ライフサイエンスコーパス: BID

1 allenge model of lung inflammation (20 mg/kg bid).

2 ia the BH3 interacting-domain death agonist (BID).

3 00 mg administered once (qd) or twice daily (bid).

4 d the barrier discharge ionisation detector (BID).

5 ng ligand, and BH3 interacting-domain death (BID).

6 ith activation by BH3 only proteins (BIM and BID).

7 rolimus (Prograf) bid, or cyclosporine (CsA) bid.

8 chondria upon caspase-mediated activation of BID.

9 1% (n = 192), or brimonidine 0.2% (n = 175) BID.

10 riptional regulation of the BH3-only protein Bid.

11 ned on day -14 while patients were under TAC BID.

12 nt intrinsic PK properties of Tac QD and Tac BID.

13 nt intrinsic PK properties of Tac QD and Tac BID.

14 43) comparing dabigatran 150 mg bid with 110 bid.

15 ned on day -14 while patients were under TAC BID.

16 6 to -0.34, p = 0.01) with dabigatran 150 mg bid.

17 2 levels and preventing cleavage of MDM2 and BID.

18 men of LBN 0.024% qpm or timolol 0.5% 1 drop BID.

19 rapy for women with IBS-C at a dose of 8 mug BID.

20 gnificantly different from dabigatran 110 mg BID.

21 d activation of caspase-8 and/or cleavage of Bid.

22 mouse model, upon dosing at 30 and 100 mg/kg BID.

23 eaved to short-lived, proapoptotic truncated Bid.

24 ics for ticagrelor 60 mg compared with 90 mg bid.

25 h levels were slightly lower with DRV QD and BID.

26 ted with pomaglumetad, 40 mg (but not 80 mg) BID.

27 HCG, suggesting a tumor-promoting effect of BID.

28 ociated protein with death domain (FADD), or Bid.

29 patocyte proliferation were not modulated by BID.

30 n etexilate, in 2 doses (150 mg twice daily [BID], 110 mg BID), and the oral Factor Xa inhibitors, ri

31 vaniprevir (300 mg twice-daily [BID], 600 mg BID, 600 mg once-daily [QD], or 800 mg QD) for 28 days,

32 d placebo or vaniprevir (300 mg twice-daily [BID], 600 mg BID, 600 mg once-daily [QD], or 800 mg QD)

33 reated with tofacitinib 0.005% QD and 0.003% BID: 71% and 67% of baseline, respectively, compared wit

34 than in patients treated qd (mean qd versus bid: 90% versus 99%, P < 10(-7)).

35 ls in the rodent with brain iron deficiency (BID), a pathogenetic model of restless legs syndrome (RL

36 In BID, a certain volume of air is introduced into the extr

37 Both the 4 mg BID ABT-894 and atomoxetine groups demonstrated signific

38 s were also significantly improved with 4 mg BID ABT-894.

39 ng EFV in combination with atovaquone 750 mg BID achieved an atovaquone C avg>18.5 microg/mL, a conce

40 Ticagrelor 60 mg bid achieved high levels of peak and trough platelet inh

41 relatively resistant to agents that require BID activation for maximal induction of apoptosis, inclu

42 le safety profile that is suitable for QD or BID administration.

43 d as a twice-daily formulation (Prograf, Tac BID), although a once-daily formulation (Advagraf, Tac Q

44 d as a twice-daily formulation (Prograf, Tac BID), although a once-daily formulation (Advagraf, Tac Q

45 4 to -0.21, p = 0.02) with dabigatran 110 mg bid and -1.08 (95% CI: -1.86 to -0.34, p = 0.01) with da

46 In patients with AF, dabigatran 110 mg bid and 150 mg bid are associated with similar rates of

47 he net clinical benefit of dabigatran 110 mg bid and 150 mg bid with that of warfarin in patients wit

48 receiving cART at atovaquone doses of 750 mg BID and 1500 mg BID, respectively (P</= .01).

49 ned with 2 reduced dronedarone doses (150 mg BID and 225 mg BID; chosen to reduce dronedarone's negat

50 Mean AUC0-24 hr was 279.8 ng mL/hr for TAC BID and 278.7 ng mL/hr for TAC QD (P=0.92).

51 Mean AUC0-24 hr was 279.8 ng mL/hr for TAC BID and 278.7 ng mL/hr for TAC QD (P=0.92).

52 CONCLUSION.: Both apremilast 20 mg BID and 40 mg QD demonstrated efficacy versus placebo an

53 sic pathway of apoptosis through cleavage of bid and activation of bax.

54 and occurred in association with cleavage of Bid and activation of caspase 9.

55 In contrast, the combined inhibition of Bid and Bax elicits an anti-apoptotic response that is e

56 Therefore, BID and BIM have nonoverlapping roles in the induction o

57 etexilate 110 mg twice daily (bid) or 150 mg bid and correlated with the clinical outcomes of ischemi

58 Choosing between dabigatran etexilate 110 mg BID and dabigatran etexilate 150 mg BID requires a caref

59 cluding the extraction of the analytes by HS-BID and GC/MS analysis of the analyte-enriched solvent,

60 -422 xenograft model when dosed at 160 mg/kg BID and is currently in Phase I clinical trials.

61 marked decrease in caspase-8, -3, cFLIP(S), Bid and Mcl-1 expression but Bak remained unchanged, alt

62 by hyperosmotic shock induces proteolysis of Bid and mono-ubiquitinated Bid at Asp-52 increasing the

63 ioavailability in steady state is similar in BID and QD formulations after conversion in stable LT re

64 ioavailability in steady state is similar in BID and QD formulations after conversion in stable LT re

65 to compare the pharmacokinetics (PK) of TAC BID and TAC QD in stable, adult LT patients.

66 to compare the pharmacokinetics (PK) of TAC BID and TAC QD in stable, adult LT patients.

67 , Gli1 inhibition affected the expression of Bid and the association of replication protein A (RPA) w

68 xpression of pro-apoptotic factors including Bid and Trb3.

69 ed 2 doses of ticagrelor, 90 mg twice a day (bid) and 60 mg bid, for long-term prevention of ischemic

70 gned 28 days of tegobuvir 40 mg twice-daily (BID) and GS-9256 75 mg BID (n = 16), tegobuvir and GS-92

71 in 2 doses (150 mg twice daily [BID], 110 mg BID), and the oral Factor Xa inhibitors, rivaroxaban and

72 In addition, proapoptotic (FasL, Bid, and activation of caspase-8 and caspase-3) and surv

73 pendent manner, and had lower levels of Bad, Bid, and Bax proapoptotic proteins compared with control

74 tion and subsequent activation of caspase-8, Bid, and Bax.

75 sion and sequential inhibition of caspase-8, Bid, and Bax.

76 downregulation; 2) activation of caspase-8, Bid, and Bax; and 3) subsequent mitochondrial depolariza

77 ptor pathway, caspase 8-mediated cleavage of BID, and BID-dependent activation of poised BAX at the m

78 tigations revealed that the presence of BAX, BID, and BIM differentially regulated the ability of BH3

79 ependent cell death constituent activated by Bid, and mitochondrial AIF expression was attenuated by

80 bitory effect on both Bax and GzmB-truncated Bid, and promotes GzmB-induced mitochondrial outer membr

81 pregulated Noxa results in the activation of Bid, and the consequent induction of apoptosis is inhibi

82 of activated pro-apoptotic proteins Bax and Bid, and to a lesser extent Bim; (iii) loss of mitochond

83 th upregulation of the proapoptotic molecule Bid, and was blocked by Bcl2 overexpression.

84 ed to compare 4 therapies: dabigatran 150 mg BID, apixaban 5 mg BID, rivaroxaban 20 mg QD, and warfar

85 ts with AF, dabigatran 110 mg bid and 150 mg bid are associated with similar rates of death.

86 ith genetic or pharmacological inhibition of BID are protected from Fas-mediated impairment of mitoch

87 -TRAF1, Asp-BRCA1, Leu-LIMK1, Tyr-NEDD9, Arg-BID, Asp-BCL(XL), Arg-BIM(EL), Asp-EPHA4, and Tyr-MET be

88 es proteolysis of Bid and mono-ubiquitinated Bid at Asp-52 increasing the release of cytochrome c and

89 tolerance mechanisms and the BCL9L/caspase-2/BID axis may limit cancer diversity and evolution.

90 uire the expression of the BH3 proteins Bim, Bid, Bad, Noxa, or Puma.

91 DTG 50 mg BID-based therapy was effective in this highly treatment

92 months of postoperative follow-up and on TAC BID-based therapy were converted to TAC QD on a 1:1 (mg/

93 months of postoperative follow-up and on TAC BID-based therapy were converted to TAC QD on a 1:1 (mg/

94 ession of B-cell lymphoma 2 family proteins (Bid, Bcl-xl, and Mcl-1) and stimulates caspase activatio

95 d-labeled Bax molecules, after activation by Bid, became localized strictly at pore edges.

96 We identified Atg5, Atg7, Bax, Bid, Bik, and Noxa as potential therapeutic targets for

97 the cooperation of multi BH3-only proteins (BID, BIK, PUMA) and the reciprocal suppression of the pr

98 apoptosis can proceed through caspase-8 and BID, but reduction in or loss of these players generally

99 ycle arrest involving activation cleavage of BID by caspase-8 and upregulation of p27, respectively.

100 ith apixaban compared with dabigatran 150 mg BID (by 26%) and rivaroxaban (by 34%), but not significa

101 Thus, our results indicate TAC BID can be safely switched to the more convenient QD for

102 Thus, our results indicate TAC BID can be safely switched to the more convenient QD for

103 Today we know that Bid can response to multiple types of proteases, which a

104 2, Cxcr7, Lgals1, Pla2g7, Rgs13, S1pr3, Spn, Bid, Cd55, Prf1, and Tlr3.

105 ced dronedarone doses (150 mg BID and 225 mg BID; chosen to reduce dronedarone's negative inotropic e

106 HARMONY tested midrange ranolazine (750 mg BID) combined with 2 reduced dronedarone doses (150 mg B

107 .82% and 0.81% with dabigatran 110 or 150 mg BID compared with 0.64% with warfarin (hazard ratio [HR]

108 nd photosensitivity were increased at 240 mg BID compared with the 240 mg QD dose.

109 mic embolism (by 26%) for dabigatran (150 mg BID) compared with rivaroxaban, as well as hemorrhagic s

110 volume at a dose of 3 mg/kg administered ip, bid, days 1-9.

111 ffect in bax-deficient neurons but protected bid-deficient neurons similarly to wild-type cells.

112 way, caspase 8-mediated cleavage of BID, and BID-dependent activation of poised BAX at the mitochondr

113 and Mfn1/2(-/-) cells show dysregulation of Bid-dependent apoptotic signaling.

114 IAP-mediated immune response by inducing the BID-dependent release of SMAC from the mitochondria.

115 ograph with barrier ionization discharge (GC-BID) detection.

116 When using the sensitive BID detector, other trace volatile compounds are observe

117 detector and under 3 min when utilising the BID detector.

118 resistant patients at the 50 mg twice daily (BID) dose.

119 epsilon(2) was high with bid dosing (mean 750 mg and 1500 mg: 98.0% and 99.8%, re

120 istent with its role in DNA damage response, Bid down-regulation in tumor cells abolished CPT-induced

121 e-blind to placebo, ranolazine alone (750 mg BID), dronedarone alone (225 mg BID), or one of the comb

122 placebo (P=0.008), whereas ranolazine 750 mg BID/dronedarone 150 mg BID reduced AFB by 43% (P=0.072).

123 Conversely, ranolazine 750 mg BID/dronedarone 225 mg BID reduced AFB by 59% versus pla

124 tain DRV 800 mg QD or switch to twice-daily (BID) DRV 600 mg; all received OBV/PTV/r + DSV + RBV for

125 n medication (fluticasone propionate 100 mug bid) during 2 weeks before the study day.

126 Thus, Bid engages a ROS-dependent, local intermitochondrial po

127 ath, provided that there is a strong caspase/Bid feedback loop; however, the efficacy of the treatmen

128 for 8 (B) or 12 weeks (C and D), or placebo BID for 12 weeks (E).

129 ) for 14 days followed by atovaquone 1500 mg BID for 14 days, or vice-versa, with a washout period in

130 apy (Proton-Pump Inhibitor + Amoxicillin 1 g bid for 5 days and Proton-Pump Inhibitor + Clarithromyci

131 7-9 days) or ticagrelor (180 mg, then 90 mg BID for 7-9 days).

132 twice-daily (BID) for 12 weeks (A), 1,000 mg BID for 8 (B) or 12 weeks (C and D), or placebo BID for

133 ergan Inc., Irvine, CA]), or vehicle control BID for 8 weeks.

134 rently recommended dose of atovaquone 750 mg BID for treatment of mild to moderate PCP may not be ade

135 solized budesonide/formoterol versus placebo bid for up to 5 days.

136 icitabine at a dosage of 500 mg twice-daily (BID) for 12 weeks (A), 1,000 mg BID for 8 (B) or 12 week

137 Oral naltrexone (30 mg/kg, bid) for 14 days also reduced ethanol intake; however, t

138 y assigned to atovaquone 750 mg twice daily (BID) for 14 days followed by atovaquone 1500 mg BID for

139 he morning or timolol instilled twice a day (BID) for 3 months.

140 th the DPPIV inhibitor sitagliptin (40 mg/kg BID) for 6 weeks, whereas the remaining rats were admini

141 mg, 10 mg, or 15 mg, or placebo twice daily (BID) for 8 weeks.

142 rotein BH3 interacting-domain death agonist (BID) for chronic liver injury (CLI) and hepatocarcinogen

143 icagrelor, 90 mg twice a day (bid) and 60 mg bid, for long-term prevention of ischemic events in pati

144 e daily (BID), placebo, or risperidone, 2 mg BID, for up to 6 weeks.

145 n be linked by caspase-8-activated truncated Bid formation.

146 for extraction for 20 min), the automated HS-BID gave low limits of detections (between 0.012 and 0.0

147 choice test MT-7716 (0, 0.3, 1, and 3 mg/kg, bid) given orally for 14 days dose-dependently decreased

148 DTG 50 mg BID had a low (3%) discontinuation rate due to adverse e

149 monidine 0.2% fixed combination administered BID had a significantly greater IOP-lowering effect than

150 eiving EFV-based cART plus atovaquone 750 mg BID had an atovaquone C avg>15 microg/mL, which has prev

151 (10 mg/mL four times a day [qid] or 12 mg/mL bid) had no significant effect.

152 nd, inhibition of caspase-8 and knockdown of Bid have no effect on DR6-induced apoptosis.

153 ics and pharmacodynamics of ticagrelor 60 mg bid have not been studied.

154 rly all patients, similar to that with 90 mg bid, helping to explain the efficacy of the lower ticagr

155 h fat diet-induced apoptosis is dependent on Bid; here we report that Bid-mediated apoptosis was requ

156 n of oxidative stress (OS) response and that BID impaired full activation of p38 after OS.

157 vidence that the tumor-promoting function of BID in CLI is not related to enhanced proliferation or a

158 s were lowest on dabigatran etexilate 110 mg BID in comparison with dabigatran etexilate 150 mg BID o

159 Conversely, complementation of Bid in Gli1-deficient cells restored CPT-induced Chk1 ph

160 This study inhibited Bid in mice using two pharmacological antagonists (BI-11

161 Dabigatran dose was 110 and 75 mg BID in patients with normal or impaired renal function (

162 ban; or rivaroxaban versus dabigatran 110 mg BID in preventing stroke and systemic embolism.

163 ences between apixaban and dabigatran 110 mg BID in safety endpoints.

164 In these conditions a significant amount of Bid in the cytosol is mono- and bi-ubiquitinated.

165 a novel connection between aberrant Gli1 and Bid in the survival of tumor cells and their response to

166 AX dimerization in response to (i) truncated BID in vitro and (ii) treatment of cancer cells with DNA

167 mg (N = 81) or placebo (N = 85) twice-daily (BID) in combination with pegylated interferon alpha-2a (

168 asone propionate (FP), (both 1 spray/nostril bid), in children with allergic rhinitis (AR).

169 n of cytochrome c release and also inhibited Bid-induced cell death, whereas both superoxide and hydr

170 Bid-induced mitochondrial membrane permeabilization and

171 Bak is critical for Bid-induced OMM permeabilization and cytochrome c releas

172 We report that Bid-induced permeabilization and cytochrome c release re

173 ll populations, the rate and lag time of the Bid-induced permeabilization are dose-dependent, but eve

174 hydrogen peroxide sensitized mitochondria to Bid-induced permeabilization.

175 In contrast, expression of Bid induces rapid caspase-3 activation, even in the abse

176 potential target for therapeutic control of Bid initiated cell death.

177 Bid is a Bcl-2 family protein that promotes apoptosis by

178 Bid is a proapopotic activator protein of the Bcl-2 fami

179 ts, whereas Bid mRNA does not, suggests that Bid is actively cleaved to short-lived, proapoptotic tru

180 Bid is also emerging-in its full-length form-as a pivota

181 Full-length Bid is cleaved in response to apoptotic stimuli into two

182 The BH3-interacting domain death agonist (Bid) is a pro-apoptotic member of the B-cell lymphoma-2

183 Tacrolimus twice-daily (TAC BID) is widely used in lung transplantation (LT), but th

184 Tacrolimus twice-daily (TAC BID) is widely used in lung transplantation (LT), but th

185 Further, mice bearing either wild-type or Bid knockout tumors responded to immunotoxin treatment w

186 he pro-apoptotic proteins (Bad, Bim, Bax and Bid) leading to cell loss.

187 tion, caspase-8 activation and truncation of BID, leading to apoptosis in both LNCaPshV and LNCaPshp5

188 e of caspase-2 and the pro-apoptotic factor, Bid, leading to subsequent release of mitochondrial cont

189 daprevir 240 mg QD/LI, 240 mg QD, and 240 mg BID/LI groups, respectively.

190 s in the 240 mg QD/LI, 240 mg QD, and 240 mg BID/LI groups, respectively.

191 ce a day [BID]), voriconazole (10 mg/kg p.o. BID), liposomal amphotericin B (10 mg/kg intraperitoneal

192 an the currently recommended dose of 1500 mg BID may achieve plasma concentrations adequate to treat

193 NF-induced JNK signaling and thereby blocked bid-mediated activation of the intrinsic mitochondrial a

194 sis is dependent on Bid; here we report that Bid-mediated apoptosis was required for complement activ

195 When administered bid, mericitabine reached a high, dose-dependent, final

196 bubble-in-drop microextraction (automated HS-BID) method, coupled to gas chromatography/mass spectrom

197 monotherapy: subcutaneous placebo injections BID + monthly 0.3 mg ranibizumab.

198 ination therapy: subcutaneous AKB-9778 15 mg BID + monthly 0.3 mg ranibizumab; or (3) ranibizumab mon

199 : subcutaneous AKB-9778 15 mg twice per day (BID) + monthly sham intraocular injections; (2) combinat

200 For tofacitinib 15 mg BID, most patients reported satisfaction or extreme sati

201 AICD-susceptible replicating blasts, whereas Bid mRNA does not, suggests that Bid is actively cleaved

202 ir 40 mg twice-daily (BID) and GS-9256 75 mg BID (n = 16), tegobuvir and GS-9256 plus RBV 1,000-1,200

203 study comparing 8 weeks of SC BNP (10 mug/kg bid) (n = 20) with placebo (n = 20) in patients with eje

204 randomized to receive atomoxetine (20-50 mg BID, N = 220) or placebo (N = 225) for 12 weeks.

205 ed to 12 weeks oral therapy with CAP (7.5 mg BID; n=6) or to no therapy (control; n=6).

206 e driven by contagion beliefs: when asked to bid on a sweater owned by a well-liked celebrity, partic

207 level impact of proapoptotic human truncated BID on the cellular network.

208 antly differ for concurrent ATV/r for 750 mg BID or 1500 mg BID when compared to the group not receiv

209 sic mitochondrial pathway by either cleaving Bid or activating Bim leading to the activation of Bak/B

210 s significantly lower with dabigatran 110 mg BID or apixaban.

211 effected by the activator BH3-only proteins BID or BIM, which have been considered to be functionall

212 ere administered deferiprone, 10 or 15 mg/kg BID or placebo, for 6 months.

213 andomized to receive either ticagrelor 90 mg BID or prasugrel 10 mg OD with a 15-day treatment period

214 comparison with dabigatran etexilate 150 mg BID or warfarin.

215 ith dabigatran etexilate 110 mg twice daily (bid) or 150 mg bid and correlated with the clinical outc

216 double-blind ranolazine (target dose 1000 mg bid) or placebo.

217 d 4 mg once daily (QD)) or 4 mg twice daily (BID) or the active comparator atomoxetine (40 mg BID) vs

218 lone (750 mg BID), dronedarone alone (225 mg BID), or one of the combinations.

219 subjects receiving placebo, apremilast 20 mg BID, or apremilast 40 mg QD; a 12-week treatment-extensi

220 lease (Astagraf XL) qd, tacrolimus (Prograf) bid, or cyclosporine (CsA) bid.

221 ticagrelor 180 mg loading followed by 90 mg bid, or prasugrel 60 mg loading followed by 10 mg od for

222 s (rivaroxaban: 20 mg QD, dabigatran: 150 mg BID, or warfarin) using 3-way propensity-matched samples

223 003%, 0.001%, 0.003%, or 0.005% twice daily [BID] or 0.005% once daily [QD]), active comparator (cycl

224 the evening was noninferior to timolol 0.5% BID over 3 months of treatment, with significantly great

225 43.5% of subjects receiving apremilast 20 mg BID (P<0.001) and 35.8% receiving 40 mg QD (P=0.002) ach

226 The ATM/ATR-Bid pathway is critically involved in preserving the qui

227 ither pomaglumetad, 40 or 80 mg twice daily (BID), placebo, or risperidone, 2 mg BID, for up to 6 wee

228 days (maintenance therapy: ticagrelor 90 mg BID plus aspirin 81 mg QD).

229 combination regimen of mericitabine 1,000 mg BID plus Peg-IFNalpha-2a/RBV is well tolerated and more

230 on preferences exist between these proteins: BID preferentially activates BAK while BIM preferentiall

231 together, these results show that as soluble Bid progresses toward a membrane-inserted state, it unde

232 An in silico analysis of the Bid promoter identified a putative Gli1 binding site, an

233 est that the caspase 8-dependent cleavage of Bid promotes intrinsic apoptotic signaling within the br

234 The BH3-only Bid protein is a critical sentinel of cellular stress in

235 The finding that full-length Bid protein significantly declines in AICD-susceptible r

236 of Fas receptor, caspases-3/7/8, and Bak/Bax/Bid proteins were determined.

237 also found in Fas-receptor and Bak, Bax, and Bid proteins; caspase mRNA decreases were also noted.

238 AUC0-24 hr and C24 for both QD (r=0.96) and BID (r=0.94) formulations.

239 AUC0-24 hr and C24 for both QD (r=0.96) and BID (r=0.94) formulations.

240 BID rats showed hypersensitivity of corticostriatal glut

241 eas ranolazine 750 mg BID/dronedarone 150 mg BID reduced AFB by 43% (P=0.072).

242 ly, ranolazine 750 mg BID/dronedarone 225 mg BID reduced AFB by 59% versus placebo (P=0.008), whereas

243 Dabigatran etexilate 150 mg BID reduced the primary outcome of stroke and systemic e

244 mice, oral pazopanib (40 mg/kg twice a day [bid]) reduced RLLR (0.84 to 0.58, P = 0.0014) and RRLR (

245 ne (99.51% vs. 90.35%) after 28 day 25 mg/Kg bid regimens with a more potent block in microfilarial p

246 veness, with mean t(1/2) = 13.9 hours in the bid regimens.

247 e 110 mg BID and dabigatran etexilate 150 mg BID requires a careful assessment of characteristics tha

248 t atovaquone doses of 750 mg BID and 1500 mg BID, respectively (P</= .01).

249 rapies: dabigatran 150 mg BID, apixaban 5 mg BID, rivaroxaban 20 mg QD, and warfarin therapy.

250 Bid's initial 'claim to fame' came from its ability-as a

251 Bid sensitivity of Bak-deficient mitochondria is regaine

252 Loss of BID significantly delayed tumor development in two mouse

253 Compared with the full-length Bid structure, a longer flexible loop between tBid helix

254 In contrast, BID suppresses p38 activity and facilitates malignant tr

255 It remains a mystery how tiny amounts of Bid synchronize the function of a large number of discre

256 d from Bcl-2 could be activated by truncated Bid (tBid) and could form BH3:groove homodimers but coul

257 al carrier homologue 2 (MTCH2) and truncated BID (tBID) was characterized.

258 teraction of fluorescently labeled truncated Bid (tBid) with a mitochondria-like supported lipid bila

259 the production of the MOMP-inducer truncated Bid (tBid), or a process that drives the spatial propaga

260 d for mitochondrial Bak import and truncated Bid (tBid)-induced apoptosis.

261 ct on the direct BAX/BAK "activators" BIM or BID (tBID).

262 antly greater IOP lowering than timolol 0.5% BID throughout the day over 3 months of treatment.

263 cin 500 mg + Metronidazole/Tinidazole 500 mg bid/tid in the following 5 days; group A) or a 10-day mo

264 aced on target selectivity and affinity in a bid to diminish off-target toxicity without compromising

265 and adjuvanticity of the formulations, in a bid to further manipulate the pharmacokinetic profiles o

266 c AUC0-24 improved after converting from Tac BID to Tac QD in stable renal transplant patients, espec

267 c AUC0-24 improved after converting from Tac BID to Tac QD in stable renal transplant patients, espec

268 ity of Tac AUC0-24 after converting from Tac BID to Tac QD.

269 ity of Tac AUC0-24 after converting from Tac BID to Tac QD.

270 9 and caspase-12, along with the cleavage of Bid to tBid, all upstream signals for caspase-3 activati

271 activates the calpain-dependent cleavage of BID to trigger the release of SMAC, which antagonizes th

272 BIM; BCL-2 interacting-domain death agonist, BID) to induce mitochondrial outer membrane permeabiliza

273 Bioinspired design (BID) traditionally has focused on a unit operation and s

274 d low-molecular-weight heparin compared with bid unfractionated heparin decreases pulmonary embolism

275 e cumulative incidence of delirium, assessed bid using the confusion assessment method for the ICU.

276 ly greater (P = 0.001) for tofacitinib 15 mg BID versus placebo.

277 on of the mitochondrial apoptotic program by Bid-via its recently identified receptor mitochondrial c

278 kg of body weight orally [p.o.] twice a day [BID]), voriconazole (10 mg/kg p.o. BID), liposomal ampho

279 or the active comparator atomoxetine (40 mg BID) vs placebo for 28 days.

280 ablations, and prescribed dabigatran 150 mg bid was admitted for an atrial fibrillation ablation pro

281 Short-term treatment with tofacitinib BID was associated with dose-dependent improvement in he

282 compared with rivaroxaban, dabigatran 110 mg BID was associated with less major bleeding (by 23%) and

283 AUC0-12 hr of TAC BID was higher than the AUC12-24 hr.

284 AUC0-12 hr of TAC BID was higher than the AUC12-24 hr.

285 ere was no in vivo or in vitro evidence that BID was involved in DNA damage response in hepatocytes a

286 was superior and dabigatran etexilate 110 mg BID was noninferior to warfarin in preventing stroke and

287 Dabigatran etexilate 110 mg BID was noninferior to warfarin in reducing stroke and s

288 rial showed that dabigatran etexilate 150 mg BID was superior and dabigatran etexilate 110 mg BID was

289 Dabigatran 150 mg BID was superior to rivaroxaban for some efficacy endpoi

290 Forty renal transplant patients on Tac BID were converted on a 1:1 (mg/mg) basis to Tac QD in a

291 Forty renal transplant patients on Tac BID were converted on a 1:1 (mg/mg) basis to Tac QD in a

292 Caspase-2 and Bid were necessary for activation of the canonical infla

293 prescription for dabigatran (110 and 150 mg bid) were compared with matched warfarin users with resp

294 r concurrent ATV/r for 750 mg BID or 1500 mg BID when compared to the group not receiving cART.

295 leaving the proapoptotic Bcl-2 family member Bid, which, together with Bax, induces mitochondrial out

296 with INI-resistant virus received DTG 50 mg BID while continuing their failing regimen (without ralt

297 : -0.80 to 0.43) comparing dabigatran 150 mg bid with 110 bid.

298 ic to grass pollen comparing OC000459 200 mg bid with placebo for 8 days.

299 benefit of dabigatran 110 mg bid and 150 mg bid with that of warfarin in patients with atrial fibril

300 240 mg QD without LI, or 240 mg twice daily (BID) with LI.