ライフサイエンスコーパス: white cell

1 nd tolerance requires a residual functioning white cell.

2 cantly higher levels in opaque cells than in white cells.

3 onversely, 152 were more highly expressed in white cells.

4 imately 10(6) times more efficiently than do white cells.

5 ive hypoglycemia and depletion of peripheral white cells.

6 othrombin time; and numbers of platelets and white cells.

7 vels and provides survival advantages to the white cells.

8 ing by opaque cells and biofilm formation by white cells.

9 and adhesion (-0.45; p<0.01), and markers of white-cell (-0.51; p<0.01), platelet (-0.61; p<0.001), a

10 n of white cells into tissues, and influence white cell activation.

11 In addition, white cell adhesiveness was measured to assess the effec

12 These extracts were free of white cell and platelet contamination.

13 iver biopsy is unsuitable or unavailable the white cell and platelet counts can be used to determine

14 Manual white cell and platelet counts, hematocrit, total protei

15 s of magnitude more efficiently than control white cells and at a frequency approaching that of opaqu

16 The premature newborn, deficient in white cells and humoral immunity, is at high risk of inf

17 ntigen, and it is expressed in virtually all white cells and in hematopoietic stem cells.

18 e bottlenecks in pheromone MAPK signaling in white cells and that alleviation of these bottlenecks en

19 HIF-1alpha but also depends on PPARgamma in white cells and the PPARgamma cofactors PGC-1alpha and P

20 In contrast, white cells (and their descendents) lack appreciable lev

21 c variants for association with 36 red cell, white cell, and platelet properties in 173,480 European-

22 plays a critical role in the development of white cells, and abnormal expression of PU.1 can lead to

23 ent rises in genetically modified red cells, white cells, and platelets in both animals, with minimal

24 poside phosphate against granulocytes, total white cells, and platelets.

25 led with mepacrine (marker for platelets and white cells), anti-hTF1(Alexa.568) (marker for tissue fa

26 , "white" and "opaque." In Candida albicans, white cells are essentially sterile, whereas opaque cell

27 These data suggest that some allostimulatory white cells are filter adherent, whereas others escape f

28 As white cells are generally more robust in a mammalian hos

29 pheromones by undergoing conjugation, while white cells are induced by pheromones to form sexual bio

30 In contrast, white cells are unable to undergo mating, but can still

31 Disorders of white cells are very common in clinical practice.

32 DA or its related compounds are recruited by white cells as a signaling molecule(s) to up-regulate st

33 ucoreduction is necessary for the removal of white-cell-associated TSE infectivity from blood; howeve

34 to become cohesive and adhesive, and enhance white cell biofilm development, a pathogenic trait.

35 f majority white cell biofilms, and majority white cell biofilms facilitate minority opaque cell chem

36 increase two-fold the thickness of majority white cell biofilms, and majority white cell biofilms fa

37 te over 1,000 times more efficiently than do white cells, but less efficiently than do opaque cells.

38 required for the alpha-pheromone response of white cells, but not that of opaque cells.

39 The white cell button was then resuspended in 4 ml of platel

40 reducing Lw/Bw by 77%, red cells by 89%, and white cells by 91% when dosed at 37.5 mg/kg orally.

41 We show that white cells co-overexpressing STE4, CST5, and CEK2 under

42 Furthermore, reconstitution of the white cell compartment of SCID mice by mutant fetal live

43 pressure, decreased deformability of red and white cells, constricted arterioles, circulating obstruc

44 e essentially purely erythroid and free from white cell contamination.

45 ed at a level higher in opaque cells than in white cells; conversely, 152 were more highly expressed

46 d glucose >150 mg/dL (8.2 mmol/L), admission white cell count >14,300 cells/mm3 (14.3 x 10(9) cells/L

47 ate >90/minute, respiratory rate >20/minute, white cell count <4 x 10(9)/L or >/= 20 x 10(9)/L, album

48 o, the S. typhi vaccination caused a rise in white cell count (11.1 +/- 0.5 x10(9)/l vs. 7.9 +/- 0.8

49 White cell count (16.2 +/- 10.5 v 6.9 +/- 3.5 (x 109/L);

50 (median 9 years vs 5 years), and had a lower white cell count (median 3.9 vs 12.4) compared with chil

51 Mutations were associated with a high white cell count (P =.006) and patients with inv(16) (P

52 rticipants with early ART initiation had CSF white cell count (WCC) >/=5/microL at day 14 (58% vs 40%

53 Mean C-reactive protein (CRP), and white cell count (WCC) were significantly higher in the

54 sedimentation rate (ESR), hemoglobin, total white cell count (WCC), estimated glomerular filtration

55 wice the upper limit of normal (2N) or more, white cell count 150 x 10(9)/L or more, abnormal chromos

56 inine, haemoglobin, potassium, sodium, urea, white cell count and an index NEWS undertaken within +/-

57 d with steroid withdrawal were reductions in white cell count and haemoglobin and increases in plasma

58 aminotransferase (ALT), blood pressure, and white cell count and lower HDL cholesterol compared with

59 0.83 (0.73, 0.94) and 0.81 (0.69, 0.93) for white cell count and platelet count respectively.

60 Vaccination resulted in elevations in white cell count and serum levels of interleukin-6 and i

61 model identified age, NEWS, albumin, sodium, white cell count and urea as significant (p<0.001) predi

62 elet count and hematocrit in addition to the white cell count during the first 3 months of therapy wi

63 lammation at 8 hours, reflected by increased white cell count in both sexes.

64 he prognostic significance of the presenting white cell count is weaker and the rate of decline in mi

65 arge were body mass index less than 28 kg/m, white cell count less than 15,000/mL, C-reactive protein

66 of C-reactive protein (CRP), fibrinogen, and white cell count to components of IRS in the nondiabetic

67 was consistent with meningitis or if the CSF white cell count was >100 cells/mm(3) (>50% neutrophils)

68 Increased circulating white cell count was associated with increased neutrophi

69 ate analysis with cytogenetic category, age, white cell count, and French-American-British subtype de

70 Serum fibrinogen, white cell count, and high-sensitivity C-reactive protei

71 status, high fungal burden, high peripheral white cell count, and older age.

72 ing and beta(2)M, hemoglobin, prior therapy, white cell count, and platelet level (P =.005).

73 type, and Ho-Tr was independent of sex, age, white cell count, and T-cell status among Ph-negative pa

74 CRLF2-d was not associated with age, sex, or white cell count, but IGH@-CRLF2 patients were older tha

75 n activator antigen, C-reactive protein, and white cell count, even after adjustment for possible con

76 s, LDL cholesterol, HbA(1c) (A1C), increased white cell count, ever having smoked, and previous retin

77 and symptoms together with laboratory tests (white cell count, neutrophil count and C-reactive protei

78 specialty (medical versus surgical), raised white cell count, or co-morbidity.

79 Decreases in white cell count, platelets and C-reactive protein were

80 ACLF grade and white cell count, were independent predictors of mortali

81 ic utility of quantifying the synovial fluid white cell count, with two recent systematic reviews rea

82 1 are older (median age 9 years), with a low white cell count.

83 itution of chemotherapy and normalization of white cell count.

84 olytic-uremic syndrome were a higher initial white-cell count (relative risk, 1.3; 95 percent confide

85 e analysis that was adjusted for the initial white-cell count and the day of illness on which stool w

86 dverse event in the entire cohort included a white-cell count of 200,000 per cubic millimeter or high

87 that fever, a virus-specific rash, and a CSF white-cell count of 5/microL or more were independent pr

88 The median cerebrospinal fluid white-cell count on the first lumbar puncture among pati

89 tive protein, and fibrinogen levels, and the white-cell count were measured at base line, along with

90 APL classified as low-to-intermediate risk (white-cell count, </=10x10(9) per liter).

91 Laboratory studies revealed a normal white-cell count, an international normalized ratio of m

92 Levels of C-reactive protein, the white-cell count, and fibrinogen levels were strong pred

93 The fetal hemoglobin level, white-cell count, and platelet count and the use of hydr

94 Multivariate analysis incorporating age, white-cell count, and treatment parameters showed that s

95 ong patients with AML, independently of age, white-cell count, induction dose, and post-remission the

96 to age, neutrophil JAK2 V617F allele burden, white-cell count, platelet count, or clonal dominance.

97 io of FLT3-ITD to wild-type FLT3 and for the white-cell count.

98 specific effects on mortality and neutrophil/white cell counts (rho = 0.48), C-reactive-protein (rho

99 ducing the time of return to normalcy of the white cell counts after chemotherapy in patients with ac

100 patients present at diagnosis with increased white cell counts and hepatosplenomegaly, and are at an

101 White cell counts and plasma lipoprotein profiles were s

102 cerebrospinal fluid comprising either raised white cell counts and/or raised levels of interferon-alp

103 We determined differential white cell counts in peripheral blood of 189 adults who

104 clinical signs of encephalitis had elevated white cell counts in the blood caused mostly by increase

105 al antibodies) was 67.9%, whereas normal CSF white cell counts ruled out Lyme neuroborreliosis with a

106 eactive protein, platelet aggregability, and white cell counts were not modified by losartan.

107 transport variables, total and differential white cell counts, and serum concentrations of TNF and I

108 In a murine MPN model, CYT387 normalized white cell counts, hematocrit, spleen size, and restored

109 linical examinations, hemoglobin levels, and white cell counts.

110 t 60 h, through comparable CSF bacterial and white cell counts.

111 ts one to nine years of age, all of whom had white-cell counts of at least 50,000 per cubic millimete

112 ALL who were either 1 to 9 years of age with white-cell counts of at least 50,000 per cubic millimete

113 outcome, but either high cerebrospinal fluid white-cell counts or severe hyponatremia did.

114 Both white-cell deficiency and overproduction can lead to dis

115 Some forms of inherited white-cell deficiency are potentially treatable with gen

116 Analysis of peripheral white cells demonstrated induction of histone acetylatio

117 White-cell development and numbers are controlled by a m

118 cells are the mating-competent form, whereas white cells do not mate but can still respond to pheromo

119 impair cerebral microcirculation and reduces white cell/endothelial activation after deep hypothermic

120 yan) cells, along with blue-yellow and black-white cells, establish three chromatic axes that are suf

121 ile consistent with oxidative metabolism and white cells expressing a fermentative one.

122 pH conditions and high temperatures promote white cell filamentation.

123 od from KO mice showed a decrease in red and white cells, hemoglobin, hematocrit, and platelets.

124 especially among patients with a paucity of white cells in cerebrospinal fluid.

125 rodynamic interface in the motion of red and white cells in microvessels, and as a mechanotransducer

126 Instead, most of the white cells in the peripheral blood of mutant mice had t

127 and linear, are capable of increasing mature white cells in the periphery and mobilizing stem/progeni

128 Among patients with few white cells in their cerebrospinal fluid (<5 per cubic m

129 hese same neurons were surrounded by a focal white cell infiltrate, indicating the presence of an ant

130 dulate the accumulation and extravasation of white cells into tissues, and influence white cell activ

131 the polymerase chain reaction (PCR) from the white cells isolated on the filters.

132 White cells, like opaque cells, possess pheromone recept

133 and development of a previously unrecognized white cell lineage is better understood, as is the impor

134 is also expressed in two other cell types of white cell lineage, mast cells, and basophils.

135 Several different white-cell lineages are recognised; each has a role in h

136 recommendations and the use of bead beating, white cell lysis buffer, and an internal control PCR.

137 nt motion of red cells or the penetration of white cell microvilli.

138 that pheromone induces cohesiveness between white cells, minority opaque cells increase two-fold the

139 to induce adhesion and biofilm formation in white cells of C. albicans.

140 ths of the rDNA clusters in peripheral blood white cells of healthy human volunteers.

141 gh the release of pheromone, signal majority white cells of opposite mating type to form a biofilm th

142 E,E-Farnesol, which is secreted by white cells only, is a potent stimulator of macrophage c

143 S) was associated with increased circulating white cell (P < 0.01) and neutrophil (P < 0.01) counts a

144 n speculating about the possible role of the white cell pheromone response, it is hypothesized that i

145 he evolution of one such pathway, namely the white-cell pheromone response pathway in Candida albican

146 Moreover, engineered white cells recapitulate the transcriptional and morphol

147 calculate the increase in resistance due to white cell rolling and adhesion.

148 To accomplish this, C. albicans white cells secrete a low-molecular-weight chemoattracti

149 same pheromones stimulate mating-incompetent white cells to become cohesive and adhesive, and enhance

150 ession of WOR3 results in mass conversion of white cells to opaque cells and that deletion of WOR3 af

151 cur during the switch from the opaque to the white cell type.

152 phenotypic switch in C. albicans, from the "white" cell type to the "opaque" cell type.

153 that opaque cells begin to globally resemble white cells well before they irreversibly commit to swit

154 bution of each factor to mating, C. albicans white cells were reverse-engineered to express elevated,

155 h-density infection (>2500 parasites per 200 white cells) with only mild symptoms before severe malar

156 e of both repressed (pink) and de-repressed (white) cells within a single colony when assayed with th

157 ating-associated genes in mating-incompetent white cells without causing G1 arrest or shmoo formation

158 chanism for their survival and whether these white cells would use any metabolites as signal molecule