コーパス検索結果 (1語後でソート)
通し番号をクリックするとPubMedの該当ページを表示します
1 orage) and late gadolinium enhancement (LGE, scar).
2 act in anisotropically resistive structures (SCARS).
3 action dose delivered to the area of culprit scar.
4 d injury contributing new cells to the glial scar.
5 otic cardiomyocytes, and a larger myocardial scar.
6 ion due to the formation of a glial-fibrotic scar.
7 recurrent strabismus secondary to stretched scar.
8 y specimens that are painful and permanently scar.
9 ntribute collagen to the forming post-injury scar.
10 o penetrate the inhibitory spinal cord glial scar.
11 as are localized to regions of prior defined scar.
12 slower CV compared with areas without dense scar.
13 repeat containing 1), and localize into the scar.
14 rgery is needed in patients with a stretched scar.
15 herapy in children with foveal toxoplasmosis scars.
16 in the treatment of hypertrophic and keloid scars.
17 CI, 37.4-100) with resulting permanent flat scars.
18 ith external features resembling modern fire scars.
19 glycans (CSPGs)-a primary component of glial scars.
20 ions including their use in the treatment of scars.
21 were at risk of progression of trachomatous scarring.
22 e are associated with post-burn pruritus and scarring.
23 ue repair due to accelerated closure without scarring.
24 analyses to evaluate inflammation and renal scarring.
25 ibrogenic cell in the liver, and drive liver scarring.
26 ract can lead to irreversible fallopian tube scarring.
27 ns (pannus and/or HPs) plus any conjunctival scarring.
28 y epidermal appendage neogenesis and lack of scarring.
29 al signs and moderate or severe conjunctival scarring.
30 st patients respond well to steroids without scarring.
31 recent rigid contact lens wear, and corneal scarring.
32 improved and finally turned to conjunctival scarring.
33 d in 1 tumor (9%, 95% CI, 0.2-50.6), and all scars (100%, 95% CI, 49.9-100) showed pigmentary changes
35 in high-risk, vascularized herpetic corneal scars achieves clinical outcomes that remain stable for
39 Moreover, noninvasive imaging of myocardial scar and hibernation can inform the risk of sudden cardi
42 dary strabismus by excision of the stretched scar and muscle fixation to the sclera using non-absorba
45 diated inflammatory responses promoted renal scarring and compromised renal function, as indicated by
47 sex, and the presence of preoperative apical scarring and environmental allergies in a multivariable
48 y response in some individuals that leads to scarring and in-turning of the eyelids in later life.
50 mulation reveals a novel mechanism of genome scarring and is critical to exploring therapies to count
51 derived from skin biopsy studies that cause scarring and may be impractical in large-scale clinical
52 or ductular regeneration, demonstrating that scarring and regeneration can be uncoupled in adult bili
53 mate human biology, as well as comparison of scarring and regenerative phenotypes to uncover master r
54 bullous keratopathy, postinfectious corneal scarring and thinning and keratoconus were the most comm
56 Due to the substantial improvement in skin scarring and well-established clinical safety profile, l
57 n a slowly progressive uveitis, with retinal scars and atrophy observed in the chronic stage by fundo
58 gonal order with specific elongated defects, scars and pleats, where the 5-valence and 7-valence vert
60 spersion mapping, to assess heterogeneity of scar, and evaluated its prognostic role in patients with
64 Moreover, we show that the mono(ADP-ribose) scars are lost from the chromatin of ARH3-defective cell
67 thesis are evident in characteristic genomic scars as insertions of 3 to 30 bp of sequence that is id
69 ty of life (EuroQol 5-level EQ-5D), surgical scar assessment (Patient and Observer Scar Assessment Sc
70 rgical scar assessment (Patient and Observer Scar Assessment Scale), and chronic pain (Douleur Neurop
71 equirement and generates distinctive genomic scars associated with pathogenic genome instability.
74 can act as an eraser of ADP-ribose chromatin scars at sites of PARP activity during DNA single-strand
75 gnificantly improved hypertrophic and keloid scars based on both subjective and objective analyses an
76 The 3D CNN identified patients with a large scar burden (>15%) with 98% accuracy (202 of 207) (95% c
77 GE cardiovascular magnetic resonance-defined scar burden is independently associated with inducible V
79 ot only poised to prevent progressive tissue scarring, but also have the potential to reverse establi
80 injury and promote the formation of ductular scars by upregulating pro-fibrogenic cytokines and posit
81 nifested as molecular "scars." Some of these scars can influence brain functions throughout the entir
82 severity of dryness, corneal ulceration and scarring, cataract, and glaucoma are factors associated
84 significant corneal injuries and subsequent scarring collectively represent a major global human hea
85 of decay with distance from the electrode in scars compared with uninjured regions, suggesting reduce
86 me season in which the individual showed new scars, confirming that the squid-white shark interaction
87 are required to exclude the other causes of scarring conjunctivitis until more sensitive and specifi
88 After surgical correction of the stretched scar, consecutive deviations in the form of consecutive
89 fibroblasts (OFs) were treated with the pro-scarring cytokine, transforming growth factor beta (TGFb
92 iopathic pulmonary fibrosis is a progressive scarring disease characterized by extracellular matrix a
93 Eleven showed progression of conjunctival scarring during a median follow-up of 42 months (range,
95 val scarring on presentation or worsening of scarring during follow-up, even in the setting of negati
96 flammatory cells significantly contribute to scar electrophysiology through coupling mediated at leas
99 ed1 profibrotic fibroblasts, responsible for scar extracellular matrix deposition, were significantly
102 nsition zones between healthy myocardium and scar form a spatially complex substrate that may give ri
103 ws the complexity of retinal fibrosis, where scar formation is regulated both by TGFbetaR and non-TGF
104 adult mouse GFPtpz-collagen donors, enhances scar formation via cell autonomous production of collage
105 erefore, understanding whether we can reduce scar formation while maintaining a pro-regenerative micr
106 cord injury in mammals is thought to trigger scar formation with little regeneration of axons(1-4).
110 duction of Wnt-ligands reduces the amount of scar formed around the bile duct, without reducing the d
112 , functional heterogeneity and regulation of scar-forming cells that occur during human kidney fibros
113 fibroblasts as the main cellular sources of scar-forming myofibroblasts during human kidney fibrosis
115 diameter and cell wall thickness in the pre-scarring fossilized wood show a response similar to that
116 eatures of wood anatomy associated with fire scars found on fossil tree trunks is likely to increase
118 strategies that could be used to facilitate scar-free healing in the adult mammalian nervous system.
119 to the spinal cord in neonatal mice leads to scar-free healing that permits the growth of long projec
125 lar scaring affects liver function; however, scar-generating portal fibroblasts also provide importan
130 q to probe unsorted cells from regenerating, scarring, homeostatic, and developing skin, we identifie
131 of the Wiskott-Aldrich syndrome protein and SCAR homolog (WASH) complex that activates actin nucleat
132 rmed involving 21 patients with hypertrophic scars (HS) (n = 9) and keloids (n = 12) resulting from v
144 study the electrophysiological properties of scars in fetal liver chimeric mice generated using conne
146 generation because it does not fibrose (i.e. scar) in response to tissue injury as most other mammals
147 P-activated protein kinase activation in the scar, increased vessel density in the penumbra, higher t
149 nsecutive and 6 recurrent cases of stretched scar -induced strabismus were identified and all cases w
150 factors, such as bacterial infection, tissue scarring, inflammation, and vasculature damage, as well
154 on of CD80 has a detrimental role in corneal scarring, likely by increasing CD8(+) T cell recruitment
155 techniques, we found the presence of evident scars made by large squids on the body of the white shar
159 ces of cranial implants, which include glial scarring, meningeal lymphangiogenesis, and increased gly
160 droitinase ABC (chABC), tested here in glial scar models, and ability of cervically-patterned scNSCs
165 t associated with the presence of myocardial scar (odds ratio per 1 SD higher, 1.12 [95% CI, 0.86-1.4
167 size, the GG homozygotes demonstrated worse scarring (odds ratio 1.88, P = 0.005) compared to AG het
168 e scar, was 0.48 +/- 0.04 mm (n = 11) in the scar of the bmpCTL group and decreased 37.5% in the bmpK
169 retion, ependymal denudation, and damage and scarring of intraventricular and parenchymal (glia-lymph
171 stitial lung disease characterized by patchy scarring of the distal lung with limited therapeutic opt
174 lmonary Fibrosis (IPF), there is unrelenting scarring of the lung mediated by pathological mesenchyma
175 ) is a complex lung disease characterized by scarring of the lung that is believed to result from an
176 atients who have Foster stage 3 conjunctival scarring on presentation or worsening of scarring during
177 oor HRQOL on multivariable analysis; pain on scars on chest (odds ratio (OR) 1.27; 95% CI 0.97-1.65),
178 ed patient cells accumulate mono(ADP-ribose) scars on core histones that are a molecular memory of re
179 ry or foraging behavior, including predation scars on trilobites [7], directionality of invertebrate
181 ) of BCG, ascertained based on presence of a scar or vaccination history, against latent tuberculosis
182 to be unique among mammals by showing little scarring or fibrosis after skin or muscle injury, but th
183 xed scar area at baseline but not changes in scar over time is associated with progressive increase i
186 cuity risk was 11.1-fold higher with macular scarring (p = 0.001) and 14-fold higher with optic atrop
188 ildren for clinical evidence of trachomatous scarring, pannus and Herbert's pits (HPs) or limbal foll
189 decreased in 12 (30%), related to subfoveal scar, persistent subretinal fluid, reactive exudation, r
191 e, absence of bacillus Calmette-Guerin (BCG) scar, presence of donor-specific antibody, and KTR group
192 s CTHRC1 as a novel regulator of the healing scar process and a target for future translational studi
194 enes that were significantly associated with scarring progression included those encoding proinflamma
195 A and PDGF were significantly upregulated in scarring progressors relative to in nonprogressors.
196 shown to contribute to myofibroblasts during scarring, promote metaplastic differentiation of airway
198 mances were evaluated with respect to manual scar quantification performed in a core laboratory setti
203 hat collagen V, a minor constituent of heart scars, regulates the size of heart scars after ischemic
204 ndergoing 21 catheter ablation procedures of scar-related VT, site of origin localization accuracy wa
208 ic injury, corneal wound healing can cause a scarring response that stiffens the tissue and impairs o
210 We demonstrate that the ADP-ribose chromatin scars result in reduced endogenous levels of important c
211 nt with this, myofibroblasts in human tendon scar samples displayed enhanced prosurvival signaling co
213 aluations were performed using the Vancouver Scar Scale, Doppler ultrasound, Cutometer, Mexameter and
215 d patients) with low DNA damage (low genomic scar score with chromosome 9 gain) and a superior outcom
220 .2 logMAR lines, P = .006) and 1.1 mm larger scar size at 3 months after controlling for baseline mea
221 3 days, 3 weeks, and 3 months, infiltrate or scar size at 3 weeks and 3 months, 3-day smear and cultu
224 h A1 and A3 showed a significant decrease in scar size versus A2; however, A1 showed a further 24% re
227 left ventricle cardiac function, reduced MI scar size, and enhanced post-MI neovascularization in MI
228 nction, inhibited cell apoptosis, reduced MI scar size, and promoted post-MI neovascularization, wher
229 ncluded 3-week and 3-month visual acuity and scar size, corneal perforation, and/or the need for ther
231 There was no difference in infiltrate or scar size, percentage of epithelialized or adverse event
234 factors and may be manifested as molecular "scars." Some of these scars can influence brain function
235 ata were analyzed in relation to progressive scarring status between baseline and the final time poin
236 fivefold over the following 4 years and bite scars suggest significantly more intraspecific fighting
237 eve demonstration shows the potential of the SCARS technology for the development of unobtrusive, wea
241 of injury was found to significantly reduce scar thickness by 24.8% (P < 0.0001) without compromisin
247 osition and the mechanical properties of the scar tissue have been implicated to inhibit neuronal reg
249 esponse in the infarct area typically yields scar tissue rather than newly formed cardiomyocytes.
251 art regeneration", replacing injured cardiac scar tissue with concomitant electrical integration.
252 Surgical correction involved excision of the scar tissue with muscle re-attachment to the sclera usin
253 ficiency alters the mechanical properties of scar tissue, and altered reciprocal feedback between mat
259 ntly no treatment to halt the progression of scarring trachoma due to an incomplete understanding of
262 r for episiotomy, and for multiparous women, scarred uterus and multiple pregnancies were risk factor
263 gly correlated with manual quantification of scar volume (r = 0.82-0.99, P < .001) and %LGE (r = 0.90
264 compared with 3D CNN, 2D CNN underestimated scar volume (r = 0.85, P < .001) and %LGE (r = 0.83, P <
265 ardiac MRI late gadolinium enhancement (LGE) scar volume is an important marker for outcome predictio
266 monstrated excellent correlation with manual scar volume quantification (r = 0.88, P < .001) and rati
267 tification (r = 0.88, P < .001) and ratio of scar volume to total left ventricle myocardial volume (%
268 st and accurate quantification of myocardial scar volume, outperforms a two-dimensional convolutional
269 the unambiguous external features of a fire scar was collected for analysis of its fossilized wood.
272 ches 37% of the amplitude at the edge of the scar, was 0.48 +/- 0.04 mm (n = 11) in the scar of the b
276 CKAP1 subunit of the pentameric cytoskeletal SCAR/WAVE complex, a major downstream target of RAC1, in
277 te how API, a SCAR2 protein component of the SCAR/WAVE complex, controls the root cell wall architect
278 ods and patches of phosphorylation-deficient Scar/WAVE last substantially longer in mutants, altering
279 Phosphorylation-deficient or phosphomimetic Scar/WAVE mutants are both normally functional and rescu
283 ant than extracellular signals at regulating Scar/WAVE's activity and that phosphorylation acts as a
285 nt modifications of the cell wall, driven by SCAR/WAVE, are important in balancing cell wall developm
289 uble coxsackievirus and adenovirus receptor (sCAR) were similar with and without FBS, but FBS amplifi
290 findings contrast with the current model of scarring, whereby collagen deposition is exclusively att
292 Adduction deficits indicate a stretched scar, which must be treated with resection and advanceme
294 o cells expressing phosphorylation-deficient Scar, with longer-lived pseudopods and patches of Scar r
296 3A)-responsive cells in driving trachomatous scarring, with potential key mechanistic roles for PDGFB
297 dentifies a trend between COMT genotype with scarring, with rs4680 genetic variation constituting an
298 ealing (ie, full epithelialisation or stable scar) without recurrence at 52 weeks after start of anti
299 rate instead of only repairing wounds with a scar, without perturbing development and homeostasis.