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 or step initiation in freezers may be due to FoG.

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

6 an explanation of excessive driving speed in fog.

7 history of falls, and 15 (16%) had observed FoG.

8 gion that is regularly inundated with marine fog.

9 locomotor region as the probable origins of FoG.

10 ents lack efficacy in patients with advanced FoG.

11 ion of the G-protein-coupled receptor ligand Fog.

12 or step initiation in freezers may be due to FoG.

13 tal and supplementary motor areas in PD with FOG.

14 ircuits are used for complex gait in PD with FOG.

15 signaling pathway in living embryos, T48 and Fog.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

72 3 trimethylation at lysine 4, GATA-1, NF-E2, FOG-1, SCL, and MTA-2 binding and consensus GATA-1-E-box

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

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

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

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

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

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

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

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

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

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

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

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

85 g the quantitatively greater requirement for FOG-1.

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

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

88 cription inhibition and require the cofactor FOG-1.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

117 FOG-2 physically interacts with thyroid hormone receptor

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

171 , 9 with FOG (aged 68 +/- 6 y) and 9 without FOG (aged 65 +/- 5 y), were included.

172 athic PD in the off-medication state, 9 with FOG (aged 68 +/- 6 y) and 9 without FOG (aged 65 +/- 5 y

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

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

175 Fog and cloud readily form under winter haze conditions,

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

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

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

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

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

181 ional VAChT expression and freezing of gait (FoG) and falls.

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

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

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

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

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

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

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

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

190 Our results suggest that fog-borne MMHg, while likely a small fraction of Hg in a

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

192 FOGs can both facilitate and antagonize GATA factor tran

193 all-thickness, acting as an artificial solid fog, capable of withstanding ~10 times the irradiance le

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

195 rticle sizes during the event, indicative of fog/cloud processing.

196 de good guidelines for developing artificial fog collectors.

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

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

199 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

200 nscription, and is not governed by regulated Fog delivery.

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

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

203 n microbial biomass C with increasing summer fog drip.

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

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

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

207 Individuals with freezing of gait (FoG) due to Parkinson's disease (PD) have small and long

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

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

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

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

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

213 and conditions favorable for low-visibility fog events.

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

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

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

217 Individuals with FoG ('freezers') may require functional reorganization o

218 Individuals with FoG ('freezers') may require functional reorganization o

219 pheric deposition, at sites with the highest fog frequencies.

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

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

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

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

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

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

226 airment (i.e., reduced stride length) in the FOG group.

227 More specifically, those with FOG had less activation of the posterior parietal cortex

228 ng new possibilities in applications such as fog harvesting and heat transfer.

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

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

231 is broadly representative for insects, that Fog has multiple morphogenetic functions.

232 Coastal marine atmospheric fog has recently been implicated as a potential source o

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

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

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

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

237 inergic systems changes underlying falls and FoG in PD.

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

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

240 Freezing of gait (FOG) in Parkinson disease (PD) often occurs during steer

241 Freezing of gait (FoG) in Parkinson's disease involves deficient anticipat

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

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

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

245 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

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

247 During gastrulation, Fog induces apical cell constrictions that drive the inv

248 ur and fur-normalized whiskers in our marine fog-influenced study region had a mean (+/-SE) total Hg

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

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

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

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

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

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

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

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

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

258 ulfate concentration consistent with "London fog" levels.

259 that atmospheric deposition of MMHg through fog may be contributing to this pattern, as we also obse

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

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

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

263 scientists alike: with each passing year the fog of progress thickens, making it easy to lose sight o

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

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

266 The Drosophila Fog pathway represents one of the best-understood signal

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

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

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

270 ental limits on our ability to image through fog, rain, dust, or the atmosphere.

271 y found for freezers between loss of PSI and FoG-ratio (r = 0.59, P = 0.0005) and loss of PSI and APA

272 Objective assessment of FoG severity (FoG-ratio) was performed.

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

274 istantly related insect species reveals that Fog's role during cellularization is widely conserved an

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

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

277 Objective assessment of FoG severity (FoG-ratio) was performed.

278 ssociated with both small APA amplitudes and FoG severity.

279 p initiation, which would be associated with FoG severity.

280 In addition, Fog signaling affects blastoderm cellularization, primor

281 g insects and recent work has suggested that Fog signaling is specific to the fast mode of gastrulati

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

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

284 FoG status is associated with reduced VAChT expression i

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 ocessing of biomass-burning phenols in cloud/fog water versus aerosol liquid water.

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

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

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

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

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

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

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

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