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 impaired soon after HTx (average in first 2 year

10 HRR was most prominent during immobility and running wit

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

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

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

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

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

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

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

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

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

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

21 measured by elevated resting HR and abnormal HRR.

22 Mortality was predicted by abnormal HRR (hazard ratio [HR] 2.5, 95% confidence interval [CI]

23 ity, and left ventricular function, abnormal HRR remained predictive of death (adjusted HR 1.6, 95% C

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

25 functional capacity, and normal or abnormal HRR.

26 sent in 421 patients (14%), whereas abnormal HRR was noted in 838 patients (29%).

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 he RAD51 paralog XRCC2 (342delT) found in an HRR-defective tumour cell line, 342delT was introduced i

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 ow the median for both exercise capacity and HRR had a 3.5-fold increased risk of cardiovascular deat

47 median levels of both exercise capacity and HRR had significantly increased risk compared with women

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

49 RAD51-dependent responses to DNA damage and HRR.

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

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

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

53 and the potential crosstalk between NHEJ and HRR, and between repair and other stress-induced pathway

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

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

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

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

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

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

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

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

62 n cells, as opposed to lower eucaryotes, but HRR has recently been implicated in critical cell signal

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

64 (HRR, 0.64; 95% CI, 0.42-0.97), and cancer (HRR, 0.49; 95% CI, 0.29-0.84), independent of age, smoki

65 ventricular function, and exercise capacity, HRR is independently predictive of mortality.

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

67 Whereas NHEJ repair appears constitutive, HRR is regulated by the cell cycle and inducible signal

68 1.32; 95% CI, 1.19-1.47) and first cousins (HRR, 1.15; 95% CI, 1.07-1.25), compared with relatives o

69 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

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

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

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

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

74 HRR, selected against cells with deregulated HRR.

75 al [CI], 0.40-0.69), cardiovascular disease (HRR, 0.64; 95% CI, 0.42-0.97), and cancer (HRR, 0.49; 95

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

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

78 ted rates of laparoscopic colectomy for each HRR.

79 ssion rates among Medicare enrollees in each HRR.

80 ucting deductibles and coinsurances) in each HRR.

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 response contributes to the highly efficient HRR in such cells.

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

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

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

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

88 at induced damage required ATM to facilitate HRR.

89 compared with 14 participants in the fastest HRR quartile.

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

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

92 nd exchange activities that are integral for HRR.

93 fficient nucleoprotein filament required for HRR.

94 apse and are transformed into substrates for HRR.

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

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

97 6-2.00) and adenomas with villous histology (HRR, 2.43; 95% CI, 1.96-3.01) also were increased in FDR

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

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

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

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

102 e results point to a direct role of IRS-1 in HRR and suggest a novel role for the IGF-IR/IRS-1 axis i

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

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

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

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

107 ; for every 10 beats per minute decrement in HRR, the hazard ratio was 1.36 (95% CI, 1.19-1.55; P<.00

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

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

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

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

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

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 further suggest a critical role for XRCC2 in HRR at replication forks, possibly in the loading of RAD

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

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

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

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

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

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

125 umour cell line, 342delT was introduced into HRR proficient cells containing a recombination reporter

126 DNA replication transformation of SSBs into HRR substrates.

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

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

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

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

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

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

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

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

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

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

137 CI, 0.56-0.82) and cardiovascular mortality (HRR, 0.62; 95% CI, 0.44-0.88) than sedentary women.

138 h visits also had lower all-cause mortality (HRR, 0.68; 95% CI, 0.56-0.82) and cardiovascular mortali

139 Nevertheless, HRR could also be faster than theta.

140 to that of individuals with baseline normal HRR.

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

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

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

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

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

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

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

148 1, which is the major enzymatic component of HRR.

149 Rad51 specifically, a critical component of HRR.

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

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

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

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

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

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

156 ocalization in nuclear foci is a hallmark of HRR.

157 ese cells were defective in the induction of HRR by either thymidine or DSBs.

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

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

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

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

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

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

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

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

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

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

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

169 Attenuated orthostatic HRR may reflect dysregulation of the parasympathetic bra

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

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

172 0.67; P (HRR > 1) < 0.01 and HRRav, 1.50; P (HRR < 1) = 0.02, respectively).

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

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

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

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

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

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

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

180 weight loss had a 24% lower mortality rate (HRR, 0.76 [95% CI, 0.60 to 0.97]) and those with uninten

181 weight loss had a 31% higher mortality rate (HRR, 1.31 [CI, 1.01 to 1.70]).

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

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

184 ortality from all causes (hazard rate ratio [HRR], 0.52; 95% confidence interval [CI], 0.40-0.69), ca

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

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

187 stability through homologous recombination (HRR).

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

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

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

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

192 exercise capacity, low heart rate recovery (HRR), and not achieving target heart rate were independe

193 rate after exercise, or heart rate recovery (HRR), has been shown to predict mortality.

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

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

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

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

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

199 (2007-2011) to the hospital referral region (HRR) level.

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

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

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

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

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

205 ignaling positively and negatively regulates HRR in human cells.

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

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

208 ,1.59-2.03), as did second-degree relatives (HRR, 1.32; 95% CI, 1.19-1.47) and first cousins (HRR, 1.

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

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

211 omologous recombination-directed DNA repair (HRR).

212 omologous recombination-directed DNA repair (HRR).

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

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 efective in homologous recombination repair (HRR) induced by DNA double-strand breaks.

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 Homologous recombination repair (HRR) is required for both the repair of DNA double stran

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

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

223 RCA2 in the homologous recombination repair (HRR) of double-strand breaks in DNA implicates this path

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 repair via homologous recombination repair (HRR).

235 1-dependent 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 (NHEJ) and homologous recombination repair (HRR).

241 (NHEJ) and homologous recombination repair (HRR).

242 joining and homologous recombination repair (HRR).

243 on disrupts homologous recombination repair (HRR).

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

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

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

247 n homology-dependent recombinational repair (HRR) of DNA double-strand breaks (DSBs).

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

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

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

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

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

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

259 to thymidine and mitomycin C and suppressed HRR induced at the recombination reporter by thymidine b

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

261 own about the molecular details of NHEJ than HRR in mammalian cells.

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

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

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

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

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

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

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

269 These results suggest that HRR pathways responding to stalled replication forks or

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

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

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

273 The HRR was abnormal if < or =12 beats/min during the first

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

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

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

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

278 1992 and 2010, the spending patterns in the HRR in which their residency program was located were as

279 lines may be a consequence of defects in the HRR pathway.

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

281 n of drug resistance and facilitation of the HRR in FTK-transformed cells.

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

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

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

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

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

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

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

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

294 ir is deficient in cells without Ku, whereas HRR is highly efficient in such cells compared with thei

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