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1 mine whether neurotransmitters influence the meibomian gland.
2 expression of almost 400 genes in the human meibomian gland.
3 y multiple changes in gene expression in the meibomian gland.
4 progesterone modulate gene expression in the meibomian gland.
5 progesterone regulate gene expression in the meibomian gland.
6 he expression of numerous genes in the mouse meibomian gland.
7 ression of more than 1590 genes in the mouse meibomian gland.
8 n of IGF-1 action in epithelial cells of the meibomian gland.
9 in the sex-related differences of the mouse meibomian gland.
10 r role in the sex-related differences of the meibomian gland.
11 significant impact on gene expression in the meibomian gland.
12 ression of more than a thousand genes in the meibomian gland.
13 ility and quality of meibum, and drop-out of meibomian glands.
14 ctopic row of hair follicles in place of the Meibomian glands.
15 r and ectopic cilia formed at the expense of Meibomian glands.
16 dant in the eyelid, which contains wax-laden meibomian glands.
17 ant second row of eyelashes arising from the meibomian glands.
18 me; and (2) trophic effects on sebaceous and Meibomian glands.
19 ed for the maintenance of both sebaceous and meibomian glands.
20 ed to the basement membranes of acini of the meibomian glands.
21 ing TH, CGRP, and SP were more sparse in the meibomian glands.
22 te associated changes of the lid margins and meibomian glands.
23 with the expressibility and the drop-out of meibomian glands.
24 automated lipid expression (Lipiflow) of the Meibomian glands.
25 n managing OSD arising from disorders of the meibomian glands.
26 ent of OSD that arises from disorders of the meibomian glands.
27 ands and contributes to the formation of the meibomian glands.
28 erior segment of the eye, and the absence of meibomian glands.
29 anterior segment defects and the absence of meibomian glands.
30 d bulbar conjunctiva, corneal epithelium and meibomian glands.
31 terations in the lipid content of the rabbit meibomian gland; 19-nortestosterone treatment modulated
32 that 1) as previously reported, mice lacked meibomian glands; 2) >80% developed corneal lesions such
36 ting stress showed hyperproliferation of the meibomian gland and ductal dilation suggesting a marked
37 he expression of numerous genes in the mouse meibomian gland and that many of these genes are involve
38 ment and the commonest was an anomaly of the meibomian glands and lacrimal drainage system defects.
42 nic eyelid closure as well in development of meibomian glands and the anterior segment of the eye.
44 exists in the epithelial cell nuclei of rat meibomian glands and, in addition, whether androgen defi
45 nance of primary epithelial cells from human meibomian glands and, second, to immortalize these cells
46 anterior eye segment defects, absence of the meibomian glands, and defects in the semilunar cardiac v
47 al and neutral lipid fractions of the rabbit meibomian gland; and androgens did not appear to influen
48 within acinar epithelial cell nuclei of rat meibomian glands; androgen deficiency was associated wit
51 ontent, and fatty acid profile of the rabbit meibomian gland, as well as the appearance of the tear f
52 luding hypertrophic salivary, sebaceous, and meibomian glands, as well as enhanced squamous tumorigen
53 essenger RNA is also present in lacrimal and meibomian glands, as well as in a number of other tissue
54 lopment and maturation of both sebaceous and meibomian glands, as well as in the formation and compos
55 B presenting over seventeen months including meibomian gland assessment using a recognized classifica
59 omarker positivity was assessed in 16 severe meibomian gland atrophy cases after being found relevant
64 was not significantly associated with severe meibomian gland atrophy vs controls (P = .34, right-eye;
67 , 11 years; 49% female): 17 cases had severe meibomian gland atrophy; 24 controls had insignificant g
69 redness, tear volume, anterior blepharitis, meibomian gland capping) and tear inflammatory cytokine
70 Consistent with this, we show that human Meibomian gland carcinoma exhibits increased Hh signalin
71 t cell cohesion is maintained differently in meibomian gland cells and indicate that Ecad is importan
72 hair growth after shaving and also enlarged meibomian glands, consistent with a nearly 80% reduction
74 stemic, T-cell-dependent process that causes meibomian gland damage and induces a robust form of ocul
75 rmore, corneal stroma neovascularization and meibomian gland degeneration were examined by immunohist
76 subbasal corneal nerve inhomogeneity (SCNI), Meibomian gland density and inhomogeneity (MGD, MGI), an
78 ents with dry eye who had rosacea-associated meibomian gland disease (MGD) or Sjogren's syndrome (SS)
80 hology, causes, and ocular surface impact of meibomian gland disease (MGD), as well as its relationsh
81 5 patients with DE, including subgroups with meibomian gland disease (MGD), Sjogren's syndrome (SS) a
83 ormal and 33 subjects with tear dysfunction (meibomian gland disease [n = 11], aqueous tear deficienc
88 positively correlated with the total eyelid meibomian gland dropout values (r = 0,208, p < 0,05 and
92 ibum from normal donors (Mn) and donors with meibomian gland dysfunction (Md) by (1)H-NMR spectroscop
93 )H-NMR spectra of meibum from 39 donors with meibomian gland dysfunction (Md) were compared to meibum
95 rading of clinical variables associated with meibomian gland dysfunction (MGD) in real-time examinati
104 h regular eyelid shampoo on the treatment of meibomian gland dysfunction (MGD) signs and symptoms.
105 and the abnormalities of these glands cause Meibomian gland dysfunction (MGD) which is responsible f
107 lated to be necessary for the development of meibomian gland dysfunction (MGD), a common form of chro
115 f depression has been found in patients with meibomian gland dysfunction (MGD); however, specific con
116 njunctivitis (OR: 3.76, 95% CI: 1.33-10.63), meibomian gland dysfunction (OR: 4.45, 95% CI: 1.9-10.40
117 oma, retinal vein occlusion, conjunctivitis, meibomian gland dysfunction and blepharitis, between pat
119 conjunctival staining, tear osmolarity, and meibomian gland dysfunction at baseline, 6 months, and 1
122 investigating the linkage of lid changes and meibomian gland dysfunction may shed new lights on the p
123 Meibum lipid compositional changes with meibomian gland dysfunction reflect changes in hydrocarb
125 time, corneal and conjunctival staining, and meibomian gland dysfunction, all in both eyes, and a com
127 igating ocular surface pathologies involving meibomian gland dysfunction, blepharitis, corneal or con
128 s, accompanied by tear hyperosmolarity, mild meibomian gland dysfunction, reduced BUT, mucus filament
129 Restasis) may also have a positive effect on meibomian gland dysfunction, the other main form of dry
132 luorescein corneal stain, and assessment for meibomian glands dysfunction (MGD) were carried out.
133 In aqueous-deficient dry eye (ADDE) and Meibomian-gland dysfunction (MGD), compositional changes
135 g), and promoted lipid accumulation in human meibomian gland epithelial cells (about 2-fold increase
138 port the hypothesis that IGF-1 acts on human meibomian gland epithelial cells and may explain why tre
143 N, SETTING, AND MATERIAL: Immortalized human meibomian gland epithelial cells were cultured in the pr
144 To test our hypotheses, immortalized human meibomian gland epithelial cells were cultured with or w
145 shes the differentiation and adipogenesis of meibomian gland epithelial cells, and both mTOR complexe
155 eyelid margin measurements, meibum quality, meibomian gland expressability, ocular surface disease i
157 Because lipid production was unaltered in meibomian glands from Dsg3-deficient mice, we establishe
159 esis in the study was that androgens control meibomian gland function, regulate the quality and/or qu
161 x, Ocular Surface Staining, Schirmer I test, Meibomian gland functionality in 757 patients (1514 eyes
163 Therapeutically, anti-inflammatory therapy, meibomian gland heating and expression, and scleral cont
166 l injections (IVI) on the ocular surface and meibomian glands in patients with neovascular age-relate
168 upper lids, total mebioscore, percentage of meibomian glands in upper and lower lids, first non-inva
169 upper lids, total meiboscore, percentage of meibomian glands in upper and lower lids, NIV-BUT of the
170 thetic preganglionic neurons that project to meibomian gland-innervating ganglion cells are located i
171 n, platinum segment insertion, correction of meibomian gland inversion (MGI), full-thickness skin gra
172 hypothesis that the androgen control of the meibomian gland involves the regulation of gene expressi
173 plications, including the destruction of the meibomian glands, irregularity of the eyelid margin, and
175 In prior work, it has been found that the meibomian gland is an androgen target organ, that androg
186 mark stem cells that play a critical role in Meibomian gland (MG) development and homeostasis, howeve
187 rneal epithelial disruption and lower eyelid meibomian gland (MG) dropout, adjusted for age and sex (
190 staining score (according to Oxford scale), meibomian gland (MG) loss rates of lower and upper eyeli
191 ation of dyslipidemia and its treatment with meibomian gland (MG) morphologic changes by standardized
192 o conclusive information about the impact of meibomian gland (MG) morphology in tear film physiology
193 esence of corneal subepithelial fibrosis and meibomian gland (MG) orifice metaplasia were recorded.
198 Meibum-a lipid secretion that is produced by Meibomian glands (MG) in a process termed meibogenesis-p
199 osynthesis of FAlc and FAld in mammals using Meibomian glands (MG) of wild-type (WT) and Sdr16c5/Sdr1
200 ime (TBUT), Tear Film Meniscus Height (TMH), Meibomian glands (MG), and Lipid Layer Thickness (LLT) w
201 result in a marked enlargement of the mouse Meibomian glands (MGs) and sebaceous glands, respectivel
205 e modeling to identify relationships between Meibomian gland morphological features and subject demog
206 77%, 76%, and 86% accuracies for predicting Meibomian gland morphological features, subject age, and
210 scosity could alter secretion of lipids from meibomian glands, or tear-film stabilization properties
213 lities in the fur texture and the absence of meibomian glands prompted us to evaluate other epidermal
214 eal staining, tear breakup time, Schirmer's, meibomian gland quality, orifice plugging, lid vasculari
215 Many pathologies can disrupt function of meibomian glands, ranging from congenital to acquired ca
216 d in the search documented an improvement in meibomian gland-related OSD after treatment with these a
224 tty acids and the fatty acid amides in human meibomian gland secretions by using electrospray mass sp
225 he production, secretion, and/or delivery of meibomian gland secretions to the ocular surface, the go
227 eral corneal, or bulbar conjunctival stroma; meibomian glands; skin; retina-choroid; or episcleral re
228 mal development of both sebaceous glands and meibomian glands, specialized sebaceous glands of the ey
230 This study highlights the need to evaluate meibomian gland structure and function in patients with
231 ith mechanical expression of lipids from the meibomian glands successfully treats dry eye symptoms an
244 lts indicate that aging mice show dropout of meibomian glands with loss of gland volume and a forward