ライフサイエンスコーパス: tear film

1 the aqueous layer (rather than the complete tear film).

2 o the complete thickness of the cornea (plus tear film).

3 y has implications in meibum behavior in the tear film.

4 primary component of the lipid layer of the tear film.

5 t lenses and, potentially, the meibum and/or tear film.

6 y responsible for the aqueous portion of the tear film.

7 etro-transport secretory IgA (sIgA) from the tear film.

8 l M cells bind and translocate sIgA from the tear film.

9 to explain the observed thinning rate of the tear film.

10 e MG is a prominent source of lipids for the tear film.

11 tation of the functions of the latter in the tear film.

12 with TL that could augment stability of the tear film.

13 ing and/or in the maintenance of the complex tear film.

14 the large secreted glycoprotein gp340 in the tear film.

15 es water, electrolytes, and protein into the tear film.

16 venly distributed, further destabilizing the tear film.

17 om for the thickness of the human precorneal tear film.

18 rotein was present in conjunctiva and in the tear film.

19 for TLs in maintaining the integrity of the tear film.

20 ils migrated from the stromal vessels to the tear film.

21 mined by recovery of infectious virus in the tear film.

22 + PPV does not affect the osmolarity of the tear film.

23 ine concentrations were also measured in the tear film.

24 itulates the aqueous and mucin layers of the tear film.

25 rs that promote an unstable and hyperosmolar tear film.

26 hich attempt to modify the properties of the tear film.

27 obial peptide LL-37, and constituents of the tear film.

28 Tear film abnormality is prevalent in patients with FES

29 ddition, in 13 subjects, the thinning of the tear film after a blink was measured.

30 ating the time-course changes of pre-corneal tear film after simultaneous phacoemulsification and lim

31 e epithelial changes further destabilize the tear film, amplify inflammation, and create a vicious cy

32 unctional tear syndrome, may destabilize the tear film and cause ocular surface epithelial disease.

33 unction, reduced BUT, mucus filaments in the tear film and conjunctival epithelium metaplasic changes

34 tudying the thickness of layers of the human tear film and cornea because of their ability to make no

35 anjo's method, interference effects from the tear film and cornea were studied, with the aim of corre

36 ine fluorescence scans centrally through the tear film and cornea, 2 microliters of 0.35% F were inst

37 to determine the thickness of layers of the tear film and cornea.

38 e source of the neutrophils infiltrating the tear film and cornea.

39 eminal damage, suggesting that assessment of tear film and corneal sensitivity as well as in vivo con

40 estrogen may have detrimental effects on the tear film and could influence the development of dry eye

41 le for the increased stability of the infant tear film and decreased stability of the tear film with

42 the concentrations, the total masses in the tear film and in the cornea derived from the area under

43 physiologic implications for the precorneal tear film and its derangements as well as for the histog

44 omes and with objective clinical findings of tear film and ocular surface damage.

45 ME activity provides expert insight into the Tear Film and Ocular Surface Society's International Wor

46 neal staining with fluorescein, a variety of tear film and ocular surface, contact lens, and patient-

47 ocular disorder characterized by an abnormal tear film and ocular surface.

48 Dimensional information of the tear film and of the upper and lower tear menisci during

49 porimeters restrict movement of air over the tear film and reduce evaporation compared to our free ai

50 neoplasms of the ocular surface and eyelids, tear film and tear production abnormalities, ocular surf

51 gest that gp340 is a normal component of the tear film and that the glycoprotein may function as a ba

52 identify the repertoire of O-glycans in the tear film and the glycosyltransferases associated with t

53 the stability and functionality of the human tear film and the tear film lipid layer.

54 combined thickness of the central cornea and tear film and the true corneal thickness obtained after

55 ements of the central corneal thickness plus tear film and the true corneal thickness obtained after

56 Spontaneous reactivation (HSV-1 recovery in tear film) and recurrence (HSV-1-specific epithelial les

57 ws eDNA and NETs to accumulate in precorneal tear film, and results in ocular surface inflammation.

58 mic medications may reach the cornea via the tear film, aqueous humor, and limbal vasculature.

59 The clinical examination included tear film assessment (tear film break-up time and Schirm

60 seems to be a poor animal model of the human tear film, at least when studying its biochemistry and b

61 Cer and FC can be elevated in meibum and the tear film because of certain pathologic processes, or ca

62 offer some protection from toxicants in the tear film, because mucins could function as acceptors fo

63 Natural antibodies, present in the tear film before immunization, may have contributed to s

64 A method to measure the tear film beneath a soft contact lens, referred to as po

65 The thinning of the precorneal tear film between blinks and tear film breakup can be lo

66 CFTRact-K089 showed sustained tear film bioavailability without detectable systemic ab

67 ols, documented baseline measures (including tear film biomarkers and quality of life).

68 escein staining, tear volume concentrations, tear film break up time analyses, and lastly, analytical

69 st corrected visual acuity, tear osmolarity, tear film break-up time (BUT), corneal fluorescein stain

70 hniques including measurement of noninvasive tear film break-up time (NIBUT), lipid layer thickness (

71 med for 11 normal eyes and 7 eyes with short tear film break-up time (SBUT) dry eye, with a tear film

72 Baseline tear film break-up time (TBUT) and Schirmer tests withou

73 disease index (OSDI) score of more than 12, tear film break-up time (TBUT) of 10 seconds or less, Sc

74 rformed using the following objective tests: tear film break-up time (TBUT), fluorescein corneal stai

75 Furthermore, tear film break-up time (TBUT), fluorescein corneal stai

76 nts were corneal fluorescein staining (CFS), tear film break-up time (TBUT), Schirmer test results, a

77 Additional clinical tests included tear film break-up time (TFBUT), ocular staining, osmola

78 nd signs (conjunctival and corneal staining, tear film break-up time [TBUT], and Schirmer test) of DE

79 d tear film stability (evaluated by means of tear film break-up time [TFBUT]) were assessed preoperat

80 The outcome measures included Schirmer test, tear film break-up time and OSDI score.

81 l examination included tear film assessment (tear film break-up time and Schirmer I test), ocular sur

82 Similar results were reported in the tear film break-up time in XG/CS (5.5 +/- 2.1 vs 7.4 +/-

83 ar film break-up time (SBUT) dry eye, with a tear film break-up time shorter than 5 seconds, using a

84 nificantly decreased (P </= .01) fluorescein tear film break-up time values (from 2.78 +/- 0.56 secon

85 and 48%; slit-lamp examination, 20% and 66%; tear film break-up time, 40% and 69%; and Schirmer's tes

86 niscus height, noninvasive first and average tear film break-up time, and Schirmer test results were

87 (Ocular Surface Disease Index questionnaire, Tear film break-up time, Ocular Protection Index, Ocular

88 ests included meibum expression and quality, tear film break-up time, ocular staining, osmolarity, Sc

89 ad test, conjunctival hyperemia, fluorescein tear film break-up time, Schirmer test, and ocular surfa

90 Scores of tear-film break-up time and Schirmer I test were signifi

91 essure measurement, indirect ophthalmoscopy, tear-film break-up time, Schirmer I testing, axial lengt

92 or simultaneous video imaging of fluorescein tear film breakup and the TFLL.

93 the precorneal tear film between blinks and tear film breakup can be logically analyzed into contrib

94 orter NITBUT values and bigger, more central tear film breakup locations were observed in the glaucom

95 visual analogue scale (VAS), and noninvasive tear film breakup time (NITBUT).

96 n, entropion, limitation of ocular motility, tear film breakup time (second), Schirmer's test (mm) ,

97 rrected visual acuity (BCVA), Schirmer test, tear film breakup time (TBUT), conjunctival congestion,

98 BCVA), tear osmolarity, the Schirmer I test, tear film breakup time (TBUT), corneal and conjunctival

99 Tear film breakup time (TBUT), corneal staining score (0

100 y testing, Schirmer test without anesthesia, tear film breakup time (TBUT), corneal staining, meibomi

101 njunctival staining, conjunctival hyperemia, tear film breakup time (TBUT), tear osmolarity, and the

102 isease Index [OSDI]), clinical examinations (tear film breakup time [TBUT], Schirmer I test, corneal

103 diseased group, the tear production rate and tear film breakup time were significantly decreased, and

104 easured by the Ocular Surface Disease Index, tear film breakup time, and meibomian gland secretion qu

105 ks after disease induction, tear production, tear film breakup time, and rose bengal staining score w

106 uate spatial and temporal progression of the tear film breakup using an automatic non-invasive device

107 determine size, location and progression of tear film breakup with automatically identified breakup

108 conjunctival staining with lissamine green, tear-film breakup time (TFBUT), Schirmer's test with ane

109 n symptoms and clinical parameters including tear-film breakup time, ocular staining and Schirmer I.

110 ars appears to play a key role in preventing tear film collapse and as a natural slow release mechani

111 Whether overlapping tear film components are involved in these defense funct

112 Tear film composition depends on water and ion transport

113 ions and pH in mice and to determine whether tear film composition is sensitive to deficiency of the

114 iameter 11.8 mm, power zero), and a constant tear film concentration of 170+/-30 mug/mL was measured

115 nea, and this led to error in estimating the tear film concentration of the dye.

116 e used to examine the relation between these tear film, contact lens, and patient-related factors ass

117 this study was to examine ocular surface and tear film, contact lens, care solution, medical, and pat

118 embers of the fatty acid amide family in the tear film could lead to additional insights into the rol

119 Viral shedding was monitored by tear film cultures.

120 ontaining 20 mug/ml NTX effectively reversed tear film deficits and restored corneal surface sensitiv

121 s care solutions or other ocular surface and tear film, demographic, or medical factors.

122 Dry eye disease is a tear film disorder which can cause discomfort to patient

123 ers that include allergic conjunctivitis and tear film disorders is associated with its high frequenc

124 er, and loss of gland function can result in tear film disorders such as dry eye syndrome, a widely e

125 trength in the orbicularis, and for improved tear film distribution.

126 d ocular surface discomfort in patients with tear film disturbances.

127 To investigate tear film dynamics using simultaneous measurements of oc

128 ansfer function (vMTF) induced by changes in tear film dynamics were calculated for a 5-mm pupil.

129 Tear film dynamics were evaluated by kinetic tear interf

130 ne contributing factor is the abnormality in tear film dynamics.

131 A variety of tear film (e.g., interferometry, osmolality, phenol red

132 pithelial cells and body fluids like saliva, tear film, ear fluid, and breast milk.

133 Studies have shown a range of tear film evaporation rates from 0.24 to 1.45 microm/min

134 Thus, slow thinning rates may be due to tear film evaporation, whereas rapid rates (which are of

135 of secretory phospholipase A2 in the normal tear film exceeded 30 microg/ml, only 1.1 ng (<0.1 nM) o

136 ocular anatomy (e.g. cornea and conjunctiva, tear film, eyelids) allows improved understanding of the

137 e, demographics, comorbidities, medications, tear film factors, and QST metrics) dropped out of these

138 mal fluorescence by the time integral of the tear film fluorescence calculated over the 20-minute exp

139 is study was to test the association between tear film fluorescence changes during tear break-up (TBU

140 Tear film fluorescence decreased (median PI) and the per

141 tear film thinning best explains decreasing tear film fluorescence during trials.

142 tical system was used for video recording of tear film fluorescence in 30 subjects.

143 bly due to multiple factors: an insufficient tear film for bacterial clearance and migration of neutr

144 measure the thinning rate of the precorneal tear film for up to 19 seconds after a blink.

145 The lipid layer of the tear film forms a barrier to evaporation.

146 e concentration of drug is maintained in the tear film from a contact lens for an extended period of

147 in the protection of conjunctival tissue and tear film from oxidant insults.

148 It could not resolve the tear film from the cornea, but in the early stages of me

149 Complete eye examination, tear film function tests, corneal staining, and Cochet-B

150 The complex superficial lipid layer of the tear film functions to prevent evaporation and maintain

151 The existence of tear film gaps and touching points were predicted in the

152 Similarly, post-lens tear film gaps at the corneal mid-periphery were present

153 Limbal post-lens tear film gaps were present in 42% of the eyes, with the

154 buildup as well as different frequencies of tear film gaps.

155 haracterized by the conjunctival buildup and tear film gaps.

156 To determine if tear film gp340 may function as a bacterial agglutinin a

157 Although classes of lipids found in the tear film have been reported, individual lipid species a

158 (DED) is a disorder characterized by loss of tear film homeostasis that causes ocular surface inflamm

159 Slow increases in tear film hyperosmolarity may cause the gradual increase

160 Tear film hypertonicity in AQP5 deficiency is likely cau

161 Tear film impairment (aqueous and lipid) and lacrimal dr

162 l epithelium in response to the hyperosmolar tear film in dry eye disease.

163 ds that target CFTR can correct the abnormal tear film in dry eye.

164 ed with those of adolescents and adults, the tear film in the younger groups is more stable and provi

165 esults can explain (partially) a less stable tear film in those subjects.

166 cribing water movement into the hyperosmolar tear film in vivo--were determined by a dye-dilution met

167 se (DED) is characterized by a dysfunctional tear film in which the corneal epithelium and its abunda

168 normal vision is the thin, but protein-rich, tear film in which the small tear glycoprotein lacritin

169 tuation, caused by the presence of an intact tear-film in vivo.

170 esents a second source of this mucin for the tear film, in addition to the corneal and conjunctival e

171 the Dry Eye Questionnaire 5 [DEQ5] score) to tear film indicators obtained by clinical examination (i

172 No significant differences in tear film indicators were found among the three groups.

173 filtration of CD4(+) lymphocytes, leading to tear film instability and destructive inflammation.

174 cular inflammatory disorder characterized by tear film instability and reduced tear production.

175 Tear film instability and tear hyperosmolarity are consi

176 itutes one of the mechanisms responsible for tear film instability in Sjogren syndrome.

177 f the central epithelium by dendritic cells, tear film instability, and increased corneal thickness a

178 sition were measured in search of markers of tear film instability.

179 nts a heterogeneous group of conditions with tear film insufficiency and signs and/or symptoms of ocu

180 delivery of lipids other than retinol to the tear film interfaces.

181 lish in situ fluorescence methods to measure tear film ionic concentrations and pH in mice and to det

182 Tear film ionic concentrations and pH were measured in a

183 The tear film is a complex mixture of secreted fluid, ions,

184 ns may play an important role in forming the tear-film layer at the air and ocular surface epithelium

185 e (DED) is caused by a persistently unstable tear film leading to ocular discomfort and is treated ma

186 Because evaporation is controlled by the tear film lipid layer (TFLL) it should therefore be expe

187 successfully applied to a complex biological tear film lipid layer extract in preparation for MALDI-T

188 nd compared with meiboscores (range 0-4) and tear film lipid layer thickness (range 0-100 nm).

189 The rabbit tear film lipid layer was assessed by interferometry.

190 functionality of the human tear film and the tear film lipid layer.

191 to exert a demonstrable effect on the rabbit tear film lipid layer.

192 mian gland, as well as the appearance of the tear film lipid layer.

193 ight into the physical behavior of the human tear-film lipid layer (TFLL).

194 Our proposed structure for the tear-film lipid layer at physiologic temperature is a hi

195 conducted to measure the adsorption of major tear film lipids to soft contact lenses over time.

196 ay function as a lipolytic enzyme, modifying tear film lipids.

197 ats, and defects in the sensory nerve and/or tear film may contribute to diabetic keratopathy and del

198 , suggesting that hyperosmolar levels in the tear film may transiently spike during tear instability,

199 In wild-type mice, tear film [Na(+)] was 139 +/- 8 mM, [K(+)] was 48 +/- 1

200 sh an in situ optical methodology to measure tear film [Na(+)], [K(+)], [Cl(-)], and pH in living mic

201 better barrier to evaporation than does the tear film of adults.

202 12-HETrE was detected in the tear film of both control and inflamed eyes, with the me

203 Plaque assay quantified HSV-1 in the tear film of infected mice.

204 e levels of infectious virus detected in the tear films of mice from days 4 to 9 postinfection.

205 t, the light refracting and immunoprotective tear film on eyes would collapse.

206 OCT images owing to media opacity, irregular tear film, or poor patient cooperation.

207 DED syndrome that can be used in studies on tear film-oriented therapies.

208 , limbal injection (P = 0.03), and increased tear film osmolality (P = 0.05).

209 oration or dewetting) resulting in increased tear film osmolality.

210 he aim of our study was to assess changes of tear film osmolarity after micro-incision 25G+ pars plan

211 Increased tear film osmolarity and lower TFBUT were found in the l

212 We did not find differences in tear film osmolarity between the operated eyes and the f

213 Tear film osmolarity was found to be the single best mar

214 Tear film osmolarity was measured in both eyes in every

215 most notable new diagnostic tests in DED are tear film osmolarity, inflammatory biomarkers, and meibo

216 re incorporated into a mathematical model of tear film osmolarity, providing insights into the pathop

217 ous humor (P = 0.03), at 16 hours PI for the tear film (P = 0.0024) and at 22 hours PI for the cornea

218 CEC allows for a thorough evaluation of tear film parameters and dry eye treatment protocols in

219 Measurement of standard tear film parameters could not explain the degree of sym

220 nnaire 5 (DEQ5) and underwent measurement of tear film parameters.

221 Four recordings of precorneal tear film (PCTF) thinning were made, followed by 1 hour

222 ens wear and then four recordings of prelens tear film (PLTF) thinning.

223 from inadequate tear mixing in the postlens tear film (PoLTF).

224 t spectacle-corrected visual acuity (BSCVA), tear film production, tear break-up time (BUT), corneal

225 y objectively has demonstrated the impact of tear film-related aberration changes on activities of da

226 eye disease is defined as an abnormality of tear film resulting in changes in the ocular surface.

227 enerator is overactive, possibly influencing tear film retention.

228 The DAGR indicates that tear film rupture is bigger and increases faster in glau

229 his tissue, and promote the formation of the tear film's lipid layer.

230 on dry eye disease models by stabilizing the tear film, scavenging ROS, up-regulating SOD, promoting

231 r 1 test showed a significant improvement of tear film secretion.

232 with Schirmer's I test with anesthesia), and tear film stability (evaluated by means of tear film bre

233 ), anxiety and depression evaluation (HADS), tear film stability (osmolarity and TBUT) and production

234 rted to result in dry eye, but its effect on tear film stability and tear production has not been stu

235 Tear film stability decreased as early as 1 week after b

236 Human tear film stability decreases with increasing age.

237 ould be detected on basic tear secretion and tear film stability in our group of patients.

238 Precorneal tear film stability is altered in the early postoperativ

239 It is reasonable that tear film stability is higher in infants than in adults.

240 Tear film stability is the key event in ocular surface d

241 se lipids and whether this action may impact tear film stability remain to be determined.

242 se in corneal sensation, tear secretion, and tear film stability several months after keratorefractiv

243 Pre-corneal tear film stability was assessed by measuring the tear b

244 ein solution to assess epithelial damage and tear film stability.

245 ecretion of lipids from meibomian glands, or tear-film stabilization properties of the lipid layer.

246 Tear film-stabilizing eye drops prior to keratometry mea

247 By month 3, visual outcome, symblepharon, tear film status, and lid abnormalities were comparable

248 ckness (LLT), and quantitative evaluation of tear film surface quality and dynamics (TFD).

249 um or contact lens), and (3) parallel to the tear film surface.

250 s a recapitulation of the ocular surface and tear film system, which can be further developed as a mo

251 ay be a shared structural abnormality of the tear film that is responsible for the instability.

252 ase of the interpalpebral ocular surface and tear film that leads to discomfort, fatigue and disturba

253 nds function to produce an aqueous layer, or tear film, that helps to nourish and protect the ocular

254 ections from four surfaces--the front of the tear film, the front and back of the contact lens, and t

255 omucin complex is also present in the ocular tear film, the rat lacrimal gland represents a second so

256 when the lipid layer is washed away from the tear film, the thinning rate, due to evaporation, would

257 ion conditions, there were no differences in tear film thickness (P = 0.09) or thinning rates (P = 0.

258 t were found to correlate significantly with tear film thickness but not with tear-thinning rate.

259 A value for the tear film thickness had to be assumed.

260 ng normal and delayed blinking sessions, the tear film thickness increased significantly after each b

261 er than that of the PCTF and average initial tear film thickness of the PLTF was less than that of th

262 Tear film thickness, thinning rate, and fluorescent inte

263 hence determining the most probable value of tear film thickness.

264 ctions were sensitive to the distribution of tear-film thickness under the lens.

265 measurement of the postlens distribution of tear-film thickness.

266 The rate of tear film thinning after a blink was measured using spec

267 Areas of tear film thinning and breakup usually matched correspon

268 tudy was to investigate the relation between tear film thinning and lipid layer thickness before and

269 sing ocular discomfort, suggesting that both tear film thinning and TBU stimulate underlying corneal

270 centration quenching of fluorescein dye with tear film thinning best explains decreasing tear film fl

271 Tear film thinning can be analyzed in terms of flow in t

272 The mean (+/-SD) tear film thinning rates for subjects was 3.22 +/- 4.27

273 pendent interference was used to measure the tear film thinning rates in 20 normal contact lens weare

274 nal water content (P = 0.002), rapid prelens tear film thinning time (P = 0.008), frequent usage of o

275 ay be explained mechanistically by increased tear film thinning times (evaporation or dewetting) resu

276 e gradual increase in discomfort during slow tear film thinning, whereas the sharp increases in disco

277 study was to test the prediction that if the tear film thins due to evaporation, rather than tangenti

278 ar trap (NET) accumulation in the precorneal tear film, thus causing ocular surface inflammation.

279 Specifically, tear film titers of 22/n199-infected mice were significa

280 Following corneal inoculation of mice, tear film titers of DoriS-I were reduced relative to wil

281 goblet cells (CGCs) secrete mucins into the tear film to preserve ocular surface homeostasis.

282 n the maintenance of the mucous layer of the tear film to sustain ocular surface homeostasis and has

283 showed a wave of neutrophils moving from the tear film toward bacteria in the central corneal stroma

284 In contrast, titers of DoriL-I(LR) in tear film, trigeminal ganglia (TG), and hindbrain were r

285 16, 18, and 21 after inoculation, and their tear film viral titers were determined on A549 cells.

286 1Delta29 vaccination decreased postchallenge tear film virus titers and ocular disease incidence and

287 The tear film was analyzed for MMP-9 by a commercially avail

288 Tear film was collected from human subjects with inflame

289 Fluorescence of the tear film was quantified by a pixel-based analysis of th

290 Various host proteins and the rabbit tear film were analyzed for their susceptibility to PASP

291 Viral titers in the tear film were determined by plaque assay.

292 r video recordings of the lipid layer of the tear film were made from 16 normal subjects, with the su

293 tion the virus is initially suspended in the tear film, where it encounters a multi-pronged immune re

294 ry to the eye, the main consideration is the tear film, which like other barriers to drug delivery, c

295 f proinflammatory cytokines and MMP-9 in the tear film, which results in dry eyes and insufficient at

296 ant tear film and decreased stability of the tear film with MGD.

297 Instability of the tear film with rapid tear break-up time is a common feat

298 for one patient, all others showed abnormal tear film, with an average tear break-up time of 2.9 +/-

299 , a high concentration of fluorescein in the tear film would show a greater reduction in fluorescent

300 and functional components of the precorneal tear film, yet little is known of their composition and