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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.
12       One eye showed increased vitreomacular traction (3 months).
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
16 lyzing the spatiotemporal evolution of their traction adhesions (TAs).
17                                    Worsening traction after treatment was defined as the occurrence w
18  noninvasive species has gained considerable traction, although few studies extend this hypothesis to
19                    One eye had vitreomacular traction and a remote history of blunt trauma.
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
23  dynamics, thus increasing cell motility and traction and enabling chemotaxis.
24 is verified experimentally by comparing cell traction and F-actin retrograde flow for two cell types
25                                        Using traction and monolayer stress microscopy, we show that S
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
29 rylation and the CSD promotes focal adhesion traction and, thereby, cancer cell motility.
30 -related macular degeneration, vitreomacular traction, and cystoid macular edema.
31 densation ridge-like interface with residual traction, and premature vitreous syneresis.
32 ived from stem cells have gained significant traction as 3D models of central nervous system (CNS) re
33                        Ultrasound is gaining traction as a neuromodulation method due to its ability
34 criptomic, and epigenomic changes and gained traction as a significant tool capable of accelerating d
35             Exon skipping by ASOs is gaining traction as a therapeutic strategy, and the use of ASOs
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
39 owed gliosis, foveal involvement, or retinal traction at 1-year follow-up.
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
48 patterns supporting a potential mechanism of traction by Muller cells in the CB.
49 thick stage 3 membranes with anteroposterior traction concerning for progression to stage 4 ROP (3 ey
50 acting rheological information directly from traction data.
51 lute, turbulent, supercritical flows causing traction-dominated deposition.
52      We discovered that the insects produced traction during the acceleration phase by piercing these
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
55                                              Traction exerted on the substrate was used to generate t
56 quisition of continuous in- and out-of-plane traction fields with high sensitivity.
57  3D full-field stress and strain and surface traction fields.
58 s mediate adhesive interactions that provide traction for cell migration.
59  engage with multiple ligands and to provide traction for emigration into diverse organs in distant p
60 such as tumor-educated platelets are gaining traction for the detection of early-stage tumors.
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
65 g network, simulations predict the resulting traction force and FN fibril formation.
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
70                                  We measured traction force generation and also performed gene expres
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
73 range over which FAs can accurately adapt to traction force generation.
74 , with reduced YAP/TAZ nuclear shuttling and traction force generation.
75 tion forces rather than a lack of sufficient traction force generation.
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
83              Across a variety of cell types, traction force measurements revealed a relationship betw
84      In this article, we present single-cell traction force measurements using breast tumor cells emb
85 ments provided results consistent with total traction force measurements.
86      Conventional force-to-strain based cell traction force microscopies have low resolution which is
87                   Cell traction recorded via traction force microscopy (TFM) commonly takes place on
88                                              Traction force microscopy (TFM) enables determination of
89 escence images are generally not used for 3D traction force microscopy (TFM) experiments due to limit
90                                              Traction force microscopy (TFM) has been instrumental fo
91                                              Traction force microscopy (TFM) is a family of methods u
92                                              Traction force microscopy (TFM) revealed that cells prod
93                                              Traction force microscopy (TFM) was used to establish th
94                      Using three-dimensional traction force microscopy and a double hydrogel sandwich
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.
97                                              Traction force microscopy and time-lapse imaging reveal
98                      While three-dimensional traction force microscopy for single cells in a nonlinea
99                                              Traction force microscopy revealed that tumor-associated
100 combination with cell migration analysis and traction force microscopy shows a wide-range of applicab
101                                              Traction force microscopy shows that lowering cholestero
102 netic control of RhoA, live-cell imaging and traction force microscopy to investigate the dynamics of
103       These cell forces can be measured with traction force microscopy which inverts the equations of
104 mp recording, phase contrast microscopy, and traction force microscopy).
105  vinculin localization at the cell membrane, traction force microscopy, and phosphorylated myosin lig
106                                        Using traction force microscopy, we show that cells exert sign
107 l, we describe stimulated emission depletion traction force microscopy-STED-TFM (STFM), which allows
108 ed using two-dimensional and micropost-based traction force microscopy.
109        This question is addressed here using traction force microscopy.
110 e compared to experimental maps obtained via traction force microscopy.
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).
113                       Our model captures the traction force patterns of small clusters of nonmotile c
114 e reciprocal effects facilitate increases in traction force production in domains exhibiting decrease
115 at may be responsible for the variability in traction force production.
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
118 ation, increased focal adhesions, and higher traction force than controls.
119 icity of the FA structure and the associated traction force to accurately sense ECM stiffness.
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
122  actin filament density, sudden decreases in traction force, and neurite retraction.
123 firm that Tpm 2.1 is a negative regulator of traction force.
124 ocal adhesion formation, cell spreading, and traction-force generation.
125 ariety of migration modes relying on diverse traction-force-generation mechanisms.
126                                     Cellular traction forces (CTFs) play an integral role in both phy
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
129 ntly and irreversibly remodelled by cellular traction forces and by macroscopic strains.
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
132 und circular obstacles, and CIL accounts for traction forces at the edge.
133 ed of motion and magnitude of the associated traction forces at the level of a single cell.
134 y a mechanism where cell migration regulates traction forces by promoting dynamic turnover of focal a
135 rin-mediated adhesion accompanied by reduced traction forces exerted through these structures.
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
138                         Here, we report that traction forces generated by T cells are regulated by dy
139 n of the E413K mutant desmin also alters the traction forces generation of single myoblasts lacking o
140 ally and temporally correlated with cellular traction forces in migrating cells.
141 mosomal protein regulates actin dynamics and traction forces in motile keratinocytes.
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%
152                Indeed, the magnitude of cell traction forces on the underlying extracellular matrix i
153 lts suggest the profound impacts of cellular traction forces on their host ECM during development and
154                               Strikingly, FA traction forces oscillate in time and space, and govern
155                    When actomyosin-dependent traction forces overcome substrate resistance, platelets
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
160 hich cells exert actin cytoskeleton-mediated traction forces to sense the ECM stiffness.
161 ver, these are largely deficient in exerting traction forces to the matrix.
162 d on a surface or to crawl, cells must apply traction forces to the underlying substrate via adhesion
163 ansion and contraction and apply coordinated traction forces to their environment.
164                                         Cell traction forces transmitted by FAs and integrin tensions
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
171 RhoA activation, decreased contractility and traction forces, and reduced metastasis.
172 including molecular binding strengths, local traction forces, and viscoelastic properties.
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
175                     Specifically, we measure traction forces, cell morphology, and invasiveness of MD
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
181 n (alpha-SMA) expression, and exerted larger traction forces.
182 n of existing focal adhesions and associated traction forces.
183 ower tension within the network, and smaller traction forces.
184 ate characterized by a broad distribution of traction forces.
185  are known that depend on substrate-mediated traction forces.
186 ckdown led to higher than normal tension and traction forces.
187 ess dynamic, and more peripherally localized traction forces.
188 rate of cellular proliferation, and cellular tractions forces.
189 yes with DME irrespective of the presence of traction formation imaged by SDOCT.
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
194                  Cell migration initiates by traction generation through reciprocal actomyosin tensio
195                                The resulting traction gradient within the growing FA favors SF format
196      Twitching bacterial groups also produce traction hotspots, but with forces around 100 pN that fl
197        Laser treatment resulted in worsening traction in a substantial proportion of eyes with FEVR.
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
200            A theory that has gained a lot of traction in recent years suggests that multi-scale integ
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
203  is one approach that has gained significant traction in recent years.
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
206                       Amyloid PET is gaining traction in the clinical arena, but validity and cost-ef
207 reality (VR) is a technology that is gaining traction in the consumer market.
208              This pursuit has recently found traction in the field of optomechanics in which a mechan
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
211 terfering RNAs (siRNA) and microRNAs gaining traction in the therapeutic market.
212                                              Traction in unraveling new and diverse classes of molecu
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.
217                                     However, traction is amplified approximately fivefold in groups.
218 = 1), and progressive vasoproliferation with traction leading to phthisis (n = 2).
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).
222                             However, past 3D traction measurements have been low throughput due to th
223 istance or remodeled fibers at a distance by traction-mediated reorientation or aligned deposition ga
224 l magnetic twisting cytometry (OMTC), and 4) traction microscopy (TM).
225 lectively, elongate substantially, and exert tractions more forcefully compared with cells many ranks
226  resonance (MR) imaging (MR arthrography and traction MR arthrography).
227  cystoid retinal edema (n = 6; 13%), retinal traction (n = 11; 23%), intralesional cavities (n = 28;
228                   None of the cases involved traction of the vitreomacular interface or posterior vit
229 g budding yeast to gain temporal and genetic traction on crossover regulation, we find that MutLgamma
230 ar tuft on the optic nerve head with induced traction on superior arcade was visible.
231         These actuators have recently gained traction on the one hand due to the technology push from
232        No preoperative evidence for vitreous traction on the optic disc or macula was seen in any eye
233 s are isolated, gliding produces low average traction on the order of 1 Pa.
234 of white vascularized tissue with associated traction on the retina and sometimes hemorrhage.
235         Retinal tear location and persistent traction on the retinal flap was evaluated with B-scan u
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
241        However, precisely how and why the FA traction oscillates is unknown.
242               This underpins the observed FA traction oscillation and, importantly, broadens the ECM
243 growth and maturation thus culminate with FA traction oscillation to drive efficient FA mechanosensin
244 her stabilizes the FA and generates a second traction peak near the center of the FA.
245 oximal growth of the FA and contributes to a traction peak near the FA's distal tip.
246 tomyosin contractility, resulting in central traction peak oscillation.
247    It has been postulated that vitreoretinal traction plays a major role in the retinal findings.
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
251                                         Cell traction recorded via traction force microscopy (TFM) co
252 asmin injection, which may be due to retinal traction release.
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
255 (9 eyes), neovascular glaucoma (5 eyes), and traction retinal detachment (4 eyes).
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
259 fibroblasts impedes enhanced cell spreading, traction stress, and fibronectin fiber formation.
260 strate that the cytoskeletal stiffness, cell traction stress, and focal adhesion area were significan
261 tributes to the net development of force and traction stress.
262 e manner of how we evaluate the magnitude of traction stress.
263 organizing the distribution and size of high-traction-stress regions at the cell periphery.
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.
272 e levels expected along the train and on the traction stresses they create at the substrate.
273 n subendothelial stiffness by increasing the traction stresses they exert on stiffer as compared to s
274 s TGF-beta2 expression and their cell-matrix traction stresses.
275 r, subject to external loads given by the 3D traction stresses.
276  required for the anisotropic orientation of traction stresses.
277 developed by the International Vitreomacular Traction Study Group by 2 independent masked observers.
278 according to the International Vitreomacular Traction Study Group.
279 examine the natural history of vitreomacular traction syndrome (VMTS) in the absence of other ocular
280                  Patients with vitreomacular traction syndrome, secondary ERM, or both were excluded.
281                                          The traction test (inverted grid with mice clinging to the u
282 at includes robust parameterisation of basal traction, the resistance to ice flow at the bed.
283 d PDR with persistent NVs and no evidence of traction to achieve regression of neovessels.
284 ave no single dominant element is giving new traction to materials discovery.
285 part of the 19(th) century, but did not gain traction until the introduction of the Schiotz tonometer
286  (FAZ) in eyes with idiopathic vitreomacular traction (VMT) after ocriplasmin injection.
287 y of patients with symptomatic vitreomacular traction (VMT) after Ocriplasmin treatment.
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
291                                      Fascial traction was used in more than 75% of cases.
292    Patients with any degree of vitreomacular traction were excluded from the analysis.
293        Epiretinal membrane and vitreomacular traction were the most common artifacts.
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
298 ll as the formation of localized contractile tractions with elongated cluster morphologies.
299 wever, HMMs have only recently begun to gain traction within the broader ecological community.
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%)

 
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