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

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

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

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

8 -12 ms), QT (73+/-27 versus 52+/-22 ms), and JT (96+/-31 versus 67+/-35 ms) dispersion.

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

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

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

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

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

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

15 T4 appeared to have shorter corrected QT and JT.

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

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

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

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

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

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

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

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

24 er these complexes exhibit static or dynamic JT distortions.

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

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

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

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

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

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

31 3 missense mutations associated with the HPT-JT syndrome are located in the region encoding CDC73-NTD

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

56 for the circuit and confirms a diagnosis of JT.

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

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

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

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

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

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

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

64 ective management strategy for postoperative JT.

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

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

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

68 dent on the H2 orientation through quadratic JT distortion.

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

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

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

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

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

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

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

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

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

78 The JT stabilization energy is estimated to be approximately

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

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

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

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

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

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

85 ame era to identify features associated with JT.

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

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

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