HUGO ID Detailed Result 7873

PMID	Match String	Actual String	Score	Flanking text	Edited by	Edit
12060810	iNOS	iNOS	1.9	inhibits microglial activation caspase-1 and inducible nitric oxide synthetase (iNOS) iNOS up-regulation and decreases infarct size after experimental ischemia in rats
12060810	iNOS	iNOS	1.9	Second minocycline inhibits caspase-1 and caspase-3 expression decreases iNOS activity and delays mortality in a transgenic mouse model of
12060810	iNOS	iNOS	1.9	Excitotoxicity microglial activation iNOS and caspase up-regulation have all been suggested to play a
12060810	iNOS	iNOS	1.9	microglia as well as the concomitant induction of caspase-1 and iNOS
12060810	iNOS	iNOS	1.9	related to an inhibition of caspases and a decrease in iNOS activity _amp_#91 5 _amp_#93
14739060	iNOS	iNOS	1.9	NO synthase (nNOS; nNOS type I inducible NO synthase (iNOS; iNOS typeII which is produced in very large amounts by activated
14739060	iNOS	iNOS	1.9	in pathologic conditions especially NO coming from activated microglia (iNOS) iNOS or and from endothelial cells (eNOS) eNOS
15453089	iNOS	iNOS	1.0	was frequently associated with that of inducible NO synthase (iNOS), iNOS suggesting that both enzymes could contribute to the progression of
15453089	iNOS	iNOS	1.0	The authors also propose that the colocalization of COX-2 and iNOS may be functionally linked to oligodendroglial excitotoxic death in MS
15453089	iNOS	iNOS	1.0	In transgenic mutated SOD1 mice COX-2 and iNOS are induced with a similar temporal pattern and co-expression of
15572176	iNOS	iNOS	2.7	such as the inducible forms of nitric oxide synthase (iNOS) iNOS and cyclooxygenase (COX-2), COX-2 display nitrotyrosine immunoreactivity and downregulate the
15572176	iNOS	iNOS	2.7	S100_amp_#x3b2 85 and express inflammatory makers such as COX-2 81 iNOS and neuronal NOS 5 and 115
15572176	iNOS	iNOS	2.7	expression of the calcium-binding protein S100A6 63 as well as iNOS and become immunoreactive for nitrotyrosine 3 and 116
15572176	iNOS	iNOS	2.7	characterized by the appearance of process-bearing cells displaying intense GFAP iNOS and nitrotyrosine immunoreactivity 19 and 20
15572176	iNOS	iNOS	2.7	LPS stimulated iNOS expression and nitrotyrosine formation suggesting a role for peroxynitrite in
15572176	iNOS	iNOS	2.7	Interestingly cytokine signaling can induce iNOS COX-2 and NMDA receptor subunit phosphorylation with different consequences in
15572176	iNOS	iNOS	2.7	Activation of iNOS in astrocytes by IL-1_amp_#x3b2 potentiates NMDA-mediated neurotoxicity in mixed cortical
15572176	iNOS	iNOS	2.7	factor-alpha (TNF-_amp_#x3b1;), TNF-_amp_#x3b1 IL-1_amp_#x3b2 and IFN_amp_#x3b3 induces IL-6 COX-2 and iNOS and makes the cells vulnerable to undergo apoptosis in response
15572176	iNOS	iNOS	2.7	In particular induction of iNOS by LPS or cytokines seems to be required for astrocytes
15572176	iNOS	iNOS	2.7	Inhibition of iNOS by nitro--arginine methyl ester and low concentrations of aminoguanidine prevented
15649489	iNOS	iNOS	3.2	Pioglitazone also reduced iNOS NF_amp_#x3ba -B and 3-nitrotyrosine immunoreactivity in the spinal cords of
15649489	iNOS	iNOS	3.2	PPARs down-regulate proinflammatory cytokines and iNOS in both macrophages and microglial cells ( Colville-Nash et al.
15649489	iNOS	iNOS	3.2	sections were immunostained with CD40 (Serotec), Serotec GFAP (DAKO), DAKO iNOS (Upstate, Upstate Waltham MA NF_amp_#x3ba B (Santa Santa Cruz CA
15649489	iNOS	iNOS	3.2	iNOS NF_amp_#x3ba -B and nitrotyrosine immunoreactivity
15649489	iNOS	iNOS	3.2	Control diet fed G93A mice showed strong immunoreactivity for iNOS NF_amp_#x3ba -B and 3-nitrotyrosine
15649489	iNOS	iNOS	3.2	Pioglitazone treatment reduced the immunoreactivity of iNOS NF_amp_#x3ba -B and 3-nitrotyrosine in the lumbar spinal cord sections
15649489	iNOS	iNOS	3.2	IL-1_amp_#x3b2 tumor necrosis factor- and iNOS levels are increased in transgenic mouse models of ALS (
15649489	iNOS	iNOS	3.2	This appears to block iNOS induction and NO-mediated toxicity
15649489	iNOS	iNOS	3.2	Fig 5._amp_#xa0 Pioglitazone treatment reduced iNOS NF_amp_#x3ba -B and 3-nitrotyrosine immunostaining in G93A mice
15649489	iNOS	iNOS	3.2	Strong iNOS NF_amp_#x3ba -B and 3-nitrotyrosine immunoreactivities in motor neurons (arrow) arrow
16014720	iNOS	iNOS	2.2	For instance NADPH oxidase and inducible nitric oxide synthase (iNOS), iNOS which are major sources of inflammatory oxidants are upregulated in
16014720	iNOS	iNOS	2.2	Studies of mice deficient in NADPH oxidase or iNOS indicate that superoxide radical (O O 2 and NO contribute
16014720	iNOS	iNOS-dependent	2.2	Pennathur et al. 1999 for the most part in an iNOS-dependent manner (Liberatore Liberatore et al. 1999
16014720	iNOS	iNOS	2.2	Remarkably detectable changes in iNOS expression and enzymatic activity are also confined to ventral midbrains
16120782	iNOS	iNOS	2.2	of cyclooxygenase 2 (COX-2) COX-2 and nitric oxide synthase (iNOS) iNOS in the spinal cord (Phul Phul et al. 2000 Almer
16120782	iNOS	iNOS	2.2	For the analysis of iNOS and COX-2 100 microg of protein samples was separated in
16120782	iNOS	iNOS	2.2	onto Immobilon-P polyvinylidene difluoride membranes and stained with a polyclonal iNOS antibody at 1 500 dilution (rabbit rabbit polyclonal antibody to
16120782	iNOS	iNOS	2.2	dilution (rabbit rabbit polyclonal antibody to C terminus of murine iNOS Santa Cruz Biotechology Heidelberg Germany or a polyclonal COX-2 antibody
16120782	iNOS	iNOS	2.2	The specificities of the iNOS and COX-2 antibodies have been confirmed by positive controls containing
16120782	iNOS	iNOS	2.2	and COX-2 antibodies have been confirmed by positive controls containing iNOS or COX-2 protein (data data not shown
16120782	iNOS	iNOS	2.2	Coinduction of COX-2 and iNOS were described in several neurodegenerative disorders including ALS as well
16120782	iNOS	iNOS	2.2	In contrast iNOS was hardly detectable in wild-type but strongly expressed by SOD1-G93A
16120782	iNOS	iNOS	2.2	In both cases Pio treatment significantly decreased COX-2 and iNOS expression in SOD1-G93A mice ( n = 4
16120782	iNOS	iNOS	2.2	= 5 for SOD1 and SOD1-Pio and of COX-2 and iNOS Western blots ( n = 4 for all groups from
16120782	iNOS	iNOS	2.2	found a marked reduction in the expression of COX-2 and iNOS two major proinflammatory enzymes after Pio treatment
16120782	iNOS	iNOS	2.2	or identical stimulators (O'Banion, O'Banion 1999 because the COX-2 and iNOS promoters share several binding sites for signal transduction factors involved
16120782	iNOS	iNOS-derived	2.2	Apart from the detrimental action of either iNOS-derived excess NO or COX-2-generated proinflammatory prostanoids the dual inhibition of
16120782	iNOS	iNOS	2.2	The latter signal transduction pathway is also involved in the iNOS and COX-2 gene regulation after inflammatory stimulation
16120782	iNOS	iNOS	2.2	antagonizing the JAK-STAT pathway contributes to the observed suppression of iNOS and COX-2 expression
16436205	iNOS	iNOS	3.2	B 4 (LTB LTB 4 inducible nitric oxide synthase (iNOS) iNOS and _amp_#x02022 NO (indexed indexed by nitrite release into the
16436205	iNOS	iNOS	3.2	Results iNOS expression and nitric oxide synthesis is increased in G93A-SOD1 glia
16436205	iNOS	iNOS	3.2	Elevated levels of iNOS protein could be detected in G93A-SOD1 astrocytes relative to nontransgenic
16436205	iNOS	iNOS	3.2	of TNF_amp_#x003b1 COX-II and to a lesser extent 5LOX and iNOS
16436205	iNOS	iNOS	3.2	Figure 3 iNOS protein expression and NO 2 -formation in cultured nontransgenic or
16624536	iNOS	iNOS	2.7	from oxidative damage resulting from inducible nitric oxide synthase (iNOS) iNOS activity 59
16624536	NOS	NOS	2.7	neurons and which is dependent on transcriptional upregulation of neuronal NOS 36
16624536	iNOS	iNOS	2.7	well as decreased mRNA expression of inflammatory products including COX-2 iNOS and I_amp_#x3ba B (an an inhibitor of NF-_amp_#x3ba B by
16624536	iNOS	iNOS	2.7	Like microglia reactive astrocytes express inflammatory markers including iNOS and COX-2 114 and can produce proinflammatory mediators including prostaglandins
16624536	iNOS	iNOS	2.7	the level of the microglia in which the up-regulation of iNOS is inhibited and at the target cell where the release
16647138	NOS	NOS	2.7	mice with deletion of the inducible nitric oxide synthase (NOS) NOS gene which suggests that COX-2 reaction products may be another
16647138	iNOS	iNOS-derived	2.7	that COX-2 reaction products may be another mechanism by which iNOS-derived nitric oxide contributes to ischemic brain injury ( Nagayama et
16753239	iNOS	iNOS	1.5	or the PPAR-_amp_#x3b3 antagonist GW9662 did not alter NO and iNOS expression in these cells
16753239	iNOS	iNOS	1.5	Recent studies demonstrated that TZDs block the production of iNOS TNF-_amp_#x3b1 IL-6 and COX-2 by primary rat microglia and astrocytes
16753239	iNOS	iNOS	1.5	the PPAR-_amp_#x3b1 agonist gemfibrozil inhibited cytokine induction of NO and iNOS by human astroglial and primary astrocytes
16753239	iNOS	iNOS	1.5	negative PPAR-_amp_#x3b1 mutant did not overcome gemfibrozil mediated inhibition of iNOS gene expression following transient transfection of astroglial cells
16766086	iNOS	iNOS	2.5	(1999) 1999 reported that PPAR_amp_#x3b3 agonists suppress cytokine evoked neuronal iNOS expression in vitro thereby preventing NO-mediated cell death of neurons
16766086	iNOS	iNOS	2.5	cerebellum resulted in induction of inducible nitric oxide synthase (iNOS) iNOS expression and subsequent neuronal death
16766086	iNOS	iNOS	2.5	it was argued to be due to the suppression of iNOS and other inflammatory gene expression ( Heneka et al. 2000
16766086	iNOS	iNOS	2.5	However PPAR_amp_#x3b3 agonist treatment was shown to suppress neuronal iNOS expression ( Heneka et al. 1999
16766086	iNOS	iNOS	2.5	Expression of inflammatory genes such as iNOS cyclooxygenase-2 (COX-2), COX-2 proinflammatory cytokines and intercellular adhesion molecule are
16766086	iNOS	iNOS	2.5	is associated with reduced expression of inflammatory mediators such as iNOS COX-2 and IL-1_amp_#x3b2 ( Fig 5
16766086	iNOS	iNOS	2.5	level troglitazone inhibited pro-inflammatory cytokine expression including IL1_amp_#x3b2 TNF_amp_#x3b1 and iNOS in the spinal cord
16766086	iNOS	iNOS	2.5	vehicle treated rats mRNA was reduced by approximately 25% for iNOS 30% for COX-2 and 50% for IL-1_amp_#x3b2 ( n =
16909005	iNOS	iNOS	1.0	Celastrol treatment reduced TNF-alpha iNOS CD40 and GFAP immunoreactivity in the lumbar spinal cord sections
17018025	iNOS	iNOS	3.7	nitric oxide by up-regulation of inducible nitric oxide synthase (iNOS) iNOS ( Zhao et al 2004
17018025	iNOS	iNOS	3.7	Figure 5 demonstrates that lipopolysaccharide enhanced iNOS protein expression and IL-4 significantly inhibited iNOS expression induced by
17018025	iNOS	iNOS	3.7	that lipopolysaccharide enhanced iNOS protein expression and IL-4 significantly inhibited iNOS expression induced by lipopolysaccharide
17018025	iNOS	iNOS	3.7	In our previous study we demonstrated that special iNOS inhibitor L-NIL significantly reduced nitric oxide production and reversed motoneuron
17018025	iNOS	iNOS	3.7	Nitric oxide is synthesized by iNOS in microglia iNOS protein expression was down-regulated by IL-4 in
17018025	iNOS	iNOS	3.7	Nitric oxide is synthesized by iNOS in microglia iNOS protein expression was down-regulated by IL-4 in activated microglia when
17018025	iNOS	iNOS	3.7	potential explanation of the increased suppressive effects of IL-4 on iNOS expression in activated microglia
17018025	iNOS	iNOS	3.7	Two studies have reported the inhibitory effects of IL-4 on iNOS in lipopolysaccharide-stimulated astrocytes and mixed glial cultures ( Brodie et
17018025	iNOS	iNOS	3.7	However simultaneous activation of iNOS (to to produce nitric oxide and NADPH oxidase (to to
17018025	NOS	NOS	2.7	that AB-stimulated microglia released TNF-A and glutamate which synergistically increased NOS expression and activity in neurons by western blot and immunocytochemistry
17018025	iNOS	iNOS	3.7	Therefore in addition to microglia iNOS expression neuronal NOS may be another source of nitric oxide
17018025	NOS	NOS	2.7	Therefore in addition to microglia iNOS expression neuronal NOS may be another source of nitric oxide contributing to motoneuron
17018025	iNOS	iNOS	3.7	also been shown that TNF-A had neurotoxic effects through up-regulating iNOS nitric oxide and production from microglia ( Kuno et al
17018025	iNOS	iNOS	3.7	Like IL-4 IL-10 inhibited iNOS expression and nitric oxide production from microglia (data data not
17191135	iNOS	iNOS	3.2	and interferon-G (IFN-G) IFN-G promotes a rapid increase in both iNOS expression and nitrite levels followed by enhancement of Hsp70 3
17191135	iNOS	iNOS-derived	2.7	3 20 whereas the modulation of HO-1 mRNA expression by iNOS-derived NO following stimulation with LPS has also been reported in
17191135	iNOS	iNOS	3.2	Moreover the early increase in iNOS protein levels observed in endothelial cells exposed to low oxygen
17191135	NOS	NOS	2.7	(ii) ii decreasing the neuronal 3-nitrotyrosine levels and therefore inducible NOS activity and (iii) iii by the well known direct free
17418957	iNOS	iNOS	1.0	also plan to evaluate apoptosis and necrosis as well as iNOS production in response to a variety of cytokines
17555556	iNOS	iNOS	2.8	by lipopolysaccharide (LPS) LPS up-regulated inducible nitric oxide synthase (iNOS) iNOS expression and released nitric oxide and superoxide which were cytotoxic
17555556	iNOS	iNOS	2.8	The iNOS inhibitor L-N 6 -(1-iminoethyl)lysine - 1-iminoethyl lysine hydrochloride (L-NIL, L-NIL
17555556	iNOS	iNOS	2.8	of the cultured microglia we measured the protein levels of iNOS in microglia which is the major source of nitric oxide
17555556	iNOS	iNOS	2.8	As demonstrated by western analyses the iNOS expression in untreated microglia was at background levels
17555556	iNOS	iNOS	2.8	_amp_#x03BC g mL LPS mSOD1 G93A microglia expressed 170% more iNOS than wild-type microglia ( p _lt_ 0.05 ( Fig 1b
17555556	iNOS	iNOS	2.8	motoneurons we tested if the addition of an inhibitor of iNOS can rescue motoneurons
17555556	iNOS	iNOS	2.8	The addition of the iNOS inhibitor L-NIL (100 100 _amp_#x03BC;g/mL) _amp_#x03BC g mL 1 h
17555556	iNOS	iNOS	2.8	leading to further cell damage ( Mhatre et al 2004 iNOS was found to be up-regulated in a transgenic mouse model
17555556	iNOS	iNOS	2.8	Up-regulation of iNOS may in turn stimulate nitric oxide production which plays a
17555556	iNOS	iNOS	2.8	present study we demonstrated that mSOD1 G93A microglia expressed more iNOS and released more nitric oxide and superoxide release relative to
17555556	iNOS	iNOS	2.8	Furthermore pre-treatment with the iNOS inhibitor (L-NIL) L-NIL prior to LPS treatment significantly decreased nitrate
17555556	iNOS	iNOS	2.8	Although two earlier reports demonstrated that gene deletion of iNOS or neuronal nitric oxide synthase (nNOS) nNOS does not alter
17555556	iNOS	iNOS	2.8	(nNOS) nNOS does not alter motoneuron disease in double transgenic iNOS _amp_#8722;/_amp_#8722; _amp_#8722 _amp_#8722 /mSOD1 mSOD1 G93A or nNOS _amp_#8722;/_amp_#8722; _amp_#8722
17555556	iNOS	iNOS	2.8	(2007) 2007 demonstrated that mSOD1 G93A mice with both iNOS alleles deleted have a delayed disease progression and a prolonged
17555556	iNOS	iNOS	2.8	a heightened sensitivity to LPS as demonstrated by superinduction of iNOS and activation of mitogen-activated protein kinase
17569578	iNOS	iNOS	1.0	In addition neuronal expression of inflammatory enzyme systems including iNOS have been described in AD 77 105 and 165
17569578	iNOS	iNOS	1.0	The experimental expression of iNOS in neurons resulted in time dependent neuronal cell death which
17569578	iNOS	iNOS	1.0	PPAR_amp_#x3b3 activation in microglial cells suppressed inflammatory cytokine expression iNOS expression and NO production and inhibition of COX2 and subsequent
17569578	iNOS	iNOS	1.0	studies suggested that neuroinflammatory changes accompanied by microglial and astroglial iNOS expression may play a pivotal role in PD 79 and
17569578	iNOS	iNOS	1.0	Since PPAR_amp_#x3b3 activation results in a profound suppression of iNOS in peripheral macrophages 37 and 142 as well as in
17569578	iNOS	iNOS	1.0	In part iNOS suppression in MPTP treated mice may have been achieved by
17569578	iNOS	iNOS	1.0	SOD1-G93A mice as were the protein levels of COX-2 and iNOS
17569578	iNOS	iNOS	1.0	chemokine expression as well as elevated expression of adhesion molecules iNOS COX2 and other inflammatory mediators which act to exacerbate the
17569578	iNOS	iNOS	1.0	infiltration of peripheral leukocytes diminished microglial activation and reduction of iNOS COX2 and cytokine expression
17574754	iNOS	iNOS	1.0	One potential mechanism is via induction of iNOS production of NO and production of reactive oxygen species alternatively
18246426	iNOS	iNOS	2.7	neuronal form (nNOS) nNOS and inducible calcium independent form (iNOS) iNOS
18436268	iNOS	iNOS	2.5	and inhibited the expression of inducible nitric oxide synthase (iNOS) iNOS and tumor necrosis factor-alpha (TNF-_amp_#x3b1;) TNF-_amp_#x3b1 in spinal cord
18436268	iNOS	iNOS	2.5	0.45 _amp_#x3bc m PVDF membrane incubated with primary antibodies of iNOS (1:5000, 1 5000 Chemicon CA USA TNF-_amp_#x3b1 (1:1000, 1 1000
18436268	iNOS	iNOS	2.5	significant increase in the_amp_#xa0 expression of inflammation-related factors such as iNOS and TNF-_amp_#x3b1 in SOD1 G93A transgenic mice ( Almer et_amp_#xa0
18436268	iNOS	iNOS	2.5	Therefore in our study we examined the protein levels of iNOS and TNF-_amp_#x3b1 in the spinal cord of the mice
18436268	iNOS	iNOS	2.5	We_amp_#xa0 observed significant reduction of iNOS and TNF-_amp_#x3b1 in FA-SOD1 group or FA SOD1 group mice
18436268	iNOS	iNOS	2.5	FA B12 was more effective in lowing the level of iNOS ( Fig._amp_#xa0 5 C
18436268	iNOS	iNOS	2.5	treatment can suppress the production of inflammatory factors such as iNOS and TNF-_amp_#x3b1 and inhibit the activation of microglia and astrocytes
18436268	iNOS	iNOS	2.5	can switch resting murine astrocytes to active state and up-regulate iNOS expression and subsequently release nitric oxide ( Falsig et_amp_#xa0 al.
18436268	iNOS	iNOS	2.5	In addition it was reported that the expression of iNOS was increased in the spinal cord of the SOD1 G93A
18436268	iNOS	iNOS	2.5	mice and activated microglia and astrocytes increased the production of iNOS which suggest that iNOS may contribute to the pathology of
18436268	iNOS	iNOS	2.5	and astrocytes increased the production of iNOS which suggest that iNOS may contribute to the pathology of ALS and represent a
18436268	iNOS	iNOS	2.5	suppressed the glial activation as well as the expression of iNOS and TNF-_amp_#x3b1 in the spinal cord of SOD1 G93A mice
18436268	iNOS	iNOS	2.5	FA B12 possessed anti-inflammatory effects through inhibiting the expression of iNOS and TNF-_amp_#x3b1 and suppressing the activation of microglia and astrocytes
18436268	iNOS	iNOS	2.5	(A) A Western blot of iNOS and TNF-_amp_#x3b1 from spinal cord samples of G93A transgenic mice
18436268	iNOS	iNOS	2.5	(C_amp_#x2013;G) C_amp_#x2013 G Quantitative data of the expression of iNOS TNF-_amp_#x3b1 Bcl-2 cleaved caspase-3 and cleaved PARP in five groups
18464922	iNOS	iNOS	2.2	of various inflammatory proteins like inducible nitric oxide synthase (iNOS), iNOS tumor necrosis factor-_amp_#x003b1 TNF-_amp_#x003b1 and matrix metalloproteinase-9 (MMP-9) MMP-9 in
18464922	iNOS	iNOS	2.2	PPRE in their promoters including those encoding for inflammation (iNOS, iNOS NF-_amp_#x003ba B COX-2 oxidative stress and apoptosis
18464922	iNOS	iNOS	2.2	Furthermore we showed that pioglitazone treatment reduced iNOS NF-_amp_#x003ba B and 3-nitotyrosine immunoreactivity in the spinal cord of
18464922	iNOS	iNOS	2.2	as well as reduction in the expression of COX-2 and iNOS 39
18464922	iNOS	iNOS	2.2	Increased levels of iNOS in HD 59 elevated oxidative damage products such as malondialdehyde
18464925	iNOS	iNOS	2.2	and TNF-_amp_#x003b1 as well as expression of the inducible enzymes iNOS and COX2 induced in LPS-stimulated astrocyte and microglial cultures 58
18464925	iNOS	iNOS	2.2	Paintlia et al 65 demonstrated that the inhibition of iNOS expression and the increase of survival of differentiating OPs induced
18464925	iNOS	iNOS	2.2	al 74 who demonstrated that this PPAR-_amp_#x003b3 natural ligand attenuates iNOS expression and the subsequent NO accumulation in the murine BV-2
18464925	iNOS	iNOS	2.2	the NO pathway it was suggested that 15d-PGJ 2 inhibits iNOS expression by a PPAR-_amp_#x003b3 independent mechanism
18464925	iNOS	iNOS	2.2	cell line in primary microglial cultures 15d-PGJ 2 prevented LPS-induced iNOS expression and TNF-_amp_#x003b1 production as well as IFN-_amp_#x003b3 -induced expression
10525172	nitric oxide synthase	nitric oxide synthase	1.0	schematic representation of the nitric oxide synthase monomer.
11173059	nitric oxide synthase	nitric oxide synthase	1.0	ion pump activity and therefore atp expenditure in dopaminergic cells with a mitochondrial dysfunction due to a defective complex i. the concomitant rise in intracellular ca 2+ levels would activate nitric oxide synthase with the subsequent generation of toxic free radicals such as peroxynitrites.
11173059	nitric oxide synthase	nitric oxide synthase	1.0	alzheimer disease since it induces microglia activation and the production of several inflammatory cytokines and chemokines including interleukin 1_amp_#x3b2; with subsequent stimulation of inducible nitric oxide synthase and further oxidative damage to neurons berger ; yates and akama .
12076984	nitric oxide synthase	nitric oxide synthase	1.0	excessive production of no as a consequence of nitric oxide synthase induction in activated glia has been attributed to participate in neurodegeneration.
15081582	nitric oxide synthase	nitric oxide synthase	1.0	prostaglandins pga 1 pga 2 and pgj 2 all can suppress nf _amp_#x3ba;b activation and thus suppress cox 2 induction as well as other inflammatory mediators including inducible nitric oxide synthase and certain cytokines.
15571972	nitric oxide synthase	nitric oxide synthase	1.0	accordingly several studies showed that minocycline reduces the expression of inducible nitric oxide synthase and subsequent nitric oxide production as well as caspase 1 activity/expression and thereby prevents the formation of interleukin 1_amp_#x3b2; amin et al. 1996 ; chen et al. 2000 _amp_#x2014;5 mg/kg/
15572176	nitric oxide synthase	nitric oxide synthase	1.0	reactive astrocytes in als contain protein inclusions express inflammatory makers such as the inducible forms of nitric oxide synthase inos and cyclooxygenase cox 2 display nitrotyrosine immunoreactivity and downregulate the glutamate transporter eaat2.
15649489	nitric oxide synthase	nitric oxide synthase	1.0	nf kappa b|neuroprotective agents|ppar gamma|thiazolidinediones|pioglitazone|3 nitrotyrosine|tyrosine|nitric oxide synthase|nitric oxide synthase type ii|nos2 protein mouse|sod1 g93a protein|superoxide dismutase|
15799549	nitric oxide synthase	nitric oxide synthase	1.0	macrophages in als spinal cord showed strong expression of cyclooxygenase 2 cox 2 one log greater than control tissues and inducible nitric oxide synthase.
16014720	nitric oxide synthase	nitric oxide synthase	1.0	for instance nadph oxidase and inducible nitric oxide synthase inos which are major sources of inflammatory oxidants are upregulated in damaged areas in both pd and the 1 methyl 4 phenyl 1 2 3 6 tetrahydropyridine mptp model of pd hunot et al. 1996 ; liberatore
16120782	nitric oxide synthase	nitric oxide synthase	1.0	activated microglia were significantly reduced at sites of neurodegeneration in pio treated sod1 g93a mice as were the protein levels of cyclooxygenase 2 and inducible nitric oxide synthase.
16120782	nitric oxide synthase	nitric oxide synthase	1.0	f als is the loss of motor neurons talbot 2002 which is accompanied by a robust glial response including activation of microglia and astrocytes as well as the expression of cyclooxygenase 2 cox 2 and nitric oxide synthase inos in the spinal cord phul et al. 2000 ; almer et al. 2001 ; yasojima et al. 2001 ; barbeito et al. 2004 .
16179515	nitric oxide synthase	nitric oxide synthase	1.0	baicalein treatment also downregulated tumor necrosis factor receptor tnfrp55 and upregulated noninducible nitric oxide synthase nnos and glutamine synthase gs .
16436205	nitric oxide synthase	nitric oxide synthase	1.0	a significant elevation in either the basal or the tumor necrosis alpha tnf_amp_#x003b1; stimulated levels of proinflammatory eicosanoids prostaglandin e 2 pge 2 and leukotriene b 4 ltb 4 ; inducible nitric oxide synthase inos and _amp_#x02022;no indexed by nitrite release into the culture medium ; and protein carbonyl products.
16624536	nitric oxide synthase	nitric oxide synthase	1.0	oic acid nmda receptor antagonists and soluble tnf receptor protect neurons from microglial conditioned media dependent death which is thought to result from oxidative damage resulting from inducible nitric oxide synthase inos activity [59] .
16637591	nitric oxide synthase	nitric oxide synthase	1.0	it has been documented that the excessive s100b promotes the expression of inducible nitric oxide synthase or pro inflammatory cytokines and exhibits detrimental effects on neurons.
16647138	nitric oxide synthase	nitric oxide synthase	1.0	the beneficial effects of ns 389 on ischemic brain injury were not apparent in mice with deletion of the inducible nitric oxide synthase nos gene which suggests that cox 2 reaction products may be another mechanism by which inos derived nitric oxide contributes to ischemic brain injury nagayama et al. 1999 .
16766086	nitric oxide synthase	nitric oxide synthase	1.0	similarly the injection of the proinflammatory stimulus lipopolysaccharide into the rat cerebellum resulted in induction of inducible nitric oxide synthase inos expression and subsequent neuronal death.
17018025	nitric oxide synthase	nitric oxide synthase	1.0	we have previously demonstrated that activated microglia produce nitric oxide by up regulation of inducible nitric oxide synthase inos zhao et al 2004 .
17034351	nitric oxide synthase	nitric oxide synthase	1.0	n mutant sod1+ glial cells may stimulate broad spectrum upregulation of proinflammatory genes including arachidonic acid metabolizing enzymes [e.g. cyclooxygenase ii cox ii and 5 lipoxygenase 5lox ]; nitric oxide synthase nos isoforms; cytokines particularly tumor necrosis factor alpha tnf alpha ; chemokines; and immunoglobulin fc receptors fcgammars .
17191135	nitric oxide synthase	nitric oxide synthase	1.0	in addition ad lymphocytes showed an increased expression of inducible nitric oxide synthase ho 1 hsp72 hsp60 and trxr [ 96 ].
17350694	nitric oxide synthase	nitric oxide synthase	1.0	ion of voltage gated l n and p/q type ca 2+ channels activation of k + channels activation of focal adhesion kinase activation of cytosolic phospholipase a 2 activation cb 1 r or inhibition cb 2 r of nitric oxide synthase.
17555556	nitric oxide synthase	nitric oxide synthase	1.0	our previous in vitro studies have demonstrated that primary microglia activated by lipopolysaccharide lps up regulated inducible nitric oxide synthase inos expression and released nitric oxide and superoxide which were cytotoxic to co cultured primary motoneurons le et al 2001 ; zhao et al 2004 .
18246426	nitric oxide synthase	nitric oxide synthase	1.0	no is synthesized from l arginine by nitric oxide synthase nos [ 22 23 ].
18436268	nitric oxide synthase	nitric oxide synthase	1.0	furthermore we found that fa or fa + b12 treatment significantly attenuated the plasma hcy level suppressed the activation of microglia and astrocytes and inhibited the expression of inducible nitric oxide synthase inos and tumor necrosis factor alpha tnf _amp_#x3b1; in spinal cord.
18464922	nitric oxide synthase	nitric oxide synthase	1.0	tzds inhibit the expression of various inflammatory proteins like inducible nitric oxide synthase inos tumor necrosis factor _amp_#x003b1; tnf _amp_#x003b1; and matrix metalloproteinase 9 mmp 9 in macrophages [ 26 ] and are beneficial in disorders such as inflammatory bowel disease [ 27 ].
18464925	nitric oxide synthase	nitric oxide synthase	1.0	= central nervous system cox= cyclooxygenase dbd= dna binding domain eae= experimental autoimmune encephalomyelitis hode= hydroxy octadecadienoic acids ifn= interferon il= interleukin inos= inducible nitric oxide synthase jak= janus activated kinases lbd= ligand binding domain lps= lipopolysaccharide mapk= mitogen activated protein kinase mcp 1= monocyte chemoattractrant protein 1 mhc= major histocompatibility complex
18539342	nitric oxide synthase	nitric oxide synthase	1.0	epiplexus cells have been shown to respond to lps or ifn gamma injection blast injury and other stimuli with ultrastructural modifications increased number hla dr and nitric oxide synthase upregulation eng ang et al. 1998 .