ライフサイエンスコーパス: SCU

1 edematous (n = 11) and nonedematous (n = 11) SCU when they were infected and malnourished (clinical p

2 edematous (n = 11) and nonedematous (n = 11) SCU when they were infected and malnourished (clinical p

3 h edematous (n = 14) or nonedematous (n = 7) SCU when they were infected and malnourished (postadmiss

4 Although SCUs may have provided unmeasured benefits to families a

5 e observe a pattern of better outcomes among SCU residents.

6 embryonal and undifferentiated small cells (SCU) progressively lose EGFR and ASAP1 expression.

7 r in the group that previously had edematous SCU than in the nonedematous group.

8 d in the group that previously had edematous SCU, but it did not change in the other group.

9 in the children who previously had edematous SCU.

10 r than the rate at recovery in the edematous SCU group, and there were no significant differences bet

11 e as when recovered, children with edematous SCU cannot.

12 At clinical phase 1, children with edematous SCU had rates of total methionine flux, flux from protei

13 and infected state, children with edematous SCU have slower methionine production than do children w

14 wer, however, in the children with edematous SCU than in those with nonedematous SCU.

15 , is much greater in children with edematous SCU than in those with nonedematous SCU.

16 sm will be slower in children with edematous SCU than in those with nonedematous SCU.

17 dimensional cationic metal organic framework SCU-103, showing ultrahigh stability in alkaline aqueous

18 n a stable cationic metal-organic framework, SCU-102 (Ni(2) (tipm)(3) (NO(3) )(4) ), which exhibits f

19 Differences in SCU among functional categories reflect differences in l

20 s reveal that PFOS anions are immobilized in SCU-8 by driving forces including electrostatic interact

21 e gBGC model explains 70% of the variance in SCU among genes.

22 ved in the speed of decline for residents in SCUs and traditional units in any of the 9 outcomes.

23 ent a mesoporous cationic thorium-based MOF (SCU-8) containing channels with a large inner diameter o

24 moplastic dispersal of a semiconductive MOF (SCU-13) through a commercially available polymer, poly(v

25 een children with edematous and nonedematous SCU and inherent differences in protein metabolism when

26 in children with edematous and nonedematous SCU.

27 ized that, in edematous but not nonedematous SCU, impaired protein breakdown leading to inadequate am

28 s of children with edematous or nonedematous SCU in the malnourished and recovered states.

29 roduction than do children with nonedematous SCU because of a slower rate of release from protein bre

30 Whereas children with nonedematous SCU can maintain arginine flux at the same rate as when

31 dematous SCU than in those with nonedematous SCU.

32 dematous SCU than in those with nonedematous SCU.

33 dematous SCU than in those with nonedematous SCU.

34 -five patients had some elements (1%-25%) of SCU identified on central review of diagnostic specimens

35 We argue that the strong heterogeneity of SCU induced by gBGC in mammalian genomes precludes any o

36 tral pathologic review for identification of SCU histology.

37 The presence of SCU did not affect event-free survival (EFS).

38 The presence of SCU histology did not correlate with age, alpha-fetoprot

39 The presence of SCU histology in HB does not appear to adversely affect

40 tification without regard to the presence of SCU histology.

41 The anion-exchange properties of SCU-8 were explored with many anions including small oxo

42 ratory, and physiologic variables at time of SCU admission, at 24 hrs, as well as vital status at the

43 Decontamination experiments confirm that SCU-102 represents the optimal Tc scavenger with the hig

44 sage, which was interpreted as evidence that SCU is adaptively constrained to optimize translation ef

45 We demonstrate here that SCU is not driven by constraints on tRNA abundance, but

46 tal status at the time of discharge from the SCU and hospital.

47 The median length of stay in the SCU was 2 days, and the median hospitalization for patie

48 The causes of admission to the SCU were pulmonary (15/43), cardiac (14/43), wound relat

49 urgical procedures required admission to the SCU.

50 ck malignant disease were transferred to the SCU.

51 h edematous severe childhood undernutrition (SCU) can maintain production rates of glycine and serine

52 ous form of severe childhood undernutrition (SCU) during food deprivation are not clear.

53 onedematous severe childhood undernutrition (SCU) have lower plasma and erythrocyte-free concentratio

54 onedematous severe childhood undernutrition (SCU) have lower plasma and erythrocyte-free concentratio

55 Small cell undifferentiated (SCU) histology in hepatoblastoma (HB) tumors has histori

56 patients admitted to the special care unit (SCU) of Memorial Sloan-Kettering Cancer Center between J

57 Alzheimer disease special care units (SCUs) in nursing homes are increasingly prevalent, but l

58 Synonymous codon usage (SCU) varies widely among human genes.

59 bryonal tumor cells are EGFR-negative, while SCU cells are EGFR-negative and ASAP1-negative.

60 e production is reduced in all children with SCU because of a decreased contribution from protein bre

61 ular nitric oxide synthesis in children with SCU.

62 ease from protein breakdown in children with SCU.

63 homocysteine remethylation in children with SCU.

64 tudies should be able to treat patients with SCU HB according to risk stratification without regard t

65 Patients with SCU histology identified at the local treating instituti

66 -risk, intermediate-risk, and high-risk with SCU HB was 86% (95% CI, 33 to 98), 81% (95% CI, 57 to 92

67 cluding 1228 residents in 48 facilities with SCUs.

68 red with EFS at 5 years for patients without SCU enrolled with low-risk, intermediate-risk, and high-