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 - 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 +/-

7 0.26) and dependent lung (RV = 6.6 +/- 2.4, FRC = 6.1 +/- 2.1, TLC = 6.4 +/- 2.6; P = 0.51).

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

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

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

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

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

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

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

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

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

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

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

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

20 Accordingly, FRC conditioning significantly enhanced the persistence

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 signaling via the IL-17 receptor, activated FRCs underwent cell cycle arrest and apoptosis, accompan

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

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

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

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

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

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

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

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

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

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

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

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

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

41 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

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

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

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

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

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

47 me (tptef/te) and maximal expiratory flow at FRC (VmaxFRC)-have been linked to increased risk for chi

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

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

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

51 measured with the subject breath-holding at FRC.

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

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

54 [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

55 mages obtained during a respiratory pause at FRC.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

70 loss of presentation of an intestinal PTA by FRCs during GVHD resulted in the activation of autoaggre

71 ompressible occluded volume when calculating FRC in infants.

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

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

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

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

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

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

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

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

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

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

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

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

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

85 1 L above FRC functional residual capacity [ FRC+1 L 1 L above FRC ], total lung capacity [ TLC total

86 4] at TLC plus functional residual capacity [FRC]; and -1.60 g/L per year [0.26] at FRC) than in the

87 l-scavenging capacity of fresh red Capsicum (FRC).

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

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

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

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

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

93 )gp38(+)CD31(-) fibroblastic reticular cell (FRC)-like cells.

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

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

96 ts secreted by fibroblastic reticular cells (FRC).

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

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

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

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

101 Fibroblastic reticular cells (FRCs) and their specialized collagen fibers termed 'cond

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

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

104 Fibroblastic reticular cells (FRCs) form a cellular network that serves as the structu

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

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

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

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

109 on of GVHD, LN fibroblastic reticular cells (FRCs) rapidly reduced expression of genes regulated by D

110 Lymph node fibroblastic reticular cells (FRCs) respond to signals from activated T cells by relea

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

112 3D network of fibroblastic reticular cells (FRCs) that are a rich cytokine source.

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

114 , particularly fibroblastic reticular cells (FRCs), during experimental autoimmune encephalomyelitis

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

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

117 ast in part to fibroblastic reticular cells (FRCs), which are a major population of the nonhematopoie

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

119 asculature and fibroblastic reticular cells (FRCs).

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

121 fully regenerated within 4 wk after complete FRC ablation.

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

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

124 s in that they resemble lymph nodes, contain FRC-like cells expressing beta-cell autoantigens, and ar

125 antly, 12-week-old Ins2-CCL21 TLOs contained FRC-like cells with higher contractility, regulatory, an

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

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

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

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

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

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

132 lorigen activation/repressor complexes (FACs/FRCs), which regulate transition to flowering in leaves

133 the development of T(H)17 cells, but failed FRC proliferation impaired germinal center formation and

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

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

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

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

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

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

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

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

142 patients performed a gentle exhalation from FRC.

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

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

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

146 g the parameters of this model, we generated FRC network representations with realistic topological p

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

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

149 from C57BL/6 mice designated as immortalized FRC.

150 brosis disrupting and damaging the important FRC network.

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

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

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

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

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

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

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

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

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

160 (PDPN) regulates actomyosin contractility in FRCs.

161 , the donor mast cell-mediated senescence in FRCs was associated with collagen 1 deposition in DLNs.

162 IL-17 signaling in FRCs was not required for the development of T(H)17 cell

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

196 Systemic administration to mice of FRCs that were expanded ex vivo decreased DLN fibrosis a

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

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

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

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

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

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

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

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

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

206 ral bZIP proteins that assemble into FACs or FRCs.

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

208 found structural alterations in perivascular FRCs and associated high endothelial venules.

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

210 g the actomyosin cytoskeleton and permitting FRC stretching.

211 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).

212 Notably, PP FRCs responded to conduit fluid flow via the mechanosens

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

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

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

216 provide a framework for simulating realistic FRC networks.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

233 Our study demonstrates that FRCs play a role beyond restricting T cell expansion-the

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

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

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

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

238 Finally, we show that FRCs normally expressed a unique PTA gene signature that

239 The FRC stromal networks are critical for proper lymphoid ar

240 The FRC% predicted was significantly higher in subjects with

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

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

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

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

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

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

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

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

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

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

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

252 cute GVHD damages and prevents repair of the FRC network, thus disabling an essential platform for pu

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

254 GVHD led to the selective elimination of the FRC population, and blocked the repair pathways required

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

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

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

258 What causes this FRC loss is unknown.

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

260 In mice, this FRC network has been found to have small-world propertie

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

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

263 Thus, FRCs effectively presented antigen along with activating

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

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

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

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

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

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

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

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

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

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

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

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

276 cell proliferation was sufficient to trigger FRC expansion.

277 interconversion of these states in wild type FRC.

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

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

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

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 Our results explain why FRC networks have small-world properties and provide a f

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

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

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

298 Here we report that encounters with FRCs enhanced cytokine production and remodeled chromati

299 Whether interactions with FRCs also support the function or differentiation of act

300 th FRCs compared with those cultured without FRCs.

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