ライフサイエンスコーパス: BID

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

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

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

4 se reduction (maximum tolerated dose 1800 mg bid).

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

6 d the barrier discharge ionisation detector (BID).

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

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

9 d via a surgically inserted gastrostomy tube BID.

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

11 patocyte proliferation were not modulated by BID.

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

13 chondria upon caspase-mediated activation of BID.

14 1% (n = 192), or brimonidine 0.2% (n = 175) BID.

15 riptional regulation of the BH3-only protein Bid.

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

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

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

19 6 to -0.34, p = 0.01) with dabigatran 150 mg bid.

20 e, we detail the fibrillation between HN and BID.

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

22 gnificantly different from dabigatran 110 mg BID.

23 anzyme B activates the proapoptotic molecule Bid.

24 QD (PM) or timolol ophthalmic solution 0.5% BID.

25 t the criteria for noninferiority to timolol BID.

26 the patient was prescribed ivacaftor 150 mg BID.

27 2 levels and preventing cleavage of MDM2 and BID.

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

29 fically, it is known to complex with BAX and BID.

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

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

32 le-blind treatment to RUX (1.5% twice daily [BID], 1.5% once daily [QD], 0.5% QD, 0.15% QD), vehicle,

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

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

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

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

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

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

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

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

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

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

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

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

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

46 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

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

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

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

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

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

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

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

67 nt was the comparison between 1.5% RUX cream BID and vehicle in mean percentage change from baseline

68 ering medication, was noninferior to timolol BID and was associated with tolerable ocular AEs.

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 CsA CE twice daily [BID, low-dose] + vehicle BID) and vehicle patients were allocated to one of these

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

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

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

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

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

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

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

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

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

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

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

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

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

85 The data show that two distinct segments of BID are incorporated into the fiber structure, whereas o

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

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

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

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

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

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

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

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

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

102 2, Cxcr7, Lgals1, Pla2g7, Rgs13, S1pr3, Spn, Bid, Cd55, Prf1, and Tlr3.

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

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

105 .82% and 0.81% with dabigatran 110 or 150 mg BID compared with 0.64% with warfarin (hazard ratio [HR]

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

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

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

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

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

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

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

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

114 24 months of 91.5% (95% CI, 70.0-97.8) with BID dosing and an ORR of 79.2% (95% CI, 57.9-92.9) and a

115 harmacokinetics (PK) profile consistent with bid dosing in patients.

116 BID dosing maintained higher BTK occupancy and achieved

117 Small increments in occupancy attained by BID dosing relative to QD dosing compounded over time to

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

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

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

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

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

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

124 implant shoulder and the buccal bone plate (BID) effect.

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

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

127 BID fibers are similar to those produced using BAX; howe

128 BID fibers display both types of secondary structure in

129 osttransplant at 40 mg TID for 1 week, 40 mg BID for 1 week, followed by 40 mg daily thereafter, alon

130 o be safe in animals with a dose of 30 mg/kg BID for 12 days in the dose tolerance study.

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

132 200 mg (cohort 2), or 1800 mg (cohort 3) NAC bid for 12 weeks and then tid for 12 weeks.

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

134 effects on ECD, CV, or %HEX when dosed QD or BID for 3 months in eyes with OHTN or OAG.

135 Subsequently, patients could apply 1.5% RUX BID for 4 additional weeks of open-label treatment.

136 % QD), vehicle, or triamcinolone cream (0.1% BID for 4 weeks, then vehicle for 4 weeks).

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

138 7-9 days) or ticagrelor (180 mg, then 90 mg BID for 7-9 days).

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

140 , 2017, and December 31, 2017, were assessed bid for delirium throughout their ICU stay using the Con

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

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

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

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

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

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

147 e efficacious at 30 mg/kg dosed twice daily (BID) for 5 days with no observable signs of toxicity up

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

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

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

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

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

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

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

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

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

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

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

159 (10 mg/mL four times a day [qid] or 12 mg/mL bid) had no significant effect.

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

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

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

163 (250 mg BID orally for 2 weeks, then 500 mg BID if automated office blood pressure (AOBP) >140/90 mm

164 Finally, we show that Bid impacts necroptotic signaling through modulation of

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

166 Patients who transitioned to 1.5% RUX BID improved in all measures.

167 through upregulation of cathepsin B, Tnf and Bid in a neutrophil-independent manner.

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

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

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

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

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

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

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

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

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

177 Bid-induced mitochondrial membrane permeabilization and

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

193 aily [QID, high-dose] or CsA CE twice daily [BID, low-dose] + vehicle BID) and vehicle patients were

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

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

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

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

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

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

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

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

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

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

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

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

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

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

213 taneous enoxaparin 4,000 international units bid or therapeutic unfractioned heparin).

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 hibitor acalabrutinib at 100 mg twice daily (BID) or 200 mg once daily (QD) in 48 patients with relap

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

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

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

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

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

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

223 ere randomized 1:1:1 to placebo, 25 mg of OM BID, or to pharmacokinetically guided dose titration (OM

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

225 ects received firibastat for 8 weeks (250 mg BID orally for 2 weeks, then 500 mg BID if automated off

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

227 43.5% of subjects receiving apremilast 20 mg BID (P<0.001) and 35.8% receiving 40 mg QD (P=0.002) ach

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

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

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

231 hibitor (Group 1, n=709); rivaroxaban 2.5 mg bid plus dual antiplatelet therapy (DAPT; Group 2, n=709

232 hibitor (group 1, n=709); rivaroxaban 2.5 mg bid plus dual antiplatelet therapy (group 2, n=709); and

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

234 s, patients received 200 mg two times a day (BID), preceded by a titration period, and ended by a tap

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

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

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

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

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

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

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

242 nstrated therapeutic benefit at week 4; 1.5% BID provided the greatest improvement in Eczema Area and

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

244 BID rats showed hypersensitivity of corticostriatal glut

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

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

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

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

249 e fiber structure, whereas other portions of BID remain solvent-exposed and retain helical structure.

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

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

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

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

254 Bid sensitivity of Bak-deficient mitochondria is regaine

255 Loss of BID significantly delayed tumor development in two mouse

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

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

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

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

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

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

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

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

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

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

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

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

268 Active caspase-6 cleaved Bid to induce cytochrome c release, generating a feedfor

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

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

271 ectives and possible directions forward in a bid to transcend what has already been achieved in this

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

273 Further deletion of the BH3-only member Bid (to generate Vav CreBaxBakBid triple-knockout [TKO]

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

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

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

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

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

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

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

281 g scale score occurred within 36 hours (1.5% BID vs vehicle, -1.8 vs -0.2; P < .0001) and were sustai

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

298 : -0.80 to 0.43) comparing dabigatran 150 mg bid with 110 bid.

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.

301 FA ranging from 10.73% (Ardestan) to 13.51% (Bid Zard).