戻る
「早戻しボタン」を押すと検索画面に戻ります。

今後説明を表示しない

[OK]

コーパス検索結果 (1語後でソート)

通し番号をクリックするとPubMedの該当ページを表示します
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
7 eron-gamma, tumor necrosis factor-alpha, and interleukins 1alpha, 6, 12, 22, 23, and 17.
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
10                                 In addition, interleukin-1alpha, a germ cell-derived cytokine, was al
11  (MABp1) cloned from a human being to target interleukin-1alpha, a mediator of chronic inflammation.
12                             The responses to interleukin-1alpha, a photoinduced cytokine, were marked
13 ar clearance and tear fluid concentration of interleukin-1alpha, a proinflammatory cytokine that has
14 sis, in part through a process that requires interleukin-1alpha activation.
15                            Neutralization of interleukin-1alpha activity suppressed the constitutive
16                                              Interleukin-1alpha, although activated in VZV-infected c
17  did poorly metastatic clones in response to interleukin 1alpha and IFN-gamma stimulation.
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
20                                    Cytokines interleukin-1alpha and -1beta, tumor necrosis factor-alp
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
24                                              Interleukin-1alpha and interleukin-1beta were first incr
25                            For example, both interleukin-1alpha and interleukin-33 exhibit 'alarmin'-
26                                    Moreover, interleukin-1alpha and interleukin-6 did not impair the
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
32                                              Interleukin-1alpha and tumor necrosis factor-alpha enhan
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
38                  Further study of MABp1 anti-interleukin-1alpha antibody therapy for advanced stage c
39           As tumor necrosis factor-alpha and interleukin-1alpha are major mediators of cutaneous infl
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
44 on exogenous microglia induced expression of interleukin-1alpha by the organotypic culture.
45                                          The interleukin-1alpha concentration remained increased unti
46  uropathogenic GBS-specific up-regulation of interleukin 1alpha during infection.
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
51                                              Interleukin-1alpha had a repulsive chemotactic effect on
52              MABp1, an antibody that targets interleukin 1alpha, has been associated with antitumour
53  expression of the bone resorptive cytokines interleukin 1alpha (IL-1alpha) (P < 0.01) and IL-1beta (
54 nduced steady increases in the expression of interleukin 1alpha (IL-1alpha) and IL-18.
55                                              Interleukin 1alpha (IL-1alpha) and IL-1beta are equally
56 ractant CCL20, and proinflammatory cytokines interleukin 1alpha (IL-1alpha) 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
59 ot have a marked effect on the expression of interleukin 1alpha (IL-1alpha) during infection.
60                                              Interleukin 1alpha (IL-1alpha) is capable of driving pro
61               Mechanistically, deficiency in interleukin 1alpha (IL-1alpha) or platelet-activating fa
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
64                                              Interleukin 1alpha (IL-1alpha), a 33 kDa precursor, is c
65  in response to tumor necrosis factor alpha, interleukin 1alpha (IL-1alpha), gamma interferon, lipopo
66 ection 3 d later as well as their content of interleukin 1alpha (IL-1alpha), IL-1beta, and IL-6.
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
72            No upregulation of antral mucosal interleukin 1alpha (IL-1alpha), IL-1beta, or tumor necro
73 ally pronounced when cells were treated with interleukin-1alpha (IL-1) plus aspirin for 24 h.
74 s (EC) to tumor necrosis factor-alpha (TNF), interleukin-1alpha (IL-1), and phorbol myristate acetate
75 posed to phorbol ester (TPA) or PDGF-BB plus interleukin-1alpha (IL-1).
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
79                              While levels of interleukin-1alpha (IL-1alpha) and IL-16 were among 10 p
80                Neutrophils unable to produce interleukin-1alpha (IL-1alpha) and IL-1beta (IL-1alpha/b
81                                              Interleukin-1alpha (IL-1alpha) and IL-1beta are potent i
82              Neutralizing antibodies against interleukin-1alpha (IL-1alpha) and IL-1beta completely b
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
85  expression of the proinflammatory cytokines interleukin-1alpha (IL-1alpha) and IL-1beta.
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
95           Aggrecan catabolism was induced by interleukin-1alpha (IL-1alpha) in normal human articular
96 ficiency enhances the early local release of interleukin-1alpha (IL-1alpha) in response to damaged ce
97         Recently, we demonstrated a role for interleukin-1alpha (IL-1alpha) in the establishment of i
98                                              Interleukin-1alpha (IL-1alpha) is a key danger signal re
99                                              Interleukin-1alpha (IL-1alpha) is a multifunctional cyto
100                                              Interleukin-1alpha (IL-1alpha) is a potent proinflammato
101                                              Interleukin-1alpha (IL-1alpha) is a powerful activator o
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
107                                     Enhanced interleukin-1alpha (IL-1alpha) production from ER-stress
108                   Here, we demonstrated that interleukin-1alpha (IL-1alpha) signaling through IL-1R a
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
111              We previously demonstrated that interleukin-1alpha (IL-1alpha) was critical for the indu
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
115 f proinflammatory cytokines, such as GRO/KC, interleukin-1alpha (IL-1alpha), and IL-1beta.
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
119                    Mouse platelets expressed interleukin-1alpha (IL-1alpha), but not IL-1beta, induce
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
125                                              Interleukin-1alpha (IL-1alpha), IL-1beta, IL-2, IL-4, IL
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
138                  Up-regulated genes included interleukin-1alpha (IL-1alpha), IL-8, and thrombomodulin
139                                        bFGF, interleukin-1alpha (IL-1alpha), IL-8, and tumor necrosis
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
144                                              Interleukin-1alpha (IL-1alpha)-stimulated stromelysin pr
145  were cultured with 1 microM RetA or in 3 nM interleukin-1alpha (IL-1alpha).
146  the surrounding tissue through the cytokine interleukin-1alpha (IL-1alpha).
147 tro produced tumor necrosis factor alpha and interleukin-1alpha (IL-1alpha).
148  lines constitutively produce high levels of interleukin-1alpha (IL-1alpha).
149 inomycin D, and the proinflammatory cytokine interleukin-1alpha (IL-1alpha).
150 itamin D(3) was the proinflammatory cytokine interleukin-1alpha (IL-1alpha).
151    It is also possible to measure release of interleukin-1alpha (IL-1alpha).
152 rtilage chondrocytes treated with or without interleukin-1alpha (IL-1alpha).
153 diated through the proinflammatory cytokine, interleukin-1alpha (IL-1alpha).
154 as stimulated to resorb with the addition of interleukin-1alpha (IL-1alpha)/oncostatin M (OSM) in the
155                                              Interleukin-1alpha (IL-1alpha)is a prototypical proinfla
156 ced by direct injection of recombinant human interleukin-1alpha (IL-1alpha, 1 microg in 2 microL) int
157                   Histamine (100 microM) and interleukin-1alpha (IL-1alpha, 10 ng/ml) significantly s
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
164                                              Interleukin-1alpha (IL1A) is both regulated by and able
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
167  inducible form of nitric-oxide synthase and interleukin-1alpha in RAW 264.7 cells.
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
170 or significantly decreased recombinant human interleukin-1alpha-induced hypercalcemia.
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
175                                              Interleukin-1alpha, interleukin-1beta, or live Pseudomon
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
179                                        Human interleukin-1alpha is transported across the murine bloo
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
186                        With the exception of interleukin-1alpha, none of the humoral factors changed
187 or 2 and interleukin 17F, without effects on interleukin 1alpha or interleukin 1beta, suggesting a di
188                               Treatment with interleukin-1alpha or interleukin-6 of cultured composit
189 ted protein kinase by tumor necrosis factor, interleukin-1alpha, or gamma-interferon.
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
192                                              Interleukin-1alpha plus ultraviolet B caused a remarkabl
193                                         Only interleukin-1alpha possibly fulfills the criteria which
194 inding domain which resembles the NLS of the interleukin-1alpha precursor.
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
198                In contrast, addition of rIL (interleukin)-1alpha, rIL-1beta, rIL-6, or rIL-12 did not
199  in an increase in tumor necrosis factor and interleukin-1alpha staining in the epidermis that was re
200                                           In interleukin-1alpha-stimulated epidermal cultures, human
201 onoclonal antibody binding for E-selectin in interleukin-1alpha-stimulated microvascular endothelium
202              We thus compared the effects of interleukin-1alpha stimulation and neuronal induction of
203                         Within five hours of interleukin-1alpha stimulation, E-selectin density incre
204 ry cytokines tumor necrosis factor alpha and interleukin 1alpha, strongly potentiated IFN-gamma-induc
205                                Without added interleukin-1alpha the two constructs produced similar b
206 ated by transforming growth factor-alpha and interleukin-1alpha, the model revealed new molecular mec
207          This and the failure of recombinant interleukin-1alpha to stimulate peripheral blood mononuc
208 h polymyositis and dermatomyositis implicate interleukin-1alpha, transforming growth factor-beta, and
209           The tumor produced transcripts for interleukin-1alpha, tumor necrosis factor-alpha, and int
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
212            Further investigation showed that interleukin-1alpha was the primary cytokine secreted by
213 els of serum tumor necrosis factor alpha and interleukin 1alpha were detected.
214                                              Interleukin-1alpha, when normalized to baseline, increas
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

WebLSDに未収録の専門用語(用法)は "新規対訳" から投稿できます。
 
Page Top