ライフサイエンスコーパス: white cell

1 nd tolerance requires a residual functioning white cell.

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

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

4 ive hypoglycemia and depletion of peripheral white cells.

5 ow which opaque cells irreversibly switch to white cells.

6 vels and provides survival advantages to the white cells.

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

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

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

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

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

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

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

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

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

16 these acute illnesses tend to follow a joint white cell and platelet trajectory that can be reduced t

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

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

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

20 hastic nature of switching by beginning with white cells and monitoring the activation of Wor1, a mas

21 resent in blood cellular components, such as white cells and platelets.

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

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

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

25 ure red cells, and myeloid/lymphoid/compound white cells) and 49 haemostasis traits (including clotti

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

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

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

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

30 and rare structural variants with red cell-, white cell-, and platelet-related quantitative traits an

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

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

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

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

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

36 ating-competent form of the species, whereas white cells are thought to be essentially "sterile".

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

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

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

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

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

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

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

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

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

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

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

48 ive regulatory T cells (nTreg) in cord blood white cells (CBWCs) measured by flow cytometry.

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

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

51 ulus, and Rattus norvegicus and adjusted for white cell concentrations.

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

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

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

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

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

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

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

59 raised platelets (3.48, 3.35 to 3.62), total white cell count (3.01, 2.89 to 3.14), and C reactive pr

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

61 C-reactive protein (n = 2), albumin (n = 2), white cell count (n = 3), neutrophils (n = 2), and plate

62 There was a significantly higher white cell count (P = 0.014) and CRP (P = 0.004) on admi

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

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

65 ts with culture-negative meningitis with CSF white cell count (WCC) above 20 cells per muL were inclu

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

67 Primary outcomes were CSF white cell count (WCC), CSF-to-serum albumin ratio, CSF

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

69 analysis adjusted for age, sex, haemoglobin, white cell count (WCC), platelet count, creatinine, and

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

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

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

73 ransporter SPNS2 are associated with reduced white cell count and hearing defects.

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

75 0.83 (0.73, 0.94) and 0.81 (0.69, 0.93) for white cell count and platelet count respectively.

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

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

78 n modeling defined a minimal model including white cell count at diagnosis, pretreatment cytogenetics

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

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

81 d in the highest and most sustained systemic white cell count increase.

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

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

84 ormal value, <8.0 mg/L [76.2 nmol/L]), and a white cell count of 7 x 10(9)/L (normal range, [4-11] x

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

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

87 Increased circulating white cell count was associated with increased neutrophi

88 ls or plasmacytosis >20% of the differential white cell count) and WHO performance status 0-3.

89 Age, white cell count, and day of illness at study enrollment

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

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

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

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

94 ncluding treponemal and lipoidal antibodies, white cell count, and protein concentration.

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

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

97 Preoperative acute phase proteins (white cell count, C-reactive protein, and albumin), cyto

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

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

100 were older, had higher admission anion-gap, white cell count, hemoglobin (hb), neutrophil/lymphocyte

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

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

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

104 aboratory data including CD4 cell count, CSF white cell count, protein, glucose, and quantitative cry

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

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

107 itution of chemotherapy and normalization of white cell count.

108 e protein, haemoglobin, platelets, and total white cell count.

109 1 are older (median age 9 years), with a low white cell count.

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

111 Elevations in CSF white-cell count and protein were reported as adverse ev

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

128 White cell counts and plasma lipoprotein profiles were s

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

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

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

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

133 re older or presented earlier and with lower white cell counts were more likely to have poor platelet

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

135 arthritis), MGA (blood pressure) and COMMD7 (white cell counts).

136 covery was associated with older ages, lower white cell counts, and earlier stages of illness at pres

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

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

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

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

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

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

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

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

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

146 Analysis of peripheral white cells demonstrated induction of histone acetylatio

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

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

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

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

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

152 pH conditions and high temperatures promote white cell filamentation.

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

154 erature, heart rate and immune: differential white cell, IL-6, TNF-alpha, IL-8, IL-10 responses (all

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

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

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

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

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

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

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

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

163 White cells, like opaque cells, possess pheromone recept

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

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

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

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

168 K pathway, play opposite roles in regulating white cell mating as TEC1 deletion or CPH1 overexpressio

169 ivation of the Cph1 repressor Dig1 increases white cell mating ~4000 fold in glucose-depleted medium

170 EC1 deletion or CPH1 overexpression promotes white cell mating.

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

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

173 ns with CSF pleocytosis (16% vs 26% with >=5 white cells/muL) and CSF opening pressure >200 mmH2O (16

174 groups had lower age- and sex-adjusted total white cells, neutrophils, lymphocytes, monocytes, and eo

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

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

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

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

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

180 anial opening pressure (P = .03), higher CSF white cells (P = .007), and lower CSF glucose (P = .0003

181 cranial opening pressure (p=.03), higher CSF white cells (p=.007), and lower CSF glucose (p=.0003) co

182 mal residual disease (1 tumor cell per 10(5) white cells) (P<0.001).

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

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

185 lume, conductivity and light scatter in four white-cell populations (eosinophils, lymphocytes, monocy

186 both opaque-to-white switching and selective white cell proliferation are required for entire populat

187 By also measuring white cell proliferation rates under each condition, we

188 usted to increase in environments that favor white cell proliferation.

189 g for age, sex, measurement batch, estimated white cell proportions, BMI, smoking and methylation pri

190 The platelet-to-white-cell ratio's association with prognosis is consist

191 Here we show that the platelet-to-white-cell ratio, which was selected based on this conse

192 Moreover, engineered white cells recapitulate the transcriptional and morphol

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

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

195 versibly lose their memory and switch to the white cell state.

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

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

198 common nutrient stress, enables C. albicans white cells to undergo efficient sexual mating.

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

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

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

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

203 iated with AIS/CES, eosinophil percentage of white cells with LAS, and thrombin-activatable fibrinoly

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

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

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

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