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1        However, the effects of the pulmonary endothelium-derived amyloid and tau proteins on brain fu
2                               Mice receiving endothelium-derived amyloid and tau proteins via intrace
3 tem tissues obtained from animals exposed to endothelium-derived amyloids to assess these issues.
4 al NOS (eNOS) activity, and in aortic rings, endothelium-derived and eNOS-mediated relaxation (EDRF)
5 ecanoate (4alpha-PDD) (5 micromol/L) and the endothelium-derived arachidonic acid metabolite 11,12 ep
6         Epoxyeicosatrienoic acids (EETs) are endothelium-derived arachidonic acid metabolites of cyto
7 lcium-activated potassium channels (KCa) and endothelium-derived autacoids to CVD.
8 We confirm that TG2 activity is modulated by endothelium-derived bioactive NO in young rat aorta.
9                     We then demonstrate that endothelium-derived bioactive NO primarily mediates its
10            In this review, multiple modes of endothelium-derived blood flow regulation is discussed,
11 poxic pulmonary vasculature and suggest that endothelium-derived BMP4 plays a direct, paracrine role
12 ated by those that do not; (iii) PQ inhibits endothelium-derived, but not NO-induced, relaxations of
13 an mass in the legs and higher levels of the endothelium-derived C-terminal-pro-endothelin-1 (both p
14 hese results demonstrate a novel function of endothelium-derived Cat S in angiogenesis.
15 as a direct tumor-promoting effect, and that endothelium-derived CC chemokine ligand 2 (CCL2) suppres
16           A combination of prothrombin time, endothelium-derived CD105-microparticles, and platelet c
17 thelial cells, aortic endothelial cells, and endothelium-derived cell line (ECV304).
18 s both resting and stimulated HUVEC, and the endothelium-derived chemokine CCL2 (monocyte chemoattrac
19        To date, however, the contribution of endothelium-derived chemokines found in these lesion to
20                                  We measured endothelium-derived clotting factors and assayed platele
21                                              Endothelium-derived CNP is involved in the regulation of
22      In contrast, TGF-beta1 did not decrease endothelium-derived constitutive NOS mRNA in organs of r
23                        Estrogen also affects endothelium-derived constrictor factors.
24                 Specifically, choroid plexus endothelium-derived EBOV infection led to viral persiste
25 cessive primary tumor growth but depended on endothelium-derived EETs at the site of metastasis.
26 tion of these routes is determined by venous endothelium-derived endothelin-1, acting through its spe
27                                              Endothelium-derived epoxyeicosatrienoic acids (EETs) rel
28       Further characterization revealed that endothelium-derived EVs (EC-EVs) suppressed monocyte act
29  Researchers recently found elevated pigment endothelium-derived factor (PEDF) associated with active
30 rived Vegf-A, and identify Hgf as a putative endothelium-derived factor that mediates the reciprocal
31 rmation and suggesting that Hgf serves as an endothelium-derived factor that signals to the epitheliu
32 ations to bradykinin by increased release of endothelium-derived factors other than nitric oxide.
33 endothelium with a higher mitotic index than endothelium derived from local sources.
34 ndings indicate novel potential functions of endothelium-derived GABA.
35                                              Endothelium-derived gene products play a critical role i
36                                        Thus, endothelium-derived HS chains and mast cell-derived hepa
37              These data further suggest that endothelium-derived hydrogen sulfide is a potential ther
38 responses were instead abolished by blocking endothelium derived hyperpolarising factor (EDHF) with a
39 rate that 10 mM propionate relaxes RMSAs via endothelium-derived hyperpolarising factor (EDHF).
40      These localized Ca(2+) events result in endothelium-derived hyperpolarization (and SMC relaxatio
41   Evidence from animal models has identified endothelium-derived hyperpolarization (EDH) as a potenti
42                  In striking contrast to the endothelium-derived hyperpolarization (EDH) characterist
43  arteries, RA-2 inhibited bradykinin-induced endothelium-derived hyperpolarization (EDH)-type relaxat
44 ATPase in humans, consistent with a role for endothelium-derived hyperpolarization in functional symp
45 1 transnitrosation activity is essential for endothelium-derived hyperpolarization.
46  present in arterial endothelium to generate endothelium-derived hyperpolarization.
47                                 Dilations to endothelium-derived hyperpolarizing factor (EDHF) are si
48                    It has been proposed that endothelium-derived hyperpolarizing factor (EDHF) contri
49 ch as acetylcholine release an unidentified, endothelium-derived hyperpolarizing factor (EDHF) which
50 r relaxation is mediated by nitric oxide and endothelium-derived hyperpolarizing factor (EDHF), and b
51 is remaining vasorelaxation activity, termed endothelium-derived hyperpolarizing factor (EDHF), is mo
52  prostanoids, but involves the release of an endothelium-derived hyperpolarizing factor (EDHF), possi
53 l compounds, including prostacyclin, NO, and endothelium-derived hyperpolarizing factor (EDHF), that
54  (NO) synthase or K(+) channels that mediate endothelium-derived hyperpolarizing factor (EDHF)-depend
55  we investigated and compared NO release and endothelium-derived hyperpolarizing factor (EDHF)-mediat
56  severe HHcy impaired nitric oxide (NO)- and endothelium-derived hyperpolarizing factor (EDHF)-mediat
57 gen peroxide (H2O2), which is proposed as an endothelium-derived hyperpolarizing factor (EDHF).
58 relaxations that are widely attributed to an endothelium-derived hyperpolarizing factor (EDHF).
59 l toxins reported to block the release of an endothelium-derived hyperpolarizing factor (EDHF).
60 derives from hyperpolarization and is termed endothelium-derived hyperpolarizing factor (EDHF).
61 crucial component of dilation resulting from endothelium-derived hyperpolarizing factor (EDHF).
62                               Thus, enhanced endothelium-derived hyperpolarizing factor activity in c
63 on in VHF rats, and blunted prostacyclin and endothelium-derived hyperpolarizing factor components in
64           This is consistent with a role for endothelium-derived hyperpolarizing factor in FID of the
65 ified C-type natriuretic peptide (CNP) as an endothelium-derived hyperpolarizing factor in the mesent
66 r-dependent effects on NO, prostacyclin, and endothelium-derived hyperpolarizing factor production, t
67 l cell surface contributes to control of the endothelium-derived hyperpolarizing factor response, alt
68 effects of nitric oxide, prostaglandins, and endothelium-derived hyperpolarizing factor were inhibite
69  increased involvement of prostaglandins and endothelium-derived hyperpolarizing factor(s).
70 ently by enhanced production of the putative endothelium-derived hyperpolarizing factor(s).
71  (e.g., endothelium-derived relaxing factor, endothelium-derived hyperpolarizing factor, and prostagl
72 n endothelial cells to produce nitric oxide, endothelium-derived hyperpolarizing factor, or prostagla
73 like" SKA-31 (half-life of 12 h) potentiated endothelium-derived hyperpolarizing factor-mediated dila
74 sent a marker for the endothelial effects of endothelium-derived hyperpolarizing factor.
75 e vasodilatory properties similar to that of endothelium-derived hyperpolarizing factor.
76  for how hydrogen peroxide can operate as an endothelium-derived hyperpolarizing factor.
77 potassium ion (K(+)) have been identified as endothelium-derived hyperpolarizing factors (EDHFs) in a
78 nd hydrogen peroxide (H2O2) both function as endothelium-derived hyperpolarizing factors (EDHFs) in t
79 on of vascular smooth muscle are mediated by endothelium-derived hyperpolarizing factors (EDHFs).
80 y cytochrome P-450 monooxygenase (P450), are endothelium-derived hyperpolarizing factors (EDHFs).
81 nd epoxyeicosatrienoic acid release and that endothelium-derived hyperpolarizing factors compensate f
82                         We hypothesized that endothelium-derived hyperpolarizing factors contribute t
83 ioisomers, which were recently identified as endothelium-derived hyperpolarizing factors in coronary
84 hanism contributes to the effects of EETs as endothelium-derived hyperpolarizing factors to hyperpola
85              We assessed the contribution of endothelium-derived hyperpolarizing factors to resting a
86 ctivating TEA-inhibitable K(+)(Ca) channels, endothelium-derived hyperpolarizing factors, together wi
87      Hence, like EETs, DHETs may function as endothelium-derived hyperpolarizing factors.
88 ) production by the endothelium, suppressing endothelium-derived inflammation and decreasing foam cel
89 time points (2-8 hours) after AECA addition, endothelium-derived interleukin-1 (IL-1) accounted for t
90 y is required to facilitate the transport of endothelium-derived lactate into pericytes.
91                                 We find that endothelium-derived lactate is taken up by pericytes, an
92  residual responses were mediated by another endothelium-derived mediator or NO released despite trea
93       This finding suggests a role for other endothelium-derived mediators and/or for endothelium-ind
94 ia-cell injury may result in an imbalance in endothelium-derived mediators, favouring vasoconstrictio
95  act by inducing the release of at least two endothelium-derived mediators, one (as-yet-unidentified)
96 take place in the occlusive lesions and that endothelium-derived mesenchymal cells can further differ
97 vage in the blood circulation by soluble and endothelium-derived NEP.
98  without nosocomial pneumonia indicated that endothelium-derived neurotoxins disrupted the postsynapt
99  salt rats were resistant to the blocking of endothelium derived nitric oxide (EDNO) with L-NAME and
100  rabbits, oral L-arginine (the substrate for endothelium derived nitric oxide) attenuates endothelial
101 fts has been attributed in part to increased endothelium-derived nitric oxide (.NO) production.
102                                      Loss of endothelium-derived nitric oxide (EDNO) contributes to t
103                      The effective action of endothelium-derived nitric oxide (EDNO) is impaired in p
104  endothelium-dependent vasodilator function, endothelium-derived nitric oxide (EDNO) production, and
105 y a role in the modulation of the release of endothelium-derived nitric oxide (EDNO).
106 n action and vasodilation may be mediated by endothelium-derived nitric oxide (EDNO).
107 portant for shear stress-mediated release of endothelium-derived nitric oxide (NO) and lowering pulmo
108                                      Loss of endothelium-derived nitric oxide (NO) and prostacyclin c
109                We tested the hypothesis that endothelium-derived nitric oxide (NO) and vasodilating p
110  a key role in the endogenous suppression of endothelium-derived nitric oxide (NO) bioactivity and ha
111                                              Endothelium-derived nitric oxide (NO) contributes to epi
112           Ageing is associated with impaired endothelium-derived nitric oxide (NO) function in human
113 bination of other nutrients known to enhance endothelium-derived nitric oxide (NO) in patients with s
114                                              Endothelium-derived nitric oxide (NO) is a potent vasodi
115                                              Endothelium-derived nitric oxide (NO) is an important re
116 ntal stress-induced vasodilation mediated by endothelium-derived nitric oxide (NO) is defective in co
117                                              Endothelium-derived nitric oxide (NO) is synthesised fro
118                                              Endothelium-derived nitric oxide (NO) may be an importan
119               The reduced bioavailability of endothelium-derived nitric oxide (NO) may play a role in
120                           The bioactivity of endothelium-derived nitric oxide (NO) reflects its rates
121                                              Endothelium-derived nitric oxide (NO) selectively enhanc
122                                              Endothelium-derived nitric oxide (NO) selectively enhanc
123              Many angiogenic factors require endothelium-derived nitric oxide (NO) to exert their eff
124          Cerebral blood flow is regulated by endothelium-derived nitric oxide (NO), and endothelial N
125 flow is a potent stimulus for the release of endothelium-derived nitric oxide (NO).
126  mutations affect vasorelaxation mediated by endothelium-derived nitric oxide (NO).
127  taken during hand hyperemia (a stimulus for endothelium-derived nitric oxide [NO] release in the ups
128 .47 mN/mm; P=0.004) attributable to impaired endothelium-derived nitric oxide activity.
129 ssociated with atherosclerosis by preserving endothelium-derived nitric oxide activity.
130             In particular, the production of endothelium-derived nitric oxide and activation of solub
131 e (ADMA), correlate with decreased levels of endothelium-derived nitric oxide and subsequent endothel
132 at is likely to be related to a reduction in endothelium-derived nitric oxide bioavailability and/or
133 gh a mechanism that is not caused by loss of endothelium-derived nitric oxide but may involve oxidati
134                              Inactivation of endothelium-derived nitric oxide by oxygen-derived free
135          Oxidatively mediated degradation of endothelium-derived nitric oxide contributes to abnormal
136                                              Endothelium-derived nitric oxide contributes to basal sy
137 is investigation sought to determine whether endothelium-derived nitric oxide contributes to hypoxia-
138                                              Endothelium-derived nitric oxide contributes to systemic
139 stress is associated with impaired action of endothelium-derived nitric oxide in patients with athero
140 dy was undertaken to investigate the role of endothelium-derived nitric oxide in the regulation of fo
141 nthase (Nos3), which suggests that decreased endothelium-derived nitric oxide is not a sufficient mec
142 rovide a mechanism by which FXR may increase endothelium-derived nitric oxide levels through modulati
143                    Decreased availability of endothelium-derived nitric oxide may contribute to the h
144               The reduced bioavailability of endothelium-derived nitric oxide may play a role in endo
145          There are some data indicating that endothelium-derived nitric oxide mediates changes in vas
146            To study the effect of endogenous endothelium-derived nitric oxide on TF expression and ac
147                     Oxidative degradation of endothelium-derived nitric oxide plays a major role in e
148 ese data suggest that enhanced production of endothelium-derived nitric oxide reduces endotoxin- and
149                               Stimulation of endothelium-derived nitric oxide with acetylcholine resu
150 ndothelium-dependent relaxation (mediated by endothelium-derived nitric oxide) is depressed during th
151               L-arginine is the precursor of endothelium-derived nitric oxide, an endogenous vasodila
152 n molecules and decreased bioavailability of endothelium-derived nitric oxide, an important regulator
153                       Hemoglobin inactivates endothelium-derived nitric oxide, participates in free-r
154 sodilates skeletal muscle vasculature via an endothelium-derived nitric oxide-dependent mechanism.
155 n smooth muscle are thought to be targets of endothelium-derived nitric oxide.
156 d cANF(4-23) were enhanced in the absence of endothelium-derived nitric oxide.
157 nt mechanism whereby hyperglycemia decreases endothelium-derived nitric oxide.
158 e endothelial dysfunction: essential role of endothelium-derived nitric oxide.
159 ized by a decrease in the bioavailability of endothelium-derived nitric oxide.
160 ial artery cannula to assess vasodilation to endothelium-derived nitric oxide.
161 sodilator function that depends partially on endothelium-derived nitric oxide.
162 structural and functional factors, including endothelium-derived nitric oxide.
163                                     Although endothelium derived NO has been shown to be of prime imp
164 at estradiol may stimulate the production of endothelium-derived NO and thereby reduce the contractil
165                                 Both p21 and endothelium-derived NO appear to have protective roles i
166 -coupled receptor-mediated, or shear-induced endothelium-derived NO bioactivity) is understood to inv
167 d antioxidant status has been shown to alter endothelium-derived NO bioactivity.
168 d the role of intracellular ascorbic acid in endothelium-derived NO bioactivity.
169                                              Endothelium-derived NO controls the contractility and gr
170                                              Endothelium-derived NO has been shown to be of crucial i
171                                              Endothelium-derived NO is considered to be primarily an
172                                          The endothelium-derived NO is detected amperometrically at a
173 nvolve, at least in part, the attenuation of endothelium-derived NO production through a calcineurin-
174 may protect against vasospasm by stimulating endothelium-derived NO release and inhibiting coronary a
175                 In these cells, VEGF and the endothelium-derived NO synergistically up-regulated the
176 nation reaction of plasma oxyhemoglobin with endothelium-derived NO to form bioinactive nitrate.
177 nyl thiol redox switch to decrease pulmonary endothelium-derived NO(.) and promote PAH.
178 ions of bradykinin, a well-known stimulus of endothelium-derived NO, activated nitric oxide synthase
179  hypertrophy through the paracrine action of endothelium-derived NO, which triggers the degradation o
180 it refractoriness and repriming depends upon endothelium-derived NO.
181 e contributes to impairment of the action of endothelium-derived NO.
182 onstriction via the possible facilitation of endothelium-derived NO.
183 that this effect of exercise is meditated by endothelium-derived NO.
184 tivation, with apparently less of a role for endothelium-derived NO.
185  vascular endothelium as a result of loss of endothelium-derived NO.
186 d in part by .O2-, likely via degradation of endothelium-derived NO.
187 t exert its action through direct effects on endothelium-derived NO.
188 nd resistance vessels is mediated in part by endothelium-derived NO.
189 reases the production and bioavailability of endothelium-derived NO.
190 poxanthine/xanthine oxidase system inhibited endothelium-derived .NO-mediated arterial relaxation eli
191 t a positional identity that is regulated by endothelium-derived Notch signalling, and that this stro
192                            However, although endothelium-derived PDGF-BB appears vital for the develo
193                                          The endothelium-derived peptide endothelin-1 (ET-1) causes v
194                    Endothelin-1 (ET-1) is an endothelium-derived peptide that constricts coronary ves
195 ciated with increased expression of ET-1, an endothelium-derived peptide with vasoconstricting, mitog
196                     We tested the role of an endothelium-derived phosphatidylserine-binding opsonin,
197                      The vasomotor effect of endothelium-derived prostacyclin was examined by monitor
198 portant physiological platelet inhibitors is endothelium-derived prostacyclin which stimulates the pl
199 ulated release and proteolytic processing of endothelium-derived Reelin.
200 isolated arteries, focusing our attention on endothelium-derived relaxation and on its antioxidant pr
201  within the current framework of NO biology, endothelium-derived relaxation factor activity (ie, G pr
202    Well over 2 decades have passed since the endothelium-derived relaxation factor was reported to be
203 y, imbalance in the relative contribution of endothelium-derived relaxing and contracting factors, an
204                             The discovery of endothelium-derived relaxing factor (EDRF) and its impor
205  or -2 regulates serum ADMA (S(ADMA)) and/or endothelium-derived relaxing factor (EDRF)/NO.
206               We sought to determine whether endothelium-derived relaxing factor (nitric oxide) exert
207       Nitric oxide (NO) is identified as the endothelium-derived relaxing factor and a neurotransmitt
208 he production and the degradation of NO, the endothelium-derived relaxing factor and a primary mediat
209 nitric oxide (NO) is considered an important endothelium-derived relaxing factor and may function to
210          The superoxide radical can scavenge endothelium-derived relaxing factor and produce potent o
211 e (Hcy) decreases the biological activity of endothelium-derived relaxing factor and that this decrea
212                        The identification of endothelium-derived relaxing factor as nitric oxide (NO)
213 cular endothelium accounts in large part for endothelium-derived relaxing factor bioactivity.
214 taglandin I2, staurosporine, wortmannin, the endothelium-derived relaxing factor congener S-nitroso-N
215  an impaired nitric oxide synthase-dependent endothelium-derived relaxing factor response and paradox
216              The vasorelaxant effects of the endothelium-derived relaxing factor S-nitrosocysteine (S
217                                        As an endothelium-derived relaxing factor, a mediator of immun
218 by signals arising in the endothelium (e.g., endothelium-derived relaxing factor, endothelium-derived
219 e (NO), the biologically active component of endothelium-derived relaxing factor, has critical roles
220 wing the discovery that NO is the prototypic endothelium-derived relaxing factor, this signaling mole
221 tes that pHi may modulate the release of the endothelium-derived relaxing factor.
222 act on the endothelium to cause synthesis of endothelium-derived relaxing factor.
223 have also been shown to influence release of endothelium-derived relaxing factor.
224                                  A number of endothelium-derived relaxing factors have been identifie
225  this study was to discover and identify new endothelium-derived relaxing factors involved in the reg
226 ienoic acids as new members of the family of endothelium-derived relaxing factors.
227 dependent on the addition of exogenous Zn2+, endothelium-derived S-SMase was partially active even in
228                  These factors will serve as endothelium derived signaling molecules in the tumor mic
229 ine mechanisms involving the upregulation of endothelium-derived stabilizing factors and the recruitm
230        Endothelial microparticles (EMPs) are endothelium-derived submicron vesicles that are released
231 indings have highlighted the contribution of endothelium-derived substances to blood flow control in
232 raction; local metabolic, red blood cell and endothelium-derived substances; and the sympathetic nerv
233              We recently identified TL1A, an endothelium-derived T cell costimulator and a ligand for
234 DAMTS-13, a metalloprotease that cleaves the endothelium-derived ultra-large multimers of von Willebr
235                    Endothelin-1 (ET-1) is an endothelium-derived vasoactive peptide with mitogenic pr
236                    Cyclooxygenase-dependent, endothelium-derived vasoconstrictor release modulates ac
237 ) influx, (2) the release (by hypoxia) of an endothelium-derived vasoconstrictor, or (3) endothelium-
238 ion is characterized by an imbalance between endothelium-derived vasodilating and vasoconstricting fa
239 increased intima/media ratio, and maintained endothelium-derived vasodilation.
240 hyporeactivity in large part mediated by the endothelium-derived vasodilator nitric oxide.
241  is that they improve the bioactivity of the endothelium-derived vasodilator NO by enhancing NO synth
242 entation of L-arginine, the precursor of the endothelium-derived vasodilator NO, reverses coronary en
243 drogen sulfide (H(2)S), a recently described endothelium-derived vasodilator, is produced by the enzy
244 constrictors, such as endothelin, antagonize endothelium-derived vasodilators and contribute to endot
245  Epoxyeicosatrienoic acids (EETs) are potent endothelium-derived vasodilators formed from cytochrome
246  denudation or pharmacological inhibition of endothelium-derived vasodilators such as nitric oxide (N
247           In the present study, the roles of endothelium-derived vasodilators, guanylyl cyclase, and
248 ular tone of mouse cerebral arteries through endothelium-derived vasodilatory mechanisms.

 
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