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1                                              DLE delays molecular clock rhythms in the heart, liver,
2                                              DLE shows the lowest CAPEX but the highest OPEX due to h
3                                              DLE-induced phase shifts are unaffected in Opn4(-/-) mic
4                                              DLE-SLE+ subjects had higher IgG autoantibodies against
5 9), SLE subjects with DLE (DLE+SLE+) (N=10), DLE subjects without SLE (DLE+SLE-) (N=11), and healthy
6 oassays in DLE-SLE+ (N=18), DLE+SLE+ (N=17), DLE+SLE- (N=23), and healthy subjects (N=22).
7 odies using immunoassays in DLE-SLE+ (N=18), DLE+SLE+ (N=17), DLE+SLE- (N=23), and healthy subjects (
8 .2 contains a di-acidic ER exit signal, (280)DLE(282), which promotes concentration of the channel in
9                                 In addition, DLE modifies patterns of hypothalamic and cortical cFos
10                                     Although DLE usually responds to topical or intralesional cortico
11  mechanism that dampens D-loop formation and DLE at hyper-resected ends.
12                                  Healthy and DLE+SLE- subjects expressed higher IgM autoantibodies ag
13 ies against selected antigens in healthy and DLE+SLE- subjects may be nonpathogenic.
14 5) allele in combined cutaneous LE (SCLE and DLE) patients with PLE was 42%, significantly lower than
15 al GST gene polymorphisms and PLE, SCLE, and DLE in a case-control study.
16  and desmoglein-3 compared with DLE+SLE+ and DLE-SLE+ subjects.
17 s coated with the Fc-optimized CD33 antibody DLE-HuM195 reveals a distinct kinetic profile.
18   These effects are particularly relevant as DLE conditions-due to artificial light exposure-are expe
19 DLE (DLE-SLE+) (N=9), SLE subjects with DLE (DLE+SLE+) (N=10), DLE subjects without SLE (DLE+SLE-) (N
20 tibody profiles of SLE subjects without DLE (DLE-SLE+) (N=9), SLE subjects with DLE (DLE+SLE+) (N=10)
21 ts has nearly 100 % drug loading efficiency (DLE) and ultrahigh drug loading content (DLC) of PTX alo
22  (DLE + EM); group 3, with DLE plus SOR-EMs (DLE + SOR-EM); and group 4, with saline solution.
23 orubicin-Lipiodol (ethiodized oil) emulsion (DLE) and SOR-EMs were sequentially injected into the hep
24 ofiles of human discoid lupus erythematosus (DLE) and lupus nephritis (LN).
25                 Discoid lupus erythematosus (DLE) is a chronic variant of cutaneous lupus erythematos
26 y of choice for discoid lupus erythematosus (DLE) is the 4-aminoquinolone antimalarial hydroxychloroq
27                 Discoid lupus erythematosus (DLE) is the most common skin manifestation of lupus.
28 ith outcomes in discoid lupus erythematosus (DLE) remains poorly understood.
29 ) patients with discoid lupus erythematosus (DLE) were reported to have milder disease.
30 c infiltrate in discoid lupus erythematosus (DLE), their contribution to pathogenesis is unknown.
31 osus (SCLE) and discoid lupus erythematosus (DLE), which may reflect a common genetic background.
32 associated with discoid lupus erythematosus (DLE).
33 e to dim artificial lighting in the evening (DLE) may perturb circadian rhythms and sleep patterns, a
34 ot for males, with disabled life expectancy (DLE) remaining stable.
35 hysical D-loop capture and D-loop extension (DLE) assays to track HR intermediates, we employed genet
36 ed as a promising direct lithium extraction (DLE) technology owing to its high lithium selectivity an
37  Thacker Pass, 4.3 for Silver Peak, 17.4 for DLE, and 17.6 for Hard Rock.
38 acker Pass, $4600 for Silver Peak, $7850 for DLE, and $6100 for Hard Rock.
39 eous manifestations, targeted treatments for DLE are lacking, likely because of a dearth of knowledge
40 e support investigations into treatments for DLE that target Th1 cells or the IFN-gamma signaling pat
41 iple mutation Ser293Asp/Ala330Leu/Ile332Glu (DLE), and developed Time-lapse Imaging Microscopy in Nan
42 G autoantibodies against nuclear antigens in DLE+SLE+ versus DLE-SLE+ subjects suggest that DLE indic
43 act mechanism driving skin carcinogenesis in DLE is unknown.
44 inflammation promotes skin carcinogenesis in DLE.
45 of studying the role of cutaneous B cells in DLE pathogenesis.
46 s without that for IL-17-associated genes in DLE.
47 01), are among the most upregulated genes in DLE.
48 pressed autoantibodies using immunoassays in DLE-SLE+ (N=18), DLE+SLE+ (N=17), DLE+SLE- (N=23), and h
49 proportionately greater B-cell infiltrate in DLE lesions.
50                         Regression models in DLE indicated increased glycolysis was correlated with k
51 olicy changes to improve patient outcomes in DLE.
52 ll types, only B cells are more prevalent in DLE.
53 Da) compared with all other groups including DLE+SLE+ subjects (P<0.05).
54 g the less educated contributed to increased DLE.
55  Here, we examine the effects of 4-h, 20-lux DLE on circadian physiology and behavior in mice and the
56 with DLE plus unloaded embolic microspheres (DLE + EM); group 3, with DLE plus SOR-EMs (DLE + SOR-EM)
57 enting this life-threatening complication of DLE.
58 h of knowledge of the molecular landscape of DLE skin.
59       Extraction of T cells from the skin of DLE patients identified a predominance of IFN-gamma-prod
60       Here, we profiled the transcriptome of DLE skin in order to identify signaling pathways and cel
61                         We show that 2 wk of DLE induces a phase delay of ~2 to 3 h in mice, comparab
62 Cs and the perilesional skin of cancer-prone DLE patients.
63 nts with treatment-refractory, biopsy-proved DLE were prescribed a novel, off-label preparation of ta
64 flammation promotes skin cancer in high-risk DLE patients, and blocking the inflammation may be criti
65 (DLE+SLE+) (N=10), DLE subjects without SLE (DLE+SLE-) (N=11), and healthy controls (N=11).
66 ticosteroids and/or oral antimalarials, some DLE is resistant to these treatments or adverse effects
67                 Together, our data show that DLE causes coordinated realignment of circadian rhythms,
68 E+SLE+ versus DLE-SLE+ subjects suggest that DLE indicates lower disease severity.
69                                          The DLE + SOR-EM-treated rats showed a superior tumor growth
70 ompared with the other treatment groups, the DLE + SOR-EM treatment group had the lowest number of mi
71                    Further comparison of the DLE transcriptome with that of psoriasis, a useful refer
72                      We demonstrate that the DLE-HuM195 antibody increases both the quality and the q
73  antigens progressively rose from healthy to DLE-SLE+ subjects.
74 ies a B-cell-predominant signature unique to DLE and highlights the importance of studying the role o
75  being used in a lotion formulation to treat DLE lesions, resulting in hair regrowth.
76 ers with areas of active inflammation in two DLE patients followed over 8 years strongly suggested th
77  against nuclear antigens in DLE+SLE+ versus DLE-SLE+ subjects suggest that DLE indicates lower disea
78                         The main outcome was DLE disease severity as codified by the validated Cutane
79                                        While DLE and hard rock methods have higher emissions, Silver
80 bolic microspheres (DLE + EM); group 3, with DLE plus SOR-EMs (DLE + SOR-EM); and group 4, with salin
81 t geospatial disadvantage is associated with DLE disease severity independent of race.
82 , race was not significantly associated with DLE disease severity.
83    NK cells encountering targets coated with DLE-HuM195 induce rapid target cell apoptosis by promoti
84  HCC model, SOR-EMs used in combination with DLE TACE were effective in treating HCC.Keywords: Chemoe
85 k cognate 70, and desmoglein-3 compared with DLE+SLE+ and DLE-SLE+ subjects.
86 injected with DLE; group 2 was injected with DLE plus unloaded embolic microspheres (DLE + EM); group
87 rats: The rats in group 1 were injected with DLE; group 2 was injected with DLE plus unloaded embolic
88           A total of 154 adult patients with DLE (128 women [83%] and 26 men [17%]; mean [SD] age, 43
89 s-sectional study included 154 patients with DLE seen between January 1, 2007, and January 1, 2024, a
90 tential therapeutic option for patients with DLE that is refractory to first-line therapies and who r
91 d pharmacogenetic study of 200 patients with DLE treated with hydroxychloroquine.
92 hout DLE (DLE-SLE+) (N=9), SLE subjects with DLE (DLE+SLE+) (N=10), DLE subjects without SLE (DLE+SLE
93 are the immune landscape of 17 subjects with DLE with that of 21 subjects with subacute cutaneous lup
94 A few of the subjects (3 of 17 subjects with DLE, and 5 of 21 subjects with subacute cutaneous lupus
95 y effect compared with the rats treated with DLE only (P < .05).
96 utoantibody profiles of SLE subjects without DLE (DLE-SLE+) (N=9), SLE subjects with DLE (DLE+SLE+) (