ライフサイエンスコーパス: venous

1 We compared different central venous access device types and these complications in th

2 Central venous access devices (CVAD) are used to deliver intrave

3 Central venous access devices, including peripherally inserted c

4 tal hemostasis and the major role of central venous access devices.

5 le alternative to intravenous (18)F-FDG when venous access is problematic.

6 mplantation strategy for totally implantable venous access ports with the optimal benefit/risk ratio

7 onstrates that the large amount of pulmonary venous admixture observed in patients with early COVID-1

8 reat omentum, our approach uses arterial and venous anastomoses which rapidly restores blood flow and

9 ded-duration rivaroxaban reduces the risk of venous and arterial fatal and major thromboembolic event

10 amines the incidence of and risk factors for venous and arterial thrombosis in patients hospitalized

11 s of R0 resection and pathologic invasion of venous and arterial walls were 52.4%, 74.2%, and 58%, re

12 Both venous and capillary blood samples were analyzed using t

13 dy using paired DBS-whole blood samples from venous and capillary sources from 49 volunteers with Hg

14 n also be used for assessing the function of venous and lymphatic valves from various species, includ

15 Arterial, endothelial, venous, angiogenic, and mural cell markers were signific

16 ontagious respiratory virus that can lead to venous/arterial thrombosis, stroke, renal failure, myoca

17 he central nervous system at this vulnerable venous barrier surface.

18 ntraretinal microvascular abnormalities, and venous beading, agreement was moderate (weighted kappa,

19 Heparinized venous blood and bone marrow were collected from the pat

20 tion is a rare condition in which splanchnic venous blood bypasses the liver draining directly into s

21 the differential assessment of arterial and venous blood flow patterns in the retina that may facili

22 leg blood flow and radial artery and femoral venous blood gases were measured.

23 Radial artery and femoral venous blood gases were measured.

24 from a primary tumor can be detected in the venous blood of cancer patients.

25 er laboratory indicators, were measured in a venous blood sample.

26 d at peak exercise from femoral arterial and venous blood samples and leg blood flow (by thermodiluti

27 Venous blood samples and urine were collected for pharma

28 moglobin concentration (Hb) in capillary and venous blood samples of HIV-negative and HIV-positive su

29 oth protocols, arterial and internal jugular venous blood samples were collected at rest and coupled

30 Serial venous blood samples were drawn from 1 to 240 min after

31 Methods: Venous blood samples were obtained from 48 patients subj

32 ontinuous arterial and discrete arterial and venous blood sampling were performed to determine a plas

33 LV(EV), distal pulmonary venous blood volume for vessels smaller than 5 mm(2) in

34 Simultaneous arterial and jugular venous bulb blood gas samples were recorded prospectivel

35 ressure, mean arterial pressure, and jugular venous bulb oxygen saturation.

36 he mean brain tissue oxygen tension, jugular venous bulb oxygen tension, and cerebral perfusion press

37 were significant differences in the jugular venous bulb oxygen tension-brain oxygen tension gradient

38 < 0.001) and in the relationship of jugular venous bulb oxygen tension-brain oxygen tension gradient

39 he mean brain tissue oxygen tension, jugular venous bulb oxygen to brain tissue oxygen tension gradie

40 or caval replacement technique without veno-venous bypass or shunts.

41 ton-wool spots, Kyrieleis plaques, irregular venous caliber with dilated and sclerotic segments, peri

42 Conversely, a subset of angiogenic venous capillary ECs and respective resident endothelial

43 nited States start hemodialysis on a central venous catheter (CVC).

44 he distribution of microorganisms in central venous catheter and arterial catheter-related bloodstrea

45 nicity are associated with time on a central venous catheter and transition to an arteriovenous fistu

46 ediatric patients with cancer with a central venous catheter from April 2015 to August 2019 at a sing

47 a catheterization with a short-term central venous catheter or peripheral arterial catheter with an

48 sidence within 1 year prior; or if a central venous catheter was present <=2 days prior.

49 Among central venous catheter, the distribution of microorganisms asso

50 ccess, and repeated life-threatening central venous catheter-associated infections requiring critical

51 No patient had central venous catheter-related deep vein thrombosis.

52 mbotic medication, and presence of a central venous catheter.

53 ly inserted central catheter: 0.73%, central venous catheter: 0.24%; p = 0.001) (peripherally inserte

54 ly inserted central catheter: 0.93%, central venous catheter: 0.52%; p = 0.001) (peripherally inserte

55 ral catheter: 10.82/1,000 line days, central venous catheter: 4.97/1,000 line days) occurred in perip

56 tral catheter: 8.65/1,000 line days, central venous catheter: 6.29/1,000 line days) and central-line

57 sists of six independent predictors: central venous catheterization (5 points), immobilization greate

58 Central venous catheterization and immobilization are potentiall

59 llowing: vasoactive infusions (88%), central venous catheters (86%), mechanical ventilation (59%), an

60 h the majority of cases secondary to central venous catheters (CVCs).

61 tion and venous thromboembolism than central venous catheters in children admitted to the PICU.

62 rally inserted central catheters and central venous catheters, are often needed in critically ill pat

63 d only a small number of artery enhancers in venous cells to prevent their activation, including a di

64 The average time for processing arterial and venous cerebral vasculature with the network was less th

65 hosis occurred (thrombocytopenia, collateral venous circulation, first degree varices oesophagii).

66 tered systemically, from the arterial to the venous circulation.

67 s, expression of Angpt2(443) caused impaired venous development, suggesting enhanced function as a co

68 breathlessness, sleep disturbance, cyanosis, venous dilatation, paresthesia, headache, and tinnitus)

69 Chronic Venous Disease (CVD) is an important cause of morbidity

70 rt disease, heart failure, valvular disease, venous disease, and peripheral artery disease) and the a

71 All cases of deep venous drainage and all those located in eloquent areas

72 in poorly formed networks, especially in the venous drainage areas, and arteriovenous malformations a

73 emodelling in utero and also indicates rapid venous drainage from the placenta, which is important be

74 on of the defect with unobstructed pulmonary venous drainage to left atrium.

75 rm defect closure and unobstructed pulmonary venous drainage, followed by deployment of a 10-zig cove

76 ed in eloquent areas, and of those with deep venous drainage; it is also highly sensitive in detectin

77 greater weight regain included: younger age, venous edema, poorer physical function, and more depress

78 By contrast, in venous endothelial cells, NR2F2 was bound to this site,

79 idence of thrombosis (including arterial and venous events) at day 30 following discharge was 2.5% (9

80 tory element of Prox1, thereby enhancing its venous expression.

81 induced by volume overload using the arterio-venous fistula model (AV-Shunt) in adult male rats.

82 maximized to 100% the use of continuous veno-venous hemodiafiltration and doubled the percentage of p

83 isruption of Rasa1 in adult mice resulted in venous hypertension and impaired VV function that was as

84 ni-osmotic pump for continuous 4-day jugular venous infusion of sEVs and determined their effects on

85 Direct venous inoculation (DVI) with PfSPZ vaccine has been saf

86 ult male volunteers were immunized by direct venous inoculation with radiation-attenuated, aseptic, p

87 ned as persistent symptoms, signs of chronic venous insufficiency, or both, occurs in 25% to 50% of p

88 iously proposed MVI signatures: radiogenomic venous invasion (RVI) and two-trait predictor of venous

89 us invasion (RVI) and two-trait predictor of venous invasion (TTPVI), using single-reader and consens

90 e analysis, baseline mrTD/mrEMVI (extramural venous invasion) status was the only significant MRI fac

91 ologic lymph nodes, perineural invasion, and venous invasion.

92 nd %IT of nonobstructed lung territories and venous %IT of obstructed lung territories were significa

93 tructurally, atorvastatin promoted favorable venous limb outward remodeling, preserved arteriovenous

94 reviews the different conditions (arterial, venous, low-flow states) that can result in reduced bloo

95 e shown to have significant differences with venous metrics (p < 0.001).

96 al (water, Na(+), and K(+)) analyses; and 2) venous occlusion plethysmography to assess peripheral mi

97 PulseCam can also detect venous or partial blood flow occlusion that is difficult

98 Neovascularization of venous origin demonstrated slower flow speeds, whereas t

99 in DeltaPCO2 (Delta - DeltaPCO2) and central venous oxygen saturation (DeltaScvO2) during spontaneous

100 to -0.49 L/min/m; p = 0.00001), and central venous oxygen saturation (mean difference, -5.07; 95% CI

101 Delta - DeltaPCO2 and central venous oxygen saturation could predict extubation failur

102 Central venous oxygen saturation decreased in the failure group

103 index; 2.9% (2.2-3.5%) (p < 0.01) for mixed venous oxygen saturation or central venous oxygen satura

104 ery index, oxygen consumption index, central venous oxygen saturation, central venous-to-arterial car

105 ion with cardiac index, lactate, and central venous oxygen saturation.

106 or mixed venous oxygen saturation or central venous oxygen saturation; -3.7% (-4.4% to -3.0%) (p < 0.

107 mL/min of CO2 (59 mL/min when normalized to venous PCO2 of 45 mm Hg), corresponding to a 29% reducti

108 ne material density (MD) images, plus portal venous phase (PVP) conventional CT images.

109 phase (PCP), arterial phase (AP), and portal venous phase (PVP) scans.

110 ccular lesions that filled slowly during the venous phase and became brightly hyperfluorescent saccul

111 of the three phases (arterial, phase 1; peak venous, phase 2; and late venous, phase 3) of the CT ang

112 ial, phase 1; peak venous, phase 2; and late venous, phase 3) of the CT angiography.

113 that D-2-hydroxyglutarate (D-2HG) is high in venous plasma from patients with isocitrate dehydrogenas

114 e profiled more than 1600 molecules in renal venous plasma obtained from human subjects.

115 Baseline and follow-up voltage mapping, venous potentials, ostial diameters, and phrenic nerve v

116 tions in IOP, suggesting elevated episcleral venous pressure (EVP).

117 RV function improved as measured by central venous pressure (from 23.4 +/- 4.9 to 10.5 +/- 3.1 mm Hg

118 the mean systemic filling pressure - central venous pressure and the number of cardiac index-responde

119 Central venous pressure and velocity-time integral were measured

120 Marked increase in central venous pressure during passive leg raising cannot identi

121 cirrhosis, and portal hypertension (hepatic venous pressure gradient [HVPG] >= 6 mm Hg) from 36 cent

122 An increase in central venous pressure greater than or equal to 4 mm Hg during

123 we hypothesized that an increase in central venous pressure greater than or equal to 5 cm H2O (i.e.,

124 By analogy with the classical central venous pressure rules to assess a fluid challenge, we hy

125 Her venous pressure was elevated, but the liver was not enla

126 turn (mean systemic filling pressure-central venous pressure), arterial load properties (systemic vas

127 overy was defined as improvements in central venous pressure, pulmonary artery systolic pressure, RV/

128 Pullers reduce central venous pressures or renal venous pressures to increase r

129 ers reduce central venous pressures or renal venous pressures to increase renal perfusion.

130 = 21) displayed higher central and pulmonary venous pressures, and more severely impaired cardiac out

131 her mammals identified differential arterial-venous proteoglycan dynamics as a determinant of these c

132 djuvant chemotherapy, 105 (89%) simultaneous venous resections, and 101 (85.5%) arterial reconstructi

133 cluding 121 multivisceral resections and 171 venous resections.

134 Upright posture reduces venous return, stroke volume, and cardiac output (CO) wh

135 er 3 months confirmed unobstructed pulmonary venous return.

136 We evaluated the gradient for venous-return (mean systemic filling pressure-central ve

137 ic disc and in each of multiple arterial and venous segments was obtained and shown to reveal a tempo

138 Of the 122 total venous segments with corresponding conventional venograp

139 timating, in a pair of adjacent arterial and venous segments, various temporal waveform metrics such

140 t case of coinciding cerebral infarction and venous sinus thrombosis unveiling the diagnosis of celia

141 ry occlusion and left transverse and sigmoid venous sinus thrombosis, along with left jugular vein th

142 These cells are positioned adjacent to dural venous sinuses: regions of slow blood flow with fenestra

143 he consequential CRVO presumably advanced by venous stasis due to decrease in arterial inflow.

144 By now, venous stasis retinopathy in children due to Valsalva ma

145 ed by Valsalva maneuver is a risk factor for venous stasis retinopathy.

146 reproducible differences among arterial and venous thrombi and emboli related to their origin, desti

147 he structure and composition of arterial and venous thrombi and pulmonary emboli using high-resolutio

148 nary emboli mirrored the most distal part of venous thrombi from which they originated, which differe

149 d in TGFbetaRII-KO endothelial cells, murine venous thrombi, or endarterectomy specimens and plasma o

150 Although arterial and venous thromboembolic disorders are among the most frequ

151 iod, one death, one nonfatal stroke, and two venous thromboembolic events occurred in the upadacitini

152 A Study of Rivaroxaban [JNJ-39039039] on the Venous Thromboembolic Risk in Post-Hospital Discharge Pa

153 equal to 4 days (4 points), prior history of venous thromboembolism (4 points), mechanical ventilatio

154 logical events (25%), arrhythmias (22%), and venous thromboembolism (9%).

155 mary efficacy outcome, symptomatic recurrent venous thromboembolism (assessed by intention-to-treat),

156 ore of 15-18 (2%) had a high (17.7%) risk of venous thromboembolism (hazard ratio, 28.1; 95% CI, 21.7

157 -14 (22%) had an intermediate (3.6%) risk of venous thromboembolism (hazard ratio, 6.7; 95% CI, 5.3-8

158 accident (HR, 6.0; 95% CI, 2.6 to 14.1), and venous thromboembolism (HR, 24.7; 95% CI, 14.0 to 43.6).

159 tive international registry of patients with venous thromboembolism (March 2001-January 2019), we exp

160 ure (OR, 1.00 [95% CI, 0.68-1.47]; P=0.996), venous thromboembolism (OR, 1.04 [95% CI, 0.77-1.39]; P=

161 An increased rate of venous thromboembolism (peripherally inserted central ca

162 Early reports describe high venous thromboembolism (VTE) and disseminated intravascu

163 y contribute to thrombotic diseases, such as venous thromboembolism (VTE) and ischemic stroke.

164 T) replacement has been suggested to prevent venous thromboembolism (VTE) and thus may increase expos

165 failure to provide defect-free postoperative venous thromboembolism (VTE) chemoprophylaxis, (2) ident

166 se 2019 (COVID-19) with an increased risk of venous thromboembolism (VTE) has resulted in specific gu

167 Venous thromboembolism (VTE) incidence in children has s

168 Venous thromboembolism (VTE) is a major preventable dise

169 Venous thromboembolism (VTE) is a significant public hea

170 rtant decision in the long-term treatment of venous thromboembolism (VTE) is how long to anticoagulat

171 nship between cholesterol levels and risk of venous thromboembolism (VTE) is uncertain.

172 ated with dabigatran etexilate for secondary venous thromboembolism (VTE) prevention.

173 However, the association between GDF-15 and venous thromboembolism (VTE) remains uncertain.

174 All patients with venous thromboembolism (VTE) should receive anticoagulan

175 role of the polymorphism at position 310 in venous thromboembolism (VTE) using the International Net

176 pulmonary embolism, collectively defined as venous thromboembolism (VTE), are the third leading caus

177 h immunomodulatory drugs are at high risk of venous thromboembolism (VTE), but data are lacking from

178 Venous thromboembolism (VTE), composed of pulmonary embo

179 For patients with venous thromboembolism (VTE), prediction of bleeding is

180 Risk factors for venous thromboembolism (VTE), such as older age, maligna

181 ias in a substantial number of patients with venous thromboembolism (VTE), the initial hope that thei

182 Venous thromboembolism (VTE), which includes both deep v

183 Venous thromboembolism (VTE), which includes deep vein t

184 eminated intravascular coagulation (DIC) and venous thromboembolism (VTE).

185 r peripheral artery disease (PAD) events and venous thromboembolism (VTE).

186 [CI], 0.8-7.6); the cumulative incidence of venous thromboembolism alone at day 30 postdischarge was

187 Obese patients are also at higher risk for venous thromboembolism and dialysis.

188 this study was to determine the frequency of venous thromboembolism and the degree of inflammatory an

189 isms for the 50% of patients with unprovoked venous thromboembolism and to better understand mechanis

190 ombus resolution, and freedom from recurrent venous thromboembolism and venous thromboembolism-relate

191 ies of patients who were at elevated risk of venous thromboembolism and were randomly assigned to eit

192 Apixaban for the treatment of venous thromboembolism associated with cancer.

193 arin for the primary outcome of incidence of venous thromboembolism at 10 to 13 days postoperatively.

194 riptive statistics outlined the frequency of venous thromboembolism at any time during severe coronav

195 associated with dialysis initiation and with venous thromboembolism but not with major adverse cardia

196 -dimer and peak D-dimer were associated with venous thromboembolism development (p < 0.05).

197 a degree of inflammatory marker elevation to venous thromboembolism development.

198 coagulation marker elevation associated with venous thromboembolism development.

199 outcome was objectively confirmed recurrent venous thromboembolism during the trial period.

200 tically significant effects of prevention on venous thromboembolism endpoints.

201 The secondary objective was to compare venous thromboembolism events and coagulation variables

202 the study was to determine the prevalence of venous thromboembolism events in patients infected with

203 that heparin reduces the risk of symptomatic venous thromboembolism for patients with cancer; however

204 Historically, venous thromboembolism has received the greatest attenti

205 ow-molecular-weight heparin for treatment of venous thromboembolism in cancer patients: an updated me

206 Treatment of venous thromboembolism in children is based on data obta

207 this study was to determine the frequency of venous thromboembolism in critically ill coronavirus dis

208 nt study aimed to describe the prevalence of venous thromboembolism in critically ill patients receiv

209 We report a 100% occurrence of venous thromboembolism in critically ill patients suppor

210 edoxaban or rivaroxaban for the treatment of venous thromboembolism in patients with cancer.

211 parin with regard to the prevention of major venous thromboembolism in these patients.

212 Venous thromboembolism is a major cause of morbidity and

213 Venous thromboembolism is associated with increased mort

214 Clinically diagnosed symptomatic venous thromboembolism occurred in 1.4% of this large po

215 verse cardiovascular events, and symptomatic venous thromboembolism occurred with high frequency in p

216 Prespecified subgroup analysis of venous thromboembolism occurrence by cancer type identif

217 ulant administration on all-cause mortality, venous thromboembolism occurrence, and bleeding related

218 urgery who were considered to be at risk for venous thromboembolism on the basis of the investigator'

219 ysis that examined significant predictors of venous thromboembolism or central-line associated bloods

220 alysis established that the causal effect of venous thromboembolism prevention on mortality was null

221 We used data from venous thromboembolism prevention trials to evaluate the

222 tion trials to evaluate the causal effect of venous thromboembolism reduction on mortality.

223 were positive, with significantly increased venous thromboembolism risk in patients in control group

224 The ICU-Venous Thromboembolism score can identify patients at in

225 The ICU-Venous Thromboembolism score consists of six independent

226 Randomisation was stratified by age and venous thromboembolism site.

227 al-line associated bloodstream infection and venous thromboembolism than central venous catheters in

228 ing risk for stroke, pulmonary embolism, and venous thromboembolism through its effect on thrombin-in

229 The primary efficacy outcome of major venous thromboembolism was a composite of symptomatic di

230 Symptomatic venous thromboembolism was defined as deep vein thrombos

231 thrombosis in 7 of 12 patients (58%) in whom venous thromboembolism was not suspected before death; p

232 Annualized rates of stent occlusion or venous thromboembolism were 7.8 (acute thrombotic), 15.0

233 All complications except venous thromboembolism were significantly reduced in the

234 pitals in 28 countries with documented acute venous thromboembolism who had started heparinisation we

235 D-dimer greater than 2,600 ng/mL predicted venous thromboembolism with an area under the receiver o

236 false-negative rate (defined as diagnosis of venous thromboembolism within 90 d).

237 Low-molecular-weight heparin reduces risk of venous thromboembolism without increasing risk of major

238 agent (which might mitigate the lethality of venous thromboembolism) and those for which mortality da

239 adjusted RR was 0.58 (95% CI 0.47-0.71) for venous thromboembolism, 1.27 (0.92-1.74) for major bleed

240 examines the effect of heparin on survival, venous thromboembolism, and bleeding in patients with ca

241 ent highlights future research priorities in venous thromboembolism, developed by experts and a crowd

242 Major arterial or venous thromboembolism, major adverse cardiovascular eve

243 In children with acute venous thromboembolism, treatment with rivaroxaban resul

244 deep-vein thrombosis, pulmonary embolism, or venous thromboembolism-related death during the treatmen

245 om from recurrent venous thromboembolism and venous thromboembolism-related death.

246 solve the pressing public health problem of venous thromboembolism.

247 can identify patients at increased risk for venous thromboembolism.

248 a, 529 patients (1.4%) developed symptomatic venous thromboembolism.

249 ildren aged birth to less than 18 years with venous thromboembolism.

250 G containing ICs may also reduce the risk of venous thromboembolism.

251 ardial injury, myocarditis, arrhythmias, and venous thromboembolism.

252 ]), which dominated the overall reduction in venous thromboembolism.

253 s standard of care in treating children with venous thromboembolism.

254 , obstructive sleep apnoea, osteoporosis and venous thromboembolism.

255 tations of standard of care in children with venous thromboembolism.

256 are potentially modifiable risk factors for venous thromboembolism.

257 l-line associated bloodstream infections and venous thromboembolism.

258 All of these patients experienced venous thromboembolism: 10 patients (76.9%) had isolated

259 (76% of the sample) had a low (0.3%) risk of venous thromboembolism; those with a score of 9-14 (22%)

260 The secondary outcome was venous thromboembolisms.

261 isease 2019 infection has been high rates of venous thromboses.

262 te ischemic infarct (23.3%), one with a deep venous thrombosis (1.4%), eight with multiple microhemor

263 VTE) using the International Network Against Venous Thrombosis (INVENT) consortium multi-ancestry gen

264 used data from the International Network on Venous Thrombosis (INVENT) consortium to examine whether

265 regimen was not related to presence of deep venous thrombosis (p = 0.35).

266 mon complication was cannula-associated deep venous thrombosis (six patients, 23.1%).

267 There was no difference in incidence of deep venous thrombosis among different pharmacologic prophyla

268 omboembolism (VTE), which includes both deep venous thrombosis and pulmonary embolism, is a common an

269 e typical of the commonest manifestations of venous thrombosis at the lower extremities.

270 Patients found to have deep venous thrombosis had no difference in time to intubatio

271 Autopsy revealed deep venous thrombosis in 7 of 12 patients (58%) in whom veno

272 Lower extremity deep venous thrombosis is prevalent in coronavirus disease 20

273 locumab reduces the risk of VTE events (deep venous thrombosis or pulmonary embolism).

274 r loop of SLC44A2 that is protective against venous thrombosis results in severely impaired binding t

275 3,176-30,770 ng/mL] for lower extremity deep venous thrombosis vs 2,087 ng/mL [interquartile range, 6

276 Venous thrombosis was induced by inferior vena cava liga

277 ves, and had no history to suggest past deep venous thrombosis).

278 traction) and the incidence of postoperative venous thrombosis, 78 patients with brain tumors that we

279 cal site infection, pulmonary embolism, deep venous thrombosis, and death.

280 s were markedly higher in patients with deep venous thrombosis, both for maximum value and value on d

281 sis, thus resulting in 38.7% with PE or deep venous thrombosis, despite 40% receiving prophylactic an

282 TE), composed of pulmonary embolism and deep venous thrombosis, is a significant cause of maternal mo

283 atomas (1 of them due to needing heparin for venous thrombosis, none required interventions).

284 results at CT pulmonary angiography had deep venous thrombosis, thus resulting in 38.7% with PE or de

285 ultrasonography of both legs showed no deep venous thrombosis.

286 45 patients (42.2%) were found to have deep venous thrombosis.

287 ge, 638-3,735 ng/mL] for no evidence of deep venous thrombosis; p < 0.0001).

288 (DOACs) have become first-line treatment for venous thrombotic events.

289 an and murine endothelial cells and improved venous thrombus resolution and pulmonary vaso-occlusions

290 x, central venous oxygen saturation, central venous-to-arterial carbon dioxide pressure difference, a

291 ch of the intestinal epithelial barrier, and venous translocation to organs.

292 Several potential mechanisms, including venous transmission of pressure and elevated intracrania

293 Chest radiography showed no pneumonia, and venous ultrasonography of both legs showed no deep venou

294 mics, we characterized arterial (A)-to-renal venous (V) gradients for >1,300 proteins in 22 individua

295 pN stage, pT stage, lymphatic invasion, and venous vascular invasion.

296 lationships between CT metrics of emphysema, venous vascular volume, and sarcopenia with the LV epica

297 l volume correlated with a loss of pulmonary venous vasculature, greater pectoralis muscle sarcopenia

298 alidate the agreement between blood sources (venous vs capillary) and matrices (whole blood vs DBS).

299 lar to background populations (i.e., MeHg in venous whole blood ranged from 0.2 to 3 mug/L with a med

300 t concentrations in the gold standard (i.e., venous whole blood) and that DBS is a suitable tool for