ライフサイエンスコーパス: CVC

1 CVC exposure was associated with a significantly elevate

2 CVC malposition was detected with different imaging moda

3 CVC remained significantly lower than the control site w

4 CVC removal is recommended when the catheter is no longe

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

6 CVC retained multipotentiality despite passaging and exp

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 CVC was not different between sites prior to (SNP: 0.42

11 CVC were immunopositive to antigens to CD29 and CD44 but

12 CVC-DVT was defined as persistent ipsilateral leg swelli

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

14 16, P < 0.001; Combo, 201 +/- 200, P < 0.001%CVC max s).

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

17 00 CVC days (95% Poisson CLs: 0.89, 3.0/1000 CVC days) in the taurolidine-citrate-heparin and heparin

18 00 CVC days (95% Poisson CLs: 0.4, 2.07/1000 CVC days; P = 0.005).

19 0 CVC days (95% Poisson CLs: 0.17, 1.21/1000 CVC days) and 1.72/1000 CVC days (95% Poisson CLs: 0.89,

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

21 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

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

23 5 catheters (2.7%) caused BSIs (5.9 per 1000 CVC days).

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

44 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(

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

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

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

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

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

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

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

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

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

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

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

56 = 0.84) (Y: NOS-I 41 +/- 4 versus C 39 +/- 4%CVC(max); P = 0.67).

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

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

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

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

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

62 y NOS-I (O: NOS-I 35 +/- 5 versus C 38 +/- 5%CVC(max); P = 0.84) (Y: NOS-I 41 +/- 4 versus C 39 +/- 4

63 ); 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

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

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

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

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

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

69 otal of 1084 accesses (185 AVF, 296 AVG, 603 CVC) were used for a total of 1381 person-years.

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

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

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

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

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

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

76 VSX1 is a CVC domain homeoprotein specifically expressed in cone b

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

78 nterviewed were unaware of the presence of a CVC.

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

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

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

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

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

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

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

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

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

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

89 After CVC removal, each lumen was sampled in vitro using the e

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

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

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

93 should include improved vascular access and CVC care.

94 All four patients with DKA and CVC-DVT were <3 yrs old.

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

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

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

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

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

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

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

102 7-NI significantly attenuated CVC increases during whole-body heat stress (P < 0.05),

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

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

105 taken during episodes of probable bacterial CVC-associated infection.

106 aised in 4 of 29 episodes in which bacterial CVC-associated infection was unlikely.

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

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

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

110 peripheral blood cultures were taken before CVC removal.

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

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

113 In Brazil, CVC became important in the early 1990s and has now expa

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

115 Cardiovascular calcification (CVC), a marker of atherosclerosis, is also more prevalen

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

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

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

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

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

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

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

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

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

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

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

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

128 long-term use of a central venous catheter (CVC), or cancer.

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

130 (6%) patients with central venous catheter (CVC)-associated UEDVT, 268 (5%) patients with non-CVC-as

131 s grafts (AVG) and central venous catheters (CVC), but whether AVF are associated independently with

132 f vascular cells (calcifying vascular cells, CVC), derived by dilutional cloning of bovine aortic med

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

134 12% for both conditions, but did not change CVC in either of the normothermic trials.

135 lella diseases, citrus variegated chlorosis (CVC) and Pierce's disease (PD) of grapevines, have emerg

136 on three of the four patients with clinical CVC-DVT, confirming the diagnosis in each case.

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

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

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

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

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

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

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

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

145 vasively and cutaneous vascular conductance (CVC) calculated as LDF/MAP.

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

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

148 n in forearm cutaneous vascular conductance (CVC) during the cold stress was significantly attenuated

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

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

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

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

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

154 ood flow and cutaneous vascular conductance (CVC) was calculated as LDF/mean arterial pressure and no

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

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

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

158 d to maximum cutaneous vascular conductance (CVC).

159 d changes in cutaneous vascular conductance (CVC).

160 e of maximal cutaneous vascular conductance (CVC).

161 monitored as cutaneous vascular conductance (CVC).

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

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

164 Cutaneous vascular conductance (CVC; LDF/mean arterial pressure) was expressed as percen

165 ry (LDF) and cutaneous vascular conductance (CVC; LDF/mean arterial pressure) was normalized to maxim

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

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

168 stress trials, isometric exercise decreased CVC by approximately 12% for both conditions, but did no

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

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

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

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

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

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

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

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

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

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

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

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

181 Four of eight patients with DKA developed CVC-DVT compared with none of the 16 control patients (p

182 Dead volumes of different CVC lumens vary considerably.

183 due to a non-specific effect of an elevated CVC secondary to SNP administration.

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

185 P = 0.01) than women (n = 282; RH = 1.0 for CVC; P = 0.92).

186 11.7% for AVF, 14.2% for AVG, and 16.1% for CVC.

187 .5 (95% confidence interval, 1.0 to 2.2) for CVC and 1.2 (0.8 to 1.8) for AVG.

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

189 arily because current diagnostic methods for CVC-associated infection are unreliable.

190 In seven subjects forearm CVC during a whole-body cold stress was assessed at two

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

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

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

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

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

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

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

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

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

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

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

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

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

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

205 trol trials resulted in similar decreases in CVC.

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

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

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

209 on with atropine, attenuated the increase in CVC during heat stress, suggesting an important role for

210 0.05) significantly attenuated increases in CVC in response to 0.25 and 5 mm MCh.

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

212 The reduction in CVC during the subsequent cold stress was significantly

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

214 The rise in CVC with low-dose SNP (deltaCVC) was significantly great

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

219 n analysis, we determined that an indwelling CVC was the strongest independent predictor of UEDVT (od

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

221 During postexercise ischaemia, CVC and MAP returned to pre-exercise levels in the PNB t

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 ation were the independent predictors of non-CVC-associated UEDVT.

238 The non-CVC-associated UEDVT patients were younger (59.2+/-18.2

239 associated UEDVT, 268 (5%) patients with non-CVC-associated UEDVT, and 4796 (89%) patients with lower

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

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

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

243 ivity of local inflammation for diagnosis of CVC-related BSI was dismal (0-3%).

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

245 The pathogenesis of CVC is complex and includes factors that promote calcifi

246 Chondrogenic potential of CVC was evidenced by expression of types II and IX colla

247 Stromogenic potential of CVC was evidenced by the ability to support growth of co

248 Leiomyogenic potential of CVC was evidenced by the expression of smooth muscle-alp

249 To determine the multilineage potential of CVC, molecular and functional markers of multiple mesenc

250 ation at the insertion site is predictive of CVC-related BSI.

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

252 ughout southern California and the spread of CVC northward from Argentina through Brazil exemplifies

253 reproduced the inhibitory effects of DHA on CVC mineralization.

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

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

256 If only one CVC lumen is sampled, a negative result does not reliabl

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

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

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

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

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

262 There was no difference in peak %CVC(max) during ACh infusion between age groups, and the

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

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

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

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

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

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

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

270 L-NAME) infusion during hyperthermia reduced CVC by approximately 32 % (65 +/- 4 % CVCmax vs. 45 +/-

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

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

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

274 In the H2 receptor antagonist studies, CVC in control sites was not significantly different fro

275 In the H1 antagonist studies, CVC in l-NAME, pyrilamine, and combined l-NAME plus pyri

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

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

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

279 We now show that CVC have the potential to differentiate along other mese

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

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

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

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

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

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

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

287 Malposition of the CVC is not common.

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

289 ning the carrier immediately upstream of the CVC.

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

291 us therapeutic interventions in reducing the CVC burden in patients with CKD.

292 erial DNA in blood samples drawn through the CVC in a population of patients receiving intravenous nu

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

294 o thrombolytic agents in treating thrombotic CVC occlusions.

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

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

297 The increased hazards associated with CVC, as compared with AVF, were stronger in men (n = 334

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

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

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