ライフサイエンスコーパス: MEM

1 MEM analyses showed that no significant differences exis

2 MEM explants treated with either inhibitor demonstrated

3 MEM is not suitable for the modeling of CEC data because

4 MEM outperforms traditional metrics in describing immune

5 MEM provides a quantitative language to communicate char

6 MEM treatment also significantly decreased elevated vitr

7 MEM-18 and 61D3 (anti-CD14 mAbs) were poor inhibitors of

8 the negative-control groups (Ng-rPorB, 13%; MEM-0, 19%; P < 0.05).

9 Among these compounds, 17, with a C-28 MEM ester moiety, and 22, with a C-28 ethyl hexanoate, i

10 ms were visualized by CLSM on 46 (92%) of 50 MEM specimens from children with OME and recurrent OM us

11 es is not greater than a minimum length of a MEM.

12 erative search algorithms" is refuted with a MEM analysis of their triexponential test case with incr

13 baseline cognitive composite scores of ADNI-MEM and ADNI-EF, (2) identifying subjects with significa

14 MPA concentrations other than 1:320 and all MEM-based tests had suboptimal sensitivities or specific

15 on of SPBN-TNF-alpha+ than of SPBN-TNF-alpha(MEM) or SPBN-TNF-alpha-, which carries an inactivated TN

16 ble membrane-bound TNF-alpha [SPBN-TNF-alpha(MEM)].

17 ow perfusion bioreactor system wherein alpha-MEM (supplemented with 10% fetal bovine serum and 1% ant

18 ow perfusion bioreactor system wherein alpha-MEM (supplemented with 10% fetal bovine serum and 1% ant

19 Similar to the calpain and MEM domains, the Linker is highly conserved in the land

20 may determine the magnitude of both EFFE and MEM cells, which arise subsequently.

21 We isolated NAI, EFFE, and MEM CD8(+) T cell subsets from human peripheral blood an

22 s that strongly differentiate NAI, EFFE, and MEM CD8(+) T cells; these genes provide previously unrec

23 rs the development of adaptive immunity, and MEM is incomplete.

24 Hodge test (MHT) was performed using IPM and MEM disks.

25 pts are illustrated using kinetic traces and MEM populations derived from the CO recombination proces

26 The LFA-1 activating antibody MEM-83, or its Fab fragment, decreased the rolling veloc

27 Monoclonal antibody MEM-265 recognizes the peptide-free conformation of the

28 The absence of a B(MEM) response to nonspecific inflammatory signals clearl

29 Memory B (B(MEM)) cells and long-lived bone marrow plasma cells (BM-

30 nflammatory signals promote memory B cell (B(MEM)) self-renewal and differentiation in an antigen-ind

31 B cell markers before generating daughter B(MEM) and differentiating into plasma cells or form struc

32 onse profiles of B-2 lineage B220(+)IgG(+) B(MEM) toward cognate protein antigen in comparison to bys

33 We report herein that long-lived B(MEM) cell survival and function are completely independe

34 tander proliferation or differentiation of B(MEM) occurred.

35 ivation, fail to induce even low levels of B(MEM) proliferation or differentiation in vivo.

36 Surprisingly, proliferating B(MEM) do not acquire germinal center (GC) B cell markers

37 After in vivo antigen encounter, quiescent B(MEM) clonally expand.

38 However, the factors supporting B(MEM) cell survival within the secondary lymphoid organs

39 ic inflammatory signals clearly shows that B(MEM) proliferation and differentiation is a process tigh

40 Thus, B(MEM) cells represent the only mature B2 lineage subset w

41 of random noise had similar effects on both MEM and NLLS results.

42 BWA-MEM alignment and raw variant calls are available at htt

43 ations in SeqLib: HTSlib for BAM access, BWA-MEM and BLAT for sequence alignment and Fermi for error

44 ing combinations of three read aligners--BWA-MEM, Bowtie2, and Novoalign--and four variant callers--G

45 ads from a CRAM file and then align with BWA-MEM.

46 on of I-GPI cells with ICAM-3 was blocked by MEM-83.

47 -67 as essential for specific recognition by MEM-265.

48 onent in the antigenic epitope recognized by MEM-265 in the peptide-free form of major histocompatibi

49 rrors in lifetime distributions recovered by MEM was compared to that in standard nonlinear least-squ

50 ements, on fluorescence lifetime recovery by MEM.

51 ntaining gel alone implanted over calvarium (MEM-GEL; n = 10); 4) implanted PLA membrane containing g

52 th sPGN and ReLPS was inhibited by anti-CD14 MEM-18 mAb, but other anti-CD14 mAbs showed differential

53 Chronic MEM treatment significantly improved retinal function an

54 the neuroprotective effect of this compound, MEM can reduce vascular changes seen in diabetic retinas

55 Biofilms were not observed on 8 control MEM specimens obtained from the patients undergoing coch

56 Uninfected (control) MEM specimens were obtained from 3 children and 5 adults

57 e is regulated by the membrane-anchored DEK1 MEM, which is connected to the calpain via the 600-amino

58 and DEK1 calpains, we propose that the DEK1 MEM-Linker complex inactivates the calpain by forcing ap

59 Arabidopsis thaliana dek1 mutants, and DEK1-MEM also failed to restore wild-type phenotypes in Arabi

60 Instead, ectopic expression of DEK1-MEM under the control of the cauliflower mosaic virus 35

61 consists of a membrane-spanning region (DEK1-MEM) and a calpain-like Cys proteinase region (DEK1-CALP

62 Since DEX, MEM and KET are currently used in humans and considered

63 nd consists of a large transmembrane domain (MEM) linked to a protease catalytic domain and a regulat

64 vested and cultured for three days in either MEM or MEM plus 10% serum.

65 -52 and Gln-64, that contribute by enhancing MEM-265 binding.

66 a and 46a could be prepared analogously from MEM ether 44c, but the sensitivity of several of the int

67 microscopic (CLSM) images were obtained from MEM biopsy specimens and were evaluated for biofilm morp

68 Bioinformatic analysis identifies MEM as a member of the Major Facilitator Superfamily, me

69 white rats (Sprague-Dawley) were cultured in MEM enriched with 5% horse serum.

70 terial OM via the activation of Erk1/Erk2 in MEM of an in vivo rat bacterial OM model.

71 Human gingival fibroblasts were incubated in MEM containing chlorhexidine concentrations ranging from

72 The arterial segments were incubated in MEM for 24 hours at 37 degrees C in the presence or abse

73 assessed whether this pathway is involved in MEM hyperplasia during bacterial OM via the activation o

74 support a role for Ras and Erk signaling in MEM hyperplasia during bacterial OM.

75 ted with increasing titers of the vectors in MEM.

76 llel to those recognized by anti-HLA-E mAbs (MEM-E/02/06/07).

77 ign of future vaccine strategies to maximize MEM cell generation.

78 sue culture milieu, Minimum Essential Media (MEM), the sensitivity of the EIS measurement was greater

79 i.n. with Eagle's minimal essential medium (MEM-0).

80 ll culture medium (minimum essential medium, MEM) and fetal calf serum (FCS) were probed by XANES and

81 To test whether chronic memantine (MEM) treatment improves retinal function and prevents ne

82 her 5 mM dextrorphan (DEX), 10 mM memantine (MEM) or 10 mM ketamine (KET) significantly attenuated fo

83 AI) T cells into effector (EFFE) and memory (MEM) cells is incompletely understood.

84 Immunological memory (MEM) development is affected by stress-induced neuroendo

85 the beta-lactams imipenem (IPM), meropenem (MEM), ertapenem (ERT), and ceftazidime (CAZ).

86 Imipenem (IPM), meropenem (MEM), ertapenem (ERT), and doripenem (DOR) were tested b

87 The maximum entropy method (MEM) further chooses a unique model from the group of fe

88 The maximum entropy method (MEM) has been used in many studies to reliably recover e

89 The maximum entropy method (MEM) is used to numerically invert the kinetics of ligan

90 The maximum entropy method (MEM) provides a robust and unbiased solution to fluoresc

91 is that combines the maximum entropy method (MEM) with nonlinear least squares (NLS) fitting has been

92 ferent ratios of the regioisomeric pairs MME/MEM, PPE/PEP, PPD/PDP, EEP/EPE and DDP/DPD (M=14:0, P=16

93 We present marker enrichment modeling (MEM), an algorithm that objectively describes cells by q

94 op individual-based movement ecology models (MEM) to explore turkey vulture (Cathartes aura) migratio

95 ucing reagent for acyclic acetal (i.e., MOM, MEM, SEM, and BOM) protected alpha-hydroxy ketones.

96 N, SETTING, AND PATIENTS: Middle-ear mucosa (MEM) biopsy specimens were obtained from 26 children (me

97 Hyperplasia of middle-ear mucosa (MEM) during otitis media (OM) is thought to be partially

98 The middle ear muscle (MEM) reflex is one of two major descending systems to th

99 Compared to NLLS, MEM afforded significant improvements for the recovery o

100 ed to the dynamic, self-modeling approach of MEM and the direction provided by the entropy criterion.

101 This effect of MEM was not seen in nondiabetic rats.

102 to identify the vasculoprotective effect of MEM.

103 his article is to (a) provide an overview of MEM reflex anatomy and physiology, (b) present new data

104 oderate proliferative response above that of MEM (P < 0.001).

105 Control cells received an equal volume of MEM without chlorhexidine for similar times at 37 degree

106 Direct detection of biofilms on MEM biopsy specimens from children with OME and recurren

107 tomy and physiology, (b) present new data on MEM reflex anatomy and physiology from our laboratory an

108 um Essential Medium (Opti-MEM-I) alone; Opti-MEM-I plus EGF, NGF, PDGF-BB, bovine pituitary extract,

109 lular uptake profiles were evaluated in Opti-MEM and demonstrate that all the click clusters efficien

110 ified Eagle's Minimum Essential Medium (Opti-MEM-I) alone; Opti-MEM-I plus EGF, NGF, PDGF-BB, bovine

111 d growth in an artificial serum medium, Opti-MEM, and a rich LB-based medium with Na(+) levels and pH

112 less IFU than the Ng-rPorB (40 x 10(6))- or MEM-0 (70 x 10(6))-immunized mice (P < 0.05).

113 ncurrently differentiate into either EFFE or MEM cells (parallel differentiation) remains unresolved.

114 diate state followed by a split into EFFE or MEM cells, hence supporting the parallel differentiation

115 and cultured for three days in either MEM or MEM plus 10% serum.

116 Additionally, an in vitro model of rat MEM in bacterial OM was treated with farnesyl transferas

117 substitutions that either improve or reduce MEM-265 recognition could be traced to differences in th

118 ent claims made by Mulligan et al. regarding MEM analyses of kinetics are shown to be unfounded.

119 + IL-1 respectively for 24 hours in Eagle's MEM at 37 degrees C.

120 SDR-MEM mice had significantly attenuated anti-influenza IgG

121 b)NP(366-74)CD8(+) T cell populations in SDR-MEM mice.

122 Moreover, during resting memory, SDR-MEM mice responded with an enhanced footpad delayed-type

123 were rechallenged with A/PR/8/34 virus, SDR-MEM mice terminated viral gene expression significantly

124 ells were starved in 0.1% fetal bovine serum/MEM for 72 h and then treated with 50-450 microM caffein

125 PLA membrane containing gel and simvastatin (MEM-SIM; n = 10); and 5) untreated mice (n = 12).

126 l gene expression significantly earlier than MEM mice and generated a greater D(b)NP(366-74)CD8(+) T

127 These results indicate that MEM could be useful for the treatment of ocular diseases

128 nships between these subsets and showed that MEM cells have gene expression patterns intermediate bet

129 imates a 3.5-residue repeat, suggesting that MEM-265 may recognize the epitope in an alpha-helical co

130 The MEM approach describes the data much better than traditi

131 The MEM reflex pathways begin with sound presented to the ea

132 The MEM resolves two barrier distributions suggestive of reb

133 ether and the t-alcohol functionality as the MEM ether to give 20, which after sequential reduction/o

134 ation of the parameter space achieved by the MEM stabilizes the introduction of each successive expon

135 We suggest how the MEM can be extended to other spatial and temporal scales

136 Revision of the MEM "prior" based on features in the data can improve th

137 show that the postulated sensory Loop of the MEM domain plays an important role in the developmental

138 recovered from noisy kinetics data with the MEM can be improved by using a simple filter when bootst

139 distribution of lifetimes obtained with the MEM.

140 ls serially differentiate into EFFE and then MEM cells (linear differentiation) or whether they concu

141 6 to an alanine actually improved binding to MEM-265.

142 eus project either directly or indirectly to MEM motoneurons located elsewhere in the brainstem.

143 the thickest point of calvarial bone, while MEM-SIM caused a highly significant (P < or = 0.0005) in

144 lar recombination traces in conjunction with MEM (maximum entropy method) analysis of kinetic populat

145 e treated either with the second VEH or with MEM (10 mg/kg daily) for another 3 to 4 weeks using mini

146 media were removed, cells washed twice with MEM supplemented with 10% FBS, and fibroblasts in treatm