to basic region leucine zipper (bZIP) family (1,2). | [
"1",
"2",
"2",
"1–3",
"1",
"3",
"4",
"5",
"2"
] | 128 | 38,813 | 0 | false | Small heterodimer partner interacting leucine zipper protein (SMILE) belongs to basic region leucine zipper (bZIP) family. | [
"1,2"
] | Small heterodimer partner interacting leucine zipper protein (SMILE) belongs to basic region leucine zipper (bZIP) family. | true | true | true | true | true | 6,683 |
0 | INTRODUCTION | 1 | 2 | [
"B1",
"B2",
"B2",
"B1 B2 B3",
"B1",
"B3",
"B4",
"B5",
"B2"
] | 19,429,690 | pmid-10871379|pmid-18657049|pmid-18657049|pmid-10871379|pmid-18657049|pmid-16282471|pmid-10871379|pmid-16282471|pmid-16343488|pmid-15705566|pmid-18657049|pmid-10871379|pmid-16282471|pmid-18657049 | SMILE gene produces two isoforms, SMILE-L (long isoform of SMILE, also known as CREBZF) and SMILE-S (short isoform of SMILE, previously known as Zhangfei), from alternative usage of initiation codons (2). | [
"1",
"2",
"2",
"1–3",
"1",
"3",
"4",
"5",
"2"
] | 204 | 38,814 | 1 | false | SMILE gene produces two isoforms, SMILE-L (long isoform of SMILE, also known as CREBZF) and SMILE-S (short isoform of SMILE, previously known as Zhangfei), from alternative usage of initiation codons. | [
"2"
] | SMILE gene produces two isoforms, SMILE-L (long isoform of SMILE, also known as CREBZF) and SMILE-S (short isoform of SMILE, previously known as Zhangfei), from alternative usage of initiation codons. | true | true | true | true | true | 6,683 |
0 | INTRODUCTION | 1 | 1–3 | [
"B1",
"B2",
"B2",
"B1 B2 B3",
"B1",
"B3",
"B4",
"B5",
"B2"
] | 19,429,690 | pmid-10871379|pmid-18657049|pmid-18657049|pmid-10871379|pmid-18657049|pmid-16282471|pmid-10871379|pmid-16282471|pmid-16343488|pmid-15705566|pmid-18657049|pmid-10871379|pmid-16282471|pmid-18657049 | Although SMILE has the ability to homodimerize like other bZIP proteins, it cannot bind to DNA as a homodimer (1–3). | [
"1",
"2",
"2",
"1–3",
"1",
"3",
"4",
"5",
"2"
] | 116 | 38,815 | 1 | false | Although SMILE has the ability to homodimerize like other bZIP proteins, it cannot bind to DNA as a homodimer. | [
"1–3"
] | Although SMILE has the ability to homodimerize like other bZIP proteins, it cannot bind to DNA as a homodimer. | true | true | true | true | true | 6,683 |
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