ライフサイエンスコーパス: vitamin K

1 er risk in relation to the dietary intake of vitamin K.

2 physiological function other than recycling vitamin K.

3 lation at the physiological concentration of vitamin K.

4 olecule with a chemical structure similar to vitamin K.

5 ylloquinone, the primary circulating form of vitamin K.

6 relation between circulating phylloquinone (vitamin K(1)) concentrations and type 2 diabetes by usin

7 asures of fasting circulating phylloquinone (vitamin K-1) and confirmed CVD events and mortality.

8 ciations of dietary intake of phylloquinone (vitamin K-1), menaquinones (vitamin K-2), and total vita

9 h the p.Arg98Trp mutation results in reduced vitamin K 2,3-epoxide reductase activity, the molecular

10 patients and results in high serum levels of vitamin K 2,3-epoxide, suggesting that supplemented vita

11 Menaquinone (MK) or vitamin K(2) is an important metabolite that controls th

12 Menaquinone (vitamin K(2)) plays a vital role in energy generation an

13 ylgeranyl pyrophosphate (GGpp) to synthesize vitamin K(2).

14 f phylloquinone (vitamin K-1), menaquinones (vitamin K-2), and total vitamin K with the development o

15 in both cell and mouse models and regulates vitamin K absorption in mice.

16 s (antithrombin dabigatran etexilate or anti-vitamin K acenocoumarol) was started 2 days before inocu

17 Vitamin K activates both hepatic coagulation factors and

18 A clinical trial could assess whether vitamin K administration improves COVID-19 outcomes.

19 Vitamin K also activates matrix Gla protein (MGP), which

20 treat analysis, with 80 allocated to receive vitamin K and 79 to receive placebo.

21 t infusion (BHI) supplemented with hemin and vitamin K, and a blend of SHI and BHI, each at 3 sucrose

22 al Direct Factor Xa Inhibition Compared With Vitamin K Antagonism for Prevention of Stroke and Emboli

23 l, Direct Factor Xa Inhibition Compared With Vitamin K Antagonism for Prevention of Stroke and Emboli

24 al Direct Factor Xa Inhibition Compared with Vitamin K Antagonism for Prevention of Stroke and Emboli

25 al Direct Factor Xa Inhibition Compared with Vitamin K Antagonism for Prevention of Stroke and Emboli

26 l, Direct Factor Xa Inhibition Compared With Vitamin K Antagonism for Prevention of Stroke and Emboli

27 synthetic cannabinoids, evidence of isolated vitamin K antagonism with or without bleeding, and detec

28 Vitamin K antagonist (eg, warfarin) use is nowadays chal

29 as compared with 14.7% of those receiving a vitamin K antagonist (hazard ratio, 0.69; 95% confidence

30 2), or standard therapy with a dose-adjusted vitamin K antagonist (once daily) plus DAPT for 1, 6, or

31 ment with low-molecular-weight heparin and a vitamin K antagonist (RR, 0.67; 95% CI, 0.37-1.20; I2 =

32 vention had less bleeding with apixaban than vitamin K antagonist (VKA) and with placebo than aspirin

33 ovascular rehospitalizations compared with a vitamin K antagonist (VKA) based triple therapy regimen.

34 ine, 37,539 patients (52%) were treated with vitamin K antagonist (VKA) monotherapy, 25,458 (35%) wit

35 The safety and effectiveness of non-vitamin K antagonist (VKA) oral anticoagulants, dabigatr

36 ry stenting traditionally are treated with a vitamin K antagonist (VKA) plus dual antiplatelet therap

37 omen treated with any of the following: 1) a vitamin K antagonist (VKA) throughout pregnancy; 2) low-

38 ing the association between switching from a vitamin K antagonist (VKA) to a direct oral anticoagulan

39 e increased risk of bleeding associated with vitamin K antagonist (VKA) treatment was particularly ev

40 s quality of anticoagulation control amongst vitamin K antagonist (VKA) users.

41 Use of low-dose aspirin, clopidogrel, a vitamin K antagonist (VKA), a direct oral anticoagulant,

42 Rapid reversal of vitamin K antagonist (VKA)-induced anticoagulation is of

43 zed ratio (INR) among subjects administrated Vitamin K antagonist (VKA)-triple therapy.

44 1.82 (95% CI, 1.76-1.89) for therapy with a vitamin K antagonist and an antiplatelet drug, 1.28 (95%

45 Trial to Evaluate the Safety of Apixaban vs Vitamin K Antagonist and Aspirin vs Aspirin Placebo in P

46 a P2Y(12) inhibitor to receive apixaban or a vitamin K antagonist and to receive aspirin or matching

47 safety profile equal or superior to that of vitamin K antagonist anticoagulants (VKAs) in the genera

48 well-controlled vitamin K antagonists or non-vitamin K antagonist anticoagulants.

49 may at least not be worse than that of major vitamin K antagonist bleeding, and probably better.

50 However, findings suggest that the UFH-vitamin K antagonist combination is associated with the

51 bination, a treatment strategy using the UFH-vitamin K antagonist combination was associated with an

52 Compared with the LMWH-vitamin K antagonist combination, a treatment strategy u

53 molecular weight heparin, fondaparinux, or a vitamin K antagonist for at least 2 months or, in childr

54 f death or hospitalization than those in the vitamin K antagonist group (23.5% vs. 27.4%; hazard rati

55 anticoagulation with warfarin or alternative vitamin K antagonist is the standard anticoagulant treat

56 In comparison with vitamin K antagonist monotherapy, adjusted hazard ratios

57 ischemic stroke-related hospitalizations in vitamin K antagonist naive patients and patients with CH

58 reater reductions with edoxaban were seen in vitamin K antagonist naive patients, patients with CHADS

59 tion of an OAC with warfarin sodium or a non-vitamin K antagonist OAC.

60 44 (59.8%) were treated with warfarin or non-vitamin K antagonist OACs.

61 09 (61.8%) were treated with warfarin or non-vitamin K antagonist OACs.

62 ence regarding ICH related to the use of non-vitamin K antagonist oral anticoagulant (NOAC) agents.

63 to determine if they are candidates for non-vitamin K antagonist oral anticoagulant (NOAC) therapy.

64 ticoagulation, either with warfarin or a non-vitamin K antagonist oral anticoagulant (NOAC), is indic

65 of rt-PA in patients who are receiving a non-vitamin K antagonist oral anticoagulant (NOAC).

66 It is unclear whether the non-vitamin K antagonist oral anticoagulant agents rivaroxab

67 In comparing the 2 non-vitamin K antagonist oral anticoagulant agents with each

68 Non-vitamin K antagonist oral anticoagulant drugs have recen

69 icular thrombus plus the availability of non-vitamin K antagonist oral anticoagulant drugs may lead t

70 ials are assessing the optimal timing of non-vitamin K antagonist oral anticoagulant initiation after

71 mic stroke and the benefit:harm ratio of non-vitamin K antagonist oral anticoagulant treatment in pat

72 Non-vitamin K antagonist oral anticoagulant-associated ICH h

73 function were excluded from the pivotal non-vitamin K antagonist oral anticoagulants (NOAC) trials,

74 The non-vitamin K antagonist oral anticoagulants (NOACs) apixaba

75 Current guidelines recommend non-vitamin K antagonist oral anticoagulants (NOACs) as the

76 Although non-vitamin K antagonist oral anticoagulants (NOACs) do not

77 farin) use is nowadays challenged by the non-vitamin K antagonist oral anticoagulants (NOACs) for str

78 These novel non-vitamin K antagonist oral anticoagulants (NOACs) have be

79 Non-vitamin K antagonist oral anticoagulants (NOACs) have pr

80 The use of non-vitamin K antagonist oral anticoagulants (NOACs) instead

81 Dose reduction of non-vitamin K antagonist oral anticoagulants (NOACs) is indi

82 The comparative effectiveness of non-vitamin K antagonist oral anticoagulants (NOACs) is unce

83 NR] >/=2) and 8290 (8.8%) were receiving non-vitamin K antagonist oral anticoagulants (NOACs) precedi

84 There are now 4 new non-vitamin K antagonist oral anticoagulants (NOACs) that ar

85 Phase III trials comparing non-vitamin K antagonist oral anticoagulants (NOACs) with wa

86 nclear whether the two once-daily dosing non-vitamin K antagonist oral anticoagulants (NOACs), edoxab

87 Of patients given OAC, 17.2% received non-vitamin K antagonist oral anticoagulants (NOACs).

88 min K antagonists, such as warfarin, and non-vitamin K antagonist oral anticoagulants (NOACs).

89 Non-vitamin K antagonist oral anticoagulants are being inves

90 Non-vitamin K antagonist oral anticoagulants are expensive a

91 Specific reversal agents for non-vitamin K antagonist oral anticoagulants are lacking.

92 Warfarin and non-vitamin K antagonist oral anticoagulants are underused a

93 Whether the use of non-vitamin K antagonist oral anticoagulants could lower the

94 Non-vitamin K antagonist oral anticoagulants have been prove

95 Guidelines caution against the use of non-vitamin K antagonist oral anticoagulants in patients wit

96 s enrolled in phase 3 clinical trials of non-vitamin K antagonist oral anticoagulants in prevention o

97 The advent of non-vitamin K antagonist oral anticoagulants, which attenuat

98 to derive a benefit from treatment with non-vitamin K antagonist oral anticoagulants.

99 umber of patients managed with uninterrupted vitamin K antagonist phenprocoumon (international normal

100 plus P2Y12 inhibitor) versus triple therapy (vitamin K antagonist plus aspirin and P2Y12 inhibitor) i

101 nt bleeding than was standard therapy with a vitamin K antagonist plus DAPT for 1, 6, or 12 months.

102 t of stents, standard anticoagulation with a vitamin K antagonist plus dual antiplatelet therapy (DAP

103 OAC in AF patients, but with low quality of vitamin K antagonist therapy and insufficient adherence

104 Long-term vitamin K antagonist therapy can be complicated by unsta

105 favorable risk-benefit profile compared with vitamin K antagonist therapy for venous thromboembolism

106 Results from this trial suggest that during vitamin K antagonist treatment INR monitoring could be r

107 gies of Rivaroxaban and a Dose-Adjusted Oral Vitamin K Antagonist Treatment Strategy in Subjects With

108 iplatelet drug, 3.73 (95% CI, 3.23-4.31) for vitamin K antagonist triple therapy, and 2.28 (95% CI, 1

109 Vitamin K antagonist use in the first trimester compared

110 nd it was amplified by diabetes and previous vitamin K antagonist use.

111 initially for 6 uninterrupted months with a vitamin K antagonist were randomized and followed up bet

112 , usually overlapping with and followed by a vitamin K antagonist) for at least 3 months.

113 ndard anticoagulants (heparin or switched to vitamin K antagonist).

114 schemic events than regimens that included a vitamin K antagonist, aspirin, or both.

115 necessitates lifelong anticoagulation with a vitamin K antagonist.

116 Warfarin, a vitamin K "antagonist" used clinically for the preventio

117 including 907 patients with AF treated with vitamin K antagonists (3,865 patient-years), to assess C

118 Patients were treated with vitamin K antagonists (48.4%), parenteral heparins (27.7

119 This holds for both vitamin K antagonists (e.g., warfarin) and direct oral a

120 ooled persistence was higher with DOACs than vitamin K antagonists (odds ratio, 1.44 [95% CI, 1.12-.8

121 difference was identified between NOACs and vitamin K antagonists (RR, 0.84; 95% CI, 0.59-1.19; I2 =

122 Overall, 43,299 AF patients initiating vitamin K antagonists (VKA) (42%), dabigatran (29%), riv

123 es to low molecular weight heparin (LMWH) or vitamin K antagonists (VKA) for treatment of cancer asso

124 Vitamin K antagonists (VKA) have long been the default d

125 acy and bleeding outcomes in comparison with vitamin K antagonists (VKA) in elderly participants (age

126 rivaroxaban or apixaban or dabigatran versus vitamin K antagonists (VKA) in patients with venous thro

127 Vitamin K antagonists (VKA) use is challenging because o

128 Thromboprophylaxis can be obtained with vitamin K antagonists (VKA, eg, warfarin) or a non-VKA o

129 ality in intracranial haemorrhage related to vitamin K antagonists (VKA-ICH).

130 t strategies for intracerebral hemorrhage on vitamin K antagonists (VKA-ICH).

131 Elderly patients in long-term treatment with vitamin K antagonists (VKAs) are at high risk of osteopo

132 erm (>/=3 months) vs short-term therapy with vitamin K antagonists (VKAs) associated with differences

133 l appendage closure (LAAC) is noninferior to vitamin K antagonists (VKAs) for preventing atrial fibri

134 a favorable risk-benefit profile compared to vitamin K antagonists (VKAs) for preventing stroke and s

135 Vitamin K antagonists (VKAs) have been used in 1% of the

136 onist oral anticoagulants (NOACs) instead of vitamin K antagonists (VKAs) in patients with atrial fib

137 Bleeding risk with vitamin K antagonists (VKAs) is closely related to the q

138 he association of prior anticoagulation with vitamin K antagonists (VKAs) or direct oral anticoagulan

139 Women receiving vitamin K antagonists (VKAs) require adequate contracept

140 ation treated with heparins, heparinoids, or vitamin K antagonists (VKAs) to prevent recurrent ischae

141 Vitamin K antagonists (VKAs), although commonly used to

142 e these drugs have several benefits over the vitamin K antagonists (VKAs).

143 ared a direct oral anticoagulant (DOAC) with vitamin K antagonists (VKAs).

144 Oral anticoagulants (both vitamin K antagonists [VKAs] and non-VKA oral anticoagul

145 ring pregnancy, and anticoagulation (LMWH or vitamin K antagonists [VKAs]) should be continued until

146 Thus, vitamin K antagonists act through mimicking the key inte

147 vidence for adding aspirin to the regimen of vitamin K antagonists and clopidogrel seems to be weaken

148 t anticoagulation with specific guidance for vitamin K antagonists and direct-acting oral anticoagula

149 aban, provide potential advantages over oral vitamin K antagonists and subcutaneous low-molecular-wei

150 Vitamin K antagonists are commonly used by clinicians to

151 For example, vitamin K antagonists are the most efficacious for preve

152 Vitamin K antagonists are widely used anticoagulants tha

153 anticoagulant therapy and have replaced the vitamin K antagonists as the preferred treatment for man

154 icoagulants, such as edoxaban, compared with vitamin K antagonists during extended therapy for venous

155 latelet drugs, dual antiplatelet therapy, or vitamin K antagonists further reduces the risk of major

156 But vitamin K antagonists have limitations, including causin

157 anticoagulants (DOACs) have largely replaced vitamin K antagonists in many indications for anticoagul

158 ATCHMAN has emerged as viable alternative to vitamin K antagonists in randomized controlled trials.

159 ndent proteins in patients not maintained on vitamin K antagonists is most commonly associated with p

160 vascular and renovascular calcification, and vitamin K antagonists may be associated with a decreased

161 lar-weight heparins, unfractionated heparin, vitamin K antagonists or fondaparinux) was compared with

162 Vitamin K antagonists or low molecular weight heparins a

163 ncreased risk of stroke with well-controlled vitamin K antagonists or non-vitamin K antagonist antico

164 acteristics and natural history of acute non-vitamin K antagonists oral anticoagulants (NOAC)-associa

165 ssion ratio >=80%), persistence, DOAC versus vitamin K antagonists persistence, and clinical outcomes

166 rial fibrillation, oral anticoagulation with vitamin K antagonists reduces the risk of stroke by more

167 mitant treatment with warfarin or equivalent vitamin K antagonists was prohibited.

168 For decades, vitamin K antagonists were the only oral option availabl

169 For these reasons, we anticipate that the vitamin K antagonists will continue to be important anti

170 Although the use of oral anticoagulants (vitamin K antagonists) has been abandoned in primary car

171 ation (parenteral anticoagulants followed by vitamin K antagonists), these agents showed improved saf

172 py (low-molecular-weight heparin followed by vitamin K antagonists).

173 2) describe the advantages of the DOACs over vitamin K antagonists, (3) summarize the experience with

174 Therapy with low-molecular-weight heparin, vitamin K antagonists, and direct-acting anticoagulants

175 Despite this, DOACs, like vitamin K antagonists, can still cause major and clinica

176 amiliarity with the dosing and monitoring of vitamin K antagonists, clinicians are accustomed to usin

177 anticoagulant treatment, and treatment with vitamin K antagonists, direct oral anticoagulants, plate

178 Recent data suggest that BPVT responds to vitamin K antagonists, emphasizing the need for reliable

179 tcome measure was the use of anticoagulants (vitamin K antagonists, factor Xa inhibitors, and direct

180 e for the different types of anticoagulants: vitamin K antagonists, heparins, fondaparinux, thrombin

181 anticoagulants, with options including LMWH, vitamin K antagonists, or direct factor Xa or direct fac

182 ical heart valves, treatment options include vitamin K antagonists, such as warfarin, and non-vitamin

183 nd clinical outcomes between NOAC-ICH versus vitamin K antagonists-ICH (VKA-ICH).

184 risk of intracranial bleeding compared with vitamin K antagonists.

185 antithrombotic therapy including the use of vitamin K antagonists.

186 coagulated with a combination of aspirin and vitamin K antagonists.

187 n inhibitors may represent an alternative to vitamin K antagonists.

188 nts to have greater benefits than risks over vitamin K antagonists.

189 (NOACs) that are attractive alternatives to vitamin K antagonists.

190 need to reverse the anticoagulant effect of vitamin K antagonists.

191 ng that has hindered usage and acceptance of vitamin K antagonists.

192 P2Y12 inhibitors compared with regimens with vitamin K antagonists.

193 7) and 30 on OAC (direct anticoagulants: 26, vitamin K antagonists: 4), with no differences in baseli

194 Vitamin K apical efflux was significantly decreased in p

195 es of phylloquinone, menaquinones, and total vitamin K, assessed with either the DQX or DHQ, were not

196 ion of a two-segment fluorogenic analogue of vitamin K, B-VKQ, prepared by coupling vitamin K3, also

197 served functional associations occur between vitamin K biosynthesis and NDC1 homologs throughout the

198 abled the quantitation of microgram level of vitamin K compounds in food.

199 sition was optimized for separation of eight vitamin K compounds on a reversed phase column in 10 min

200 MS) method was developed for the analysis of vitamin K compounds: phylloquinone (PK) and menaquinones

201 Higher vitamin K concentrations can restore up to 60% of coagul

202 n fecal menaquinone concentrations and serum vitamin K concentrations, gut microbiota composition, an

203 assigned patients in a 1:1 ratio to receive vitamin K concomitant with a single dose of either 4F-PC

204 itamin K epoxide reductase (VKOR) drives the vitamin K cycle, activating vitamin K-dependent blood cl

205 Vitamin K deficiency associated with lower relative cMGP

206 Functional vitamin K deficiency may further contribute to their sus

207 ceiving dialysis and examined the effects of vitamin K deficiency on MGP carboxylation.

208 In conclusion, vitamin K deficiency-mediated reduction in relative cMGP

209 Protein C, a secretory vitamin K-dependent anticoagulant serine protease, inact

210 VKOR) drives the vitamin K cycle, activating vitamin K-dependent blood clotting factors.

211 reductase (VKOR) is an essential enzyme for vitamin K-dependent carboxylation, while the physiologic

212 In addition, VKOR variants can cause vitamin K-dependent clotting factor deficiency or alter

213 here for protein C have general relevance to vitamin K-dependent clotting factors containing epiderma

214 Vitamin K-dependent coagulation factors deficiency is a

215 bit calcification requires the activity of a vitamin K-dependent enzyme, which mediates MGP carboxyla

216 Analyses of vitamin K-dependent factors in 6 cancer patients with av

217 Vitamin K-dependent factors protect against vascular and

218 Inactive vitamin K-dependent MGP (dp-ucMGP) and prothrombin (PIVK

219 anin-A[rs9658644], Cystatin-C[rs2424577] and Vitamin K-Dependent Protein S[rs6123] in the schizophren

220 Activation of Axl by its ligand Gas6, a vitamin K-dependent protein, is inhibited at doses of wa

221 frozen plasma (mFFP), PCC, mixtures of human vitamin K-dependent proteins (VKDP) (prothrombin, FVII,

222 TAM receptors can be activated by the vitamin K-dependent proteins Gas6 and protein S.

223 Severe deficiency of vitamin K-dependent proteins in patients not maintained

224 e cancer cells, and an altered expression of vitamin K-dependent proteins in prostate tumors has been

225 Vitamin K-dependent proteins in vascular tissue affect v

226 No binding of PTX2 to other vitamin K-dependent proteins was observed.

227 e to the analogous sequence present in other vitamin K-dependent proteins, contains a disproportionat

228 cate impairment of the functional, secreted, vitamin K-dependent, gamma-carboxylated form of periosti

229 mechanism of pneumonia-induced extrahepatic vitamin K depletion leading to accelerated elastic fiber

230 st time that ABCB1 is involved in enterocyte vitamin K efflux in both cell and mouse models and regul

231 tamin K transintestinal efflux and a biliary vitamin K efflux were observed, but the specific involve

232 to explore whether ABCB1 is also involved in vitamin K efflux.

233 Vitamin K epoxide reductase (VKOR) drives the vitamin K

234 oralis, and revealed the essential role of a vitamin K epoxide reductase (VKOR) gene in pilus assembl

235 Vitamin K epoxide reductase (VKOR) is an essential enzym

236 Human vitamin K epoxide reductase (VKOR) is the target of warf

237 Using the mammalian membrane protein vitamin K epoxide reductase (VKORc1) as a reporter, we d

238 ctions of vIL-6 with the ER membrane protein vitamin K epoxide reductase complex subunit 1 variant 2

239 eviously uncharacterized ER membrane protein vitamin K epoxide reductase complex subunit 1 variant 2

240 ociates with a novel membrane protein termed vitamin K epoxide reductase complex subunit 1 variant 2

241 largely uncharacterized ER-resident protein vitamin K epoxide reductase complex subunit 1 variant 2

242 n the ER with a nonsignaling receptor called vitamin K epoxide reductase complex subunit 1 variant 2

243 transducer and the novel ER membrane protein vitamin K epoxide reductase complex subunit 1 variant-2

244 macromolecular interactions by inhibition of vitamin K epoxide reductase, cellular responses includin

245 s are widely used anticoagulants that target vitamin K epoxide reductases (VKOR), a family of integra

246 Despite knowledge of the importance of vitamin K for various health parameters, few studies hav

247 suggests novel roles for bacterially derived vitamin K forms known as menaquinones in health and dise

248 The method was used to screen and quantitate vitamin K from 17 fermented food products.

249 Vitamin K has multiple important physiological roles, in

250 ex, and diet are determinants of circulating vitamin K; however, there is still large unexplained int

251 agonists, clinicians are accustomed to using vitamin K if there is a need to reverse the anticoagulan

252 stinal microbes possess the genes to produce vitamin K in the form of menaquinone (MK).

253 apid progression to end-stage liver disease, vitamin K-independent coagulopathy, low-to-normal serum

254 Vitamin K inhibits prostate cancer cells, and an altered

255 In times of vitamin K insufficiency, hepatic procoagulant factors ar

256 n COVID-19 patients, indicating extrahepatic vitamin K insufficiency, which was related to poor outco

257 ncrease) variable or after outliers of total vitamin K intake (defined as a value that falls above th

258 The present study does not suggest that vitamin K intake influences the occurrence of total and

259 However, little is known about the effect of vitamin K intake on prostate cancer in human populations

260 ese results remained virtually the same when vitamin K intake was modeled as a categorical (divided i

261 Vitamin K is a cofactor for proteins involved in prevent

262 K 2,3-epoxide, suggesting that supplemented vitamin K is reduced in vivo.

263 methylation of the demethylated precursor of vitamin K is strictly dependent on the reduced form of i

264 or the Adequate Intake level) of vitamin A, vitamin K, magnesium, zinc, and copper was associated wi

265 We hypothesized that vitamin K may be implicated in coronavirus disease 2019

266 , siderophore biosynthesis, bioluminescence, vitamin K metabolism, brominated compound metabolism, pl

267 Vitamin K occurs in the diet as phylloquinone and menaqu

268 However, the effect of vitamin K on vascular calcification is unknown.

269 Non-vitamin K oral anticoagulants (NOACs) are commonly presc

270 Non-vitamin K oral anticoagulants (NOACs) are now widely use

271 ials will assess the risk and benefit of non-vitamin K oral anticoagulants among patients at high ris

272 Non-vitamin K oral anticoagulants and warfarin have also ent

273 lighting the greater absolute benefit of non-vitamin K oral anticoagulants in patients with type 2 di

274 ents who have both and the potential for non-vitamin K oral anticoagulants to have greater benefits t

275 al anticoagulants (NOACs), also known as non-vitamin K oral anticoagulants, were at least noninferior

276 able a better understanding of the role that vitamin K plays in biological redox reactions ubiquitous

277 In vivo, the vitamin K postprandial response was higher in male Abcb1

278 eversible redox behavior on par with that of vitamin K, provides a high-sensitivity fluorescence sign

279 of menaquinones produced by gut bacteria to vitamin K requirements and inflammation is undetermined.

280 Growing evidence of vitamin K's importance in human health beyond blood coag

281 wal of VKAs and high-dose vitamin K2 improve vitamin K status in patients on hemodialysis, but have n

282 We investigated the effect of vitamin K status on VC progression in 132 patients on he

283 nversely related to extrahepatic and hepatic vitamin K status, respectively.

284 ther health outcomes in individuals with low vitamin K status.

285 e unexplained interindividual variability in vitamin K status.

286 GP levels were quantified to assess vascular vitamin K status.

287 ontaining protein-1 (UBIAD1) synthesizes the vitamin K subtype menaquinone-4 (MK-4).

288 sults obtained from the patient treated with vitamin K, suggesting that the D153G alteration in GGCX

289 Whether vitamin K supplementation can prevent and/or treat calci

290 Whether or not vitamin K supplementation could improve arterial stiffne

291 Vitamin K supplementation increased in ALGS after PEBD (

292 To determine if vitamin K supplementation might improve arterial stiffne

293 he updated meta-analysis showed no effect of vitamin K supplementation on vascular stiffness or vascu

294 Daily supraphysiological vitamin K supplementation restores clotting for VKCFD2 p

295 uthentic step in the biosynthetic pathway of vitamin K, that this reaction is enzymatically driven, a

296 Finally, a vitamin K transintestinal efflux and a biliary vitamin K

297 genital/acquired FX deficiency or after anti-vitamin K treatment) were characterized by concomitantly

298 s, a cellular process requiring reduction of vitamin K (VK) by a second enzyme, a reductase called VK

299 Dietary intake of vitamin K was assessed with the Dietary Questionnaire (D

300 K-1), menaquinones (vitamin K-2), and total vitamin K with the development of prostate cancer among