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10.1002%2Fglia.21117
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_:vb17571953 _:vb17571948 _:vb17571932 _:vb17571973
Subject Item
_:vb17571932
rdf:type
n5:Section
dc:title
introduction
n5:contains
_:vb17571934 _:vb17571935 _:vb17571933 _:vb17571946 _:vb17571947 _:vb17571944 _:vb17571945 _:vb17571938 _:vb17571939 _:vb17571936 _:vb17571937 _:vb17571942 _:vb17571943 _:vb17571940 _:vb17571941
Subject Item
_:vb17571933
rdf:type
n2:Context
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Although many therapeutic approaches have been explored, there has been no major improvement in survival over the last 30 years (DeAngelis, >>2001<<; Legler et al., 1999).
n2:mentions
n3:11150363
Subject Item
_:vb17571934
rdf:type
n2:Context
rdf:value
Although many therapeutic approaches have been explored, there has been no major improvement in survival over the last 30 years (DeAngelis, 2001; Legler et al., >>1999<<).
n2:mentions
n3:10451443
Subject Item
_:vb17571935
rdf:type
n2:Context
rdf:value
Gliomas are infiltrated by MG/MP, and the extent of MG/MP infiltration correlates positively with malignancy (Morimura et al., >>1990<<; Morris and Esiri, 1991; Roggendorf et al., 1996). Microglia are capable of antigen presentation to T cells patrolling the CNS (Kreutzberg, 1996).
n2:mentions
n3:2399810
Subject Item
_:vb17571936
rdf:type
n2:Context
rdf:value
Gliomas are infiltrated by MG/MP, and the extent of MG/MP infiltration correlates positively with malignancy (Morimura et al., 1990; Morris and Esiri, >>1991<<; Roggendorf et al., 1996). Microglia are capable of antigen presentation to T cells patrolling the CNS (Kreutzberg, 1996).
n2:mentions
n3:2027027
Subject Item
_:vb17571937
rdf:type
n2:Context
rdf:value
Gliomas are infiltrated by MG/MP, and the extent of MG/MP infiltration correlates positively with malignancy (Morimura et al., 1990; Morris and Esiri, 1991; Roggendorf et al., >>1996<<). Microglia are capable of antigen presentation to T cells patrolling the CNS (Kreutzberg, 1996).
n2:mentions
n3:8870831
Subject Item
_:vb17571938
rdf:type
n2:Context
rdf:value
Microglia are capable of antigen presentation to T cells patrolling the CNS (Kreutzberg, >>1996<<). Upon injury, microglia undergo activation characterized by changes in morphology, gene expression, proliferation, phagocytic capacity, and migration towards the injury site (Kreutzberg, 1996; Streit et al., 1999).
n2:mentions
n3:8843599
Subject Item
_:vb17571939
rdf:type
n2:Context
rdf:value
Upon injury, microglia undergo activation characterized by changes in morphology, gene expression, proliferation, phagocytic capacity, and migration towards the injury site (Kreutzberg, >>1996<<; Streit et al., 1999).
n2:mentions
n3:8843599
Subject Item
_:vb17571940
rdf:type
n2:Context
rdf:value
Upon injury, microglia undergo activation characterized by changes in morphology, gene expression, proliferation, phagocytic capacity, and migration towards the injury site (Kreutzberg, 1996; Streit et al., >>1999<<).
n2:mentions
n3:10221782
Subject Item
_:vb17571941
rdf:type
n2:Context
rdf:value
Moreover, GIMs have been proposed to promote glioma growth by secreting growth factors, immune-suppressive cytokines and angiogenic factors (Alterman and Stanley, >>1994<<; Demuth et al., 2007; Galasso et al., 2000; Lafuente et al., 1999; Wagner et al., 1999; Wesolowska et al., 2008), thus stimulating interest in therapies that modulate MG/MP activity/function.
n2:mentions
n3:8086034
Subject Item
_:vb17571942
rdf:type
n2:Context
rdf:value
Moreover, GIMs have been proposed to promote glioma growth by secreting growth factors, immune-suppressive cytokines and angiogenic factors (Alterman and Stanley, 1994; Demuth et al., >>2007<<; Galasso et al., 2000; Lafuente et al., 1999; Wagner et al., 1999; Wesolowska et al., 2008), thus stimulating interest in therapies that modulate MG/MP activity/function.
n2:mentions
n3:17406030
Subject Item
_:vb17571943
rdf:type
n2:Context
rdf:value
Moreover, GIMs have been proposed to promote glioma growth by secreting growth factors, immune-suppressive cytokines and angiogenic factors (Alterman and Stanley, 1994; Demuth et al., 2007; Galasso et al., >>2000<<; Lafuente et al., 1999; Wagner et al., 1999; Wesolowska et al., 2008), thus stimulating interest in therapies that modulate MG/MP activity/function.
n2:mentions
n3:10683275
Subject Item
_:vb17571944
rdf:type
n2:Context
rdf:value
Moreover, GIMs have been proposed to promote glioma growth by secreting growth factors, immune-suppressive cytokines and angiogenic factors (Alterman and Stanley, 1994; Demuth et al., 2007; Galasso et al., 2000; Lafuente et al., >>1999<<; Wagner et al., 1999; Wesolowska et al., 2008), thus stimulating interest in therapies that modulate MG/MP activity/function.
n2:mentions
n3:10691304
Subject Item
_:vb17571945
rdf:type
n2:Context
rdf:value
have been proposed to promote glioma growth by secreting growth factors, immune-suppressive cytokines and angiogenic factors (Alterman and Stanley, 1994; Demuth et al., 2007; Galasso et al., 2000; Lafuente et al., 1999; Wagner et al., >>1999<<; Wesolowska et al., 2008), thus stimulating interest in therapies that modulate MG/MP activity/function.
n2:mentions
n3:10360813
Subject Item
_:vb17571946
rdf:type
n2:Context
rdf:value
glioma growth by secreting growth factors, immune-suppressive cytokines and angiogenic factors (Alterman and Stanley, 1994; Demuth et al., 2007; Galasso et al., 2000; Lafuente et al., 1999; Wagner et al., 1999; Wesolowska et al., >>2008<<), thus stimulating interest in therapies that modulate MG/MP activity/function. However, such approaches yielded conflicting results:
n2:mentions
n3:17684491
Subject Item
_:vb17571947
rdf:type
n2:Context
rdf:value
oligonucleotides, which stimulate MG/MP, induced glioma apoptosis and prolonged survival times of tumor-bearing animals in one report, whereas the same approach caused increased animal tumor size in others (El Andaloussi et al., >>2006<<; Ginzkey et al., 2009).
n2:mentions
n3:16906541
Subject Item
_:vb17571948
rdf:type
n5:Section
dc:title
materials and methods
n5:contains
_:vb17571950 _:vb17571951 _:vb17571949 _:vb17571952
Subject Item
_:vb17571949
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n2:Context
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CD11b-HSVTK transgenic mice were described previously (Heppner et al., >>2005<<). Female CD11b-HSVTK (+/−) mice were bred with male C57BL/6 mice and the offspring genotyped by PCR using primers 5′-GACTTCCGTGGCTTCTTGCTGC-3′ and 5′-GTGCTGGCATTACAGGCGTGAG-3′.
n2:mentions
n3:15665833
Subject Item
_:vb17571950
rdf:type
n2:Context
rdf:value
Mixed cortical cultures from newborn C57BL/6 mice (day 0–3) were made using standard protocols (Rogove and Tsirka, >>1998<<). Ten days after plating, primary microglia were isolated by treatment with 15mM lidocaine (Sigma) and gentle rocking.
n2:mentions
n3:9427623
Subject Item
_:vb17571951
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n2:Context
rdf:value
In brief, after isolation of primary microglia, the cells were resuspended at a density of 5×104 cells/ml in DMEM with 1% FBS and 20μg/ml mini-ruby (Invitrogen) (Ullrich et al., >>2001<<). After 48 hours, the medium was removed and 2×104 GL261-EGFP cells seeded on top of the microglia in DMEM with 10% FBS and desired treatments, such as 150μg/ml tuftsin, MIF/TKP (Bachem), or 4μg/ml CCL21 neutralizing antibody (PeproTech).
n2:mentions
n3:11781564
Subject Item
_:vb17571952
rdf:type
n2:Context
rdf:value
3×104 GL261-EGFP cells were delivered in 1μl PBS at a depth of 3mm over 2minutes (modified from El Andaloussi et al., >>2006<<).
n2:mentions
n3:16906541
Subject Item
_:vb17571953
rdf:type
n5:Section
dc:title
results
n5:contains
_:vb17571966 _:vb17571967 _:vb17571964 _:vb17571965 _:vb17571962 _:vb17571963 _:vb17571960 _:vb17571961 _:vb17571958 _:vb17571959 _:vb17571956 _:vb17571957 _:vb17571954 _:vb17571955 _:vb17571972 _:vb17571970 _:vb17571971 _:vb17571968 _:vb17571969
Subject Item
_:vb17571954
rdf:type
n2:Context
rdf:value
Resting microglia appear rod-shaped in culture, and upon activation, they transform into an ameboid shape with pseudopodia (Siao and Tsirka, >>2002<<). At time 0, resting microglia had elongated cell bodies and thin processes; no change in the morphology was obvious 24 h later in the same medium (microglia, DMEM+1% FBS) or in GL261 control medium (DMEM+10% FBS) (Fig. 1A, B). When
n2:mentions
n3:11978811
Subject Item
_:vb17571955
rdf:type
n2:Context
rdf:value
Iba1 (ionized calcium binding adaptor molecule 1) is a MG/MP marker that is upregulated upon activation (Ito et al., >>1998<<). Iba1 expression levels increased 3–4 fold with GCM treatment (Fig. 1B, C), concomitant with morphological changes. However, no increase in Iba1 was observed when the microglia switched from 1% to 10% FBS, or were cultured with boiled
n2:mentions
n3:9630473
Subject Item
_:vb17571956
rdf:type
n2:Context
rdf:value
As part of the innate immune response, they phagocytose pathogens and release proteases, cytokines and molecules that function to protect the host (Kreutzberg, >>1996<<); this function may be compromised in a glioma-harboring environment (Hussain et al., 2006).
n2:mentions
n3:8843599
Subject Item
_:vb17571957
rdf:type
n2:Context
rdf:value
immune response, they phagocytose pathogens and release proteases, cytokines and molecules that function to protect the host (Kreutzberg, 1996); this function may be compromised in a glioma-harboring environment (Hussain et al., >>2006<<). To directly assess the effect of glioma cells on microglial function, we co-cultured rhodamine-labeled microglia and glioma GL261-EGFP cells.
n2:mentions
n3:16573834
Subject Item
_:vb17571958
rdf:type
n2:Context
rdf:value
The CD11b-HSVTK transgenic mice express the herpes simplex thymidine kinase (HSVTK) protein in monocytic cells such as MG/MP (Heppner et al., >>2005<<). When these animals are exposed to ganciclovir (GCV), the cells that express HSVTK are eliminated. Systemic administration (100μg/g GCV i.p. every 2days) resulted in death of all proliferating monocytic cells, which led to severe anemia
n2:mentions
n3:15665833
Subject Item
_:vb17571959
rdf:type
n2:Context
rdf:value
every 2days) resulted in death of all proliferating monocytic cells, which led to severe anemia and death around 10days after the GCV injection (Heppner et al., >>2005<<). We modified this protocol by performing local infusion of GCV (Mirrione et al., 2010) at the tumor injection site, which ablated MG/MP in and around the tumor.
n2:mentions
n3:15665833
Subject Item
_:vb17571960
rdf:type
n2:Context
rdf:value
We modified this protocol by performing local infusion of GCV (Mirrione et al., >>2010<<) at the tumor injection site, which ablated MG/MP in and around the tumor.
n2:mentions
n3:20382223
Subject Item
_:vb17571961
rdf:type
n2:Context
rdf:value
Administration of clodronate for depletion of microglia was reported to attenuate glioma invasion in organotypic brain slices (Markovic et al., >>2005<<), potentially by depriving the glioma cells of microglia-produced MT1-MMP (Markovic et al., 2009).
n2:mentions
n3:16141784
Subject Item
_:vb17571962
rdf:type
n2:Context
rdf:value
of clodronate for depletion of microglia was reported to attenuate glioma invasion in organotypic brain slices (Markovic et al., 2005), potentially by depriving the glioma cells of microglia-produced MT1-MMP (Markovic et al., >>2009<<). We next performed a detailed evaluation of tumor growth in the presence and absence of microglia.
n2:mentions
n3:19617536
Subject Item
_:vb17571963
rdf:type
n2:Context
rdf:value
Tuftsin (threonine-lysine-proline-arginine, TKPR), which is derived from the proteolytic degradation of immunoglobulin G (Nishioka et al., >>1973<<), is a potent stimulator of MG/MP, enhancing the phagocytic activity, migration and antigen presentation of monocytic cells (Siemion and Kluczyk, 1999).
n2:mentions
n3:4710594
Subject Item
_:vb17571964
rdf:type
n2:Context
rdf:value
is derived from the proteolytic degradation of immunoglobulin G (Nishioka et al., 1973), is a potent stimulator of MG/MP, enhancing the phagocytic activity, migration and antigen presentation of monocytic cells (Siemion and Kluczyk, >>1999<<). Tuftsin has been widely used as an anti-tumor agent in animal cancer models (Banks et al., 1985; Noyes et al., 1981; Wleklik et al., 1986).
n2:mentions
n3:10465518
Subject Item
_:vb17571965
rdf:type
n2:Context
rdf:value
Tuftsin has been widely used as an anti-tumor agent in animal cancer models (Banks et al., >>1985<<; Noyes et al., 1981; Wleklik et al., 1986).
n2:mentions
n3:3858577
Subject Item
_:vb17571966
rdf:type
n2:Context
rdf:value
Tuftsin has been widely used as an anti-tumor agent in animal cancer models (Banks et al., 1985; Noyes et al., 1981; Wleklik et al., >>1986<<). GL261-EGFP cells cultured with tuftsin did not exhibit alterations in cell proliferation (data not shown). We thus examined whether tuftsin stimulation of microglia affected growth of GL261-EGFP cells, using a tissue-culture insert
n2:mentions
n3:3746258
Subject Item
_:vb17571967
rdf:type
n2:Context
rdf:value
MIF/TKP (tuftsin fragment 1–3) is a tripeptide, that blocks the activity of monocytic cells in vitro and in vivo (Thanos et al., >>1993<<; Rogove and Tsirka, 1998; Bhasin et al., 2007).
n2:mentions
n3:7678855
Subject Item
_:vb17571968
rdf:type
n2:Context
rdf:value
MIF/TKP (tuftsin fragment 1–3) is a tripeptide, that blocks the activity of monocytic cells in vitro and in vivo (Thanos et al., 1993; Rogove and Tsirka, >>1998<<; Bhasin et al., 2007).
n2:mentions
n3:9427623
Subject Item
_:vb17571969
rdf:type
n2:Context
rdf:value
MIF/TKP (tuftsin fragment 1–3) is a tripeptide, that blocks the activity of monocytic cells in vitro and in vivo (Thanos et al., 1993; Rogove and Tsirka, 1998; Bhasin et al., >>2007<<). The infusion of MIF/TKP to the site of excitotoxic injury inhibits microglia activation, and MIF/TKP treatment of primary microglia inhibits lipopolysaccharide (LPS)-mediated TNF-α release (Rogove and Tsirka, 1998). As shown above, an
n2:mentions
n3:17634104
Subject Item
_:vb17571970
rdf:type
n2:Context
rdf:value
The infusion of MIF/TKP to the site of excitotoxic injury inhibits microglia activation, and MIF/TKP treatment of primary microglia inhibits lipopolysaccharide (LPS)-mediated TNF-α release (Rogove and Tsirka, >>1998<<). As shown above, an indirect (segregated) and direct (physical interaction) co-culture system was utilized to assess the effects of MIF/TKP on glioma growth. In the indirect system, in the presence of MIF/TKP and microglia the growth of
n2:mentions
n3:9427623
Subject Item
_:vb17571971
rdf:type
n2:Context
rdf:value
The chemokine CCL21 is expressed by many cancers, including breast cancer and melanoma, which was recently shown to function as an immune suppressive chemokine, facilitating the immune escape of tumors (Shields et al., >>2007<<; 2010). Here we examined whether the tuftsin or MIF/TKP treatment could modulate CCL21 expression in glioma tissue.
n2:mentions
n3:17560334
Subject Item
_:vb17571972
rdf:type
n2:Context
rdf:value
The chemokine CCL21 is expressed by many cancers, including breast cancer and melanoma, which was recently shown to function as an immune suppressive chemokine, facilitating the immune escape of tumors (Shields et al., 2007; >>2010<<). Here we examined whether the tuftsin or MIF/TKP treatment could modulate CCL21 expression in glioma tissue.
n2:mentions
n3:20339029
Subject Item
_:vb17571973
rdf:type
n5:Section
dc:title
discussion
n5:contains
_:vb17572014 _:vb17572015 _:vb17572012 _:vb17572013 _:vb17572010 _:vb17572011 _:vb17572008 _:vb17572009 _:vb17572006 _:vb17572007 _:vb17572004 _:vb17572005 _:vb17572002 _:vb17572003 _:vb17572000 _:vb17572001 _:vb17572026 _:vb17572027 _:vb17572024 _:vb17572025 _:vb17572022 _:vb17572023 _:vb17572020 _:vb17572021 _:vb17572018 _:vb17572019 _:vb17572016 _:vb17572017 _:vb17571982 _:vb17571983 _:vb17571980 _:vb17571981 _:vb17571978 _:vb17571979 _:vb17571976 _:vb17571977 _:vb17571974 _:vb17571975 _:vb17571998 _:vb17571999 _:vb17571996 _:vb17571997 _:vb17571994 _:vb17571995 _:vb17571992 _:vb17571993 _:vb17571990 _:vb17571991 _:vb17571988 _:vb17571989 _:vb17571986 _:vb17571987 _:vb17571984 _:vb17571985
Subject Item
_:vb17571974
rdf:type
n2:Context
rdf:value
Among the stromal cells, macrophages have been shown to have dual roles, which are both tumor-rejecting and tumor-promoting (Allavena et al., >>2008<<; Solinas et al., 2009).
n2:mentions
n3:18364000
Subject Item
_:vb17571975
rdf:type
n2:Context
rdf:value
Among the stromal cells, macrophages have been shown to have dual roles, which are both tumor-rejecting and tumor-promoting (Allavena et al., 2008; Solinas et al., >>2009<<). Macrophages secrete anti-tumor cytokines and interact with T cells to destroy tumor cells (Galani et al., 2009). On the other hand they can be recruited by tumor-released chemokines and switch to tumor-supporting behavior in the tumor
n2:mentions
n3:19741157
Subject Item
_:vb17571976
rdf:type
n2:Context
rdf:value
On the other hand they can be recruited by tumor-released chemokines and switch to tumor-supporting behavior in the tumor microenvironment (Demuth and Berens, >>2004<<; Pollard, 2004).
n2:mentions
n3:15674479
Subject Item
_:vb17571977
rdf:type
n2:Context
rdf:value
On the other hand they can be recruited by tumor-released chemokines and switch to tumor-supporting behavior in the tumor microenvironment (Demuth and Berens, 2004; Pollard, >>2004<<).
n2:mentions
n3:14708027
Subject Item
_:vb17571978
rdf:type
n2:Context
rdf:value
stimulating factor-1, granulocyte-macrophage stimulating factor, monocyte chemoattractant protein-1, and hepatocyte growth factor/scatter factor, which recruit and promote the growth of tumor-infiltrating MG/MP (Alterman and Stanley, >>1994<<; Badie et al., 1999; Kielian et al., 2002; Leung et al., 1997; Nitta et al., 1992).
n2:mentions
n3:8086034
Subject Item
_:vb17571979
rdf:type
n2:Context
rdf:value
granulocyte-macrophage stimulating factor, monocyte chemoattractant protein-1, and hepatocyte growth factor/scatter factor, which recruit and promote the growth of tumor-infiltrating MG/MP (Alterman and Stanley, 1994; Badie et al., >>1999<<; Kielian et al., 2002; Leung et al., 1997; Nitta et al., 1992). Moreover, tumor-infiltrating MG/MP are commonly activated and proliferate in gliomas (Klein and Roggendorf, 2001).
n2:mentions
n3:10232541
Subject Item
_:vb17571980
rdf:type
n2:Context
rdf:value
stimulating factor, monocyte chemoattractant protein-1, and hepatocyte growth factor/scatter factor, which recruit and promote the growth of tumor-infiltrating MG/MP (Alterman and Stanley, 1994; Badie et al., 1999; Kielian et al., >>2002<<; Leung et al., 1997; Nitta et al., 1992). Moreover, tumor-infiltrating MG/MP are commonly activated and proliferate in gliomas (Klein and Roggendorf, 2001).
n2:mentions
n3:11949821
Subject Item
_:vb17571981
rdf:type
n2:Context
rdf:value
monocyte chemoattractant protein-1, and hepatocyte growth factor/scatter factor, which recruit and promote the growth of tumor-infiltrating MG/MP (Alterman and Stanley, 1994; Badie et al., 1999; Kielian et al., 2002; Leung et al., >>1997<<; Nitta et al., 1992). Moreover, tumor-infiltrating MG/MP are commonly activated and proliferate in gliomas (Klein and Roggendorf, 2001).
n2:mentions
n3:9144591
Subject Item
_:vb17571982
rdf:type
n2:Context
rdf:value
protein-1, and hepatocyte growth factor/scatter factor, which recruit and promote the growth of tumor-infiltrating MG/MP (Alterman and Stanley, 1994; Badie et al., 1999; Kielian et al., 2002; Leung et al., 1997; Nitta et al., >>1992<<). Moreover, tumor-infiltrating MG/MP are commonly activated and proliferate in gliomas (Klein and Roggendorf, 2001).
n2:mentions
n3:1377084
Subject Item
_:vb17571983
rdf:type
n2:Context
rdf:value
Moreover, tumor-infiltrating MG/MP are commonly activated and proliferate in gliomas (Klein and Roggendorf, >>2001<<). In our study, we show that glioma conditioned medium, but not astrocyte-derived medium, activated microglia, as previously reported (Klein and Roggendorf, 2001). In the GL261 mouse glioma model, as in human glioma specimens, activated
n2:mentions
n3:11307624
Subject Item
_:vb17571984
rdf:type
n2:Context
rdf:value
In our study, we show that glioma conditioned medium, but not astrocyte-derived medium, activated microglia, as previously reported (Klein and Roggendorf, >>2001<<). In the GL261 mouse glioma model, as in human glioma specimens, activated MG/MP infiltrated within and around the tumor, and the density of MG/MP in the tumor area was higher than the MG/MP density that surrounded relatively normal brain
n2:mentions
n3:11307624
Subject Item
_:vb17571985
rdf:type
n2:Context
rdf:value
Patients with gliomas often have deficiency in immunologic responses against the tumor (Morford et al., >>1997<<). Although up to one third of all cells in glioma specimens were MG/MP, T cells were rarely seen in gliomas (Morimura et al., 1990; Roggendorf et al., 1996). Independent studies showed that the microglial antigen-presenting function was
n2:mentions
n3:9379040
Subject Item
_:vb17571986
rdf:type
n2:Context
rdf:value
Although up to one third of all cells in glioma specimens were MG/MP, T cells were rarely seen in gliomas (Morimura et al., >>1990<<; Roggendorf et al., 1996).
n2:mentions
n3:2399810
Subject Item
_:vb17571987
rdf:type
n2:Context
rdf:value
Although up to one third of all cells in glioma specimens were MG/MP, T cells were rarely seen in gliomas (Morimura et al., 1990; Roggendorf et al., >>1996<<). Independent studies showed that the microglial antigen-presenting function was compromised in gliomas, since the major histocompatibility complex (MHC) class II molecules and co-stimulatory molecules exhibited decreased expression
n2:mentions
n3:8870831
Subject Item
_:vb17571988
rdf:type
n2:Context
rdf:value
showed that the microglial antigen-presenting function was compromised in gliomas, since the major histocompatibility complex (MHC) class II molecules and co-stimulatory molecules exhibited decreased expression levels (Badie et al., >>2002<<; Flugel et al., 1999).
n2:mentions
n3:12446006
Subject Item
_:vb17571989
rdf:type
n2:Context
rdf:value
antigen-presenting function was compromised in gliomas, since the major histocompatibility complex (MHC) class II molecules and co-stimulatory molecules exhibited decreased expression levels (Badie et al., 2002; Flugel et al., >>1999<<). The studies on GIM innate immune responses demonstrated that GIMs expressed Toll-like receptors (TLR) and mediated phagocytosis, but lacked IL-1β and TNF-α production, which are important cytokines for tumor rejection (Frei et al.,
n2:mentions
n3:10571416
Subject Item
_:vb17571990
rdf:type
n2:Context
rdf:value
The studies on GIM innate immune responses demonstrated that GIMs expressed Toll-like receptors (TLR) and mediated phagocytosis, but lacked IL-1β and TNF-α production, which are important cytokines for tumor rejection (Frei et al., >>1994<<; Hussain et al., 2006). Moreover in a CD11b-HSVTK glioma model, Markovic et al. (2009) reported that activation of MMPs in glioma is promoted via activation of TLRs and MT1-MMP in microglia.
n2:mentions
n3:8072666
Subject Item
_:vb17571991
rdf:type
n2:Context
rdf:value
innate immune responses demonstrated that GIMs expressed Toll-like receptors (TLR) and mediated phagocytosis, but lacked IL-1β and TNF-α production, which are important cytokines for tumor rejection (Frei et al., 1994; Hussain et al., >>2006<<). Moreover in a CD11b-HSVTK glioma model, Markovic et al. (2009) reported that activation of MMPs in glioma is promoted via activation of TLRs and MT1-MMP in microglia.
n2:mentions
n3:16573834
Subject Item
_:vb17571992
rdf:type
n2:Context
rdf:value
Moreover in a CD11b-HSVTK glioma model, Markovic et al. (>>2009<<) reported that activation of MMPs in glioma is promoted via activation of TLRs and MT1-MMP in microglia.
n2:mentions
n3:19617536
Subject Item
_:vb17571993
rdf:type
n2:Context
rdf:value
could be anti-inflammatory cytokines released by glioma cells, such as interleukin (IL)-6, IL-11, leukemia inhibitory factor, oncostatin-M, and TGF-β, which can inhibit cytotoxic T-cell activation and MG/MP activation (Constam et al., >>1992<<; Goswami et al., 1998; Halfter et al., 1998; Hao et al., 2002; Murphy et al., 1995).
n2:mentions
n3:1538124
Subject Item
_:vb17571994
rdf:type
n2:Context
rdf:value
cytokines released by glioma cells, such as interleukin (IL)-6, IL-11, leukemia inhibitory factor, oncostatin-M, and TGF-β, which can inhibit cytotoxic T-cell activation and MG/MP activation (Constam et al., 1992; Goswami et al., >>1998<<; Halfter et al., 1998; Hao et al., 2002; Murphy et al., 1995).
n2:mentions
n3:9798907
Subject Item
_:vb17571995
rdf:type
n2:Context
rdf:value
by glioma cells, such as interleukin (IL)-6, IL-11, leukemia inhibitory factor, oncostatin-M, and TGF-β, which can inhibit cytotoxic T-cell activation and MG/MP activation (Constam et al., 1992; Goswami et al., 1998; Halfter et al., >>1998<<; Hao et al., 2002; Murphy et al., 1995).
n2:mentions
n3:9760066
Subject Item
_:vb17571996
rdf:type
n2:Context
rdf:value
such as interleukin (IL)-6, IL-11, leukemia inhibitory factor, oncostatin-M, and TGF-β, which can inhibit cytotoxic T-cell activation and MG/MP activation (Constam et al., 1992; Goswami et al., 1998; Halfter et al., 1998; Hao et al., >>2002<<; Murphy et al., 1995).
n2:mentions
n3:11810184
Subject Item
_:vb17571997
rdf:type
n2:Context
rdf:value
(IL)-6, IL-11, leukemia inhibitory factor, oncostatin-M, and TGF-β, which can inhibit cytotoxic T-cell activation and MG/MP activation (Constam et al., 1992; Goswami et al., 1998; Halfter et al., 1998; Hao et al., 2002; Murphy et al., >>1995<<).
n2:mentions
n3:7501271
Subject Item
_:vb17571998
rdf:type
n2:Context
rdf:value
On the other hand, glioma infiltrating microglia/macrophages (GIMs) release many factors, such as cytokines, growth factors and proteases, which directly or indirectly influence tumor progression (Graeber et al., >>2002<<). It has been shown that GL261 cell migration occurred earlier and faster in the presence of primary microglia or microglia-conditioned medium, which indicated that microglia-released soluble factors can promote glioma migration
n2:mentions
n3:12379912
Subject Item
_:vb17571999
rdf:type
n2:Context
rdf:value
shown that GL261 cell migration occurred earlier and faster in the presence of primary microglia or microglia-conditioned medium, which indicated that microglia-released soluble factors can promote glioma migration (Bettinger et al., >>2002<<). GIMs are the major source of IL-10, an immunosuppressive cytokine that promotes glioma proliferation and migration (Huettner et al., 1997; Wagner et al., 1999).
n2:mentions
n3:11904754
Subject Item
_:vb17572000
rdf:type
n2:Context
rdf:value
GIMs are the major source of IL-10, an immunosuppressive cytokine that promotes glioma proliferation and migration (Huettner et al., >>1997<<; Wagner et al., 1999).
n2:mentions
n3:9413151
Subject Item
_:vb17572001
rdf:type
n2:Context
rdf:value
GIMs are the major source of IL-10, an immunosuppressive cytokine that promotes glioma proliferation and migration (Huettner et al., 1997; Wagner et al., >>1999<<). Moreover, the glioma- and GIM-derived TGF-β has multiple effects on glioma progression: it can inhibit microglia proliferation and release of cytokines in vitro (Suzumura et al., 1993), can also induce metalloproteinase (MMPs)
n2:mentions
n3:10360813
Subject Item
_:vb17572002
rdf:type
n2:Context
rdf:value
Moreover, the glioma- and GIM-derived TGF-β has multiple effects on glioma progression: it can inhibit microglia proliferation and release of cytokines in vitro (Suzumura et al., >>1993<<), can also induce metalloproteinase (MMPs) expression and promote the invasion of glioma (Markovic et al., 2009; Wesolowska et al., 2008; Wick et al., 2001).
n2:mentions
n3:8345199
Subject Item
_:vb17572003
rdf:type
n2:Context
rdf:value
effects on glioma progression: it can inhibit microglia proliferation and release of cytokines in vitro (Suzumura et al., 1993), can also induce metalloproteinase (MMPs) expression and promote the invasion of glioma (Markovic et al., >>2009<<; Wesolowska et al., 2008; Wick et al., 2001). Both GIMs and glioma cells secrete vascular endothelial growth factor (Lafuente et al., 1999; Tsai et al., 1995) that mediates angiogenesis.
n2:mentions
n3:19617536
Subject Item
_:vb17572004
rdf:type
n2:Context
rdf:value
it can inhibit microglia proliferation and release of cytokines in vitro (Suzumura et al., 1993), can also induce metalloproteinase (MMPs) expression and promote the invasion of glioma (Markovic et al., 2009; Wesolowska et al., >>2008<<; Wick et al., 2001). Both GIMs and glioma cells secrete vascular endothelial growth factor (Lafuente et al., 1999; Tsai et al., 1995) that mediates angiogenesis.
n2:mentions
n3:17684491
Subject Item
_:vb17572005
rdf:type
n2:Context
rdf:value
microglia proliferation and release of cytokines in vitro (Suzumura et al., 1993), can also induce metalloproteinase (MMPs) expression and promote the invasion of glioma (Markovic et al., 2009; Wesolowska et al., 2008; Wick et al., >>2001<<). Both GIMs and glioma cells secrete vascular endothelial growth factor (Lafuente et al., 1999; Tsai et al., 1995) that mediates angiogenesis.
n2:mentions
n3:11716069
Subject Item
_:vb17572006
rdf:type
n2:Context
rdf:value
Both GIMs and glioma cells secrete vascular endothelial growth factor (Lafuente et al., >>1999<<; Tsai et al., 1995) that mediates angiogenesis.
n2:mentions
n3:10691304
Subject Item
_:vb17572007
rdf:type
n2:Context
rdf:value
Both GIMs and glioma cells secrete vascular endothelial growth factor (Lafuente et al., 1999; Tsai et al., >>1995<<) that mediates angiogenesis.
n2:mentions
n3:7714613
Subject Item
_:vb17572008
rdf:type
n2:Context
rdf:value
The results presented here agree with recent data (Markovic et al., >>2009<<), but provide more detailed characterization of the model.
n2:mentions
n3:19617536
Subject Item
_:vb17572009
rdf:type
n2:Context
rdf:value
It was shown that macrophage depletion in CD11b-TKmt-30 mice via systemic GCV injection resulted in glioma growth increase (Galarneau et al., >>2007<<). These results agree with the early-time points of our data, but the final outcome is different.
n2:mentions
n3:17875729
Subject Item
_:vb17572010
rdf:type
n2:Context
rdf:value
for glioma are–among others - manipulations of the activity of tumor-associated macrophages, including inhibition of their recruitment to and survival in tumor tissue and restoration of their anti-tumor immunity (Allavena et al., >>2005<<; Sessa et al., 2005; Wu et al., 2009). However, the development of therapeutic anti-glioma options by modulating the activity of GIM has not been thoroughly investigated.
n2:mentions
n3:15805300
Subject Item
_:vb17572011
rdf:type
n2:Context
rdf:value
others - manipulations of the activity of tumor-associated macrophages, including inhibition of their recruitment to and survival in tumor tissue and restoration of their anti-tumor immunity (Allavena et al., 2005; Sessa et al., >>2005<<; Wu et al., 2009). However, the development of therapeutic anti-glioma options by modulating the activity of GIM has not been thoroughly investigated.
n2:mentions
n3:15774779
Subject Item
_:vb17572012
rdf:type
n2:Context
rdf:value
of the activity of tumor-associated macrophages, including inhibition of their recruitment to and survival in tumor tissue and restoration of their anti-tumor immunity (Allavena et al., 2005; Sessa et al., 2005; Wu et al., >>2009<<). However, the development of therapeutic anti-glioma options by modulating the activity of GIM has not been thoroughly investigated.
n2:mentions
n3:19454672
Subject Item
_:vb17572013
rdf:type
n2:Context
rdf:value
For example, the injection of CpG ODN to GL261 mouse glioma cells resulted in contradictory data in a 9L rat glioma model (El Andaloussi et al., >>2006<<; Ginzkey et al., 2009), which suggests that MG/MP stimulators may have different effects on MG/MP activities depending on the tumor microenvironment.
n2:mentions
n3:16906541
Subject Item
_:vb17572014
rdf:type
n2:Context
rdf:value
Although tuftsin has been widely used in anticancer studies (Banks et al., >>1985<<; Noyes et al., 1981; Wleklik et al., 1986), its infusion into the glioma model presented here exaggerated tumor growth and shortened the survival time of tumor-bearing mice.
n2:mentions
n3:3858577
Subject Item
_:vb17572015
rdf:type
n2:Context
rdf:value
Although tuftsin has been widely used in anticancer studies (Banks et al., 1985; Noyes et al., 1981; Wleklik et al., >>1986<<), its infusion into the glioma model presented here exaggerated tumor growth and shortened the survival time of tumor-bearing mice.
n2:mentions
n3:3746258
Subject Item
_:vb17572016
rdf:type
n2:Context
rdf:value
Tuftsin activates monocytes and macrophages leading to IL-1, TNF-α and nitric oxide release (Cillari et al., >>1994<<; Robey et al., 1987; Wleklik et al., 1987), which possibly contributed to the initial slowing down of glioma growth.
n2:mentions
n3:8188392
Subject Item
_:vb17572017
rdf:type
n2:Context
rdf:value
Tuftsin activates monocytes and macrophages leading to IL-1, TNF-α and nitric oxide release (Cillari et al., 1994; Robey et al., >>1987<<; Wleklik et al., 1987), which possibly contributed to the initial slowing down of glioma growth.
n2:mentions
n3:3034878
Subject Item
_:vb17572018
rdf:type
n2:Context
rdf:value
Tuftsin activates monocytes and macrophages leading to IL-1, TNF-α and nitric oxide release (Cillari et al., 1994; Robey et al., 1987; Wleklik et al., >>1987<<), which possibly contributed to the initial slowing down of glioma growth.
n2:mentions
n3:3627109
Subject Item
_:vb17572019
rdf:type
n2:Context
rdf:value
Similar results were obtained in a mouse model of multiple sclerosis, where tuftsin infusion altered the host immune response towards favoring the expression of immunosuppressive Th2 genes (Bhasin et al., >>2007<<).
n2:mentions
n3:17634104
Subject Item
_:vb17572020
rdf:type
n2:Context
rdf:value
Delivery of MIF/TKP to the tumor inhibited tumor proliferation and induced GIM apoptosis, in agreement with the current trend of tumor therapy (Allavena et al., >>2005<<; Meng et al., 2010; Miselis et al., 2008).
n2:mentions
n3:15805300
Subject Item
_:vb17572021
rdf:type
n2:Context
rdf:value
Delivery of MIF/TKP to the tumor inhibited tumor proliferation and induced GIM apoptosis, in agreement with the current trend of tumor therapy (Allavena et al., 2005; Meng et al., >>2010<<; Miselis et al., 2008).
n2:mentions
n3:20145121
Subject Item
_:vb17572022
rdf:type
n2:Context
rdf:value
Delivery of MIF/TKP to the tumor inhibited tumor proliferation and induced GIM apoptosis, in agreement with the current trend of tumor therapy (Allavena et al., 2005; Meng et al., 2010; Miselis et al., >>2008<<). Similarly, it was shown that MIF/TKP delivery to the injury site after intracerebral hemorrhage (ICH) inhibited MG/MP infiltration and activation, and afforded neuroprotection (Wang and Tsirka, 2005).
n2:mentions
n3:18375821
Subject Item
_:vb17572023
rdf:type
n2:Context
rdf:value
Similarly, it was shown that MIF/TKP delivery to the injury site after intracerebral hemorrhage (ICH) inhibited MG/MP infiltration and activation, and afforded neuroprotection (Wang and Tsirka, >>2005<<).
n2:mentions
n3:15692122
Subject Item
_:vb17572024
rdf:type
n2:Context
rdf:value
A recent report (Shields et al., >>2010<<) showed that melanoma cells could shift their microenvironment to an immune tolerant one by expressing CCL21.
n2:mentions
n3:20339029
Subject Item
_:vb17572025
rdf:type
n2:Context
rdf:value
Previously it has been shown that CCL21 is up-regulated in neurons after injury, which activates microglia through the chemokine receptor CXCR3 and induces microglia migration (Biber et al., >>2001<<; de Jong et al., 2005; Rappert et al., 2002).
n2:mentions
n3:11307161
Subject Item
_:vb17572026
rdf:type
n2:Context
rdf:value
Previously it has been shown that CCL21 is up-regulated in neurons after injury, which activates microglia through the chemokine receptor CXCR3 and induces microglia migration (Biber et al., 2001; de Jong et al., >>2005<<; Rappert et al., 2002).
n2:mentions
n3:16107642
Subject Item
_:vb17572027
rdf:type
n2:Context
rdf:value
Previously it has been shown that CCL21 is up-regulated in neurons after injury, which activates microglia through the chemokine receptor CXCR3 and induces microglia migration (Biber et al., 2001; de Jong et al., 2005; Rappert et al., >>2002<<). We found here that glioma and surrounding stromal cells expressed CCL21 two weeks after glioma inoculation, which suggested that the glioma microenvironment is immune suppressive.
n2:mentions
n3:11907075
Subject Item
_:vb635007791
rdf:type
n2:RelevantBibliographicResource
n2:RelevantScore
23
n2:hasRelevantPaperId
n3:19617536
Subject Item
_:vb635007792
rdf:type
n2:RelevantBibliographicResource
n2:RelevantScore
22
n2:hasRelevantPaperId
n3:24056773
Subject Item
_:vb635007793
rdf:type
n2:RelevantBibliographicResource
n2:RelevantScore
21
n2:hasRelevantPaperId
n3:20667896
Subject Item
_:vb635007794
rdf:type
n2:RelevantBibliographicResource
n2:RelevantScore
21
n2:hasRelevantPaperId
n3:16141784
Subject Item
_:vb635007795
rdf:type
n2:RelevantBibliographicResource
n2:RelevantScore
17
n2:hasRelevantPaperId
n3:15758009
Subject Item
_:vb635007796
rdf:type
n2:RelevantBibliographicResource
n2:RelevantScore
16
n2:hasRelevantPaperId
n3:12379912
Subject Item
_:vb635007797
rdf:type
n2:RelevantBibliographicResource
n2:RelevantScore
16
n2:hasRelevantPaperId
n3:16775224
Subject Item
_:vb635007798
rdf:type
n2:RelevantBibliographicResource
n2:RelevantScore
16
n2:hasRelevantPaperId
n3:21901144
Subject Item
_:vb635007799
rdf:type
n2:RelevantBibliographicResource
n2:RelevantScore
16
n2:hasRelevantPaperId
n3:22573310
Subject Item
_:vb635007800
rdf:type
n2:RelevantBibliographicResource
n2:RelevantScore
16
n2:hasRelevantPaperId
n3:26713745
Subject Item
_:vb635007801
rdf:type
n2:RelevantBibliographicResource
n2:RelevantScore
15
n2:hasRelevantPaperId
n3:18553315
Subject Item
_:vb635007802
rdf:type
n2:RelevantBibliographicResource
n2:RelevantScore
15
n2:hasRelevantPaperId
n3:17684491
Subject Item
_:vb635007803
rdf:type
n2:RelevantBibliographicResource
n2:RelevantScore
15
n2:hasRelevantPaperId
n3:22294205
Subject Item
_:vb635007804
rdf:type
n2:RelevantBibliographicResource
n2:RelevantScore
14
n2:hasRelevantPaperId
n3:21446047
Subject Item
_:vb635007805
rdf:type
n2:RelevantBibliographicResource
n2:RelevantScore
14
n2:hasRelevantPaperId
n3:25658639
Subject Item
_:vb635007806
rdf:type
n2:RelevantBibliographicResource
n2:RelevantScore
14
n2:hasRelevantPaperId
n3:8870831
Subject Item
_:vb635007807
rdf:type
n2:RelevantBibliographicResource
n2:RelevantScore
14
n2:hasRelevantPaperId
n3:15959903
Subject Item
_:vb635007808
rdf:type
n2:RelevantBibliographicResource
n2:RelevantScore
12
n2:hasRelevantPaperId
n3:10764271
Subject Item
_:vb635007809
rdf:type
n2:RelevantBibliographicResource
n2:RelevantScore
12
n2:hasRelevantPaperId
n3:20129251
Subject Item
_:vb635007810
rdf:type
n2:RelevantBibliographicResource
n2:RelevantScore
12
n2:hasRelevantPaperId
n3:23864876
Subject Item
_:vb635007811
rdf:type
n2:RelevantBibliographicResource
n2:RelevantScore
12
n2:hasRelevantPaperId
n3:12953273
Subject Item
_:vb635007812
rdf:type
n2:RelevantBibliographicResource
n2:RelevantScore
11
n2:hasRelevantPaperId
n3:17875729
Subject Item
_:vb635007813
rdf:type
n2:RelevantBibliographicResource
n2:RelevantScore
11
n2:hasRelevantPaperId
n3:20966214
Subject Item
_:vb635007814
rdf:type
n2:RelevantBibliographicResource
n2:RelevantScore
11
n2:hasRelevantPaperId
n3:22664874
Subject Item
_:vb635007815
rdf:type
n2:RelevantBibliographicResource
n2:RelevantScore
11
n2:hasRelevantPaperId
n3:22159219
Subject Item
_:vb635007816
rdf:type
n2:RelevantBibliographicResource
n2:RelevantScore
10
n2:hasRelevantPaperId
n3:21527731
Subject Item
_:vb635007817
rdf:type
n2:RelevantBibliographicResource
n2:RelevantScore
10
n2:hasRelevantPaperId
n3:20184883
Subject Item
_:vb635007818
rdf:type
n2:RelevantBibliographicResource
n2:RelevantScore
10
n2:hasRelevantPaperId
n3:24316889
Subject Item
_:vb635007819
rdf:type
n2:RelevantBibliographicResource
n2:RelevantScore
10
n2:hasRelevantPaperId
n3:18772890
Subject Item
_:vb635007820
rdf:type
n2:RelevantBibliographicResource
n2:RelevantScore
10
n2:hasRelevantPaperId
n3:23650109
Subject Item
_:vb635007821
rdf:type
n2:RelevantBibliographicResource
n2:RelevantScore
9
n2:hasRelevantPaperId
n3:19926287
Subject Item
_:vb635007822
rdf:type
n2:RelevantBibliographicResource
n2:RelevantScore
9
n2:hasRelevantPaperId
n3:26718201
Subject Item
_:vb635007823
rdf:type
n2:RelevantBibliographicResource
n2:RelevantScore
9
n2:hasRelevantPaperId
n3:11455617
Subject Item
_:vb635007824
rdf:type
n2:RelevantBibliographicResource
n2:RelevantScore
9
n2:hasRelevantPaperId
n3:17965659
Subject Item
_:vb635007825
rdf:type
n2:RelevantBibliographicResource
n2:RelevantScore
9
n2:hasRelevantPaperId
n3:11904754
Subject Item
_:vb635007826
rdf:type
n2:RelevantBibliographicResource
n2:RelevantScore
8
n2:hasRelevantPaperId
n3:10353745
Subject Item
_:vb635007827
rdf:type
n2:RelevantBibliographicResource
n2:RelevantScore
8
n2:hasRelevantPaperId
n3:422981
Subject Item
_:vb635007828
rdf:type
n2:RelevantBibliographicResource
n2:RelevantScore
8
n2:hasRelevantPaperId
n3:25580734
Subject Item
_:vb635007829
rdf:type
n2:RelevantBibliographicResource
n2:RelevantScore
8
n2:hasRelevantPaperId
n3:23983766
Subject Item
_:vb635007830
rdf:type
n2:RelevantBibliographicResource
n2:RelevantScore
8
n2:hasRelevantPaperId
n3:10232541
Subject Item
_:vb635007831
rdf:type
n2:RelevantBibliographicResource
n2:RelevantScore
8
n2:hasRelevantPaperId
n3:18669428
Subject Item
_:vb635007832
rdf:type
n2:RelevantBibliographicResource
n2:RelevantScore
8
n2:hasRelevantPaperId
n3:15549107
Subject Item
_:vb635007833
rdf:type
n2:RelevantBibliographicResource
n2:RelevantScore
7
n2:hasRelevantPaperId
n3:17107968
Subject Item
_:vb635007834
rdf:type
n2:RelevantBibliographicResource
n2:RelevantScore
7
n2:hasRelevantPaperId
n3:21636707
Subject Item
_:vb635007835
rdf:type
n2:RelevantBibliographicResource
n2:RelevantScore
7
n2:hasRelevantPaperId
n3:28292436
Subject Item
_:vb635007836
rdf:type
n2:RelevantBibliographicResource
n2:RelevantScore
7
n2:hasRelevantPaperId
n3:19199469
Subject Item
_:vb635007837
rdf:type
n2:RelevantBibliographicResource
n2:RelevantScore
7
n2:hasRelevantPaperId
n3:21157378
Subject Item
_:vb635007838
rdf:type
n2:RelevantBibliographicResource
n2:RelevantScore
7
n2:hasRelevantPaperId
n3:21376230
Subject Item
_:vb635007839
rdf:type
n2:RelevantBibliographicResource
n2:RelevantScore
7
n2:hasRelevantPaperId
n3:19424580
Subject Item
_:vb635007840
rdf:type
n2:RelevantBibliographicResource
n2:RelevantScore
7
n2:hasRelevantPaperId
n3:28235764
Subject Item
_:vb635007841
rdf:type
n2:RelevantBibliographicResource
n2:RelevantScore
6
n2:hasRelevantPaperId
n3:9413151
Subject Item
_:vb635007842
rdf:type
n2:RelevantBibliographicResource
n2:RelevantScore
6
n2:hasRelevantPaperId
n3:17618441
Subject Item
_:vb635007843
rdf:type
n2:RelevantBibliographicResource
n2:RelevantScore
6
n2:hasRelevantPaperId
n3:19306372
Subject Item
_:vb635007844
rdf:type
n2:RelevantBibliographicResource
n2:RelevantScore
6
n2:hasRelevantPaperId
n3:24360280
Subject Item
_:vb635007845
rdf:type
n2:RelevantBibliographicResource
n2:RelevantScore
6
n2:hasRelevantPaperId
n3:24722970
Subject Item
_:vb635007846
rdf:type
n2:RelevantBibliographicResource
n2:RelevantScore
6
n2:hasRelevantPaperId
n3:9144591
Subject Item
_:vb635007847
rdf:type
n2:RelevantBibliographicResource
n2:RelevantScore
6
n2:hasRelevantPaperId
n3:27157931
Subject Item
_:vb635007848
rdf:type
n2:RelevantBibliographicResource
n2:RelevantScore
6
n2:hasRelevantPaperId
n3:25477239
Subject Item
_:vb635007849
rdf:type
n2:RelevantBibliographicResource
n2:RelevantScore
6
n2:hasRelevantPaperId
n3:24193082
Subject Item
_:vb635007850
rdf:type
n2:RelevantBibliographicResource
n2:RelevantScore
6
n2:hasRelevantPaperId
n3:15831717
Subject Item
_:vb635007851
rdf:type
n2:RelevantBibliographicResource
n2:RelevantScore
6
n2:hasRelevantPaperId
n3:17051156
Subject Item
_:vb635007852
rdf:type
n2:RelevantBibliographicResource
n2:RelevantScore
5
n2:hasRelevantPaperId
n3:18794121
Subject Item
_:vb635007853
rdf:type
n2:RelevantBibliographicResource
n2:RelevantScore
5
n2:hasRelevantPaperId
n3:12835669
Subject Item
_:vb635007854
rdf:type
n2:RelevantBibliographicResource
n2:RelevantScore
5
n2:hasRelevantPaperId
n3:19269895
Subject Item
_:vb635007855
rdf:type
n2:RelevantBibliographicResource
n2:RelevantScore
5
n2:hasRelevantPaperId
n3:21056915
Subject Item
_:vb635007856
rdf:type
n2:RelevantBibliographicResource
n2:RelevantScore
5
n2:hasRelevantPaperId
n3:19748528
Subject Item
_:vb635007857
rdf:type
n2:RelevantBibliographicResource
n2:RelevantScore
5
n2:hasRelevantPaperId
n3:10360813
Subject Item
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rdf:type
n2:RelevantBibliographicResource
n2:RelevantScore
5
n2:hasRelevantPaperId
n3:11810184
Subject Item
_:vb635007859
rdf:type
n2:RelevantBibliographicResource
n2:RelevantScore
5
n2:hasRelevantPaperId
n3:10802656
Subject Item
_:vb635007860
rdf:type
n2:RelevantBibliographicResource
n2:RelevantScore
5
n2:hasRelevantPaperId
n3:26449250
Subject Item
_:vb635007861
rdf:type
n2:RelevantBibliographicResource
n2:RelevantScore
5
n2:hasRelevantPaperId
n3:16520032
Subject Item
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rdf:type
n2:RelevantBibliographicResource
n2:RelevantScore
5
n2:hasRelevantPaperId
n3:16734735
Subject Item
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rdf:type
n2:RelevantBibliographicResource
n2:RelevantScore
5
n2:hasRelevantPaperId
n3:29260225
Subject Item
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n2:RelevantBibliographicResource
n2:RelevantScore
5
n2:hasRelevantPaperId
n3:22379614
Subject Item
_:vb635007865
rdf:type
n2:RelevantBibliographicResource
n2:RelevantScore
5
n2:hasRelevantPaperId
n3:17400655
Subject Item
_:vb635007866
rdf:type
n2:RelevantBibliographicResource
n2:RelevantScore
5
n2:hasRelevantPaperId
n3:21909104
Subject Item
_:vb635007867
rdf:type
n2:RelevantBibliographicResource
n2:RelevantScore
4
n2:hasRelevantPaperId
n3:11716069
Subject Item
_:vb635007868
rdf:type
n2:RelevantBibliographicResource
n2:RelevantScore
4
n2:hasRelevantPaperId
n3:15895084
Subject Item
_:vb635007869
rdf:type
n2:RelevantBibliographicResource
n2:RelevantScore
4
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