ライフサイエンスコーパス: PAD

1 PAD after neoadjuvant treatment is safe.

2 PAD events and VTE occurred in 246 and 92 patients, resp

3 PAD is a major risk factor for diabetic foot ulceration

4 PAD is common among patients undergoing commercial TAVR

5 PAD patients with carotid constriction showed more cardi

6 PAD severity and medical treatment were comparable betwe

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

8 PAD-scan had a lower specificity (77%, CI 67 to 84%) com

9 PAD-scan had a significantly higher sensitivity (95%, CI

10 PAD-scan has superior diagnostic utility and is a valid

11 PAD-scan may be advantageous over current tests as it al

12 erval (CI): 1.46 to 6.39]; p(trend) = 0.002; PAD HR(Q4): 2.58 [95% CI: 1.18 to 5.63]; p(trend) = 0.01

13 replicated in an independent sample of 5,117 PAD cases and 389,291 controls from the UK Biobank.

14 A total of 172 PAD patients (68 +/- 10 years, 67% male) underwent the C

15 We identified 19 PAD loci, 18 of which have not been previously reported.

16 Of 44 PAD participants randomized (mean age, 72.3 years [+/-7.

17 median follow-up of 26 years, there were 492 PAD cases, 1,798 CHD cases, and 1,106 stroke cases.

18 and progression of kidney disease (HR, 0.78, PAD; HR, 0.76, no-PAD; P-interaction=0.84) were consiste

19 th dapagliflozin for CV death/HHF (HR, 0.86, PAD; HR, 0.82, no-PAD; P-interaction=0.79) and progressi

20 Aberrant PAD activity is associated with rheumatoid arthritis, mu

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

22 eas the control group received no adjunctive PAD.

23 st group received two sessions of adjunctive PAD (red LED, 635 nm, photosensitive dye, 0.01% tolonium

24 cal and microbiological effect of adjunctive PAD in the treatment of periodontitis with a red LED as

25 The positive effect of adjunctive PAD regarding clinical parameters was reported in recent

26 ent, without beneficial effect of adjunctive PAD.

27 enzyme activity and immune responses against PAD enzymes will be important to fully comprehend the pa

28 ects (10 in group A, and six in group B).All PAD cases were detected by the two readers.

29 In a prespecified analysis, PAD events (critical limb ischemia, limb revascularizati

30 None of the previously reported ABI and PAD associations in whites generalized to Hispanics/Lati

31 (GWAS) of the ankle brachial index (ABI) and PAD (defined as an ABI < 0.90) have not been conducted i

32 e were stepwise increases in risk of CKD and PAD with higher LDL-C (both p for trend <0.001), with ha

33 comprising CHD, cerebrovascular disease, and PAD events until December 31, 2017.

34 the association between flavonoid intake and PAD hospitalizations and investigate if the association

35 sociation between total flavonoid intake and PAD hospitalizations differed according to baseline smok

36 death), and individual outcomes (MI, IS, and PAD).

37 RA at both genetic and cellular levels, and PAD inhibitors have shown therapeutic efficacy in mouse

38 comes in patients with diabetes mellitus and PAD in the EXSCEL trial (Exenatide Study of Cardiovascul

39 L-C was significantly associated with MI and PAD (MI hazard ratio [HR](Q4): 3.05 [95% confidence inte

40 TRL-C strongly associates with future MI and PAD events, whereas sdLDL-C strongly associates with MI

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

42 UK Biobank for retinopathy, neuropathy, and PAD gave similar results.

43 e 2, serine protease, virus replication, and PAD-4.

44 the risk of VTE and the composite of VTE and PAD events.

45 LC3 and PADs were further shown to partially co-localize in the

46 subsets of patients with RA, suggesting anti-PAD antibodies as possible biomarkers for RA diagnosis a

47 1 participants had been hospitalized for any PAD.

48 was associated with a 32% lower risk of any PAD hospitalization (HR: 0.68; 95% CI: 0.60, 0.77), a 26

49 sis, we assessed the association of baseline PAD with rates of MACE, LEA, and the effects of exenatid

50 calculated by transfer function gain between PAD and SV index; SV index and sBP; and sBP and RR inter

51 Brain-PAD at study entry predicted time-to-disability progress

52 Greater annualized brain-PAD increases were associated with greater annualized ED

53 Relationships between brain-PAD and Expanded Disability Status Scale (EDSS) were exp

54 We compared brain-PAD among patients with MS and patients with CIS and hea

55 hether brain-predicted age difference (brain-PAD) was sensitive to the presence of MS, clinical progr

56 dicate brain-predicted age difference (brain-PAD).

57 ed the brain-predicted age difference (brain-PAD: predicted age-chronological age) of the HCs and 318

58 A higher brain-PAD at baseline was associated with more rapid disabilit

59 average, MDD patients showed a higher brain-PAD of +1.08 (SE 0.22) years (Cohen's d = 0.14, 95% CI:

60 Patients with MS had markedly higher brain-PAD than healthy controls (mean brain-PAD +10.3 years; 9

61 PME had a higher brain-PAD than JME (22.0 vs. 9.3 years).

62 rosis presented a significantly higher brain-PAD than several other categories.

63 progression and the rate of change in brain-PAD related to worsening disability.

64 lepsy showed a significant increase in brain-PAD.

65 PNES showed a comparable mean brain-PAD (10.6 years) to that of epilepsy patients.

66 brain-PAD than healthy controls (mean brain-PAD +10.3 years; 95% confidence interval [CI] = 8.5-12.1

67 The mean brain-PAD in TLE with inter-ictal psychosis was 10.9 years, wh

68 We compared the brain-PAD values based on the research questions.

69 her assess the clinical value of these brain-PAD estimates.

70 The highest brain-PADs were in secondary-progressive MS (+13.3 years; 95%

71 using synthetic peptide T-cell epitopes (Cat-PAD) from the major cat allergen Fel d 1 has been shown,

72 eceptor CRTh2, we assessed the impact of Cat-PAD on the frequency and functional phenotype of Fel d 1

73 ouble-blind, placebo-controlled trial of Cat-PAD, we employed Fel d 1 MHC II tetramers and flow cytom

74 Peptide immunotherapy with Cat-PAD does not significantly alter the frequency or phenot

75 Among patients with chronic PAD for whom the goal of antithrombotic therapy is secon

76 including coronary heart disease (CHD), CKD, PAD and neuropathy.

77 poxia serum starvation, in vivo pre clinical PAD models, and adoptive transfer of VEGF(165)b-expressi

78 Conversely, PAD is exposed in pathological tau and plays an essentia

79 Currently, PAD patient identification relies on diagnosis/procedure

80 Predominantly antibody deficiencies (PADs) are the most prevalent primary immunodeficiencies,

81 patients with primary antibody deficiencies (PADs) experience frequent respiratory tract infections,

82 em failure in primary antibody deficiencies (PADs) has been linked to recurrent infections, autoimmun

83 Protein arginine deiminase (PAD) enzymes catalyze the conversion of protein-bound ar

84 Protein arginine deiminases (PADs) hydrolyze the side chain of arginine to form citru

85 Peptidylarginine deiminases (PADs) have an important role in the pathogenesis of rheu

86 Peptidylarginine deiminases (PADs), a family of calcium-dependent enzymes, catalyze c

87 enzymes called peptidylarginine deiminases (PADs), is the conversion of arginine into citrulline res

88 c inhibition of peptidylarginine deiminases (PADs), the enzymes mediating citrullination, through BB-

89 The Peace-Athabasca Delta (PAD) is a large inland wetland complex in northern Alber

90 reased percentage of aggregates destruction (PAD) than CC treatment.

91 ch foods may have a lower risk of developing PAD.

92 n-specific IgG repertoires between different PAD entities.

93 njection-flow (AI), pneumatic-air-discharge (PAD), optical (OP) and X-ray-computed microtomography (M

94 Patients with peripheral arterial disease (PAD) are at increased risk of cardiovascular morbidity a

95 Patients with peripheral arterial disease (PAD) have increased risk on future cerebro- and cardiova

96 he detection of peripheral arterial disease (PAD) in diabetes.

97 ease (CKD), and peripheral arterial disease (PAD) in the general population.

98 the severity of peripheral arterial disease (PAD) symptomology, however, the biological mechanisms re

99 he diagnosis of peripheral arterial disease (PAD).

100 -, 3- or 4-vessel peripheral artery disease (PAD) (ABI of <=0.9).

101 lue = 0.008), and peripheral artery disease (PAD) (OR = 2.35, 95% CI, 1.38-4.01, P value = 0.002).

102 ey disease (CKD), peripheral artery disease (PAD) and neuropathy.

103 Patients with peripheral artery disease (PAD) are at heightened risk for ischemic events related

104 Patients with peripheral artery disease (PAD) are at heightened risk of cardiovascular complicati

105 Patients with peripheral artery disease (PAD) are at risk of major adverse cardiac and cerebrovas

106 Lower extremity peripheral artery disease (PAD) burden differs by race/ethnicity.

107 e are at risk for peripheral artery disease (PAD) events and venous thromboembolism (VTE).

108 Patients with peripheral artery disease (PAD) have a higher risk of major adverse cardiovascular

109 h lower-extremity peripheral artery disease (PAD) have greater functional impairment, faster function

110 Patients with peripheral artery disease (PAD) have greater incidence of diabetes mellitus and ris

111 lood flow such as peripheral artery disease (PAD) impact nearly 10 million people in the United State

112 Peripheral artery disease (PAD) is a leading cause of cardiovascular morbidity and

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

114 Peripheral artery disease (PAD) is associated with increased risk for atherosclerot

115 Peripheral artery disease (PAD) is associated with increased risk of mortality, car

116 Peripheral artery disease (PAD) is underrecognized, undertreated, and understudied:

117 , associated with peripheral artery disease (PAD), leads to the release of proinflammatory mediators

118 ary prevention of peripheral artery disease (PAD), the third leading cause of atherosclerotic cardiov

119 is exaggerated in peripheral artery disease (PAD).

120 flex in rats with peripheral artery disease (PAD).

121 g risk factor for peripheral artery disease (PAD).

122 stroke (IS), and peripheral artery disease (PAD).

123 in patients with peripheral artery disease (PAD).

124 for patients with peripheral artery disease (PAD).

125 cidence of 3 major atherosclerotic diseases (PAD, CHD, and stroke).

126 Photoactivated disinfection (PAD) could support the periodontal treatment outcome.

127 Distinct PAD defective B-cell patterns were identified that are a

128 , termed the "phosphatase activation domain (PAD)", is hidden within native Tau in a 'paperclip'-like

129 the origin and consequences of dysregulated PAD enzyme activity and immune responses against PAD enz

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

131 Of the five PAD enzyme isoforms, PAD2 and PAD4 are the most strongly

132 for CKD, and 2.09 (95% CI: 1.30 to 2.38) for PAD.

133 d p = 0.05 (unadjusted p = 7.5 x 10(-5)) for PAD in MESA Hispanics.

134 for CKD, and 1.41 (95% CI: 1.23 to 1.62) for PAD in individuals with LDL-C above the 95th percentile

135 to 30 years following smoking cessation for PAD and up to 20 years for CHD.

136 rs according to established risk factors for PAD.

137 starvation was used as an in vitro model for PAD.

138 d 3 outcomes, with the strongest results for PAD.

139 t to which genetic factors increase risk for PAD is largely unknown.

140 evidence that supports a pathogenic role for PAD enzymes in RA as both promoters and targets of the a

141 of the variants appeared to be specific for PAD, including F5 p.R506Q, highlighting the pathogenic r

142 Xa inhibition as a therapeutic strategy for PAD.

143 isk due to smoking lasted up to 30 years for PAD and 20 years for CHD.

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

145 H2 PAD can also facilitate elucidation of fundamental bioch

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

147 HPAEC-PAD analysis showed a maximum bioconversion rate of 49%

148 HPAEC-PAD analysis showed that 8% of the total amount of starc

149 The current work presents an HPAEC-PAD method based on gradient elution of aqueous solvents

150 nd characterized by using HPSEC-RI and HPAEC-PAD/MS.

151 imazethapyr (IMT) with determination by HPLC-PAD (High performance liquid chromatography - photodiode

152 Carotid vasoconstriction identifies PAD patients with a 4-fold increased risk for future car

153 rd can learn models that accurately identify PAD patients at risk of future major adverse cardiac and

154 ualized rate of major amputation was 0.6% in PAD overall, 3.9% in the CLI at baseline group, and 0.5%

155 ponse to muscle contraction is alleviated in PAD.

156 he arterial injection of alphabeta-me ATP in PAD rats.

157 sed risk for future cardiovascular events in PAD patients is likely related to endothelial dysfunctio

158 function) predicts cardiovascular events in PAD patients.

159 F(165)b in regulating macrophage function in PAD.

160 ulating macrophage phenotype and function in PAD.

161 asal muscle temperature (T(m) ) was lower in PAD rats than in control rats.

162 ession with increased M1-like macrophages in PAD versus non-PAD (controls) muscle biopsies.

163 (BP) response to contraction was observed in PAD rats.

164 ict cardiovascular events and progression in PAD patients.

165 ibits angiogenesis and perfusion recovery in PAD muscle.

166 Reduction in PAD events with alirocumab was associated with baseline

167 aggeration of the exercise pressor reflex in PAD and a reduction in the activity of the P2X receptor

168 aggeration of the exercise pressor reflex in PAD and a reduction of the activity of the P2X receptor

169 n the exaggerated exercise pressor reflex in PAD rats.

170 ated the amplification of the BP response in PAD rats.

171 diode (LED) as an innovative light source in PAD is under discussion.

172 porting the use of antithrombotic therapy in PAD, as well as a clinical framework for analysis and tr

173 n the EUCLID (Examining Use of Ticagrelor in PAD) trial.

174 with the strongest effect size for incident PAD.

175 ion, intensity, and cessation) with incident PAD were quantified and contrasted with CHD and stroke u

176 history of 1, 2, and 3 conditions including PAD, CHD, and cerebrovascular disease was 40.8 (95% conf

177 ations were evaluated for total CVD (MI, IS, PAD, and CVD death), coronary and cerebrovascular diseas

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

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

180 the PADs as therapeutic targets and multiple PAD inhibitors are known.

181 kidney disease (HR, 0.78, PAD; HR, 0.76, no-PAD; P-interaction=0.84) were consistent regardless of P

182 or CV death/HHF (HR, 0.86, PAD; HR, 0.82, no-PAD; P-interaction=0.79) and progression of kidney disea

183 reased M1-like macrophages in PAD versus non-PAD (controls) muscle biopsies.

184 A total of 16 cases of PAD (22.2%) were found in the evaluated of subjects (10

185 omography (CT) scanning for the diagnosis of PAD with the lowest possible radiation and contrast volu

186 e test, 202 (66.2%) patients had evidence of PAD.

187 We performed a GWAS of PAD and the ABI in 7,589 participants aged >45 years fro

188 no significant interactions by a history of PAD versus not (P-interactions=0.30 and 0.093, respectiv

189 dicare health insurance who had a history of PAD, CHD, or cerebrovascular disease on December 31, 201

190 death in macrophages and that inhibition of PAD enzyme activity by Cl-amidine, a pan-PAD inhibitor,

191 yet patients with clinical manifestations of PAD (e.g., claudication and limb ischemia) have limited

192 ts with ligated femoral arteries (a model of PAD).

193 mulation of P2X in muscle afferent nerves of PAD rats.

194 X currents in the muscle afferent neurons of PAD rats.

195 increased P2X currents in the DRG neurons of PAD rats.

196 aspects of care and longer term outcomes of PAD patients.

197 findings provide insight in the potential of PAD inhibition for treating autoimmune diseases like typ

198 similar rates of MACE and LEA, regardless of PAD status.

199 eraction=0.84) were consistent regardless of PAD.

200 Alirocumab reduced risk of PAD events (hazard ratio [HR], 0.69 [95% CI, 0.54-0.89];

201 with recent acute coronary syndrome, risk of PAD events is related to lipoprotein(a) level and is red

202 whether PCSK9 inhibition reduces the risk of PAD events or VTE after acute coronary syndrome, and if

203 In the placebo group, risk of PAD events was related to baseline quartile of lipoprote

204 on was consistently related to lower risk of PAD, CHD, and stroke, but a significantly elevated risk

205 , may be a key strategy to lower the risk of PAD.

206 nd genetically associated with high risks of PAD and CKD, suggesting that LDL-C is causally involved

207 e correlated with clinical manifestations of PADs.

208 herein was to determine the impact of CKD on PAD pathology in mice.

209 ecutive patients undergoing PAR (n = 195) or PAD (n = 190) of the encased artery for LAPC between Jan

210 of PAD enzyme activity by Cl-amidine, a pan-PAD inhibitor, blocks NLRP3 inflammasome assembly and pr

211 esection were used as an in vivo preclinical PAD model, and hypoxia serum starvation was used as an i

212 by-beat pulmonary artery diastolic pressure (PAD), stroke volume index (SV index), systolic blood pre

213 tient care as well as efficient, large-scale PAD research.

214 ultrasound test (podiatry ankle duplex scan; PAD-scan) against commonly used bedside tests for the de

215 e perfusion recovery in patients with severe PAD.

216 ations (0-800 muM) of Cl-amidine, a specific PAD inhibitor.

217 ts were referred for evaluation of suspected PAD with CT angiography.

218 underwent revascularization for symptomatic PAD.

219 underwent revascularization for symptomatic PAD.

220 national cohort of patients with symptomatic PAD after revascularization.

221 ontrolled trial in patients with symptomatic PAD undergoing lower extremity revascularization randomi

222 r SET programs for patients with symptomatic PAD.

223 quality of life in patients with symptomatic PAD.

224 icate the need for public statements to take PAD into account when acknowledging the impact of smokin

225 The PAD method generated highly vulnerable VCs, the AI metho

226 Despite its geographic isolation, the PAD is threatened by encroachment of oil sands mining in

227 irectly measured midday embolism levels, the PAD and AI methods substantially overestimated embolism,

228 erability estimated using the AI but not the PAD method.

229 nt difference in the size or location of the PAD between the two groups; the average image noise was

230 e together may impede the reliability of the PAD method.

231 oCT methods for tropical plants, whereas the PAD and AI need further mechanistic testing.

232 These pathologies established the PADs as therapeutic targets and multiple PAD inhibitors

233 homeostasis of human epidermis, where three PADs are expressed, namely PAD1, 2, and 3.

234 is known about the genetic susceptibility to PAD, especially in non-European descent populations.

235 m time of entry into the health system up to PAD diagnosis were used for modeling.

236 ion between total flavonoid intake and total PAD hospitalizations was nonlinear, reaching a plateau a

237 Eighty-two PAD patients demonstrated carotid constriction and 90 pa

238 All of the 190 patients undergoing PAD (100%) and 95 of the 195 patients undergoing PAR (48

239 alpation and ankle waveform assessment using PAD-scan and Doppler devices (audible and visual wavefor

240 69 (1.1%) had 3-, and 69 (1.1%) had 4-vessel PAD, respectively.

241 VOYAGER PAD was a phase 3, international, double-blind, placebo-

242 The VOYAGER PAD trial (Vascular Outcomes Study of ASA Along With Riv

243 In the VOYAGER PAD trial, rivaroxaban plus aspirin reduced the risk of

244 predictive model accurately determined which PAD patients would go on to develop major adverse cardia

245 ctronic health record data-to identify which PAD patients are most likely to develop major adverse ca

246 of 6861 patients in our health system whose PAD status had previously been adjudicated were used to

247 diabetes mellitus, including 1025 (6%) with PAD, were randomized.

248 Patients in the placebo arm with PAD versus those without tended to have higher adjusted

249 Among patients with PAD and CHD, with PAD and cerebrovascular disease, and with CHD and cerebr

250 he pathogenesis of autoimmune diabetes, with PAD inhibition leading to disease prevention through mod

251 ta were derived from patients diagnosed with PAD at 2 tertiary care institutions.

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

253 EXSCEL participants with PAD had higher rates of all-cause mortality and LEA comp

254 ed clinical trial in which participants with PAD were randomized to either cocoa beverage versus plac

255 EXSCEL included 2800 patients with PAD (19% of the trial population).

256 EUCLID enrolled 13,885 patients with PAD (28% women [n = 3,888]).

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

258 for delivering SET programs to patients with PAD according to Centers for Medicare & Medicaid Service

259 Among patients with PAD and CHD, with PAD and cerebrovascular disease, and w

260 Further, patients with PAD are at risk for not only major adverse cardiovascula

261 dverse outcomes; nevertheless, patients with PAD are often undertreated.

262 ns including statin therapy in patients with PAD are warranted.

263 mprove our ability to identify patients with PAD compared with an approach using structured data alon

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

265 Patients with PAD had a higher risk of limb events, with no consistent

266 Patients with PAD had higher all-cause mortality (adjusted hazard rati

267 ng to more accurately identify patients with PAD in an electronic health record system compared with

268 Statin use was lower in patients with PAD only (33.9%) versus those with cerebrovascular disea

269 The ASCVD event rate among patients with PAD only, CHD only, and cerebrovascular disease only was

270 s and the use of statins among patients with PAD versus those with coronary heart disease (CHD) or ce

271 ng high risk for ASCVD events, patients with PAD were less likely to be taking a statin versus those

272 ce on how to implement SET for patients with PAD, including the SET protocol, options for outcome mea

273 ding antithrombotic therapy in patients with PAD.

274 implementing SET programs for patients with PAD.

275 and accurate identification of patients with PAD.

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

277 improved walking performance in people with PAD, compared with placebo.

278 cocoa on walking performance in people with PAD.

279 improves walking performance in people with PAD.

280 different populations, including those with PAD.

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

282 sting ~32 million DNA sequence variants with PAD (31,307 cases and 211,753 controls) across veterans

283 le Cox models, higher number of vessels with PAD was associated with higher risk of mortality (P for

284 Although women with PAD are at lower risk for MACE and all-cause mortality,

285 e respiratory exacerbations in patients with PADs and chronic infection-related pulmonary diseases.

286 We investigated patients with PADs for the distribution of 41 blood B-cell and plasma

287 Blood samples from 139 patients with PADs, 61 patients with common variable immunodeficiency

288 se azithromycin prophylaxis in patients with PADs.

289 classes were identified in all patients with PADs.

290 Within PAD populations, data from trials may be difficult to in

291 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=

292 -related events in patients with and without PAD in an exploratory analysis.

293 versus placebo in patients with and without PAD.

294 rates of MACE compared with patients without PAD (13.6% versus 11.4%, respectively) as well as a high

295 d poorer quality of life than people without PAD.

296 sclerosis Risk In Communities) study without PAD, CHD, or stroke at baseline (1987 to 1989) were incl

297 anish Diet, Cancer, and Health Study without PAD, recruited from 1993 to 1997, were cross-linked with

298 ortality and LEA compared with those without PAD.

299 ar events (MACE) compared with those without PAD.

300 Patients with versus without PAD are at a higher risk of CV death of CV death, HHF, a