ライフサイエンスコーパス: JT

1 JT and Jtag cells were CD28(null) and CD28(lo), respecti

2 JT/Bcl-2 and JT/Bcl-X(L) cells are susceptible to NO-med

3 s provides insight into the reactivity of 1: JT-induced symmetry lowering provides an orbital selecti

4 Active-site forces induce a JT distortion that localizes the odd electron in a singl

5 riations in heart rate (HR) or reliance on a JT-normalized time scale.

6 JT/Bcl-2 and JT/Bcl-X(L) cells are susceptible to NO-mediated apoptos

7 Exposure of JT/Bcl-2 and JT/Bcl-X(L) cells to the NO donor, S-nitroso-N-acetylpen

8 nger QT (3.01 ms [95% CI, 2.03 to 3.99]) and JT (2.89 ms [1.91 to 3.87]) intervals.

9 epolarization, estimated by QRS duration and JT interval, respectively.

10 , rate-corrected QT (QTc), QRS duration, and JT interval.

11 ncy (XSCID) lymphoblastoid cell line JT, and JT cells reconstituted with gamma c (JT/gamma c).

12 -12 ms), QT (73+/-27 versus 52+/-22 ms), and JT (96+/-31 versus 67+/-35 ms) dispersion.

13 e technique indicated AVNRT in 1 patient and JT in 7 patients, and the test was indeterminate in 1 pa

14 dispersion of QT and its components QRS and JT, in an attempt to determine whether any association e

15 Furthermore, increased QT, QRS, and JT dispersions, combined with a QRS > or = 180 ms, refin

16 cid was associated with rate-adjusted QT and JT intervals (QTrr and JTrr, respectively).

17 entrations are associated with longer QT and JT intervals in the general population.

18 morphologies and prolongation of the QT and JT intervals when measured in vivo, but not in isolated

19 The differences in QT and JT, and JTp intervals should also be corrected for race.

20 els appeared to have longer corrected QT and JT, and men in the lowest category of T4 appeared to hav

21 observed in established pathways for QT and JT, and previously unreported genes indicated in insulin

22 T4 appeared to have shorter corrected QT and JT.

23 or QRS, QT, and JT duration and QRS, QT, and JT dispersion.

24 ynchronous ECG was analyzed for QRS, QT, and JT duration and QRS, QT, and JT dispersion.

25 QRS, QT, and JT intervals and their dispersions were measured from 12

26 The arranged JT complexes, Fe(2+)O(4), their adiabatic potential ener

27 Wei B, Bernert JT, Blount BC, Sosnoff CS, Wang L, Richter P, Pirkle JL.

28 lysis of the RMC supercell reveals that both JT ions disproportionate to higher and lower valence sta

29 JT, and JT cells reconstituted with gamma c (JT/gamma c).

30 istortion induced by a cooperative collinear JT distortion, similar to that seen in NNO.

31 We propose that this collinear JT ordering is also present in solid-state synthesized L

32 allow for variation in heart rate, corrected JT interval (JTc) was defined as QTc-QRSd.

33 e to PACs during tachycardia can distinguish JT and AVNRT with 100% specificity in adult patients.

34 er these complexes exhibit static or dynamic JT distortions.

35 ients with 44 tachycardias suggesting either JT or AVNRT based on a short ventriculo-atrial interval

36 J; odds ratio [OR] = 3.66), T16126C+G13368A (JT; OR = 10.27), A4917G+A73G (T4; OR = 5), and T3197C+A1

37 HPT-JT is caused by mutations of the cell division cycle 73

38 Hyperparathyroidism-jaw tumor syndrome (HPT-JT) is an autosomal dominant disease characterized by th

39 The HPT-JT gene (HRPT2) maps to chromosome 1q25-q31.

40 on of CDC73 and its association with the HPT-JT syndrome and other diseases.

41 3 missense mutations associated with the HPT-JT syndrome are located in the region encoding CDC73-NTD

42 ry of primary hyperparathyroidism or the HPT-JT syndrome at presentation.

43 line mutations in HRPT2 and may have the HPT-JT syndrome or a phenotypic variant.

44 nd uterine neoplasms that develop in the HPT-JT syndrome, provide in vivo models for future studies o

45 s directly involved in predisposition to HPT-JT and in development of some sporadic parathyroid tumor

46 ated with hyperparathyroidism-jaw tumor (HPT-JT) syndrome, an autosomal dominant disorder.

47 yroidism--hyperparathyroidism-jaw tumor (HPT-JT) syndrome--that carries an increased risk of parathyr

48 with the hyperparathyroidism-jaw tumor (HPT-JT) syndrome.

49 The hyperparathyroidism-jaw tumour (HPT-JT) syndrome is an autosomal dominant disorder character

50 and the hyperparathyroidism-jaw tumour (HPT-JT) syndrome, which is associated with renal and uterine

51 We describe further investigation of two HPT-JT families (K3304 and K3349) identified through the lit

52 A single locus associated with HPT-JT (HRPT2) was previously mapped to chromosomal region 1

53 a single gene in fourteen families with HPT-JT.

54 ed TG-induced NO production and apoptosis in JT/Neo cells.

55 milar to the QT interval, the differences in JT, JTp and Tpe intervals should be corrected for sex.

56 tion mediates apoptosis after TG exposure in JT/Neo cells.

57 lted in apoptosis comparable to that seen in JT/Neo cells.

58 JAK3, and downstream activation of STAT5, in JT/gamma c cells as well as BaF3/IL-21R alpha and primar

59 re dramatically reduced compared to those in JT/Neo cells.

60 JT)-active Cu(2+) and the octahedral site is JT-active Mn(3+).

61 kat cells overexpressing Bcl-2 and Bcl-X(L) (JT/Bcl-2 or JT/Bcl-X(L)), NO production, late (36-h) Ca(

62 odeficiency (XSCID) lymphoblastoid cell line JT, and JT cells reconstituted with gamma c (JT/gamma c)

63 t PR interval, PR segment, and QRS, and long JT.

64 ascular mortality in smokers, including long JT, QRS, and QTc, and short QRS, whereas only short JT p

65 ate the JAK-STAT pathway in nonreconstituted JT cells.

66 clinically obvious AVNRT, clinically obvious JT, and clinically indeterminate rhythm.

67 In the 9 cases of clinically obvious JT, the sensitivity and specificity were 100% and 100%,

68 Ablation of JT is associated with a lower success rate and a higher

69 for the circuit and confirms a diagnosis of JT.

70 Exposure of JT/Bcl-2 and JT/Bcl-X(L) cells to the NO donor, S-nitros

71 e evolved, but because of a low incidence of JT, large studies of the most efficient therapeutic sequ

72 rapy was defined as a sustained reduction of JT rate <170 beats/min within 2 h.

73 approximately 10% longer compared to that of JT (p < 0.001).

74 erexpressing Bcl-2 and Bcl-X(L) (JT/Bcl-2 or JT/Bcl-X(L)), NO production, late (36-h) Ca(2+) accumula

75 ension, neither haplogroups H1, H2, UK, K or JT were associated with any DR, NPDR, PDR or DME.

76 between thyroid hormones and corrected QT or JT was found, except that men in the highest category of

77 Postoperative JT is a transient arrhythmia that may be fatal after ope

78 Postoperative JT was strongly associated with young age, transient atr

79 ective management strategy for postoperative JT.

80 n data for evaluation of newer and promising JT options, such as intravenous amiodarone.

81 QRS duration and QT/QRS/JT dispersion were measured manually from standard ECGs

82 fy 177, 156 and 121 independent loci for QT, JT and QRS, respectively, including a male-specific X-ch

83 d Holter recordings were used to measure QT, JT, JTp, and Tpe intervals preceded by both stable and v

84 te the causal effect of serum calcium on QT, JT, and QRS intervals using an inverse-weighted method i

85 ectronic structure, which reveal a quadratic JT distortion and significant e-e mixing, thus reaching

86 dent on the H2 orientation through quadratic JT distortion.

87 A protocol for rapid JT (>170 beats/min) was adopted in 1986, and was tested

88 , and QTc, and short QRS, whereas only short JT predicted mortality in nonsmokers.

89 SM, JT and JJ were supported by the Austrian Federal Ministr

90 The studyEvans JT, Mouchti S, Blom AW, et al.

91 Above T(JT) where NaNiO(2) is rhombohedral, diffraction measurem

92 order-disorder, Jahn-Teller transition at T(JT).

93 ow its Jahn-Teller transition temperature, T(JT), NaNiO(2) has a monoclinic layered structure consist

94 tiate non-re-entrant junctional tachycardia (JT) and typical atrioventricular node re-entry tachycard

95 toperative automatic junctional tachycardia (JT) using conventional drugs and techniques, and 2) iden

96 ovel type of sub-lattice of the Jahn-Teller (JT) centers was arranged in Ti-doped barium hexaferrite

97 nation compound is subject to a Jahn-Teller (JT) distortion of its doubly degenerate (2)E ground stat

98 t place, through a second-order Jahn-Teller (JT) distortion, which slides the Ta ion along the axial

99 E ground state susceptible to a Jahn-Teller (JT) distortion.

100 al (R3m) bulk structure and the Jahn-Teller (JT) distortions of the NiO(6) octahedra inferred on the

101 tructure below 140 K due to the Jahn-Teller (JT) instability arising from the (t2g)(4)(eg)(2) configu

102 d Fe-H2 show that both have the Jahn-Teller (JT)-active (2)E ground state (idealized C3 symmetry) wit

103 doublet, which renders R(3)S(0) Jahn-Teller (JT)-active and therefore subject to vibronically induced

104 ng that the tetrahedral site is Jahn-Teller (JT)-active Cu(2+) and the octahedral site is JT-active M

105 We hypothesized that JT can be distinguished from AVNRT based on specific res

106 The JT complexes are sensitive to external stress and applie

107 The JT stabilization energy is estimated to be approximately

108 In these circumstances, the JT interval has been proposed as a more valid way to ass

109 Here, we show the versatility of the JT and Jtag cell lines in tracking CD28(null) <--> CD28(

110 be controlled by the amount and state of the JT complexes.

111 ct to the [Formula: see text] problem of the JT effect.

112 s the vibronic interactions that lead to the JT distortions, and addresses whether these complexes ex

113 is analysis predicts CsTaS(3) to undergo the JT metal-to-semiconductor transition at temperatures bel

114 valence states as a means of avoiding their JT tendency, particularly on the tetrahedral site.

115 eliminate nonproductive stages, the time to JT control was significantly shortened for the last 30 p

116 sis in Jurkat cells transfected with vector (JT/Neo).

117 ame era to identify features associated with JT.

118 so correlated with QRS duration but not with JT dispersion.

119 up were contrasted with all patients without JT from this same era to identify features associated wi

120 transduction of wild-type gamma c into XSCID JT cells restored function to the IL-21R, as shown by IL