ライフサイエンスコーパス: outflow facility

1 (TM) cell volume and NO-induced increases in outflow facility.

2 duction in SC cell volume may also influence outflow facility.

3 hwork (TM) cells increases the aqueous humor outflow facility.

4 its can be explained mainly by a decrease in outflow facility.

5 est that ADAMTS-4 is a potential modifier of outflow facility.

6 tility in ocular pulse-associated changes in outflow facility.

7 recombinant ADAMTSs to determine effects on outflow facility.

8 ceptor stimulation facilitated aqueous humor outflow facility.

9 C is involved in the NO-induced increases in outflow facility.

10 sed a transient enhancement of aqueous humor outflow facility.

11 sGC in mediating the NO-induced increases in outflow facility.

12 act of ocular pulsation on human and porcine outflow facility.

13 with IDAPS (500 microg/mL) had no effect on outflow facility.

14 eptor in the trabecular meshwork to increase outflow facility.

15 matrix turnover and increases aqueous humor outflow facility.

16 y demonstrated to be involved in controlling outflow facility.

17 extracellular matrix significantly influence outflow facility.

18 or the CB1 receptor, increases aqueous humor outflow facility.

19 cular pressure primarily by increasing total outflow facility.

20 6)-cyclohexyladenosine (CHA) on conventional outflow facility.

21 advantageous over drugs that do not increase outflow facility.

22 asure the effects of JWH015 on aqueous humor outflow facility.

23 myosin II in the regulation of aqueous humor outflow facility.

24 (3-6 attacks) was due to reduced tonographic outflow facility.

25 inoid agonist JWH015 increases aqueous humor outflow facility.

26 ressures, allowing calculation of trabecular outflow facility.

27 iable loss of canal cells but did not change outflow facility.

28 l physiological homeostasis of aqueous humor outflow facility.

29 with the extracellular matrix in influencing outflow facility.

30 n AHF, trabecular outflow facility, or total outflow facility.

31 by which latanoprost reduces IOP and alters outflow facility.

32 ociated with a significant increase in total outflow facility.

33 lism and have been shown to increase aqueous outflow facility.

34 spected to have abnormally low aqueous humor outflow facility.

35 production in the TM, which in turn improves outflow facility.

36 response is mediated in part by increases in outflow facility.

37 this process to restore normal aqueous humor outflow facility.

38 equesters actin monomers) similarly increase outflow facility.

39 dose of Jas increases rather than decreases outflow facility.

40 , or 500 nM Jas had no significant effect on outflow facility.

41 fect is greater in eyes with higher baseline outflow facility.

42 us flow followed by a subsequent increase in outflow facility.

43 ho kinase in the modulation of aqueous humor outflow facility.

44 cted to be an important factor in regulating outflow facility.

45 outflow resistance, and thus restores normal outflow facility.

46 be a direct effect of muscarinic agonists on outflow facility.

47 tem has been shown to increase aqueous humor outflow facility.

48 nt, and correlated with reduced conventional outflow facility.

49 Fbeta2 on transcellular pressure changes and outflow facility.

50 (GPBS) at 15 mm Hg to establish the baseline outflow facility.

51 serve as a novel parameter to correlate with outflow facility.

52 al antagonism on the PEA-induced increase of outflow facility.

53 over suggests that the mechanism is enhanced outflow facility.

54 g vectors caused similar opposite effects on outflow facility.

55 e eyes resulted in a significant decrease in outflow facility.

56 the more SC that it dilates, the greater the outflow facility.

57 lyburide inhibited diazoxide from increasing outflow facility.

58 ay appears to contribute to PG regulation of outflow facility.

59 al remodeling and MMP-mediated modulation of outflow facility.

60 involvement of versican and CS GAG chains in outflow facility.

61 d IOP, consistent with an 2-fold increase in outflow facilities.

62 an 20 photon units/msec (n = 21) had a lower outflow facility (0.17 +/- 0.07 microl/min x mm Hg) than

63 is necessary for the NO-induced increases in outflow facility (0.3215 microL/min per mm Hg [baseline

64 ility (0.3215 microL/min per mm Hg [baseline outflow facility]+/-0.0837 [SEM]).

65 used a significant increase in aqueous humor outflow facility (110%) compared with control eyes, in a

66 ne expression caused a transient decrease of outflow facility (30% +/- 22%, P = 0.02), which resolved

67 ficant increase (P < 0.01, n = 7) in aqueous outflow facility (53% and 64%, respectively) from the ba

68 e maximum effect (151.08 +/- 11.12% of basal outflow facility) achieved at 30 nM of PEA.

69 flow facility (P > 0.35) or on the change in outflow facility after 1 hour at 0 mm Hg (P > 0.15).

70 f matrix-matrix separation and the change in outflow facility after 1 hour of 0 mm Hg.

71 H-7 significantly increased outflow facility after single or sequential doses, with

72 some individuals by decreasing aqueous humor outflow facility, although a causal relationship cannot

73 rs partially blocked PEA-induced increase in outflow facility and abolished PEA-induced phosphorylati

74 rfused with carbachol (10(-9)-10(-5) M), and outflow facility and cAMP levels in the perfusate were m

75 l outflow were higher, and fluorophotometric outflow facility and CCT were not different during the d

76 The increase in outflow facility and decrease in resistance supports the

77 , AAV-mediated expression of MMP-3 increased outflow facility and decreased IOP, and controlled expre

78 Increases in outflow facility and EFL demonstrated a positive correla

79 mined the effects of ADAMTS-1, -4, and -5 on outflow facility and investigated their mRNA levels and

80 The effect of ICP elevation on outflow facility and IOP is blocked by TTX.

81 ent study was undertaken to evaluate aqueous outflow facility and its age dependence in these mice.

82 stiffness of the TM correlated with a higher outflow facility and less IOP elevation-induced variatio

83 TRPV4 inhibition enhanced the outflow facility and lowered perfusate pressure in biomi

84 ive effort, which may reflect a reduction in outflow facility and may contribute to the development o

85 actors of elevated IOP and decreased aqueous outflow facility and may potentially serve as a model fo

86 t on aqueous humor production or tonographic outflow facility and may thus indicate a drug-induced in

87 Outflow facility and outflow resistance were measured ag

88 Using a constant pressure perfusion method, outflow facility and outflow resistance were measured in

89 oth PEA-induced enhancement of aqueous humor outflow facility and PEA-induced phosphorylation of p42/

90 Nitric oxide signaling alterations in outflow facility and retinal blood flow autoregulation a

91 dministration of AEA increases aqueous humor outflow facility and that this effect of AEA involves CB

92 At peak IOP, aqueous outflow facility and total TGFbeta2 levels in aqueous hu

93 ithout any significant effect on tonographic outflow facility and uveoscleral outflow.

94 sed on outflow resistance (the reciprocal of outflow facility) and the effect of age on the rate of c

95 TM cell markers, and maintained normal IOP, outflow facility, and extracellular matrix.

96 of ECHO treatment further restored baseline outflow facility, and the outflow facility response to H

97 Aqueous humor dynamics (aqueous flow, outflow facility, and uveoscleral outflow), IOP, and pac

98 Outflow facility appears to be normal in patients with a

99 Main outcome measures were tonographic outflow facility, aqueous humor flow rate, and uveoscler

100 nd EP(4) receptor activation on conventional outflow facility, as observed in human eyes.

101 contribution of changes in aqueous flow and outflow facility associated with the ocular hypotensive

102 Changes in IOP, aqueous flow, and total outflow facility at various times after CHA administrati

103 re in nonhuman primate eyes, which increases outflow facility but has no effect on aqueous secretion

104 rog/mL) and PPRARI (500 microg/mL) increased outflow facility by 31% +/- 13% (n = 9, P < 0.05) and 24

105 eceptors, 3,7-dithiaPGE(1) (10 nM) increased outflow facility by 51% +/- 18% over baseline levels in

106 Concurrent H-7 enhanced outflow facility by 73% +/- 18% (n = 12, P < 0.005) beyo

107 ve been suggested to contribute to decreased outflow facility by altering the contractility of the TM

108 Bimatoprost increased outflow facility by an average of 40% +/- 10% within 48

109 nd inhibition of the CHA-induced increase in outflow facility by the adenosine A(1) antagonist confir

110 he inhibition of the CHA-induced increase in outflow facility by the MMP inhibitor GM-6001 provides e

111 Studies on total outflow facility by the two-level, constant-pressure per

112 iscleral venous pressure (EVP), conventional outflow facility (C(t)), aqueous humor production (F(a))

113 Tonographic outflow facility (C) and fluorophotometric aqueous humor

114 hwork (TM) stiffness and its relationship to outflow facility (C) in perfused normal human and porcin

115 Outflow facility (C) was determined based on constant pr

116 Outflow facility (C) was determined by constant-pressure

117 Mouse outflow facility (C) was determined by multiple flow-rat

118 pulated by varying reservoir height, and eye outflow facility (C) was determined from the pump flow r

119 an anterior segments to determine changes in outflow facility (C).

120 H-7 increased outflow facility, causing a partial loss of the endothel

121 vivo perfusion-cultured human eyes decreased outflow facility, concomitant with reduced levels of bet

122 Total outflow facility corrected for control eye washout was i

123 The reduction in outflow facility correlates with an increase in intraocu

124 An increase in outflow facility (decrease in IOP) is demonstrated in a

125 Mean outflow facility decreased from 0.23 +/- 0.08 muL/min/mm

126 Tonographic outflow facility did not change in a 24-hour period in t

127 ificant trend toward a nocturnal decrease of outflow facility (diurnal, 0.27 +/- 0.11 microL/min/mm H

128 therefore the association between flare and outflow facility does not appear to be an indirect refle

129 Decreasing outflow facility during acute IOP elevation coincides wi

130 undertaken to investigate whether changes in outflow facility, episcleral venous pressure, or uveoscl

131 lobe, decreased ocular compliance, increased outflow facility, extracellular matrix (ECM) abnormaliti

132 Outflow facility for phosphate-buffered saline (0.0027 +

133 Measurement of the outflow facility found no significant change in facility

134 sal or superior quadrant of the TM increased outflow facility from 0.16 +/- 0.05 muL/min/mm Hg to 0.3

135 he Hydrus Microstent significantly increased outflow facility from 0.33 +/- 0.17 muL/min/mm Hg to 0.5

136 The 1 iStent showed a greater increase in outflow facility from baseline (0.10+/-0.04 mul/minute p

137 uced a significant decrease in aqueous humor outflow facility from baseline of 37% (n = 6) and 31% (n

138 The compounds also increase outflow facility in a pig eye perfusion assay.

139 rade extracellular matrix (ECM) and increase outflow facility in anterior segment perfusion culture.

140 contribution of each of the HAS proteins to outflow facility in anterior segment perfusion culture.

141 Outflow facility in anterior segments treated with Hep I

142 yme unique to CS GAG biosynthesis, increased outflow facility in both species.

143 Steroid treatment significantly decreases outflow facility in C57BL/6 mice despite having small ef

144 tive site in the HepII domain that regulates outflow facility in cultured anterior segments and disru

145 suggests that the HepII domain may increase outflow facility in cultured anterior segments by alteri

146 Decreased outflow facility in cyclically pulsed anterior segments

147 sion system was used to measure conventional outflow facility in enucleated mouse eyes ex vivo.

148 molol, an aqueous humor flow suppressant, on outflow facility in healthy eyes.

149 Timolol reduces outflow facility in healthy human eyes, and this effect

150 Versican silencing decreased outflow facility in human and increased facility in porc

151 Recombinant ADAMTS-4 increased outflow facility in human and porcine anterior segments,

152 ine whether K(ATP) channel openers influence outflow facility in human anterior segment culture and i

153 a second-generation bypass stent, increased outflow facility in human anterior segment culture.

154 K(ATP) channel openers increased outflow facility in human anterior segments (0.14 +/- 0.

155 Treatment with 4MU decreased outflow facility in human anterior segments but increase

156 Muscarinic agonists increase outflow facility in human eyes by a direct stimulation o

157 ostent provided an effective way to increase outflow facility in human eyes ex vivo.

158 macologic compounds that affect conventional outflow facility in human eyes exert similar effects in

159 Y27632 increases outflow facility in human eyes.

160 ions that reduce aqueous humor production on outflow facility in living human eyes is unclear.

161 in part explains the S1P-induced decrease of outflow facility in organ culture.

162 ermore, no difference was identified between outflow facility in patients with active uveitis (those

163 he effect(s) of ocular pulse on conventional outflow facility in perfused anterior segments.

164 ine whether muscarinic agonists could change outflow facility in perfused human ocular anterior segme

165 ological agonists of Edg receptors, decrease outflow facility in perfused porcine eyes in association

166 hosphorylation in TM cells, and decreased AH outflow facility in perfused porcine eyes.

167 Disrupting GAG chain biosynthesis increased outflow facility in perfusion culture and induced atypic

168 ity in human anterior segments but increased outflow facility in porcine eyes.

169 chanism driven by ICP regulates conventional outflow facility in rats.

170 , possibly underlie the reported increase in outflow facility in response to Fsk perfusion ex vivo.

171 sure the effects of statins on aqueous humor outflow facility in the anterior segments of porcine eye

172 ut also to drugs that increase aqueous humor outflow facility in the eyes of primates and humans.

173 The Hep II domain of fibronectin increases outflow facility in the human anterior segment.

174 and other muscarinics substantially increase outflow facility in the isolated human outflow system de

175 (110%, P < 0.001) and reduced aqueous humor outflow facility in the mouse.

176 ist CHA significantly increases conventional outflow facility in the perfused bovine eye.

177 The mean outflow facility in the sitting and supine positions wer

178 ver the 12- to 56-week study period, IOP and outflow facility in the transgenic mice were inversely c

179 data suggest that AQP1 expression may affect outflow facility in vivo.

180 Aqueous humor outflow facility increased (40%-80%) in enucleated porci

181 enic mice returned to normal levels, whereas outflow facility increased by 36.0%.

182 r 300 nM of noladin ether, the aqueous humor outflow facility increased concentration dependently.

183 After Hydrus placement, the outflow facility increased from 0.23+/-0.03 mul/minute p

184 Outflow facility increased from baseline facility in eye

185 Outflow facility increased in porcine eyes with chlorate

186 Outflow facility increased, in a dose-dependent manner,

187 racranial pressure (ICP) lowers conventional outflow facility (increases aqueous outflow resistance)

188 retion of substances into the AH that govern outflow facility independent of pressure.

189 concentration- and time-dependent changes in outflow facility induced by CHA were determined.

190 receptors are involved in the enhancement of outflow facility induced by JWH015.

191 In addition, the enhancement of outflow facility induced by noladin ether was blocked by

192 the hypothesis that increases in uveoscleral outflow facility induced by PG administration involves t

193 ow that noladin ether-induced enhancement of outflow facility is mediated through the trabecular mesh

194 Outflow facility is reduced in transgenic Col1a1(r/r) mi

195 Outflow facility is significantly reduced in patients wi

196 eye, including the TM; however, its role in outflow facility is unknown.

197 Outflow facility measured by tonography does not decreas

198 H-7 partially restored baseline outflow facility measured during subsequent perfusions w

199 low to develop with no significant change in outflow facility measured until after 60 minutes of CHA

200 Aqueous humor outflow facility measured with electronic Schiotz tonogr

201 The outflow facility measurement in each eye after drug admi

202 t cholinergics may indeed exert an effect on outflow facility, mediated by cAMP, which is independent

203 Neither the tonographic outflow facility nor the uveoscleral outflow was signifi

204 Ps contributing to the increased uveoscleral outflow facility observed after topical latanoprost.

205 Outflow facility of eyes in animals receiving bilateral

206 ion with exposure duration, yet conventional outflow facility of implanted eyes was normal (24.1 +/-

207 Ocular pulse decreases outflow facility of perfused anterior segments.

208 e trabecular meshwork (TM) and the effect on outflow facility of silencing the versican gene were eva

209 Outflow facility (OF) was decreased by approximately 40%

210 equired to verify the influence of increased outflow facility on intraocular pressure fluctuation and

211 trol eyes were significant for IOP and total outflow facility only.

212 rrelation was found between aqueous flow and outflow facility (ONT, R (2) = 0.24; OHT, R(2) = 0.10).

213 29 doses showed no change in AHF, trabecular outflow facility, or total outflow facility.

214 anterior segments produced a 28% increase in outflow facility over basal levels.

215 h RGE control, RGD had no apparent effect on outflow facility (P > 0.35) or on the change in outflow

216 5 mm Hg coincided with a twofold decrease in outflow facility (P < 0.0001), a 33% to 57% decrease in

217 Outflow facility (P = 0.01) and EFL (P < 0.05) were sign

218 inflow (acetazolamide, timolol) or increase outflow facility (pilocarpine, latanoprost) in primates

219 e was a linear correlation between flare and outflow facility (r = -0.50, P = 0.005).

220 lity was negatively correlated with baseline outflow facility (r = -0.51; P < 0.001).

221 Outflow facility remained high during Hep II domain perf

222 consistent with the age-related decrease in outflow facility reported in both humans and monkeys.

223 Outflow facility response to H-7 was measured by two-lev

224 restored baseline outflow facility, and the outflow facility response to H-7.

225 The effect was reversible, with outflow facility returning to baseline after drug remova

226 n organization in TM cells, and decreases AH outflow facility, revealing a potentially important role

227 Outflow facility significantly increased after short-dur

228 NAs targeting ZO-1 and tricellulin increased outflow facility significantly.

229 r outflow pathway leads to increased aqueous outflow facility, suggesting a critical role for myosin

230 es results in small and transient changes in outflow facility, suggesting suitability of this class o

231 the time-course for NO-induced increases in outflow facility, suggesting that the NO-induced reducti

232 ated with AA (with or without TA) had higher outflow facility than animals treated with TA (P < 0.05)

233 The increase in outflow facility that occurs during washout in the bovin

234 d TM cells, which may contribute to reducing outflow facility through the TM.

235 t the stiffer the ECM, the lower the aqueous outflow facility through the TM.

236 TP) channel openers, these channels increase outflow facility through the trabecular outflow pathway

237 of a second iStent inject further increased outflow facility to 0.78 +/- 0.66 muL/min/mm Hg (n = 2).

238 ol1a1(+/+) mice (P < 0.01), whereas the mean outflow facility was 25.4% lower than in control mice (P

239 The percent increase in outflow facility was 79+/-21% for the Hydrus and 11+/-16

240 ive dose of the actin depolymerizer Lat B on outflow facility was also determined.

241 or without bilateral TA injection and their outflow facility was also determined.

242 The AEA-induced enhancement of outflow facility was blocked by SR141716A, a CB1 antagon

243 se curves demonstrated that this increase in outflow facility was concentration-dependent, with an EC

244 ferent pressures (7, 15, 30, 45 mm Hg) while outflow facility was continuously recorded.

245 Baseline outflow facility was decreased by 46% +/- 7% (n = 12, P

246 Outflow facility was determined by a two-level, constant

247 Outflow facility was determined by both fluorophotometry

248 re determined by laser flare photometry, and outflow facility was determined by Schiotz tonography.

249 Total outflow facility was determined by two-level constant pr

250 Outflow facility was determined by two-level, constant-p

251 Outflow facility was determined using simultaneous press

252 Conventional outflow facility was evaluated in isolated bovine anteri

253 The effect of inhibition of CD73 on outflow facility was evaluated in perfused living mouse

254 on between the amount of canal cell loss and outflow facility was found.

255 The outflow facility was increased dose dependently within 1

256 Aqueous outflow facility was increased significantly in eyes per

257 The decrease in outflow facility was independent of blood pressure, reve

258 The tonographic outflow facility was lower in Group 1 compared to the ot

259 Outflow facility was lower in patients with uveitis (0.2

260 leral outflow were higher, fluorophotometric outflow facility was lower, and CCT was thinner in both

261 Outflow facility was measured before (baseline control)

262 Total outflow facility was measured by the two-level, constant

263 Total outflow facility was measured by two-level constant-pres

264 Total outflow facility was measured by two-level, constant-pre

265 Outflow facility was measured for 60 minutes after each

266 Outflow facility was measured in enucleated glaucomatous

267 Using a constant pressure perfusion method, outflow facility was measured in paired eyes from human

268 Outflow facility was measured in perfused porcine and hu

269 Outflow facility was measured in porcine eyes using the

270 Outflow facility was measured under general anesthesia b

271 Aqueous humor outflow facility was measured using enucleated porcine e

272 The outflow facility was measured with the participant in th

273 The change in outflow facility was negatively correlated with baseline

274 simple relationship between canal cells and outflow facility was not found; canal cells probably int

275 A consistent decrease in outflow facility was observed in response to cyclic intr

276 Synergism in outflow facility was observed with TNF-alpha and IL-1alp

277 n FAAH inhibitor, the effect of 10 nM AEA on outflow facility was prolonged by at least 4 hours.

278 ever, by 3.5 hours after CHA administration, outflow facility was significantly increased by 85%.

279 h 8-SPT, the epinephrine-induced increase in outflow facility was significantly reduced by 60% when c

280 Combined cytokine effects on outflow facility were appraised in perfused anterior seg

281 s of 4MU treatment and HAS gene silencing on outflow facility were assessed in human and porcine perf

282 Fu and trabecular outflow facility were calculated from these measurements

283 Nocturnal IOP, flow rate, and outflow facility were compared to the same variables dur

284 Changes in aqueous humor outflow facility were determined in enucleated porcine e

285 ues for the initial steady state IOP and the outflow facility were determined using standard tables a

286 The effects of LPA and S1P on aqueous humor outflow facility were evaluated by perfusion of enucleat

287 the current study, transgene expression and outflow facility were evaluated in perfused human anteri

288 Agonist effects on outflow facility were examined in paired human donor eye

289 he effects of noladin ether on aqueous humor outflow facility were measured in a porcine anterior-seg

290 The effects of PEA on outflow facility were measured using a porcine anterior

291 Aqueous humor flow rate, IOP, and outflow facility were measured with pneumatonometry, ant

292 Total and trabecular outflow facility were unchanged.

293 in whole eye organ culture models decreases outflow facility, whereas S1P promotes stress fiber form

294 uveoscleral outflow but does increase total outflow facility, which accounts for a substantial propo

295 a novel mechanism for negative regulation of outflow facility, which may contribute to overall physio

296 antly reduced IOP and improved aqueous humor outflow facility, which was sustained for at least 9 wk.

297 Outflow facility with 1 iStent (0.38+/-0.07 mul/minute p

298 o investigate the variation of aqueous humor outflow facility with body position changes.

299 exercises support substantial impairment in outflow facility with increased HTM stiffness.

300 sed a concentration-dependent enhancement of outflow facility, with the maximum effect (151.08 +/- 11