ライフサイエンスコーパス: VAD

1 VAD (retinol <1.05 mumol/L) was present in 10% of this p

2 VAD and Rpe65(-)/(-) mice are different in cone photorec

3 VAD causes major reductions in levels of the VA intracel

4 VAD implantation (mean, 129+/-99 days) reduced serum adi

5 VAD infection increased 1-year mortality (adjusted hazar

6 VAD infection is a serious consequence because it advers

7 VAD mice showed more prominent downregulation of middle

8 VAD modulates chromatin structure in cis and activates g

9 VAD reduced serum IgE and IgG1 responses, pulmonary eosi

10 VAD therapy is an effective strategy for patients with A

11 VAD was 65% and 0% according to TLRs and SR, respectivel

12 VAD were implanted in 502 patients with AMI: 443 left ve

13 VAD-free or HTx-free survival of patients with peak VO(2

14 VADs are an option for patients with advanced heart fail

15 VADs are well-established treatment for end-stage heart

16 removal for patients with midlines per 1000 VAD days than those with PICCs.

17 er for patients with midlines (6.90 per 1000 VAD days) than for PICCs (2.89 per 1000 VAD days).

18 1000 VAD days) than for PICCs (2.89 per 1000 VAD days).

19 Presented as per 1000 VAD days, patients with PICCs and midlines had similar r

20 se events (14 and 11 adverse events per 1000 VAD days, respectively).

21 here were 76 deaths, 52 transplantations, 14 VAD placements, and 684 cardiac hospitalizations.

22 7%), followed by bloodstream infections (24% VAD related, and 22% non-VAD related).

23 Thirty-three patients (22%) developed 34 VAD-related infections with an incidence rate of 0.10 pe

24 They caused 3 of 6 VAD-related infections.

25 SR as a VAD indicator may depend on infection rates, which shoul

26 A total of 5735 patients had a VAD placed during the 10-year period (0.3% cardiac surge

27 o 14 mL/min per kg and low BNP levels have a VAD-free or HTx-free survival similar to post-HTx surviv

28 Among 2,507 patients who received a VAD at 103 centers during the study period, the in-hospi

29 Serum retinol-a VAD marker-increases in kidney disease and decreases in

30 We identified patients undergoing a VAD procedure after cardiac surgery at US hospitals part

31 A focus on enhancing quality of life with a VAD will be critical to widespread application of mechan

32 Sharing status 1 patients not bridged with a VAD with respect to post-transplant mortality.

33 and found this conditioning led to an acute VAD state.

34 6 patients with advanced HF before and after VAD implantation and 10 healthy control subjects.

35 expression in adipose tissue decreased after VAD implantation (-65%; P<0.03).

36 Overall survival rate to discharge after VAD placement was 54.1%.

37 VAD implantation and in serial fashion after VAD implantation.

38 rol subjects; P<0.05), which increased after VAD placement.

39 Short- and long-term mortality after VAD implantation among Medicare beneficiaries improved,

40 jects (+25%; P<0.01), which normalized after VAD implantation.

41 or relationship with cardiac stability after VAD explantation.

42 ts with the potential to remain stable after VAD explantation.

43 Also, VAD blocked pulmonary hyperresponsiveness following meth

44 prove the survival and quality of life among VAD-supported patients.

45 period between best cardiac improvement and VAD explantation and also during the final off-pump tria

46 itutions: 14 with subsequent LV recovery and VAD removal and 14 clinically matched VAD-dependent pati

47 erentially expressed between LV recovery and VAD-dependent patients in the test cohort.

48 hallenges, increased coordination of STH and VAD interventions represents an important public health

49 on the complex relationship between STH and VAD.

50 associated with death, transplantation, and VAD placement (adjusted hazard ratio [HR]: 3.0; 95% conf

51 Differential expression of miRs at VAD placement may provide markers to assess recovery pot

52 Additionally, b-VAD-fmk failed to label any activated initiator caspase

53 ble biotinylated general caspase inhibitor b-VAD-fmk (biotin-Val-Ala-Asp(OMe)-CH(2)F) both inhibited

54 However, some patients with LVEF >45 before VAD explantation show early recurrence of heart failure

55 s showed relevant instability already before VAD explantation during the time period between best car

56 ation, anti-HLA antibodies are common before VAD implantation in pediatric patients.

57 site were cultured for S. epidermidis before VAD insertion and at 7 times after surgery.

58 during the final off-pump trial just before VAD explantation.

59 ction and can improve decision making before VAD implantation if preoperative RV pressure load and tr

60 adiponectin was higher in HF patients before VAD implantation compared with control subjects (13.3+/-

61 for anti-HLA antibodies was performed before VAD implantation and in serial fashion after VAD implant

62 nstable improvement can be recognized before VAD explantation.

63 Benzyloxycarbiny-VAD-fluoromethyl ketone had no effect on erlotinib-induc

64 Caspase 3 inhibitor benzyloxycarbonyl-VAD failed to prevent the Abeta42-induced BACE1 increase

65 y the pancaspase inhibitor benzyloxycarbonyl-VAD, indicating that caspase-independent pathways were a

66 he broad caspase inhibitor benzyloxycarbonyl-VAD.

67 t cells in the presence of benzyloxycarbonyl-VAD, a pan-caspase inhibitor.

68 inotropes, biventricular assist devices (Bi-VADs) and the total artificial heart (TAH).

69 In contrast to patients with Bi-VADs, patients with the TAH have no postoperative inotro

70 ty-labeled with the active site probe biotin-VAD-fluoromethyl ketone, suggesting that this fragment i

71 iveness of a bridge-to-transplantation (BTT)-VAD approach relative to direct heart transplantation in

72 BTT-VAD therapy is associated with improved survival and inc

73 evaluate survival benefits and costs for BTT-VAD versus nonbridged heart transplant recipients.

74 Over a 20-year time horizon, BTT-VAD therapy increased survival at an increased cost rela

75 estimated a 59%, 54%, and 43% chance of BTT-VAD therapy being cost-effective for high-, medium-, and

76 accepted willingness-to-pay thresholds, BTT-VAD therapy is likely to be cost-effective relative to n

77 h June 2012, 143 patients received CentriMag VAD.

78 lt patients who underwent surgical CentriMag VAD insertion as bridge-to-decision therapy.

79 The next destination after the CentriMag VAD was myocardial recovery in 30%, device exchange to a

80 l ventricular assist device (VAD), CentriMag VAD (Thoratec Corp., Pleasanton, CA), in patients with v

81 Bridge-to-decision therapy with CentriMag VAD is feasible in a variety of refractory cardiogenic s

82 ntinuous-flow ventricular assist devices (CF-VADs) in the treatment of refractory cardiogenic shock i

83 Clinical evidence supporting the use of CF-VADs still remains at the level of small case series, bu

84 us short-term, percutaneous, and surgical CF-VADs.

85 Short-term CF-VADs have several favorable features, but, most notably,

86 trates that infection frequently complicates VAD placement and is a continuing problem despite the us

87 In conclusion, VAD diminished and high-level dietary vitamin A enhanced

88 her IFN-alpha levels were induced in control VAD versus VAS piglet sera at postchallenge day 2.

89 ineage ALL treated with either conventional (VAD/CVAD) or intensive (hyper-CVAD) frontline chemothera

90 0.52; VLD, rho = -0.54; P < 0.001) and deep (VAD, rho = -0.50; VLD, rho = -0.50; P < 0.001) networks.

91 Vitamin A deficiency (VAD) and soil-transmitted helminthiasis (STH) represent

92 Vitamin A deficiency (VAD) can produce a Th1 bias, whereas high-level dietary

93 tial tool for fighting vitamin A deficiency (VAD) in developing countries.

94 n of the prevalence of vitamin A deficiency (VAD) is important in planning and implementing intervent

95 ow prenatally acquired vitamin A deficiency (VAD) modulates innate immune responses and human rotavir

96 urden of malnutrition: vitamin A deficiency (VAD) prevails, whereas the nutrition-related chronic con

97 hed model of embryonic vitamin A deficiency (VAD).

98 reschool children have vitamin A deficiency (VAD).

99 ied in rat fetuses made vitamin A deficient (VAD) after embryonic day (E) 10.5 (late VAD).

100 , whereas transfer into vitamin A-deficient (VAD) hosts caused diversion to the CD11b(-)CD8alpha(+) l

101 inal phenotypes between vitamin A-deficient (VAD) mice and Rpe65(-)/(-) mice under normal diet.

102 rentiation identical to vitamin A-deficient (VAD) mice; (2) the blockage of spermatogonial differenti

103 present study, pregnant vitamin A-deficient (VAD) rats were maintained during early pregnancy on the

104 FAZ area, vessel area density (VAD), vessel length density (VLD), and visual acuity.

105 Dietary VA deprivation (VAD) causes greatly decreased pancreatic VA levels, hype

106 dlines are a type of vascular access device (VAD) used exclusively in one treatment facility within A

107 c stability after ventricular assist device (VAD) explantation is a major goal.

108 n patients with a ventricular assist device (VAD) placed for post-cardiac surgery shock.

109 ts at the time of ventricular assist device (VAD) placement would differentiate those who remained VA

110 ansplantation, or ventricular assist device (VAD) placement; and 2) cardiac hospitalization.

111 en pre-transplant ventricular assist device (VAD) support and mortality after heart transplantation.

112 ng without HTx or ventricular assist device (VAD) support was compared with survival of 743 de novo H

113 ansplantation and ventricular assist device (VAD) therapy.

114 ous-flow external ventricular assist device (VAD), CentriMag VAD (Thoratec Corp., Pleasanton, CA), in

115 received durable ventricular assist devices (VAD).

116 iaries receiving ventricular assist devices (VADs) and associations between hospital-level procedure

117 and durability, ventricular assist devices (VADs) are being implanted with increasing frequency.

118 Ventricular assist devices (VADs) are increasingly being used in pediatric patients

119 Ventricular assist devices (VADs) are now available for all ages, which can improve

120 Ventricular assist devices (VADs) have revolutionized heart failure management in ad

121 Ventricular assist devices (VADs) improve survival and quality of life in patients w

122 t 10 years, with ventricular assist devices (VADs) reaching an impressive degree of sophistication an

123 implantation of ventricular assist devices (VADs) would reverse adipocyte activation and correct adi

124 nd refinement of ventricular assist devices (VADs), medical devices capable of maintaining circulator

125 tation is use of ventricular assist devices (VADs).

126 rials, including ventricular assist devices (VADs).

127 d with long-term ventricular assist devices (VADs).

128 vincristine, doxorubicin, and dexamethasone (VAD) group of the HOVON65/GMMG-HD4 trial (thalidomide in

129 vincristine, doxorubicin, and dexamethasone (VAD) or bortezomib, doxorubicin, and dexamethasone (PAD)

130 one v vincristine-doxorubicin-dexamethasone [VAD] induction), HOVON-65/GMMG-HD4 (bortezomib-doxorubic

131 oboma and retinal folding represent distinct VAD-dependent defects.

132 CCM patients with cardiac improvement during VAD support by analyzing the pre-explant stability of se

133 lformations not previously observed in early VAD or genetic models.

134 amined in PSC.The relation between estimated VAD and CRP and AGP deciles followed a linear pattern in

135 ct of adjusting for malaria on the estimated VAD after adjusting for CRP and AGP.The use of regressio

136 n adjusting for inflammation when estimating VAD with the use of RBP.

137 Specificity of SR to evaluate VAD was high, but additional research is needed to inves

138 ic pulsatile pumps (e.g., Berlin Heart EXCOR VAD, Berlin Heart GmbH, Berlin, Germany) are most common

139 n well described with the Berlin Heart EXCOR VAD, the most commonly used VAD in pediatric patients.

140 Extracorporeal VADs are associated with higher mortality within 6 month

141 Extracorporeal VADs were associated with an HR of 1.91 (95% CI: 1.53 to

142 and 448 patients bridged with extracorporeal VADs with 9,455 United Network for Organ Sharing status

143 Adult mice fed VAD diets display remodeling of the endocrine pancreas,

144 and caspase-3 were detected in situ by FITC-VAD-fmk staining and caspase-3 substrate, respectively.

145 Seventy-five VAD recipients at 4 geographically diverse US cardiac ce

146 ity with currently available continuous-flow VADs are evident, as compared with first-generation devi

147 of complications specific to continuous-flow VADs, including bleeding and aortic insufficiency.

148 tal liver reserves (TLRs) were evaluated for VAD in children from Thailand (n = 37) and Zambia (n = 1

149 One hundred fifty patients scheduled for VAD implantation were enrolled (2006-2008) at 11 US card

150 is review is to describe the indications for VADs in children, types of devices available, current ou

151 Among 96 patients weaned from VADs since 1995, a relatively homogenous group of 53 pat

152 may also contribute to the design of future VADs that are less thrombogenic.

153 atients were supported with the Berlin Heart VAD; 13 met inclusion criteria.

154 d 108 Heartmate II (HM II) and 105 HeartWare VAD (HVAD).

155 In patients with hypertension, VAD might be underestimated because of increased serum r

156 th heart failure who received an implantable VAD between 2006 and 2011.

157 ry in 30%, device exchange to an implantable VAD in 15%, and heart transplantation in 18%.

158 Importantly, VAD inhibits the incorporation of the repressive histone

159 The depressed LRAT activity in VAD mice was partially rescued by the intraperitoneal in

160 ments of photoreceptors were disorganized in VAD mice and were not disorganized in Rpe65(-)/(-) mice,

161 hmias, when present, are also efficacious in VAD-supported hearts.

162 ndritic cells (cDCs and pDCs) were higher in VAD piglets prechallenge, but decreased substantially po

163 Numbers of necrotic MNCs were higher in VAD pigs in spleen (coincident with splenomegaly in othe

164 There has been a dramatic increase in VAD utilization in children over the last decade.

165 10, we observed reduced IFN-alpha levels in VAD pigs that coincided with decreased TLR3(+) MNC frequ

166 th both increased mortality and morbidity in VAD-supported patients.

167 Increasingly, VADs are being used to bridge patients to heart transpla

168 Importantly, although we induced VAD in the entire animal, the pancreatic beta-cells are

169 Intracorporeal VADs are associated with a small increase in mortality i

170 Intracorporeal VADs were associated with an HR of 1.20 (95% confidence

171 ent (VAD) after embryonic day (E) 10.5 (late VAD).

172 In addition, late VAD fetuses displayed both anteriorization of cervical r

173 All late VAD-induced malformations were prevented by the addition

174 ate of late fetal vitamin A deficiency (late VAD) was induced in the organs of developing fetuses.

175 gulated in the periocular mesenchyme in late VAD embryos, and dissolution of the basal lamina does no

176 The optic fissure does not close in late VAD embryos, and severe folding and collapse of the reti

177 genes (Hoxd3 and Hoxb4) was altered in late VAD embryos, with a reduction in Hoxd3 noted as early as

178 nd folding of the retina that occurs in late VAD fetuses.

179 The addition of ROL to late VAD embryos by E12.5 restores Pitx2 expression, supports

180 , 25.7% had been transplanted, 1.6% had left VAD explanted for recovery, and 20.7% had died on device

181 ht ventricular failure post-implantable left VAD in 13.

182 isolated right VAD in 26%, and isolated left VAD in 8%.

183 ry and VAD removal and 14 clinically matched VAD-dependent patients.

184 Mean VAD was lower in diabetic eyes compared with control eye

185 Maintenance consisted of thalidomide 50 mg (VAD) once per day or bortezomib 1.3 mg/m(2) (PAD) once e

186 eam infections (24% VAD related, and 22% non-VAD related).

187 higher VirHRV fecal titers in nonvaccinated VAD piglets.

188 lls (MNCs) isolated from spleen and blood of VAD pigs prechallenge also produced more IFN-alpha.

189 No cases of VAD were identified by both TLRs and SR (true positives)

190 One potential complication of VAD therapy is the development of antibodies directed ag

191 ents randomly assigned either to 3 cycles of VAD or to TAD.

192 , current outcomes, and future directions of VAD therapy.

193 um creatinine were independent predictors of VAD infection (adjusted hazard ratio=2.8 [P=0.007] and 1

194 of adjustment on the estimated prevalence of VAD (defined as <0.7 mumol/L) was examined in PSC.The re

195 ation (CRP+AGP), the estimated prevalence of VAD decreased by a median of 11-18 percentage points in

196 inflammation, to estimate the prevalence of VAD in PSC in regions with inflammation and malaria is s

197 d renal dysfunction may increase the risk of VAD infection.

198 tissues further exacerbates the severity of VAD and thus the embryonic malformations of RBP(-/-) mic

199 nd smaller cardiomyocyte size at the time of VAD placement were associated with subsequent LV functio

200 A higher volume of VAD implants was associated with lower risk of mortality

201 were prospectively followed up to 1 year of VAD support.

202 of adverse events and unexpected removal of VADs.

203 this article, we discuss 1) the spectrum of VADs for outpatient therapy, including their basic physi

204 w describes the currently available types of VADs, their current clinical use, the patient selection

205 the external drive line will make the use of VADs a superior option to heart transplant and even to m

206 th less severe heart failure, and the use of VADs for myocardial recovery in combination with novel p

207 t selection process, the trend toward use of VADs in patients with less severe heart failure, and the

208 The utilization of VADs in complex circulations, such as single ventricle p

209 zation (the development of new antibodies on VAD) occurred in 69%.

210 While on VAD support, new anti-HLA antibodies formed in a majorit

211 atch positive for antibodies formed while on VAD.

212 independently associated with death, HTx, or VAD requirements (hazard ratio, 3.5 and 0.6; 95% CI, 1.2

213 pleen (coincident with splenomegaly in other VAD animals) prechallenge and intestinal tissues (coinci

214 o receive VAD have outcomes similar to other VAD populations, despite being more critically ill pre-i

215 Although overall outcomes of pediatric VADs are favorable, complication rates remain high.

216 No true positive VAD cases occurred; thus, sensitivity was 0% and indeter

217 At 1 month post-VAD, 91.8% of AMI patients were alive with ongoing devic

218 ubgroup analyses indicated that risk of post-VAD and transplantation complications, waiting time, ren

219 At 1-year post-VAD, 52% of AMI patients were alive with ongoing device

220 Evidence of sensitization pre-VAD was found in 69%; new-onset sensitization (the devel

221 Thus, prenatal VAD caused an imbalance in innate immune responses and e

222 Patients with AMI who receive VAD have outcomes similar to other VAD populations, desp

223 uded and compared with patients who received VAD for non-AMI indications.

224 Recently, VADs have similarly taken a prominent role in the manage

225 ement would differentiate those who remained VAD-dependent from those with subsequent left ventricula

226 ts with nonischemic cardiomyopathy requiring VAD support consisting of test and validation cohorts fr

227 nfiguration was BiVAD in 67%, isolated right VAD in 26%, and isolated left VAD in 8%.

228 Yet, several VAD-specific morbidities and technological challenges, w

229 ely 75% of countries with moderate or severe VAD are coendemic for STH.

230 he vascular density in both the superficial (VAD, rho = -0.52; VLD, rho = -0.54; P < 0.001) and deep

231 modynamic support (ECMO, ventilator support, VAD support vs. medical therapy), cardiac diagnosis (rep

232 hese data do not provide evidence supporting VAD implantation in stable United Network for Organ Shar

233 t devices (HR, 5.00; P<0.0001) and temporary VADs (HR, 7.72; P<0.0001).

234 vices, total artificial heart, and temporary VADs were also analyzed.

235 dioverter defibrillators (ICDs) in long-term VAD patients to mitigate the risks associated with ventr

236 As the application of long-term VAD support continues to grow, it will be increasingly i

237 s VAD piglets postchallenge, indicating that VAD may interfere with homing (including intestinal) phe

238 We show that VAD, a novel antisense vlincRNA strongly induced during

239 The VAD and vitamin A-sufficient (VAS) Gn pigs were vaccinat

240 The VAD mice were fed with a vitamin A-deprived diet after b

241 lowed by maintenance with interferon for the VAD arm or thalidomide for the TAD arm.(1) This study to

242 In the VAD mice, the reductions in pancreatic islet sizes and t

243 Demographic and clinical data regarding the VAD course were collected.

244 er leakage and dislodgement) and whether the VAD was removed unexpectedly.

245 pplementation failed to compensate for these VAD effects.

246 Retinal folding due to VAD is preceded by an overall reduction in the percentag

247 atic beta-cells are exquisitely sensitive to VAD-associated apoptosis compared with other cell types

248 ion of beta-cell mass by reintroducing VA to VAD mice does not involve increased beta-cell proliferat

249 Reintroduction of dietary VA to VAD mice restores pancreatic VA levels, glycemic control

250 ove the prediction of postexplant transplant/VAD-free outcome in CCM patients with cardiac improvemen

251 records of all pediatric patients undergoing VAD support using the Berlin Heart device at our institu

252 Circulatory Support) registry who underwent VAD placement in the setting of AMI were included and co

253 rlin Heart EXCOR VAD, the most commonly used VAD in pediatric patients.

254 -HD4 (bortezomib-doxorubicin-dexamethasone v VAD), and PETHEMA GEM05MENOS65 (bortezomib-thalidomide-d

255 in alphaEbeta7) expressing DCs in VAS versus VAD piglets postchallenge, indicating that VAD may inter

256 4-fold; and 195, -1.8-fold; all p < 0.04 vs. VAD dependent).

257 r to LV recovery patients (both p < 0.04 vs. VAD dependent).

258 ) were superior for hyper-CVAD compared with VAD/CVAD; rates were particularly favorable for the CD20

259 cal management have allowed individuals with VADs to be managed in their communities.

260 ), whereas those with BNP>/=506 showed worse VAD-free or HTx-free survival (1 year: 79.7%; P<0.001 ve

261 um pharmacological inhibitor of apoptosis, Z-VAD.

262 d breaks using an alkaline comet assay (+/-z-VAD-fmk cotreatment) and by levels of iododeoxyuridine-D

263 ctivation by NK92 treatment was blocked by Z-VAD treatment in D54-CR cells.

264 eavage of ORF57 in KSHV(+) BCBL-1 cells by z-VAD, z-DEVD, or caspase-7 small interfering RNA led to i

265 MEHP treatment was profoundly inhibited by Z-VAD-FMK, suggesting that 15d-PGJ(2) activates apoptosis

266 of apoptosis as it could not be rescued by z-VAD.

267 Inhibition of caspase-8 with either Z-VAD-fmk or IETD-fmk resulted in necrosis of activated mi

268 se inhibition by the pan-caspase inhibitor Z-VAD fails to prevent photoreceptor death; thus, we inves

269 re activated and the pan-caspase inhibitor z-VAD reduced cell death.

270 and inhibited by the pan-caspase inhibitor z-VAD(OMe)-fluoromethyl ketone.

271 RF57 is prevented by pan-caspase inhibitor z-VAD, caspase-3 and caspase-7 inhibitor z-DEVD, and caspa

272 rescued with the general caspase inhibitor z-VAD, suggesting that reduced cornification was not entir

273 ROS scavengers, and the caspase inhibitor z-VAD-fmk (where z and fmk are benzyloxycarbonyl and fluor

274 Cotreatment with the caspase-3 inhibitor Z-VAD-FMK abrogated the effect of FTY720 on facilitating P

275 The general caspase inhibitor Z-VAD-FMK and caspase-3 inhibitor Z-DEVD-FMK decreased avi

276 d 86%, respectively, pan-caspase inhibitor Z-VAD-fmk completely abolished the induced apoptosis.

277 Moreover, the pan-Casp inhibitor Z-VAD-FMK delayed cornification, and corneocytes were stru

278 The pan-caspase inhibitor Z-VAD-FMK largely restored the growth of ADdlUL38 in norma

279 atment with either a pan-caspase inhibitor z-VAD-fmk or a more specific caspase 3 inhibitor Ac-DEVD-C

280 r Z-DEVD-FMK and general caspase inhibitor Z-VAD-FMK or Fas-deficient mice abrogated the complete dis

281 The pan-caspase inhibitor z-VAD-fmk suppressed liver injury induced by polyI:C/posth

282 not inhibited by the pancaspase inhibitor Z-VAD-FMK, suggesting cell necrosis.

283 at is blocked by the pan-caspase inhibitor Z-VAD-fmk.

284 f this effect by the pan-caspase inhibitor Z-VAD-fmk.

285 itor Z-YVAD-fmk, and pan-caspase inhibitor Z-VAD-fmk.

286 arkedly prevented by the caspase inhibitor z-VAD-FMK.

287 bited apoptosis using pancaspase inhibitor Z-VAD-FMK.

288 o treatment with the pan-caspase inhibitor Z-VAD-FMK.

289 Caspase inhibitor, z-VAD, did not inhibit cell damage from hypoxia/reoxygenat

290 ministration of the pan caspase inhibitor, Z-VAD-FMK into normal mice protected against Chlamydia-ind

291 as inhibited by the pan-caspase inhibitor, z-VAD-FMK suggesting that ABT-263 potentiated caspase-depe

292 ked partially with LDL (P < 0.01) or LDL + z-VAD-fmk (P < 0.001) but not with z-VAD-fmk alone.

293 , and this was reversed with LDL and LDL + z-VAD-fmk (P < 0.001).

294 poptotic cells in the CL group, the use of z-VAD-FMK had no effect on the frequency of these cells.

295 cell death was reduced by the addition of Z-VAD-FMK in chondroitinase ABC-treated explants and was a

296 The z-VAD-fmk inhibitor blocked caspase-3 activities in the ho

297 In R28 cultures, the z-VAD-fmk treatment did not blocked 7kCh-induced caspase-3

298 ssessment of detached retinas treated with Z-VAD showed decreased apoptosis but significantly increas

299 r LDL + z-VAD-fmk (P < 0.001) but not with z-VAD-fmk alone.

300 Inhibition of caspases with Z-VAD-fmk did not kill non-activated microglia, or astrocy