ライフサイエンスコーパス: -injured

1 In CoCl(2) -injured retinas, blockade of endogenous extracellular AT

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

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

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

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

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

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

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

9 cGAS) drives IRF3 activation in both alcohol-injured hepatocytes and the neighboring parenchyma via a

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

38 cohort study randomly selected 10,000 battle-injured United States military personnel.

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

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

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

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

43 dies on altered gene expression in the blast-injured rat cochlea may provide insights into new therap

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

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

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

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

48 lveolar epithelial type I cells in bleomycin-injured mouse lungs and in lung sections from IPF patien

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

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

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

52 When introduced into dermis or bleomycin-injured lungs of mice, collectins MBL and SP-D were endo

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

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

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

56 Brain-injured patients experienced a maturation defect of the

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

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

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

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

61 All brain-injured mice that consumed BCAAs demonstrated cognitive

62 150 healthy controls and communicative brain-injured subjects in various states of conscious wakefuln

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

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

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

66 ocesses and has therapeutic effects in brain-injured mice without displaying overt side effects.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

88 7 were administered to splenectomized, brain-injured rats.

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

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

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

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

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

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

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

96 atient outcomes in older traumatically brain-injured patients.

97 rbidity and mortality in traumatically brain-injured patients.

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

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

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

101 Burn-injured Sprague Dawley rats were randomized into treatme

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

117 e regeneration when grafted into cardiotoxin-injured muscle.

118 regeneration when injected into cardiotoxin-injured skeletal muscle.

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

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

121 ling and adhesion, were found reduced in CCI-injured juvenile compared to CCI-injured adult immune ce

122 Genome-wide comparison of CCI-injured peripheral whole blood showed a significant incr

123 and on infiltrating immune cells in the CCI-injured juvenile cortex.

124 uced in CCI-injured juvenile compared to CCI-injured adult immune cells.

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

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

127 Consistently, in cisplatin-injured renal tubular cells in vitro, lithium enhanced a

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

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

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

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

132 unction and molecular changes in spinal cord-injured (SCI) rats were investigated.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

147 jured and destabilized medial meniscus (DMM)-injured knees from 8-wk-old C57BL/6J and MRL/MpJ mice.

148 pSMAD5-positive cells were found in the DMM-injured AC in MRL/MpJ mice than in normal mice.

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

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

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

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

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

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

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

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

157 Head-injured animals display features characteristic of mamma

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

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

160 magnesium favourably affects outcome in head-injured patients.

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

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

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

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

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

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

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

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

169 hils infiltrate the intracerebral hemorrhage-injured brain.

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

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

172 lammation and oxidative stress in ifosfamide-injured bladder, which are reversed by pretreatment with

173 emia diminished the ferroptotic damage in IR-injured lung tissue, consistent with the protective effe

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

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

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

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

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

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

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

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

182 quantified by intravital microscopy of laser-injured arterioles.

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

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

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

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

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

188 initiator of osteoarthritis in the ligament-injured patient.

189 The ligation-injured lacrimal glands temporarily decreased in weight

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

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

192 2 in bronchial alveolar lavage fluids in LPS-injured lung compared with wild-type mice.

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

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

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

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

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

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

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

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

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

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

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

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

205 Nerve-injured HCN3 knockout mice exhibited similar levels of m

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

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

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

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

210 gen alleviated mechanical allodynia in nerve-injured animals.

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

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

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

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

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

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

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

218 story of exposure to TBI was selected as non-injured controls (n = 32).

219 t, surgery, and their combination impact non-injured bones will improve treatment strategies for astr

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

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

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

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

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

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

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

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

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

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

230 The lateral tract on the opposite (non-injured) side was minimally affected by the injury.

231 and fracture surgery/healing on several non-injured bones within the axial and appendicular skeleton

232 nt, corneal NV occurred only through the non-injured aspect of the limbus.

233 ot significantly differ from that in the non-injured control mice.

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

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

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

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

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

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

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

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

242 , 21.2% of head-injured and 16.3% of nonhead-injured patients fulfilled the DSM-IV diagnosis of PCS;

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

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

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

246 Notch signaling on lin28a expression in post-injured retina.

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

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

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

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

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

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

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

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

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

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

257 which co-expressed Prox-1 in the DG of rmTBI-injured mice which coincided with enhanced cFos expressi

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

259 p inhibited neuronal inflammation in scratch-injured neurons.

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

261 ommon and portends poor outcomes in severely-injured children.

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

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

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

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

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

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

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

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

270 TBI by midline fluid percussion or were sham-injured.

271 s unchanged in CCI models compared with sham-injured animals.

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

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

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

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

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

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

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

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

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

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

282 s become functionally integrated into stroke-injured brain circuitry is poorly understood.

283 nections after transplantation in the stroke-injured brain.

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

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

286 ized with adherent bacteria in superficially-injured corneas.

287 surface only if the cornea was superficially-injured.

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

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

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

291 physiology could significantly shape how VML-injured patients and clinicians approach regenerative me

292 on of PGC1-alpha as a limiting factor in VML-injured muscle's adaptive capacity to exercise and provi

293 Herein, the data indicated that VML-injured muscle has diminished mitochondrial content and

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.