ライフサイエンスコーパス: MSV

1 MSV enablement increased nAb-PTX efficacy and survival i

2 MSV-nAb-PTX also augmented the accumulation of paclitaxe

3 MSVs provided both a high degree of sensitivity and rapi

4 MSVs, conventional culture, and direct immunofluorescenc

5 the blood were unchanged after administering MSV-nAb-PTX or nAb-PTX.

6 Whole-brain ANOVA revealed that AS and MSV interacted in the inferior frontal, inferior parieta

7 augmented the accumulation of paclitaxel and MSV in the liver, specifically in macrophages, whereas p

8 ogists individually evaluated DBT images and MSVs of 67 masses (30 malignant, 37 benign) in 67 women

9 transformed Madin-Darby canine kidney cells (MSV-MDCK) have highly reduced levels of E-cadherin and b

10 oloney sarcoma virus-transformed MDCK cells (MSV-MDCK) express low levels of Na,K-ATPase beta(1)-subu

11 thesized two of the most extreme conceivable MSV chimeras, each effectively carrying 182 recombinatio

12 and collagen increased in plaques from ESTA-MSV/miRs-treated vs. vehicle-treated mice.

13 Treatment with miRs packaged in ESTA-MSV but not in PEG/PEI reduced atherosclerotic plaque si

14 Likewise, miR-146a/-181b packaged in ESTA-MSV efficiently suppressed the chemokines, CCL2, CCL5, C

15 Targeted delivery of STAT3 siRNA in ESTA-MSV resulted in knockdown of STAT3 expression in 48.7% o

16 (PEG/PEI) nanoparticles and loaded into ESTA-MSV microparticles.

17 Accumulation of ESTA-MSV inside the bone marrow correlated with the E-selecti

18 Weekly systemic administration of ESTA-MSV/STAT3 siRNA significantly extended survival of mice

19 Our data supported our hypothesis that ESTA-MSV microparticle-mediated delivery of miR-146a/-181b am

20 ioaptamer-conjugated multistage vector (ESTA-MSV) drug carrier to bone marrow for the treatment of br

21 E-selectin-targeting multistage vector (ESTA-MSV) to inflamed endothelium covering atherosclerotic pl

22 d ECs with miRs was more efficient with ESTA-MSV than with the PEG/PEI.

23 somal fraction in beta(1)-subunit expressing MSV-MDCK cells compared with MSV-MDCK cells, indicating

24 pha(1)-subunit in beta(1)-subunit expressing MSV-MDCK cells was six- to sevenfold higher compared wit

25 e in MSV-MDCK and beta(1)-subunit expressing MSV-MDCK cells.

26 ) ranged 0.36-0.52 for DBT and 0.25-0.40 for MSV (P >/= .20).

27 ) ranged 0.89-0.93 for DBT and 0.88-0.93 for MSV (P >/= .23).

28 imum speedup of 37.5, 23.1 and 11.6-fold for MSV, SSV and P7Viterbi respectively.

29 yields upto 440 GCUPS for SSV, 277 GCUPS for MSV and 14.3 GCUPS for P7Viterbi all with 100 % accuracy

30 here, offers a finer-grained parallelism for MSV/SSV and Viterbi algorithms.

31 s, confirming the importance of splicing for MSV infection.

32 Forced expression of E-cadherin in MSV-MDCK cells did not reestablish epithelial polarity o

33 alpha(1)-subunit protein were comparable in MSV-MDCK and beta(1)-subunit expressing MSV-MDCK cells.

34 on of both early and late gene expression in MSV and DSV.

35 e lamellipodia and suppress cell motility in MSV-MDCK cells, independent of Na,K-ATPase ion transport

36 d invasiveness, and reduced cell motility in MSV-MDCK cells.

37 virus-transformed Madin-Darby canine kidney (MSV-MDCK) cells suppressed their motility.

38 murine sarcoma and leukemia virus complex (M-MSV/M-MuLV), and the induced immune response was monitor

39 When M-MSV/M-MuLV-challenged mice were treated with the immunos

40 in (EGFP) gene expression compared with MLV, MSV LTR, phosphoglycerate kinase, and CMV promoters in T

41 to a nanoporous solid multistage nanovector (MSV) to enable the passage of the drug through the tumor

42 tilizes heuristic-pipeline which consists of MSV/SSV (Multiple/Single ungapped Segment Viterbi) stage

43 gnificantly affect murine osteosarcomavirus (MSV).

44 DNA binding motifs into the Rep78-resistant MSV long terminal repeat results in a promoter that has

45 was up to 5-fold enrichment of the targeted MSV in the bone marrow of mice bearing early or late sta

46 Preliminary findings suggest that MSV might not be necessary for mass characterization whe

47 The MSV and its parent one-site version are equivalent for d

48 The MSV is an example of a promising therapeutic platform th

49 a biologically active form of c-ski and the MSV LTR are required for the development of the muscular

50 Our results indicate that MyoD-E12 binds the MSV enhancer with higher affinity and higher cooperativi

51 application to actual FA titration data, the MSV function is simulated, and its predictive ability is

52 ndition of a static quenching mechanism, the MSV postulates an underlying 1:1 fulvic acid (FA)/copper

53 of c-ski expressed under the control of the MSV LTR.

54 MyoD-E12 versus Myogenin-E12 binding to the MSV enhancer.

55 llular transcription factor Sp1, whereas the MSV long terminal repeat promoter did not.

56 of MyoD, as a heterodimer with E12, with the MSV enhancer, which has six E-box targets for MyoD famil

57 -9) in mice exhibiting positive responses to MSV-EphA2 siRNA treatment.

58 " AS) and format ("message sensation value," MSV) of anti-smoking ads in humans.

59 rous silicon particle- or multistage vector (MSV) - enabled EphA2 siRNA therapy.

60 by primarily focusing on multistage vectors (MSVs).

61 ink lung and A549 cell lines in shell vials (MSVs) for the detection of respiratory viruses in 159 sp

62 carcinoma virus MH2 and murine sarcoma virus MSV 3611.

63 under the control of a murine sarcoma virus (MSV) long terminal repeat (LTR) express the transgene in

64 -ski oncogene from the murine sarcoma virus (MSV) promoter-enhancer display preferential hypertrophy

65 repeat (LTR) promoters-murine sarcoma virus (MSV), MoMLV (MLV), and the LTR (termed Rh-MLV) that is d

66 Here, we used a maize streak virus (MSV) experimental model to explore both the extremes of

67 In maize streak virus (MSV)-infected maize plants, approximately 80% of the com

68 e intensive tasks within the pipeline (viz., MSV/SSV and P7Viterbi stages) still stand to benefit fro

69 work, we modify the multisite Stern-Volmer (MSV) equation for fitting fluorescence titration curves.

70 unit expressing MSV-MDCK cells compared with MSV-MDCK cells, indicating that in mammalian cells the N

71 s was six- to sevenfold higher compared with MSV-MDCK cells.

72 y better with DBT (range, 3.2-4.4) than with MSV (range, 3.8-4.8) for all four readers, with one read

73 masses as BI-RADS 4 or 5 with DBT than with MSV, at a cost of five false-positive biopsy recommendat

74 s demonstrated that macrophages treated with MSV-nAb-PTX remained viable and were able to internalize

75 the supernatants of macrophage treated with MSV-nAB-PTX.

76 assessment with DBT was similar to that with MSVs.