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 can exacerbate extrinsic AD by augmenting Th2-mediat

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 patients and their caregivers were randomized to SBM

10 VAD patients have an acceptable risk profile for abdomin

11 VAD therapy has increased survival but is associated wit

12 VAD therapy is an effective strategy for patients with A

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

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

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

16 VADs are an option for patients with advanced heart fail

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

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

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

20 1000 VAD days) than for PICCs (2.89 per 1000 VAD days).

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

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

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

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

25 The SBML group completed a pretest on 3 VAD self-care skills (controller, power source, and dres

26 ML and usual training groups took the same 3 VAD self-care skills tests.

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

28 They caused 3 of 6 VAD-related infections.

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

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

31 We compared the effectiveness of a VAD simulation-based mastery learning (SBML) self-care t

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

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

34 The DTE approach was applied to a VAD (MIN(DTE)) design with a favorable thromboresistance

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

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

37 6 patients with advanced HF before and after VAD implantation and 10 healthy control subjects.

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

39 VAD implantation and in serial fashion after VAD implantation.

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

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

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

43 or relationship with cardiac stability after VAD explantation.

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

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

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

47 CE1 activity is a common feature of LOAD and VAD, thus underlying a further pathogenic link between t

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

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

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

51 on the complex relationship between STH and VAD.

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

53 -17 mRNA between OVA-treated skin of VAN and VAD mice.

54 blished AD model on both normal VA (VAN) and VAD feeding mast cell deficiency mice (ckit(w-sh/w-sh) )

55 mergently performed in the same admission as VAD placement and analyzed separately.

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

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

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

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

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

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

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

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

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

65 nstable improvement can be recognized before VAD explantation.

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

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

68 ifferences in the above measurements between VAD and VAN group.

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

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

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

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

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

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

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

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

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

78 tween races and ethnicities (P = 0.037), but VAD was not (P < 0.05).

79 h June 2012, 143 patients received CentriMag VAD.

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

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

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

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

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

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

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

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

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

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

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) has been hypothesized to play a role in the pathoph

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 Vitamin A deficiency (VAD) is one of the most prevalent nutrition-related heal

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

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

98 reschool children have vitamin A deficiency (VAD).

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

100 Vitamin A deficient (VAD) mice fared worst with more rapid disease progressio

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

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

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

104 s a separate disease from vascular dementia (VAD).

105 Vessel area density (VAD) and vessel length were calculated for retinal vascu

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

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

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

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

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

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

112 their caregivers ventricular assist device (VAD) self-care skills.

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

114 Ventricular assist device (VAD) technology has evolved significantly over the past

115 Ventricular assist device (VAD) therapy has become an important tool for end-stage

116 ansplantation and ventricular assist device (VAD) therapy.

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

118 Ventricular assist devices (VAD), a mainstay of therapy for advanced and end-stage h

119 received durable ventricular assist devices (VAD).

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

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

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

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

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

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

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

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

128 rials, including ventricular assist devices (VADs).

129 s supported with ventricular assist devices (VADs).

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

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

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

133 alysis of all patients who underwent durable VAD placement between 2005 and 2014.

134 alysis of all patients who underwent durable VAD placement between 2005-2014.

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

136 In the DVC, VAD and VLD also varied significantly with age (P < 0.00

137 E) is a device design approach for enhancing VAD thromboresistance.

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

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

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

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

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

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

144 Here we tested DTE efficacy in experimental VAD designs.

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

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

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

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

149 linical impact of these antibodies following VAD insertion.

150 ed class I panel reactive antibody following VAD support.

151 ignificantly increased Class I PRA following VAD support.

152 iagnostic accuracy was 77% for LOAD, 83% for VAD, and 77% for MIXED dementia.

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

154 iocapillaris (CC) images were quantified for VAD and flow deficit metrics.

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

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

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

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

159 L/6 mouse AD model, compared with VAN group, VAD mice manifested significantly more mast cells accumu

160 43% versus 32% of patients had VADs as a destination therapy.

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

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

163 ward worse SCD/VT/VF (p = 0.062) and DHF/HTx/VAD (p = 0.061) was found in carriers.

164 tricular assist device implantation (DHF/HTx/VAD); and 3) sudden cardiac death/sustained ventricular

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

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

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

168 Importantly, VAD inhibits the incorporation of the repressive histone

169 idity and mortality associated with improper VAD self-care.

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

171 higher not only in LOAD (+ 30%), but also in VAD (+ 35%) and MIXED dementia (+ 22%) (p < 0.001 for al

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

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

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

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

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

177 10, we observed reduced IFN-alpha levels in VAD pigs that coincided with decreased TLR3(+) MNC frequ

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

179 Chronic in vivo studies in VAD implanted calves, revealed MIN(DTE) calf surviving w

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

181 g group completed the existing institutional VAD self-care teaching protocol.

182 , 25.7% had been transplanted, 1.6% had left VAD explanted for recovery, and 20.7% had died on device

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

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

185 40), MIXED (LOAD/VAD) dementia (n.

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

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

188 ng physical prototypes in vitro by measuring VAD thrombogenicity using the modified prothrombinase as

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

190 In PCA model, VAD mice showed remarkable more blue dye leakage than th

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

192 higher VirHRV fecal titers in nonvaccinated VAD piglets.

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

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

195 In a cohort of VAD patients receiving leukocyte-reduced blood products

196 In a cohort of VAD patients receiving leukocyte-reduced blood products

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

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

199 e current state of the art of the effects of VAD support and cell therapy on the reverse remodeling o

200 ling myocardium, as only a small fraction of VAD-supported patients demonstrate reverse structural re

201 Here, we evaluated the impact of VAD on the immune response to the BRSV-NP vaccine and su

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

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

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

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

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

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

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

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

210 of adverse events and unexpected removal of VADs.

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

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

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

214 passive cutaneous anaphylaxis (PCA) model on VAD and vitamin A supplementation (VAS) model in wild-ty

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

216 atch positive for antibodies formed while on VAD.

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

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

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

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

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

222 teria included availability of pre- and post-VAD HLA antibody results.

223 e incidence of HLA antibody development post-VAD insertion, across the age spectrum, in patients rece

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

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

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

227 Pre-VAD sensitization, age, sex (pediatrics), and transfusio

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

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

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

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

232 f end-stage heart failure patients receiving VADs, an increasing number of these patients require sur

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

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

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

236 Therapeutic VAS can rescue VAD-aggravated eAD.

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

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

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

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

241 SBML provided superior VAD self-care skills learning outcomes compared with usu

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

243 In the SVC, VAD and VLD varied significantly with age (P < 0.001) an

244 omparisons were made, survival after all TCS-VAD types continued to be superior to ECMO (p = 0.019) a

245 le LVAD, 84 +/- 3% and 71 +/- 4% for all TCS-VAD types, 79 +/- 9% and 73 +/- 14% for biventricular TC

246 +/- 9% and 73 +/- 14% for biventricular TCS-VAD, and 68 +/- 3% and 61 +/- 8% for ECMO.

247 tory support-ventricular assist devices (TCS-VAD) have a survival advantage over extracorporeal membr

248 lanted, nonendovascular support devices (TCS-VAD) to higher listing statuses.

249 tality in the Cox analysis compared with TCS-VAD (hazard ratio 2.40; 95% confidence interval: 1.44 to

250 Post-transplant survival with TCS-VAD is superior to ECMO and similar to LVAD in a nationa

251 ), 177 (0.7%) with ECMO, 203 (0.8%) with TCS-VAD, 44 (0.2%) with percutaneous endovascular devices, a

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

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

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

255 h theoretically the combination of long-term VAD support and cell therapy may offer significant advan

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

257 at in selected patients undergoing long-term VAD support, improvement of myocardial structure and fun

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

259 Our results show that VAD calves are unable to respond to the mucosal BRSV-NP

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

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

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

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

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

265 ced stresses (statistically representing the VAD 'Thrombogenic Footprint').

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

267 pplementation failed to compensate for these VAD effects.

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

269 D (VADD) had disease progression similar to VAD mice.

270 en well-nourished individuals susceptible to VAD.

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

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

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

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

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

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

277 ML) self-care training curriculum with usual VAD self-care training.

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

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

280 4-fold; and 195, -1.8-fold; all p < 0.04 vs. VAD dependent).

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

282 We sought to verify whether VAD can exacerbate AD development, and explore the possi

283 Compared with VAD group, the above-mentioned inflammatory measurements

284 t review across 3 hospitals of patients with VADs who underwent abdominal surgeries between 2003 and

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

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

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

288 Caspase inhibition (Z-VAD-FMK, 50 um) attenuated cell death with immunostainin

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

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

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

292 cotreatment with the pan-caspase inhibitor Z-VAD-FMK.

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

294 as suppressed by the pan-caspase inhibitor Z-VAD-FMK.

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

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

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

298 ly inhibited by the pan-caspase inhibitor, z-VAD-FMK, and has no cross-reactivity with other known pr

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

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