ライフサイエンスコーパス: fog

1 ed from atmospheric sources (e.g., rainfall, fog).

2 was fast-twitch oxidative-glycolytic fibres (FOG).

3 stimulation frequency alone could affect the FOG.

4 lts by showing that car drivers slow down in fog.

5 an explanation of excessive driving speed in fog.

6 locomotor region as the probable origins of FoG.

7 ents lack efficacy in patients with advanced FoG.

8 signaling pathway in living embryos, T48 and Fog.

9 all the cacti are able to harvest water from fog.

10 transcription factor GATA-1 and its cofactor FOG-1 (friend of GATA-1).

11 naturally occurring mutant that cannot bind FOG-1 (GATA-1(V205G)), we reveal that FOG-1 intricately

12 FOG-1 (ZFPM1), a co-factor for the haematopoietic factor

13 germline survival and prevent apoptosis with fog-1 and fog-3 and that simultaneous loss of fshr-1 and

14 s can override the canonical requirement for fog-1 and fog-3 in the execution of the male-germline fa

15 FOG-1 and its interactor Mi-2beta, a chromatin remodelin

16 he capacity of GATA-1 to recruit and utilize FOG-1 and Med1 at activated and repressed target genes.

17 Med1 to activated genes, and the kinetics of FOG-1 and Med1 recruitment were similar.

18 ences between GATA-1-mediated recruitment of FOG-1 and Med1 to chromatin, with a fundamental differen

19 s show that NuRD is a critical co-factor for FOG-1 and underscore the versatile use of NuRD by lineag

20 Moreover, we demonstrate that FOG-1 antagonizes the fate choice of multipotential prog

21 GATA-1 and its cofactor FOG-1 are required for the differentiation of erythrocyt

22 A mutation of GATA-1 V205G that disrupts FOG-1 binding and K137 mutations yielded similar phenoty

23 hough sumoylation was FOG-1 independent, and FOG-1 binding did not require sumoylation.

24 A GATA-1 mutant defective in FOG-1 binding occupied a Tac-2 regulatory region at leve

25 The nuclear protein FOG-1 binds transcription factor GATA-1 to facilitate er

26 cell precursors, while variations in GATA-1/FOG-1 complex composition and concentrations drive their

27 of genes repressed by GATA-1 independent of FOG-1 defines a novel mode of GATA-1-mediated transcript

28 n examples of GATA-1-mediated repression are FOG-1 dependent.

29 In turn, FOG-1 displaces pRb/E2F-2 from GATA-1, ultimately releas

30 wever, little is known about the function of FOG-1 during myeloid and lymphoid development or how FOG

31 ring myeloid and lymphoid development or how FOG-1 expression is regulated in any tissue.

32 levels higher than wild-type GATA-1, whereas FOG-1 facilitated chromatin occupancy at a distinct targ

33 Whereas knocking-down FOG-1 had catastrophic effects on GATA-1-mediated activa

34 es a cooperative function with GATA-1 and/or FOG-1 in a developmental stage-specific manner.

35 Remarkably, ectopic expression of FOG-1 in committed mast cell progenitors redirects them

36 We further show that exogenous expression of FOG-1 in mast cells leads to displacement of GATA-1 from

37 with that site of action, we detect FBF and FOG-1 in the germ line but not in the VPCs.

38 ionally interrogate whether GATA-1 regulates FOG-1 in vivo, we used bioinformatics combined with tran

39 similar phenotypes, although sumoylation was FOG-1 independent, and FOG-1 binding did not require sum

40 t bind FOG-1 (GATA-1(V205G)), we reveal that FOG-1 intricately regulates the chromatin occupancy of G

41 While FOG-1 is an established GATA-1 coregulator, the importan

42 We found that FOG-1 is dispensable for endoderm specification but is r

43 Zebrafish FOG-1 is expressed in early hematopoietic cells, as well

44 ds myeloid-progenitor cells, indicating that FOG-1 is required during erythroid/myeloid commitment.

45 ertain GATA-1 target genes have little to no FOG-1 requirement for expression, presumably additional

46 mponents at both repressed and active GATA-1/FOG-1 target genes in vivo.

47 e repression and activation of select GATA-1/FOG-1 target genes.

48 HSC platelet programming through loss of the FOG-1 transcription factor is accompanied by increased l

49 To examine whether FOG-1 via NuRD controls HBG1 and HBG2 silencing in vivo,

50 Homozygous FOG-1(R3K5A) mice were found to have splenomegaly, extra

51 pecifically disrupts FOG-1/NuRD interaction (FOG-1(R3K5A)).

52 FOG-1(R3K5A/R3K5A) megakaryocytes and erythroid progenit

53 ly recruited to a mast cell gene promoter in FOG-1(R3K5A/R3K5A) megakaryocytes, suggesting that FOG-1

54 eraction with the cofactor friend of GATA-1 (FOG-1) for its essential role in erythroid and megakaryo

55 e transcriptional co-factor Friend of GATA1 (FOG-1) has been shown to interact with subunits of the n

56 GATA-1-interacting protein Friend Of GATA-1 (FOG-1) is essential for the proper transcriptional activ

57 ssion, and the coregulator Friend of GATA-1 (FOG-1) selectively mediated repression.

58 crucial GATA-1 coregulator Friend of GATA-1 (FOG-1), a component of the Mediator complex, Med1, facil

59 0, a Cys(2)HisCys ZBD from Friend of GATA-1 (FOG-1), and from both Cys(4) ZBDs of GATA-1.

60 multi-zinc finger protein Friend of GATA-1 (FOG-1), the histone acetyltransferase CREB binding prote

61 tions with the coregulator Friend of GATA-1 (FOG-1).

62 or without the coregulator Friend of GATA-1 (FOG-1).

63 requiring the coregulator Friend of GATA-1 (FOG-1).

64 ription factors GATA-1 and Friend of GATA-1 (FOG-1).

65 and its essential cofactor Friend of GATA-1 (FOG-1).

66 GATA-1 and its coregulator Friend of GATA-1 (FOG-1).

67 binding a protein complex containing GATA-1, FOG-1, and Mi2 at the -566/-567 GATA sites of the proxim

68 AC transgenic mice demonstrated that GATA-1, FOG-1, and Mi2 were recruited to the (A)gamma-globin -56

69 ic transcription factor GATA-1, its cofactor FOG-1, and the associated chromatin remodeling complex N

70 GATA-1 used different combinations of SetD8, FOG-1, and the FOG-1-interacting nucleosome remodeling a

71 n factors gata-2 and pu.1, but not gata-1 or fog-1, are necessary for early MC development.

72 In contrast to FOG-1, GATA-1 evicted Med1 during transcriptional repres

73 Similar to FOG-1, GATA-1 recruited Med1 to activated genes, and the

74 The suppression of FOG-1, in the presence of normal GATA-1 levels, induces

75 ites and show that GATA-1, in the absence of FOG-1, occupies GATA-1(V205G)-selective sites, but not G

76 3 trimethylation at lysine 4, GATA-1, NF-E2, FOG-1, SCL, and MTA-2 binding and consensus GATA-1-E-box

77 Cooccupancy with FOG-1, SCL, and MTA-2 was found at all regions of GATA-1

78 tive erythropoiesis, phenocopying aspects of FOG-1- and GATA-1-deficient animals.

79 While FOG-1- and SUMO-1-dependent genes migrated away from the

80 nuclear periphery upon erythroid maturation, FOG-1- and SUMO-1-independent genes persisted at the per

81 ER) chimeras of either wild-type GATA-1 or a FOG-1-binding defective mutant of GATA-1 repressed sever

82 est that, unexpectedly, NuRD is required for FOG-1-dependent activation of adult-type globin gene exp

83 GATA-1 chromatin occupancy at select sites, FOG-1-dependent gene expression, and were rescued by tet

84 on assay in GATA-1-null cells, GATA-1 expels FOG-1-dependent target genes from the nuclear periphery

85 e show a direct requirement of NuRD also for FOG-1-dependent transcriptional activation.

86 Although FOG-1-independent activation by GATA-1 has been describe

87 y repressed genes that GATA-1 represses in a FOG-1-independent manner.

88 ing that GATA-1-mediated Med1 recruitment is FOG-1-independent.

89 ferent combinations of SetD8, FOG-1, and the FOG-1-interacting nucleosome remodeling and deacetylase

90 Repression also occurred in a FOG-1-null cell line expressing ER-GATA-1 and during ex

91 velopment requires GATA-1 and the absence of FOG-1.

92 g the quantitatively greater requirement for FOG-1.

93 T and OGA interact with Mi2beta, GATA-1, and FOG-1.

94 ntrol the tissue-specific gene expression of FOG-1.

95 trol the expression of their partner protein FOG-1.

96 r310, thereby increasing GATA-1 affinity for FOG-1.

97 cription inhibition and require the cofactor FOG-1.

98 ted by modulating the assembly of the GATA-1.FOG-1.Mi2beta repressor complex at the -566 GATA motif w

99 amma-globin gene silencing involves a GATA-1.FOG-1.Mi2beta repressor complex that binds to the -566 G

100 encing in vivo, we created mice in which the FOG-1/NuRD complex is disrupted and crossed these with a

101 e with a mutation that specifically disrupts FOG-1/NuRD interaction (FOG-1(R3K5A)).

102 To test the importance of FOG-1/NuRD interaction for haematopoiesis in vivo, we ge

103 ese results underscore the importance of the FOG-1/NuRD interaction for the re-enforcement of lineage

104 We found that the FOG-1/NuRD interaction is dispensable for the silencing

105 Mice in which the FOG-1/NuRD interaction is disrupted display defects simi

106 R3K5A/R3K5A) megakaryocytes, suggesting that FOG-1/NuRD interaction is required for the direct suppre

107 ssed increased levels of GATA2, showing that FOG-1/NuRD interaction is required for the earlier descr

108 In addition, ablation of FOG-1/NuRD interaction led to inappropriate expression o

109 how that independent of MBD2-NuRD and GATA-1/FOG-1/NuRD, Mi2beta binds directly to and positively reg

110 ng complexes, including MBD2-NuRD and GATA-1/FOG-1/NuRD, play a role in gamma-globin gene silencing,

111 have increased expression of friend of GATA (FOG)-2, a cardiac nuclear hormone receptor corepressor p

112 Whereas FOG-2 acts through GLD-1 in C. elegans, SHE-1 does not b

113 ase (NuRD) complex physically interacts with FOG-2 and is necessary for FOG-2 mediated repression of

114 strate that SERCA2 is an important target of FOG-2 and that increased FOG-2 expression may contribute

115 In addition, we demonstrate that FOG-2 can directly repress the activity of the Cdkn1a ge

116 ration, differentiation, or apoptosis in the FOG-2 deficient cushions when compared to wild-type cont

117 ously shown that the endocardial cushions in FOG-2 deficient mice are hyperplastic and fail to remode

118 rease in atrioventricular cushion EMT in the FOG-2 deficient mice when compared with wild-type mice.

119 ts upstream of tra-2 in C. briggsae, just as fog-2 does in C. elegans.

120 important target of FOG-2 and that increased FOG-2 expression may contribute to a decline in cardiac

121 wever, the relevance of this interaction for FOG-2 function in vivo has remained unclear.

122 in promoting EMT, these results suggest that FOG-2 functions in cardiac valve formation as an attenua

123 Cardiac-specific overexpression of FOG-2 in transgenic mice led to depressed cardiac functi

124 FOG-2 is a multi-zinc finger protein that binds the tran

125 epaired the loss-of-function mutation in the fog-2 locus, thereby reestablishing hermaphroditism as t

126 ly interacts with FOG-2 and is necessary for FOG-2 mediated repression of GATA4 activity in vitro.

127 were reduced in FOG-2 transgenic hearts, and FOG-2 overexpression impaired T3-mediated SERCA2 express

128 FOG-2 physically interacts with thyroid hormone receptor

129 ization of mice homozygous for a mutation in FOG-2 that disrupts NuRD binding (FOG-2(R3K5A)).

130 ranscript and protein levels were reduced in FOG-2 transgenic hearts, and FOG-2 overexpression impair

131 ately outcrossing populations of C. elegans [fog-2(lf)] spontaneously repaired the loss-of-function m

132 cardiomyocyte proliferation in wild-type and FOG-2(R3K5A) developing hearts.

133 p21(cip1)) is up-regulated 2.0+/-0.2-fold in FOG-2(R3K5A) hearts.

134 is notion, the genetic ablation of Cdkn1a in FOG-2(R3K5A) mice leads to an improvement in left ventri

135 cyte proliferation was reduced by 31+/-8% in FOG-2(R3K5A) mice.

136 utation in FOG-2 that disrupts NuRD binding (FOG-2(R3K5A)).

137 Although C. elegans hermaphrodites require fog-2, which encodes an F box protein that regulates the

138 nd evolution of the species-specific protein FOG-2.

139 mRNAs, the related species C. briggsae lacks fog-2.

140 including GATA4 and its interacting partner FOG-2.

141 ur results define a novel mechanism in which FOG-2/NuRD interaction is required for cardiomyocyte pro

142 his report, we demonstrate the importance of FOG-2/NuRD interaction through the generation and charac

143 a gene promoter, suggesting a model by which FOG-2/NuRD promotes ventricular wall thickening by repre

144 Importantly, FOG-3 activity must be maintained for the continued prod

145 red in fog-3/+ heterozygotes, again for both fog-3 alleles, revealing a haplo-insufficient effect on

146 Here we report that FOG-3 also regulates proliferation in the germline tissu

147 Finally, we show that FOG-3 and FBF work together to promote tumor formation i

148 urvival and prevent apoptosis with fog-1 and fog-3 and that simultaneous loss of fshr-1 and the fbfs

149 We find that overexpressed FOG-3 blocks proliferation in fbf-1 fbf-2 mutants; where

150 We next overexpressed FOG-3 by removal of FBF, the collective term for FBF-1 a

151 utants possess small tumors, suggesting that FOG-3 can act as a tumor suppressor.

152 We conclude that FOG-3 can either promote or inhibit proliferation in a m

153 The discovery of these FOG-3 effects on proliferation has implications for our

154 romotes proliferation, and two copies of the fog-3 gene are required for this function.

155 phosphorylated and unphosphorylated forms of FOG-3 in nematodes.

156 ride the canonical requirement for fog-1 and fog-3 in the execution of the male-germline fate.

157 Our findings suggest that unphosphorylated FOG-3 initiates the sperm fate program and that phosphor

158 ts vertebrate Tob/BTG cousins, overexpressed FOG-3 is 'antiproliferative'.

159 We first demonstrate that FOG-3 is a positive regulator of germline proliferation.

160 e sperm fate program and that phosphorylated FOG-3 maintains that program for continued sperm product

161 A FOG-3 mutant with its four consensus ERK phosphorylation

162 A different FOG-3 mutant with its sites substituted to glutamates, c

163 Therefore, FOG-3 normally promotes proliferation, and two copies of

164 e decrease observed for each of two distinct fog-3 null alleles.

165 we assayed FOG-3 transgenes for rescue of a fog-3 null mutant.

166 Thus, fog-3 null mutants possess fewer germ cells than normal,

167 Here we investigate FOG-3 phosphorylation and its effect on sperm fate speci

168 We then interrogated the role of FOG-3 phosphorylation in sperm fate specification.

169 WDR-5.1 associates with the fog-3 promoter and is required for TRA-1 to bind to fog-

170 romoter and is required for TRA-1 to bind to fog-3 promoter.

171 Wild-type FOG-3 rescued both initiation and maintenance of sperm f

172 Specifically, we assayed FOG-3 transgenes for rescue of a fog-3 null mutant.

173 ulation of other regulators; therefore, this FOG-3 tumor-promoting effect is context dependent.

174 Thus, when FOG-3(4A) and FOG-3(4E) were both introduced into the sa

175 cuing activity on its own, but together with FOG-3(4A) rescue was complete.

176 lation sites substituted to alanines, called FOG-3(4A), rescued partially: sperm were made transientl

177 Thus, when FOG-3(4A) and FOG-3(4E) were both introduced into the same animals, sp

178 its sites substituted to glutamates, called FOG-3(4E), had no rescuing activity on its own, but toge

179 phenotype is caused by ectopic expression of fog-3, a direct target of TRA-1 repression.

180 gle Caenorhabditis elegans Tob/BTG ortholog, FOG-3, by contrast, was identified from its loss-of-func

181 FOG-3, the single Caenorhabditis elegans Tob/BTG protein

182 A similar decrease also occurred in fog-3/+ heterozygotes, again for both fog-3 alleles, rev

183 Indeed, some fog-3; fbf-1 fbf-2 mutants possess small tumors, suggest

184 ble mutants, they continue to proliferate in fog-3; fbf-1 fbf-2 triple mutants.

185 hemoglobin (HbO2) and deoxyhemoglobin (HbR), FOG allows label-free imaging.

186 ssociated with the presence of summer marine fog along the Pacific coast of California.

187 mutant strains lacking FOG or PG showed that FOG and PG both activate the procoagulant branch of the

188 Two surface proteins of GGS, protein FOG and protein G (PG), were found to bind contact syste

189 to define the genetic relationships between Fog and PTP52F, and the results suggest that PTP52F is a

190 the Rho-GTPase-signaling pathway not through Fog and RhoGEF2, but rather by inhibiting Rho GTPase act

191 lity of life is impaired in PD patients with FOG and that optimizing dopaminergic therapy and avoidin

192 DNA microarrays, digital lab-on-a-chip, anti-fogging and fog-harvesting, inkjet printing and thin-fil

193 communities from halites exposed to coastal fogs and high relative humidity were more diverse; their

194 , sized, and quantified in airborne aerosol, fog, and cloud water, strongly suggesting that they domi

195 and the aqueous phase (atmospheric aerosols, fog, and clouds) in the atmosphere.

196 , self-cleaning, anti-smudge, low-drag, anti-fog, and oil-water separation applications.

197 lications in anti-fouling, anti-smudge, anti-fog, and self-cleaning.

198 formed through aqueous chemistry in clouds, fogs, and wet aerosols, yet the gas-particle partitionin

199 ning, water harvesting, anti-corrosion, anti-fogging, anti-icing and thermal management.

200 rties are of interest for anti-fouling, anti-fogging, anti-icing, self-cleaning, anti-smudge, and oil

201 A car driving through the fog appears to move more slowly than one driving on a cl

202 ric liquid crystals, also known as the "blue fog," are among the rising stars in materials science th

203 at the commonly used frequency of 130 Hz and FOG can be ameliorated by 60 Hz stimulation in some pati

204 FOGs can both facilitate and antagonize GATA factor tran

205 Using an artificial anti-fog-that is, fog characterized by better visibility for distant than

206 efective in interaction with Friend of Gata (FOG) cofactors rescued the EMT defect, but resulted in a

207 de good guidelines for developing artificial fog collectors.

208 au Index score, Gunning Fog Index score, New Fog Count, New Dale-Chall Readability Formula score, FOR

209 , Coleman-Liau Index, Gunning Fog Index, New Fog Count, New Dale-Chall Readability Formula, FORCAST s

210 e Gunning Fog Index; 8.2 to 16.0 for the New Fog Count; 11.2 to 16.0 for the New Dale-Chall Readabili

211 moisture content, and received more frequent fog drip inputs than the site with less cloud cover.

212 icrobial metabolism was highly responsive to fog drip, illustrated by an observed ~3-fold increase in

213 n microbial biomass C with increasing summer fog drip.

214 n is accomplished in nanostructures, whereas fog droplets are gathered in areas where a high density

215 f hair from humid atmospheres; collection of fog droplets on leaf hairs; collection of splash water f

216 s of NAP SOA compounds dissolved in cloud or fog droplets.

217 Of 672 PD patients, 257 reported FOG during the onstate (38.2%), which was significantly

218 single-RBC functional imaging capability of FOG enables numerous biomedical studies and clinical app

219 es, show variability in gait metrics between FoG episodes and a substantial reduction in step length

220 h with frequent trembling of the legs during FoG episodes.

221 tive humidity (c. 93%) for 5 h, simulating a fog event.

222 and conditions favorable for low-visibility fog events.

223 that the transcriptional dynamics of t48 and fog expression foreshadow the coordinated invagination o

224 are induced to form a single vulva, but, in fog; fbf mutants, four or five VPCs are typically induce

225 may be the germ-line signal to the VPCs: the fog; fbf Muv phenotype depends on LIN-3 activity, and th

226 The fog; fbf Muv phenotype is generated by aberrant inductio

227 trate that the germ line is critical for the fog; fbf Muv phenotype.

228 of, anti-bio-fouling, drag-reducing, or anti-fogging, for smartphone screens, eye glasses, windshield

229 GATA and Friend of GATA (FOG) form a transcriptional complex that plays a key rol

230 t stressed under a summer climate of reduced fog frequency and greater evaporative demand.

231 Here we present a novel record of summer fog frequency in the coast redwood region upon the basis

232 Our analysis shows that coastal summer fog frequency is a remarkably integrative measure of Uni

233 nd temperatures, we infer a 33% reduction in fog frequency since the early 20th century.

234 ave previously established a requirement for FOG (Friend Of GATA) cofactors during mouse development.

235 Whether ATOH8 modulates GATA-FOG function at other sites or in more subtle ways in ma

236 identify ATOH8 as a novel regulator of GATA-FOG function that is required for cardiac development in

237 nstration of GATA:FOG regulation of Runx and Fog gene expression.

238 zygotic function of the folded gastrulation (fog) gene, which encodes a putative secreted protein.

239 Adaptive liquid repellency and programmable fog harvesting are demonstrated as application examples

240 ays, digital lab-on-a-chip, anti-fogging and fog-harvesting, inkjet printing and thin-film lubricatio

241 Fog has a distinct set of functions in CNS neurons.

242 Two cases of PD who developed FOG immediately upon activation of the newly placed STN

243 d for the effect of stimulation frequency on FOG in both 'off' and 'on' medication status.

244 Dopaminergic therapy improved FOG in most patients with motor fluctuations, especially

245 effect of stimulation frequency on immediate FOG in newly activated STN DBS patient with PD and deter

246 itation techniques can alleviate symptoms of FoG in some patients, but these treatments lack efficacy

247 Item 14 scores for FOG in the off condition were also collected in patients

248 ata show that reduction or overexpression of Fog in these neurons produces axon guidance phenotypes.

249 Measure of Gobbledygook (SMOG), and Gunning Fog Index (GFOG).

250 ook grade, Coleman-Liau Index score, Gunning Fog Index score, New Fog Count, New Dale-Chall Readabili

251 bbledygook test, Coleman-Liau Index, Gunning Fog Index, New Fog Count, New Dale-Chall Readability For

252 man-Liau Index; 12.4 to 18.7 for the Gunning Fog Index; 8.2 to 16.0 for the New Fog Count; 11.2 to 16

253 In contrast, only FOG induced cleavage of high molecular weight kininogen,

254 Here we show that Fog is also required for nervous system development.

255 Fog is an essential autocrine signal that induces cytosk

256 It is not clear whether the development of FOG is due to the disease progression or the chronic sti

257 Fog is expressed by longitudinal glia in the central ner

258 Freezing of gait (FOG) is a common axial symptom of Parkinson disease (PD)

259 Freezing of gait (FoG) is a unique and disabling clinical phenomenon chara

260 Smoke, fog, jelly, paints, milk and shaving cream are common ev

261 rrant MC gene expression persisted in mature Fog(ki/ki) MK and erythroid progeny.

262 Gene expression profiling of Fog(ki/ki) MK-erythroid progenitors revealed inappropria

263 hich the FOG1/NuRD interaction is disrupted (Fog(ki/ki)) produce MK-erythroid progenitors that give r

264 ributed to the representation of the morning fog layer, and to more accurate characterization of conv

265 The morning fog layer, present in the wet season but absent in the d

266 ulfate concentration consistent with "London fog" levels.

267 ifferential spatial accumulations of t48 and fog mRNAs along the DV axis, similar to the distribution

268 trated by the suppression of death in Apaf-1(fog) mutant pro-B cells.

269 have early VF phenotypes like those seen in fog mutants.

270 s routinely compromised when body fluids and fogging occlude the lens, requiring lengthy cleaning pro

271 commonly used 130 Hz stimulation could cause FOG or make it worse.

272 asma and isogenic GGS mutant strains lacking FOG or PG showed that FOG and PG both activate the proco

273 Glial Fog overexpression produces a disorganized glial lattice

274 Here we show that the Friend of GATA (FOG) protein U-shaped (Ush) is expressed in circulating

275 GATA transcription factors interact with FOG proteins to regulate tissue development by activatin

276 , GATA-1 functions completely independent of FOG proteins.

277 dedicated co-factors, termed Friend of GATA (FOG) proteins, control cell fate and differentiation in

278 ies that have elucidated mechanisms by which FOGs regulate GATA factor function and discuss how these

279 This is the first demonstration of GATA:FOG regulation of Runx and Fog gene expression.

280 The FOG score improved by more than 50% in 43.7% of patients

281 The FOG score improved from the off to on states in 148 of 1

282 that PTP52F is a downstream component of the Fog signaling pathway in CNS neurons.

283 le but limited water resources (such as dew, fog, snow and rain), yet the mechanisms for water collec

284 on a dry world, even a small amount of rain, fog, snow, and even atmospheric humidity can be adequate

285 While exposure to fog strongly compromises the water-repellency of hydroph

286 al photosynthesis (CO2 photoreduction), anti-fogging surfaces, heat transfer and heat dissipation, an

287 pends on a Rho GTPase signaling pathway (T48/Fog) that is deployed by the developmental regulatory ge

288 Using an artificial anti-fog-that is, fog characterized by better visibility for

289 from seeing over short distances in a dense fog to seeing over long distances on a clear day.

290 for distant objects, as is the case in real fog, visual speed is actually overestimated, prompting d

291 This frequency effect on FOG was present in both 'off' and 'on' statuses and rema

292 us SOA (aqSOA) formation is observed both in fog water and in wet aerosol.

293 Patients with FOG were identified as those with a score of 1 or greate

294 Scores for FOG were missing in 11 patients who were not included in

295 oped single-RBC photoacoustic flowoxigraphy (FOG), which can image oxygen delivery from single flowin

296 Patients with FoG, which is a feature of parkinsonian syndromes, show

297 frequency stimulation of 60 Hz could improve FOG, while the commonly used 130 Hz stimulation could ca

298 Both patients developed severe FOG with the commonly used 130 Hz stimulation.

299 s disease (PD) may develop freezing of gait (FOG) with chronic deep brain stimulation (DBS) of the su

300 requency to 60 Hz immediately alleviated the FOG, without change in contacts, voltages and pulse widt