ライフサイエンスコーパス: CVC

1 CVC administration regimens prevented the increase in in

2 CVC exposure was associated with a significantly elevate

3 CVC increased liver T-cell numbers and attenuated Il-2 e

4 CVC malposition was detected with different imaging moda

5 CVC removal is recommended when the catheter is no longe

6 CVC responses to each NP and NS trial were averaged into

7 CVC should be placed by well-trained providers, and the

8 CVC was calculated as flux/mean arterial pressure and no

9 CVC was calculated from blood flow and blood pressure.

10 C(max)), compared to older fit (46.2 +/- 7.0%CVC(max), P < 0.05) and young subjects (41.2 +/- 5.2%CVC

11 16, P < 0.001; Combo, 201 +/- 200, P < 0.001%CVC max s).

12 to both normocholesterolaemic (0.09 +/- 0.02%CVC(max) /%(baseline) ; P = 0.024) and statin-treated (0

13 hypercholesterolaemic adults (0.02 +/- 0.03%CVC(max) /%(baseline) ) compared to both normocholestero

14 P = 0.024) and statin-treated (0.12 +/- 0.05%CVC(max) /%(baseline) ; P = 0.03) adults.

15 1, NOS-I + COX-I 16 +/- 2 versus C 10 +/- 1%CVC(max); P < 0.001) but not in the young, suggesting an

16 normal = 36 +/- 1%CVC(max) , high = 32 +/- 1%CVC(max) , statin = 38 +/- 1%CVC(max) ; P < 0.01).

17 eltaT(or) = 1.0 degrees C: normal = 36 +/- 1%CVC(max) , high = 32 +/- 1%CVC(max) , statin = 38 +/- 1%

18 high = 32 +/- 1%CVC(max) , statin = 38 +/- 1%CVC(max) ; P < 0.01).

19 e heparin arm, with an incidence of 1.0/1000 CVC days (95% Poisson CLs: 0.4, 2.07/1000 CVC days; P =

20 00 CVC days (95% Poisson CLs: 0.89, 3.0/1000 CVC days) in the taurolidine-citrate-heparin and heparin

21 00 CVC days (95% Poisson CLs: 0.4, 2.07/1000 CVC days; P = 0.005).

22 reduced the incidence 4.56-fold to 0.09/1000 CVC-days (P < .03).

23 0 CVC days (95% Poisson CLs: 0.17, 1.21/1000 CVC days) and 1.72/1000 CVC days (95% Poisson CLs: 0.89,

24 espite the low CLABSI incidence of 0.41/1000 CVC-days in patients randomized to ACH, the IMD further

25 The CVC removal rates were 0.52/1000 CVC days (95% Poisson CLs: 0.17, 1.21/1000 CVC days) and

26 CLs: 0.17, 1.21/1000 CVC days) and 1.72/1000 CVC days (95% Poisson CLs: 0.89, 3.0/1000 CVC days) in t

27 dence limits (CLs): 2.12, 2.71 episodes/1000 CVC days].

28 substance P combined with L-NAME (20 +/- 2% CVC(max)) and was significantly reduced compared to the

29 substance P combined with L-NAME (27 +/- 2% CVC(max); P < 0.001).

30 with substance P increased CVC to 48 +/- 2% CVC(max), which was significantly greater than for sites

31 (BH(4): 60 +/- 5% CVC(max); combo 58 +/- 2% CVC(max), both P < 0.001).

32 ect in NC subjects (plateau BH(4): 90 +/- 2% CVC(max); combo 95 +/- 3% CVC(max); NO-dependent vasodil

33 eau HC: 70 +/- 5% CVC(max) vs. NC: 95 +/- 2% CVC(max); NO HC: 45 +/- 5% CVC(max) vs. NC: 64 +/- 5% CV

34 both groups (COX-I O: 29 +/- 3, Y: 22 +/- 2%CVC(max) versus C; P < 0.001 both groups; NOS-I + COX-I

35 NOS-I + COX-I O: 32 +/- 3 versus Y: 29 +/- 2%CVC(max); versus C; P < 0.001 both groups).

36 , P < 0.05) and young subjects (41.2 +/- 5.2%CVC(max), P < 0.05), whereas exercise training in the ol

37 HC with arginase inhibition (92+/-2, 67+/-2%CVC(max), P < 0.001), L-arginine (93+/-2, 71+/-5%CVC(max

38 E sites was significantly reduced (32 +/- 3% CVC(max); P < 0.001) compared to both control sites and

39 Sites pretreated with substance P (48 +/- 3% CVC(max)) were significantly reduced compared to control

40 ) and NO-dependent vasodilatation (68 +/- 3% CVC(max), P < 0.001).

41 NO-dependent vasodilatation BH(4): 68 +/- 3% CVC(max); combo 58 +/- 4% CVC(max), all P > 0.05 vs. con

42 CVC in control sites increased to 69 +/- 3% CVC(max).

43 ndent vasodilatation in HC (BH(4): 74 +/- 3% CVC(max); combo 76 +/- 3% CVC(max), both P < 0.001), but

44 (BH(4): 74 +/- 3% CVC(max); combo 76 +/- 3% CVC(max), both P < 0.001), but there was no effect in NC

45 (BH(4): 93 +/- 3% CVC(max); combo 89 +/- 3% CVC(max), both P < 0.001) and NO-dependent vasodilatatio

46 ombo augmented the plateau (BH(4): 93 +/- 3% CVC(max); combo 89 +/- 3% CVC(max), both P < 0.001) and

47 u BH(4): 90 +/- 2% CVC(max); combo 95 +/- 3% CVC(max); NO-dependent vasodilatation BH(4): 68 +/- 3% C

48 cts (low dose 3.2 +/- 1.3 versus 6.6 +/- 1.3%CVC(max); mid dose 11.4 +/- 2.4 versus 21.6 +/- 4.5%CVC(

49 (HTN, 32 +/- 4%CVC(max) versus AMN, 23 +/- 3%CVC(max), P<0.05).

50 different between the groups (HTN, 43 +/- 3%CVC(max) versus AMN, 45 +/- 3%CVC(max), P>0.05).

51 (HTN, 43 +/- 3%CVC(max) versus AMN, 45 +/- 3%CVC(max), P>0.05).

52 (HTN, 65 +/- 5%CVC(max) versus AMN, 48 +/- 3%CVC(max), P<0.05).

53 (HTN, 49 +/- 5%CVC(max) versus AMN, 49 +/- 3%CVC(max), P > 0.05).

54 (HTN, 60 +/- 7%CVC(max) versus AMN, 61 +/- 3%CVC(max), both P<0.05 versus respective control sites).

55 rolaemic subjects (HC: 76+/-2 vs. NC: 94+/-3%CVC(max), P < 0.001) as was NO-dependent vasodilatation

56 n Control (4109 +/- 2777 versus 1295 +/- 368%CVC max s).

57 n BH(4): 68 +/- 3% CVC(max); combo 58 +/- 4% CVC(max), all P > 0.05 vs. control site).

58 an increase in the plateau in HC (96 +/- 4% CVC(max), P < 0.001) and NO-dependent vasodilatation (68

59 was greater in the HTN group (HTN, 32 +/- 4%CVC(max) versus AMN, 23 +/- 3%CVC(max), P<0.05).

60 nt vasodilatation (HC: 43+/-5 vs. NC: 62+/-4%CVC(max), P < 0.001).

61 s on HD were enrolled and followed for 43738 CVC-days.

62 vs. NC: 95 +/- 2% CVC(max); NO HC: 45 +/- 5% CVC(max) vs. NC: 64 +/- 5% CVC(max); both P < 0.001).

63 fter the drug intervention (BH(4): 60 +/- 5% CVC(max); combo 58 +/- 2% CVC(max), both P < 0.001).

64 NO HC: 45 +/- 5% CVC(max) vs. NC: 64 +/- 5% CVC(max); both P < 0.001).

65 educed in HC subjects (plateau HC: 70 +/- 5% CVC(max) vs. NC: 95 +/- 2% CVC(max); NO HC: 45 +/- 5% CV

66 ); mid dose 11.4 +/- 2.4 versus 21.6 +/- 4.5%CVC(max); high dose 35.2 +/- 6.0 versus 52.6 +/- 7.9%CVC

67 ect %CVC(max) in either group (HTN, 49 +/- 5%CVC(max) versus AMN, 49 +/- 3%CVC(max), P > 0.05).

68 erence between control sites (88+/-4, 61+/-5%CVC(max)) and localized microdialysis treatment sites (a

69 VC(max) only in the HTN group (HTN, 65 +/- 5%CVC(max) versus AMN, 48 +/- 3%CVC(max), P<0.05).

70 001) and combined treatments (94+/-4, 65+/-5%CVC(max), P < 0.001) but not in NC.

71 max), P < 0.001), L-arginine (93+/-2, 71+/-5%CVC(max), P < 0.001) and combined treatments (94+/-4, 65

72 heir respective control sites (HTN, 60 +/- 7%CVC(max) versus AMN, 61 +/- 3%CVC(max), both P<0.05 vers

73 yperaemic responses in Control (1389 +/- 794%CVC max s) were significantly greater compared to TEA, E

74 longed heating at 42 degrees C (26.9 +/- 3.9%CVC(max)), compared to older fit (46.2 +/- 7.0%CVC(max),

75 ks: 13.7 +/- 3.6, 28.9 +/- 5.3, 56.1 +/- 3.9%CVC(max), P < 0.05).

76 ; high dose 35.2 +/- 6.0 versus 52.6 +/- 7.9%CVC(max), P < 0.05) and training reversed this (12 weeks

77 nicians are aware that their patients have a CVC is unknown.

78 by well-trained providers, and the use of a CVC clinical care bundle is recommended.

79 nterviewed were unaware of the presence of a CVC.

80 Female patients spend a longer time on a CVC and are less likely to transition to permanent acces

81 ged >=66 years who started hemodialysis on a CVC in July 2010 through 2013.

82 Women spent a significantly longer time on a CVC than men.

83 to an arteriovenous graft, 32.1% stayed on a CVC, and 24.5% died.

84 ents, minorities also spend longer time on a CVC, but are more likely to eventually transition to per

85 minority spent significantly more days on a CVC.

86 hen we accounted for propensity to receive a CVC and limited the cohort to individuals at high risk o

87 s, 60.4% of patients were dialyzed through a CVC.

88 initiation, 409 (66%) patients were using a CVC, 122 (20%) were using an AVG, and 85 (14%) were usin

89 After 6 mo, 34% were using a CVC, 40% were using an AVG, and 26% were using an AVF.

90 ed 479 patients starting hemodialysis with a CVC at a large medical center (during 2004-2012) who sub

91 for patients initiating hemodialysis with a CVC, a scenario occurring in over 70% of United States d

92 mong patients initiating hemodialysis with a CVC, the annual cost of access-related procedures and co

93 G (n=105) placed or no arteriovenous access (CVC group, n=71).

94 ildren determined a 21.9% incidence of acute CVC-related thrombosis.

95 atment of occult DVT will prevent additional CVC-related complications and prolong the duration of ca

96 L-Arg alone did not affect %CVC(max) in either group (HTN, 49 +/- 5%CVC(max) versus

97 eloped a pneumothorax with hydrothorax after CVC placement for PBSC collection.

98 bble (MB) enhanced sonothrombolysis for aged CVC associated thrombi in vivo.

99 US+systemic MB facilitates reduction of aged CVC associated thrombi in vivo.

100 SI (HR = 1.6; 95% CI, 1.2-2.2; P = .002) and CVC malfunction (HR = 2.0; 95% CI, 1.6-2.4; P < .001).

101 vertebrae (46%), AB: L4 vertebrae (63%), and CVC: L4 vertebrae (52%).

102 should include improved vascular access and CVC care.

103 cidence of catheter-related VTE, CLABSI, and CVC malfunction over TLs.

104 was measured by laser-Doppler flowmetry, and CVC was the ratio of skin blood flow to mean arterial pr

105 gasdermin D [GSDMD] cleavage) in livers, and CVC prevented both of these forms of cell death.

106 s C, [ATP](d) averaged 18.93 +/- 4.06 nm and CVC averaged 12.57 +/- 1.59% peak.

107 The absolute increase in cardiac output and CVC were similar between groups, whereas FVC increased t

108 e discharge home were similar in the PAC and CVC groups (27.4 percent and 26.3 percent, respectively;

109 monstrate blunted increases in both SSNA and CVC during passive heating and (2) chronic statin treatm

110 ss the comparative efficacy of antimicrobial CVC impregnations in reducing catheter-related infection

111 neous vascular conductance was calculated as CVC = LDF/MAP and expressed as per cent change from base

112 in 2 children (1 symptomatic, 1 asymptomatic CVC-related thrombosis), however, neither had functional

113 thrombotic syndrome (PTS), from asymptomatic CVC-related thrombosis is unknown.

114 as children identified to have asymptomatic CVC-related thrombosis were not treated (clinical team k

115 d to determine the frequency of asymptomatic CVC-related thrombosis during hospital admission, and th

116 at critically ill children with asymptomatic CVC-related thrombosis require anticoagulant treatment,

117 nm) co-infused with l-NNA further attenuated CVC during 0.25, 5 and 100 mm MCh administration relativ

118 7-NI significantly attenuated CVC increases during whole-body heat stress (P < 0.05),

119 A-I alone augmented %CVC(max) only in the HTN group (HTN, 65 +/- 5%CVC(max) v

120 Combined A-I + L-arg augmented %CVC(max) in both subject groups compared with their resp

121 was added as an NO donor to restore baseline CVC at one site.

122 ase (P < 0.05) in CVC at sites with baseline CVC restored, while, as in Part 1, there was no change (

123 Baseline %CVC(max) was increased in the O at COX-I sites (COX-I 16

124 was used to examine the relationship between CVC use and infections, with CVC exposure as a time-depe

125 At the end of each 500 W exercise bout, CVC was attenuated with l-NAME ( approximately 35% CVCma

126 ntly decreased %CVC(max) in both groups but %CVC(max) was greater in the HTN group (HTN, 32 +/- 4%CVC

127 erase [ALT]) and steatosis were prevented by CVC whether administered as "prevention" throughout the

128 Cardiovascular calcification (CVC) contributes to morbidity and mortality in patients

129 d cutaneous vascular conductance calculated (CVC = LDF/MAP).

130 taneous vascular conductance was calculated (CVC = flux/MAP) and normalized to maximal CVC (28 mM SNP

131 taneous vascular conductance was calculated (CVC = flux/mean arterial pressure) and normalized to max

132 rsely, removal of a central venous catheter (CVC) (OR, 0.50; 95% CI, .35-.72; P = .0001) and treatmen

133 hemodialysis with a central venous catheter (CVC) and subsequently undergo placement of a new arterio

134 ncy in contaminated central venous catheter (CVC) coupons.

135 s 2.4 episodes/1000 central venous catheter (CVC) days [95% Poisson confidence limits (CLs): 2.12, 2.

136 also observed after central venous catheter (CVC) placement for PBSC collection.

137 tula, AV graft, and central venous catheter (CVC) strategies for patients initiating hemodialysis wit

138 Central venous catheter (CVC) thrombi result in significant morbidity in children

139 s a complication of central venous catheter (CVC) use in children with cancer, but its clinical signi

140 agement guided by a central venous catheter (CVC) using an explicit management protocol.

141 through a prevalent central venous catheter (CVC) were randomly assigned to have their CVC locked bet

142 agents, presence of central venous catheter (CVC), site of cancer, stage of cancer, leukocyte and hem

143 Asymptomatic central venous catheter (CVC)-related thrombosis in children varies in incidence

144 t hemodialysis on a central venous catheter (CVC).

145 ith the dual CCR2/5 inhibitor, cenicriviroc (CVC), would attenuate ALD.

146 NS did not change CVC (Delta = 0.002 +/- 0.005 a.u. mmHg(-1); P = 0.63).

147 bladder of the contractile vacuole complex (CVC) of Trypanosoma cruzi, the etiologic agent of Chagas

148 gi produce numerous caveola-vesicle complex (CVC) structures within the surface of the infected eryth

149 The apparent critical vesicle concentration (CVC) increased in the presence of positively-charged nan

150 Cutaneous vascular conductance (CVC = flux/mean arterial pressure) was expressed as a ch

151 d to maximum cutaneous vascular conductance (CVC(max)).

152 Cutaneous vascular conductance (CVC) and sweat rate were assessed in three protocols: in

153 per group), cutaneous vascular conductance (CVC) and sweat rate were evaluated at four intradermal f

154 e of maximal cutaneous vascular conductance (CVC) at each site (28 mm sodium nitroprusside; 43 degree

155 Cutaneous vascular conductance (CVC) declines in response to local cooling (LC).

156 Cutaneous vascular conductance (CVC) decreases during isometric handgrip exercise in hea

157 relation to cutaneous vascular conductance (CVC) during passive heat stress is unknown.

158 increase in cutaneous vascular conductance (CVC) during whole-body heat stress, this vascular bed is

159 Cutaneous vascular conductance (CVC) was calculated (laser Doppler flux/mean arterial pr

160 owmetry, and cutaneous vascular conductance (CVC) was calculated (laser-Doppler flux/mean arterial pr

161 ontinuously; cutaneous vascular conductance (CVC) was calculated as laser-Doppler flowmetry/mean arte

162 Cutaneous vascular conductance (CVC) was calculated as LDF/mean arterial pressure and no

163 owmetry, and cutaneous vascular conductance (CVC) was calculated as RBC flux/mean arterial pressure a

164 uced rise in cutaneous vascular conductance (CVC) was diminished in the older sedentary subjects afte

165 Cutaneous vascular conductance (CVC) was monitored at four forearm skin sites continuous

166 e of maximal cutaneous vascular conductance (CVC).

167 monitored as cutaneous vascular conductance (CVC).

168 d to maximum cutaneous vascular conductance (CVC).

169 d changes in cutaneous vascular conductance (CVC).

170 ography) and cutaneous vascular conductance (CVC, laser-Doppler) were measured before and after rapid

171 Cutaneous vascular conductance (CVC; LD flux/mean arterial pressure) was expressed as pe

172 e evaluated cutaneous vascular conductance (%CVC(max) ) with laser Doppler flowmetry during low dose

173 artery (SMA), vena cava inferior confluence (CVC), abdominal aorta bifurcation (AB), and iliolumbar l

174 Conversely, CVC was elevated with Ascorbate ( approximately 72% CVCm

175 al pressure) and normalized to maximal CVC (%CVC(max)) (28 mm sodium nitroprusside + local heating to

176 During whole-body heating, NP decreased CVC (by 0.16 +/- 0.04 a.u. mmHg(-1); (P < 0.05), whereas

177 During normothermia, NP decreased CVC by 0.032 +/- 0.007 arbitrary units (a.u.) mmHg(-1);

178 NOS-I significantly decreased %CVC(max) in both groups but %CVC(max) was greater in the

179 stem is engaged and is capable of decreasing CVC during an orthostatic challenge in heat-stressed ind

180 ine, young: 41 +/- 2, older: 36 +/- 3% Delta CVC(base)) and tyrosine (cold, young: 37 +/- 4, older: 3

181 ing (young: 39 +/- 3, older: 17 +/- 3% Delta CVC(base); P < 0.01) and tyramine infusion (young: 41 +/

182 ine, young: 40 +/- 4, older: 45 +/- 4% Delta CVC(base)) both resolved the age-related decrease in cut

183 ion (young: 41 +/- 3, older: 21 +/- 4% Delta CVC(base); P < 0.01).

184 ressure) and normalized to baseline (% Delta CVC(base)).

185 ine, young: 36 +/- 3, older: 36 +/- 5 Delta %CVC(base)).

186 The Delta%CVC(max) between the control and NOS-I site was calculat

187 The Delta%CVC(max) between the control and NOS-I sites was attenua

188 Dead volumes of different CVC lumens vary considerably.

189 ng confirmed the absence of any pre-existing CVC thrombus.

190 ated thrombosis during admission and femoral CVC placement was predictive of residual thrombosis 2 ye

191 .5 (95% confidence interval, 1.0 to 2.2) for CVC and 1.2 (0.8 to 1.8) for AVG.

192 Cardiac arrest was a risk factor for CVC-related thrombosis during admission and femoral CVC

193 Patient length of stay and indication for CVC were not recorded.

194 here was a higher risk of complications from CVC placement before apheresis.

195 ups, with a 1 percent rate of crossover from CVC- to PAC-guided therapy.

196 US-guided CVC placement in children is associated with decreased n

197 Throughout, whole body heating %CVC(max) was not different between the groups (HTN, 43 +

198 TX-A-treated site during whole-body heating, CVC at this site was elevated to a similar level relativ

199 During whole-body heating, CVC in control sites increased to 69 +/- 3% CVC(max).

200 Importantly, CVC at the BT + L-NAME sites was unaffected by LC (P > 0

201 that the minocycline-rifampicin-impregnated CVC appears to be the most effective in preventing CRBSI

202 here was a 24 +/- 10% decrease (P < 0.05) in CVC at sites with baseline CVC restored, while, as in Pa

203 eptor stimulation elicits dynamic changes in CVC and that these changes are more apparent during whol

204 In this thermal state, changes in CVC are reported to be due to withdrawal of active vasod

205 caused a significant (P < 0.05) decrease in CVC at control sites (68 +/- 4%) and at the BT treated s

206 n of L-NAME elicited a 35 +/- 4% decrease in CVC at the L-NAME and BT + L-NAME sites (P < 0.05); subs

207 er 23 +/- 5% of initial baseline decrease in CVC at the L-NAME treated sites (P < 0.05).

208 trol trials resulted in similar decreases in CVC.

209 was accompanied by significant elevations in CVC (38.90 +/- 1.37% peak and 60.32 +/- 1.95% peak, resp

210 n to 35 degrees C resulted in an increase in CVC (17.63 +/- 1.27% peak; P < 0.05), but no change in [

211 The increase in CVC at eNOS-inhibited (41 +/- 3%CVCmax) and non-selectiv

212 0.05) significantly attenuated increases in CVC in response to 0.25 and 5 mm MCh.

213 Prostacyclin-induced increases in CVC were similar between groups (all concentrations, P >

214 and capable of contributing to reductions in CVC during an orthostatic challenge of heat-stressed ind

215 tid hypertension) will decrease and increase CVC, respectively, during normothermic and whole-body he

216 . mmHg(-1); (P < 0.05), whereas NS increased CVC by 0.07 +/- 0.03 a.u. mmHg(-1); (P < 0.05).

217 Pretreatment with substance P increased CVC to 48 +/- 2% CVC(max), which was significantly great

218 injected with vitamin D (days 1-3) to induce CVC were infused with saline or SNF472 (days 1-12).

219 It also induced CVC proliferation based on 3H-thymidine incorporation.

220 A model of chronic indwelling CVC in the low superior vena cava with thrombus in situ

221 rn babies who needed a peripherally inserted CVC (PICC) were allocated randomly (1:1) to receive eith

222 identity of a predominantly expressed 95 kDa CVC protein.

223 loss of Chx10/Vsx2, demonstrating that Prd-L:CVC genes, although important, are not absolutely requir

224 and Vsx1 are the only Paired-like CVC (Prd-L:CVC) homeobox genes in the mouse genome.

225 Chx10/Vsx2 and Vsx1 are the only Paired-like CVC (Prd-L:CVC) homeobox genes in the mouse genome.

226 ), 39%) from cutaneous vasoconstrictor-like (CVC(like), 28%) SPNs.

227 diatrics often requires central venous line (CVC - Central Venous Catheter) implantation for carrying

228 d TEA, as well as their combination, lowered CVC in young males at all prostacyclin concentrations (P

229 e of three vascular access choices: maintain CVC, attempt fistula, or attempt graft.

230 In older males, CVC during prostacyclin administration was not influence

231 Maximal CVC was attenuated in the HTN subjects by approximately

232 arterial pressure) and normalized to maximal CVC (%CVC(max)) (28 mm sodium nitroprusside + local heat

233 d (CVC = flux/MAP) and normalized to maximal CVC (28 mM SNP + local heating to 43 degrees C).

234 arterial pressure) and normalized to maximal CVC (CVCmax, 28.0 mM sodium nitroprusside + local heatin

235 Mechanical CVC occlusions need cause-specific treatment, whereas th

236 < 0.04); however, Ascorbate did not modulate CVC during exercise ( approximately 60% CVCmax ; both P

237 R = 23; 95% CI, 4-127; P < .001), multilumen CVC (HR = 3.9; 95% CI, 1.8-8.9; P = .003), and leukemia

238 In contrast, the activity of CVC(like) SPNs was underpinned by rhythmical membrane po

239 e physicians were more likely to be aware of CVC presence than general medicine physicians (12.6% vs.

240 nce of a CRBSI or right-censoring because of CVC removal.

241 ctions in PICCs and TLs, and risk factors of CVC-related VTE.

242 The incidence of CVC-related VTE was 5.9% +/- 0.63%.

243 pressure (Finapres) was used as an index of CVC.

244 g: 75%), which correlated with inhibition of CVC (r = 0.401, P = 0.003).

245 ization, which correlated with inhibition of CVC (r = 0.628, P = 0.005).

246 crystallization in plasma and inhibition of CVC both in a rat model and in humans, supporting the us

247 Inhibition of CVC was 50-65% with SNF472 3 mg/kg and ~ 80% with SNF472

248 collagen-1) were normalized by both modes of CVC administration.

249 larger confirmatory study of nontreatment of CVC-related thrombosis in critically ill children is jus

250 variate analysis, only age, KPS, presence of CVC, and Khorana score retained significance.

251 Increased risk of CVC-related VTE was found in patients with a prior histo

252 reproduced the inhibitory effects of DHA on CVC mineralization.

253 heat stress (P < 0.05), but had no effect on CVC increases induced by local skin warming (P > 0.05).

254 ements, and its correlations with effects on CVC in rats or humans.

255 RK or PI3K pathway reversed IGF-I effects on CVC proliferation and AP activity, suggesting a common d

256 re is insufficient evidence to recommend one CVC type or insertion site; femoral catheterization shou

257 dren with CVCs commonly experience two other CVC-related complications: occlusion and infection.

258 ous proteins PvPHIST/CVC-81(95) and PcyPHIST/CVC-81(95) , analysed their structural features, includi

259 Peak CVC responses (3 s average) to NP and NS were compared t

260 COX-I and NOS-I + COX-I attenuated the peak CVC response to ACh in both groups (COX-I O: 29 +/- 3, Y

261 raphy (ET), and used immuno-ET to show PHIST/CVC-81(95) localizes to the cytoplasmic side of the CVC

262 This suggests that PHIST/CVC-81(95) is essential for survival of these malaria pa

263 C-terminal PHIST domain, and show that PHIST/CVC-81(95) is most highly expressed in trophozoites.

264 All drug sites attenuated plateau CVC from the control site (86 +/- 1%) to 79 +/- 3% with

265 axis with thrombolytic flushes might prevent CVC infections and catheter-related thromboses, but conf

266 eparin arm, respectively, tending to prolong CVC survival in the taurolidine arm (P = 0.06).

267 We named the orthologous proteins PvPHIST/CVC-81(95) and PcyPHIST/CVC-81(95) , analysed their stru

268 flow was matched between sites, LBNP reduced CVC at both the BTX-A-treated (Delta15.3 +/- 4.6%max) an

269 LBNP reduced CVC at the BTX-A-treated sites (Delta4.2 +/- 2.9%max), a

270 tal admission, and the incidence of residual CVC-related thrombosis and clinically significant PTS 2

271 ults showed that IGF-I inhibited spontaneous CVC differentiation and mineralization as evidenced by d

272 The slope of the SSNA:CVC relation was blunted in hypercholesterolaemic adults

273 e response range and sensitivity of the SSNA:CVC relation.

274 We examined the impact of long-term CVC use on infection risk, independent of other risk fac

275 Long-term CVC use was associated with an increased risk of infecti

276 was associated with more complications than CVC-guided therapy.

277 The CVC group had the highest median annual overall access-r

278 The CVC removal rates were 0.52/1000 CVC days (95% Poisson C

279 The CVC response to whole-body heat stress in L-NAME sites w

280 The CVC response to whole-body heating was nearly abolished

281 The CVC(like) have longer after-hyperpolarisations (314 +/-

282 Above the CVC, initial vesicle formation rates were faster in the

283 hromboses includes proper positioning of the CVC and prevention of infections; anticoagulation prophy

284 Malposition of the CVC is not common.

285 95) localizes to the cytoplasmic side of the CVC tubular extensions.

286 s: use of an echinocandin and removal of the CVC.

287 ning the carrier immediately upstream of the CVC.

288 treated with antimicrobial therapy while the CVC remains in place.

289 r (CVC) were randomly assigned to have their CVC locked between dialysis sessions with an antimicrobi

290 o thrombolytic agents in treating thrombotic CVC occlusions.

291 to fewer admission days related to treating CVC-related complications (P = 0.02).In patients with in

292 In vitro, CVC inhibited CCL2-induced increases in hepatocyte fatty

293 ine firing frequencies (2.52 +/- 0.33 Hz vs. CVC(like) 1.34 +/- 0.17 Hz, P = 0.007).

294 Risk factors associated with CVC-related thrombosis were also identified.

295 Children with CVC-related DVT frequently have recurrent catheter compl

296 Of 21 patients (7%) diagnosed with CVC-related DVT, only five had specific signs or symptom

297 ionship between CVC use and infections, with CVC exposure as a time-dependent predictor.

298 nical evidence for CCR2/CCR5 inhibition with CVC as a potent intervention to ameliorate alcohol-induc

299 In patients with CVC (N = 274), infusion of SNF472 during hemodialysis fo

300 We found that prevention and treatment with CVC reversed alcohol-related increases in liver mRNA and