ライフサイエンスコーパス: CCB

1 CCB did not alter PAP or PVR/SVR from baseline values.

2 CCB long-term response was found in 54.3% of patients.

3 CCB showed better predictive value (positive predictive

4 CCB-bound GLUT4 exhibits an inward-open conformation.

5 CCBs should be avoided among patients taking cyclosporin

6 mic agents (17.4% versus 16.8% versus 8.0%), CCB (14.8% versus 14.4% versus 8.0%) and anticonvulsants

7 r (eight groups) 0.67 (0.56-0.80, p<0.0001); CCB (nine groups): 0.75 (0.62-0.90, p=0.002); placebo (n

8 09), beta blockers (1.97%; 0.97, 0.88-1.07), CCBs (2.11%; 1.05, 0.96-1.13), diuretics (2.02%; 1.00, 0

9 10), beta blockers (1.23%; 0.93, 0.80-1.08), CCBs (1.27%; 0.96, 0.82-1.11), diuretics (1.30%; 0.98, 0

10 While all 4 CCBs exerted similar inhibition on calcium kinetics, ver

11 of adults experienced cost burdens (and 3.5% CCB); 17.4% (and 9.9% CCB) experienced these outcomes (r

12 cost burdens (and 3.5% CCB); 17.4% (and 9.9% CCB) experienced these outcomes (respectively) at least

13 ive a thiazide-type diuretic (n = 15 002), a CCB (n = 8898), or an ACE inhibitor (n = 8904) for plann

14 , of whom 3165 started a diuretic and 2710 a CCB.

15 ent: a Mg2+-supplemented diet; amlodipine, a CCB; and N-acetylcysteine, an antioxidant.

16 d the lowest among tacrolimus users not on a CCB (15%).

17 17.9%; 95% CI, 15.3%-20.8%) received only a CCB, and 295 mothers (weighted percentage, 37.6%; 95% CI

18 advanced CKD, using a diuretic rather than a CCB on top of RASi may improve kidney outcomes without c

19 Using a CCB cohort, our previously validated models have demonst

20 ded low dosage and not in combination with a CCB may not be associated with a significant risk for GE

21 profiling cardiomyocyte transcriptome after CCB treatment, we identified little overlap in their tra

22 dropyridine calcium channel blocking agents (CCBs) appears to reduce reinfarction in patients with is

23 M pairing with controls was achieved for all CCB users.

24 tory method showed good sensitivity: CCa and CCB ranging from 0.03 to 4.80 ng g(-1) and from 0.12 to

25 assessed the association of hypertension and CCB use with all-cause and infection-related mortality d

26 assessed the association of hypertension and CCB use with all-cause and infection-related mortality d

27 esolution of mebudipine revealed that MR and CCB activity reside in opposite enantiomers.

28 iteria used to identify acute responders and CCB use are insufficiently studied.

29 nteraction between clopidogrel treatment and CCB (HR for patients not on CCBs, 0.87; 95% CI, 0.62-1.2

30 r CCBs at 3 years; beta-blockers, 1.47%; and CCBs, 1.48% at 5 years).

31 t among patients receiving beta-blockers and CCBs (0.38% for both beta-blockers and CCBs at 1 year; 0

32 s and CCBs (0.38% for both beta-blockers and CCBs at 1 year; 0.91% for beta-blockers and 0.93% for CC

33 revalence among those taking cyclosporin and CCBs (76%) and the lowest among tacrolimus users not on

34 of ARBs, ACEi, beta blockers, diuretics, and CCBs.

35 yme inhibitors (ACEIs), calcium antagonists (CCBs) and alpha-blockers in preventing one or more major

36 hyperlipidemia, and hypertension, use of any CCBs remained associated with an increased risk of devel

37 In bivariate analysis, use of any CCBs was associated with an increased risk of POAG (odds

38 ent of yttrium in coals and their associated CCBs.

39 o a small molecule inhibitor cytochalasin B (CCB) at resolutions of 3.3 angstrom in both detergent mi

40 onocarboxylate transport and cytochalasin B (CCB) to inhibit glucose transport, we examined the role

41 Our clinical counseling-based (CCB) cohort consists of 3,297 individuals across 124 fam

42 Massachusetts Bay (MB) and Cape Cod Bay (CCB) together comprise one of seven areas in the Gulf of

43 d analysis, there was no association between CCB use for 2-<12 years and breast cancer: All 95% confi

44 ts have reported strong associations between CCB use and bladder hyperactivity, opposing expectations

45 e performed to evaluate associations between CCB use and POAG.

46 oncern about a potential causal link between CCB use and an increased risk for cancer development.

47 es of Caco-2 cell membrane-coated biosensor (CCB) using electrochemical impedance spectroscopy (EIS).

48 : 48 demonstrated complete conduction block (CCB) and 27 demonstrated intact Purkinje activation (IPA

49 ence and level of complete conduction block (CCB) in the His-Purkinje system.

50 children includes calcium channel blockade (CCB) for acute responders with vasodilator testing and c

51 ), beta-blocker, or calcium channel blocker (CCB) from 2010 to 2017.

52 a T-type and L-type calcium channel blocker (CCB) released in the United States in 1997 for managemen

53 ble prognosis using calcium-channel blocker (CCB) therapy.

54 s were matched with calcium channel blocker (CCB) users using propensity score matching (PSM).

55 22,941, or 7.05%), calcium-channel blocker (CCB, 2791 of 38,607, or 7.23%), placebo (1686 of 24,767,

56 itro potency and no calcium channel-blocker (CCB) activity.

57 Calcium channel blockers (CCB) are considered the agents of choice to treat hypert

58 Calcium channel blockers (CCB) are widely prescribed anti-hypertensive agents.

59 Calcium channel blockers (CCB) improve TB treatment outcomes in pre-clinical model

60 Calcium channel blockers (CCB) improve TB treatment outcomes in preclinical models

61 c oxide (iNO), and calcium channel blockers (CCB) in 10 patients with BPD who underwent cardiac cathe

62 poglycemic agents, calcium channel blockers (CCB), insulin, and diuretics were significantly higher i

63 Treatment with calcium channel blockers (CCB), proven to be beneficial in a subset of patients wi

64 ut respond well to calcium channel blockers (CCB).

65 r the past decade, calcium channel blockers (CCBs) and ACE inhibitors have been used increasingly in

66 for the effect of calcium channel blockers (CCBs) and supragingival plaque.

67 Calcium channel blockers (CCBs) are an important class of drugs in managing cardio

68 Calcium channel blockers (CCBs) are prescribed to patients with Marfan syndrome fo

69 overactivity with calcium channel blockers (CCBs) have been unsuccessful, creating an unsolved myste

70 ive agents such as calcium channel blockers (CCBs) in patients with chronic kidney disease (CKD).

71 ent with high-dose calcium channel blockers (CCBs) is recommended.

72 h long-term use of calcium channel blockers (CCBs) or angiotensin-converting enzyme inhibitors (ACEis

73 Calcium channel blockers (CCBs) represent a chemically and pharmacologically diver

74 ilar results using calcium channel blockers (CCBs) such as amlodipine, which inhibited prosurvival ER

75 The potential of calcium channel blockers (CCBs) to induce gingival enlargement (GE) as well as the

76 beta-blockers, and calcium channel blockers (CCBs) were identified.

77 ut associations of calcium channel blockers (CCBs) with outcomes in patients with heart failure and p

78 (ACE) inhibitors, calcium channel blockers (CCBs), alpha-blockers, and angiotensin receptor blockers

79 diones (TZDs), and calcium channel blockers (CCBs), on the risk of developing diabetic macular edema

80 h also metabolizes calcium channel blockers (CCBs).

81 me inhibitors, and calcium channel blockers [CCBs]) were matched to each other using propensity score

82 lytic (atosiban vs calcium channel blockers [CCBs]).

83 ockers, diuretics, calcium channel blockers [CCBs], alpha-agonists, angiotensin-converting enzyme inh

84 i], beta blockers, calcium-channel blockers [CCBs], or diuretics) with follow-up of at least 1 year.

85 se who received either ACEIs, beta-blockers, CCBs, or a combination of these antihypertensive medicat

86 come individuals); catastrophic cost burden (CCB) defined as OOP spending greater than 40% of postsub

87 PGE2 in the brain and this was abrogated by CCB.

88 owest for ARB and ACE inhibitors followed by CCB and placebo, beta blockers and diuretics in rank ord

89 of REE including coal combustion byproducts (CCBs).

90 ext, a selective COX-2 inhibitor, Celecoxib (CCB), was used with social stress.

91 This study aimed to simulate chronic CCB treatment and to examine both the functional and tra

92 DHP-CCB use may lower all-cause mortality in TB patients wit

93 There was no association between DHP-CCB use and infection-related mortality (HR 0.78, 95%CI:

94 There were no associations between DHP-CCB use and infection-related mortality (HR, 0.78; 95% C

95 Dihydropyridine-CCB (DHP-CCB) use was associated only with reduced all-cause mort

96 Dihydropyridine-CCB (DHP-CCB) use was associated with reduced all-cause mortality

97 Is were predominantly male and had diabetes, CCB users were generally older (eg, >65 years), and beta

98 m cell lines and exposed them to 4 different CCBs-nifedipine, amlodipine, diltiazem, and verapamil-at

99 fy the transcriptome signatures of different CCBs in human cardiomyocytes.

100 1 or more CCB, 28.2% used a dihydropyridine CCB, and 2.2% used a nondihydropyridine CCB.

101 rogression is not known, but dihydropyridine CCB should be used cautiously in African Americans with

102 A number of known 1,4-dihydropyridine CCBs were identified as having comparable potency to the

103 ; 95% CI, 1.04-2.14) but not dihydropyridine CCBs (hazard ratio, 1.04; 95% CI, 0.83-1.32).

104 d by type of CCB, the use of dihydropyridine CCBs (OR: 1.31, 95% CI: 1.14-1.50, P < 0.001) was associ

105 Use of dihydropyridine CCBs was associated with a significantly higher risk of

106 ta-blockers who began taking dihydropyridine CCBs.

107 her divided into exposure to dihydropyridine CCBs and nondihydropyridine CCBs, and subgroup analyses

108 Dihydropyridine-CCB (DHP-CCB) use was associated only with reduced all-c

109 Dihydropyridine-CCB (DHP-CCB) use was associated with reduced all-cause

110 s were 23.7, 21.6, and 23.8 in the diuretic, CCB, and ACE inhibitor groups, respectively, at 23 years

111 e trapped in the endoplasmic reticulum (ER), CCB-1 and UNC-36 fail to colocalize with UNC-2 in the ER

112 rs, and 11.2% lived in families experiencing CCBs.

113 rd ratio [AHR], 0.97 [95% CI, 0.89-1.05] for CCB vs diuretic; AHR, 1.06 [95% CI, 0.97-1.15] for ACE i

114 Propensity scores for CCB initiation, calculated for each of the 7514 patients

115 year; 0.91% for beta-blockers and 0.93% for CCBs at 3 years; beta-blockers, 1.47%; and CCBs, 1.48% a

116 Advertising for CCBs increased from 4.6% of advertising pages in 1985 to

117 art failure, new discharge prescriptions for CCBs had no associations with composite or individual en

118 nts received new discharge prescriptions for CCBs.

119 ing and not receiving CCBs (hazard ratio for CCBs, 1.03; 95% confidence interval, 0.92-1.14).

120 Extraction of REE from CCBs can be advantageous as it involves reusing a waste

121 ason when right whales congregate to feed in CCB.

122 f 8.6 (6, 11.5) and 8.2 (5.9, 11.2) years in CCB users and controls, respectively.

123 iterature reports on the abundance of REE in CCBs globally, studies examining the key factors which c

124 Exposures included CCB or ACEi use of 1-12 years' duration, determined from

125 ty response criteria and received an initial CCB alone (n=123) or in combination with another PAH the

126 emained on CCB monotherapy, 14.7% on initial CCB plus another initial PAH therapy, and the remaining

127 was defined as alive with unchanged initial CCB therapy with or without other initial PAH therapy an

128 ug.kg(-1) and capability of detection limit (CCB) ranged 0.032-0.233 ug.kg(-1).

129 rted EPSPs after administration of 50 microM CCB, whereas CCB failed to alter the slow decay of pyruv

130 ong patients with POAG, 32.6% used 1 or more CCB, 28.2% used a dihydropyridine CCB, and 2.2% used a n

131 Moreover, CCB reduced RSD-induced Hypothalamic-Pituitary-Adrenal (

132 The effect of a new CCB, amlodipine, has not been established.

133 those receiving amlodipine and nonamlodipine CCBs.

134 dine CCB, and 2.2% used a nondihydropyridine CCB.

135 dihydropyridine CCBs and nondihydropyridine CCBs, and subgroup analyses were performed using chi-squ

136 ified potential effect of nondihydropyridine CCBs on diverticulosis risk could have clinical implicat

137 sociation was specific to nondihydropyridine CCBs (hazard ratio 1.49 considering thiazide diuretic ag

138 Nonetheless, CCB blocked anxiety-like behavior in response to RSD.

139 Two percent (n = 397) of CCB users and 1.9% (n = 1,733) of ACEi users developed b

140 a(1) localizes to AZs even in the absence of CCB-1/beta or UNC-36/alpha(2)delta, albeit at low levels

141 cated that Rab11 is positioned downstream of CCB within this axonal transport system.

142 y the limited information on the duration of CCB exposure in this cohort.

143 ly evaluate associations between duration of CCB or ACEi use and breast cancer in hypertensive women

144 ria and cutoffs on the estimated duration of CCB use.

145 mber 31, 2008), 7514 had no prior history of CCB use.

146 required for the presynaptic localization of CCB-1 and UNC-36.

147 The site of CCB was localized to the level of the left-sided His fib

148 When stratified by type of CCB, the use of dihydropyridine CCBs (OR: 1.31, 95% CI:

149 The presence of hypertension or the use of CCB did not result in a significant change in microbiolo

150 lthough the acute pharmacological actions of CCBs in the hearts are well-defined, little is known abo

151 hospitalization, regardless of the class of CCBs.

152 As) and veins (MVs) to the dilator effect of CCBs.

153 this review demonstrated that the effects of CCBs on apoptosis are complex as both increases and decr

154 Long-acting formulas of CCBs appear to decrease congestive heart failure in pati

155 risk status at 12 months after initiation of CCBs.

156 association was stronger for monotherapy of CCBs with direct cardiac effects (OR, 1.96; 95% CI, 1.23

157 t an effect (either positive or negative) of CCBs on apoptosis requires doses in the supra-pharmacolo

158 Increasing promotion of CCBs has mirrored trends in physician prescribing.

159 detail the unsuccessful urological trials of CCBs and the promise of Cav1.2 agonists as potential nov

160 relationship between the therapeutic use of CCBs and an increased incidence of cancer development as

161 tentially harmful association between use of CCBs and glaucoma prevalence.

162 nificant risk factors for GE were the use of CCBs and the widespread presence of abundant supragingiv

163 imally adjusted multivariable models, use of CCBs was associated with a higher prevalence of glaucoma

164 univariate analysis stratified by the use of CCBs, but multivariate analysis revealed that the only s

165 r differences between patients on and not on CCB, there was still no evidence of an interaction betwe

166 At 12 months, 53.2% remained on CCB monotherapy, 14.7% on initial CCB plus another initi

167 Treatment success on CCB decreased significantly when acute responders became

168 Among the 580 patients (27%) on CCBs at enrollment, at 28 days, the combined end point w

169 f clopidogrel was similar in patients not on CCBs at 1 year (HR, 0.78; 95% CI, 0.56-1.09).

170 el treatment and CCB (HR for patients not on CCBs, 0.87; 95% CI, 0.62-1.23; HR for patients on CCBs,

171 lopidogrel in patients on CCBs versus not on CCBs.

172 eatment effect of clopidogrel in patients on CCBs versus not on CCBs.

173 0.87; 95% CI, 0.62-1.23; HR for patients on CCBs, 0.74; 95% CI, 0.45-1.21).

174 ment in patients with T2DM, whereas those on CCBs experienced an increased risk.

175 ificant damage during glucose deprivation or CCB administration.

176 reated with RASi, who initiated diuretics or CCB.

177 itiated on GLP-1 RAs, fenofibrates, TZDs, or CCBs.

178 switching patients to amlodipine from other CCB for reasons of cost.

179 Among patients with LBB block pattern, CCB within the proximal left conduction system was obser

180 ECG criteria for LBBB incompletely predicted CCB, and intracardiac data might be useful in refining p

181 In the absence of UNC-2, presynaptic CCB-1 and UNC-36 are profoundly diminished to barely det

182 received beta-blockers, and 448 589 received CCBs.

183 81% of patients receiving and not receiving CCBs (hazard ratio for CCBs, 1.03; 95% confidence interv

184 omen; 10% black) receiving and not receiving CCBs, balanced on 114 baseline characteristics.

185 mcitabine resistance and suggest that select CCBs may provide a clinical benefit to PDAC patients rec

186 l death and damage to myofilament structure, CCBs elicited line-specific inhibition on calcium kineti

187 m acute degradation of the CaV2 beta-subunit CCB-1.

188 of inherited thoracic aortic aneurysm taking CCBs display increased risk of aortic dissection and nee

189 ong older women with hypertension, long-term CCB use does not increase breast cancer risk and long-te

190 ork supporting the CCB system and found that CCB colocalizes and coimmunoprecipitates with Rab11.

191 l to provide support for the hypothesis that CCB use is associated with an increased susceptibility f

192 This study reveals that CCB is part of a novel transport system that delivers ce

193 In this manuscript, we show that CCB is involved in axonal trafficking of FasII and synap

194 In CREDO, there was no evidence that CCBs decrease the efficacy of clopidogrel.

195 There is little evidence at present that CCBs offer a major advantage over other antihypertensive

196 eclinical studies, it has been proposed that CCBs may work differently in humans by interfering with

197 Several studies have reported that CCBs reduce the ability of clopidogrel to inhibit platel

198 t platelet aggregability; one suggested that CCBs reduce the efficacy of clopidogrel.

199 the CCB had an excellent limit of detection of ~11.46 nM and

200 In addition, the CCB showed high selectivity against various interfering

201 therapy, and the remaining patients had the CCB withdrawn and/or PAH therapy added.

202 y analyzed data from 107 193 patients in the CCB cohort, 76 583 in the GLP-1 agonists cohort, 25 657

203 ear (mean [95% confidence intervals]) in the CCB users and -0.35 (-0.37 to -0.33) dB/year in the matc

204 Determining causality of the CCB association should be a research priority.

205 herapeutic concentrations (nanomolar) of the CCB nifedipine while higher than therapeutic concentrati

206 UK Biobank identified an association of the CCB standardized genetic risk score with increased risk

207 Overall, the CCB has excellent potential for practical use such as po

208 tigated the molecular network supporting the CCB system and found that CCB colocalizes and coimmunopr

209 We propose that the CCB/Rab11/SPIRE system regulates axonal trafficking of s

210 The long-term stability of the CCBs was also verified for 3 weeks using EIS.

211 is transferred in bulk from the coals to the CCBs.

212 B pattern, ranging from no discrete block to CCB.

213 Compared to CCB, diuretic use was associated with a lower risk of MA

214 n venous SMCs to confer venous resistance to CCB-induced dilation, a fundamental drug property that w

215 d to atosiban compared with those exposed to CCBs (RR, 0.94; 95% CI, 0.67-1.32; P = .71).

216 esolve the mechanism of venous resistance to CCBs.

217 eactivity response for long-term response to CCBs and other outcomes.

218 Long-term response to CCBs was defined as alive with unchanged initial CCB the

219 sustained satisfactory clinical response to CCBs.

220 difference in odds of OH with vasodilators (CCBs, ACE inhibitors/ARBs, SSRIs), compared to placebo.

221 eta-blocker, and 601 002 patients for ARB vs CCB.

222 s, 28,423 were ACEi/ARB users, and 7565 were CCB users.

223 ter administration of 50 microM CCB, whereas CCB failed to alter the slow decay of pyruvate-supported

224 Whether CCB treatment is detrimental to human lymphatic vessel f

225 g and prescribing patterns could explain why CCBs have supplanted better-substantiated therapies for

226 ted with CCB (40 of 48 patients [83.3%] with CCB vs 13 of 27 patients [48.1%] with IPA had a notch or

227 plexes of lateral leads were associated with CCB (40 of 48 patients [83.3%] with CCB vs 13 of 27 pati

228 te of VF mean deviation (MD) associated with CCB use and other covariates (for the MV analysis).

229 d major adverse cardiac events compared with CCB use.

230 (HR: 0.97, 95% CI: 0.86-1.10) compared with CCB.

231 hypertension has significantly improved with CCB and epoprostenol.

232 The site of block in patients with CCB was at the level of the left His bundle in 72% and i

233 ents with LBBB pattern and 85% of those with CCB (94% left intrahisian, 62% proximal left bundle-bran

234 For acute responders treated with CCB (n=31), survival at 1, 5, and 10 years was 97%, 97%,

235 ts with excellent survival when treated with CCB therapy.

236 acute responders, only 23% were treated with CCB without additional PAH-targeted therapy.

237 who had excellent outcome when treated with CCB.

238 en who are acute responders are treated with CCB; they are treated with epoprostenol if they become n

239 ponders to AVT and subsequent treatment with CCB therapy demonstrated large discrepancies with curren

240 OR 1.14, 95% CI 1.04-1.24; p=0.004) and with CCBs (1.06, 1.01-1.12; p=0.02).

241 Compared with CCBs, low-dose diuretics were associated with reduced ri

242 Unexpectedly, Marfan mice treated with CCBs show accelerated aneurysm expansion, rupture, and p

243 ng was assessed in patients with and without CCB in the left bundle.