ライフサイエンスコーパス: HRR

1 HRR and nonhomologous end joining (NHEJ) were also deter

2 HRR does not appear to identify patients likely to have

3 HRR gene expression was significantly deregulated in Msh

4 HRR is blunted soon after HTx but normalizes at approxim

5 HRR is closely related to workload, the limitation of wh

6 HRR is most prominent in the dentate gyrus, especially w

7 HRR readmission rates ranged from 11 to 32% for congesti

8 HRR usually depends on BRCA1/2-RAD51, and RAD52-RAD51 se

9 HRR was calculated as the maximal HR achieved minus the

10 HRR was impaired soon after HTx (average in first 2 year

11 HRR was most prominent during immobility and running wit

12 (95% CI, 0.52 to 0.73), and for non-BRCA1/2 HRR, the HR was 0.65 (95% CI, 0.51 to 0.85).

13 BRCA1/2, HRR, and CD31 were not predictive of bevacizumab activit

14 for sick-child visits increased risk by 30% (HRR = 1.30, 95% CI:1.11 to 1.53).

15 ge-adjusted analyses for AJCC stages 2 to 4 (HRR, 4.88, 3.60, and 2.04, respectively); and in Kaplan-

16 R2 may improve the anti-cancer activity of 4-HRR and other DHC-inducing agents.

17 Abnormal HRR was also associated with increased all-cause mortali

18 Among patients with an abnormal HRR at baseline, failure to normalize after rehabilitati

19 able adjustment, the presence of an abnormal HRR at exit was predictive of death in all patients (haz

20 evidence of myocardial ischemia, an abnormal HRR is associated with a nonsignificant trend toward blu

21 ciated with elevated resting HR and abnormal HRR after adjusting for age, sex, cardiovascular risk fa

22 th impaired exercise tolerance, and abnormal HRR predicts increased all-cause mortality in RT patient

23 Both elevated resting HR and abnormal HRR were associated with reduced exercise capacity in RT

24 measured by elevated resting HR and abnormal HRR.

25 There was a strong association of abnormal HRR at exit with all-cause mortality.

26 functional capacity, and normal or abnormal HRR.

27 Patients with abnormal HRR at baseline who normalized afterward had survival ra

28 Patients with abnormal HRR at baseline who normalized HRR with exercise had a m

29 90), whereas ischemic patients with abnormal HRR did not (HR 0.78, 95% CI 0.47 to 1.29); however, the

30 ding to DNA is the first step for activating HRR and Ku binding to DNA is the first step for initiati

31 The risk of adenomas (HRR, 1.82; 95% CI, 1.66-2.00) and adenomas with villous

32 Adjusted HRR-level brand-name statin use ranged (from the 5th to

33 used linear regression to estimate adjusted HRR-level 30-day outcomes, to identify HRR-level charact

34 The mean adjusted HRR-level 30-day mortality and readmission rates were 10

35 Patient quintiles of adjusted HRR utilization were used to evaluate differences in pat

36 , the measles vaccine group had an admission HRR of 0.70 (95% confidence interval [CI], .52-.95), wit

37 significant for measles infection (admission HRR, 0 [95% CI, 0-.24]) and respiratory infections (admi

38 -.24]) and respiratory infections (admission HRR, 0.37 [95% CI, .16-.89]).

39 ren who had not received NVAS, the admission HRR was 0.53 (95% CI, .34-.84), with an effect of 0.30 (

40 CI: 1.88 to 2.09, P < 0.0001) of CNLD and an HRR of 2.16 (1.86 to 2.52, P < 0.0001) of hepatocellular

41 hese unexpected findings establish XPG as an HRR protein with important roles in genome stability and

42 propriate prostate imaging if he lived in an HRR in the fourth, third, or second quartiles, respectiv

43 In line with an HRR defect in these tumors, UBQLN4 overexpression is ass

44 Diabetes was associated with an HRR of 1.98 (95% CI: 1.88 to 2.09, P < 0.0001) of CNLD a

45 The opening of a cardiac hospital within an HRR is associated with increasing population-based rates

46 1) the association of exercise capacity and HRR is much weaker in severe CHF compared to normal left

47 RAD51-dependent responses to DNA damage and HRR.

48 ine the intricate interface between FANC and HRR proteins in maintaining chromosome stability.

49 important roles in RAD51 focus formation and HRR of DNA double-strand breaks (DSBs).

50 The HRA and HRR regions are necessary and sufficient to activate and

51 n formation and show that, as for D-NHEJ and HRR, the function of B-NHEJ facilitates the recovery fro

52 study, we showed that although wild-type and HRR-deficient mice or DT40 cells are more sensitive to h

53 cise to 1 minute of recovery was measured as HRR and was expressed as Z score calculated from referen

54 We assessed HRR after pediatric heart transplantation (HTx) and its

55 treated with caffeine, an inhibitor of ATM, HRR was reduced, whereas NHEJ was not.

56 Of 544 patients with abnormal baseline HRR, 225 (41%) had normal HRR after rehabilitation.

57 udies to assess: 1) the relationship between HRR and exercise capacity in CHF; and 2) the effect of i

58 CA1 and dentate gyrus are modulated by both HRR and theta.

59 When excessive and uncontrolled, BRCA1 HRR activity promotes illegitimate recombination and gen

60 on contribute to the kinetics by which BRCA1 HRR-sustaining complexes normally concentrate in nuclear

61 s in CA1 and dentate gyrus were modulated by HRR and theta oscillations.

62 ATM-specific inhibitor KU-55933 compromised HRR up to 90% in growth-arrested cells, whereas this eff

63 1.32; 95% CI, 1.19-1.47) and first cousins (HRR, 1.15; 95% CI, 1.07-1.25), compared with relatives o

64 UBQLN4 therefore curtails HRR activity through removal of MRE11 from damaged chrom

65 ted in a 25% reduction in the risk of death (HRR = 0.73, 95% CI:0.58 to 0.91) and accounted for 30% o

66 abnormalities, cell-cycle delays, defective HRR, inability to overcome replication fork stalling, an

67 egulating EMI1 and restoring RAD51-dependent HRR.

68 the Shu proteins in a Rad51/Rad54-dependent HRR pathway(s) to repair MMS-induced lesions during S-ph

69 A deregulated HRR phenotype could be partially recapitulated in MMR-co

70 an selection against clones with deregulated HRR suggests that persistence and expansion of unstable

71 HRR, selected against cells with deregulated HRR.

72 then restrict the amplitude of BRCA1-driven HRR.

73 the US to estimate the deficit in beds each HRR will likely encounter given the demand for hospital

74 assessed providers' use of imaging for each HRR after creating an imaging referral index (IRI) to ad

75 Models were constructed for each HRR for three seasons: nonbreeding season (NBS), early a

76 For each HRR, a Herfindahl-Hirschman index, a measure of market c

77 ted rates of laparoscopic colectomy for each HRR.

78 ucting deductibles and coinsurances) in each HRR.

79 ssion rates among Medicare enrollees in each HRR.

80 < 0.05) between all HRV(DO) measures to each HRR measure and are presented in ranges: lnSDNN (r = 0.4

81 AF/MEK/ERK pathway is critical for efficient HRR and for radiation-induced ATM activation, suggestive

82 ctions with other paralogs and for efficient HRR.

83 rocessing of HRR intermediates, and elevated HRR-associated mutagenesis, is detectable in a yeast mod

84 therapy nitrogen mustard predicted to elicit HRR, selected against cells with deregulated HRR.

85 features that reduce predation risk explain HRR size throughout the breeding period.

86 at BLM collaborates with RAD51 to facilitate HRR and promotes the resistance of BCR/ABL-positive leuk

87 at induced damage required ATM to facilitate HRR.

88 compared with 14 participants in the fastest HRR quartile.

89 ectasia mutated (ATM) kinase is critical for HRR.

90 ), suggesting that ATM is also important for HRR outside of the S and G(2) cell cycle phases.

91 nd exchange activities that are integral for HRR.

92 fficient nucleoprotein filament required for HRR.

93 apse and are transformed into substrates for HRR.

94 Furthermore, HRR was inhibited by caffeine in serum-starved cells arr

95 sk (adjusted hazard ratio compared with high HRR/high METs for women 8.51, 95% CI 3.65 to 19.84; for

96 6-2.00) and adenomas with villous histology (HRR, 2.43; 95% CI, 1.96-3.01) also were increased in FDR

97 motifs in the functional domains (OSA, HRA, HRR, bZIP).

98 sponse (OSA) and meiotic recombination (HRA, HRR).

99 usted HRR-level 30-day outcomes, to identify HRR-level characteristics associated with 30-day outcome

100 including BRCA1 and BRCA2, lead to impaired HRR that can genetically be complemented for (i.e. suppr

101 ose a model in which the Shu proteins act in HRR to promote the formation of HRR intermediates that a

102 This late decline in HRR Z score is associated with worse outcome.

103 A subsequent decline in HRR Z score was noted from 6 years after HTx (rate of Z=

104 of agreement = 0.90 per 1 point decrement in HRR score, P < 0.001; odds of agreement = 0.30 for medic

105 Defects in HRR have long been known to contribute to genomic instab

106 A high mutation rate is detected in HRR products in BCR/ABL-positive cells, but not in the n

107 Differences in HRR between cohorts were greater in the initial five int

108 g exhibited by RecA and is less efficient in HRR reactions in vitro.

109 better understanding of missing heredity in HRR-associated cancers (e.g., heredity breast and ovaria

110 c RAF-1, an approximately 2-fold increase in HRR was observed.

111 expression of several key genes involved in HRR including BRCA1, PALB2, and TOPBP1.

112 Mutations in HRR genes can result in increased mutation rate and geno

113 To determine the role of MAPK signaling in HRR, we used a human in vivo I-SceI-based repair system.

114 An important early step in HRR is the formation of single-stranded DNA (ss-DNA) coa

115 ty of deep end-resection-the initial step in HRR.

116 Upstream in HRR, XPG interacts directly with BRCA1.

117 We examined the variation in HRR readmission rates that was explained by overall hosp

118 Secondary outcomes included HRR according to stage, grade, and age and hazard rate o

119 mal left ventricular function; 2) increasing HRR using rate-adaptive pacing (versus fixed-rate pacing

120 Furthermore, PARP inhibitor-induced HRR is abolished in ATM, but not DNA-PK, inhibited cells

121 RAD54 prevented the formation of MMS-induced HRR intermediates (X-molecules) arising during replicati

122 tive ATM expressed from adenovirus inhibited HRR by 45%, also having little to no effect on NHEJ.

123 vated levels of RAD51 in tumors with initial HRR defects limits genomic instability during carcinogen

124 DNA replication transformation of SSBs into HRR substrates.

125 ion, coupled with a putative block in a late HRR step.

126 Individuals with low (median or less) HRR or METs experienced 91% of all cardiovascular diseas

127 Low HRR/low METs was also associated with an increased relat

128 After FRS adjustment, low HRR and METs individually were highly significant predic

129 significant predictors of CVD death, but low HRR and METs together were associated with substantially

130 -adjusted CVD death risk associated with low HRR/low METs was less than at 20 years but remained sign

131 Lower HRR scores and higher D15 CCI (both indicating worse col

132 hat the dox-induced ATRkd cells have a lower HRR efficiency compared with the cells without dox induc

133 ul recombination-dependent repair mechanisms HRR and SSA, and enhances the loss of DNA bases during N

134 focused on CtIP (RBBP8 gene), which mediates HRR through the end resection of DNA double-strand break

135 e Tuscaloosa HRR to 3.7 in the Royal Oak, MI HRR.

136 We modeled HRR to the stand by age group, cardiovascular disease bu

137 Nevertheless, HRR could also be faster than theta.

138 to that of individuals with baseline normal HRR.

139 abnormal baseline HRR, 225 (41%) had normal HRR after rehabilitation.

140 es similar to those of the group with normal HRR at baseline and after cardiac rehabilitation (P=0.14

141 Ischemic patients with normal HRR had significantly lower mortality with revasculariza

142 with abnormal HRR at baseline who normalized HRR with exercise had a mortality similar to that of ind

143 To map novel HRR genes systematically, we developed clade phylogeneti

144 erent fibre activation were balanced, a null HRR was evoked (defined as 'neural fulcrum') during whic

145 The application of HRR/METs information to FRS assessment identified those

146 This temporal attenuation of HRR may contribute to the accumulation mutations after D

147 1, which is the major enzymatic component of HRR.

148 Rad51 specifically, a critical component of HRR.

149 CLL cells to clinically achievable doses of HRR-inducing chemotherapeutic agents in vitro and in viv

150 d Ku determine the different efficiencies of HRR and NHEJ to repair high-LET radiation induced DSBs.

151 igh-LET IR does not affect the efficiency of HRR remains unclear.

152 ereby DNA MMR loss promotes the emergence of HRR gene superexpressing clones, with concomitant chromo

153 We could thus demonstrate the existence of HRR in awake animals, namely, a respiration-entrained sl

154 teins act in HRR to promote the formation of HRR intermediates that are processed by the Sgs1-Rmi1-To

155 ocalization in nuclear foci is a hallmark of HRR.

156 Furthermore, aberrant processing of HRR intermediates, and elevated HRR-associated mutagenes

157 y for androgenization) and the proportion of HRR, covered by antipredatory features (shrubs and falle

158 Patients in the lowest quartile of HRR Z score had a much higher 5-year event rate (event-f

159 between the lowest and highest quintiles of HRR utilization were negligible, and there was no differ

160 gnaling are important positive regulators of HRR in growth-arrested cells.

161 ate (MMS), indicating the broad relevance of HRR to genotoxicity.

162 Speed of HRR in the immediate 20 s after standing was a strong pr

163 ay generated an almost 2-fold stimulation of HRR.

164 plication forks and may function upstream of HRR in the repair of certain types of double-strand brea

165 down cells exhibited increased dependence on HRR, as evidenced by elevated levels of cisplatin-induce

166 formation deriving from defects in D-NHEJ or HRR in cells irradiated in the G2-phase and identify B-N

167 Attenuated orthostatic HRR may reflect dysregulation of the parasympathetic bra

168 Speed of orthostatic HRR predicts mortality and may aid clinical decision mak

169 thin this time frame, NHEJ predominated over HRR in the range of 3-50-fold.

170 0.67; P (HRR > 1) < 0.01 and HRRav, 1.50; P (HRR < 1) = 0.02, respectively).

171 ogical prognostic variables (HRRav, 0.67; P (HRR > 1) < 0.01 and HRRav, 1.50; P (HRR < 1) = 0.02, res

172 ociated with good prognosis (HRRav, 0.67; P (HRR >1) < 0.01) and high VEGFA expression to poor progno

173 xpression to poor prognosis (HRRav, 1.84; P (HRR < 1) = 0.02), also after multivariate analysis inclu

174 The HRR surface peaked (HRR, 13.0) for younger sexagenarian relatives related to

175 The number of physicians per HRR ranged from 135 in Minot, North Dakota, to 8197 in B

176 brand-name drug use than the 5th-percentile HRR in Medicare.

177 For each drug group, the 95th-percentile HRR in the VA had lower brand-name drug use than the 5th

178 ention of MRE11, promoting non-physiological HRR activity in vitro and in vivo.

179 al, age-specific, 10-year hazard rate ratio (HRR) surface representing the relative risk of AD in rel

180 e, stage, and tumor site [hazard rate ratio (HRR), 2.97; 95% CI, 2.05-4.32]; in stage-specific, age-a

181 an increased risk of CRC (hazard rate ratio [HRR], 1.79; 95% confidence interval [CI],1.59-2.03), as

182 Hazard rate ratios (HRR) were determined in Cox proportional hazard survival

183 stability through homologous recombination (HRR).

184 beats/min) and abnormal heart rate recovery (HRR) at 1 min (</=12 beats/min if active cool-down, or <

185 line measures of HRV to heart rate recovery (HRR) following maximal exercise.

186 A blunted heart rate recovery (HRR) from peak exercise is associated with adverse outco

187 Abnormal heart rate recovery (HRR) has been shown to predict mortality.

188 Although heart rate recovery (HRR) predicts mortality after exercise testing, its abil

189 uivalents, or METs) and heart rate recovery (HRR).

190 cytometry demonstrated that caffeine reduced HRR by 90% under conditions when ATM kinase activity was

191 dly reduces RAD51 and BRCA2 foci and reduces HRR of DSBs by 20- to 100-fold.

192 th status-adjusted hospital referral region (HRR) brand-name drug use was compared, and changes in sp

193 th Dartmouth Atlas Hospital Referral Region (HRR) files.

194 d capacity of each Hospital Referral Region (HRR) in the US to estimate the deficit in beds each HRR

195 (2007-2011) to the hospital referral region (HRR) level.

196 te, for each local hospital referral region (HRR), the 30-day, 60-day, and 90-day readmission rates a

197 In a hospital referral region (HRR)-level analysis, our dependent variable was HRR-leve

198 ion ratio for each hospital referral region (HRR).

199 nd PRR2) that flank a histidine-rich region (HRR), and a C-terminal domain.

200 tors and the size of two home-range regions (HRR), defined as areas of different intensities of use.

201 Home ranges were split into two regions (HRR): the 'core', representing the most intensively used

202 ignaling positively and negatively regulates HRR in human cells.

203 tly, ATM plays a critical role in regulating HRR but not NHEJ throughout the cell cycle.

204 rimary end point was hazard rate of relapse (HRR) for BC by study cohort according to biomarker statu

205 ,1.59-2.03), as did second-degree relatives (HRR, 1.32; 95% CI, 1.19-1.47) and first cousins (HRR, 1.

206 volved in recombination-mediated DNA repair (HRR) and replication fork maintenance.

207 n the homologous recombinational DNA repair (HRR) pathway, is the major strand-transferase required f

208 omologous recombination-directed DNA repair (HRR).

209 omologous recombination-mediated DSB repair (HRR).

210 e, homologous recombination-mediated repair (HRR) of DNA double-stranded breaks (DSBs).

211 ed homologous recombination-mediated repair (HRR), since silencing MYB impaired the formation of RAD5

212 nt inhibits homologous recombination repair (HRR) and increases sensitivity to cisplatin in BCR/ABL-p

213 sential for homologous recombination repair (HRR) and is frequently disrupted in breast cancers.

214 lian cells: homologous recombination repair (HRR) and nonhomologous end joining (NHEJ).

215 -stimulated homologous recombination repair (HRR) and nonhomologous end-joining (NHEJ) mechanisms.

216 etection of homologous recombination repair (HRR) by GFP expression.

217 utations in homologous recombination repair (HRR) genes.

218 d breaks by homologous recombination repair (HRR) is critical to the long-term survival of the cell.

219 Homologous recombination repair (HRR) is functional during the S- and G2-phases, when a s

220 -D2-G-X3 in homologous recombination repair (HRR) is supported by our finding that FANCG and the RAD5

221 Homologous recombination repair (HRR) maintains chromosomal stability by the repair of DN

222 inhibit the homologous recombination repair (HRR) pathway (such as PI3K inhibitors) might sensitise H

223 The homologous recombination repair (HRR) pathway repairs DNA double-strand breaks in an erro

224 TM-mediated homologous recombination repair (HRR) pathway.

225 he cellular homologous recombination repair (HRR) pathway.

226 Homologous recombination repair (HRR) protects cells from the lethal effect of spontaneou

227 esponse and homologous recombination repair (HRR) via decreasing DICER-generated small RNAs at the da

228 (NHEJ) and homologous recombination repair (HRR), contribute to repair ionizing radiation (IR)-induc

229 rmation and homologous recombination repair (HRR), EGFR-mutant cells also exhibited an impaired RAD51

230 r pathways, homologous recombination repair (HRR), nonhomologous end-joining (NHEJ), and single-stran

231 t factor of homologous recombination repair (HRR), preferentially sensitized stable R2-knockdown p53(

232 plicated in homologous recombination repair (HRR), their precise role(s) within this pathway remains

233 ficiency of homologous recombination repair (HRR), which is associated with the cellular sensitivity

234 a result is homologous recombination repair (HRR).

235 joining and homologous recombination repair (HRR).

236 repair and homologous recombination repair (HRR).

237 and trigger homologous recombination repair (HRR).

238 sential for homologous recombination repair (HRR).

239 d to induce homologous recombination repair (HRR).

240 repair via homologous recombination repair (HRR).

241 on disrupts homologous recombination repair (HRR).

242 1-dependent homologous recombination repair (HRR).

243 nd rad5), homologous recombinational repair (HRR) (rad51 and rad54), base excision repair (BER) (apn1

244 decreased homologous recombinational repair (HRR) activity, down-regulated XIAP expression, and sensi

245 Homologous recombinational repair (HRR) of DNA damage is critical for maintaining genome st

246 tebrates, homologous recombinational repair (HRR) requires RAD51 and five RAD51 paralogs (XRCC2, XRCC

247 Homologous recombinational repair (HRR) restores chromatid breaks arising during DNA replic

248 Conversely, UBQLN4 overexpression represses HRR and favors non-homologous end joining.

249 Inhibition of RAD51 degradation restores HRR in BRCA1-depleted cells.

250 ncies of the hippocampal respiration rhythm (HRR) overlap with classical theta oscillations, but both

251 h we named "hippocampal respiration rhythm" (HRR), also occurs in awake mice.

252 Limited heart rate (HR) rise (HRR) during exercise, known as chronotropic incompetence

253 cy, as determined by the Hardy-Rand-Rittler (HRR) score and Lanthony D15 color confusion index (D15 C

254 ) and 1 SNP in African Americans (rs7250581; HRR = 1.60, P = 0.05) were significantly associated with

255 ay (such as PI3K inhibitors) might sensitise HRR-proficient epithelial ovarian cancers to PARP inhibi

256 A 1-bpm slower HRR between 10 and 20 s after standing increased the haz

257 Sixty-nine participants in the slowest HRR quartile died during the observation period compared

258 demonstrates that PARP1 inhibits spontaneous HRR events, and supports the model of DNA replication tr

259 strate an increased frequency of spontaneous HRR in vivo in the absence of PARP1 using the p(un) assa

260 To target HRR in tumor cells, a phenomenon called "synthetic letha

261 Altogether, these results demonstrate that HRR contributes substantially to DSB repair in human gli

262 esults confirm the a priori expectation that HRR acts in an error-free manner to repress three classe

263 Although small studies have found that HRR can be improved with cardiac rehabilitation, it is u

264 We propose that HRR becomes important for recovery from cisplatin-DNA le

265 ranger directionality analysis revealed that HRR is caused by the OB and that theta oscillations in O

266 Directionality analysis shows that HRR is caused by the OB.

267 ut improved afterward (Z=+0.52/y), such that HRR Z score normalized in most patients by 6 years after

268 Our analysis suggests that HRR-based policies may be too crudely targeted to promot

269 The HRR decreased in C2 compared with C1 for all disease sta

270 The HRR surface peaked (HRR, 13.0) for younger sexagenarian

271 For relatives aged in their late 80s, the HRR fell lower than 2.0 regardless of proband onset age

272 th complex evolutionary dynamics such as the HRR.

273 At the HRR level, inappropriate prostate cancer imaging rates w

274 thought that an HRG fragment containing the HRR, released via plasmin-mediated cleavage, acts as a n

275 (Kip1) levels and resulted in decreasing the HRR efficiency.

276 1992 and 2010, the spending patterns in the HRR in which their residency program was located were as

277 ese genes are expected to play a role in the HRR pathway and might lead to a better understanding of

278 n together, our results implicate ATM in the HRR-mediated rescue of replication forks impaired by thy

279 For the overall population, the HRR approximately halved in all yearly intervals to year

280 Despite intensive research, the HRR pathway is not yet fully mapped.

281 Furthermore, we found that the HRR events that occur in Parp1 nullizygous mice are asso

282 f unrecognized genes that coevolved with the HRR pathway, either globally across all eukaryotes or lo

283 (DO) displayed the strongest correlations to HRR therefore, averaged resting HRV measures do not stre

284 ty are independent of NHEJ but are linked to HRR that may be affected by the deficient S and G(2) che

285 s independent of NHEJ but might be linked to HRR.

286 ute in a nonessential but critical manner to HRR proficiency.

287 pending HRRs, the difference across training HRR levels was not significant ($533; 95% CI, -$46 to $1

288 ction ratios ranged from 0 in the Tuscaloosa HRR to 3.7 in the Royal Oak, MI HRR.

289 > DSBs in proliferating cells --> unfaithful HRR and NHEJ repair.

290 moylated causes DNA damage, whose repair via HRR produces an intermediate that generates tandem copie

291 on, chromatin remodelling and DSB-repair via HRR; effectively phenocopying loss of TIP60.

292 ory testing was performed using the Waggoner HRR Diagnostic Test color plates (Home Vision Care).

293 Our independent variable was HRR-level imaging rate among patients with low-risk brea

294 )-level analysis, our dependent variable was HRR-level imaging rate among patients with low-risk pros

295 We sought to determine whether HRR can identify patients likely to have improved surviv

296 e aim of this study was to determine whether HRR could be improved with cardiac rehabilitation and wh

297 d (defined as 'neural fulcrum') during which HRR approximately 0.

298 .63), compared with older than age 60 years (HRR, 1.77; 95% CI, 1.58-1.99).

299 developed CRC at younger than age 60 years (HRR, 2.11; 95% CI, 1.70-2.63), compared with older than

300 For the follow-up after 6 years, HRR Z score was the only predictor of death/re-heart tra