ライフサイエンスコーパス: MOI

1 MOI estimates were derived by PCR at the msp-1 and -2 lo

2 MOI inactivates the enzyme to a limit of 14% activity.

3 When transduced with Ad5p53 alone at 1 MOI, the cell lines grew rapidly.

4 lines at a low multiplicity of infection (1 MOI).

5 tly suppressed by high MOI, (i.e., MOI [0.1]/MOI [0.1] > or = 2, P < 0.006).

6 Maximal immunoreactivity was observed at 100 MOI AdMnSOD with both techniques.

7 parental cell levels that also peaked at 100 MOI AdMnSOD.

8 LacZ reporter gene construct (AdLacZ) at 100 MOI.

9 decreased approximately two-thirds with 100 MOI AdMnSOD (P < 0.001).

10 day 13 decreased approximately 50% with 100 MOI AdMnSOD (P < 0.05) compared with parental cells.

11 all appeared to show maximal effect with 100 MOI AdMnSOD.

12 ling time increased from 38 to 44 h with 100 MOI AdMnSOD.

13 as increased 5-fold after infection with 100 MOI of AdCat as compared with control.

14 Five days after infection with 100 MOI of AdCat, cell numbers were reduced as compared with

15 re infected at a moderate (10) or high (100) MOI.

16 and LNCaP cells were infected with 10 and 2 MOI of Ad-PML.

17 uent AEC monolayers (R(t) > 2 kOmega. cm(2); MOI = 10) revealed efficient transduction only when VSV-

18 ty (MOI) of 0, 10, 25, 50, 100, 150, and 200 MOI or with the adenovirus-LacZ reporter gene construct

19 Adv-caPKCdelta infection (1 to 25 MOI, 4 to 48 hours) increased total PKCdelta levels in a

20 exposure to 100 J/m(2) of UV light and 10(3) MOIs for 8 days.

21 Adv-caPKCdelta (5 MOI) induced a 29-fold increase in phosphorylated p54 JN

22 At a MOI of 500, 10% to 70% of the CLL B cells from different

23 t, even at very low MOI (>95% infection at a MOI of 6) and did not reduce viability.

24 As expected, increasing the AAV MOI resulted in an increase in the percentage of cells i

25 Additional MOI only marginally effected a further increase in perce

26 empirical power) is approximately 0 for all MOI, there are parameter settings for which the power di

27 After an MOI of 1, GFP expression was high with the human CMV enh

28 However, because one must assume an MOI, the application of LOD-score analysis to complex di

29 growth occurs in macrophages infected at an MOI of </=1.

30 However, at an MOI of 0.05, viruses lacking CR3 showed replication defe

31 cation defect of MAV-1 in Sur2-/- MEFs at an MOI of 0.05.

32 1A null mutant viruses in Sur2-/- MEFs at an MOI of 0.05.

33 of infection (MOI) of 0.5 and 80-fold at an MOI of 0.1.

34 At an MOI of 1, >3-fold regulation was found for five group 1

35 d at about 49% at an MOI of 130 and 2% at an MOI of 1.3.

36 At an MOI of 10, at which 80% of cells are infected, less than

37 s infected, with 80% of cells infected at an MOI of 10.

38 At an MOI of 100 or greater, however, 35 to 40% of clonal cell

39 ssages) coronary VSMCs were transduced at an MOI of 100 with a recombinant adenovirus encoding human

40 requencies were estimated at about 49% at an MOI of 130 and 2% at an MOI of 1.3.

41 At an MOI of 130 IU, nearly all cells expressed tNGFR immediat

42 radually from an MOI of 0.02 to a peak at an MOI of 200 (reaching an average of two bacteria internal

43 ss was apparently saturated within 2 h at an MOI of 200, indicating stringent host cell limitations o

44 At an MOI of 30, neutrophils loaded with AZM failed to kill si

45 At an MOI of 5, all genes from group 1 and four of five genes

46 ion (MOI) of 50 to 500 and by 633 only at an MOI of 5,000, while both viruses infected essentially 10

47 were infected with HCMV (strain AD169) at an MOI of 5.

48 infected essentially 100% of BHK cells at an MOI of 5.

49 icity of infection (MOI) of 0.1 to 99% at an MOI of 50 for AEC grown on plastic.

50 At an MOI of 90, neutrophils loaded with AZM killed significan

51 itionally, kinetic studies showed that at an MOI of approximately 400, maximal S. typhi entry is virt

52 mma)* mRNA in mature colonies but only at an MOI of greater than 5 x 10(7).

53 ge of BALB/c mice with HSV-IL-2 alone, at an MOI that resulted in only 13% survival when parental vir

54 ampylobacter CFU increased gradually from an MOI of 0.02 to a peak at an MOI of 200 (reaching an aver

55 similarly well at a high MOI, suggesting an MOI-dependent importance of pUL38-TSC2 interaction in su

56 Survival with an MOI of 10 was 39+/-8.7 days.

57 cellular multiplicity of infection (MOI) and MOI model selection, suggested that low levels of cellul

58 At a comparable titer and MOI, transduction of these cells by a similarly pseudoty

59 rse linear relationship with virus titer and MOI.

60 linkage, and (3) adequacy of the approximate MOI for the true MOI.

61 /2) genes is a standard method for assessing MOI, despite the apparent problem of underestimation.

62 ion for linkage analysis is that the assumed MOI at the disease locus being tested is approximately c

63 At MOI 50, the protein levels of pro-MMP-1, -3, and -9 also

64 ciency of internalization was the highest at MOI of 0.02 and decreased steadily at higher MOIs, presu

65 IMP-1 and PAI-1 protein levels, increased at MOI 25.

66 ase in cytolysis within 24 h was observed at MOI > or = 25.

67 not impaired following exposure to AdGFP at MOIs of 1 to 1,000.

68 T cell proliferation to exogenous antigen at MOIs as low as 1.0.

69 nd was not observed with epithelial cells at MOIs of as high as 2000.

70 ict physical limitation on S. typhi entry at MOIs of >/=40.

71 t only limited rotavirus replication even at MOIs of 100 or 500, but delivery of rotavirus particles

72 , we found very low levels of integration at MOIs of less than 10.

73 ls were infected after 2 h with C. jejuni at MOIs of 200 to 2,000.

74 Application of these four phages at MOIs of 5-15 significantly reduced Gordonia host levels

75 resulting antiviral effect was only seen at MOIs greater than 10 PFU/cell.

76 cell lines including U87, U118, and U251 at MOIs 0.1, 1, and 10 resulted in significant cytopathic e

77 The k for inactivation by MOI is decreased 20-fold by S-hexylglutathione but only

78 changes in chromatin condensation induced by MOIs of 10:1 and 1:1 required more time and had a reduce

79 w multiplicity of infection (MOI) challenge (MOI = 0.1) results in substantial production of IL-8 and

80 Positive control challenges (MOI = 10) induced levels of IL-8 that were comparable to

81 rossing risk including the number of clones (MOI), their relative proportions and genetic divergence.

82 type profiles in cells infected at different MOIs are correlated with differences in interferon-stimu

83 4.7 murine macrophage cell line at different MOIs.

84 ion efficiency was dependent on the UV dose, MOI, and time.

85 significantly suppressed by high MOI, (i.e., MOI [0.1]/MOI [0.1] > or = 2, P < 0.006).

86 rrier injury to repair following endotoxemic MOI.

87 chain reaction-based approaches to estimate MOI can lack sensitivity.

88 Here, we present a method to estimate MOI, which considers unique combinations of polymorphism

89 re not independently associated with fasting MOI, although they were independently inversely associat

90 skin, lungs, and colon, demonstrating fatal MOI induced by CD103-independent mechanism.

91 , accelerating barrier restoration following MOI.

92 contrast to its effect on the pi class GST, MOI inactivates much less rapidly and extensively alpha

93 Incorporation of [(3)H]MOI up to approximately 1 mol/mol of enzyme dimer concom

94 tionation of the proteolytic digest of [(3)H]MOI-modified GST pi yielded Trp38 as the only labeled am

95 that osteosarcoma (OS) tumors with IGF2/H19 MOI exhibit allele-specific differential methylation of

96 Even though at a high MOI (10 PFU/cell), the murine CMV enhancer was as effici

97 or with 2009 pandemic H1N1 viruses at a high MOI (10 PFU/cell).

98 (MOI), but it grew similarly well at a high MOI, suggesting an MOI-dependent importance of pUL38-TSC

99 integration was markedly improved at a high MOI.

100 Apoptosis at high MOI differs markedly from low MOI apoptosis: it is poten

101 these working parts are dispensable at high MOI, partly because of compensatory stimulation of MIE p

102 At high MOI, stochastic influences appear to dictate the virus's

103 At high MOI, the macrophage growth defect was not apparent.

104 At high MOI, viral infection suppressed the interferon (IFN)-med

105 s regulatory function is unnecessary at high MOI.

106 obustly and significantly suppressed by high MOI, (i.e., MOI [0.1]/MOI [0.1] > or = 2, P < 0.006).

107 Caspase inhibitors failed to prevent high MOI apoptosis, and macrophages deficient in caspase-3, M

108 apies must remain effective against the high MOI observed during cell-to-cell transmission to inhibit

109 ne therapy of nondividing cells, a very high MOI or improvements in basic aspects of AAV-based vector

110 ) markedly inhibited apoptosis, whereas high MOI (> or =75) potentiated apoptosis.

111 + population expanded 10- to 15-fold at high MOIs (500 to 1,000), indicating multiple copies of the t

112 Stop infection of murine fibroblasts at high MOIs was substantially more cytotoxic than infection wit

113 t competition between genomes occurs at high MOIs.

114 gene in erythroid cells, but only when high MOIs are used.

115 While high MOIs caused cytotoxicity and irreversible host cell deat

116 onsensus sequences of the viruses after high-MOI passages, and mutation rates increased under low-MOI

117 ever, infection of BALB/c BMDC with a higher MOI of 50 PFU/cell resulted in a productive infection wi

118 e subtypes than cells infected at the higher MOI.

119 MOI of 0.02 and decreased steadily at higher MOIs, presumably due to reported C. jejuni autoagglutina

120 the macrophage-Candida interaction at higher MOIs, we introduced a luciferase reporter gene into wild

121 per epithelial cell) and decreased at higher MOIs.

122 However, MOI greater than 100 resulted in a significant inhibitio

123 (22.1%; OR, 4.4; P < .0001), and high-impact MOIs (16.5%; OR, 3.1; P < .0001) were independent predic

124 nisms involved in maintenance of imprinting (MOI) and loss of imprinting (LOI) are unresolved.

125 1.5h for each order of magnitude decrease in MOI.

126 ctions between the IGF2 promoter and ICR1 in MOI cells, while the model of LOI lung cancer cells is f

127 s infection of RDC increased with increasing MOIs.

128 Transfer of Sf CD4(+) T cells induced MOI more rapidly than CD103(-)CD4(+) T cells, indicating

129 ere, the multiplicity of cellular infection (MOI) and population bottlenecks were quantified during p

130 f vector at a low multiplicity of infection (MOI = 5).

131 mycobacteria at multiplicities of infection (MOI) < or = 10 triggers TNF-alpha-mediated apoptosis whi

132 After a low multiplicity of infection (MOI) (0.01 PFU/cell), recombinant human CMV with the mur

133 cubated with RSV (multiplicity of infection (MOI) = 10) induced IL-8, macrophage inflammatory protein

134 , or zero (0.0) multiplicities of infection (MOI) and harvested at different times after infection (1

135 at low or high multiplicities of infection (MOI) and measured viral genomic replication and infectio

136 s of the cellular multiplicity of infection (MOI) and MOI model selection, suggested that low levels

137 normally at high multiplicity of infection (MOI) but replicate poorly at low MOI in comparison to wi

138 own how the viral multiplicity of infection (MOI) can affect IFN induction.

139 Multiplicity of infection (MOI) can be an indicator of immune status and transmissi

140 dicate that a low multiplicity of infection (MOI) challenge (MOI = 0.1) results in substantial produc

141 d in terms of the multiplicity of infection (MOI) derived by PCR-based genotyping.

142 for 48 hours at a multiplicity of infection (MOI) from 0.1 to 10.0 pfu/cell.

143 passaged at high multiplicity of infection (MOI) in cells permitting high titer growth.

144 at a high or low multiplicity of infection (MOI) in human foreskin fibroblast (HFF)- or NTera2-deriv

145 nfection at a low multiplicity of infection (MOI) in the presence of acyclovir results in a quiescent

146 ging from 4% at a multiplicity of infection (MOI) of 0.1 to 99% at an MOI of 50 for AEC grown on plas

147 h as 50-fold at a multiplicity of infection (MOI) of 0.5 and 80-fold at an MOI of 0.1.

148 At a multiplicity of infection (MOI) of 1 at 24 h postinfection (p.i.), the expression o

149 At a multiplicity of infection (MOI) of 1, viruses containing CR3 replicated better in S

150 retion was at the multiplicity of infection (MOI) of 1,000:1 in bacterial dose response studies using

151 ion with SV5 at a multiplicity of infection (MOI) of 10 PFU/cell compared to BALB/c BMDC, as determin

152 ntly greater at multiplicities of infection (MOI) of 10 PFU/cell or greater, and the resulting antivi

153 s and primed at a multiplicity of infection (MOI) of 10(2) with different A. actinomycetemcomitans or

154 the corresponding multiplicity of infection (MOI) of 10.

155 280 +/- 43% at a multiplicity of infection (MOI) of 10.0 plaque forming units (pfu)/cell at 48 hours

156 s infected with a multiplicity of infection (MOI) of 100 of AdGFP show that 78% of megakaryocytic (CD

157 th AAV-tNGFR at a multiplicity of infection (MOI) of 13 infectious units (IU), 26 to 38% of cells exp

158 s infected with a multiplicity of infection (MOI) of 25:1 developed chromatin condensation and DNA fr

159 fected by TE at a multiplicity of infection (MOI) of 50 to 500 and by 633 only at an MOI of 5,000, wh

160 nfection with 100 multiplicity of infection (MOI) of AdCat, cellular catalase activity was increased

161 nd because a high multiplicity of infection (MOI) of H. pylori is needed to induce apoptosis in vitro

162 dependent on the multiplicity of infection (MOI) of rAAV.

163 the effect of the multiplicity of infection (MOI) on costimulatory ligand upregulation and inflammato

164 itted at a higher multiplicity of infection (MOI) that, in vitro, results in a higher number of provi

165 depending on the multiplicity of infection (MOI) used for transduction, and 0.13 to 0.19 for the ret

166 ne tested and the multiplicity of infection (MOI) used.

167 a function of the multiplicity of infection (MOI) with the rAAV.

168 V at increasing multiplicities of infection (MOI) without or with IFN-beta or IFN-lambda.

169 es were infected (multiplicity of infection (MOI), 100; 24 h) with replication-defective adenoviruses

170 rrelates with the multiplicity of infection (MOI), and optimal chlamydial growth occurs in macrophage

171 ects the observed multiplicity of infection (MOI), as well as the relationship between the MOI and th

172 pe virus at a low multiplicity of infection (MOI), but it grew similarly well at a high MOI, suggesti

173 cription at a low multiplicity of infection (MOI), but this increase is not mediated by the CREs; (ii

174 y used measure of multiplicity of infection (MOI), computed as the ratio of the number of phage to th

175 ulation at a high multiplicity of infection (MOI), eh2-AcNPV replicates efficiently in both the Sf-9

176 ationship between multiplicity of infection (MOI), gene expression, and unselected genome integration

177 of 2, 10, and 100 multiplicity of infection (MOI), respectively.

178 mutants at a low multiplicity of infection (MOI), so that individual plaques were formed, reactivate

179 nt virus at a low multiplicity of infection (MOI), there is a marked delay in the production of infec

180 ls, even at a low multiplicity of infection (MOI), though a reduction in titer was observed.

181 cularly for low multiplicities of infection (MOI), where few virus particles initiate the infection.

182 rophages at low multiplicities of infection (MOI), yielding 0.1 to 1.0% of wild-type levels.

183 e by using a high multiplicity of infection (MOI).

184 pe virus at a low multiplicity of infection (MOI).

185 pe virus at a low multiplicity of infection (MOI).

186 lication at low multiplicities of infection (MOI).

187 e with increasing multiplicity of infection (MOI).

188 st notable at low multiplicity of infection (MOI).

189 viruses at a high multiplicity of infection (MOI).

190 a relatively high multiplicity of infection (MOI).

191 function of viral multiplicity of infection (MOI); efficiency of site-specific integration; and disru

192 viruses at a low multiplicity of infection (MOI; 0.0001 PFU/cell) or with 2009 pandemic H1N1 viruses

193 nge of starting multiplicities of infection (MOI; from 0.02 to 20,000 bacteria/epithelial cell).

194 fected (100 multiplicity of viral infection (MOI); 24 h) with a replication-deficient adenovirus expr

195 (1 to 25 multiplicities of viral infection (MOI); 4 to 48 hours) increased total PKCepsilon levels i

196 segments using multiplicities of infection (MOIs) 25 or 50.

197 culture at low multiplicities of infection (MOIs) and found that 73.Stop growth was impaired in muri

198 ns at different multiplicities of infection (MOIs) and initial ratios of the wild type to the mutant

199 at high and low multiplicities of infection (MOIs) for 11 generations and the genome sequences, growt

200 ls at different multiplicities of infection (MOIs) have revealed a strict physical limitation on S. t

201 antibiotic) at multiplicities of infection (MOIs) of 30 and 90 bacteria per neutrophil.

202 macrophages at multiplicities of infection (MOIs) of as low as 20 and was not observed with epitheli

203 th AdCTLA4Ig at multiplicities of infection (MOIs) ranging from 0.1 to 10 were transplanted into stre

204 cted at various multiplicities of infection (MOIs) with rAAV containing the enhanced green fluorescen

205 ication at high multiplicities of infection (MOIs), analyses of plaque morphology and intra- and extr

206 albicans at low multiplicities of infection (MOIs).

207 titers of virus (multiplicity of infection [MOI] of 100).

208 ve C. pneumoniae (multiplicity of infection [MOI], 5), UVCP (MOI, 5), or cHSP60 for 24 h, and the exp

209 ae cultures (at multiplicities of infection [MOIs] of 0.01, 0.1, and 1.0) were incubated with mouse b

210 (AdMnSOD) at multiplicities of infectivity (MOI) of 0, 10, 25, 50, 100, 150, and 200 MOI or with the

211 s and develop fatal multiorgan inflammation (MOI) mediated by CD4(+) T cells.

212 g concentrations of markers of inflammation (MOI) than do lean children.

213 inding linkage when the mode of inheritance (MOI) is known.

214 ominant and a recessive mode of inheritance (MOI), (b) ASP methods, and (c) nonparametric linkage (NP

215 to be a consequence of either a low initial MOI or a high superinfecting MOI.

216 cords were reviewed for mechanism of injury (MOI).

217 tion is a hallmark of multiple organ injury (MOI).

218 Low MOI also induced cellular proliferation.

219 Low MOI reduced mitochondrial membrane depolarization, caspa

220 In the superficial chondrocytes, a low MOI and 200 J/m(2) of UV light increased the transductio

221 ontext of MHV if cells are infected at a low MOI and accelerates disease in mice transgenic for the h

222 rs also replicated less efficiently at a low MOI and expressed lower levels of GFP from the UL127 pro

223 the human CMV enhancer and promoter at a low MOI are discussed.

224 d increase in viral DNA replication at a low MOI but only when basal levels of MIE promoter activity

225 herefore, we propose a mechanism where a low MOI gonococcal challenge results in diminished AP-1 acti

226 RNA levels in a CRE-specific manner at a low MOI in both HFF- and NTera2-derived neuronal cells; and

227 ad a direct effect on HIV-1 virions at a low MOI in the absence of serum.

228 At a low MOI, IL-1beta secretion was minimal in CFT073-infected m

229 However, at a low MOI, only one of the genomes is delivered into the cells

230 M-G52, were tested for the ability, at a low MOI, to progressively infect the culture over time, caus

231 ring infection with the VRS mutants at a low MOI.

232 the transduction efficiency 2-fold at a low MOI.

233 hancer, the impairment in replication at low MOI corresponds to a deficiency in production of MIE RNA

234 infection (MOI) but replicate poorly at low MOI in comparison to wild-type virus (WT) or HCMVs that

235 ene expression and genome replication at low MOI, but this regulatory function is unnecessary at high

236 At low MOI, stochastic influences appear as kinetic effects whi

237 At low MOI, the transcription rates of ICP6 and tk were compara

238 At low MOI, these working parts likely function in cis to direc

239 poptosis and undergoing proliferation at low MOI, whereas CD3+ T cells did not exhibit this pattern.

240 xamined were protected from apoptosis at low MOI.

241 mediated host antiviral response seen at low MOI.

242 ion of viral US3 RNA was also evident at low MOI.

243 ion of viral components was observed for low MOI stochastic simulations.

244 ptosis at high MOI differs markedly from low MOI apoptosis: it is potently induced by virulent M. tub

245 Induction of IL-8 expression in low MOI challenges was not mediated by an autocrine response

246 virus is required to complete infection (low MOI), the 3'CS is retained due to the need for NSP1 to b

247 The protective effect of low MOI on apoptosis persisted even when B cells were isolat

248 els of HCMV DNA replication at a high or low MOI in HFF.

249 Analysis of various MAPKs indicated that low MOI challenges were able to efficiently activate both th

250 vels of IL-8 that were comparable to the low MOI challenges, but now induced significant levels of TN

251 fection was very efficient, even at very low MOI (>95% infection at a MOI of 6) and did not reduce vi

252 biphasic response to H. pylori, in which low MOI (1-10) markedly inhibited apoptosis, whereas high MO

253 limits the efficiency of reactivation at low MOIs and that competition between genomes occurs at high

254 oductively infected these macrophages at low MOIs but yielded few viable elementary bodies (EBs) when

255 n viral spread during HSV-1 infection at low MOIs.

256 observed in 3 macaques using relatively low MOIs (5-10) in a 48-hour ex vivo transduction protocol.

257 rgeting that we achieved with relatively low MOIs suggest that combining rAAV vectors with DSBs is a

258 longed survival was even found with very low MOIs of 0.1 and 0.5, with survivals of 24+/-4.2 and 25+/

259 ages, and mutation rates increased under low-MOI-passage conditions.

260 Cells infected at the lower MOI induced more subtypes than cells infected at the hig

261 in human foreskin fibroblast cells, at lower MOIs, the murine CMV enhancer was less efficient.

262 ines in which IGF2 imprinting is maintained (MOI), essentially all of the 3C interactions seen in nor

263 ts place, we propose an alternative measure, MOI(actual), that takes into account the cell concentrat

264 The compound 3-methyleneoxindole (MOI), a photooxidation product of the plant auxin indole

265 ll death, macrophages infected at a moderate MOI did not show signs of cytotoxicity until late in the

266 idarum in macrophages infected at a moderate MOI, implying that chlamydial growth was blocked by acti

267 ent following infection at low multiplicity (MOI = 0.1 PFU/cell) inhibited HCMV in a dose-dependent m

268 In addition, the concept of MOI(actual) allows us to write simple formulas for compu

269 MDP did not induce IFN-beta, irrespective of MOI.

270 that explain the demonstrated usefulness of MOI at high cell densities, as well as some unexpected c

271 the neonatal cells infected with Ad.RSV.PL (MOI, 10 pfu/cell) were characterized by (1) a significan

272 te the relations of fasting and postprandial MOI with total and regional adiposity and insulin sensit

273 ssociated with both fasting and postprandial MOI.

274 hether adiposity influences the postprandial MOI response is unknown.

275 The postprandial MOI response may be influenced by central adiposity in c

276 ed by infection and normalized by the PreS1*-MOI, which is the multiplicity of infection that reflect

277 nfected hepatocytes normalized by the PreS1*-MOI.

278 At the highest relative MOI of 400, survival was prolonged to 58+/-10 days.

279 rolongation was found at the lowest relative MOIs of 0.2 and 1, but there was dose-dependent prolonga

280 Similarly, MOI may bind in this substrate site.

281 r a low initial MOI or a high superinfecting MOI.

282 Our data demonstrate that MOI-dependent TLR2 activation of macrophages results in

283 (hydroxyethyl)ethacrynic acid indicates that MOI reacts in the active site region involving both the

284 allizable sequencing technologies means that MOI can be detected genome wide by considering the abund

285 These results show that MOI reacts preferentially with GST pi.

286 fold by S-methylglutathione, suggesting that MOI does not react entirely within the glutathione site.

287 OI), as well as the relationship between the MOI and the risk of subsequent malaria.

288 ild type is very sensitive to changes in the MOI (i.e., the degree of complementation) but depends li

289 critical factor in LOD-score analysis is the MOI at the linked locus, not that of the disease or trai

290 istinct antiviral responses depending on the MOI.

291 e increase was inversely proportional to the MOI.

292 h live organisms and was proportional to the MOI.

293 ore the relationship between the traditional MOI and F(WS) approaches.

294 f LOD scores to detect linkage when the true MOI was complex but a LOD score analysis assumed simple

295 adequacy of the approximate MOI for the true MOI.

296 (multiplicity of infection [MOI], 5), UVCP (MOI, 5), or cHSP60 for 24 h, and the expression of costi

297 The cells infected at the lower viral MOI induced the IFNAR2-dependent IFN-alpha subtypes 4, 6

298 esent the novel finding that different viral MOIs differentially activate JAK/STAT signaling through

299 Infection of CD34(+) progenitor cells with MOIs of 1 to 100 did not impair clonogeneic efficiency o

300 Prolonged survival with MOIs as low as 0.1 and 0.5 indicates that only a minorit