ライフサイエンスコーパス: -injured

1 MSCs were infused intraportally into CCl(4) -injured mice with and without neutralizing antibodies.

2 Alveolar macrophages from acid-injured Akt2(-/-) mice demonstrated the alternative acti

3 plasma and the bronchoalveolar fluid of acid-injured mice (Spearman's rho = -0.73 and -0.69, respecti

4 ificant differences in T2 values between ACL-injured and control knees were found.

5 ompartments at baseline and follow-up in ACL-injured knees and were compared with measures acquired i

6 bearing medial femorotibial cartilage in ACL-injured knees were significantly elevated at 1-year foll

7 f the posterolateral tibial cartilage in ACL-injured knees were significantly elevated at baseline co

8 sprouting, whereas puromycin aminonucleoside-injured podocyte supernatant decreased these GEN respons

9 neointimal formation in balloon angioplasty-injured rat carotid arteries (0.172 +/- 29.9, versus 0.3

10 The antibody-injured pericytes had reduced efficacy in inhibiting T c

11 PCs from APAP+ISO-treated mice to other APAP-injured mice improved AILI, an effect antagonized by DKK

12 proportionately sampled group of non-assault-injured youth enrolled from September 2009 through Decem

13 or violent reinjury among high-risk, assault-injured youth is poorly understood.

14 o attenuate intimal hyperplasia in a balloon-injured artery was determined.

15 P, in rat embryonic aortas and adult balloon-injured carotid arteries compared with quiescent adult a

16 reover, a PCL sheath deployed around balloon-injured rat carotid arteries was associated with a minim

17 Finally, restoration of miR-145 in balloon-injured arteries via Ad-miR-145 inhibits neointimal grow

18 MC growth and intimal hyperplasia in balloon-injured carotid arteries of streptozotocin-treated rats,

19 s inhibited by warfarin treatment in balloon-injured carotids.

20 In balloon-injured rabbit arteries, cell proliferation (51%) and le

21 n cultured rat VSMCs in vitro and in balloon-injured rat carotid arteries in vivo, we demonstrate tha

22 f Id3a inhibited lesion formation in balloon-injured rat carotid arteries in vivo.

23 apoptosis of VSMCs in culture and in balloon-injured rat carotid arteries, thus contributing to Mfn-2

24 PGC-1beta expression was observed in balloon-injured rat carotid arteries.

25 lammation and neointima formation in balloon-injured rat carotid arteries.

26 of rno-miR-31 is verified in vivo in balloon-injured rat carotid arteries.

27 ts were further confirmed in vivo in balloon-injured rat carotid arteries.

28 ifferentially expressed sequences in balloon-injured versus normal arteries.

29 expression levels are upregulated in balloon-injured vs. uninjured VSMCs.

30 In balloon-injured, atherosclerosis-free porcine arteries, COX-1 ge

31 erized in vitro and then seeded into balloon-injured rat carotid arteries to determine the effects on

32 ession increases in the neointima of balloon-injured rat carotids.

33 owth factor (VEGF) expression in the balloon-injured carotid artery of female Zucker fatty rats.

34 cible TN-C protein expression in the balloon-injured rat artery wall.

35 Indeed, delivery of Ad-p27-126TS to balloon-injured arteries in rats not only induced faster and mor

36 Local NO-ELIP administration to balloon-injured carotid arteries attenuated the development of i

37 ks after perivascular application to balloon-injured rat common carotid arteries, halofuginone versus

38 ecular mechanism of PESDA binding to balloon-injured vasculature.

39 teration developed in saline-treated balloon-injured rat aortas (20.3+/-8.0%), and psiepsilonRACK sig

40 time that neointimal formation using balloon-injured rat carotid arteries was associated with a signi

41 sphorylation were observed in 1-week balloon-injured arteries compared with uninjured arteries, and t

42 of ERK activation in stellate cells from BDL-injured liver led to a decrease in expression of endothe

43 Conditional ablation of MSLN+ aPFs in BDL-injured mice attenuated liver fibrosis by approximately

44 maximum pupil constriction diameter in blast-injured mice using red light or blue light stimuli 24 ho

45 rformed in a homogeneous population of blast-injured polytrauma inpatients.

46 Further, BLEO-injured il17a(-/-) mice had diminished levels of circula

47 of CLF-1/CLC to both uninjured and bleomycin-injured mice led to the pulmonary accumulation of CD4(+)

48 ivity in fibroblasts isolated from bleomycin-injured lung with induced telomerase activity.

49 CCL2 expression increased in bleomycin-injured bronchoalveolar lavage (BAL), but significantly

50 and Smad3 levels were increased in bleomycin-injured lungs.

51 PC species that increase in BAL of bleomycin-injured mice were discordant, inconsistent with a substr

52 fibroblasts isolated from lungs of bleomycin-injured mice, effects that are inhibited in bleomycin-AG

53 increases markedly in the lungs of bleomycin-injured mice.

54 RNA patterns were seen in lungs of bleomycin-injured wild-type, but not CD103(-/-) or Mmp7(-/-), mice

55 other day for 1 week in normal or bleomycin-injured mice maintains significantly higher lung sphingo

56 or vitronectin-binding activity to bleomycin-injured mice genetically deficient in PAI-1.

57 and C5aR in lung fibrosis by using bleomycin-injured mice with fibrotic lungs, elevated local C3a and

58 Brain-injured animals had significantly increased caspase-medi

59 Brain-injured patients experienced a maturation defect of the

60 Brain-injured patients ventilated more than 24 hours were eval

61 (iv) Finally, a brain-injured adult with glutaric aciduria type 1 had regional

62 ence for the conscious experience of a brain-injured patient, who had remained entirely behaviorally

63 t are extremely challenging in acutely brain-injured patients.

64 tely isolated living slices from adult brain-injured mice.

65 All brain-injured mice that consumed BCAAs demonstrated cognitive

66 ury status of the host brain, although brain-injured animals had significantly fewer graft cells than

67 l death was observed in both sham- and brain-injured animals, and caspase-mediated graft cell death w

68 150 healthy controls and communicative brain-injured subjects in various states of conscious wakefuln

69 Transfer of blood-borne EVs from brain-injured animals was also enough to suppress exploratory

70 eripheral blood mononuclear cells from brain-injured patients with nosocomial pneumonia generated sig

71 SAS, and GCS scores in critically ill brain-injured patients, with and without sedation.

72 her serum levels of GFAP and UCH-L1 in brain-injured children compared with controls and also demonst

73 EL(+) pyramidal and granule neurons in brain-injured mice were amplified and compared with those from

74 nulomas was significantly decreased in brain-injured patients with nosocomial pneumonia (3% [range: 1

75 range: 8%-61%]) and was not altered in brain-injured patients with nosocomial pneumonia (31% [range:

76 l pneumonia (1% [range: 0%-7%]) and in brain-injured patients with nosocomial pneumonia (4% [range: 2

77 ultinucleated giant cells was lower in brain-injured patients without nosocomial pneumonia (1% [range

78 ) and was not significantly altered in brain-injured patients without nosocomial pneumonia (26% [rang

79 cells were significantly increased in brain-injured patients without nosocomial pneumonia (66% [rang

80 verall immune response to pathogens in brain-injured patients, and assessed its relationship to nosoc

81 e functions that are often impaired in brain-injured patients.

82 can offer prolonged WM improvement in brain-injured patients.

83 ssessment of level of consciousness in brain-injured patients.

84 tural killer cells were not altered in brain-injured patients.

85 arotoxin increased BBB permeability in brain-injured rats, while PNU-282987 injection decreased such

86 unction assayed using these methods in brain-injured subjects.

87 the extent of functional activation of brain-injured circuits is a consequence of initial disruption

88 science and the neurointensive care of brain-injured human patients.

89 As PIE affects as many as 20% of brain-injured patients, reliable biomarkers are imperative bef

90 tone in the management of the severely brain-injured patient and should be used to compliment other t

91 oxyglucose PETs obtained from severely brain-injured patients (BIs) and 10 normal volunteers (NVs).

92 We studied seven severely brain-injured patients and a control group of 14 subjects usin

93 ommunication capacity in some severely brain-injured patients who may not retain sufficient motor fun

94 in a continuous sample of 143 severely brain-injured patients with DOC (and 96 volunteers), across 2

95 gnized cognitive abilities in severely brain-injured patients with very limited or no motor responses

96 7 were administered to splenectomized, brain-injured rats.

97 Specifically, the brain-injured subjects dissociated bedside and functional magn

98 ndent responses without exception, the brain-injured subjects showed a wide variation in the correlat

99 of exogenous IL-1beta and TNF-alpha to brain-injured animals worsened Evans Blue dye extravasation, s

100 Almost 50% of traumatic brain-injured (TBI) patients are alcohol intoxicated.

101 thy subjects is preserved in traumatic brain-injured patients.

102 degenerating neurons in the traumatic brain-injured tissue with the absence of staining in our sham-

103 sity of care provided to traumatically brain-injured adults and to determine the influence of intensi

104 atient outcomes in older traumatically brain-injured patients.

105 rbidity and mortality in traumatically brain-injured patients.

106 e infancy and early childhood, whereas brain-injured children had an early velocity peak (18 months)

107 onia (3% [range: 1%-9%]) compared with brain-injured patients without nosocomial pneumonia (16% [rang

108 fewer mature granulomas compared with brain-injured patients without nosocomial pneumonia and with h

109 Burn-injured Sprague Dawley rats were randomized into treatme

110 In Experiment 1, burn-injured young rats received once daily saline or morphin

111 e collected for a 10-year period on all burn-injured patients admitted to the Birmingham Burn Centre

112 CFU of E. coli, whereas the LD(50) for burn-injured mice was 50 x 10(3) CFU at 7 days postinjury.

113 In contrast, spleen cells from burn-injured CD4(-/-) mice produced cytokines at significantl

114 ndicated that splenocytes prepared from burn-injured CD8(-/-) mice displayed TLR-induced cytokine pro

115 Lymph node cells from burn-injured mice also produced higher levels of Th2-type cyt

116 Moreover, the peritoneal neutrophils in burn-injured mice were more highly activated than neutrophils

117 common sites of secondary infection in burn-injured patients.

118 istry; Western blot) was upregulated in burn-injured young rats receiving morphine alone or in combin

119 ve found that prophylactic treatment of burn-injured mice with the DC growth factor FLT3 ligand (FL)

120 Data obtained from the urine of burn-injured rats and pediatric burn patients match previousl

121 We have demonstrated that burn-injured adults remain hyperglycemic, are insulin resista

122 We found that burn-injured mice had higher numbers of circulating neutrophi

123 ructured, multidisciplinary approach to burn-injured patients, early surgical excision and wound clos

124 phrenic motor recovery was present in all C2-injured rats via crossed spinal synaptic pathways that c

125 rrow cells to skeletal muscle in cardiotoxin-injured anterior tibialis muscle in a green fluorescent

126 ssion and muscle regeneration in cardiotoxin-injured beta3-integrin-null mice are impaired, as indica

127 that gene transfer of GEFT into cardiotoxin-injured mouse tibialis anterior muscle exerts a powerful

128 e regeneration when grafted into cardiotoxin-injured muscle.

129 regeneration when injected into cardiotoxin-injured skeletal muscle.

130 on of these committed cells into cardiotoxin-injured skeletal muscles of NOD/SCID mice reveals surviv

131 ells isolated from dystrophic or cardiotoxin-injured muscle fail to undergo myogenesis.

132 rgeted mice, we show that in ferric chloride-injured veins platelet adhesion to subendothelium is dec

133 Hepatocytes that reside in a chronically-injured liver have altered growth responses compared to

134 In E. coli-injured human lungs, mesenchymal stem cells restored alv

135 nd samples from extremity injuries in combat-injured U.S. service members.

136 orresponding mRNAs in the IgG immune complex-injured lung, compared with wild-type mice.

137 chia coli UTI was modeled in the spinal cord-injured (SCI) rat with the hypothesis that SCI animals w

138 In this study, we show that in spinal cord-injured C57BL/6 mice, both ApoE S1 and ApoE S3 transcrip

139 athing cells) in a population of spinal cord-injured companion dogs that accurately model many of the

140 duction in F4/80+ macrophages in spinal cord-injured MMP-9 knock-out mice (by 36%) or wild-type mice,

141 s after long-term engraftment in spinal cord-injured NOD-scid mice.

142 a significant improvement for a spinal cord-injured patient.

143 Spinal cord-injured rats had fewer myelinated axons in the medullary

144 -reflex can modify locomotion in spinal cord-injured rats.

145 ing a model for VAP prediction in critically-injured trauma patients, and to identify differentially

146 veloped that accurately predicted critically-injured trauma patients that went on to develop VAP (VAP

147 ate or NMDA was injected directly into crush-injured rat sciatic nerves, ERK1/2 phosphorylation was o

148 olated them as GFP(+)EpCAM(-) cells from DDC-injured livers of Sox9-EGFP mice.

149 x9(+) cells surrounded luminal spaces in DDC-injured liver while they expressed HNF4alpha.

150 d compensatory proliferation observed in DEN-injured ERRalpha-null livers is concomitant with increas

151 cle cells was readily observed in denudation-injured carotid arteries at 7 and 14 days.

152 ing of diffuse-injured circuits into diffuse-injured tissue likely establishes maladaptive circuits r

153 The sprouting of diffuse-injured circuits into diffuse-injured tissue likely esta

154 se an inflammatory response in intact or DSS-injured mouse colon.

155 d recruitment of neutrophils to the elastase-injured aortic wall and impaired local production of CXC

156 oupled receptor 6(GPR6) expression in fAbeta-injured neurons.

157 verexpressing animals compared with non-FasL-injured littermates.

158 avital microscopy to ferric chloride (FeCl3)-injured mesenteric arterioles and laser-induced injury o

159 Control and FPI-injured rats at 1 year of age displayed large-amplitude

160 Here we demonstrate that, in freeze-injured muscle, CCR2 co-localized with Mac-3, a marker o

161 were also observed in an in vivo gentamicin-injured animal model.

162 ediated overexpression of NoxA1 in guidewire-injured mouse carotid arteries significantly increased s

163 sabled (n = 12) and vegetative (n = 10) head-injured patients who survived between 6 h and 3 years, a

164 ted into the rehabilitation program for head-injured military personnel who will be returned to duty,

165 new data reveal safety and efficacy in head-injured patients.

166 magnesium favourably affects outcome in head-injured patients.

167 input resistance in controls but not in head-injured rats.

168 cal penetrating head injuries and a non-head-injured control group for the Val66Met BDNF polymorphism

169 ower rates of pneumonia compared to non-head-injured trauma patients and suggest that the mechanism o

170 This study examines the profile of head-injured (HI) trauma patients and their actual need for t

171 e months following the trauma, 21.2% of head-injured and 16.3% of nonhead-injured patients fulfilled

172 CT imaging of head-injured children has risks of radiation-induced malignan

173 ed the DSM-IV diagnosis of PCS; 8.8% of head-injured patients fulfilled the diagnostic criteria for P

174 lei in severely disabled and vegetative head-injured patients.

175 o be an active process in which viable, heat-injured cells induce a signal cascade and/or mediator th

176 hils infiltrate the intracerebral hemorrhage-injured brain.

177 on and axonal excitability in chronically HX-injured rats, (2) that antibody treatment increased the

178 d improvement of synaptic transmission in HX-injured spinal cord.

179 Ischemia-injured porcine ileal mucosa was mounted in Ussing chamb

180 ing recovery of barrier function in ischemia-injured intestine through a mechanism involving stimulat

181 inal Cl - secretion restores TER in ischemia-injured intestine.

182 the recovery of barrier function in ischemia-injured porcine ileum.

183 hat vascular survival and growth in ischemia-injured tissue may be stimulated by suppressing PHD2 in

184 rtery ligation and reperfusion, the ischemia-injured heart elaborates the cardioprotective polypeptid

185 Application of PGE 2 to ischemia-injured ileal mucosa stimulated increases in Isc, an ind

186 from airspaces of fluorescein isothiocyanate-injured CCR2(+/+) mice than from CCR2(-/-) mice.

187 ring stem cells (SASCs) from both laceration-injured and control noninjured skeletal muscles in mice

188 Laser-injured frog eyes were employed to test the potential of

189 ctivity was present in both normal and laser-injured mice at the laser burn site and at the ganglion

190 latelet-mediated thrombus formation in laser-injured arterioles by > 75% (P < 0.001).

191 map localized photoreceptor lesion in laser-injured frog eyes.

192 In vivo microthrombus formation in laser-injured vessels significantly increased in fibrinogen-tr

193 IOS imaging of laser-injured frog eyes indicated that the confocal IOS could

194 permeability compared with retinas of laser-injured mouse retinas injected with control plasmid.

195 Four days postinjury, laser-injured mouse retinas injected with IGFBP-3NB plasmid de

196 were anesthetized, ventilated, saline lavage-injured, and randomized into groups: group 1 (convention

197 rectly with a parenchymal probe in the least-injured hemisphere.

198 The ligament-injured joint is at high risk for osteoarthritis.

199 initiator of osteoarthritis in the ligament-injured patient.

200 The ligation-injured lacrimal glands temporarily decreased in weight

201 urotrophic factor (GDNF) stimulation of long-injured axons.

202 For successful regeneration, long-injured axons must overcome their poor intrinsic growth

203 2 in bronchial alveolar lavage fluids in LPS-injured lung compared with wild-type mice.

204 reduced inflammation and lung injury in LPS-injured mice.

205 ophils in both the blood and airspace of LPS-injured mice and that Ab-mediated SDF-1 blockade signifi

206 -derived EVs before adoptive transfer to LPS-injured mice.

207 cally lower in Lum-/- - compared with Lum+/+-injured cornea.

208 Lum-/- -injured corneas showed significantly lower caspase-3/7 a

209 ees from its phase three location and mildly-injured animals were impaired.

210 One day after phase three, sham- and mildly-injured animals were tested on a phase four conflict act

211 Control and mildly-injured rats learned this task within four ten-minute tr

212 Moderately-injured animals were also impaired if tested 3 weeks aft

213 thin four ten-minute trials while moderately-injured animals were impaired.

214 ilat on macrophage-conditioned medium (MPCM)-injured human mesangial cells can be modulated by this r

215 ition of receptor-associated protein to MPCM-injured mesangial cells with and without ACE-I increased

216 analysis of the steady-state and naphthalene-injured trachea to evaluate the predictions of this mode

217 of lineage relationships in the naphthalene-injured tracheal epithelium demonstrated that two multip

218 n of hundreds of genes across sham and nerve-injured groups, which can be difficult to validate, part

219 e in both lamina I and II neurons from nerve-injured animals than in controls, suggesting that endoge

220 excitability, and against neurons from nerve-injured rats.

221 On- and off-cells recorded in nerve-injured animals exhibited novel responses to innocuous m

222 gen alleviated mechanical allodynia in nerve-injured animals.

223 induced NMDA receptor-dependent LTP in nerve-injured rats.

224 sitivity in a dose-dependent manner in nerve-injured rats.

225 na I of the spinal cord dorsal horn in nerve-injured versus control animals, suggesting a functional

226 ges in primary afferents from naive or nerve-injured rats, respectively, thus confirming the predicte

227 and exhibited enhanced migration toward NMDA-injured hippocampal cultures.

228 We studied injured and non-injured Amish glutaric aciduria type 1 patients using ma

229 cifically collect individual injured and non-injured nociceptive DRG neurons and to define their gene

230 ely express this transcription factor in non-injured adult DRG neurons.

231 a(V) were not significantly different in non-injured and SNL-injured DRG neurons.

232 ed with atherosclerotic plaque growth in non-injured arteries.

233 owing experimental pressure responses in non-injured human subjects or to data from people with SCI.

234 postinjury but was still higher than in non-injured mice.

235 In non-injured muscle, muscle-specific kinase expression was si

236 found minimal transcriptional changes in non-injured neurons at 7 days after SNI.

237 In non-injured patients, middle cerebral artery velocities were

238 mg/kg, intraperitoneal) lowered cAMP in non-injured rats to injury amounts, which were unchanged by

239 while producing no significant change in non-injured rats.

240 the injured hemisphere compared with the non-injured hemisphere, while the hyperpolarized bicarbonate

241 lly evoked activity that extended to the non-injured hemisphere; by 8 weeks, significant recovery was

242 others like GAP-43, was increased in the non-injured neurons.

243 in abnormal neuronal hypoactivity in the non-injured primary somatosensory cortex (S1).

244 llular markers of neuroplasticity in the non-injured S1 compared to TBI rats that did not receive the

245 (i) Three children (two non-injured) had low cerebral blood flow, prolonged mean tra

246 ponse to pressure in people with SCI vs. non-injured control subjects, and thus may serve as novel di

247 of hedgehog activation, consistent with non-injured controls.

248 , 21.2% of head-injured and 16.3% of nonhead-injured patients fulfilled the DSM-IV diagnosis of PCS;

249 egion of the unilateral ureteral obstruction-injured kidney in mice correlating with SMAD3 and p53(Se

250 these results indicate that while LFP in P19-injured animals does not lead to significant cell death,

251 ated that regardless of injury severity, P19-injured rats exhibited a significant increase in escape

252 er eight strains tested, especially when pre-injured.

253 obal gene expression changes in the pressure-injured ONH.

254 active caspase-3 protein was enhanced in I/R-injured and CsA-treated kidneys, but decreased by Tac, R

255 that miR-494 was downregulated in murine I/R-injured and human infarcted hearts.

256 tion of full-length caspase-3 widened in I/R-injured kidneys from normal distal tubules and collectin

257 ficantly increased in uninephrectomy and I/R-injured kidneys, they were not significantly affected by

258 nitrosylated mitochondrial proteins from I/R-injured mouse livers with or without MnTMPyP pretreatmen

259 Tumor was differentiated from radiation-injured tissue by histopathology (n = 13) or 1-y clinica

260 the vitreous of retinal ischemia-reperfusion-injured adult nonobese diabetic-severe combined immunode

261 metastases residing in ischemia-reperfusion-injured liver lobes acquired CSC characteristics.

262 Scratch-injured mouse eyes were infected with the six P. aerugin

263 p inhibited neuronal inflammation in scratch-injured neurons.

264 ged 3 weeks later by inoculating the scratch-injured cornea with P. aeruginosa.

265 f acute lung injury on mortality in severely-injured trauma patients beyond baseline severity of illn

266 ements, the animals were allocated to a sham-injured group (n = 5), an injured and saline-treated gro

267 ed hemorrhagic hypotension (n = 8), and sham-injured control animals receiving anesthesia and surgery

268 s, the animals were allocated to either sham-injured, nontreated controls (sham), injured, nontreated

269 ion, we show herein that the LD(50) for sham-injured mice was 10(3) CFU of E. coli, whereas the LD(50

270 vents (EEEs) that are never observed in sham-injured animals and have electrographic appearance simil

271 sue with the absence of staining in our sham-injured brains.

272 ad significantly fewer graft cells than sham-injured animals.

273 e-mediated graft cell death compared to sham-injured animals.

274 eral cortex and hippocampus compared to sham-injured controls 24h after mTBI.

275 cal tissue loss (p < .01) compared with sham-injured animals.

276 rall survival of TBI mice compared with sham-injured mice.

277 Neuronal cells dissociated from SNE-injured and contralateral L4 and L5 dorsal root ganglia

278 gnificantly different in non-injured and SNL-injured DRG neurons.

279 imulated with conditioned medium from spinal-injured tissue explants.

280 tent effects on restoring function to spinal-injured adult mammals.

281 todomain [aa 27-310; NgR(310)ecto] to spinal-injured rats.

282 ized the SSc epidermis and asked whether SSc-injured epidermal cells release factors capable of promo

283 t reactive glial cells in the cortex of stab-injured or Alzheimer's disease (AD) model mice can be di

284 s should guide future experiments on stretch-injured axons.

285 Rapidly stretch-injured rat pheochromocytoma (PC12) cells express cellul

286 nections after transplantation in the stroke-injured brain.

287 to promote detrimental actions in the stroke-injured brain.

288 y revealed that monocytes home to the stroke-injured hemisphere., and that infiltration peaks 3 d aft

289 ized with adherent bacteria in superficially-injured corneas.

290 surface only if the cornea was superficially-injured.

291 lls in normal liver, in carbon tetrachloride-injured liver, and in several models of OC activation.

292 chanisms underlying TAI in the traumatically-injured immature brain.

293 nd SMA in both injured (ipsilesional) and un-injured (contralesional) hemispheres.

294 st endothelial cells in vein grafts and wire-injured arteries.

295 ia were evaluated in cultured VSMCs and wire-injured mouse carotid arteries from wild-type (WT, C57BL

296 rmed at 2 and 4 wk after injury in both wire-injured ApoE(-/-) and wild-type C57BL/6 mice.

297 io was significantly greater in femoral wire-injured arteries from P2Y(12)(+/+) compared with P2Y(12)

298 elets inhibited endothelial recovery in wire-injured carotid arteries, but this effect was also abrog

299 nd vascular cell adhesion molecule 1 in wire-injured carotid arteries.

300 r antiglaucoma drugs were determined on zinc-injured retinal cells.