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 has probably retained its MC160 gene to inhibit NF-k

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

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

6 MCV lacks the agnoprotein sequence but generates miRNAs.

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 was found to act downstream in the mammalian targ

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

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

19 MCV sT-PP2A interactions can be functionally distinguish

20 MCV was associated with more permanent pacemakers (22.5%

21 MCV was significantly lower in the postfortification per

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

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

24 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

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

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

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

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

29 In the context of an MCV infection in vivo, MC160 protein expression may damp

30 ncreased hemoglobin concentration, %HbF, and MCV, and decreased reticulocytes, WBC, and platelets (p<

31 e differences in hematocrit, hemoglobin, and MCV among women were slightly less.

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

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

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

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

36 f CHr, ferritin, transferrin saturation, and MCV demonstrates that CHr has the highest overall sensit

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 sing chemical family for development of anti-MCV agents.

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

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

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

44 rats injected with labeled MSCs, as well as MCV and hemoglobin, alkaline phosphatase, aspartate amin

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

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

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

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

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

50 82; p = 0.340) or life-threatening bleeding (MCV, 13.7% vs. ESV, 8.8%; HR: 1.644; 95% CI: 0.878 to 3.

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 eotide substrates indicates that cleavage by MCV topoisomerase is favored just 3' of the sequence 5'

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

55 echanism for evasion of the immune system by MCV.

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

57 .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.

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

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

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

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

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

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

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

65 minate viral replication among tumor-derived MCV.

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

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

68 ith severe immunodeficiency and disseminated MCV.

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

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

71 id implementation of a mandatory second-dose MCV requirement probably limited the extent of this outb

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

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

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

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

76 gregating with thrombocytopenia and elevated MCV.

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

78 5.3-131.6]; P<0.001) and the self-expandable MCV prosthesis during implantation (MCV(TF), 397.1 [302.

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

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

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

82 We have cloned the gene for MCV topoisomerase, overexpressed and purified the protei

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

84 omerase, an enzyme likely to be required for MCV replication.

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

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

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

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

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

90 0828; P < 1E - 13 for Hgb, hematocrit (Hct), MCV, RBC count and red cell distribution width (RDW)] we

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

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

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

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

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

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

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

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

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

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

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

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

103 ports also document efficacy of rituximab in MCV.

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

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

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

107 essure within tumors to abrogate independent MCV replication.

108 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

109 e mechanism by which sansalvamide A inhibits MCV topoisomerase.

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

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

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

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

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

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

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

117 More MCV-4 recipients had passive protective activity against

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

119 2.984; p = 0.352), cardiovascular mortality (MCV, 6.9% vs. ESV, 6.4%; HR: 1.083; 95% CI: 0.496 to 2.3

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

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

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

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

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

125 agonized the cell transformation activity of MCV sT.

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

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

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

129 ized to receive (arm 1, n=61 ) two cycles of MCV before 39.6-Gy pelvic irradiation with concurrent ci

130 Two cycles of MCV neoadjuvant chemotherapy were not shown to increase

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

132 ified, 31 had been vaccinated with 1 dose of MCV, 1 had received 2 doses, and vaccination status was

133 50.4% and 45.5% had received >or=2 doses of MCV before measles introduction at the schools.

134 among persons vaccinated with >or=2 doses of MCV compared with 1 dose was 0.06 (95% confidence interv

135 for studies of the mechanism of function of MCV topoisomerase and the development of medically usefu

136 eins encoded by the MC53L and MC54L genes of MCV, as well as their human and murine homologs.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

154 Only MCVs exhibited rCBF increases in the left amygdala.

155 Optimal MCV replication requires coexpression of MCV small T pro

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

174 ssociated with the Merkel cell polyomavirus (MCV).

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

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

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

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

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

180 3 ligases enhances LT stability and promotes MCV genome replication.

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

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

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

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

185 Mean diameters of the SV, SMV, MCV, and FJV were significantly larger in the cirrhosis

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

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

188 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.

189 arison was conducted separately by subgroup, MCVs and FNVs with PTSD exhibited these medial frontal g

190 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

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

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

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

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

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

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

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

198 Previous studies revealed that MCV encodes a family of proteins with homology to mammal

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

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

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

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

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

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

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

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

207 The MCV origin provides a novel model for eukaryotic replica

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

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

210 nnection between a CSMC extension (along the MCV or PCV) and the ventricle.

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

212 8 (82%), in the PCV in 13 (11%), in both the MCV and PCV in 6 (5%), and in the CS in 3 (2%) of 120 pa

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

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

215 Significant QTL were identified for the MCV trait only, suggesting that RBC membrane characteris

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

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

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

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

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

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

222 ), like an AP potential, was recorded in the MCV in 98 (82%), in the PCV in 13 (11%), in both the MCV

223 (AP) potential or earliest activation in the MCV or PCV and late activation at anular endocardial sit

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

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

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

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

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

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

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

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

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

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

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

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

236 harbor mutations prematurely truncating the MCV LT helicase.

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

238 r the need for permanent pacemakers with the MCV.

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

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

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

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

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

244 Like other eukaryotic type I topoisomerases, MCV topoisomerase can relax both positive and negative s

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

246 d natural products from microorganisms using MCV topoisomerase assays in vitro.

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

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

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

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

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

252 f >or=2 doses of measles-containing vaccine (MCV) compared with 1 dose.

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

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

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

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

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

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

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

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

261 C-related mixed cryoglobulinemic vasculitis (MCV).

262 SMC extending along the middle cardiac vein (MCV) or posterior coronary vein (PCV) and the ventricle.

263 ticoduodenal vein, in 22; middle colic vein (MCV), in 29; and first jejunal vein (FJV), in 36.

264 lbous enlargement of the small cardiac vein, MCV, or CS in 15 (9%) patients.

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

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

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

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

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

270 Molluscum contagiosum virus (MCV) is a common, human poxvirus that causes small papul

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

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

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

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

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

276 Molluscum contagiosum virus (MCV), a member of the human poxvirus family, encodes the

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

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

279 ogenic poxvirus molluscum contagiosum virus (MCV).

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

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

282 in patients with high mean cellular volume (MCV) or red cell disorders such as thalassemia.

283 oglobin (Hb F), and mean corpuscular volume (MCV) and decreased reticulocytes, white blood cells (WBC

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

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

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

287 n concentration and mean corpuscular volume (MCV) in the rats injected with labeled MSCs, as well as

288 4 +/- 1.3 g/dL, and mean corpuscular volume (MCV) is 112 +/- 9 fL.

289 2 (<258 pmol/L) and mean corpuscular volume (MCV) measured between 1995 and 2004 were identified from

290 globin, hematocrit, mean corpuscular volume (MCV), and mean corpuscular hemoglobin content (MCHC) was

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

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

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

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

295 ing the hemoglobin, mean corpuscular volume (MCV), serum transferrin saturation (TS), serum ferritin,

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

299 However, when patients with MCV more than 100 fL are excluded, receiver operator cur

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