ライフサイエンスコーパス: intensive therapy

1 d therapy) with 80 mg of atorvastatin daily (intensive therapy).

2 y the degree of weight gain while undergoing intensive therapy.

3 n maintain this high survival rate with less intensive therapy.

4 1540 patients in three prospective trials of intensive therapy.

5 myeloid leukemia (AML) necessitate maximally intensive therapy.

6 be due, in part, to increased intolerance of intensive therapy.

7 onship with motor deficits across 28 days of intensive therapy.

8 ;22), or a t(1;19), and most received highly intensive therapy.

9 marrow on day 7) have a poor outcome despite intensive therapy.

10 that these patients are candidates for less intensive therapy.

11 ecent studies have shown improved outcome on intensive therapy.

12 nce of early and sustained implementation of intensive therapy.

13 g-term survival is approximately 40% despite intensive therapy.

14 for these patients who cannot tolerate more intensive therapy.

15 th lower DFS because these patients received intensive therapy.

16 d (OS of 100% at 6-year follow-up) with less-intensive therapy.

17 in the setting of combined modality or more intensive therapy.

18 esigned to examine thalidomide combined with intensive therapy.

19 the development of reliable organ-protective intensive therapy.

20 at 12 weeks, as compared with usual care or intensive therapy.

21 60) as compared with usual care but not with intensive therapy.

22 eks as compared with usual care but not with intensive therapy.

23 hypoglycemic clamp studies before and after intensive therapy.

24 RCs with BRD4-NUT are highly lethal, despite intensive therapies.

25 ed with significant myelosuppression in dose-intensive therapies.

26 k factor despite treatment with contemporary intensive therapies.

27 with 48% and 38% in those who received less-intensive therapies.

28 and adults in persistence of the benefits of intensive therapy 10 years after completion of the Diabe

29 owever, for the 17 patients who received non-intensive therapy, 16 (94%) of M1 clones had a response

30 tients, low-education patients received less intensive therapy (30% v 48%; adjusted odds ratio, 0.65;

31 act extraction (adjusted risk reduction with intensive therapy, 48%; 95% CI, 23 to 65; P=0.002); 29 p

32 n patients who received R-CHOP compared with intensive therapy (56% v 88%; P = .002).

33 performed in 63 of 711 patients assigned to intensive therapy (8.9%) and 189 ocular operations in 98

34 Despite intensive therapy, 80% of affected children die, often w

35 trial with sequential randomization to more intensive therapy achieved greater than 80% power and un

36 Complications Trial (DCCT) demonstrated that intensive therapy aimed at improved glucose control mark

37 CT) demonstrated that a mean of 6.5 years of intensive therapy aimed at near-normal glucose levels re

38 ices could lead to earlier implementation of intensive therapies and improved clinical outcomes.

39 23 to 65; P=0.002); 29 patients who received intensive therapy and 50 who received conventional thera

40 Forty-two patients who received intensive therapy and 61 who received conventional thera

41 L, particularly SR patients who require more intensive therapy and are now treated on HR COG ALL prot

42 alpha-tocopherol in patients undergoing dose-intensive therapy and hematopoietic stem cell transplant

43 tis the demyelinating episodes required more intensive therapy and resulted in more residual deficits

44 atients elected standard therapy, 21 elected intensive therapy, and 53 patients declined therapy.

45 effects to the overall clinical efficacy of intensive therapy are presently unclear.

46 e that occur with excessive weight gain with intensive therapy are similar to those seen in the insul

47 We evaluated the effect of intensive therapy as compared with conventional therapy

48 attempting to cure metastatic patients with intensive therapy as facilitated by peripheral stem cell

49 hough selected older adults can benefit from intensive therapies, as a group they experience increase

50 arction 22 (PROVE IT-TIMI 22) study compared intensive therapy (atorvastatin, 80 mg) and moderate the

51 s to prevent marrow relapse by administering intensive therapy before delayed craniospinal radiation.

52 cts for long-term survival are poor and that intensive therapy cannot be tolerated and so is not just

53 significantly for patients in the R-CHOP or intensive therapy cohorts when analyzed by receipt of au

54 iovascular events for participants receiving intensive therapy compared with moderate-dose therapy.

55 Intensive therapy conferred no survival advantage over s

56 Intensive therapy did not reduce the risk of advanced me

57 Intensive therapy during the DCCT resulted in decreased

58 ficantly less in the group that had received intensive therapy during the DCCT than in the group that

59 onventional therapy (dietary restriction) or intensive therapy (either sulfonylurea or insulin or, in

60 re acute pancreatic might benefit from early intensive therapy, enteral nutrition and timely transfer

61 rst and fourth quartiles of weight gain with intensive therapy except for a higher hemoglobin A1c in

62 The benefits of former intensive therapy extend to measures of CAN up to 14 yea

63 us 5-FU (500 mg/m2 per day) for 4 months; 2) intensive therapy: external beam radiation therapy to th

64 um to reduce mucositis in patients receiving intensive therapy for hematologic cancers.

65 led 1441 participants to address the role of intensive therapy for type 1 diabetes mellitus on the on

66 Intensive therapy for type 1 diabetes results in greater

67 ed hemoglobin (Hb A1c) concentrations during intensive therapy for type 1 diabetes.

68 In 90 patients treated with dose-intensive therapy from diagnosis at MSKCC, the use of MI

69 , with lower all-cause mortality risk in the intensive therapy group (hazard ratio [HR] = 0.67 [95% C

70 ut with a greater increase of sTNF-R1 in the intensive therapy group (P=0.002).

71 The intensive therapy group had no survival advantage when c

72 by EDIC Study year 10) vs. 31 controls (DCCT intensive therapy group subjects without complication pr

73 andard-therapy group and 235 patients in the intensive-therapy group (hazard ratio in the intensive-t

74 ce in glycated hemoglobin levels between the intensive-therapy group and the standard-therapy group a

75 Over a median follow-up of 9.8 years, the intensive-therapy group had a significantly lower risk o

76 rates of minimal response were lower in the intensive-therapy group than in the standard-therapy gro

77 d progression-free survival (P<0.001) in the intensive-therapy group than in the standard-therapy gro

78 ates of complete response were higher in the intensive-therapy group than in the standard-therapy gro

79 The goal in the intensive-therapy group was an absolute reduction of 1.5

80 intensive-therapy group (hazard ratio in the intensive-therapy group, 0.88; 95% confidence interval [

81 l mortality was evident (hazard ratio in the intensive-therapy group, 1.05; 95% CI, 0.89 to 1.25; P=0

82 The costs of surgery were 32% lower in the intensive-therapy group.

83 n the standard-therapy group and 6.9% in the intensive-therapy group.

84 the standard-therapy group and 24.1% in the intensive-therapy group.

85 Patients were eligible for 3F8/GM-CSF if intensive therapy had not eradicated potentially lethal

86 Patients who had more intensive therapy had significantly (P<0.01) better cont

87 subgroup analyses among subjects undergoing intensive therapy, hsCRP levels increased among those wh

88 Intensive therapy (IIP or MDI) for 1 year.

89 The benefit of intensive therapy in carriers was significant as early a

90 Intensive therapy in patients with type 1 diabetes melli

91 Intensive therapy in patients with type 1 diabetes was a

92 We defined SCAP as receipt of intensive therapy in the intensive care unit.

93 reased cardiovascular mortality in trials of intensive therapy in type 2 diabetes mellitus (T2DM).

94 ing subsequent hypoglycemia before and after intensive therapy in type 2 diabetic patients and in non

95 ents with ALL benefitted from receiving more intensive therapy in UKALL2003.

96 In refractory or unresponsive TTP, more intensive therapies including twice-daily plasma exchang

97 re designed to test the hypothesis that more intensive therapy, including dose intensification of che

98 Multi-targeted intensive therapy is imperative; however, unfortunately

99 However, when dose-intensive therapy is initiated at diagnosis, the reliabl

100 e hypothesis that increased weight gain with intensive therapy might be explained, in part, by geneti

101 rticipants were randomly assigned to receive intensive therapy (n = 711) aimed at achieving glycemia

102 ngs appear to corroborate early reports that intensive therapy of HIV-Burkitt lymphoma is feasible an

103 have shown that early diagnosis and timely, intensive therapy of rheumatoid arthritis can modify dis

104 tment outcome for such patients treated with intensive therapy on consecutive Children's Cancer Group

105 These data demonstrate that the effect of intensive therapy on inflammation is complex and, to the

106 The present study examined the effect of intensive therapy on levels of several markers of inflam

107 The effects of intensive therapy on measures of cardiac function and st

108 ontinued to show persistent benefit of prior intensive therapy on neuropathy, retinopathy, and nephro

109 cohort, reported persistent benefit of prior intensive therapy on retinopathy and nephropathy in type

110 We examined the effect of intensive therapy on the change in levels of the inflamm

111 ven secondary measures at study end favoured intensive therapy (p<0.05).

112 Among intensive therapy patients (n = 1,567), antecedent myelo

113 Limited to intensive therapy patients, we compared chance of comple

114 The benefit of intensive therapy progressively declined as baseline LDL

115 Intensive therapy reduced (P < 0.05) ANS and metabolic c

116 Prior DCCT intensive therapy reduced the risks of incident CAN by 3

117 They show that the less-intensive therapy reduces early mortality without impair

118 tment for baseline levels and other factors, intensive therapy remained associated with a significant

119 ailored according to response, with the most intensive therapies reserved for patients predicted to h

120 uces major vascular events, but whether more intensive therapy safely produces extra benefits is unce

121 Microvascular benefits of intensive therapy should be weighed against the increase

122 Dose-intensive therapy should currently be considered as the

123 nce of minimal residual disease (MRD) during intensive therapy still have a poor prognosis.

124 With intensive therapy, subjects with a family history of typ

125 he stability of the latent reservoir despite intensive therapy suggests that new strategies are neede

126 ears, six male/six female) across 28 days of intensive therapy targeting arm motor deficits.

127 For the 20 patients who received intensive therapy, there was no difference between the p

128 ery high-risk patients require novel or more intensive therapy to improve outcome.

129 dy tested the hypothesis that 1) 6 months of intensive therapy to lower A1C <7.0% would blunt autonom

130 those with the E2A-PBX1 fusion require more intensive therapy to obtain a good outcome.

131 roup, our findings do not support the use of intensive therapy to reduce the adverse effects of diabe

132 ed and relapsed patients, whether treated by intensive therapy (total therapy II) or novel agents (bo

133 Data for intensive therapy unit and hospital length of stay were

134 ollected from patients admitted to the liver intensive therapy unit at King's College Hospital in Lon

135 ove mortality, infectious complications, and intensive therapy unit length of stay in comparison with

136 With respect to intensive therapy unit length of stay, no differences we

137 Duration of liver intensive therapy unit stay (p = 0.175), survival (p = 0

138 t the MELD was significantly associated with intensive therapy unit stay but not eventual outcome; th

139 ritically ill adult patients admitted to the intensive therapy unit, given in addition to their routi

140 nd acute neurological illness managed in the intensive therapy unit.

141 aemopoietic-cell transplantation (HCT) is an intensive therapy used to treat high-risk haematological

142 After adjustment for DCCT baseline factors, intensive therapy was associated with a reduction in the

143 tin therapy induced EAT regression, although intensive therapy was more effective than moderate-inten

144 Intensive therapy was stopped before study end because o

145 end of the DCCT, after a mean of 6.5 years, intensive therapy was taught and recommended to all part

146 The beneficial effects of intensive therapy were fully attenuated after adjustment

147 utations predominated in mice receiving less intensive therapy, whereas high-dose treatment selected

148 M-1 decreased among participants assigned to intensive therapy, whereas they did not change among tho

149 with relapsed multiple myeloma eligible for intensive therapy, which might help to guide clinical de

150 hose patients whose prognosis justifies more intensive therapy, while predictive profiles may soon be

151 increased risk was significantly reduced by intensive therapy with atorvastatin 80 mg beyond that ac

152 These results indicate that intensive therapy with insulin, which establishes normog

153 al nervous system complications responded to intensive therapy with intravenous (IV) pulse methylpred

154 Recent clinical trials suggest that intensive therapy with statins may provide incremental b

155 capable of surviving within the body despite intensive therapy with the appropriate antimicrobial dru