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1 bstrate junctions with no apparent effect on traction.
2 ts to discover inhibitors have gained little traction.
3 al epiretinal membranes and/or vitreomacular traction.
4 ially in those without obvious vitreomacular traction.
5 ernal rounding forces and cell-intercalation traction.
6 change currently have considerable political traction.
7 the cohorts with and those without worsening traction.
8 ithout the need to explicitly determine cell tractions.
9 of variations in matrix stiffness with cell tractions.
10 ting both individual and collective cellular tractions.
11 contractile, protrusive, and circumferential tractions.
13 spite treatment (3 eyes), the development of traction (5 eyes), and the development of a dense vitreo
14 s (57.1%), vasculitis (57.1%), vitreoretinal traction (57.1%), and chronic macular edema (ME) (71.4%)
15 roduced by actin polymerization can generate traction across the plasma membrane by transmission thro
18 noninvasive species has gained considerable traction, although few studies extend this hypothesis to
20 hanced iOCT imaging revealed strong vitreous traction and adhesion above the macula and optic disc.
21 al was to determine if 2 widely used midline-traction and bilateral-thrust OA designs differ in effec
22 was developed to evaluate the vitreoretinal traction and determine whether the distribution of force
24 is verified experimentally by comparing cell traction and F-actin retrograde flow for two cell types
26 c retinopathy, vitreous hemorrhage, combined traction and rhegmatogenous retinal detachment, or lens
27 wed ILM reattachment with release of retinal traction and the development of severe diffuse retinal a
28 ever, this theory failed to gain substantial traction and was largely disregarded by the AD research
32 ived from stem cells have gained significant traction as 3D models of central nervous system (CNS) re
34 criptomic, and epigenomic changes and gained traction as a significant tool capable of accelerating d
36 ptical coherence tomography (OCT) has gained traction as an important adjunct for clinical decision m
37 ime correlated random walks" are now gaining traction as models of scale-finite animal movement patte
38 ssive loss of protrusive and circumferential tractions, as well as the formation of localized contrac
40 hree-dimensional displacement and 3D surface tractions at high spatial frequency from epifluorescence
41 M) revealed that cells produced the greatest tractions at the cell periphery, where distinct types of
42 forces in motile tissues and show that such traction-based stresses match those calculated from inst
43 ith bronchiectasis due to cystic fibrosis or traction bronchiectasis associated with another respirat
44 intralobular lines, lobular distortion, and traction bronchiectasis may occur as the illness evolves
45 clinical practice who had possible UIP with traction bronchiectasis on HRCT and had not undergone su
46 f nintedanib if they had honeycombing and/or traction bronchiectasis plus reticulation, without atypi
47 lar profiling technologies are gaining rapid traction, but the manual process by which resulting cell
49 thick stage 3 membranes with anteroposterior traction concerning for progression to stage 4 ROP (3 ey
53 this study was to evaluate the extension and traction effects of posterior vitreous detachment (PVD)
54 hole diameter and presence of vitreomacular traction, epiretinal membrane (ERM), and cystoid macular
59 engage with multiple ligands and to provide traction for emigration into diverse organs in distant p
61 al cells on stiff substrates decreased their traction force (from 300 nN to 100 nN) and spread area (
62 ls with inhibited myosin II motors increased traction force (from 41 nN to 63 nN) and slightly reorie
63 , to our knowledge, a novel method to assess traction force after long-term (24 h) uniaxial or biaxia
64 stretch, the cells had similar decreases in traction force and area and reoriented perpendicular to
66 study, we examined the relationship between traction force and vinculin-paxillin localization to sin
67 However, the study of how cell-generated traction force changes in response to stretch is general
68 d moment analysis, our results revealed that traction force dominates in regulating cell active trans
69 hanism by which FN fibril assembly regulates traction force dynamics in response to mechanical stimul
71 model that predicts the dynamics of cellular traction force generation and subsequent assembly of fib
72 he talin rod R3 subdomain decreases cellular traction force generation, which affects talin and vincu
76 dity promotes myosin II activity to increase traction force in a process negatively regulated by trop
77 HspB1 is recruited to sites of increased traction force in cells geometrically constrained on mic
78 combined results indicate that the change in traction force in response to external cyclic stretch is
79 to determine how cells actively alter their traction force in response to long-term physiological cy
80 dies introduce a new model for regulation of traction force in which local actin assembly forces buff
81 ubsequently leads to the engagement with the traction force machinery and focal adhesion maturation.
82 and paxillin FA area did not correlate with traction force magnitudes at single FAs, and this was co
89 escence images are generally not used for 3D traction force microscopy (TFM) experiments due to limit
95 e whole-mount imaging, genetic ablation, and traction force microscopy and atomic force microscopy, w
96 igh nuclear tension that matches trends from traction force microscopy and from increased lamin-A,C.
100 combination with cell migration analysis and traction force microscopy shows a wide-range of applicab
102 netic control of RhoA, live-cell imaging and traction force microscopy to investigate the dynamics of
105 vinculin localization at the cell membrane, traction force microscopy, and phosphorylated myosin lig
107 l, we describe stimulated emission depletion traction force microscopy-STED-TFM (STFM), which allows
111 t PKC activity is necessary for increases in traction force normally associated with these growth res
112 ative implementation of a new TFM technique: traction force optical coherence microscopy (TF-OCM).
114 e reciprocal effects facilitate increases in traction force production in domains exhibiting decrease
116 cells cultured on soft gels increased their traction force significantly, from 15 nN to 45 nN, doubl
117 stent rise in the radial component of inward traction force signifies successful actin-cable segment
120 of NM-II into actin stress fiber provides a traction force to promote actin retrograde flow and foca
121 ess (1100 nN) and exhibited a larger drop in traction force with uniaxial stretch, but the percentage
127 ine both the intercellular and extracellular traction forces acting on individual cells within an end
128 reduces the ability of PSCs to generate high traction forces and adapt to extracellular mechanical cu
130 h monolayers exhibit oscillatory patterns of traction forces and intercellular stresses that tend to
131 e tumor cells exert higher integrin-mediated traction forces at the bulk and molecular levels, consis
134 y a mechanism where cell migration regulates traction forces by promoting dynamic turnover of focal a
136 ocal mechanical forces, I show that cellular traction forces exhibit stick-slip dynamics resulting in
137 twork stiffness, which in turn augmented the traction forces generated by human adipose stem cells (h
139 n of the E413K mutant desmin also alters the traction forces generation of single myoblasts lacking o
142 tribution of cellular stresses from measured traction forces in motile tissues and show that such tra
143 We mapped the orientation of integrin-based traction forces in mouse fibroblasts and human platelets
144 us studies, cell spread area, alignment, and traction forces increase, whereas apoptotic activity dec
145 iderable variability in measurements of cell-traction forces indicates that they may not be the optim
146 (intercellular) and cell-ECM (extracellular) traction forces individually and cooperatively regulate
147 ges in length and spatiotemporal dynamics of traction forces measured in chemotaxing unicellular amoe
148 s of cell migration speeds, cell shapes, and traction forces measured simultaneously with fields of m
149 ermined the three-dimensional spatiotemporal traction forces of motile neutrophils at unprecedented r
150 their actin cytoskeletons in order to exert traction forces on and move directionally over the dermi
151 ing wild-type tandem pairs, each cell exerts traction forces on stationary sites ( approximately 80%
153 lts suggest the profound impacts of cellular traction forces on their host ECM during development and
156 ility of soft elastomer substrates to resist traction forces rather than a lack of sufficient tractio
157 ound that U251 cells are capable of exerting traction forces that locally pull on their environment,
158 tment of actin and myosin but also increased traction forces that rapidly propagate across the cell v
159 latform is described that harnesses cellular traction forces to activate growth factors, eliminating
162 d on a surface or to crawl, cells must apply traction forces to the underlying substrate via adhesion
165 e computational method allowing inference of traction forces with high sensitivity directly from the
166 lity of this method to correlatively overlap traction forces with spatial localization of proteins re
167 behaviors and parameters (e.g., adhesion and traction forces) to the collective migration of small gr
168 symmetric distribution of basal protrusions, traction forces, and apical aspect ratios that decreased
169 usly measured the cytoskeleton organization, traction forces, and cell-rigidity responses at both the
170 ons where associated changes in cell shapes, traction forces, and migration velocities have yet to pe
173 antly and irreversibly remodeled by cellular traction forces, as well as by macroscopic strains.
174 eases cytoskeletal remodeling, intracellular traction forces, cell migration and invasion, and anchor
176 that was associated with reduced cell-matrix traction forces, decreased levels of integrin beta1 and
177 n over a substrate by generating alternating traction forces, of up to 1.4 kPa, at each flank of the
178 ayers on stiffer substrates showed increased traction forces, vinculin at the cell membrane, and vinc
179 or receptor alpha-mediated contractility and traction forces, which are transduced to Fn through alph
180 in driving polarized motility and generating traction forces, yet little is known about how tension b
190 owever, most ice-sheet models estimate basal traction from satellite-derived surface velocity, withou
191 rporating gravitational potential energy and tractions from plate motions or relative mantle flow, su
192 We demonstrate this technique by measuring tractions generated by both single human neutrophils and
193 n (HFR) as well as movement trajectories and traction generation of individual HPCs, we find that the
196 Twitching bacterial groups also produce traction hotspots, but with forces around 100 pN that fl
198 ution, these technologies are likely to gain traction in cutaneous oncology research and practice.
199 -like receptor 9 (TLR9) agonists have gained traction in recent years as potential adjuvants for the
201 gamification" of science has gained a lot of traction in recent years, and games that convey scientif
202 ch to decreasing cancer mortality has gained traction in recent years, evidenced by its inclusion in
204 n, we find that individual cells exert local traction in small hotspots with forces on the order of 5
205 -drug conjugates (ADCs) have recently gained traction in the biomedical community due to their promis
209 mpact of microbes on plants have gained much traction in the research literature, supporting diverse
210 hed sensitivity to schizophrenia have gained traction in the study of CHR-P and its clinical outcomes
213 iting membrane (ILM) detachment with retinal traction, in association with other specific changes in
214 c vitreomacular adhesion (VMA)/vitreomacular traction, including full-thickness macular hole (FTMH).
215 d 2.1 can control intracellular pressure and traction independently, suggesting these myosin II-depen
216 auses a rapid and local increase in cellular traction, intercellular tension and tissue compaction.
219 of foveal detachment in patients with myopic traction maculopathy without posterior vitreous detachme
220 d with PVD can occur in cases of high myopic traction maculopathy, especially in those without obviou
221 xerted on the substrate was used to generate traction maps (along the cell-substrate interface).
223 istance or remodeled fibers at a distance by traction-mediated reorientation or aligned deposition ga
225 lectively, elongate substantially, and exert tractions more forcefully compared with cells many ranks
227 cystoid retinal edema (n = 6; 13%), retinal traction (n = 11; 23%), intralesional cavities (n = 28;
229 g budding yeast to gain temporal and genetic traction on crossover regulation, we find that MutLgamma
236 ultrasonography and OCT revealed persistent traction on the retinal tear flap in 19 and 15 eyes, res
237 lacements and both in-plane and out-of-plane tractions on nominally planar transparent materials usin
238 reatment of retinoblastoma and may result in traction or rhegmatogenous retinal detachment along with
239 sistent despite CS or in case of threatening traction or visually significant epimacular membrane (28
240 nce of vitreomacular adhesion, vitreomacular traction, or epiretinal membrane; (3) presence, location
243 growth and maturation thus culminate with FA traction oscillation to drive efficient FA mechanosensin
248 pathic Epiretinal Membrane and Vitreomacular Traction Preferred Practice Pattern(R) (PPP) guidelines,
249 PATHIC EPIRETINAL MEMBRANE AND VITREOMACULAR TRACTION PREFERRED PRACTICE PATTERN(R) GUIDELINES: New e
250 pontaneous resolution (defined by release of traction), progression to full-thickness macular hole, a
253 , or RhoA overexpression caused increases in traction reported by TM and stiffness reported by sharp-
254 ) of vimentin in MEFs caused a diminution of traction reported by TM, as well as stiffness reported b
256 lly perturbed by using drugs, biasing toward traction signatures of different epithelial or mesenchym
257 the dependence on substrate stiffness of the tractions' spatial distribution, contractile moment of t
258 to provide truly quantitative forecasts for traction stress, a far more detailed description of inte
260 strate that the cytoskeletal stiffness, cell traction stress, and focal adhesion area were significan
264 microscopy (TFM) was used to establish that traction stresses are limited primarily to leading edge
265 rphology, as well as to quantify the dynamic traction stresses exerted by cells under different exper
266 monolayer stress from measurements of the 3D traction stresses exerted by the cells on a flexible sub
267 the spatial and temporal evolution of the 3D traction stresses generated by the leukocytes and VECs t
268 ) with antisense morpholinos results in high traction stresses in follower row cells, misdirected pro
269 ment, consequently orchestrating anisotropic traction stresses that drive cell orientation and direct
270 tional description for the various levels of traction stresses that have been reported and of the eff
271 cell motility is to govern the alignment of traction stresses that permit single-cell migration.
273 n subendothelial stiffness by increasing the traction stresses they exert on stiffer as compared to s
277 developed by the International Vitreomacular Traction Study Group by 2 independent masked observers.
279 examine the natural history of vitreomacular traction syndrome (VMTS) in the absence of other ocular
285 part of the 19(th) century, but did not gain traction until the introduction of the Schiotz tonometer
288 ent the management options for vitreomacular traction (VMT) and to recommend an individualized approa
289 f participants were graded for vitreomacular traction (VMT), macular hole (MH), and epiretinal membra
290 ation, and real-time deformability, and cell traction was measured using two-dimensional and micropos
294 ration of adhesion complexes and actin fiber traction, whereas the fast amoeboid mode, observed exclu
295 e of MGS is caused primarily by the vitreous traction with further possible formation of the retinal
296 domized crossover trial using either midline-traction with restricted mouth opening (MR) or bilateral
297 hanges (9 eyes, 69.2%), including tangential traction with temporal vessel straightening concerning f
300 Ex vivo measurements of such multicellular tractions within three-dimensional (3D) biomaterials cou
301 %), media opacity without RD (28%), vitreous traction without RD (11%), intraocular foreign body (5%)