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1  the aqueous layer (rather than the complete tear film).
2 o the complete thickness of the cornea (plus tear film).
3 t lenses and, potentially, the meibum and/or tear film.
4 y responsible for the aqueous portion of the tear film.
5 etro-transport secretory IgA (sIgA) from the tear film.
6 l M cells bind and translocate sIgA from the tear film.
7 to explain the observed thinning rate of the tear film.
8 e MG is a prominent source of lipids for the tear film.
9 tation of the functions of the latter in the tear film.
10  with TL that could augment stability of the tear film.
11 ing and/or in the maintenance of the complex tear film.
12 the large secreted glycoprotein gp340 in the tear film.
13 hich attempt to modify the properties of the tear film.
14 es water, electrolytes, and protein into the tear film.
15 ine concentrations were also measured in 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 itulates the aqueous and mucin layers of the tear film.
23 rs that promote an unstable and hyperosmolar tear film.
24 obial peptide LL-37, and constituents of the tear film.
25 y has implications in meibum behavior in the tear film.
26  primary component of the lipid layer of the tear film.
27                                              Tear film abnormality is prevalent in patients with FES
28 ddition, in 13 subjects, the thinning of the tear film after a blink was measured.
29 e epithelial changes further destabilize the tear film, amplify inflammation, and create a vicious cy
30 unctional tear syndrome, may destabilize the tear film and cause ocular surface epithelial disease.
31 unction, reduced BUT, mucus filaments in the tear film and conjunctival epithelium metaplasic changes
32 tudying the thickness of layers of the human tear film and cornea because of their ability to make no
33 anjo's method, interference effects from the tear film and cornea were studied, with the aim of corre
34 ine fluorescence scans centrally through the tear film and cornea, 2 microliters of 0.35% F were inst
35  to determine the thickness of layers of the tear film and cornea.
36 e source of the neutrophils infiltrating the tear film and cornea.
37 eminal damage, suggesting that assessment of tear film and corneal sensitivity as well as in vivo con
38 estrogen may have detrimental effects on the tear film and could influence the development of dry eye
39 le for the increased stability of the infant tear film and decreased stability of the tear film with
40  the concentrations, the total masses in the tear film and in the cornea derived from the area under
41 omes and with objective clinical findings of tear film and ocular surface damage.
42 ME activity provides expert insight into the Tear Film and Ocular Surface Society's International Wor
43 neal staining with fluorescein, a variety of tear film and ocular surface, contact lens, and patient-
44 ocular disorder characterized by an abnormal tear film and ocular surface.
45               Dimensional information of the tear film and of the upper and lower tear menisci during
46 porimeters restrict movement of air over the tear film and reduce evaporation compared to our free ai
47 neoplasms of the ocular surface and eyelids, tear film and tear production abnormalities, ocular surf
48 gest that gp340 is a normal component of the tear film and that the glycoprotein may function as a ba
49  identify the repertoire of O-glycans in the tear film and the glycosyltransferases associated with t
50 the stability and functionality of the human tear film and the tear film lipid layer.
51 combined thickness of the central cornea and tear film and the true corneal thickness obtained after
52 ements of the central corneal thickness plus tear film and the true corneal thickness obtained after
53  Spontaneous reactivation (HSV-1 recovery in tear film) and recurrence (HSV-1-specific epithelial les
54 ws eDNA and NETs to accumulate in precorneal tear film, and results in ocular surface inflammation.
55 mic medications may reach the cornea via the tear film, aqueous humor, and limbal vasculature.
56            The clinical examination included tear film assessment (tear film break-up time and Schirm
57 seems to be a poor animal model of the human tear film, at least when studying its biochemistry and b
58 Cer and FC can be elevated in meibum and the tear film because of certain pathologic processes, or ca
59  offer some protection from toxicants in the tear film, because mucins could function as acceptors fo
60           Natural antibodies, present in the tear film before immunization, may have contributed to s
61                      A method to measure the tear film beneath a soft contact lens, referred to as po
62               The thinning of the precorneal tear film between blinks and tear film breakup can be lo
63                CFTRact-K089 showed sustained tear film bioavailability without detectable systemic ab
64 ols, documented baseline measures (including tear film biomarkers and quality of life).
65 st corrected visual acuity, tear osmolarity, tear film break-up time (BUT), corneal fluorescein stain
66 med for 11 normal eyes and 7 eyes with short tear film break-up time (SBUT) dry eye, with a tear film
67                                     Baseline tear film break-up time (TBUT) and Schirmer tests withou
68  disease index (OSDI) score of more than 12, tear film break-up time (TBUT) of 10 seconds or less, Sc
69                                 Furthermore, tear film break-up time (TBUT), fluorescein corneal stai
70 nts were corneal fluorescein staining (CFS), tear film break-up time (TBUT), Schirmer test results, a
71 d tear film stability (evaluated by means of tear film break-up time [TFBUT]) were assessed preoperat
72 The outcome measures included Schirmer test, tear film break-up time and OSDI score.
73 l examination included tear film assessment (tear film break-up time and Schirmer I test), ocular sur
74         Similar results were reported in the tear film break-up time in XG/CS (5.5 +/- 2.1 vs 7.4 +/-
75 ar film break-up time (SBUT) dry eye, with a tear film break-up time shorter than 5 seconds, using a
76 nificantly decreased (P </= .01) fluorescein tear film break-up time values (from 2.78 +/- 0.56 secon
77 and 48%; slit-lamp examination, 20% and 66%; tear film break-up time, 40% and 69%; and Schirmer's tes
78 ad test, conjunctival hyperemia, fluorescein tear film break-up time, Schirmer test, and ocular surfa
79                                    Scores of tear-film break-up time and Schirmer I test were signifi
80 essure measurement, indirect ophthalmoscopy, tear-film break-up time, Schirmer I testing, axial lengt
81 or simultaneous video imaging of fluorescein tear film breakup and the TFLL.
82  the precorneal tear film between blinks and tear film breakup can be logically analyzed into contrib
83 visual analogue scale (VAS), and noninvasive tear film breakup time (NITBUT).
84 rrected visual acuity (BCVA), Schirmer test, tear film breakup time (TBUT), conjunctival congestion,
85 BCVA), tear osmolarity, the Schirmer I test, tear film breakup time (TBUT), corneal and conjunctival
86                                              Tear film breakup time (TBUT), corneal staining score (0
87 y testing, Schirmer test without anesthesia, tear film breakup time (TBUT), corneal staining, meibomi
88 njunctival staining, conjunctival hyperemia, tear film breakup time (TBUT), tear osmolarity, and the
89 isease Index [OSDI]), clinical examinations (tear film breakup time [TBUT], Schirmer I test, corneal
90 diseased group, the tear production rate and tear film breakup time were significantly decreased, and
91 easured by the Ocular Surface Disease Index, tear film breakup time, and meibomian gland secretion qu
92 ks after disease induction, tear production, tear film breakup time, and rose bengal staining score w
93  conjunctival staining with lissamine green, tear-film breakup time (TFBUT), Schirmer's test with ane
94                          Whether overlapping tear film components are involved in these defense funct
95                                              Tear film composition depends on water and ion transport
96 ions and pH in mice and to determine whether tear film composition is sensitive to deficiency of the
97 iameter 11.8 mm, power zero), and a constant tear film concentration of 170+/-30 mug/mL was measured
98 nea, and this led to error in estimating the tear film concentration of the dye.
99 e used to examine the relation between these tear film, contact lens, and patient-related factors ass
100 this study was to examine ocular surface and tear film, contact lens, care solution, medical, and pat
101 embers of the fatty acid amide family in the tear film could lead to additional insights into the rol
102              Viral shedding was monitored by tear film cultures.
103 s care solutions or other ocular surface and tear film, demographic, or medical factors.
104 ers that include allergic conjunctivitis and tear film disorders is associated with its high frequenc
105 er, and loss of gland function can result in tear film disorders such as dry eye syndrome, a widely e
106 trength in the orbicularis, and for improved tear film distribution.
107 d ocular surface discomfort in patients with tear film disturbances.
108                               To investigate tear film dynamics using simultaneous measurements of oc
109 ansfer function (vMTF) induced by changes in tear film dynamics were calculated for a 5-mm pupil.
110                                              Tear film dynamics were evaluated by kinetic tear interf
111 ne contributing factor is the abnormality in tear film dynamics.
112                                 A variety of tear film (e.g., interferometry, osmolality, phenol red
113 pithelial cells and body fluids like saliva, tear film, ear fluid, and breast milk.
114                Studies have shown a range of tear film evaporation rates from 0.24 to 1.45 microm/min
115      Thus, slow thinning rates may be due to tear film evaporation, whereas rapid rates (which are of
116  of secretory phospholipase A2 in the normal tear film exceeded 30 microg/ml, only 1.1 ng (<0.1 nM) o
117 ocular anatomy (e.g. cornea and conjunctiva, tear film, eyelids) allows improved understanding of the
118 e, demographics, comorbidities, medications, tear film factors, and QST metrics) dropped out of these
119 mal fluorescence by the time integral of the tear film fluorescence calculated over the 20-minute exp
120 is study was to test the association between tear film fluorescence changes during tear break-up (TBU
121                                              Tear film fluorescence decreased (median PI) and the per
122  tear film thinning best explains decreasing tear film fluorescence during trials.
123 tical system was used for video recording of tear film fluorescence in 30 subjects.
124 bly due to multiple factors: an insufficient tear film for bacterial clearance and migration of neutr
125  measure the thinning rate of the precorneal tear film for up to 19 seconds after a blink.
126                       The lipid layer of the tear film forms a barrier to evaporation.
127 e concentration of drug is maintained in the tear film from a contact lens for an extended period of
128 in the protection of conjunctival tissue and tear film from oxidant insults.
129                     It could not resolve the tear film from the cornea, but in the early stages of me
130                    Complete eye examination, tear film function tests, corneal staining, and Cochet-B
131   The complex superficial lipid layer of the tear film functions to prevent evaporation and maintain
132                             The existence of tear film gaps and touching points were predicted in the
133                         Similarly, post-lens tear film gaps at the corneal mid-periphery were present
134                             Limbal post-lens tear film gaps were present in 42% of the eyes, with the
135  buildup as well as different frequencies of tear film gaps.
136 haracterized by the conjunctival buildup and tear film gaps.
137                              To determine if tear film gp340 may function as a bacterial agglutinin a
138      Although classes of lipids found in the tear film have been reported, individual lipid species a
139                            Slow increases in tear film hyperosmolarity may cause the gradual increase
140                                              Tear film hypertonicity in AQP5 deficiency is likely cau
141                                              Tear film impairment (aqueous and lipid) and lacrimal dr
142 l epithelium in response to the hyperosmolar tear film in dry eye disease.
143 ds that target CFTR can correct the abnormal tear film in dry eye.
144 ed with those of adolescents and adults, the tear film in the younger groups is more stable and provi
145 esults can explain (partially) a less stable tear film in those subjects.
146 cribing water movement into the hyperosmolar tear film in vivo--were determined by a dye-dilution met
147 normal vision is the thin, but protein-rich, tear film in which the small tear glycoprotein lacritin
148 tuation, caused by the presence of an intact tear-film in vivo.
149 esents a second source of this mucin for the tear film, in addition to the corneal and conjunctival e
150 the Dry Eye Questionnaire 5 [DEQ5] score) to tear film indicators obtained by clinical examination (i
151                No significant differences in tear film indicators were found among the three groups.
152 filtration of CD4(+) lymphocytes, leading to tear film instability and destructive inflammation.
153                                              Tear film instability and tear hyperosmolarity are consi
154 itutes one of the mechanisms responsible for tear film instability in Sjogren syndrome.
155 f the central epithelium by dendritic cells, tear film instability, and increased corneal thickness a
156 sition were measured in search of markers of tear film instability.
157 nts a heterogeneous group of conditions with tear film insufficiency and signs and/or symptoms of ocu
158 delivery of lipids other than retinol to the tear film interfaces.
159 lish in situ fluorescence methods to measure tear film ionic concentrations and pH in mice and to det
160                                              Tear film ionic concentrations and pH were measured in a
161                                          The tear film is a complex mixture of secreted fluid, ions,
162 ns may play an important role in forming the tear-film layer at the air and ocular surface epithelium
163     Because evaporation is controlled by the tear film lipid layer (TFLL) it should therefore be expe
164 successfully applied to a complex biological tear film lipid layer extract in preparation for MALDI-T
165                                   The rabbit tear film lipid layer was assessed by interferometry.
166 functionality of the human tear film and the tear film lipid layer.
167 to exert a demonstrable effect on the rabbit tear film lipid layer.
168 mian gland, as well as the appearance of the tear film lipid layer.
169 ight into the physical behavior of the human tear-film lipid layer (TFLL).
170               Our proposed structure for the tear-film lipid layer at physiologic temperature is a hi
171 conducted to measure the adsorption of major tear film lipids to soft contact lenses over time.
172 ay function as a lipolytic enzyme, modifying tear film lipids.
173 ats, and defects in the sensory nerve and/or tear film may contribute to diabetic keratopathy and del
174 , suggesting that hyperosmolar levels in the tear film may transiently spike during tear instability,
175                           In wild-type mice, tear film [Na(+)] was 139 +/- 8 mM, [K(+)] was 48 +/- 1
176 sh an in situ optical methodology to measure tear film [Na(+)], [K(+)], [Cl(-)], and pH in living mic
177  better barrier to evaporation than does the tear film of adults.
178                 12-HETrE was detected in the tear film of both control and inflamed eyes, with the me
179         Plaque assay quantified HSV-1 in the tear film of infected mice.
180 e levels of infectious virus detected in the tear films of mice from days 4 to 9 postinfection.
181 OCT images owing to media opacity, irregular tear film, or poor patient cooperation.
182 , limbal injection (P = 0.03), and increased tear film osmolality (P = 0.05).
183 oration or dewetting) resulting in increased tear film osmolality.
184               We did not find differences in tear film osmolarity between the operated eyes and the f
185                                              Tear film osmolarity was found to be the single best mar
186 most notable new diagnostic tests in DED are tear film osmolarity, inflammatory biomarkers, and meibo
187 re incorporated into a mathematical model of tear film osmolarity, providing insights into the pathop
188 ous humor (P = 0.03), at 16 hours PI for the tear film (P = 0.0024) and at 22 hours PI for the cornea
189                      Measurement of standard tear film parameters could not explain the degree of sym
190 nnaire 5 (DEQ5) and underwent measurement of tear film parameters.
191                Four recordings of precorneal tear film (PCTF) thinning were made, followed by 1 hour
192 ens wear and then four recordings of prelens tear film (PLTF) thinning.
193  from inadequate tear mixing in the postlens tear film (PoLTF).
194 t spectacle-corrected visual acuity (BSCVA), tear film production, tear break-up time (BUT), corneal
195 y objectively has demonstrated the impact of tear film-related aberration changes on activities of da
196  eye disease is defined as an abnormality of tear film resulting in changes in the ocular surface.
197 enerator is overactive, possibly influencing tear film retention.
198 his tissue, and promote the formation of the tear film's lipid layer.
199 with Schirmer's I test with anesthesia), and tear film stability (evaluated by means of tear film bre
200 rted to result in dry eye, but its effect on tear film stability and tear production has not been stu
201                                              Tear film stability decreased as early as 1 week after b
202                                        Human tear film stability decreases with increasing age.
203 ould be detected on basic tear secretion and tear film stability in our group of patients.
204                        It is reasonable that tear film stability is higher in infants than in adults.
205 se lipids and whether this action may impact tear film stability remain to be determined.
206 se in corneal sensation, tear secretion, and tear film stability several months after keratorefractiv
207 ein solution to assess epithelial damage and tear film stability.
208 ecretion of lipids from meibomian glands, or tear-film stabilization properties of the lipid layer.
209    By month 3, visual outcome, symblepharon, tear film status, and lid abnormalities were comparable
210 um or contact lens), and (3) parallel to the tear film surface.
211 s a recapitulation of the ocular surface and tear film system, which can be further developed as a mo
212 ay be a shared structural abnormality of the tear film that is responsible for the instability.
213 nds function to produce an aqueous layer, or tear film, that helps to nourish and protect the ocular
214 ections from four surfaces--the front of the tear film, the front and back of the contact lens, and t
215 omucin complex is also present in the ocular tear film, the rat lacrimal gland represents a second so
216 when the lipid layer is washed away from the tear film, the thinning rate, due to evaporation, would
217 ion conditions, there were no differences in tear film thickness (P = 0.09) or thinning rates (P = 0.
218 t were found to correlate significantly with tear film thickness but not with tear-thinning rate.
219                              A value for the tear film thickness had to be assumed.
220 ng normal and delayed blinking sessions, the tear film thickness increased significantly after each b
221 er than that of the PCTF and average initial tear film thickness of the PLTF was less than that of th
222                                              Tear film thickness, thinning rate, and fluorescent inte
223 hence determining the most probable value of tear film thickness.
224 ctions were sensitive to the distribution of tear-film thickness under the lens.
225  measurement of the postlens distribution of tear-film thickness.
226                                  The rate of tear film thinning after a blink was measured using spec
227                                     Areas of tear film thinning and breakup usually matched correspon
228 tudy was to investigate the relation between tear film thinning and lipid layer thickness before and
229 sing ocular discomfort, suggesting that both tear film thinning and TBU stimulate underlying corneal
230 centration quenching of fluorescein dye with tear film thinning best explains decreasing tear film fl
231                                              Tear film thinning can be analyzed in terms of flow in t
232                             The mean (+/-SD) tear film thinning rates for subjects was 3.22 +/- 4.27
233 pendent interference was used to measure the tear film thinning rates in 20 normal contact lens weare
234 nal water content (P = 0.002), rapid prelens tear film thinning time (P = 0.008), frequent usage of o
235 ay be explained mechanistically by increased tear film thinning times (evaporation or dewetting) resu
236 e gradual increase in discomfort during slow tear film thinning, whereas the sharp increases in disco
237 study was to test the prediction that if the tear film thins due to evaporation, rather than tangenti
238 ar trap (NET) accumulation in the precorneal tear film, thus causing ocular surface inflammation.
239                                Specifically, tear film titers of 22/n199-infected mice were significa
240       Following corneal inoculation of mice, tear film titers of DoriS-I were reduced relative to wil
241 showed a wave of neutrophils moving from the tear film toward bacteria in the central corneal stroma
242        In contrast, titers of DoriL-I(LR) in tear film, trigeminal ganglia (TG), and hindbrain were r
243  16, 18, and 21 after inoculation, and their tear film viral titers were determined on A549 cells.
244 1Delta29 vaccination decreased postchallenge tear film virus titers and ocular disease incidence and
245                                          The tear film was analyzed for MMP-9 by a commercially avail
246                                              Tear film was collected from human subjects with inflame
247                          Fluorescence of the tear film was quantified by a pixel-based analysis of th
248         Various host proteins and the rabbit tear film were analyzed for their susceptibility to PASP
249                          Viral titers in the tear film were determined by plaque assay.
250                          Viral titers in the tear film were determined by plaque assay.
251 r video recordings of the lipid layer of the tear film were made from 16 normal subjects, with the su
252 ry to the eye, the main consideration is the tear film, which like other barriers to drug delivery, c
253 f proinflammatory cytokines and MMP-9 in the tear film, which results in dry eyes and insufficient at
254 ant tear film and decreased stability of the tear film with MGD.
255                           Instability of the tear film with rapid tear break-up time is a common feat
256  for one patient, all others showed abnormal tear film, with an average tear break-up time of 2.9 +/-
257 , a high concentration of fluorescein in the tear film would show a greater reduction in fluorescent
258  and functional components of the precorneal tear film, yet little is known of their composition and

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