ライフサイエンスコーパス: WBC

1 WBC and PLT counts were the most actionable routine test

2 WBC count is also a complex trait that varies among indi

3 WBC count was independently associated with somatic depr

4 WBC count was measured at baseline in 160,117 postmenopa

5 WBC separated from whole blood was trapped by the paper

6 WBC trapped on the paper leads to the ion diffusion bloc

7 WBC, CRP, ESR and DNI were higher in APN than in lower U

8 ratio, 19.7 [95% CI, 4.4-87.4]; p < 0.0001), WBCs more than 12,000/mm3 (odds ratio, 11.6 [95% CI, 2.8

9 n ESBL gene by uropathogen; (3) pyuria (>=10 WBC/hpf); and (4) dysuria and fever plus at least one of

10 (hazard ratio [HR] = 1.67; P = .04], log(10)(WBC) (HR = 1.33; P = .02), and trisomy 22 (HR = 0.54; P

11 C count and of the mean of baseline + year 3 WBC count.

12 times the number of RBCs; CNS3a to 3c, >/= 5 WBCs/muL plus blasts with/without >/= 10 RBCs/muL or cli

13 blasts with/without >/= 10 RBCs/muL or >/= 5 WBCs/muL plus blasts, with WBCs >/= 5 times the number o

14 ts in a nontraumatic sample) nor CNS-3 (>/=5 WBCs/muL with blasts in a nontraumatic sample or the pre

15 Patients with overt CNS disease (CNS3; >= 5 WBCs/muL with blasts) received HDMTX and were randomly a

16 s follows: CNS1, no blasts; CNS2a to 2c, < 5 WBCs/muL and blasts with/without >/= 10 RBCs/muL or >/=

17 Neither CNS-2 (less than 5 WBCs/muL with blasts in a nontraumatic sample) nor CNS-3

18 Our results indicate that as little as 10(5) WBC and 100 mul of blood collected from asymptomatic scr

19 that the intravenous administration of 10(5) WBCs is sufficient to cause scrapie in recipient sheep.

20 When combined with MRD and a WBC count >/=200 x 10(9)/L, it identifies a significant

21 Fourteen patients (8.0%) had a WBC count of >50.0 x 10(9)/microL.

22 whereas animals injected with PYKK081 had a WBC count that resembled that of the uninfected control.

23 Patients harboring a WBC count >/=200 x 10(9)/L, gHiR classifier, and MRD >/=

24 of 46%, whereas the 58 patients (30%) with a WBC count <200 x 10(9)/L, gLoR classifier, and MRD <10(-

25 reater than 20.0 U combined with an abnormal WBC further improved Sepsis-2 detection (area under the

26 lbuminema, elevated creatinine, and abnormal WBC were all significant predictors (P < 0.0001) of incr

27 duction of mortality with bivalirudin across WBC tertiles was independent of major bleeding, and a si

28 its specificity for malignant and activated WBCs, LtxA is being investigated as a therapeutic agent

29 how LtxA preferentially recognizes activated WBCs is not known.

30 LtxA preferentially targets activated WBCs and is being developed as a therapeutic agent for t

31 on between bivalirudin therapy and admission WBC count was apparent for 1-year mortality.

32 Age, WBC count, secondary AML, Eastern Cooperative Oncology G

33 d 8 other prognostic factors, including age, WBC count, cytogenetics, and gene mutations, into surviv

34 ivariable Cox regression analysis, sex, age, WBC count, and cytogenetic risk category were related to

35 compared with age >60 years, secondary AML, WBC >50 G/L, European LeukemiaNet risk groups, and Easte

36 blood samples from three studies to analyze WBC DNA methylation of two ATM intragenic loci (ATMmvp2a

37 utropenia (42%), thrombocytopenia (38%), and WBC count decreased (34%).

38 2), hematocrit levels (P = 9.5 x 10(-7)) and WBC count (P = 3.1 x 10(-5)).

39 e, 0.63) followed by albumin, bilirubin, and WBC count (area under the receiver operating characteris

40 induced blood and organ cytokine content and WBC composition changes, including lymphocyte subsets in

41 n 5th POD, PCT has a better AUC than CRP and WBC (0.862 vs 0.806 vs 0.611).

42 correlation between appendiceal diameter and WBC was 80% (P=0.01 <0.05).

43 nce status, lactate dehydrogenase level, and WBC count, were confirmed as independent prognostic fact

44 clinical tumor growth rate, lymphocytes, and WBC.

45 fied the inverse association between MDS and WBC count and partially accounted for the association wi

46 PLT and WBC counts were both inversely related to MD adherence (

47 association between the MD and both PLT and WBC counts.

48 perative level for 1 year posttransplant and WBC counts were significantly lower for 3 years after tr

49 gnostic factors such as cytogenetic risk and WBC count, neither the presence of EMD nor the number of

50 the six studied PCB congeners were sex- and WBC type specific.

51 8), C-reactive protein (odds ratio 1.3), and WBCs (odds ratio 1.4).

52 eraction analysis between different PCBs and WBCs provides only a small overlap between sexes.

53 are identified in association with PCBs and WBCs.

54 9 deficiency is a common finding in RBCs and WBCs in patients with chronic hemolysis suffering from p

55 neously obtained myocardial core samples and WBCs were compared for SCN5A variants C (VC) and D (VD).

56 ly diagnosed, low- or intermediate-risk APL (WBC at diagnosis </= 10 x 10(9)/L).

57 combinations of temporal biomarkers, such as WBC, oxygen content, mean arterial pressure, and heart r

58 The genetic factors underlying basal WBC traits in Hispanics/Latinos are unknown.

59 Leptin increased basal WBCs, decreased basal and AMD3100-mobilized LSK cells, a

60 The associations between baseline WBC and MACE (composite of cardiac death, stent thrombos

61 Children had significantly higher baseline WBC counts (P < .001).

62 hazards associated with deciles of baseline WBC count and of the mean of baseline + year 3 WBC count

63 The association between WBC and MACE was consistent in acute coronary syndrome a

64 The association between WBC count and MDS disappeared when further adjusted for

65 ence is increasing for a correlation between WBC count and thrombosis, but prospective data are lacki

66 ause mortality and cardiac mortality between WBC and bivalirudin therapy.

67 nes do not change >10% of rank range between WBC and OO; only 878 (3.9%) change rank >50%.

68 vention had higher expression levels of both WBC-derived SCN5A variants compared with patients with H

69 stpartum (n = 43) by whole body calorimetry (WBC).

70 White blood cell (WBC) analysis provides rich information in rapid diagnos

71 ugh onset, and higher peak white blood cell (WBC) and lymphocyte counts.

72 jection criteria, based on white blood cell (WBC) and platelet (PLT) counts, were developed and prosp

73 tigated whether aortic and white blood cell (WBC) CoQ is programmed by suboptimal early nutrition and

74 diagnosis was defined as a white blood cell (WBC) count >20/uL, a CSF protein reading >50 mg/dL, or a

75 io [HR] = 0.58, P = .002), white blood cell (WBC) count <10 x 10(9)/L (HR = 0.60, P = .005), and ETV6

76 n, including decreased CSF white blood cell (WBC) count (P < .001), interleukin (IL)-4 (P = .02), IL-

77 I, 8.26-10.49), and higher white blood cell (WBC) count (per 1000/muL: beta = 0.95; 95% CI, 0.74-1.16

78 be an interaction between white blood cell (WBC) count and bivalirudin for the risk of mortality, an

79 White blood cell (WBC) count appears to predict total mortality and corona

80 ive values of a normal CSF white blood cell (WBC) count for ME panel targets were 100% (195/195) for

81 White blood cell (WBC) count is a common clinical measure used as a predic

82 Elevated white blood cell (WBC) count is associated with increased major adverse ca

83 Average white blood cell (WBC) count was 37.7 x 10(9)/microL.

84 and HIV disease markers or white blood cell (WBC) count were examined using mixed-effects and linear

85 otein (CRP) concentration, white blood cell (WBC) count, and absolute neutrophil cell (ANC) count for

86 hsCRP), lipid profile, and white blood cell (WBC) count, at baseline and 1, 3, and 6 months.

87 antly elevated circulating white blood cell (WBC) count, whereas animals injected with PYKK081 had a

88 , platelet count (PLT) and white blood cell (WBC) count.

89 netic classifier, MRD, and white blood cell (WBC) count.

90 30% bone marrow blasts and white blood cell (WBC) counts </=15 x 109/L (AZA-AML-001 study).

91 xin(+) patients had higher white blood cell (WBC) counts (12.5 x 10(3) versus 9.3 x 10(3) cells/mul;

92 Circulating white blood cell (WBC) counts (neutrophils, monocytes, lymphocytes, eosino

93 ration, hematocrit levels, white blood cell (WBC) counts and platelet counts in 31,340 individuals ge

94 Platelet (PLT) and white blood cell (WBC) counts are 2 markers of inflammation and have been

95 c variation in circulating white blood cell (WBC) counts from large samples of otherwise healthy indi

96 ith electrocardiogram, and white blood cell (WBC) counts with hematology analyzer.

97 ein (hsCRP) levels, higher white blood cell (WBC) counts, and lower serum albumin levels, are associa

98 es were ELN risk group and white blood cell (WBC) counts; treatment with midostaurin had no influence

99 Pleocytosis with white blood cell (WBC) levels of >=5 cells/mm(3) and >=10 cells/mm(3) were

100 ntitis, hours of sleep and white blood cell (WBC) markers among a nationally representative sample of

101 f over one quarter-million white blood cell (WBC) nuclei together with CD15/CD16 protein expression f

102 he generalizability of the white blood cell (WBC) transcriptome to the general, multiorgan transcript

103 bin, red blood cell (RBC), white blood cell (WBC), and platelet counts with an accuracy > 95% as comp

104 en BBB opening, pattern of white blood cell (WBCs) entry into the brain and seizure occurrence.

105 <30%) or first leukopenia (white blood cell [WBC] count <3000 cells/mm), which required clinical inte

106 onal inflammatory markers (white blood cell [WBC] count, erythrocyte sedimentation rate [ESR], C-reac

107 retic peptide [NT-proBNP], white blood cell [WBC], platelet counts) in 1265 AMI patients.

108 normal CSF was defined as white blood cells (WBC) >20/uL, CSF protein >50 mg/dL, or reactive CSF Vene

109 Ms-RvD3, RvD4 and PD1-and white blood cells (WBC) and platelets.

110 etween DNA methylation in white blood cells (WBC) and the risk of breast cancer.

111 avenous administration of white blood cells (WBC) resulted in efficient disease transmission.

112 rostate cancer cells from white blood cells (WBC) through forces generated by ultrasonic resonances i

113 articular distribution of white blood cells (WBC), as well as random effects.

114 omes latent in peripheral white blood cells (WBC).

115 s, more specifically from white blood cells (WBC).

116 dum 16S RNA in CSF or CSF white blood cells (WBCs) >20/uL or a reactive CSF-Venereal Disease Research

117 tion antigen-1 (LFA-1) on white blood cells (WBCs) and causes cell death.

118 -1 (LFA-1; CD11a/CD18) on white blood cells (WBCs) and causing cell death.

119 Proper circulation of white blood cells (WBCs) in the pulmonary vascular bed is crucial for an ef

120 White blood cells (WBCs) play an important role in host immune responses ea

121 cells (PBMCs) and of CSF white blood cells (WBCs) that were activated monocytes (CD14+CD16+) was det

122 DNA methylation in white blood cells (WBCs) was associated with total IgE levels in an epigeno

123 l mRNA splice variants in white blood cells (WBCs) with risk of arrhythmias in heart failure (HF).

124 crobial response in human white blood cells (WBCs).

125 that specifically targets white blood cells (WBCs).

126 ine oxime [HMPAO]-labeled white blood cells [WBC]).

127 for baseline and procedural characteristics, WBC remained independently associated with MACE (hazard

128 sex, blood pressure, serum HDL cholesterol, WBC count, and history of current cigarette smoking; and

129 genetic mechanisms that regulate circulating WBC counts and suggest a prominent shared genetic archit

130 levels strongly correlated with circulating WBC samples for both VC and VD variants (r = 0.78 and 0.

131 Because circulating WBCs demonstrate similar SCN5A splicing patterns, we hyp

132 t the sepsis-induced decrease in circulating WBCs, augment the early (6 hr postcecal ligation and pun

133 The circulating WBCs and LSKs, and CFUs were reduced in both models with

134 itory to define two datasets for comparison, WBC and OO (Other Organ) sets.

135 quantification to achieve rapid and low-cost WBC analysis at the point-of-care under resource limited

136 White blood count (WBC), C-reactive protein (CRP) and PCT levels were measu

137 r in patients with a white blood cell count (WBC) <50 Giga per liter (G/L) (P < .0001) and in older p

138 individual's maximum white blood cell count (WBC) as a continuous measure.

139 appendicoliths, and white blood cell count (WBC) were significantly correlated with the inflammation

140 interleukin (IL)-6, white blood cell count (WBC), vascular cell adhesion molecule (VCAM)-1, and inte

141 62P) concentrations; white blood cell count (WBC); heart rate; and blood pressure.

142 umin ratio, and CSF white blood cell counts (WBC), neopterin levels, and concentrations of chemokines

143 CRP, WBC and percentage of neutrophils were analyzed in the t

144 on; however, patients with CNS3 disease (CSF WBC >= 5/muL with blasts or cranial nerve palsies, brain

145 Among those living with HIV, CSF WBC counts and CSF-VDRL reactivity were more likely to n

146 elationship between the normalization of CSF WBC counts and CD4+ T cell counts may indicate continued

147 Among those with HIV, CSF WBCs and CSF-VDRL reactivity were more likely to normali

148 he relationship between normalization of CSF WBCs and CD4+ T cell count may indicate continued imprec

149 uals treated with either PenG or APPG-P, CSF WBCs and CSF-VDRL reactivity normalized within 12 months

150 defined as undetectable CSF T. pallidum, CSF WBCs </=5/uL and nonreactive CSF-VDRL.

151 Unexpectedly, CSF WBCs were more likely to normalize in those with low CD4

152 Unexpectedly, CSF WBCs were more likely to normalize in those with low CD4

153 Current WBC counting method relies on bulky instrument and train

154 Western boundary currents (WBCs) redistribute heat and oligotrophic seawater from t

155 up by the investigators because of decreased WBC counts, mostly outside of study protocol criteria, d

156 or high risk (HR) on the basis of diagnostic WBC count.

157 time of BBB-induced epileptiform discharges, WBCs populated the perivascular space of a leaky BBB.

158 label-free smartphone based electrochemical WBC counting device on microporous paper with patterned

159 Elevated WBC count during follow-up was correlated with thrombosi

160 underlying pathophysiologic role of elevated WBC across a spectrum of coronary artery disease present

161 t therapy, grade 3/4 hepatic encephalopathy, WBC count, and albumin.

162 pigenome-wide association study adjusted for WBC types (including eosinophils), methylation changes i

163 However, adjustment for WBC types resulted in markedly fewer significant sites.

164 nd the MD was not affected by adjustment for WBCs.

165 No frank WBCs extravasation in the brain parenchyma was observed.

166 to discriminate and divert tumor cells from WBCs using erythrocyte-lysed blood from healthy voluntee

167 rich both viable and fixed cancer cells from WBCs with very high recovery and purity.

168 Whole-genome methylation of DNA from WBCs was measured by using the Illumina Infinium HumanMe

169 of cancer cells from cell culture lines from WBCs with a recovery rate better than 83%.

170 fluorescent protein (GFP)-labeled WBCs (GFP-WBCs) suspended in Evans Blue we found that, at time of

171 accompanied by improvements in CSF glucose, WBC, protein, cellular and soluble inflammatory markers

172 In PR-GOAL WBC types (ie, neutrophils, eosinophils, basophils, lymp

173 ore including ASXL1 status, age, hemoglobin, WBC, and platelet counts defines three groups of CMML pa

174 Her WBC count was 10,370/muL, with a differential showing 5%

175 A high WBC count, raised serum ALT, raised serum total bilirubi

176 Lower haemoglobin (Hb) and high WBC counts were also significantly different between the

177 Higher WBC counts were significantly associated with positive b

178 Higher WBC, KIT, and/or FLT3-ITD/TKD gene mutations, and a less

179 P=0.004), having lower BMI (P=0.003), higher WBC (P=0.005) and higher D-dimer levels (P=0.044) were a

180 positively associated with older age, higher WBC and platelet counts, intermediate-risk and normal cy

181 re each independently associated with higher WBC counts in adjusted models (P < .01); the highest qua

182 Patients with higher WBC were more often younger, smokers, and with less como

183 st of the added value from the (99m)Tc-HMPAO-WBC scan for decision making was seen in patients in who

184 We assessed the value of (99m)Tc-HMPAO-WBC scintigraphy including SPECT/CT acquisitions in a se

185 (99m)Tc-HMPAO-WBC scintigraphy results were correlated with transthora

186 lts demonstrate the ability of (99m)Tc-HMPAO-WBC scintigraphy to reduce the rate of misdiagnosed case

187 aphy but correctly negative at (99m)Tc-HMPAO-WBC scintigraphy: these patients had marantic vegetation

188 hsCRP, WBC count, and serum albumin were measured at baseline i

189 expression of antimicrobial factors in human WBCs and reveal a distinctive role, not shared with ET,

190 s found to be abundantly expressed in IgM(+) WBC from CyHV-3 latently infected koi.

191 e terminal repeat was investigated in IgM(+) WBC from koi with latent CyHV-3 infection.

192 The presence of the CyHV-3 genome in IgM(+) WBC was about 20-fold greater than in IgM(-) WBC.

193 3 latency was further investigated in IgM(+) WBC.

194 WBC was about 20-fold greater than in IgM(-) WBC.

195 etes remitters had significant reductions in WBC and platelet counts whereas five non-remitters did n

196 l8, Il10, Pghs2, Tnfa, and Crp expression in WBCs, elevated plasma levels of IL-1beta, IL-6, and IL-8

197 ation between genome-wide DNA methylation in WBCs and total IgE levels in 2 studies of Hispanic child

198 T/ MR), recruitment of immune cells ((111)In-WBC SPECT), or enhanced glycolytic flux seen in inflamma

199 Increased WBC is an independent predictor of MACE after percutaneo

200 acteremia, altered liver function, increased WBC counts, pathogen-specific Ab (IgM and IgG), and cell

201 nted with lower hemoglobin levels, increased WBC and platelet counts, and were more likely to have DN

202 (WT) or Tet2(+/-) BM cells, led to increased WBC counts, monocytosis, and splenomegaly in WT recipien

203 lly increases HR, reduces HRV, and increases WBC.

204 Infected WBCs can also function as 'Trojan horses' and carry viru

205 Age, initial WBC count, genetic aberrations, and minimal residual dis

206 s that included age, race/ethnicity, initial WBC, and day-29 minimal residual disease < 0.1%, CSF bla

207 We demonstrate that several previously known WBC-associated genetic loci (e.g. the African Duffy anti

208 sing green fluorescent protein (GFP)-labeled WBCs (GFP-WBCs) suspended in Evans Blue we found that, a

209 patients with immune deficiency or leukemia WBC should be persistently monitored.

210 eic HCT, ELN favorable-risk group, and lower WBC counts as significant favorable factors.

211 EVI1(-) t(9;11) AMLs had lower WBC counts, more commonly FAB M5 morphology, and frequen

212 but not in patients in the mid-WBC or lower WBC tertiles.

213 risk factors compared with those with lower WBC.

214 0) and increased odds of being in the lowest WBC-count group (IMI: odds ratio = 1.41; 95% confidence

215 ut PCOS who had higher inflammatory markers (WBC and CRP), HDL and insulin resistance (p < 0.001).

216 High deciles of both baseline and mean WBC count were positively associated with total mortalit

217 ered from MLD(-) patients only by lower mean WBC counts, not by biologic characteristics, cytogenetic

218 The weighted mean WBC count was 7,130 cells/uL, with the WBC 5-part differ

219 ly; P<0.0001) but not in patients in the mid-WBC or lower WBC tertiles.

220 coding variants) associated with one or more WBC traits, the majority of which are pleiotropically as

221 festyle, and health characteristics, neither WBC markers nor periodontitis were related to hours of s

222 In this branched vascular network, WBCs have to strongly deform to pass through the narrowe

223 Normal WBC and monocyte distribution width inferred a six-fold

224 Notably, WBC CoQ levels correlated with aortic telomere-length (P

225 e, confirmed that high MRD values (> 0.1% of WBC) were associated with a higher risk of relapse after

226 The association of WBC count with mortality was independent of smoking and

227 th Initiative to examine the associations of WBC count with total mortality, CHD mortality, and cance

228 view demonstrated that rejection criteria of WBC >=11 000 cells/uL or PLT >=300 000 cells/uL would ha

229 The evaluation of WBC DNA methylation as a biomarker of cancer risk is of

230 el tracks the evolution of the morphology of WBC subpopulations as a patient transitions from a healt

231 Our PheWAS of WBC found expected results, including associations with

232 ed models (P < .01); the highest quartile of WBC counts (>/=6500 cells/microL) was associated with in

233 ression resulted in decreased recruitment of WBC to the sites of inflammation and improvement in card

234 as a therapeutic agent for the treatment of WBC diseases such as hematologic malignancies and autoim

235 e conclude that climate-driven expansions of WBCs will expand the range of tropical oligotrophic micr

236 increased G-CSF- or AMD3100-mobilization of WBCs and LSKs, compared to the untreated.

237 (myeloperoxidase activity), total number of WBCs, and neutrophils in bronchoalveolar lavage fluids c

238 symptoms were not associated with hs-CRP or WBC count.

239 igh-risk categories were defined as hsCRP or WBC levels above the 75th percentile (5.1 mg/L and 6.9 x

240 differentiation, or clearance of particular WBC lineages (myeloid, lymphoid) and also potentially in

241 In multivariate analyses, peak WBC count, birth weight, intubation, and receipt of nitr

242 spital lengths of stay) and incremental peak WBC counts (hospital length of stay only).

243 utations in other genes, or had a presenting WBC of < 10 x 10(9) L(-1).

244 esponses occurred in AML with low presenting WBC count.

245 Distributions of sex, age, race, presenting WBC count, risk group, treatment arm, and compliance wit

246 RD monitoring was far superior to presenting WBC (hazard ratio, 1.02; 95% CI, 1.00 to 1.03; P = .02),

247 older age (P < .001) and higher pretreatment WBC (P = .04) compared with wild-type TET2 (TET2-wt).

248 ningfully associated with hs-CRP, NT-proBNP, WBC, or platelet counts 1 month after AMI, suggesting th

249 We are able to rapidly quantify WBC concentrations covering the common physiological and

250 Recuperated WBCs also had reduced CoQ (74+/-5.8%; P<0.05).

251 se variants in CXCR2 associated with reduced WBC count (gene-based P = 2.6 x 10(-13)).

252 Laboratory work revealed WBC 30.4 k/muL, hemoglobin 7.9 g/dL, and platelets 16 k/

253 77 days post transmission) had CSF HIV RNA, WBC, neopterin, and CXCL10 concentrations similar to the

254 duals and hospitalized patients with similar WBC counts can be robustly classified based on their WBC

255 RL21A did not stain WBCs (total WBCs) or normal tissues from deceased HLA-A2

256 range, 17 to 85 years), performance status, WBC count, and mutation status of NPM1, CEBPA, and FLT3-

257 operative Oncology Group performance status, WBC count, creatinine clearance, albumin, AST, number of

258 Strengthening WBCs have been implicated in the poleward range expansio

259 In the GALA II study WBC types were imputed.

260 Here we show that the major subtropical WBC of the South Pacific Ocean, the East Australian Curr

261 lysis, age, symptoms >48 hours, temperature, WBC, Alvarado score, and appendicolith were predictive o

262 rve (AUC) (0.775 vs 0.772), both better than WBC (0.601); in 5th POD, PCT has a better AUC than CRP a

263 Together, our findings indicate that WBC DNA methylation levels at ATM could be a marker of b

264 The WBC differential showed 64% blasts and 24% promyelocytes

265 to keep the platelet count, and arguably the WBC count, within the normal range.

266 We examined the WBC- and NLR-BC relationships.

267 pression rank and correlation profile in the WBC dataset.

268 We show that the WBC nucleus images alone can be used to replicate CD exp

269 mean WBC count was 7,130 cells/uL, with the WBC 5-part differential estimated in terms of percentage

270 ts can be robustly classified based on their WBC population dynamics.

271 plicing patterns, we hypothesized that these WBC-derived splice variants might further stratify patie

272 Patients were stratified according to WBC tertiles.

273 s and suggests that the toxin contributes to WBC depletion.

274 t for neutrophil count) are generalizable to WBC traits in Hispanics/Latinos.

275 trast, periodontitis was directly related to WBC count and %neutrophils and inversely related to %lym

276 Periodontitis may be directly related to WBC count and %neutrophils and inversely related to %lym

277 low-frequency power by 90% (P = 0.01), total WBC count by 139% (P = 0.006), and lymphocyte count by 1

278 med a genome-wide association study of total WBC and differential counts in a large, ethnically diver

279 an exome array-based meta-analysis of total WBC and subtype counts (neutrophils, monocytes, lymphocy

280 erform a trans-ethnic meta-analysis of total WBC, neutrophil and monocyte counts.

281 onse to blood neutrophils (rather than total WBC) was also not well correlated between humans and mic

282 Reduction in triglyceride, VLDL, total WBC, lymphocyte, and neutrophil counts and increase in h

283 RL21A did not stain WBCs (total WBCs) or normal tissues from deceased HLA-A2 donors, sub

284 001)] and reduction of therapeutic toxicity [WBC decrease (P = 0.04); gastrointestinal adverse reacti

285 patients enrolled in the HORIZONS-AMI trial, WBC count was available in 3433 (95.3%) patients.

286 ptional and signaling pathways that underlie WBC development and lineage specification can contribute

287 IIb/IIIa inhibitors in patients in the upper WBC tertile (all-cause death: 4.1% versus 9.3%, respecti

288 Using WBC levels of >=5 cells/mm(3), 63.4% (59/93) of positive

289 Therefore, defining which WBCs are permissive to Zika virus (ZIKV) is critical.

290 have identified genomic loci associated with WBC and its subtypes, but much of the heritability of th

291 gnals within loci previously associated with WBC or its subtypes were identified.

292 ribution width alone and in combination with WBC count for early sepsis detection in the emergency de

293 Abnormal glucose in combination with WBC levels of >=10 cells/mm(3) showed high specificity (

294 er than 20.0 U, alone or in combination with WBC, improves early sepsis detection by Sepsis-2 criteri

295 -induced nor chronic seizures correlate with WBC brain parenchymal migration while albumin and IgG br

296 In tandem with WBC, monocyte distribution width is further predicted to

297 RBCs/muL or >/= 5 WBCs/muL plus blasts, with WBCs >/= 5 times the number of RBCs; CNS3a to 3c, >/= 5

298 nt responses to the interaction of PCBs with WBCs, suggesting a role of the immune system in PCB-rela

299 iAMP21 was associated with age >/= 10 years, WBC less than 50,000/muL, female sex, and detectable MRD

300 ed ASXL1 mutations, age older than 65 years, WBC count greater than 15 x10(9)/L, platelet count less