ライフサイエンスコーパス: PAD

1 PAD by EMDC-dispatched lay first responders could be a p

2 PAD is associated with low CD34+ and CD34+/VEGFR2+ PC co

3 PAD is common among patients undergoing commercial TAVR

4 PAD prevalence among persons living less than 150 m from

5 PAD symptoms remained stable or improved in the majority

6 PAD was associated with a clinically relevant reduction

7 PAD was divided into 3 groups according to who applied t

8 PAD-induced spiking is assumed to override presynaptic i

9 ular delivery of miR93 in miR106b-93-25(-/-) PAD mice increased angiogenesis, arteriogenesis, and the

10 2 x 10(-4)), COPD (OR=3.22, P=2.9 x 10(-4)), PAD (OR=3.47, P=9.2 x 10(-3)) and AAA (OR=6.44, P=6.3 x

11 A total of 2,977 and 2,966 PAD-free participants who were aged 45-74 years in 1989-

12 Aberrant PAD exposure induces a signaling cascade that leads to d

13 Females had a 1.53-fold greater adjusted PAD risk compared with males (95% confidence interval, 1

14 o qualified studies reporting survival after PAD by EMDC-dispatched lay first responders.

15 Patients with CAD and PAD had significantly lower PC counts compared with thos

16 athological link between type 2 diabetes and PAD.

17 2.50) increases in the risk of mortality and PAD-related events, respectively.

18 with increased cardiovascular mortality, and PAD risk factors overlap with those for aortic stenosis.

19 a sensitive change in the alignment-averaged PADs, which can be measured and used to retrieve the for

20 llinated antigens: ACPAs could arise because PADs are recognized by T cells, which help the productio

21 roups; and (2) study the association between PAD and functional capacity as well as health status.

22 HPR were not significantly different between PAD and no PAD groups.

23 formed to determine the relationship between PAD, platelet reactivity, and subsequent adverse events

24 ropensity-adjusted multivariable model, both PAD and HPR were independent predictors of myocardial in

25 nges in PCs differentiate patients with both PAD and CAD from those with CAD alone is unknown.

26 rates were highest among subjects with both PAD and HPR.

27 val of 40% for patients with OHCA treated by PAD.

28 ction of autoantibodies to proteins bound by PADs, according to a "hapten/carrier" model.

29 visits for patients with PAD alone, comorbid PAD and CAD were more likely to be prescribed antiplatel

30 whether those changes necessarily compromise PAD-mediated inhibition.

31 tients with prior MI, those with concomitant PAD have heightened ischemic risk.

32 ronary syndromes with or without concomitant PAD from December 2006 to December 2008.

33 an ankle brachial index <0.90 or a confirmed PAD event, with death as a competing event.

34 itrullination by protein arginine deiminase (PAD)4, exocytosis of chromatin and enzymes as neutrophil

35 at Cl-amidine, a peptidylarginine deiminase (PAD) inhibitor, improves survival in a mouse model of ce

36 ic sequencing of peptidylarginine deiminase (PAD)-modified protein.

37 e generated by peptidyl arginine deiminases (PAD).

38 Primary afferent depolarization (PAD) normally mediates inhibition via sodium channel ina

39 The most common reasons cited for desiring PAD were activities of daily living were not enjoyable (

40 (HPAEC) with pulsed amperometric detection (PAD).

41 s with coronary artery disease (CAD) develop PAD.

42 dian follow-up of 5.9 years, 17.8% developed PAD, 13.0% were lost to follow-up and 11.1% died.

43 colorimetric paper-based analytical device (PAD) combined with immunomagnetic separation (IMS) for d

44 first time a paper-based analytical device (PAD) for the non-enzymatic detection of glucose by modif

45 Paper-based analytical devices (PAD) emerge in the scientific community since 2007 as lo

46 assay using paper-based analytical devices (PADs) that can test for the presence of beta-lactamase-m

47 he ankle-brachial index was used to diagnose PAD (ankle-brachial index </= 0.9).

48 evaluate the effect of PAD and the different PAD strategies on survival after OHCA.

49 Instead, diminished PAD caused by reduction of gGABA poses a greater risk to

50 treatments for peripheral arterial disease (PAD) and are more likely to present with the most severe

51 re is linked to peripheral arterial disease (PAD) and cardiovascular disease.

52 Patients with peripheral arterial disease (PAD) are at a high risk for cardiovascular events, yet,

53 Peripheral arterial disease (PAD) causes significant morbidity and is an important ri

54 ith concomitant peripheral arterial disease (PAD) experience worse cardiovascular outcomes after perc

55 Patients with peripheral arterial disease (PAD) have high rates of adverse cardiovascular events af

56 Peripheral arterial disease (PAD) is a clinical manifestation of extracoronary athero

57 Peripheral arterial disease (PAD) is a costly source of morbidity and mortality among

58 Peripheral arterial disease (PAD) is caused by atherosclerosis that results in ischem

59 to symptomatic peripheral arterial disease (PAD) over the longer term.

60 to symptomatic peripheral arterial disease (PAD) over the longer term.

61 e management of peripheral arterial disease (PAD).

62 n patients with peripheral arterial disease (PAD).

63 ectively assessed peripheral artery disease (PAD) and its clinical relevance in patients with chronic

64 Patients with peripheral artery disease (PAD) are at heightened risk of acute limb ischemia (ALI)

65 h lower extremity peripheral artery disease (PAD) are unclear.

66 in patients with peripheral artery disease (PAD) as well as the effect on major adverse limb events.

67 The prevalence of peripheral artery disease (PAD) continues to increase worldwide.

68 the incidence of peripheral artery disease (PAD) in chronic kidney disease differs according to sex

69 in patients with peripheral artery disease (PAD) in the United States.

70 Peripheral artery disease (PAD) is associated with heightened ischemic and bleeding

71 Peripheral artery disease (PAD) is associated with increased cardiovascular mortali

72 femoral arteries: peripheral artery disease (PAD) model.

73 ct on the risk of peripheral artery disease (PAD) remains unclear.

74 Patients with peripheral artery disease (PAD) show an exaggerated EPR, sometimes report pain when

75 alence ratios for peripheral artery disease (PAD), coronary artery calcification (CAC), and abdominal

76 ients with severe peripheral artery disease (PAD).

77 in patients with peripheral artery disease (PAD).

78 drug delivery in peripheral artery disease (PAD).

79 in patients with peripheral artery disease (PAD).

80 P=9.3 x 10(-4)), peripheral artery disease (PAD; P=0.090) and abdominal aortic aneurysms (AAAs; P=0.

81 nesis to treat peripheral arterial diseases (PAD) by increasing the vascular endothelial growth facto

82 d a web resource called Proximal And Distal (PAD) clustering to identify their co-localization at the

83 n using photoelectron angular distributions (PADs) that have averaged over partial alignments of isol

84 known as the phosphatase-activating domain (PAD).

85 pharmacologically by PP2A-activating drugs (PADs).

86 ate tissue loss and ischemic myopathy during PAD.

87 s states have pending physician-aided dying (PAD) legislation.

88 h biophysical changes are required to enable PAD-induced spiking and whether those changes necessaril

89 icient, sensitive and low-cost non-enzymatic PAD has great potential for the development of point-of-

90 eased M1-like macrophages after experimental PAD.

91 rease angiogenesis in human and experimental PAD.

92 In experimental PAD, delivery of an isoform-specific monoclonal antibody

93 evascularize ischemic muscle in experimental PAD.

94 esis, and perfusion recovery in experimental PAD.

95 ion strategy for symptomatic lower extremity PAD is not established.

96 ion strategy for symptomatic lower extremity PAD is not established.

97 ted hazard ratio of ischemic lower-extremity PAD (1.54 [95% CI, 1.14-2.10]) (p = 0.005).

98 e follow-up period, ischemic lower-extremity PAD developed in 24.4% of hemodialysis patients.

99 h the occurrence of ischemic lower-extremity PAD in hemodialysis patients.

100 is patients in whom ischemic lower-extremity PAD occurred (3.03% [IQR, 2.36-4.54], n = 22) than in he

101 l the occurrence of ischemic lower-extremity PAD.

102 medical therapy and lifestyle counseling for PAD patients in the United States from 2005 through 2012

103 ke initiation properties) were necessary for PAD-induced spiking, whereas increased GABAAR conductanc

104 , since the high value of gGABA required for PAD-induced spiking still mediates strong inhibition, we

105 fficult but the biophysical requirements for PAD-induced spiking are arguably similar in soma and axo

106 th men were at a markedly increased risk for PAD at younger ages; however, at ages >70 years, the ris

107 er low PC counts are useful in screening for PAD needs to be investigated.

108 f ambulatory visits in the United States for PAD was 3,883,665.

109 el strategy to improve MSC-based therapy for PAD, possibly through autophagy modulation in MSCs.

110 n-induced arthritis of the second generation PAD inhibitor, BB-Cl-amidine.

111 genesis and to reduce tissue loss in genetic PAD models.

112 Older men had a substantially greater PAD risk compared with younger men.

113 H2 PAD can also facilitate elucidation of fundamental bioch

114 H2 PAD-enabled discovery of hydrogenase and FNR mutants tha

115 gh-throughput H2 production assay device (H2 PAD) is presented that enables simultaneous evaluation o

116 a CCD camera and image analysis software, H2 PAD senses the chemo-optical response of Pd/WO3 thin fil

117 d six hundred forty-two patients (13.2%) had PAD (1505 with no prior myocardial infarction or stroke)

118 dergoing transfemoral TAVR, 4810 (24.5%) had PAD; 3730 (47.9%) of 7780 patients undergoing nontransfe

119 emic Consequences-Comorbidities Network) had PAD.

120 patients undergoing nontransfemoral TAVR had PAD.

121 Patients were identified as having PAD at baseline if they had intermittent claudication an

122 83% (P=0.002) increase in the odds of having PAD, respectively.

123 es with chronic kidney disease have a higher PAD risk compared with males at younger ages.

124 A chromatographic method by HPAEC-PAD was developed and in-house validated for the quantif

125 In human PAD versus control muscle biopsies, VEGF165b: (1) is ele

126 METHODS AND In human PAD versus control muscle biopsies, VEGF165b: (1) is ele

127 omatography-Pulsed Amperometry Detection (IC-PAD) method for direct determination of free cyanide in

128 hether misfolding in the amino terminus (ie, PAD exposure) occurs in non-AD tauopathies.

129 minant receptor in postnatal angiogenesis in PAD.

130 xercise may augment the effects of GM-CSF in PAD, since exercise-induced ischemia enhances progenitor

131 These sex-related differences in PAD risk also differed by age (P=0.013).

132 Rapidly, electrodes were introduced in PAD for electrochemical measurements.

133 ibits angiogenesis and perfusion recovery in PAD muscle.

134 t known to modulate arteriogenic response in PAD, and the extent of arteriogenic response induced by

135 tween HPR and adverse events were similar in PAD and no PAD groups, without evidence of interaction;

136 are consistent with the data showing that in PAD calf muscles secrete mostly VEGF165b over total VEGF

137 Experimental measurements show that in PAD human muscle biopsies the VEGF165b isoform is at lea

138 apelin facilitated AD-MSCs-based therapy in PAD, possibly through promoting survival of AD-MSCs by w

139 EUCLID trial (Examining Use of Ticagrelor In PAD) randomized 13 885 patients with peripheral artery d

140 rovides a computational model of VEGF165b in PAD supported by experimental measurements of VEGF165b i

141 nce of anti-angiogenic isoform (VEGF165b) in PAD muscle tissues is a potential cause for the failure

142 Incident PAD was determined by an ankle-brachial index <0.9 asses

143 A total of 286 and 206 incident PAD cases were identified for ABI <0.9 and ABI >1.4, res

144 ow-to-moderate arsenic exposure and incident PAD by ankle brachial index (ABI).

145 itual dietary intake at midlife and incident PAD over approximately 20 y of follow-up.Among 14,082 pa

146 n other food groups or patterns and incident PAD.In this prospective cohort study, greater meat consu

147 19.9 y, 1569 participants developed incident PAD.

148 95 and 1997-1999, respectively, for incident PAD defined as either ABI <0.9 or ABI >1.4.

149 food groups, the HRs (95% CIs) for incident PAD increased across quintiles of meat consumption [quin

150 d 1-6 drinks/wk had a lower risk of incident PAD [0.78 (0.68, 0.89)].

151 was associated with a lower risk of incident PAD.

152 none was inversely associated with incident PAD [quintile 5 compared with quintile 1: 0.84 (0.75, 1.

153 PAD with consistency across type, including PAD resulting from surgical graft thrombosis and in-situ

154 sphingosine analog FTY720 is the best known PAD and we have shown that FTY720 represses production o

155 A total of 1,143 patients (5%) had known PAD.

156 ounts of CAD patients with and without known PAD.

157 tent effects in those with and without known PAD.

158 LE-PAD was significantly more prevalent in the lowest terti

159 ns between infrarenal aortic diameter and LE-PAD are limited, especially in large sample populations

160 pically an ABI </= 0.90 is used to define LE-PAD.

161 ower-extremity peripheral artery disease (LE-PAD).

162 primary noninvasive test for diagnosis of LE-PAD is the ankle-brachial index (ABI) at rest and typica

163 The prevalence of LE-PAD was found to significantly decrease as the aortic di

164 iameter) is significantly associated with LE-PAD in Chinese hypertensive adults.

165 A first-generation 3D Light PAD was fabricated using the photoactivatable dye N-phen

166 light photoactivatable dye display (3D Light PAD) is reported.

167 , vascular morbidity and mortality and local PAD outcomes.

168 sis and VEGF distribution in human and mouse PAD model.

169 nd adverse events were similar in PAD and no PAD groups, without evidence of interaction; however, ad

170 t significantly different between PAD and no PAD groups.

171 ar adverse outcomes compared with absence of PAD.

172 However, the burden of PAD in sub-Saharan Africa is poorly understood.

173 Conformational display of PAD is an early marker of pathological tau in Alzheimer

174 matic review aimed to evaluate the effect of PAD and the different PAD strategies on survival after O

175 ggest that these immunoregulatory effects of PAD inhibition in CIA are complex, but primarily mediate

176 Risk in Communities) Study initially free of PAD, dietary intake was assessed at baseline in 1987-198

177 A history of PAD was associated with ischemic and bleeding outcomes 2

178 History of PAD was obtained at baseline.

179 Among 8582 patients, 10.2% had a history of PAD.

180 ship between sex and cumulative incidence of PAD differed according to age.

181 sed to determine the cumulative incidence of PAD, defined by an ankle brachial index <0.90 or a confi

182 sized as potential noncovalent inhibitors of PAD enzymes.

183 ing to the epidemiology and/or management of PAD in sub-Saharan Africa was performed.

184 The management of PAD patients should include an exercise program, guideli

185 n, targeted screening, medical management of PAD, and defining essential vascular care.

186 ities in presentation with and management of PAD.

187 The number of PAD prescriptions written in Oregon has increased annual

188 nse experiments reveal an ordered pattern of PAD-mediated deimination events culminating in citrullin

189 Presence of PAD (n=308) was determined by history, review of medical

190 We aimed to: (1) assess the prevalence of PAD in COPD compared with distinct control groups; and (

191 The prevalence of PAD in sub-Saharan Africa may be equal to or higher than

192 ith ticagrelor was consistent, regardless of PAD, patients with PAD had a greater absolute risk reduc

193 e Fine and Gray model determined the risk of PAD according to sex.

194 linking type 2 diabetes and the severity of PAD manifestation are not well understood.

195 Status of PAD was associated with a higher risk of death and ische

196 oth documented significant undertreatment of PAD as a cardiovascular disease risk factor.

197 ttle research has been done regarding use of PAD, or ways to improve the process and/or results.

198 demonstrated that the modified electrode on PADs had excellent electrocatalytic activity towards the

199 iously described the photoactivated depot or PAD approach that allows for the light control of therap

200 To evaluate results of Oregon PAD, the longest running US program; to disseminate resu

201 In the Study of Health in Pomerania, PAD ranged from 1.8 to 4.2%.

202 ions) and in vivo experiments in preclinical PAD models (unilateral femoral artery ligation and resec

203 proved risk prediction metrics for prevalent PAD.

204 Importantly, such changes did not prevent PAD from inhibiting other spiking or from blocking spike

205 t of a public access defibrillation program (PAD) is recommended by international guidelines.

206 seminate results; and to determine promising PAD research areas.

207 mine the effect of such programs on reducing PAD-related morbidity, mortality, and health care costs.

208 tal of 41 studies were included; 18 reported PAD by nondispatched lay first responders, 20 reported P

209 dispatched lay first responders, 20 reported PAD by EMDC-dispatched professional first responders (fi

210 tein binding profiles in our online resource PAD.

211 ion of measured racial disparities in severe PAD in MA.

212 enhanced perfusion in animal model of severe PAD (Balb/c strain) without activating VEGFR2 signaling

213 entage-point decreased probability of severe PAD (P = 0.042) relative to concurrent trends in control

214 obability of patients presenting with severe PAD and resolution of measured racial disparities in sev

215 In some, we simulated PAD by ligating a femoral artery for 72 h before the exp

216 e exaggeration of EPR in rats with simulated PAD.

217 n a contemporary population with symptomatic PAD and whether protease-activated receptor 1 antagonism

218 In selected patients with symptomatic PAD and without atrial fibrillation, ALI occurs at a rat

219 Patients with symptomatic PAD who were enrolled in the Systematic Assessment of Va

220 xar reduces ALI in patients with symptomatic PAD with consistency across type, including PAD resultin

221 For patients with symptomatic PAD, previous peripheral revascularization, smoking, and

222 le patients, including 3787 with symptomatic PAD.

223 We suggest that targeting PADs is a promising strategy for the treatment of chroni

224 Among patients undergoing transfemoral TAVR, PAD is associated with a higher incidence of 1-year adve

225 mediates strong inhibition, we conclude that PAD-induced spiking does not represent failure of presyn

226 ce, FTY720-P enhances PP2A activity and that PADs can repress production of pro-inflammatory cytokine

227 ulation-based studies that better define the PAD burden in sub-Saharan Africa, health systems should

228 In the PAD calf compartment of human and mouse models, most VEG

229 ry depending on the clinical severity of the PAD and the anatomic distribution of the disease.

230 trate that the conformational display of the PAD in tau represents a common pathological event in man

231 To demonstrate viability, the PAD was used to detect beta-lactam resistance in wastewa

232 Additionally, the PADs were applied to quantify glucose in honey, white wi

233 ith PADs developed antibodies and T cells to PAD and IgG antibodies to citrullinated fibrinogen pepti

234 Thus, T cell immunization to PAD proteins may trigger ACPAs through a hapten/carrier

235 tructure, promoting exposure of R502/R510 to PAD modification and subsequent autoantibody binding.

236 particles as an alternative therapy to treat PAD.

237 Patients use PAD for reasons related to quality of life, autonomy, an

238 tion, we show that it is advantageous to use PADs obtained from multiple photon polarization directio

239 = 22) than in hemodialysis patients in whom PAD did not occur (1.13% [IQR, 0.90-1.83], n = 68) (p <

240 ) and the key secondary end point (3.5% with PAD, 1.4% without PAD).

241 uctions for the primary end point (3.5% with PAD, 1.6% without PAD) and the key secondary end point (

242 , white and non-white patients admitted with PAD in Massachusetts (MA) and 4 control states.

243 The prevalence and outcomes associated with PAD in a population undergoing transcatheter aortic valv

244 mediate the exaggerated EPR associated with PAD.

245 tched cohorts of Medicare beneficiaries with PAD from 2006 through 2009.

246 tched cohorts of Medicare beneficiaries with PAD from 2006 through 2009.

247 Patients with COPD with PAD had a significantly shorter 6-minute-walk distance (

248 patients with COPD, 8.8% were diagnosed with PAD, which is higher than the prevalence in control subj

249 ixty-six participants 65 years or older with PAD were randomized to receive a daily capsule of resver

250 rformance in patients 65 years or older with PAD.

251 827 persons evaluated, 210 participants with PAD were randomized (mean age, 67.0 [SD, 8.6] years; 141

252 primary efficacy end point in patients with PAD (19 [16.1%] vs 35 [27.3%]; HR, 0.54; 95% CI, 0.31-0.

253 3, or 5 bleeding occurred in 6 patients with PAD (5.2%) receiving prolonged DAPT relative to 8 (6.9%)

254 mary end point consistently in patients with PAD (hazard ratio [HR] 0.79; 95% confidence interval [CI

255 Compared with visits for patients with PAD alone, comorbid PAD and CAD were more likely to be p

256 d major adverse limb events in patients with PAD and a prior MI.

257 Patients with PAD are at high risk of cardiovascular events, and PCSK9

258 It is important to identify patients with PAD because of the increased risk of myocardial infarcti

259 readmission, and bleeding, for patients with PAD compared with those without, adjusting for baseline

260 ion to critical limb ischemia, patients with PAD continue to be under-recognized and undertreated.

261 matched with up to 2 (control) patients with PAD from other Ontario tertiary vascular centers not enr

262 consistent, regardless of PAD, patients with PAD had a greater absolute risk reduction of 4.1% (numbe

263 Patients with PAD had higher 2-year rates of all-cause mortality, myoc

264 Because of their higher risk, patients with PAD had larger absolute risk reductions for the primary

265 sis was significantly lower in patients with PAD treated with prolonged compared with short DAPT (HR,

266 antiplatelet therapy (DAPT) in patients with PAD undergoing PCI.

267 Patients with PAD undergoing TAVR via nontransfemoral access did not h

268 At 1-year follow-up, patients with PAD undergoing TAVR via transfemoral access had a higher

269 -reduction program targeted at patients with PAD was associated with fewer cardiovascular and limb ev

270 eline-recommended therapies in patients with PAD was much lower than expected, which highlights an op

271 1,982 outpatient visits among patients with PAD were obtained from the National Ambulatory Medical C

272 Patients with PAD were older and more likely to have comorbid conditio

273 In both groups, patients with PAD were significantly more likely to have coronary and

274 In the patients with PAD, mean (SD) age was 73.2 (9.2) in the prolonged group

275 Among patients with PAD, supervised treadmill exercise significantly improve

276 to treat walking impairment in patients with PAD.

277 rgeons, family physicians, and patients with PAD.

278 gram on long-term outcomes for patients with PAD.

279 approach to the management of patients with PAD.

280 crease in arterial pressure in patients with PAD.

281 tion of food intake or dietary patterns with PAD.We examined the relation between habitual dietary in

282 rol to Improve Outcomes in Older People With PAD (RESTORE), was conducted at Northwestern University.

283 Among current smokers with PAD, smoking cessation counseling or medication was used

284 In the placebo arm, those with PAD (n = 404) had higher rates of MACE at 3 years than t

285 re 0.73 (0.59-0.91; P=0.0040) for those with PAD and 0.81 (0.73-0.90; P<0.0001) for those without PAD

286 o hospital discharge after OHCA treated with PAD showed a median survival of 40.0% (range, 9.1-83.3).

287 C3H mice immunized with PADs developed antibodies and T cells to PAD and IgG ant

288 ndary end point (3.5% with PAD, 1.4% without PAD).

289 imary end point (3.5% with PAD, 1.6% without PAD) and the key secondary end point (3.5% with PAD, 1.4

290 erval [CI], 0.66-0.94; P=0.0098) and without PAD (HR 0.86; 95% CI, 0.80-0.93; P=0.0003; Pinteraction=

291 rised 246 and 1724 patients with and without PAD, respectively.

292 nterventions among subjects with and without PAD.

293 1-0.95; P = .03) but not in patients without PAD (81 [9.3%] vs 63 [7.4%]; HR, 1.28; 95% CI, 0.92-1.77

294 In the patients without PAD, mean (SD) age was 67.1 (11.2) years in the prolonge

295 ion (P = .04) compared with patients without PAD.

296 r readmission compared with patients without PAD.

297 .18; P<0.001) compared with patients without PAD.

298 0.81 (0.73-0.90; P<0.0001) for those without PAD (Pinteraction=0.41).

299 In women, PAD risk did not vary with age.

300 th predicted changes were necessary to yield PAD-induced spiking.