ライフサイエンスコーパス: FRC

1 FRC use is associated with deeper PDs, more clinical AL,

2 FRC was measured using open-circuit N2 washout.

3 FRC/TLC ratios allow an estimation of the degree of pulm

4 FRCs are activated within hours after the onset of infla

5 vitationally intermediate (RV = 8.9 +/- 3.1, FRC = 8.1 +/- 2.9, TLC = 7.4 +/- 3.6; P = 0.26) and depe

6 21%, FEV1 increased 34%, TLC decreased 13%, FRC decreased 23%, and FRC(trapped gas) and RV decreased

7 - 5.9), FVC (93.6 +/- 8.9 to 98.6 +/- 8.3%), FRC (45.4 +/- 18.5 to 62.1 +/- 15.3%), and TLC (84.8 +/-

8 0.26) and dependent lung (RV = 6.6 +/- 2.4, FRC = 6.1 +/- 2.1, TLC = 6.4 +/- 2.6; P = 0.51).

9 al residual capacity ("FRC") to 1.5 and 0.5 "FRC" by changing positive end-expiratory pressure.

10 EVL from 1.5 "FRC" to "FRC" and then to 0.5 "FRC" caused a significant (p < 0.01) upward shift in the

11 In addition, increases in EEVL from 0.5 "FRC" to 1.5 "FRC" caused a significant (p < 0.05) increa

12 on, increases in EEVL from 0.5 "FRC" to 1.5 "FRC" caused a significant (p < 0.05) increase in the apn

13 were not affected, decreasing EEVL from 1.5 "FRC" to "FRC" and then to 0.5 "FRC" caused a significant

14 ren without obstruction (flow at FRC >/= 0.9 FRC/s, n = 16), the slope of FRC versus length was 6.61.

15 total of 66% of these healthy infants had a FRC that was below the predicted normal range.

16 using a mouse model to conditionally ablate FRCs, we demonstrated their indispensable role in antivi

17 onal residual capacity and FRC+1 L 1 L above FRC (R(2) = 0.44, P < .001).

18 tional residual capacity [ FRC+1 L 1 L above FRC ], total lung capacity [ TLC total lung capacity ])

19 R imaging was performed at FRC+1 L 1 L above FRC by using a two-dimensional gradient-echo sequence.

20 RC functional residual capacity ], 1 L above FRC functional residual capacity [ FRC+1 L 1 L above FRC

21 +) T cells through CD40-CD40L, and activated FRC interacted directly with CD4(+) T cells to support T

22 on FRC and agonistic anti-CD40 mAb activated FRC, which supported CD4(+) T-cell proliferation, wherea

23 (+) T cells via CD40-CD40L, thereby altering FRC gene expression of immune regulatory molecules.

24 Although FRCs are targets of multiple viral infections, little is

25 Average AL was higher among FRC users than among non-FRC users (1.8 versus 1.6 mm; P

26 , and >/=8 mm was significantly higher among FRC users than among non-FRC users (mean difference in n

27 To initiate studies of interactions among FRCs, viruses, and immune cells, we isolated and immorta

28 an immune response depend on FRCs, but is an FRC independent and possibly cell-autonomous response of

29 he replacement of Trp-48 by Gln-48 yields an FRC variant for which oxalate-dependent substrate inhibi

30 %, TLC decreased 13%, FRC decreased 23%, and FRC(trapped gas) and RV decreased by 57 and 28%, respect

31 between FRC functional residual capacity and FRC+1 L 1 L above FRC (R(2) = 0.44, P < .001).

32 ally overlap with CCL21-expressing FRCs, and FRC VEGF is attenuated with IL-1beta deficiency or block

33 Both RV-HI and FRC-HI were observed in 48% of the 305 patients (mean +/

34 we show that blood vascular, lymphatic, and FRC growth are coordinately regulated and identify two d

35 birth had similar PCO2, lung mechanics, and FRC values.

36 ctional residual capacity (FRC) + 500 ml and FRC + 1 litre] on the change in pulmonary perfusion dist

37 nal residual capacity (FRC), FRC+500 ml, and FRC+1.0 l.

38 cted residual volume (RV), RV/TLC ratio, and FRC, after adjusting for HDL, but not after adjusting fo

39 lated significantly with decreases in RV and FRC(trapped gas) after LVRS (r = 0.67, p < 0.03).

40 annual rate of lung density loss at TLC and FRC combined did not differ between groups (A1PI -1.50 g

41 was self-reported cannabis use, defined as "FRC use" versus "non-FRC use." Bivariate and multivariab

42 At FRC, changes in CVP had no significant effect on either

43 city [FRC]; and -1.60 g/L per year [0.26] at FRC) than in the delayed-start group (-2.26 g/L per year

44 C plus FRC, and -2.05 g/L per year [0.28] at FRC).

45 acement of a sagittal lung slice acquired at FRC to the larger volumes was calculated.

46 lt of peripheral airways that were closed at FRC.

47 solated spontaneous diaphragm contraction at FRC displaced the lower ribs cranially and outward, but

48 FEFs at FRC increased with increasing levels of CPAP; however, t

49 those children without obstruction (flow at FRC >/= 0.9 FRC/s, n = 16), the slope of FRC versus leng

50 conductance, and maximal expiratory flow at FRC (Vmax (FRC)).

51 Maximal flow at FRC by rapid thoracoabdominal compression was used to di

52 eumonia had lower levels of maximal flows at FRC at mean age of 2 mo (albeit not significantly) and a

53 rent diffusion coefficient (ADC) of (3)He at FRC (n = 109), and average diffusion distance of helium

54 measured with the subject breath-holding at FRC.

55 ted whether the increase in flow measured at FRC (V FRC) with CPAP could be explained by the increase

56 substantiated by lung density measurement at FRC alone or by the two measurements combined.

57 (tdi) was measured to the nearest 0.1 mm at FRC (t(di)FRC) and TLC (t(di)TLC).

58 [95% CI 0.06-1.42], p=0.03), but was not at FRC alone (A1PI -1.54 g/L per year [0.24]; placebo -2.02

59 mages obtained during a respiratory pause at FRC.

60 ion, we measured baseline Pdimax and PdiT at FRC.

61 transdiaphragmatic twitch pressure (PdiT) at FRC (using a reduction of PdiT as an index of LFF) and m

62 (3)He MR imaging was performed at FRC+1 L 1 L above FRC by using a two-dimensional gradien

63 acheal stimulation was an "apneic" period at FRC, during which the PCA, a laryngeal abductor, showed

64 Removing tidal stresses at FRC after MCh challenge is sufficient to change the norm

65 ficantly lower in non-dependent lung than at FRC or RV (3.6 +/- 3.3, 7.7 +/- 1.5, 7.9 +/- 2.0, respec

66 d to the collapse of dependent lung units at FRC, (2) OA injury did not steepen the vertical gradient

67 ertical gradient in regional lung volumes at FRC, and (3) during sinusoidal oscillation of the OA-inj

68 Because FRC loss correlates with loss of both naive CD4 and CD8

69 ion analysis revealed an association between FRC and duration of asthma that was independent of the d

70 ealed positive (harmful) association between FRC use and severe periodontitis in the entire sample (o

71 ilitated bidirectional communication between FRC and CD4(+) T cells via CD40-CD40L, thereby altering

72 results from (1)H signal difference between FRC functional residual capacity and FRC+1 L 1 L above F

73 KGF + PFT-beta treatment restored both FRC and CCL21 expression, findings that correlated with

74 matory cytokine and chemokine expressions by FRC, which were inhibited by anti-CD40L mAb.

75 Notably, in vivo expression of NOS2 by FRCs and LECs regulated the size of the activated T cell

76 oss of FRCs and the loss of IL-7 produced by FRCs may thus perpetuate a vicious cycle of depletion of

77 ompressible occluded volume when calculating FRC in infants.

78 ship between frequent recreational cannabis (FRC) (marijuana and hashish) use and periodontitis preva

79 l (RV-HI) or a functional residual capacity (FRC) >120% predicted (FRC-HI).

80 ung inflation [functional residual capacity (FRC) + 500 ml and FRC + 1 litre] on the change in pulmon

81 ndent 11 cm at functional residual capacity (FRC) and almost all the lung at residual volume (RV).

82 e performed at functional residual capacity (FRC) and at the end of a tidal inspiration (VTei) under

83 ned intervals, functional residual capacity (FRC) and forced expiratory flow were measured 86 times i

84 olumes between functional residual capacity (FRC) and total lung capacity.

85 city (TLC) and functional residual capacity (FRC) combined, and the two separately, at 0, 3, 12, 21,

86 f sleep onset, functional residual capacity (FRC) fell and Rlp rose more than would be expected for t

87 lung volume at functional residual capacity (FRC) in infants.

88 lows (FEFs) at functional residual capacity (FRC) increase with increasing CPAP in infants with trach

89 Functional residual capacity (FRC) measurements made using helium dilution indicated l

90 (FEV(1)), and functional residual capacity (FRC) were measured in 20 patients aged 15.1 +/- 2.8 y (x

91 iciency index, functional residual capacity (FRC), and pressure-volume curves than piglets in the BOL

92 right lung at functional residual capacity (FRC), FRC+500 ml, and FRC+1.0 l.

93 an increase in functional residual capacity (FRC); however, no previous studies have described positi

94 approximated functional residual capacity ("FRC") to 1.5 and 0.5 "FRC" by changing positive end-expi

95 ual volume ], functional residual capacity [ FRC functional residual capacity ], 1 L above FRC functi

96 1 L above FRC functional residual capacity [ FRC+1 L 1 L above FRC ], total lung capacity [ TLC total

97 4] at TLC plus functional residual capacity [FRC]; and -1.60 g/L per year [0.26] at FRC) than in the

98 Loss of the fibroblastic reticular cell (FRC) network in lymphoid tissues during HIV-1 infection

99 on the stromal fibroblastic reticular cell (FRC) network on which T cells traffic.

100 lements of LTs, fibroblastic reticular cell (FRC) network, not only form the architectural framework

101 tor IL-7 on the fibroblastic reticular cell (FRC) network, resulting in apoptosis and depletion of T

102 ignaling in the fibroblastic reticular cell (FRC) stromal subset was required for proper lymph node s

103 f a network of fibroblastic reticular cells (FRC) and reticular fibers linking sinuses to blood vesse

104 l targeting of fibroblastic reticular cells (FRC) in the lymphoid organs.

105 ts secreted by fibroblastic reticular cells (FRC).

106 is, fibroblast-type reticular stromal cells (FRC) in the T zone and medullary cords are the principal

107 of T-cell zone fibroblastic reticular cells (FRCs) and CCL21 expression in lymphoid stroma.

108 ing in stromal fibroblastic reticular cells (FRCs) and its modulation by CLEC-2 expressed on dendriti

109 Fibroblastic reticular cells (FRCs) and lymphatic endothelial cells (LECs) are nonhema

110 Fibroblastic reticular cells (FRCs) are known to inhabit T cell-rich areas of lymphoid

111 Fibroblastic reticular cells (FRCs) are lymphoid stromal cells essential to T-cell mig

112 n lymph nodes, fibroblastic reticular cells (FRCs) form a collagen-based reticular network that suppo

113 r lymph nodes, fibroblastic reticular cells (FRCs) form a network in the T cell zone (periarteriolar

114 Fibroblastic reticular cells (FRCs) form the cellular scaffold of lymph nodes (LNs) an

115 Fibroblastic reticular cells (FRCs) in the T cell zone of lymph nodes (LNs) are pivota

116 Fibroblastic reticular cells (FRCs) showed enrichment for higher expression of genes r

117 3D network of fibroblastic reticular cells (FRCs) that are a rich cytokine source.

118 p38(+) stromal fibroblastic reticular cells (FRCs) that express VEGF are enriched for Thy1(+) cells a

119 , particularly fibroblastic reticular cells (FRCs), provide critical structural support and regulate

120 Fibroblastic reticular cells (FRCs), through their expression of CC chemokine ligand (

121 We report that fibroblastic reticular cells (FRCs), which reside in the T cell zone of the LN, ectopi

122 asculature and fibroblastic reticular cells (FRCs).

123 nts obtained from the Field Research Center (FRC) in Oak Ridge, TN.

124 fully regenerated within 4 wk after complete FRC ablation.

125 The integrity of fiber-reinforced composite (FRC) prostheses is dependent, in part, on flexural rigid

126 Field-reversed configuration (FRC) plasmas are potentially attractive as a reactor con

127 can be verified by Fourier Ring Correlation (FRC), illustrating the statistical independence of the c

128 In cultured FRC, TG is induced 5- to 20-fold and becomes colocalized

129 describe a model for conditionally depleting FRCs from LNs based on their expression of the diphtheri

130 measured to the nearest 0.1 mm at FRC (t(di)FRC) and TLC (t(di)TLC).

131 ta t(di)) was calculated as (t(di)TLC - t(di)FRC)/t(di)FRC.

132 was calculated as (t(di)TLC - t(di)FRC)/t(di)FRC.

133 ssing the PDPN receptor CLEC-2, PDPN endowed FRCs with contractile function and exerted tension withi

134 ore stringent than the corresponding enzyme (FRC) in Oxalobacter in employing formyl-CoA and oxalate

135 and partially overlap with CCL21-expressing FRCs, and FRC VEGF is attenuated with IL-1beta deficienc

136 As expected, depleting FAP(+) FRCs causes the loss of naive T cells, B cells, and dend

137 In contrast, depleting FAP(+) FRCs during an ongoing influenza infection does not dimi

138 V1 <60% predicted (93% for RV-HI and 71% for FRC-HI, vs 21% and 41% in patients with a FEV1 > 80%).

139 aken together, these data suggest a role for FRC as paracrine regulators of lymph node endothelial ce

140 The coefficient of variation for FRC measurements for all infants was 3.90 +/- 2.80% (ran

141 e of lymphotoxin-beta, a survival factor for FRCs during SIV infection in rhesus macaques.

142 (+) T cells and indicating a unique role for FRCs.

143 lung at functional residual capacity (FRC), FRC+500 ml, and FRC+1.0 l.

144 patients performed a gentle exhalation from FRC.

145 dal oscillation of the OA-injured lungs from FRC, dependent regions did not undergo cyclic reopening

146 In the case of the G260A FRC variant, the new conformation identified by simulati

147 formed on the G258A, G259A, G260A, and G261A FRC variants both to examine the energetic effects of re

148 We measured arterial blood gases, FRC, Rrs, and Crs in supine and prone positions in 30 pa

149 ere, we demonstrate that during homeostasis, FRCs also suppress T cell activation via producing high

150 d between Tw Pdi and dynamic hyperinflation (FRC: r = -0.65, P = 0.005) and arterial carbon dioxide p

151 from C57BL/6 mice designated as immortalized FRC.

152 brosis disrupting and damaging the important FRC network.

153 There was no correlation between changes in FRC and changes in AaPO2 (r = 0.225, p = 0.23).

154 studies have described positional changes in FRC in children with severe lung disease or in those und

155 There were no significant differences in FRC or TLC at baseline.

156 more than would be expected for the fall in FRC.

157 ot associated with a significant increase in FRC in the cohort of 30 patients, nor in any of the subg

158 h CPAP could be explained by the increase in FRC with CPAP.

159 on, with decreases in PaCO2 and increases in FRC.

160 increased by 0.19% for every 1% increment in FRC (95% confidence interval [CI], 0.13-0.25), whereas t

161 logy, may contribute to viral persistence in FRC during chronic infection.

162 d as a decrease in RV >20% or a reduction in FRC >10%.

163 d that only CD4 T-cell depletion resulted in FRC loss in both species and that this loss was caused b

164 PN-mediated contractility, which resulted in FRC relaxation and reduced tissue stiffness.

165 hat PDPN induces actomyosin contractility in FRCs via activation of RhoA/C and downstream Rho-associa

166 (PDPN) regulates actomyosin contractility in FRCs.

167 ll types of this reticular network including FRC, endothelial cells and sinus lining cells.

168 Conversely, anti-CD40L mAb inhibited FRC inflammatory responses.

169 es that adaptive immunity requires an intact FRC network and identifies a subset of FRCs that control

170 in the plasma core, mainly due to the large FRC ion orbits, resulting in near-classical thermal ion

171 ological properties and robustness of the LN FRC network in mice.

172 There was a trend toward a lower V max(FRC) (95% CI: -2; 67 ml/s(-)(1) in the CM group.

173 We obtained 500 measurements of V'max,(FRC) by rapid thoracic compression in 285 children ages

174 V'max,(FRC) rose with height in a linear relationship.

175 flow at functional residual capacity (V'max,(FRC)).

176 Mean FRC/TLC was significantly elevated in the obstructive gr

177 vated in the obstructive group, whereas mean FRC alone did not differ from the group without lung dis

178 tions express IL-1beta and directly modulate FRC function to help promote the initiation of vascular-

179 esized that DST and anti-CD40L mAb-modulated FRC interactions with CD4(+) T cells in mice.

180 Reduced compliance near FRC with normal elastic recoil at high lung volumes does

181 In addition, new FRC-rich environments were observed in the expanded medu

182 AL was higher among FRC users than among non-FRC users (1.8 versus 1.6 mm; P = 0.004).

183 cantly higher among FRC users than among non-FRC users (mean difference in number of PD sites: 6.9, 5

184 nnabis use, defined as "FRC use" versus "non-FRC use." Bivariate and multivariable regression models

185 ticular, downregulation of the expression of FRC-derived chemokine CCL21 and cytokine IL-7 were accom

186 ults in tolerance in mice, identification of FRC-T cell interactions provides a new research target f

187 otoxin-beta, a key factor for maintenance of FRC network, we hypothesized that loss of naive T cells

188 on testing has focused on the measurement of FRC alone in ventilated infants and children.

189 thelial cells and suggest that modulation of FRC VEGF expression may be a means to regulate lymph nod

190 High numbers of FRC were infected by LCMV clone 13, which causes a chron

191 sticity as well as the complex regulation of FRC networks allowing the rapid LN hyperplasia that is c

192 The slope of FRC (in milliliters) versus body length (in centimeters)

193 at FRC >/= 0.9 FRC/s, n = 16), the slope of FRC versus length was 6.61.

194 Comparative transcriptional analysis of FRCs from non-draining LNs and TDLNs demonstrated reprog

195 panied by the rapid activation and growth of FRCs, leading to an expanded but similarly organized net

196 A hallmark of FRCs is their propensity to contract collagen, yet this

197 ion via PGE2, underscoring the importance of FRCs in shaping the suppressive milieu of lymphoid organ

198 Unexpectedly, loss of FRCs also attenuated humoral immunity due to impaired B

199 The resulting loss of FRCs and the loss of IL-7 produced by FRCs may thus perp

200 However, in vivo manipulation of FRCs has been limited by a dearth of genetic tools that

201 viously unappreciated intrinsic mechanism of FRCs shared between mice and humans for suppressing T ce

202 ction altered the homeostasis and spacing of FRCs and T cells, which resulted in an expanded reticula

203 ntact FRC network and identifies a subset of FRCs that control B cell homeostasis and follicle identi

204 her, these results demonstrated that CD40 on FRC facilitated bidirectional communication between FRC

205 lude that prone positioning has no effect on FRC and in this series of 30 patients significantly impr

206 CD40 was expressed on FRC and agonistic anti-CD40 mAb activated FRC, which sup

207 Here we focused on FRC functions and hypothesized that DST and anti-CD40L m

208 ed death ligand 1, which was up-regulated on FRC after infection, reduced early CD8(+) T cell-mediate

209 pression, suggesting that LTbetaR signals on FRC regulate lymph node VEGF levels and, thereby, lymph

210 e initiation of an immune response depend on FRCs, but is an FRC independent and possibly cell-autono

211 xpansion, its retention no longer depends on FRCs or their chemokines, CCL19 and CCL21.

212 addition, lung density at relaxed (passive) FRC was lower for infants with CF than for control infan

213 CLEC-2 modulation of PDPN signalling permits FRC network stretching and allows for the rapid lymph no

214 g the actomyosin cytoskeleton and permitting FRC stretching.

215 significant differences in plethysmographic FRC, initial inspiratory airway resistance (Raw), or res

216 t TLC; -2.16 g/L per year [0.26] at TLC plus FRC, and -2.05 g/L per year [0.28] at FRC).

217 nal residual capacity (FRC) >120% predicted (FRC-HI).

218 h TLC 7.3 +/- 1.1 L (140 +/- 12% predicted); FRC 5.6 +/- 0.8 L (177 +/- 30% predicted); and RV 5.2 +/

219 tidal volume (VT), airways resistance (Raw), FRC, and mask leak.

220 Stimulations delivered at relaxed FRC produced a correlation coefficient (r) between Paw(t

221 Follicle-resident FRCs established a favorable niche for B lymphocytes via

222 At the initiation of immune responses, FRC remain the principal VEGF mRNA-expressing cells in l

223 Restoring FRC to presleep values either at an early (half-hour) or

224 flation was present at residual volume (RV), FRC, and TLC in all subjects.

225 in the right lung during breath-holds at RV, FRC and TLC.

226 Association of Th1/Th2 ratio with RV, FRC, and inspiratory capacity was attenuated after adjus

227 Mean (SD) FRC was 19.6 (3.4) ml/kg (within subject coefficient of

228 Significantly, FRCs of human lymphoid organs manifest similar COX-2/PGE

229 Patients in both groups had similar FRC (5.7 +/- 1.6 versus 5.0 +/- 1.5 L), V O(2)max (0.58

230 hatic vascular growth in part by stimulating FRCs to upregulate VEGF.

231 Strikingly, FRCs showed reduced stimulation of T cells after Toll-li

232 Surprisingly, FRC expansion depends mainly on trapping of naive lympho

233 Here, we show that FRC plasmas have unique, beneficial microstability prope

234 Finally, we show that FRC VEGF expression is upregulated during initiation and

235 essing cells in lymph nodes, suggesting that FRC may play an important role in regulating vascular gr

236 cloned cell lines, we have established that FRCs express the major histocompatibility complex (MHC)

237 Here we found that FRCs specifically of TDLNs proliferated in response to t

238 Here we report that FRCs and LECs inhibited T cell proliferation through a t

239 These data reveal that FRCs form a substrate for T cells in the spleen, guiding

240 The FRC stromal networks are critical for proper lymphoid ar

241 The FRC% predicted was significantly higher in subjects with

242 icious cycle of depletion of T cells and the FRC network.

243 s an interdependent relationship between the FRC stromal network and CD4(+) T lymphocytes for their s

244 eport the effects of replacing Trp-48 in the FRC active site with the glutamine residue that occupies

245 licular lymphoma (14 of 15 cases) and in the FRC and endothelium of classical Hodgkin's disease, two

246 Furthermore, T cells in the FRC environment where Cox-2 is genetic inactivated are m

247 nopathology and prevented destruction of the FRC architecture in the spleen.

248 The function of the FRC conduit network was altered after clone 13 infection

249 veals the high topological robustness of the FRC network and the critical role of the network integri

250 folds in size, but the fate and role of the FRC network during immune response is not fully understo

251 leads to collagen deposition and loss of the FRC network itself.

252 We further found the same dependence of the FRC network on CD4 T cells in HIV-1-infected patients be

253 naive T cells is responsible for loss of the FRC network.

254 We found that the FRC network exhibits an imprinted small-world topology t

255 s but instead traffic to that site using the FRC-rich MZ bridging channels (MZBCs).

256 olerate a loss of approximately 50% of their FRCs without substantial impairment of immune cell recru

257 What causes this FRC loss is unknown.

258 Different from T cell dysfunction, this FRC-mediated suppression is surmountable by enhancing th

259 inspiratory capacity (IC) decreased and thus FRC increased with increasing CPAP.

260 Thus, FRC phenotype was altered by interaction with CD4(+) T c

261 Thus, FRCs effectively presented antigen along with activating

262 can directly induce cultured gp38(+)Thy1(+) FRCs to upregulate VEGF.

263 f measurements of total lung capacity (TLC), FRC, and their ratio, we determined both lung volumes in

264 Mean values of TLC, FRC, and RV were 94 +/- 12, 88 +/- 13, and 94 +/- 41%, r

265 from a lung volume at 30 cm H(2)O (V(30)) to FRC.

266 ring a passive exhalation from +40 cm H2O to FRC measured by N2 washout.

267 pressure-volume (PV) curves from near TLC to FRC in 49 healthy, sedated, spontaneously breathing infa

268 The expired volume from V30 to FRC was defined as V30E.

269 Passive deflation from V30 to FRC was then interrupted by multiple brief occlusions at

270 lling of lymph nodes by delivering CLEC-2 to FRCs.

271 egative CD31(-) LNSCs showed similarities to FRCs but lacked expression of interleukin 7 (IL-7) and w

272 affected, decreasing EEVL from 1.5 "FRC" to "FRC" and then to 0.5 "FRC" caused a significant (p < 0.0

273 O. formigenes formyl coenzyme A transferase (FRC).

274 site of formyl-CoA:oxalate CoA transferase (FRC) play an important role in the catalytic cycle of th

275 cell proliferation was sufficient to trigger FRC expansion.

276 interconversion of these states in wild type FRC.

277 determine if the flexure behavior of uniform FRC beams with restrained or simply supported ends and v

278 ) T-cell proliferation, whereas unstimulated FRC did not.

279 ther the increase in flow measured at FRC (V FRC) with CPAP could be explained by the increase in FRC

280 Vmax FRC was also reduced in exposed infants (mean [SD], 85.2

281 Maximal forced expiratory flow (Vmax FRC) and time to peak tidal expiratory flow as a proport

282 e, and maximal expiratory flow at FRC (Vmax (FRC)).

283 nd length were important predictors of Vmax (FRC), which was, on average, 20% higher in girls than in

284 (Vmax(FRC))0.5 (ml x second(-1)) = 4.22 + 0.00210 x length2 (c

285 l flow at functional residual capacity (Vmax(FRC)) from partial forced expiratory maneuvers remain th

286 flows at functional residual capacity (Vmax(FRC)) in 169 of these infants by the chest compression t

287 To address this problem, we collated Vmax(FRC) data from 459 healthy infants (226 boys) tested on

288 e sex-specific prediction equations for Vmax(FRC) may preclude detection of clinically significant ch

289 normal" range (z scores of 0 +/- 2) for Vmax(FRC), during infancy should also improve interpretation

290 Participants who had infant Vmax(FRC) in the lowest quartile also had lower values for th

291 subjects has limited interpretation of Vmax(FRC) results in both clinical practice and research.

292 se data and essential covariates, 26.8% were FRC users.

293 Under resting conditions, when FRCs are unlikely to encounter mature DCs expressing the

294 y was obtained in 38% of the asthmatics with FRC-HI and 29% of the asthmatics with RV-HI, whereas FEV

295 Similarly, increase of (X(rms)) with FRC was significantly less than the predicted increase i

296 isolated T cells or T cells co-cultured with FRCs compared with those cultured without FRCs.

297 th FRCs compared with those cultured without FRCs.

298 ed but similarly organized network of T-zone FRCs that maintains its vital function for lymphocyte tr