ライフサイエンスコーパス: LAD

1 LAD coronary blood flow velocity and free-breathing myoc

2 LAD group had modest but significant slowing in conducti

3 LAD stenosis and additional diagonal graft remained pred

4 LAD stenosis during hyperemia decreased LCx probe flow (

5 LAD wall-thickening (27+/-3 to 46+/-6%, P<0.05) and EF (

6 LAD-2 may thus function in the semaphorin complex by com

7 LAD-III, which presents with bleeding similar to that in

8 LADs are constructed using either a single lignocellulos

9 LADs are simple, low-cost, easy to use, provide rapid re

10 bjects with leukocyte adhesion deficiency-1 (LAD-I) do not express beta2 integrins because of mutatio

11 Leukocyte adhesion deficiency type-1 (LAD-1) is an autosomal recessive immunodeficiency caused

12 ata that shows that L1-like adhesion gene 2 (LAD-2), a Caenorhabditis elegans L1CAM, functions in axo

13 We studied 3 LAD-1 patients with markedly diminished neutrophil CD18

14 ed flow differences (LAD/LCX, 3.38 +/- 0.83; LAD/septal, 1.26 +/- 0.49).

15 s of Skap2 function is sufficient to cause a LAD-like phenotype in mice.

16 Eight dogs were prepared with a LAD stenosis, and contrast-enhanced MDCT imaging was per

17 thly depot LHRH agonist leuprorelin acetate (LAD-3M; n = 299) and chemotherapy with cyclophosphamide,

18 unction, SCM is indistinguishable from acute LAD-territory MI.

19 tudies of DNA base adducts in late-stage AD (LAD) brain show elevations of 8-hydroxyguanine (8-OHG),

20 Several lung adenocarcinoma (LAD) cell lines were screened to characterize epidermal

21 oncogenic addiction in lung adenocarcinoma (LAD).

22 Although LAD syndromes are rare maladies, their investigation is

23 packed with Juniperus chinensis branches: An LAD that was uniformly distributed, linearly increasing

24 plaque distribution in coronary arteries and LAD predisposition to plaque formation.

25 grin CD18 adhesion molecule in both CLAD and LAD lead to recurrent, life-threatening bacterial infect

26 ocardial PBS injections (control group), and LAD ligation followed by NP12 administration (NP12 group

27 s in their expression levels between IMA and LAD, which included the TES gene encoding Testin.

28 nes differentially expressed between IMA and LAD.

29 on at 1 and 8 weeks post-MI than the LCx and LAD groups, along with early and severe impairment of LA

30 In the LCx and LAD groups, LA dysfunction was less pronounced and not c

31 pe of the relationship between flow rate and LAD, SAD, and volume was significantly different accordi

32 tolic stiffness were elevated in the SCM and LAD MI groups compared with the control group.

33 d diastolic stiffness were higher in SCM and LAD MI patients than in control subjects but no differen

34 SCM and LAD MI show severe diastolic dysfunction.

35 eft ventricular ejection fraction in SCM and LAD MI were 40.8+/-12.3% and 49.6+/-5.6%, respectively,

36 coupling were similarly abnormal in SCM and LAD MI.

37 ic dysfunction is equally reduced in SCM and LAD MI.

38 Moreover, attempts to reconcile TADs and LADs to replication-timing data have not revealed a comm

39 First, considerable overlap between TADs and LADs was observed with the TAD repositioning as a unit.

40 e, 63+/-12 years), those with left anterior (LAD) ST-segment-elevation MI (n=36; mean age, 63+/-10 ye

41 represents the first structural data on any LAD and provides a molecular basis for understanding the

42 he left anterior descending coronary artery (LAD) followed by reperfusion.

43 ic left anterior descending coronary artery (LAD) occlusion have a high rate of SCD that parallels th

44 he left anterior descending coronary artery (LAD) perfusion territory before microembolization and is

45 he left anterior descending coronary artery (LAD) was followed by 3-h reperfusion in 16 open-chest do

46 he left anterior descending coronary artery (LAD)-fed myocardium and the stenosed LCX-fed myocardium.

47 he left anterior descending coronary artery (LAD).

48 he left anterior descending coronary artery (LAD).

49 he left anterior descending coronary artery (LAD).

50 he left anterior descending coronary artery (LAD).

51 he left anterior descending coronary artery (LAD).

52 CAB) of the left anterior descending artery (LAD) coupled with percutaneous coronary intervention (PC

53 tion of the left anterior descending artery (LAD) ligation to induce an anterior wall myocardial infa

54 nfarct with left anterior descending artery (LAD) occlusion followed by reperfusion (group 4), or the

55 wine with a left anterior descending artery (LAD) stenosis to produce chronic hibernating myocardium

56 h a chronic left anterior descending artery (LAD) stenosis to produce hibernating myocardium underwen

57 tion with a left anterior descending artery (LAD) stenosis when flow (LAD, 0.7+/-0.2 versus 1.2+/-0.1

58 tion of the left anterior descending artery (LAD) to induce a sizable left ventricular (LV) infarct.

59 osis of the left anterior descending artery (LAD) underwent vasodilator challenges with hypercapnia a

60 ated in the left anterior descending artery (LAD), and 20 contrast material-enhanced volume scans wer

61 erritories: left anterior descending artery (LAD), left circumflex artery (LCX), and right coronary a

62 stly in the left anterior descending artery (LAD), then in the right coronary artery (RCA), circumfle

63 ry (LCX) or left anterior descending artery (LAD).

64 der of glycosylation, CDG-IIc (also known as LAD-II), which is also the result of a GFR deficiency.

65 nonmalignant hematopoietic diseases such as LAD.

66 GEDDs correlate with the lamina-associated (LADs) and replication domains of mammalian cells.

67 of 0.7 mg/kg intraperitoneally 30 min before LAD occlusion.

68 of the GPI tirofiban, starting 45 min before LAD reopening.

69 onal MR signal intensity differences between LAD and LCX-fed myocardium (1.24 +/- 0.08) were signific

70 different (P < .01) from differences between LAD and septal-fed myocardium (1.02 +/- 0.07), which was

71 Canyons mostly form between LADs and are enriched in genes and enhancers.

72 S), responses to isoproterenol were blunted (LAD, 83+/-6 versus 146+/-25 pmol/mg per minute in remote

73 Subjects with LAD-III show symptoms of both LAD-I and Glanzmann's thrombasthenia.

74 C57BL/6 mice underwent 30 min of ischemia by LAD coronary artery ligation followed by various periods

75 gh cell-to-cell consistency, interspersed by LADs with more variable NL interactions.

76 mples from swine instrumented with a chronic LAD stenosis.

77 ing was depressed under baseline conditions (LAD 3.7+/-0.3 versus 6.6+/-0.3 in remote regions, P<0.01

78 umber of site-directed variants of N. crassa LAD that are capable of utilizing NADP(+) as cofactor, y

79 To establish a last appearance date (LAD) for M. americanum regionally, we obtained 53 new (1

80 egrin lead to leukocyte adhesion deficiency (LAD) syndrome and mutations in beta(3) integrin cause th

81 e hallmark of leukocyte adhesion deficiency (LAD) syndrome in humans, characterized by impaired leuko

82 F REVIEW: The leukocyte adhesion deficiency (LAD) syndromes are rare genetically determined condition

83 human disease leukocyte adhesion deficiency (LAD).

84 L-arabinitol 4-dehydrogenase (LAD) catalyzes the conversion of l-arabinitol into l-xyl

85 terogeneity in horizontal leaf area density (LAD) within the canopy impacts the ultrafine particle (U

86 ng myocardium were confirmed, with depressed LAD wall thickening and no significant infarction.

87 for bypassing the left anterior descending (LAD) artery in patients undergoing coronary artery bypas

88 a canine model of left anterior descending (LAD) artery stenosis, during first-pass, contrast-enhanc

89 A) grafting of the left anterior descending (LAD) at reoperative coronary artery bypass grafting (CAB

90 sclerosis, whereas left anterior descending (LAD) coronary arteries are athero-prone.

91 ting branch of the left anterior descending (LAD) coronary artery most commonly perfuses the right bu

92 In eight dogs, the left anterior descending (LAD) coronary artery was occluded for 90 minutes, and 15

93 to catheterize the left anterior descending (LAD) coronary artery with x-ray guidance and to delineat

94 nt ligation of the left anterior descending (LAD) coronary artery, and 100 microL of saline, hydrogel

95 e evolution in the left anterior descending (LAD) coronary artery.

96 gery (sham group), left anterior descending (LAD) ligation of the coronary artery followed by intramy

97 LCx group); and 3) left anterior descending (LAD) occlusion (LAD group).

98 of stenosis of the left anterior descending (LAD) or circumflex (LCx) coronary arteries during adenos

99 A noncritical left anterior descending (LAD) stenosis was created in 10 dogs.

100 rresponding to the left anterior descending (LAD), circumflex (LCX), and right coronary (RCA) territo

101 onary territories (left anterior descending [LAD], left circumflex, and right coronary artery [RCA]).

102 evation, 15 min left anteriorior descending, LAD, occlusion in rabbits) with EC50 values of 190 and 8

103 ) and nonoccluded (left anterior descending; LAD) perfused myocardium of SED and EX animals.

104 usly in patients with the recently described LAD type III (LAD-III).

105 the model by the Least Absolute Deviations (LAD) approach and implement the computation by median po

106 of lignocellulose-based analytical devices (LADs) for rapid bioanalysis in low-resource settings.

107 ial fibrillation (AF), left atrial diameter (LAD) and low voltage area (LVA) are intermediate phenoty

108 Increased left atrial diameter (LAD) is associated with elevated risk of atrial fibrilla

109 s with AF had a larger left atrial diameter (LAD), waist circumference, and body mass index, and a lo

110 Long-axis diameter (LAD), short-axis diameter (SAD), and volume were measure

111 ncreased MADP by 19.8+/-2.3%, mean diastolic LAD flow by 37.2+/-3.9%, and EVR by 21.4+/-3.0% (P<0.000

112 re (MADP) by 26.5+/-3.5%, the mean diastolic LAD flow by 48.4+/-7.2%, and endocardial viability ratio

113 significantly increased MADP, mean diastolic LAD flow, and EVR.

114 with microsphere-measured flow differences (LAD/LCX, 3.38 +/- 0.83; LAD/septal, 1.26 +/- 0.49).

115 ations of left and right anterior digastric (LAD, RAD), masseter, buccinator, and genioglossus (GG) m

116 hnology called light-activated dimerization (LAD) to artificially induce protein hetero- and homodime

117 ere untreated (control) or treated by direct LAD infusion of (i) nitroglycerin (NTG) (0.5 microg.kg(-

118 n about how these lamina-associated domains (LADs) are directed to the nuclear lamina.

119 sm by which these lamina associated domains (LADs) are established remains to be elucidated.

120 Such lamina-associated domains (LADs) are thought to help organize chromosomes inside th

121 ermore, we mapped Lamina-associated domains (LADs) in mouse liver cells and found that boundaries of

122 " Mesas form at lamin B1-associated domains (LADs) in replicative senescence and oncogene-induced sen

123 , the coverage of lamina-associated domains (LADs) in the genome increases from 53.1% to 68.6%, and a

124 focused either on lamina-associated domains (LADs) or on topologically associated domains (TADs), def

125 entral regions of lamina-associated domains (LADs), which are enriched for Lys9 trimethylation on his

126 d with H3K9me2 and lamin-associated domains (LADs).

127 hundreds of large lamina-associated domains (LADs).

128 n correlates with lamina-associated domains (LADs).

129 y mapped lamin-associated chromatin domains (LADs) into two HiLands, HiLands-B and HiLands-P, which a

130 chniques, we find that low alcohol drinking (LAD) mice have dramatically higher ventral tegmental are

131 ed with manganese-enhanced MR imaging during LAD artery occlusion and 2 hours after reperfusion corre

132 and the blood (P < .01) were measured during LAD artery occlusion and at least 2 hours after reperfus

133 R imaging can depict the area at risk during LAD artery occlusion and at least 2 hours after reperfus

134 Absolute decreases in mid-wall Ecc LAD and RCA and global Ecc were 3.0%, 3.4%, and 2.8%, re

135 ruitment of YY1 proteins facilitated ectopic LAD formation dependent on histone H3 lysine 27 trimethy

136 The engineered LAD mutants with altered cofactor specificity should be

137 xploratory overall survival analysis favored LAD-3M (HR, 1.50; 95% CI, 1.13 to 1.99; P = .005).

138 descending artery (LAD) stenosis when flow (LAD, 0.7+/-0.2 versus 1.2+/-0.1 mL/min per gram in norma

139 Sex-specific growth curves for LAD were estimated for individuals with low, intermediat

140 number of positive sites in the E group for LAD, RAD, and GG muscles in face-M1 and face-S1 at days

141 ay that reached statistical significance for LAD and LVA in both enrichment tools and was also signif

142 tal stent; 536 (41%) randomized patients had LAD lesions.

143 After increasing PaO2 to >300 mm Hg, LAD flow decreased in all animals.

144 om 2.4+/-0.04 to 4.7+/-0.7 mm in hibernating LAD regions (P<0.05) whereas remote wall-thickening was

145 als genetically null for the L1CAM homologue LAD-1, exhibit variably penetrant pleiotropic phenotypes

146 ils to leukocyte adhesion deficiency type I (LAD-I), a complex inherited disorder in which reduced or

147 ed in the leukocyte adhesion deficiency III (LAD-III) disorder, leading to widespread infection due t

148 disorder leukocyte adhesion deficiency III (LAD-III), integrins on platelets and leukocytes are expr

149 ople with leukocyte adhesion deficiency III (LAD-III).

150 ts with the recently described LAD type III (LAD-III).

151 ENT) IV trial participants who underwent IMA-LAD revascularization and had 12- to 18-month angiograph

152 sfunction by Ecc was noted (p < or = 0.01 in LAD and RCA territories).

153 integrins, which are deficient or absent in LAD-I, and new beta(2) integrin-dependent functions of n

154 associated positively with 4-year change in LAD (P<0.001).

155 AD flow reserve, with no immediate change in LAD wall thickening.

156 We also related risk factors to changes in LAD during a 4-year period in 3365 participants.

157 In addition, segmental function in LAD and RCA regions was reduced when individuals in the

158 R signaling maintained aerobic glycolysis in LAD cells.

159 A (VTA-NAc) neurons is selectively higher in LAD mice.

160 is reduced after TAXUS stent implantation in LAD lesions.

161 treatment experienced a greater increase in LAD with age (0.95 versus 0.63 mm per 10-year age increm

162 Men had a greater increase in LAD with BMI than women (2.02 versus 1.77 mm in women, p

163 cally more severe bleeding manifestations in LAD-III patients, in which all platelet integrins are fu

164 scovery of 3 cases of reversion mutations in LAD-1 at one center suggests that this may be a relative

165 ough the bleeding disorder is more severe in LAD-III patients, classic aggregometry or perfusion of G

166 defective selectin binding and signaling in LAD-II are now apparent.

167 polymer-based, paclitaxel-eluting stents in LAD lesions is safe, and reduces angiographic restenosis

168 showed higher TES expression in IMA than in LAD.

169 nternal nuclear organization, and changes in LADs during T-cell activation may provide an important a

170 Third, genes and a putative enhancer in LADs that were released from the periphery during T-cell

171 As a result, pravastatin increased LAD myocyte nuclear density from 830+/-41 to 1027+/-55 n

172 The Gialpha2/Gsalpha ratio increased (LAD, 1.8+/-0.3 versus 0.99+/-0.3 in remote myocardium; P

173 imarily governed by the spatially integrated LAD when differences in aerodynamic attributes (e.g., fo

174 onary artery bypass grafting in intermediate LAD stenosis without functional evidence of ischemia.

175 cularization, and patients with intermediate LAD stenosis or with an additional bypass graft to the d

176 r baseline HSP27S was associated with larger LAD, whereas baseline HSP27S was not correlated with LAD

177 rox or HDAC3 results in dissociation of LASs/LADs from the nuclear lamina.

178 l arrhythmias, equal groups of animals (LCX; LAD; and sham-operated) underwent sequential electrophys

179 ells and increased myocardial tissue levels (LAD CD133(+) cells from 140+/-33 to 884+/-167 cells/10(6

180 To address this, we mapped LADs using Lamin B1-DamID during Jurkat T-cell activatio

181 For RF ablation lesions, the mean LAD, SAD, and volume demonstrated a significant inverse

182 elegans divergent L1 cell adhesion molecule LAD-2 acting as a non-canonical ephrin receptor to EFN-4

183 t role in aerobic glycolysis in EGFR-mutated LAD cells.

184 the global metabolic pathway in EGFR-mutated LAD cells.

185 herapies to treat patients with EGFR-mutated LAD.

186 primary CABG and whose anterior myocardium (LAD) was at risk at reoperation: 2,389 had LITA grafting

187 In the SDQL neuron, LAD-2 mediates dorsal axon guidance via the secreted MAB

188 Whereas basal cAMP production was normal (LAD, 87+/-18 versus 91+/-19 pmol/mg per minute; P=NS), r

189 Revascularization normalized LAD flow reserve, with no immediate change in LAD wall t

190 3) left anterior descending (LAD) occlusion (LAD group).

191 n 3-IPRR is unable to restore the ability of LAD-III B cells to adhere to and migrate on LFA-1 ligand

192 ifying the KINDLIN-3 protein as the cause of LAD-III in Maltese and Turkish subjects.

193 n the KINDLIN3 (FERMT3) gene is the cause of LAD-III in patients from the Middle East, Malta, and Tur

194 reperfusion (group 4), or the combination of LAD occlusion and 32-mm(3) microemboli followed by reper

195 e EMG responses in different combinations of LAD, RAD, and GG muscles.

196 We evaluated clinical correlates of LAD for a 16-year period in 4403 Framingham Study partic

197 greater BMI as key modifiable correlates of LAD, suggesting that maintaining optimal levels of these

198 arding the short- or long-term correlates of LAD.

199 s IgE- and calcium-mediated degranulation of LAD-2 cells, in a dose-dependent manner.

200 ) as cofactor, yielding the first example of LAD with an almost completely switched cofactor specific

201 ittermates in 9 dogs with the canine form of LAD known as CLAD and demonstrate that in the 3 dogs wit

202 rolein/guanine adducts in the hippocampus of LAD subjects compared to age-matched controls.

203 first-pass MDCT imaging in a canine model of LAD stenosis.

204 The proximal part of LAD was the most commonly affected coronary artery (14 c

205 Location was not a significant predictor of LAD, SAD, or volume (P >/= .4).

206 interaction is increased in the presence of LAD-2, which can interact independently with MAB-20 and

207 (mtDNA) isolated from vulnerable regions of LAD brain compared to age-matched normal control subject

208 in repair of 8-OHG in vulnerable regions of LAD brain.

209 posed model needed in discerning the role of LAD heterogeneity on UFP collection.

210 Here we report the crystal structure of LAD from the filamentous fungus Neurospora crassa at 2.6

211 .7% of LV mass +/- 2.6 compared with that of LAD territory (P = .03).

212 te and platelet functions similar to that of LAD-III patients.

213 e significantly decreased after treatment of LAD cells with EGFRTKI.

214 use liver cells and found that boundaries of LADs are enriched for macroH2A.

215 Here, we demonstrate the implementation of LADs for food and water safety (i.e., nitrite assay in h

216 Fine-scale mapping of LADs reveals numerous lamina-associating sequences (LASs

217 The overall position of LADs was not altered in trisomic cells; however, the H3K

218 Here, we discuss the properties of LADs, the molecular mechanisms that determine their asso

219 location, ablation device, and flow rate on LAD, SAD, and volume.

220 ic aggregometry or perfusion of Glanzmann or LAD-III platelets over collagen-coated slides under phys

221 Adhesion Deficiency-III syndrome (LAD-III or LAD-1/variant) present with increased bleeding tendency

222 nary artery disease findings in 16 patients; LAD was affected in 16 (72.3%), RCA in 14 (63.3%), and L

223 a core architecture consisting of gene-poor LADs that contact the NL with high cell-to-cell consiste

224 e EFN-4 engineered to be soluble can promote LAD-2-mediated axon guidance.

225 whether controlled infarction in a proximal LAD septal perforator caused RBBB or LBBB.

226 ze than LBBB is, and occlusion of a proximal LAD septal perforator causes RBBB.

227 In the proximal LAD subgroup (n = 126), the one-year target vessel revas

228 Thus, proximal LAD occlusions should cause RBBB, not LBBB.

229 Regional LAD wall thickening slowly improved but remained depress

230 Regional LAD wall thickening was depressed under baseline conditi

231 ontribution to electroanatomical remodeling (LAD, LVA) and AF type via the calcium signaling pathway.

232 was present as reflected by reduced resting LAD flow (0.75+/-0.14 versus 1.19+/-0.14 mL x min(-1) x

233 3 (GLUT3) was downregulated in TKI-sensitive LAD cells.

234 n the number of high-affinity binding sites (LAD, 40+/-4% versus 53+/-7% in normal remote; P<0.05).

235 Leukocyte Adhesion Deficiency-III syndrome (LAD-III or LAD-1/variant) present with increased bleedin

236 These results suggest that LAD-2 functions as a MAB-20 coreceptor to secure MAB-20

237 g genomic repositioning assays, we show that LADs, spanning the developmentally regulated IgH and Cyp

238 The LAD perfusion territory was 35% of left ventricular (LV)

239 The LAD-III lesion has been attributed to a C --> A mutation

240 e difference in lesion frequency between the LAD and the LCx as these are both parts of the left coro

241 that this change is not responsible for the LAD-III disorder.

242 In the LAD and LCx, plaques tend to cluster within the proximal

243 MCE acoustic intensity in the LAD and left circumflex (LCx) regions were fit to the fo

244 ptal branches generate disturbed flow in the LAD and PDA in a similar fashion to the myocardial bridg

245 associated with lower (absolute) Ecc in the LAD and RCA regions (regression coefficient 0.37 per uni

246 Smokers had lower Ecc in the LAD and RCA regions compared with nonsmokers.

247 In the LAD group, LA remodeling was not observed by cardiac mag

248 bolic agent was selectively delivered in the LAD in six pigs.

249 number of side branches is lower than in the LAD or RCA and there are no septal perforators with intr

250 eneous but was particularly prominent in the LAD region in men (test for trend, P<0.001) and in women

251 , no significant association was seen in the LAD territory (P=0.16).

252 The Ecc's in the LAD territory of participants with DBP <80, 80 to 84, 85

253 ervention are more common for lesions in the LAD than other native coronary arteries, and often neces

254 Perfusion measurements in the LAD, left circumflex artery (LCx), right coronary artery

255 tegrin-related adhesion and migration in the LAD-III patient's T and B lymphocytes.

256 that the left circumflex artery, and not the LAD, group had atrial infarction.

257 ar courses like in the proximal third of the LAD and the posterior descending artery (PDA).

258 nsitive inversion-recovery MR imaging of the LAD arterial territory was performed before occlusion, d

259 At 20 years, LITA grafting of the LAD at reoperation resulted in an absolute mortality ris

260 MI was induced by permanent occlusion of the LAD coronary artery.

261 trumented dogs by permanent occlusion of the LAD coronary artery.

262 dothelium, which are impaired in each of the LAD syndromes, continues to be refined.

263 ance images of the midapical segments of the LAD territory.

264 TECAB of the LAD was performed using the left internal mammary artery

265 Results: The LAD territory was 32.4% +/- 3.8(stadard error of the mea

266 , a LITA should be used to revascularize the LAD at coronary reoperations.

267 ary DNA but not CALDAGGEF1 cDNA reverses the LAD-III defect, restoring integrin-mediated adhesion and

268 We show that the LAD estimator is robust in the sense that it has bounded

269 LITA grafting to the LAD is the gold standard for primary CABG, but its value

270 nd 1,084 saphenous vein (SV) grafting to the LAD.

271 demonstrated the following compared with the LAD or control groups: greater slowing in atrial conduct

272 Thus, these LAD-III patient mutations have highlighted functionally

273 normal remote; P<0.05) and wall thickening (LAD, 15.5 [corrected]+/-3.2% versus 40.0+/-5.5% in remot

274 h IL-18-neutralizing antibodies 1 h prior to LAD ligation.

275 diabetes, and antihypertensive treatment to LAD.

276 3D space through differences in proximity to LADs along chromosomes.

277 reduced correlation of replication timing to LADs and heterochromatin.

278 LITA-to-LAD grafting at reoperation is safe and confers a risk-a

279 studies before SCD (n=7) demonstrated total LAD occlusion and collateral-dependent myocardium (n=5),

280 cumulative effects on activity (eg, "total" LAD PDC activity was 21.9+/-3.1 versus 42.8+/-1.9 mU, P<

281 um, but flow during adenosine was unchanged (LAD 1.45+/-0.27 versus 1.46+/-0.23 mL/min per g and remo

282 injected into the hearts of mice undergoing LAD ligation (n=15 per group).

283 Female FVB mice (n=70) underwent LAD ligation and intramyocardially received one cell typ

284 from borders of fibroblast-specific variable LADs that are sufficient to target these ectopic sites t

285 Predictors of IMA graft failure were LAD stenosis <75% (odds ratio, 1.76; 95% confidence inte

286 ggregates upon collagen stimulation, whereas LAD-III platelets were not.

287 .e. CACNA1C, RyR2) that were associated with LAD, LVA and AF type.

288 SNPs found significantly associated with LAD, LVA or AF type were used for gene-based association

289 factor burden was positively associated with LAD.

290 BOLD MR signal changes in canines with LAD stenosis during hypercapnia and adenosine infusion w

291 reas baseline HSP27S was not correlated with LAD in controls.

292 The HSP27S levels were correlated with LAD, left atrial voltage, and fractionated intervals, an

293 Swine were chronically instrumented with LAD and LCX stenoses to produce viable dysfunctional myo

294 Baseline characteristics of patients with LAD lesions were well-matched between the randomized gro

295 nt (0.54 mm) were associated positively with LAD (P<0.001).

296 sweating were initially more pronounced with LAD-3M.

297 Subjects with LAD-III show symptoms of both LAD-I and Glanzmann's thro

298 demonstrated the utility of this system with LAD constructs that can recruit the small G-protein Rac1

299 rvival was similar for patients treated with LAD-3M or CMF (hazard ratio [HR], 1.19; 95% CI, 0.94 to

300 cal time-matched surgical procedures without LAD ligation.