ライフサイエンスコーパス: FSS

1 FSS and SHS mutations affect different myosin residues,

2 FSS applied to endothelial cells (ECs) triggers signalin

3 FSS demonstrated a better predictive accuracy for MACE c

4 FSS increased prostaglandin (PG) E2 release in WT cells

5 FSS rapidly increases the intracellular calcium concentr

6 FSS was determined by only counting ischemia-producing l

7 FSS-stimulated apical endocytosis was initiated between

8 V-1 Frameshift Stimulating Signal", or HIV-1 FSS) controls the frameshift efficiency and has been hyp

9 ounds displaying high affinity for the HIV-1 FSS.

10 We exposed MPT cells to 0.2 dynes/cm(2) FSS for 3 h and performed confocal microscopy and Wester

11 Scale 7 (FSS-7) score >5; low fatigue n=20, FSS-7 score <3) participated in the study.

12 high fatigue n=21, Fatigue Severity Scale 7 (FSS-7) score >5; low fatigue n=20, FSS-7 score <3) parti

13 junctional buttressing" model explains why a FSS of only 1/10 of that used in the EC study can cause

14 losing yield gaps, these regions can achieve FSS, which also reduces international trade and increase

15 "minor limitations with strenuous activity" (FSS=9); and 15% scored </=8.

16 l significantly reduced 4 but not 24 h after FSS.

17 An FSS of greater than 4.0 was not observed in controls (me

18 Abnormal fatigue, defined as an FSS score >or=4, was present in 67% of the subjects.

19 cores in each POPC or PCPC interval, with an FSS score increase with each worsening POPC/PCPC rating.

20 ficantly better scores on both the SF-36 and FSS.

21 ith a phenotype intermediate between DA1 and FSS.

22 a significant (P < .001) difference between FSS scores in each POPC or PCPC interval, with an FSS sc

23 -like cells, we found that Akt activation by FSS occurred through two parallel pathways; one required

24 ional connections were severely disrupted by FSS.

25 tors for the WT and three of the most common FSS mutants: R672H, R672C, and T178I.

26 nship between the FSS neurologic components (FSS-CNS) and the PCPC.

27 PT cells exposed to continuous FSS also acquired an extensive brush border and basolate

28 we show that cells cultured under continuous FSS develop an expanded apical endocytic pathway and inc

29 In contrast, FSS-induced V-ATPase redistribution and expression are l

30 R FSS-supplemented media compared to control FSS-supplemented media.

31 C scores and the baseline and PICU discharge FSS scores, the dispersion of FSS scores within each of

32 gned to identify miRNAs involved in elevated FSS-induced collateral vessel growth in rat hind limbs.

33 t Akt phosphorylation and were necessary for FSS to induce nuclear translocation of beta-catenin, c-f

34 eover, addition of ATP bypassed the need for FSS in enhancing endocytic capacity.

35 dentify factors associated with abnormal FS (FSS</=8) post-HT.

36 ompared with the more objective and granular FSS.

37 % of patients in the low-, medium-, and high-FSS groups, respectively (p < 0.001).

38 ning of the endocytic response by changes in FSS may contribute to glomerulotubular balance in vivo.

39 ted cells is rapidly modulated by changes in FSS.

40 an intact microtubule network is critical in FSS-induced modulation of V-ATPase in proximal tubule ce

41 Sustained increases or decreases in FSS induce vessel remodeling to maintain proper perfusio

42 Increases in FSS scores occur with each higher POPC and PCPC rating a

43 showed 94 differentially expressed miRNAs in FSS-stressed collaterals including miRNA-352 which was d

44 ctin cytoskeleton plays an important role in FSS-induced NHE3 and Na/K-ATPase trafficking, and an int

45 sion models explained 62% of the variance in FSS and 78% of the variance in ProF-S scores.

46 Variations in FSS may also contribute to the maturation of PT cells du

47 arting at the 5' resolution, we investigated FSS from the lowest administrative levels to continents.

48 t types replicated less (P < 0.05) with IUGR FSS-supplemented media compared to control FSS-supplemen

49 ent, 64% were "fully active/no limitations" (FSS=10), 21% had "minor limitations with strenuous activ

50 Mean FSS score was 6.6.

51 Moreover, FSS provides an essential stimulus in the differentiatio

52 cy for MACE compared with SS (Harrell's C of FSS, 0.677 vs. SS, 0.630, p = 0.02; integrated discrimin

53 satility, and directional characteristics of FSS are constantly sensed by the endothelium.

54 PICU discharge FSS scores, the dispersion of FSS scores within each of the POPC/PCPC ratings, and the

55 The dispersion of FSS scores within each POPC and PCPC rating was substant

56 The effect of FSS on NOR performance was further examined in mice lack

57 tubule cells (PTCs) were subjected to 5 h of FSS (1 dyn/cm(2)) to investigate the dynamic responses o

58 lines to physiologically relevant levels of FSS led to dramatically increased internalization of the

59 Culture under suboptimal levels of FSS led to intermediate phenotypes, suggesting a thresho

60 After 30 min of FSS, P2X7R-mediated pore formation was observed in wild

61 iated between 15 and 30 min postinduction of FSS, occurred via a clathrin- and dynamin-dependent path

62 Only FSS and procedure time were independent predictors of 1-

63 atients with STS in whom carefully performed FSS may serve as definitive therapy and in whom adjuvant

64 was used to compare Fatigue Severity Scale (FSS) and SF-36 scores during treatment by treatment grou

65 mpact Profile (SIP), Fatigue Severity Scale (FSS), and neurological examination.

66 al analog scale, the Fatigue Severity Scale (FSS), and the Profile of Fatigue (ProF).

67 as self-rated by the Fatigue Severity Scale (FSS).

68 Fatigue severity score (FSS) was 5.0 +/- 1.4 in patients with SLE, with 14 of th

69 2005 to 2014 with a functional status score (FSS) available at 3 time points (listing, transplant, >/

70 core (SS), termed "functional SYNTAX score" (FSS), would predict clinical outcome better than the cla

71 ts by applying Functional Source Separation (FSS) to their EEG recordings.

72 ining 10% control or IUGR fetal sheep serum (FSS).

73 gether called frameshift stimulating signal (FSS).

74 Fluid shear stress (FSS) from blood flow acting on the endothelium criticall

75 GFR and the accompanying fluid shear stress (FSS) modulate acute changes in PT ion transport thought

76 l fluid flow, leading to fluid shear stress (FSS) of osteoblasts.

77 del to study the role of fluid shear stress (FSS) on apical NHE3 and V-ATPase and basolateral Na/K-AT

78 erts a frictional force, fluid shear stress (FSS), on the endothelial cells that line the blood and l

79 tly enhanced by elevated fluid shear stress (FSS), the underlying regulatory mechanism of this proces

80 udy, we demonstrate that fluid shear stress (FSS)-induced actin cytoskeletal reorganization and junct

81 within 1 min of onset of fluid shear stress (FSS).

82 onse to acute changes in fluid shear stress (FSS); however, it is not known whether GFR modulates PT

83 ter exposure to repeated forced swim stress (FSS).

84 cal food supply using food self-sufficiency (FSS) as an indicator.

85 s type 1 (DA1) and Freeman-Sheldon syndrome (FSS) are the two most common known causes of inherited m

86 Freeman-Sheldon syndrome (FSS) is a disease associated with missense mutations in

87 (MYH3) gene cause Freeman-Sheldon syndrome (FSS), one of the most severe multiple congenital contrac

88 nherited disorder, Freeman-Sheldon syndrome (FSS).

89 We found that FSS also affects apical endocytosis in PT cells.

90 Our hypothesis is that FSS stimulates both apical and basolateral transporter e

91 Immunofluorescence analysis revealed that FSS caused basal stress fiber disruption, more densely d

92 Our findings show that FSS leads to an increment in the amount of protein expre

93 The FSS and POPC/PCPC system are closely associated.

94 The FSS scores for the good and mild disability POPC/PCPC ra

95 The relationship between the PCPC and the FSS-CNS paralleled the relationship between the FSS and

96 -CNS paralleled the relationship between the FSS and POPC/PCPC system.

97 PC ratings, and the relationship between the FSS neurologic components (FSS-CNS) and the PCPC.

98 ignificant (P < .001) difference between the FSS-CNS scores between each of the PCPC ratings with inc

99 isrupting actin by cytochalasin D blocks the FSS-induced changes in NHE3 and Na/K-ATPase, but not V-A

100 After determining the FSS for each patient, 32% moved to a lower-risk group as

101 ch of the PCPC ratings with increases in the FSS-CNS score for each higher PCPC rating.

102 However, the dispersion of the FSS scores indicated a lack of precision in the POPC/PCP

103 es were observed for EX or NEX groups on the FSS.

104 In contrast, rapamycin did not prevent the FSS-induced increase in Na(+)/K(+)-ATPase levels.

105 , and was rapidly reversed upon removing the FSS.

106 ngest predictors of fatigue according to the FSS and the somatic fatigue domain of the ProF (ProF-S),

107 All three FSS mutations show dramatic changes in kinetic propertie

108 Dyn gene-disrupted mice exposed to FSS did not show the subsequent learning and memory defi

109 Cells exposed to FSS expressed higher levels of key proteins necessary fo

110 Exposure to FSS also caused a rapid elevation in intracellular Ca(2+

111 However, 1 h after exposure to FSS, vehicle-pretreated mice displayed a significant def

112 ZO-1, E-cadherin, vinculin, and paxillin to FSS.

113 +)]i and purinergic signaling in response to FSS-dependent ciliary bending triggers a rapid and rever

114 EC responses to FSS are mediated in part by a junctional mechanosensory

115 ters in control cells and cells subjected to FSS.

116 Using FSS as a proof-of-concept, we show that candidate genes

117 ctional buttressing" model for PTCs in which FSS enables the DPABs, TJs, and AJs to become more tight

118 The 7% LR rate after treatment of STS with FSS without RT reported herein is comparable to publishe

119 alized disease, 74 of whom were treated with FSS without RT (31%).