ライフサイエンスコーパス: MCV

1 MCV can sense stresses in its intracellular environment,

2 MCV has evolved a novel mechanism to target hVam6p that

3 MCV is clonally integrated into MCC tumor cells, which t

4 MCV is similar to simian virus 40 (SV40) and encodes a n

5 MCV lacks the agnoprotein sequence but generates miRNAs.

6 MCV large T up-regulated Sox2 through its retinoblastoma

7 MCV lesions persist because of virally encoded immune ev

8 MCV LT translocates hVam6p to the nucleus, sequestering

9 MCV provides qualitative and quantitative insights into

10 MCV sequences were detected in 8 of 10 (80%) MCC tumors

11 MCV should not be used as a marker for vitamin B-12 insu

12 MCV sT binds through its Large T stabilization domain re

13 MCV sT has a restricted range for PP2A B subunit substit

14 MCV sT instead transforms tumor cells through another re

15 MCV sT is also required for efficient MCV DNA replicatio

16 MCV ST recruits the MYC homologue MYCL (L-Myc) to the EP

17 MCV sT was found to act downstream in the mammalian targ

18 MCV sT, however, only displaces a restricted subset of P

19 MCV sT-associated 4E-BP1 serine 65 hyperphosphorylation

20 MCV sT-PP2A interactions can be functionally distinguish

21 MCV was associated with more permanent pacemakers (22.5%

22 MCV was significantly lower in the postfortification per

23 MCV-positive MCC expresses small T antigen (ST) and a tr

24 When the patient was not receiving CMX-001, MCV DNA was detected in 50% of samples.

25 Compared with MPSV-4, MCV-4 elicited greater persistence of antibody activity

26 9 [184.8-334.9]; ES(TA), 206.1[162.5-249.7]; MCV(TF), 78.5 [25.3-131.6]; P<0.001) and the self-expand

27 In addition, MCV-positive MCC cells expressed high levels of MDM4.

28 younger than 9 months followed by additional MCV doses results in high seropositivity, vaccine effect

29 m 42+/-16 mm Hg before to 18+/-8 mm Hg after MCV implantation (P<0.001), in those with AR the level d

30 Notably, all MCV-positive MCC cell lines underwent growth arrest and/

31 Although MCV is caused by direct inoculation of virus into skin i

32 Although MCV is known to integrate into the tumor cell genome and

33 count (PLT), red blood cell indices (MCH and MCV) and HDL cholesterol.

34 thy participants demonstrated higher PPC and MCV and shorter LMCV in central compared with peripheral

35 RP patients, test point in which the PPC and MCV were lower than 4 standard errors from the mean of h

36 In healthy participants, higher PPC and MCV were measured in response to blue compared with red

37 KIV, WUV and MCV are all widespread in humans.

38 assay panel combining anti-dsDNA, ANA, anti-MCV, EC4d, and BC4d is sensitive and specific for the di

39 dendritic cells have prominent roles in anti-MCV responses, and these features characterize the infla

40 ated with ANA positivity (>/=20 units), anti-MCV negativity (</=70 units), and elevated levels of bot

41 The absence of inflammation around MCV lesions suggests the presence of potent inhibitors o

42 eting capacity of viral oncoproteins such as MCV sT, which may contribute to Merkel cell carcinogenes

43 Because MCV cannot be propagated in cell culture, MC159 was expr

44 ties and differences in PP2A binding between MCV and SV40 sT.

45 This study reveals a key difference between MCV LT and simian vacuolating virus 40 LT, which activat

46 rotein-protein interface is observed between MCV OBDs when bound to the central region of the origin.

47 The study found that 5.2 billion MCV doses must be administered during 2010-2025 to maint

48 t increase in viral DNA replication for BKV, MCV and HPyV7.

49 82; p = 0.340) or life-threatening bleeding (MCV, 13.7% vs. ESV, 8.8%; HR: 1.644; 95% CI: 0.878 to 3.

50 We find that SIAs have boosted MCV coverage in some places, but not in others, particul

51 umors displayed very low mutation rates, but MCV-negative tumors exhibited a high mutation burden ass

52 ere more likely to be HPyV9-seropositive but MCV-seronegative, and HPyV7 seropositivity was associate

53 luding S6K and 4E-BP2, was also increased by MCV sT.

54 rified with subunits PP2A Aalpha and PP2A C, MCV sT coimmunopurified with PP2A Aalpha, PP2A Abeta, an

55 .785 to 2.407; p = 0.266) or cardiovascular (MCV, 8.3% vs. ESV, 7.4%; HR: 1.145; 95% CI: 0.556 to 12.

56 ear, there were no differences in all-cause (MCV, 16.2% vs. ESV, 12.3%; HR: 1.374; 95% CI: 0.785 to 2

57 differences in major vascular complications (MCV, 9.3% vs. ESV, 12.3%; HR: 0.735; 95% CI: 0.391 to 1.

58 We show that evolutionarily conserved MCV LT phosphorylation sites are constitutively recogniz

59 CC tumor cells, which then require continued MCV oncoprotein expression to survive.

60 tation (TAVI) using the Medtronic CoreValve (MCV) system might represent an alternative to convention

61 e implantation with the Medtronic CoreValve (MCV) versus the Edwards SAPIEN/SAPIEN XT transcatheter h

62 underwent transfemoral (Medtronic CoreValve [MCV(TF)], n=32; Edwards Sapien [ES(TF)], n=26) and trans

63 anemia pattern seen in complete blood count (MCV 70.2 fl, MCH 21.4 pg).

64 minate viral replication among tumor-derived MCV.

65 uorescence and electron microscopy detecting MCV membranes and actin polymerization.

66 olyomaviruses have recently been discovered: MCV was found in Merkel cell carcinoma samples, while Ka

67 ith severe immunodeficiency and disseminated MCV.

68 ng MMR vaccine and vaccine uptake for 2-dose MCV and single-dose varicella vaccine, focusing on timel

69 Following program implementation, 2-dose MCV coverage at age 36 months exceeded that obtained at

70 e effectiveness after two-dose or three-dose MCV schedules.

71 fferent from seropositivity after a two-dose MCV schedule starting later (p=0.087).

72 imate derived from two studies of a two-dose MCV schedule with MCV1 vaccination before 9 months of ag

73 To address this question, we knocked down MCV T-antigen (TA) expression in MCV-positive MCC cell l

74 MCV sT is also required for efficient MCV DNA replication by the multifunctional MCV LT helica

75 In six of eight MCV-positive MCCs, viral DNA was integrated within the t

76 tected during infection of cells with either MCV isolated from human lesions or with a recombinant MC

77 gregating with thrombocytopenia and elevated MCV.

78 evels and stabilizes LT, leading to enhanced MCV replication and transmission.

79 5.3-131.6]; P<0.001) and the self-expandable MCV prosthesis during implantation (MCV(TF), 397.1 [302.

80 , transfemoral TAVI with the self-expandable MCV prosthesis resulted in the greatest number of HITS,

81 We find MCV sT to be a promiscuous E3 ligase inhibitor targeting

82 (48%) were too young to receive their first MCV dose, 11 914 (8%) received their first dose and were

83 on coefficients were 0.7 for PPC and 0.5 for MCV.

84 rth, vaccination status, and eligibility for MCV doses in the country reporting the case.

85 compared with that in the control group (for MCV-4 recipients vs. controls, P<.01; for MPSV-4 recipie

86 ian virus 40 (SV40), but is not required for MCV sT-induced rodent cell transformation.

87 howed that 4E-BP1 inhibition is required for MCV transformation.

88 nctionally distinguished by mutagenesis from MCV sT LSD-dependent 4E-BP1 hyperphosphorylation and vir

89 ell lines used include three newly generated MCV-infected cell lines and one MCV-negative cell line f

90 The study projected global MCV demand through 2025 with and without a global eradic

91 We found males to have significantly greater MCV and CON than females (p < 0.05).

92 0828; P < 1E - 13 for Hgb, hematocrit (Hct), MCV, RBC count and red cell distribution width (RDW)] we

93 erence standards for hemoglobin, hematocrit, MCV, and TS and the white blood cell count do not apply

94 The hematocrit, hemoglobin, MCV, TS, and white blood cell counts of African-American

95 and greatly expands our understanding of how MCV so effectively evades human immunity.

96 Adoptive transfer of purified human MCV autoantibodies into mice induced osteopenia and incr

97 pandable MCV prosthesis during implantation (MCV(TF), 397.1 [302.1-492.2]; ES(TF), 88.2 [70.2-106.3];

98 led evidence from diverse sources implicates MCV as an etiological agent of Merkel cell carcinoma.

99 ene mutations and copy number alterations in MCV-positive (n = 13) and -negative (n = 21) MCC tumors

100 We observed that depletion of EP400 in MCV-positive MCC cell lines led to increased p53 target

101 nocked down MCV T-antigen (TA) expression in MCV-positive MCC cell lines using three different short

102 There was a significant increase in MCV from 1988-1994 to 1999-2004 in men (from 90.2 to 90.

103 t and lymphocyte counts, and to increases in MCV and monocytes.

104 uld play a direct role in producing pores in MCV membranes, facilitating M. marinum escape from the v

105 actericidal titers <1 : 4 (63% protective in MCV-4 recipients vs. 31% protective in MPSV-4 recipients

106 of p53, leading to an apoptotic response in MCV-positive MCC cells and MCC-derived xenografts in mic

107 ports also document efficacy of rituximab in MCV.

108 The knockdown of Sox2 in MCV(+) MCCs mimicked T antigen knockdown by inducing MCC

109 T protein levels and eliminates synergism in MCV DNA replication as well as sT-induced cell transform

110 ns render the virus replication-incompetent, MCV is not a "passenger virus" that secondarily infects

111 The cause of increased MCV in men, and in older persons of both sexes, warrants

112 essure within tumors to abrogate independent MCV replication.

113 to 2.364; p = 0.842), myocardial infarction (MCV, 0.5% vs. ESV, 1.5%; HR: 0.330; 95% CI: 0.034 to 3.2

114 mical treatments of MMP-9 markedly inhibited MCV sT-induced cell migration and invasion.

115 gases through a sT domain that also inhibits MCV large T oncoprotein turnover.

116 pression activates replication of integrated MCV DNA in MKL-1 cells.

117 Seropositivity to JC, MCV, and HPyV7 increased with age.

118 irus, as well the human polyomaviruses BK/JC/MCV, human adenoviruses, and human papillomaviruses.

119 ll as increase in virus replication for JCV, MCV, TSV and HPyV7.

120 utants isolated from MCC tumors, full-length MCV LT shows a decreased potential to support cellular p

121 ), latency (LAT), average (ACV) and maximum (MCV) constriction velocities, average dilation velocity

122 Finally, we show that ATM kinase-mediated MCV LT Ser-816 phosphorylation may contribute to the ant

123 We mapped a 71-bp minimal MCV replication core origin sufficient for initiating eu

124 f an MCC cell line (MKL-1) having monoclonal MCV integration and the signature LT mutation allowed us

125 More MCV-4 recipients had passive protective activity against

126 More MCV-4 recipients had W-135 bactericidal titers > or =1 :

127 2.984; p = 0.352), cardiovascular mortality (MCV, 6.9% vs. ESV, 6.4%; HR: 1.083; 95% CI: 0.496 to 2.3

128 were no differences in all-cause mortality (MCV, 8.8% vs. ESV, 6.4%; hazard ratio [HR]: 1.422; 95% c

129 t MCV DNA replication by the multifunctional MCV LT helicase protein.

130 n resulted in a regression of MCV(+) but not MCV(-) MCCs in vivo.

131 olio3 p=0.0089), but doctor density was not (MCV p=0.7953; DTP3 p=0.7971; polio3 p=0.7885).

132 In this study, we identified a novel MCV LT phosphorylation site at Ser-816 in the C-terminal

133 agonized the cell transformation activity of MCV sT.

134 other polyomaviruses, the large T-antigen of MCV recognizes the viral origin of replication by bindin

135 MCC and that MCV is the infectious cause of MCV-positive MCC.

136 mal MCV replication requires coexpression of MCV small T protein (sT), together with LT.

137 t support the need for an additional dose of MCV in HIV-infected adolescents and adults.

138 en use of MMRV vaccine as the second dose of MCV in toddlers and an increased risk of FSs.

139 titres after one or two subsequent doses of MCV than when measles vaccination is started at age 9 mo

140 follows: (1) received at least two doses of MCV; (2) too young for first dose; (3) received one dose

141 We report the identification of MCV protein MC005 as an inhibitor of the pathways leadin

142 While the impact of MCV and viral T-antigens on MCC development has been ext

143 aphy was performed to evaluate the impact of MCV on hemodynamics after transcatheter aortic valve imp

144 (MCV; in pixels per second), and latency of MCV (LMCV; in seconds).

145 pression is necessary for the maintenance of MCV-positive MCC and that MCV is the infectious cause of

146 However, only a small number of MCV immunomodulatory genes have been characterized in de

147 The persistence of MCV has been attributed to viral downregulation of host

148 cost-effective for large-scale production of MCV.

149 e necessary for the oncogenic progression of MCV-associated cancers.

150 n TA knockdown, whereas the proliferation of MCV-negative cell lines remained unaffected.

151 chain homology domain to a unique region of MCV LT adjacent to the retinoblastoma binding site.

152 on of Multiferon resulted in a regression of MCV(+) but not MCV(-) MCCs in vivo.

153 the prevention, diagnosis, and treatment of MCV-related cancers.

154 studies that evaluated the immunogenicity of MCVs among seronegative HIV-infected adults, measles ser

155 cts of IFNs on MCC cell lines, especially on MCV-positive (MCV(+)) lines.

156 ly, this inhibitory effect of type I IFNs on MCV(+) MCC cell lines was associated with a reduced expr

157 ly generated MCV-infected cell lines and one MCV-negative cell line from MCC tumors.

158 Of these viruses, only MCV has thus far been strongly linked to cancer.

159 Optimal MCV replication requires coexpression of MCV small T pro

160 We performed MCV sT FLAG-affinity purification followed by mass spect

161 sons, in a severely immunocompromised person MCV DNA was present in blood and may spread by viremia.

162 TM kinase is responsible for phosphorylating MCV LT at Ser-816.

163 hese volumes are within existing and planned MCV-manufacturing capacity, although there are risks.

164 virus that we call Merkel cell polyomavirus (MCV or MCPyV).

165 Merkel cell polyomavirus (MCV) causes an aggressive human skin cancer, Merkel cell

166 Merkel cell polyomavirus (MCV) causes an aggressive skin cancer after prolonged in

167 d DNA polyomavirus Merkel cell polyomavirus (MCV) causes Merkel cell carcinoma, an aggressive but rar

168 Merkel cell polyomavirus (MCV) contributes to approximately 80% of all Merkel cell

169 nal integration of Merkel cell polyomavirus (MCV) DNA into the host genome has been observed in at le

170 lonally integrated Merkel cell polyomavirus (MCV) genome have low mutation burden and require viral T

171 Merkel cell polyomavirus (MCV) has been recently described as the cause for most h

172 Merkel cell polyomavirus (MCV) infection and DNA integration into the host genome

173 Merkel cell polyomavirus (MCV) is a newly discovered human cancer virus encoding a

174 Merkel cell polyomavirus (MCV) is a recently discovered human polyomavirus causing

175 Merkel cell polyomavirus (MCV) is a virus discovered in our laboratory at the Univ

176 strated that human Merkel cell polyomavirus (MCV) is clonally integrated in approximately 80% of MCC

177 Merkel cell polyomavirus (MCV) is the first polyomavirus directly linked to human

178 Merkel cell polyomavirus (MCV) is the recently discovered cause of most Merkel cel

179 Merkel cell polyomavirus (MCV) small T (sT) oncoprotein induces centrosome overdup

180 Merkel cell polyomavirus (MCV) small T antigen (sT) is the main oncoprotein for th

181 no virus (TTV) and Merkel cell polyomavirus (MCV) were detected by qPCR in 49% and 19% of cases, resp

182 ssociated with the Merkel cell polyomavirus (MCV).

183 MCC cell lines, especially on MCV-positive (MCV(+)) lines.

184 rther clarify how the human-adapted poxvirus MCV can so effectively evade antiviral immunity and supp

185 iral with activity against other poxviruses, MCV DNA was detected in 20% of plasma samples.

186 Despite this curious presentation, MCV is very poorly characterized in terms of host-pathog

187 Previously, MCV sT was shown to induce the migratory and invasive ph

188 viral genome increase LT levels and promote MCV virion production and transmission, which can be neu

189 3 ligases enhances LT stability and promotes MCV genome replication.

190 pants of a randomized trial who had received MCV-4 (n=52) or polysaccharide vaccine (MPSV-4; n=48) an

191 ring 2000-2009, >57 million persons received MCV through SIAs in 16 countries.

192 than periodic follow-up SIAs for the second MCV dose.

193 s following MMRV vaccine given as the second MCV to toddlers.

194 Unlike the closely related SV40 sT, MCV sT transformed rodent fibroblasts to anchorage- and

195 hat activation of the ATM pathway stimulated MCV LT phosphorylation at Ser-816, whereas inhibition of

196 95% CI: 0.034 to 3.200; p = 0.339), stroke (MCV, 2.9% vs. ESV, 1.0%; HR: 3.061; 95% CI: 0.610 to 15.

197 nths on their immune responses to subsequent MCV doses.

198 10 to 15.346; p = 0.174), or device success (MCV, 95.6% vs. ESV, 96.6%; HR: 0.770; 95% CI: 0.281 to 2

199 (+)-METH HSMO9 (3) and its use to synthesize MCV will be applicable for conjugated vaccines of small

200 coprotein, Merkel cell polyomavirus small T (MCV sT).

201 Compared to the N-terminal MCV LT fragment that is usually preserved in mutants iso

202 the maintenance of MCV-positive MCC and that MCV is the infectious cause of MCV-positive MCC.

203 We conclude that MCV sT is required for Merkel cell carcinoma growth, but

204 Our results demonstrate that MCV LT-induced DDR activates p53 pathway, leading to the

205 We found that MCV-positive tumors displayed very low mutation rates, b

206 We report here that MCV LT binds to RB, leading to increased levels of ARF,

207 Our structural analysis reveals that MCV sT also displaces the B subunit of PP2A to inhibit P

208 ranscript mapping was performed to show that MCV expresses transcripts in MCCs similar to large T (LT

209 In this study, we show that MCV infection leads to the activation of host DNA damage

210 Here, we show that MCV small T (sT) antigen is expressed in most MCC tumors

211 In this study, we show that MCV sT protein stimulates differential expression of epi

212 Here, we showed that MCV(+) MCC cells cocultured with keratinocytes undergo n

213 Our study shows that MCV sT-mediated MMP-9 activation is driven through the L

214 These results suggest that MCV sT contributes to the activation of MMP-9 as a resul

215 Our findings suggest that MCV-positive MCC tumor cells undergo selection for LT mu

216 genome in a clonal pattern, suggesting that MCV infection and integration preceded clonal expansion

217 The MCV LT-activated DNA damage kinases, in turn, led to enh

218 The MCV MC159 protein suppresses NF-kappaB activation, a pow

219 The MCV origin provides a novel model for eukaryotic replica

220 g alanine mutagenesis at 29 sites across the MCV sT protein revealed that PP2A-binding domains lie on

221 In addition, the MCV produced a substantially greater immunological respo

222 sfemoral and transapical TAVI or between the MCV and ES prostheses.

223 le limpet hemocyanin (IC(KLH)) to create the MCV ICKLH-SOO9.

224 For example, the MCV MC159 protein inhibits TNF-R1-induced NF-kappaB acti

225 OBD) in complex with a DNA fragment from the MCV origin of replication.

226 esponse that could last for months (from the MCV).

227 essential role in M. marinum escape from the MCV.

228 sthesia was used to retrogradely implant the MCV system into the failing bioprosthetic valve.

229 on of STs, most of which also existed in the MCV communities.

230 th full recovery at 3-month follow-up in the MCV group.

231 Integration of the MCV genome frequently results in mutations in the large

232 inal DNA binding and helicase domains of the MCV large T antigen (LT), suggesting a selective pressur

233 port here the 2.9 A crystal structure of the MCV large T-antigen origin binding domain (OBD) in compl

234 te to the anti-tumorigenic properties of the MCV LT C-terminal domain.

235 C-terminal helicase-containing region of the MCV LT.

236 associated with a reduced expression of the MCV LTA as well as an increased expression of promyelocy

237 ming activities lie on opposite faces of the MCV sT molecule and can be genetically separated from ea

238 MALDI-TOF mass spectrometry analysis of the MCV synthesized using 3 showed there was a high and cont

239 rt, why truncation mutations that remove the MCV LT C-terminal region are necessary for the oncogenic

240 ur laboratory and others have shown that the MCV LT C-terminal helicase domain contains growth-inhibi

241 We show here that the MCV MC159 protein interacts with the NEMO subunit of the

242 We suspected that the MCV ST-MYCL-EP400 complex could functionally inactivate

243 CC cell lines show oncogene addiction to the MCV T antigens, pharmacologic interference of the large

244 harbor mutations prematurely truncating the MCV LT helicase.

245 While the MCV-truncated LT can bind and inhibit RB, it does not bi

246 were included: 453 (57.1%) treated with the MCV and 340 (42.9%) with the ESV.

247 r the need for permanent pacemakers with the MCV.

248 nd a monoclonal antibody generated from this MCV in mice showed a very high affinity for (+)-METH (K(

249 ggesting a selective pressure to remove this MCV LT region during tumor development.

250 Thus, MCV has evolved a regulatory system involving SCF(Fbw7)

251 Thus, MCV may be a contributing factor in the pathogenesis of

252 Thus, MCV sT is an oncoprotein, and its effects on dysregulate

253 proportion of infants seropositive after two MCV doses, with MCV1 administered before 9 months of age

254 DNA replication in the presence of wild-type MCV large T protein (LT).

255 ted with coverage of all three vaccinations (MCV p=0.0024; DTP3 p=0.0004; polio3 p=0.0008).

256 ted with coverage of all three vaccinations (MCV p=0.0097; DTP3 p=0.0083; polio3 p=0.0089), but docto

257 n combination with a METH-conjugate vaccine (MCV) to safely improve the overall quality and magnitude

258 r PCV7 or a meningococcal conjugate vaccine (MCV).

259 uadrivalent meningococcal conjugate vaccine (MCV-4) is recommended for United States teenagers.

260 onths and meningococcal A conjugate vaccine (MCV-A) at 15 months, in addition to measles-rubella vacc

261 rted coverage of measles-containing vaccine (MCV) and progress towards elimination of measles, 172 93

262 ditional dose of measles-containing vaccine (MCV) for human immunodeficiency virus (HIV)-infected chi

263 ), with those of measles-containing vaccine (MCV) for which SIAs are also undertaken.

264 ies (SIAs) using measles-containing vaccine (MCV) have had a substantial impact on reducing mortality

265 e second dose of measles-containing vaccine (MCV) in Australia.

266 d and supply for measles-containing vaccine (MCV).

267 ee vaccinations--measles-containing vaccine (MCV); diphtheria, tetanus, and pertussis (DTP3); and pol

268 its use to prepare METH-conjugated vaccines (MCV) from maleimide-activated proteins.

269 e from the Mycobacterium-containing vacuole (MCV) into the host cell cytosol, polymerize actin, and s

270 The method of continuous variation (MCV) was used in conjunction with (6)Li NMR spectroscopy

271 ions of the method of continuous variations (MCV or the Method of Job) to problems of interest to org

272 on with the method of continuous variations (MCV), x-ray crystallography, and density functional theo

273 C-related mixed cryoglobulinemic vasculitis (MCV).

274 il size (PPC), maximum contraction velocity (MCV; in pixels per second), and latency of MCV (LMCV; in

275 dies against mutated citrullinated vimentin (MCV) not only bound to osteoclast surfaces, but also led

276 (KIV), WU virus (WUV) and Merkel cell virus (MCV)) to a class that previously had only two disease-ca

277 Molluscum contagiosum virus (MCV) causes persistent neoplasms in healthy and immunoco

278 FLIP MC159 from molluscum contagiosum virus (MCV) in mice enhanced rather than inhibited the innate i

279 Molluscum contagiosum virus (MCV) is a dermatotropic poxvirus that causes benign skin

280 irus.IMPORTANCE Molluscum contagiosum virus (MCV) is a human-specific poxvirus that causes persistent

281 Molluscum contagiosum virus (MCV) is a poxvirus that causes localized papules in heal

282 Molluscum contagiosum virus (MCV) is a poxvirus that causes tumor-like skin lesions.

283 Molluscum contagiosum virus (MCV) is the only known extant poxvirus specifically adap

284 Molluscum contagiosum virus (MCV), the only known extant human-adapted poxvirus, caus

285 fected with the molluscum contagiosum virus (MCV), this poxvirus is expected to produce proteins that

286 Merkel cell polyoma virus (MCV) has been implicated in a majority of MCC tumors; ho

287 three red cell parameters: mean cell volume (MCV), red cell distribution width (RDW) and mean cell he

288 globin, hematocrit, mean corpuscular volume (MCV) and prevalences and likelihood of anemia and macroc

289 The mean corpuscular volume (MCV) and serum ferritin values were significantly lower

290 a, high erythrocyte mean corpuscular volume (MCV) and two occurrences of B cell-precursor acute lymph

291 2 (<258 pmol/L) and mean corpuscular volume (MCV) measured between 1995 and 2004 were identified from

292 ace area, decreased mean corpuscular volume (MCV), cell dehydration, and increased osmotic fragility.

293 n (Hgb), RBC count, mean corpuscular volume (MCV), MCH and MCHC] and the G6PD locus on Xq28 [lead SNP

294 , hematocrit (Hct), mean corpuscular volume (MCV), mean corpuscular hemoglobin (MCH), mean corpuscula

295 ncentration (MCHC), mean corpuscular volume (MCV), platelet count (PLT) and white blood cell (WBC) co

296 /L [+0.2 g/dL]) and mean corpuscular volume (MCV; 1.0 fL) compared with seronegative participants.

297 emia, associated with decreased RBCs volume (MCV) and reticulocytosis; the flow-cytometric assay show

298 istered with YFV at 9 months of age and with MCV-A at 15 months of age.

299 osomal processing as a novel interactor with MCV LT but not SV40 LT.

300 prevalence of 10 human PyVs (BK, JC, KI, WU, MCV, HPyV6, HPyV7, TSV, HPyV9, and HPyV10) among control