ライフサイエンスコーパス: TEN

1 TEN had a significantly higher number of cases with mild

2 TEN PATIENTS WHO REQUIRED two or more anterior teeth ext

3 A total of 20 SJS and 12 TEN cases were included.

4 /TEN: 16.5 +/- 1.0 days, $58,954 +/- $5,238; TEN: 16.2 +/- 1.0 days, $53,695 +/- $4,037) were observe

5 A TEN domain physically separate from the TERT core can ca

6 Suppression of a TEN-domain mutation with a compensatory charge-swap muta

7 HLA-B*1502 and carbamazepine-induced SJS and TEN and that reported sufficient data for calculating th

8 502 allele and carbamazepine-induced SJS and TEN in Han-Chinese, Thai, and Malaysian populations.

9 tay, comorbidities, and mortality of SJS and TEN in US adults.

10 HLA-B*1502 and carbamazepine-induced SJS and TEN was 79.84 (95% CI, 28.45-224.06).

11 ommon during the acute phase in both SJS and TEN.

12 ry outcome was carbamazepine-induced SJS and TEN.

13 f the acute ocular manifestations of SJS and TEN.

14 acute ocular manifestations between SJS and TEN.

15 fication codes to identify SJS, SJS/TEN, and TEN (n = 2,591, n = 502, and n = 564, respectively).

16 SJS, SJS/TEN, and TEN pose a substantial health care burden.

17 an estimated incidences of SJS, SJS/TEN, and TEN were 9.2, 1.6, and 1.9 per million adults per year,

18 holoenzyme reconstitution in vitro to assess TEN domain sequence requirements in the physiological en

19 ase and tensin homolog deleted on chromosome TEN) is a delayed step causatively leading to excitotoxi

20 e and tensin homologue deleted on chromosome TEN) is the major negative regulator of phosphatidylinos

21 e and TENsin homologue deleted on chromosome TEN) mutations predispose to phenotypically diverse diso

22 failed to interact strongly with the cognate TEN domains.

23 Under resting conditions, TEN significantly suppressed basal sympathetic tone comp

24 ical interaction assays pinpoint a conserved TEN domain surface required for holoenzyme subunit assoc

25 Collectively these observations demonstrate TEN can dampen basal sympathetic tone and attenuate symp

26 in vitro in a manner dependent on the Est2p TEN domain interaction.

27 8% for SJS, 19.4% for SJS/TEN, and 14.8% for TEN.

28 Ileal bacteria from TEN and TPN piglets were also examined for their ability

29 igh expression of RIP3 in keratinocytes from TEN patients potentiates MLKL phosphorylation/activation

30 is highly upregulated in skin sections from TEN patients and may therefore contribute to the patholo

31 Histologically, the skin from TEN patients exhibits separation at the dermo-epidermal

32 hosphorylation was observed in the skin from TEN patients, indicating the presence of RIP3-dependent

33 an-fish telomerases that contained the human TEN domain were active but not stimulated by POT1-TPP1,

34 ring between the moderate (15% in SJS, 0% in TEN) and severe groups (20% in SJS, 33% in TEN).

35 n TEN) and severe groups (20% in SJS, 33% in TEN).

36 ses with mild involvement (5% in SJS, 42% in TEN, p = 0.01), while no statistically significant diffe

37 ore contribute to the pathological damage in TEN through activation of programmed necrotic cell death

38 associated bacteria (100 colonies tested) in TEN ileal samples grew on mucin.

39 ndrome (SJS) and toxic epidermal necrolysis (TEN) among carbamazepine users, especially in some racia

40 Toxic epidermal necrolysis (TEN) and Stevens-Johnson Syndrome (SJS) are rare, acute,

41 ndrome (SJS) and toxic epidermal necrolysis (TEN) are life-threatening disorders.

42 ndrome (SJS) and toxic epidermal necrolysis (TEN) are rare but life-threatening conditions that initi

43 ndrome (SJS) and toxic epidermal necrolysis (TEN) are rare but life-threatening mucocutaneous disease

44 n syndrome (SJS)/toxic epidermal necrolysis (TEN) as a model to study the pathologic role of HLA in d

45 Toxic epidermal necrolysis (TEN) is a severe adverse drug reaction involving extensi

46 syndrome (SJS), toxic epidermal necrolysis (TEN), and graft-versus-host disease (GVHD) are distinct

47 syndrome (SJS), toxic epidermal necrolysis (TEN), drug rash with eosinophilia and systemic symptoms

48 syndrome (SJS), toxic epidermal necrolysis (TEN), or drug rash with eosinophilia and systemic sympto

49 ndrome (SJS) and toxic epidermal necrolysis (TEN).

50 syndrome (SJS) or toxic epidermal necrosis (TEN) is even rarer and not well studied.

51 The transmural extent of necrosis (TEN) (%) was measured by triphenyltetrazolium chloride s

52 this transdermal electrical neurosignaling (TEN) method on sympathetic physiology under different ex

53 s of piglets fed by total enteral nutrition (TEN; n = 6) or TPN (n = 5) were compared with the use of

54 Overall, 40% of SJS and 75% of TEN patients had acute ocular surface inflammation.

55 tructure was equally complex in the ileum of TEN and TPN piglets, but profiles clustered according to

56 t significantly different in skin lesions of TEN.

57 Importantly, in an in vitro model of TEN, dabrafenib, an inhibitor of RIP3, prevented RIP3-me

58 The roles of TEN domain surface residues in primer binding and produc

59 presents a potential target for treatment of TEN.

60 SJS (<30% body surface area involvement) or TEN (> = 30% involvement), who were treated at one terti

61 The studies included 227 SJS or TEN cases, 602 matched control subjects, and 2949 popula

62 nese race/ethnicity, no patients with SJS or TEN were carriers of the HLA-B*1502 allele.

63 In addition, P-TEN exhibited a high degree of substrate specificity, sh

64 thermore, we demonstrate that mutations in P-TEN, identified from primary tumors, tumor cells lines,

65 , demonstrating that enzymatic activity of P-TEN is necessary for its ability to function as a tumor

66 Here we show that recombinant P-TEN dephosphorylated protein and peptide substrates phos

67 didate tumor suppressor from 10q23, termed P-TEN, was isolated, and sequence homology was demonstrate

68 ne, and tyrosine residues, indicating that P-TEN is a dual-specificity phosphatase.

69 WE RECOGNISE TEN SPECIES IN THIS GROUP: S. aureitomentosum Bitter, S.

70 Ocular involvement in SJS, TEN, and Overlap syndrome is common and the ocular manif

71 ick Children between 2001 and 2011 with SJS, TEN, and Overlap syndrome were reviewed.

72 SJS/TEN mostly manifest as a reaction to new drug use, but l

73 SJS/TEN was associated with nonwhite race, particularly Asia

74 (15 drug-induced liver injury [DILI], 33 SJS/TEN, 20 hypersensitivity syndrome, and 46 nevirapine-ind

75 we calculated an incidence rate of 5.76 SJS/TEN cases per million person-years between 1995 and 2013

76 SJS: 9.8 +/- 0.3 days, $21,437 +/- $807; SJS/TEN: 16.5 +/- 1.0 days, $58,954 +/- $5,238; TEN: 16.2 +/

77 Causality assessment for DILI and SJS/TEN was carried out with the Roussel Uclaf Causality Ass

78 tically significant associations between SJS/TEN and pre-existing depression, lupus erythematosus, re

79 cytotoxicity in in vitro models of both SJS/TEN (elicited by drug-specific antigen) and GVHD (elicit

80 were penicillins and cephalosporins for SJS/TEN and AGEP; glycopeptides for DRESS.

81 possible immunomodulating treatments for SJS/TEN and estimate their effects on mortality compared wit

82 national experts, a case report form for SJS/TEN has been created to help standardize the collection

83 lating therapies or supportive care) for SJS/TEN were selected.

84 with epilepsy and gout, odds ratios for SJS/TEN were significantly increased only in the presence of

85 ed mortality was 4.8% for SJS, 19.4% for SJS/TEN, and 14.8% for TEN.

86 systemic immunomodulating treatments for SJS/TEN, which is of great relevance for treating physicians

87 ages looking for treatment proposals for SJS/TEN.

88 systemic immunomodulating therapies for SJS/TEN.

89 e 69 cases of PPI-related DHR, including SJS/TEN (n=27) and DRESS (n=10).

90 es (CTLs) from patients with CBZ-induced SJS/TEN and analyzed the interaction between HLA-B and CBZ a

91 as a risk factor for nevirapine-induced SJS/TEN in a Malawian HIV cohort.

92 orrelations for CBZ-related drug-induced SJS/TEN.

93 syndrome and toxic epidermal necrolysis (SJS/TEN) are rare but severe adverse reactions with high mor

94 syndrome and toxic epidermal necrolysis (SJS/TEN), although a detailed description is lacking in the

95 The OR for absolute risk of SJS/TEN associated with carriage of HLA-C*04:01 was 5.17 (95

96 servational study on the epidemiology of SJS/TEN contributes to the understanding of this still under

97 ality based on an international panel of SJS/TEN experts who performed a Delphi consensus-building ex

98 servational study on the epidemiology of SJS/TEN using data from the UK-based Clinical Practice Resea

99 Asian patients were at a 2-fold risk of SJS/TEN when compared with white patients.

100 d 86 patients (167 eyes) with history of SJS/TEN who underwent PROSE treatment from January 1, 2006,

101 After remission of SJS/TEN, a complete ENT mucosal healing occurred in 36 patie

102 ate and useful" for documenting cases of SJS/TEN, making it more reliable and valuable for future res

103 15, 36 (4.8%) had associated features of SJS/TEN.

104 y findings to improve prognostication of SJS/TEN.

105 yspnea is observed at the acute stage of SJS/TEN.

106 ical Modification codes to identify SJS, SJS/TEN, and TEN (n = 2,591, n = 502, and n = 564, respectiv

107 SJS, SJS/TEN, and TEN pose a substantial health care burden.

108 The mean estimated incidences of SJS, SJS/TEN, and TEN were 9.2, 1.6, and 1.9 per million adults p

109 Fatality was more frequent in the SJS/TEN group.

110 hronic ocular surface disease related to SJS/TEN, PROSE treatment offers sustained and significant la

111 f highly cited manuscripts pertaining to SJS/TEN.

112 Among 551 validated SJS/TEN patients, we calculated an incidence rate of 5.76 SJ

113 s who developed DILI in association with SJS/TEN from a registry of DILI patients from a single cente

114 Retrospective study of 49 patients with SJS/TEN hospitalized in a referral care center from 2005 to

115 ce of DILI occurring in association with SJS/TEN including the etiologic agents, clinical and biochem

116 DILI associated with SJS/TEN is rare and associated with a high death rate, parti

117 himera on CTL responses in patients with SJS/TEN or GVHD.

118 temic inflammation seen in patients with SJS/TEN or GVHD.

119 vity, such as that seen in patients with SJS/TEN, as well as the alloreactivity seen in patients with

120 In patients with SJS/TEN, higher mortality was associated with old age and un

121 t when subjects were experimentally stressed TEN produced a significant suppression of heart rate var

122 s three hypothetical consensus motifs (SVTK, TEN, and KTG) that typically form the active center of o

123 thyl ether (AME), altenuene (ALT), tentoxin (TEN), and tenuazonic acid (TeA), five alternaria toxins

124 We demonstrate that the TERT N-terminal (TEN) domain determines active-site use of the atypically

125 The telomerase essential N-terminal (TEN) domain is a conserved region of TERT proposed to me

126 he purified telomerase essential N-terminal (TEN) domain of Est2p in vitro.

127 ranscriptase (TERT) core, a TERT N-terminal (TEN) domain, and additional subunits of the telomerase h

128 thesis does not require the TERT N-terminal (TEN) domain, but RNA-dependent positioning of the TEN do

129 We find that TEN domain sequence substitutions in the Tetrahymena tel

130 ions are consistent with the hypothesis that TEN modulates noradrenergic signaling to suppress sympat

131 The TEN method involved delivering high-frequency pulsed ele

132 he docked state is further buttressed by the TEN domain and mutations within the TEN domain substanti

133 tation of a conserved glycine, Gly100 in the TEN (telomerase essential N-terminal) domain of TERT, ab

134 tify separation-of-function mutations in the TEN-domain of human telomerase reverse transcriptase (hT

135 domain, but RNA-dependent positioning of the TEN domain captures substrate and allows repeat synthesi

136 meric DNA complex and the G100 region of the TEN domain of TERT is necessary for high-processivity te

137 nked to telomeric DNA in the presence of the TEN domain.

138 ng assays to investigate the function of the TEN domain.

139 determinants of processivity lie outside the TEN domain.

140 requency dead regions, as assessed using the TEN(HL) test.

141 We propose a model in which the TEN domain stabilizes short RNA-DNA duplexes in the acti

142 t3 homologues form stable complexes with the TEN domain of telomerase reverse transcriptase.

143 We propose that interaction with the TEN domain unmasks a functionally important nucleic acid

144 d by the TEN domain and mutations within the TEN domain substantially alter the DNA substrate structu

145 positive IVC velocity correlated better with TEN (r = -0.94, p < 0.0001) than it did S (r = -0.70, p

146 ak negative velocity) highly correlated with TEN, during ischemia (r = -0.78, p < 0.001) and during r

147 lar involvement, including all patients with TEN (n = 7).

148 different experiment, subjects treated with TEN reported significantly lower levels of tension and a

149 IVC velocity was zero in ischemic walls with TEN >20%.