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1 n of cyclooxygenase-2 after stimulation with interleukin-1alpha.
2 ion, such as tumor necrosis factor-alpha and interleukin-1alpha.
3 were subjected to hypoxia and treatment with interleukin-1alpha.
4 imulation with the microenvironmental factor interleukin-1alpha.
5 elial (TBE) cells with a panel of cytokines (interleukin-1alpha, 1beta, 2, 3, 4, 5, 6, 7, 8, 9, 10, 1
6 ed levels of proinflammatory cytokine mRNAs (interleukins 1alpha, 1beta, and 6 and tumor necrosis fac
8 pression of acute proinflammatory cytokines (interleukins 1alpha, 6, and 8, tumor necrosis factor alp
9 and in accumulation of epithelial-associated interleukin-1alpha, a cytokine that inhibits Smad2 signa
11 (MABp1) cloned from a human being to target interleukin-1alpha, a mediator of chronic inflammation.
13 ar clearance and tear fluid concentration of interleukin-1alpha, a proinflammatory cytokine that has
18 gnificantly lower levels of 2 key cytokines--interleukin 1alpha and interleukin 8--at wound sites.
19 tein was shown to stimulate the secretion of interleukin 1alpha and RANTES, whereas purified F (fusio
21 amycin-treated mice reduced plasma levels of interleukin-1alpha and -beta and granulocyte-colony stim
22 vely, by basic fibroblast growth factor plus interleukin-1alpha and antisense oligonucleotides to PKC
23 r necrosis, and resulted in up-regulation of interleukin-1alpha and down-regulation of anti-apoptotic
27 ocused on the role of bacterial lipases, and interleukin-1alpha and matrix metalloproteinases in the
28 ooth muscle cells following stimulation with interleukin-1alpha and platelet-derived growth factor.
29 man corneal fibroblasts after treatment with interleukin-1alpha and subjected to DNA microarray analy
30 production of the pro-inflammatory cytokines interleukin-1alpha and tumor necrosis factor alpha in th
31 as accompanied by decreased plasma levels of interleukin-1alpha and tumor necrosis factor alpha, and
33 (KC), macrophage cationic peptide-1 (MCP-1), interleukin 1alpha, and interleukin 6) involved in monoc
34 macrophage inflammatory proteins 1 and 2 and interleukin-1alpha, and higher levels of putative protec
35 igand, macrophage colony-stimulating factor, interleukin-1alpha, and interleukin-6 mRNA compared with
36 or necrosis factor-alpha, interleukin-15 and interleukin-1alpha, and transforming growth factor-beta.
37 espectively) and was effective in inhibiting interleukin-1alpha- and oncostatin M-induced C1,C2 relea
40 mokines and we report the failure to release interleukin-1alpha as a common immunological phenotype.
41 ased expression of c-myc (5- to 12-fold) and interleukin-1alpha/beta (600-fold) by real-time polymera
42 tumor necrosis factor-alpha (TNF-alpha) and interleukin-1alpha/beta (IL-1alpha/beta) that contribute
43 ess the safety and tolerability of MABp1 for interleukin-1alpha blockade in a refractory cancer popul
47 ry cytokines tumor necrosis factor-alpha and interleukin-1alpha elevate RANKL and OPG expression 5-40
48 ctive MMP activity on the aggrecan IGD; (ii) interleukin-1alpha exposure induces both aggrecanase and
49 Our results demonstrate that regulation of interleukin-1alpha expression is primarily dependent on
50 d growth factor-BB, insulin growth factor-1, interleukin-1alpha) failed to augment the adhesion or pr
53 expression of the bone resorptive cytokines interleukin 1alpha (IL-1alpha) (P < 0.01) and IL-1beta (
57 results indicated the presence of mRNAs for interleukin 1alpha (IL-1alpha) and transforming growth f
58 in multiple cell types after treatment with interleukin 1alpha (IL-1alpha) as compared with tumor ne
62 o immunomodulatory therapeutics.The cytokine interleukin 1alpha (IL-1alpha) plays an important role i
63 g greater lung damage, vascular leakage, and interleukin 1alpha (IL-1alpha) release than the low-viru
65 in response to tumor necrosis factor alpha, interleukin 1alpha (IL-1alpha), gamma interferon, lipopo
67 ctor (GM-CSF), gamma interferon (IFN-gamma), interleukin 1alpha (IL-1alpha), IL-1beta, IL-6, and IL-1
68 d secretion of the proinflammatory cytokines interleukin 1alpha (IL-1alpha), IL-1beta, IL-6, IL-12p70
69 led significant differences in expression of interleukin 1alpha (IL-1alpha), IL-1beta, IL-6, IL-1Ra,
70 weight (LW/BW) ratio, and elevated levels of interleukin 1alpha (IL-1alpha), IL-1beta, IL-6, tumor ne
71 sets of monocytes by assessing intracellular interleukin 1alpha (IL-1alpha), IL-1beta, interleukin 6
74 s (EC) to tumor necrosis factor-alpha (TNF), interleukin-1alpha (IL-1), and phorbol myristate acetate
76 Cytokines that were upregulated included interleukin-1alpha (IL-1alpha) and -1beta, IL-1 receptor
77 eolar macrophages (AMs), which then released interleukin-1alpha (IL-1alpha) and caused inducible bron
78 temic levels of the proinflammatory cytokine interleukin-1alpha (IL-1alpha) and higher levels of the
83 in increased circulating cytokines, such as interleukin-1alpha (IL-1alpha) and IL-1beta, and increas
84 nensis-infected DCs secreted lower levels of interleukin-1alpha (IL-1alpha) and IL-1beta, were less p
86 ificant induction of mRNAs for the cytokines interleukin-1alpha (IL-1alpha) and IL-6 and the chemokin
87 colony-stimulating factor, interferon-gamma, interleukin-1alpha (IL-1alpha) and IL-6, compared with m
88 ious levels constitutively with considerable interleukin-1alpha (IL-1alpha) and tumor necrosis factor
89 icular cartilage explants were cultured with interleukin-1alpha (IL-1alpha) and/or oncostatin M (OSM)
90 Blocking experiments with neutralizing anti-interleukin-1alpha (Il-1alpha) antibodies and IL-1Ra, an
91 Expression of the genes for collagenase and interleukin-1alpha (IL-1alpha) are induced as stromal ce
92 and tested for the presence of TNFalpha and interleukin-1alpha (IL-1alpha) by enzyme-linked immunoso
93 This study was performed to determine if interleukin-1alpha (IL-1alpha) combined with other proin
94 Intratracheal LPS induced release of pro-interleukin-1alpha (IL-1alpha) from necrotic alveolar ma
96 ficiency enhances the early local release of interleukin-1alpha (IL-1alpha) in response to damaged ce
102 nal protein production in response to either interleukin-1alpha (IL-1alpha) or lipopolysaccharide (LP
103 % O(2) (normoxia) in media supplemented with interleukin-1alpha (IL-1alpha) or tumor necrosis factor
104 ingest apoptotic eosinophils was enhanced by interleukin-1alpha (IL-1alpha) or tumor necrosis factor
105 emonstrate that the proinflammatory cytokine interleukin-1alpha (IL-1alpha) plays an essential role i
106 d bone marrow-derived neutrophils exposed to interleukin-1alpha (IL-1alpha) produced chemokines in an
109 role in BTB restructuring via the action of interleukin-1alpha (IL-1alpha) since germ cells are know
110 elease from megakaryocytes can be induced by interleukin-1alpha (IL-1alpha) via a new rupture mechani
112 f the TNF-induced transcripts analyzed, only interleukin-1alpha (IL-1alpha) was modulated in response
113 treating (a) bovine articular cartilage with interleukin-1alpha (IL-1alpha), (b) purified bovine COMP
114 ransforming growth factor-alpha (TGF-alpha), interleukin-1alpha (IL-1alpha), and IL-1 receptor antago
116 ed to thrombopoietin (TPO), kit ligand (KL), interleukin-1alpha (IL-1alpha), and IL-3 in serum-free c
117 of tumor necrosis factor alpha (TNF-alpha), interleukin-1alpha (IL-1alpha), and IL-6 in DCs, althoug
118 r chondrocytes were cultured with or without interleukin-1alpha (IL-1alpha), and the relative express
120 rophages with Legionella pneumophila induced interleukin-1alpha (IL-1alpha), IL-10, monocyte chemotac
121 d against interferon-alpha, interferon-beta, interleukin-1alpha (IL-1alpha), IL-12p35, IL-12p40, and
122 creased expression of mRNA for the cytokines interleukin-1alpha (IL-1alpha), IL-1beta, and IL-8 but n
123 nes tumor necrosis factor alpha (TNF-alpha), interleukin-1alpha (IL-1alpha), IL-1beta, and IL-8 were
124 Fibroblasts from relb(-/-) mice overexpress interleukin-1alpha (IL-1alpha), IL-1beta, and tumor necr
126 is reflected at the translational level, as interleukin-1alpha (IL-1alpha), IL-1beta, IL-6, and tumo
127 ing antisense RNA probes specific for bovine interleukin-1alpha (IL-1alpha), IL-1beta, IL-6, gamma in
128 gene c-myc and the proinflammatory cytokines interleukin-1alpha (IL-1alpha), IL-1beta, IL-6, IFN-gamm
129 ater proportion of RA cases versus controls: interleukin-1alpha (IL-1alpha), IL-1beta, IL-6, IL-10, I
130 ificant up-regulation in gene expression for interleukin-1alpha (IL-1alpha), IL-1beta, IL-6, IL-10, t
131 ansgenic mice showed identical expression of interleukin-1alpha (IL-1alpha), IL-1beta, interferon gam
132 ed, immature DCs exhibited higher amounts of interleukin-1alpha (IL-1alpha), IL-1beta, tumor necrosis
133 is, we examined expression of genes encoding interleukin-1alpha (IL-1alpha), IL-2, IL-4, IL-5, IL-6,
134 for tumor necrosis factor alpha (TNF alpha), interleukin-1alpha (IL-1alpha), IL-4, IL-6, IL-8, macrop
135 hallenged with IOE had lower levels of serum interleukin-1alpha (IL-1alpha), IL-6, and IL-10 compared
136 ators of the acute-phase response, including interleukin-1alpha (IL-1alpha), IL-6, and tumor necrosis
137 pared to the attenuated mutant were noted in interleukin-1alpha (IL-1alpha), IL-6, IL-8, and tumor ne
140 ized expression of proinflammatory cytokines interleukin-1alpha (IL-1alpha), macrophage inflammatory
141 actor receptor-associated protein 1 (TRAF1), interleukin-1alpha (IL-1alpha), MCP-2, N-cadherin, and b
142 to be highly synergistic in the induction of interleukin-1alpha (IL-1alpha), type II (inducible) nitr
143 tion-polymerase chain reaction (RT-PCR) with interleukin-1alpha (IL-1alpha)-specific primers using to
154 as stimulated to resorb with the addition of interleukin-1alpha (IL-1alpha)/oncostatin M (OSM) in the
156 ced by direct injection of recombinant human interleukin-1alpha (IL-1alpha, 1 microg in 2 microL) int
158 various stimuli, including cytokines (e.g., interleukin-1alpha [IL-1alpha] and tumor necrosis factor
159 nce and absence of added exogenous cytokine (interleukin-1alpha [IL-1alpha] or tumor necrosis factor
160 oattractant protein 1]) and three cytokines (interleukin-1alpha [IL-1alpha], IL-10, and granulocyte c
161 were analyzed for cytokine production (i.e., interleukin-1alpha [IL-1alpha], IL-1beta, IL-6, IL-8, IL
162 e markers within 8 candidate cytokine genes (interleukin-1alpha [IL-1alpha], IL-2, IL-4, IL-6, IL-10,
163 x (MAC) bacteremia, the levels of IL-1alpha (interleukin-1alpha), IL-6, IL-10, tumor necrosis factor
165 [CKB], angiotensin-converting enzyme [DCP1], interleukin-1alpha [IL1A], low-density lipoprotein recep
166 is initiated by the paracrine signalling of interleukin 1alpha (IL1alpha), which activates both skin
168 cted mice produced tumor necrosis factor and interleukin-1alpha in response to T4SS-sufficient, but n
169 king synergy between ultraviolet B and added interleukin-1alpha in the induction of transcription by
171 tumor necrosis factor-alpha (TNF-alpha)- and interleukin-1alpha-induced NF-kappaB activity and an enh
172 in synergy with lipopolysaccharide (LPS) or interleukin 1alpha induces Cox-2 expression in mouse per
173 ormants was stimulated by several cytokines (interleukin 1alpha, interleukin 6, and tumor necrosis fa
174 o induce inflammation-related genes, such as interleukin-1alpha, interleukin-1beta, interleukin-6, an
176 in the expression of inflammatory cytokines (interleukin-1alpha, interleukin-1beta, or tumor necrosis
177 reversed increases in inflammatory mediators interleukin-1alpha, interleukin-1beta, tissue necrosis f
178 r cells was induced by a single injection of interleukin-1alpha into the lacrimal gland and that this
180 tumor necrosis factor alpha levels and serum interleukin-1alpha levels compared with animals with art
181 decrease in tumor necrosis factor-alpha and interleukin-1alpha levels in the oxazalone-treated epide
182 xide synthase, the proinflammatory cytokines interleukin-1alpha, macrophage inflammatory protein 1-al
183 (PKC) in basic fibroblast growth factor- and interleukin-1alpha-mediated MMP production from cultured
184 tatic cancer (18 tumour types) received anti-interleukin-1alpha monotherapy in dose-escalation and ex
185 ophages in the dermis and a reduced level of interleukin-1alpha mRNA expression, compared with WT mic
187 or 2 and interleukin 17F, without effects on interleukin 1alpha or interleukin 1beta, suggesting a di
190 Tumor necrosis factor-alpha (TNF-alpha), interleukin-1alpha, or interleukin-1beta caused a time-d
191 genes proximal to SMILR was also altered by interleukin-1alpha/platelet-derived growth factor treatm
195 alysis of the corneal fibroblast response to interleukin-1alpha provides important insight into model
196 S to uroepithelium and vigorous induction of interleukin 1alpha represents the initial stages of GBS
197 untreated or treated with recombinant human interleukin-1alpha (rHuIL-1alpha), was assessed by radio
199 in an increase in tumor necrosis factor and interleukin-1alpha staining in the epidermis that was re
201 onoclonal antibody binding for E-selectin in interleukin-1alpha-stimulated microvascular endothelium
204 ry cytokines tumor necrosis factor alpha and interleukin 1alpha, strongly potentiated IFN-gamma-induc
206 ated by transforming growth factor-alpha and interleukin-1alpha, the model revealed new molecular mec
208 h polymyositis and dermatomyositis implicate interleukin-1alpha, transforming growth factor-beta, and
210 ctor-alpha (TGF-alpha), but not by cytokines interleukin-1alpha, tumor necrosis factor-alpha, interfe
211 increase in DNA binding, but treatment with interleukin-1alpha, tumor necrosis factor-alpha, or phor
215 pa B-dependent transcriptional regulation of interleukin-1alpha, which, in an autocrine manner, induc
216 toinduced cytokine, were markedly different: interleukin-1alpha without ultraviolet produced a 15-fol
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