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1                                  To evaluate vascular abnormalities at superficial (SCP) and deep (DC
2 perforation, device dislocation, and femoral vascular access site complications.
3 cardiovascular events, hospitalizations, and vascular access thrombosis, respectively.
4 s an individualized approach to hemodialysis vascular access, on the basis of each patient's unique b
5               The links between cellular and vascular ageing reflect a complex interaction between ge
6  suggest that the links between cellular and vascular ageing reflect a complex interaction between ge
7  Thus, Ets transcription factors specify non-vascular, amniotic cells to EC-like cells, whereas Sox17
8  bone microstructure, including the sizes of vascular and lacunar (cellular) spaces, provide useful i
9                                         Both vascular and neurological aetiologies of this pain have
10 wound duration and type of surgery (general, vascular and orthopaedic).
11 gh renal actions involving increased GFR and vascular and tubular effects.
12                      Ninety-day quantitative vascular angiography results showed a lower percent diam
13 atomical mapping, the complete evaluation of vascular anomalies includes hemodynamic characterization
14 viewed include cholestatic diseases, tumors, vascular anomalies, and acquired diseases.
15  entity, referred to as perifoveal exudative vascular anomalous complex (PEVAC) by describing multimo
16 smembrane receptor NOTCH1 directly regulates vascular barrier function through a non-canonical, trans
17 in-2 levels in endothelial cells compromises vascular barrier function.
18 in EC, was not anticipated to have a role in vascular barrier.
19  differentially expressed in tissue-specific vascular beds, but its expression is induced in hematopo
20 current understanding of neuroprotection and vascular biology in general.
21                                              Vascular brain injury results in loss of structural and
22 a novel mechanism by which laminins modulate vascular branching and endothelial cell proliferation du
23 rficial vascular plexus and consequently the vascular branching density is increased.
24  across all seven hierarchical orders of the vascular branching.
25 o strong confidence in the ability to assess vascular calcific morphology in all studies with complem
26                          The extent to which vascular calcification is reversible and the possible me
27 sents an extreme model for arteriosclerosis, vascular calcification, and bone disorders, all of which
28 ship between both static and dynamic retinal vascular caliber and the severity of obstructive sleep a
29 layers of the skin, the root endodermis, the vascular cambium and the epidermis of the stem.
30                             The plexuses are vascular, carry erythrocytes, are enclosed within a base
31 le tumor necrosis factor receptor-1, soluble vascular cell adhesion molecule-1, granulocyte colony-st
32                                Periostin and vascular cell adhesion protein 1 (VCAM-1), molecules tha
33 a novel KIT D816V-dependent key regulator of vascular cell migration and angiogenesis in SM.
34 noceptor expressions within 5 hours in human vascular cells in a nuclear factor-kappaB pathway-depend
35                                  To evaluate vascular cells, von Willebrand factor (vWF) and vascular
36 nnexin43, a major known gap junction unit in vascular cells.
37 findings in AMN, with attention to choroidal vascular changes.
38 orting its potential use in the treatment of vascular cognitive impairment.
39 es vessel growth in the infundibulum, aiding vascular communication among the PT, PD, and brain.
40 (3.57% to 2.15%), bleeding (9.56% to 5.08%), vascular complications (6.11% to 4.20%), and stroke (2.0
41 e (Lotus, 1.5%; ES3, 2.1%; P=0.62), or major vascular complications (Lotus, 2.9%; ES3, 2.4%; P=0.69).
42  long-term outcome and prognosis factors for vascular complications in patients with TA.
43 cally study transfusion-associated pulmonary vascular complications in susceptible patient population
44          Diabetic nephropathy (DN) is one of vascular complications of diabetes and is caused by abno
45 irs inflammation and progression of diabetic vascular complications, cardiovascular disease (CVD), an
46 thophysiological aspects of diabetes-related vascular complications.
47 ediating adverse effects to the neuronal and vascular components of the retina.
48 d with the reduction in both its stromal and vascular components.
49 gesting interstitial hypertension results in vascular compression and decreased molecular delivery in
50 ous occlusion plethysmography) and cutaneous vascular conductance (CVC, laser-Doppler) were measured
51 oppler ultrasound) and calculated changes in vascular conductance (FVC) to intra-arterial infusion of
52     Cardiac output (thermodilution), forearm vascular conductance (FVC, venous occlusion plethysmogra
53 ulation of Gq/11-evoked Ca(2+) signaling and vascular contraction.
54  ejection fraction (P=0.045) and ventricular-vascular coupling ratio (P=0.042).
55                      We examined the role of vascular CXCR4 in atherosclerosis and plaque composition
56 dualized NK cell-targeted therapies to limit vascular damage in highly responsive sensitized patients
57 ts, MI, stroke or transient ischemic attack, vascular deaths, and major vascular events as defined by
58 2 knockouts phenocopy blood and/or lymphatic vascular defects seen in Fgfr1/Fgfr3 double mutant mice,
59 veral of these mutants also display yolk sac vascular defects, suggesting a role for thrombin signali
60 e two drugs effectively attenuate neural and vascular deficits in chronic and acute mouse models of C
61 = 1.11 [1.03-1.19], p = 0.0044) and mixed or vascular dementia (HR = 1.21 [1.04-1.41], p = 0.0163).
62 loid PET analysis, especially in subcortical vascular dementia (SVaD) patients.
63           Diagnoses of Alzheimer disease and vascular dementia were secondary outcome measures.
64 hippocampus and corpus callosum in rats with vascular dementia.
65 ery occlusion (BCCAO) was used as a model of vascular dementia.
66 tral nervous system injury in a rat model of vascular dementia.
67 y contribute to early cognitive decline and (vascular) dementia.
68 sed growth was associated with reductions in vascular density and branching suggestive of vessel norm
69          Furthermore, loss of AIBP increased vascular density and facilitated the recovery of blood v
70 tinal thickness measurements correlated with vascular density of the fovea, parafovea, and temporal a
71  by reducing liver metastatic colony growth, vascular density, and branching.
72 ntrol GATA4 exercises over specialized liver vascular development and function.
73 that are believed to play important roles in vascular development and stability.
74  cytokine biosynthesis, and angiogenesis and vascular development in (adjusted P<0.1).
75                   Many genes associated with vascular development in other species show enriched expr
76 gh the importance of neuronal progenitors in vascular development within the CNS is well recognized,
77  cell (SMC) differentiation is essential for vascular development, and TGF-beta signaling plays a cri
78 logical responses, the involvement of EVs in vascular development, growth, and maturation has been wi
79 ad range of investigations of mural cells in vascular development, neurovascular coupling and neuropa
80  cuticle formation and epidermal patterning, vascular development, programmed cell death, organ absci
81 cs have led to a deeper understanding of how vascular disease affects cognition.
82                             Atherothrombotic vascular disease is often triggered by a distinct type o
83 )] and greater odds of large-vessel cerebral vascular disease or history of cardiovascular disease bu
84 des insights into the influence of pulmonary vascular disease, spontaneous respiration and dynamic st
85             In 2 young children with retinal vascular disease, the MIOCTA images showed more detailed
86 cardiometabolic risk factors and subtypes of vascular disease, thereby suggesting differing roles in
87 now More Than We Can Tell About Diabetes and Vascular Disease," on Sunday, 12 June 2016.Diabetes is a
88 l cells, this phenomenon might contribute to vascular disease.
89 elopment of TAAD and proliferative occlusive vascular disease.
90 erating room for young children with retinal vascular disease.
91 rtant atheroprotective potential in diabetic vascular disease.
92 or an anti-inflammatory approach in diabetic vascular disease.
93 ntribute to different VSMC behavior and thus vascular disease.
94 ism (PE) is a serious and prevalent cause of vascular disease.
95 ease but lower odds of small-vessel cerebral vascular disease.
96 om the ADVANCE study (Action in Diabetes and Vascular Disease: Peterax and Diamicron MR Controlled Ev
97                                      Retinal vascular diseases are among the leading causes of acquir
98 lar inflammation and associated inflammatory vascular diseases are not well defined.
99 rged as a significant contributor to retinal-vascular diseases in the previous 2 decades.
100 te the PHACTR1 locus (6p24) in risk for five vascular diseases, including coronary artery disease, mi
101 rtension, stroke, myocardial infarction, and vascular diseases.
102 ammation in a target organ (eg, the skin) on vascular diseases.
103 n inflammation (eg, in the skin) may improve vascular diseases; however, randomized clinical trials a
104 proves endothelial Fli1 deficiency-dependent vascular disintegrity, implying its potential as a disea
105 rrier function and to the development of the vascular disorder Cerebral Cavernous Malformation (CCM).
106 striction, two abnormalities contributing to vascular dysfunction.
107 opulation as well as the adverse cardiac and vascular effects of MM itself.
108  co-localized and co-immunoprecipitated with vascular endothelial cadherin-based complexes, including
109 se BRB disintegration, it sensitizes retinal vascular endothelial cells (ECs) to VEGF-A, leading to u
110 pression of Slco2a1 in the tumour-associated vascular endothelial cells.
111 ures, tumor microvascular density (MVD), and vascular endothelial growth factor (VEGF) expression) fr
112                                              Vascular endothelial growth factor (VEGF) is implicated
113  of CCN1 as a negative feedback regulator of vascular endothelial growth factor (VEGF) receptor activ
114                             We also show how vascular endothelial growth factor (VEGF) regulates PRKC
115                        Because deficiency of vascular endothelial growth factor (VEGF) results in thr
116 r data further demonstrate the importance of Vascular Endothelial Growth Factor (VEGF) secretion for
117 ous signaling transducers and isoforms along vascular endothelial growth factor (VEGF) signaling path
118                                         Anti-vascular endothelial growth factor (VEGF) therapy has de
119  stromal cell-derived factor 1 (SDF-1alpha), vascular endothelial growth factor (VEGF), hypoxia-induc
120 ucible protein 10, interleukin (IL)-6, IL-8, vascular endothelial growth factor (VEGF), monocyte chem
121                                              Vascular endothelial growth factor (VEGF)-A has been imp
122          Alternate splicing in the exon-8 of vascular endothelial growth factor (VEGF)-A results in p
123 nhanced cell proliferation by regulating the vascular endothelial growth factor (VEGF)-A, VEGF-C, FGF
124 cular cells, von Willebrand factor (vWF) and vascular endothelial growth factor (VEGF)-C expression w
125                                              Vascular endothelial growth factor (VEGF)-D is capable o
126 esis of periodontal diseases, supported with vascular endothelial growth factor (VEGF-A) and tumor ne
127  cancer cells where it was shown to modulate vascular endothelial growth factor (VEGFR)-2 and epiderm
128               Inadequate tumor uptake of the vascular endothelial growth factor antibody bevacizumab
129                             Up-regulation of vascular endothelial growth factor enhances the therapeu
130                                              Vascular endothelial growth factor has emerged as a sign
131 sed HA levels and mesenchymal cells, but not vascular endothelial growth factor in Hyal2(-/-) embryon
132 ed patient experiences specific to receiving vascular endothelial growth factor inhibitors (anti-VEGF
133 have been raised that intravitreal dosing of vascular endothelial growth factor inhibitors in DME cou
134 amount of intervention requiring 1 or 2 anti-vascular endothelial growth factor injections only.
135 es including intravitreal injections of anti-vascular endothelial growth factor or verteporfin photod
136  niche formation (evidenced by a decrease in vascular endothelial growth factor receptor 1 positive (
137          To evaluate if the up-regulation of vascular endothelial growth factor strengthens the prote
138 iogenesis factors (fibroblast growth factor, vascular endothelial growth factor, and platelet-derived
139 s of TrpRS by enhancing its interaction with vascular endothelial-cadherin.
140 miR-204 protects against tunicamycin-induced vascular/endothelial ER stress, associated impairment of
141                                              Vascular endothelium activation and lymphocyte attractio
142 ular parameters for schizont adhesion to the vascular endothelium and to predict bond dynamics in the
143                                          The vascular endothelium is critical for induction of approp
144 nflammatory and anti-atherogenic molecule in vascular endothelium.
145 the retinal pigment epithelium (RPE), or the vascular endothelium.
146 ing in increased monocyte recruitment to the vascular endothelium.
147  All patients are alive and well with no new vascular events and resolution of hematological and immu
148  ischemic attack, vascular deaths, and major vascular events as defined by the Antiplatelet Trialists
149         Of 3096 acute cerebral or peripheral vascular events, 748 (24.2%) were AF-related.
150        Computational modeling evaluates drug vascular extravasation and diffusive transport as key RF
151                      Analysis of the stromal vascular fraction from periprostatic white adipose tissu
152 dative metabolism in animals and may enhance vascular function in humans.
153  nearby Sox consensus sites and enhances the vascular function of converted cells.
154 gh-fat (50 g total fat) meal on postprandial vascular function, as well as triglyceride, glucose, and
155 erties in endothelial cells is essential for vascular function.
156 rived cells confirmed its role in regulating vascular function.
157 obromine and caffeine, which may also affect vascular function.
158                  Hemodynamic forces regulate vascular functions.
159 onstrating that the enzymatically controlled vascular gateway specifically opens by cleavage of NPY b
160               Postcapillary PH with elevated vascular gradients and pulmonary vascular resistance def
161 of this study was to set up a mouse model of vascular graft infections that closely mimics the human
162 is the ability of cancerous cells to promote vascular growth, to disseminate and invade to distant or
163   We compared the biomechanical behavior and vascular healing profile of a novel thin-walled (115 mic
164 confirm a central role of Fli1 in regulating vascular homeostasis.
165                                 The proposed vascular image registration method based on network stru
166 uggest biventricular cardiac dysfunction and vascular impairment in baboons who were IUGR at birth be
167          The molecular mechanisms underlying vascular inflammation and associated inflammatory vascul
168 utrophils damage the endothelium, leading to vascular inflammation and necrosis.
169  urate hydroperoxide might be a key event in vascular inflammation, where there is large amount of ur
170 h as atherosclerosis, but the control of the vascular inflammatory state is still largely unclear.
171 odies, mTOR inhibition significantly reduced vascular injury, ERM phosphorylation, and macrophage inf
172 is one of the first lines of defence against vascular injury.
173  NPY2 and NPY5 receptor antagonists restored vascular integrity and limited HSPC mobilization, demons
174 n, which has been previously shown to affect vascular integrity and regenerative signaling, is here s
175 olecule targeted by many pathogens, promotes vascular interactions of the Lyme disease spirochete Bor
176  hypertrophic chondrocyte layer and impaired vascular invasion.
177 itional multimodal imaging did not show each vascular layer and any leakage in these cases.
178 ng of post-ischemic kidneys revealed reduced vascular leak with alphavbeta5 antibody treatment.
179 t, myeloperoxidase activity by luminescence, vascular leakage by fluorescence in vivo imaging, histop
180 re models, we show here that VEGF165-induced vascular leakage requires both VEGFR2 and NRP1, includin
181 urthermore, NE deletion prevents HFD-induced vascular leakage.
182 ed at the central nervous system, renal, and vascular levels, but the cell-specific role of Nox2 in B
183 the right ventricle adapts to the increasing vascular load by enhancing contractility ("coupling") to
184 hythm Disorders, Valvular Heart Disease, and Vascular Medicine (1-84).
185 here remain gaps in knowledge concerning how vascular morphology evolves during carcinogenesis.
186 red as a distinct area of hyperfluorescence (vascular network) in early to intermediate frames and as
187  of the major vessels of the trunk lymphatic vascular network, including the later-developing collate
188 eristics of polypoidal structures, branching vascular networks (BVNs), and origin of PCV using optica
189 ased approach to generate endothelialized 3D vascular networks within cell-laden hydrogel biomaterial
190 t its expression is induced in hematopoietic vascular niches after myelosuppressive injury.
191                     There was no increase in vascular occlusive events with tranexamic acid, with no
192                          Patients with extra-vascular OCTA signal identified on en face OCTA images w
193  subset of high-mortality inpatient general, vascular, or thoracic procedures.
194 pecimens collected during the Folic Acid for Vascular Outcome Reduction in Transplantation trial, we
195 e importance of p66Shc lysine acetylation in vascular oxidative stress and diabetic vascular pathophy
196                     Therefore, prevention of vascular oxidative stress and improvement of endothelial
197            TTP was inversely correlated with vascular patency and verteporfin uptake, suggesting inte
198  brain accumulation of aggregated amylin and vascular pathology in HIP rats.
199 on in vascular oxidative stress and diabetic vascular pathophysiology.
200 ease, the MIOCTA images showed more detailed vascular patterns than were visible on the fluorescein a
201  function, aggravated mucus production, peri-vascular, peri-bronchial, and allergic inflammation that
202                      Pathological changes in vascular permeability are driven by growth factors such
203 enhanced T1-weighted MRI, we determined that vascular permeability is not homogeneous but rather conf
204 EH inhibitor prevented the pericyte loss and vascular permeability that are characteristic of non-pro
205                   Dengue can cause increased vascular permeability that may lead to hypovolemic shock
206 of inflammatory cells in the lung, increased vascular permeability, and induced histologic ALI in nai
207 lity during IAV infection and show decreased vascular permeability, fewer pulmonary neutrophils, and
208  the blood-brain barrier (BBB) via increased vascular permeability, with the magnitude of changes dep
209 lies, which correspond to 33% of the 383,671 vascular plant species known worldwide.
210 uggest that horizontal gene transfer between vascular plants is not a rare event, that it is not nece
211 esponse to changes in light intensity and in vascular plants, is primarily triggered by a pH gradient
212 nated by extinct lineages of early-diverging vascular plants.
213  of the mitogenome in the common ancestor of vascular plants.
214                       To our knowledge, this vascular plasticity is unique among mammalian tissues, a
215 gamma3-null (Lamc3(-/-)) retinal superficial vascular plexus and consequently the vascular branching
216 ations make obestatin a promising target for vascular prevention in obesity and diabetes.
217 equisite to initiate SMCs reprogramming into vascular progenitors and that members of the Notch signa
218 ndothelium and coordinate the timing of both vascular pruning and barrier maturation.
219 tive inhibition of VEGFR2 despite equivalent vascular pruning, but were accompanied by suppression of
220     In arterial SMCs, CXCR4 sustained normal vascular reactivity and contractile responses, whereas C
221                                              Vascular reactivity was significantly decreased in the o
222 va or iliac veins and 2 had previous complex vascular reconstructions before transplantation for mida
223 ype, but not Tnfa(-/-), granulocytes induced vascular recovery, and wild-type granulocyte transfer di
224  The pattern of alteration observed suggests vascular redistribution efforts in response to challenge
225 te transfer did not prevent death or promote vascular regeneration in Tnfr1(-/-); Tnfr2(-/-) mice.
226       Before injury, leukocytes are near the vascular region, that is, approximately 100-300 mum away
227 ate and p-AMPK/AMPK, as well as Ach-mediated vascular relaxation.
228         We conclude that the pathogenesis of vascular remodeling in hypoxic PH involves an early comp
229 e dysregulation has been linked to occlusive vascular remodeling in pulmonary arterial hypertension (
230       Following transplantation, appropriate vascular remodeling is crucial to ensure the survival an
231                                         This vascular remodeling is reversible, and hydrogen sulfide
232                      IUGR is associated with vascular remodeling of the stem villus arteries.
233 rombus resolution by increasing inflammatory vascular remodeling of venous thrombi in vivo, and the p
234 ith right ventricular dysfunction, pulmonary vascular remodeling was not more severe.
235 induced pulmonary hypertension and pulmonary vascular remodeling were not or only slightly affected b
236 n HF, PH is associated with global pulmonary vascular remodeling, but the severity of PH correlates m
237                         EVP cells arose from vascular-resident beds that could not be transferred by
238 g) and 28 (34%) also had increased pulmonary vascular resistance >3.0 WU.
239 th elevated vascular gradients and pulmonary vascular resistance defines combined post- and precapill
240                       Midlife and concurrent vascular risk factor associations were determined by Poi
241 associations disappeared after adjusting for vascular risk factors (HR = 1.07 [0.98-1.17], p = 0.1374
242            To determine whether prespecified vascular risk factors and cardiac abnormalities are more
243               This result was independent of vascular risk factors and was attenuated after adjustmen
244                                              Vascular risk factors at ARIC baseline (age 45-64 years;
245  birth, race, educational level, and midlife vascular risk factors data were collected between 1964 a
246          At baseline, 65 participants had no vascular risk factors, 123 had 1, and 134 had 2 or more;
247 variate models adjusted for demographics and vascular risk factors, higher levels of NT-proBNP (RR, 3
248 surrogate biomarker of cerebral and systemic vascular risk in patients with OSA requiring further com
249 anth Medical [AMA]) to Absorb (bioresorbable vascular scaffold [BVS]) using different experimental mo
250 genic compared with the Absorb bioresorbable vascular scaffold in an ex vivo porcine arteriovenous sh
251 tial pressure continuously with a fast intra-vascular sensor in the carotid artery of anaesthetized,
252 ukocytes and platelets with endothelia under vascular shear stress requires mechanically specialized
253 sporter GLUT2 is located at the basolateral, vascular side, while SGLT1 is exposed to luminal glucose
254            Brain imaging techniques that use vascular signals to map changes in neuronal activity rel
255 rge to increase phosphorylation of myosin in vascular smooth muscle (VSM) cells, causing persistent c
256                                              Vascular smooth muscle cell (VSMC) apoptosis precipitate
257 resulting in pathophysiologic stimulation of vascular smooth muscle cell (VSMC) migration and prolife
258 ammation (PROCR, rs867186 (p.Ser219Gly)) and vascular smooth muscle cell differentiation (LMOD1, rs28
259              MicroRNAs are key regulators of vascular smooth muscle cells (VSMCs) phenotypic switch,
260                                 ABSTRACT: In vascular smooth muscle cells (VSMCs), stimulation of can
261                                           In vascular smooth muscle cells (VSMCs), stimulation of SOC
262  binding, real-time imaging was performed in vascular smooth muscle cells expressing a FRET-biosensor
263 ctive of this study was to determine whether vascular smooth muscle cells in cultured microvascular n
264  knockdown and pharmacological inhibition in vascular smooth muscle cells reveal that cytochrome b5 r
265 ts in a modest reduction of proliferation in vascular smooth muscle cells, but given low proliferativ
266 oltage-gated Ca(2+) channels in the adjacent vascular smooth muscle cells, causing vasoconstriction.
267 (8.6 +/- 1.3% of vessels with recruitment of vascular smooth muscle cells; VSMCs) in the presence of
268 In this study, we evaluated BKCa function in vascular smooth muscle from small resistance adipose art
269 widely mammalian cells, including epithelia, vascular smooth muscle tissue, electrically excitable ce
270 cular transit time, fractional volume of the vascular space, and fractional volume of the interstitia
271  most tumor cells-they undergo senescence in vascular sprouts and vessels, which suggests that pathol
272 ore possible correlations between the neural vascular structure and the pathogenesis of congenital op
273 and stability of bacterial interactions with vascular surfaces.
274 ral surgery, and 42801 procedures (18.1%) in vascular surgery.
275                                    Using the vascular system and organs of a plant, we manufactured o
276 ibe the changing properties of the pulmonary vascular system and the right ventricle, as well as thei
277                                The lymphatic vascular system is a hierarchically organized complex ne
278 l progenitor cells, damage to the developing vascular system of the brain, and altered cellular posit
279 bending) and the water pressure in the plant vascular system.
280 in the separation of the blood and lymphatic vascular systems, and the lymphatic valves.
281 us treatment were randomly assigned (1:1) to vascular-targeted photodynamic therapy (4 mg/kg padelipo
282 , 2013, we randomly assigned 206 patients to vascular-targeted photodynamic therapy and 207 patients
283                                              Vascular-targeted photodynamic therapy was well tolerate
284                                              Vascular-targeted photodynamic therapy, a novel tissue-p
285 ested as an increasing number of symptomatic vascular territories was associated with a graded increa
286 tantly, simultaneous patients had more renal vascular thromboses (4.4% vs 1.3% tx alone, 0% pre; P =
287 nd noncell-autonomously to control embryonic vascular tissue formation and root initiation, respectiv
288 e regulation enriched for genes expressed in vascular tissues and identify potential therapeutic targ
289  was expressed in various tissues, including vascular tissues, and PRX17 was localized to the cell wa
290 ygb has a critical role in the regulation of vascular tone and disease.
291 olar myogenic response and during changes in vascular tone induced by vasomotor agonists.
292 ical processes, including neuronal activity, vascular tone, inflammation, and energy metabolism.
293                                              Vascular tortuosity increased significantly in high-risk
294 e thromboembolic complications, cardiac, and vascular toxic effects.
295 ificantly lower arterial fraction and higher vascular transit time, fractional volume of the vascular
296  resulting high drug concentration can alter vascular transport rate constants along with having dire
297 elioid hemangioendothelioma (HEHE) is a rare vascular tumor which has an intermediate aggressive beha
298                          Novel 3-dimensional vascular ultrasound (3DVUS) provides accurate volumetric
299  interaction of circulating cells within the vascular wall is a critical event in chronic inflammator
300 hich tumor cells tether, roll, and adhere to vascular walls.

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