ライフサイエンスコーパス: myometrial

1 A switch from myometrial quiescence to myometrial activation is required to establish uterine c

2 ation between the onset of preterm labor and myometrial activation of the inflammatory transcription

3 fect only myometrial quiescence, can promote myometrial activation over time by increasing the expres

4 oteins and connexin 43 is a critical step in myometrial activation, allowing for a maximal contractil

5 oteins and connexin 43 is a critical step in myometrial activation, allowing for a maximal contractil

6 During myometrial activation, proteins that prime the smooth mu

7 ed in the premature occurrence of labor-type myometrial activity and increases in maternal plasma est

8 dly, peripheral estrogen infusions increased myometrial activity but did not produce preterm delivery

9 hanism by which Hsp20 acetylation can affect myometrial activity by liberating cofilin is described a

10 aternal endocrinology, a nocturnal switch in myometrial activity from low amplitude, infrequent contr

11 brane biochemical changes, and alteration of myometrial activity patterns.

12 slational modification that can affect human myometrial activity.

13 aglandins that could significantly influence myometrial activity.

14 Myometrial aging leads to fewer contractile capillary ce

15 ivate proinflammatory pathways in both human myometrial and amnion cells, which suggests that the pro

16 NF-kappaB and p38 kinase activation in both myometrial and amnion cells.

17 isoform (mK44) is expressed predominantly in myometrial and aortic smooth muscle and forms a function

18 Data for the imaging evaluation of myometrial and cervical invasion were abstracted indepen

19 by the downregulation of Fabp4 and Fatp4 in myometrial and decidual tissues, respectively; this supp

20 Viability of myometrial and fibroid cells was not greatly affected by

21 Using matched pairs of human myometrial and leiomyoma smooth muscle cells from the sa

22 Only Thy-1(+) human myometrial and orbital fibroblasts were capable of myofi

23 descriptive and quantitative analysis of the myometrial and placental changes including volumetric an

24 Immunohistochemistry localized Cav3.1 to myometrial and vascular smooth muscle cells whilst Cav3.

25 , neutrophils, and mature dendritic cells to myometrial and/or decidual tissues.

26 ly activates AP-1 but not NFkB, we show that myometrial AP-1 activation drives production of cytokine

27 f the low T2* in the placental bed and other myometrial areas, high intensity vessel-like structures

28 channels, we assessed the vasodilatation of myometrial arteries from appropriate for gestational age

29 rease in K(ATP) -dependent vasodilatation in myometrial arteries from high versus low altitude, where

30 de, K(+) channel-dependent vasodilatation of myometrial arteries is increased compared to those from

31 ed the localization of these channels in the myometrial arteries using immunofluorescence.

32 ial markers was reduced in the high-altitude myometrial arteries, which suggested that the functional

33 Chorionic plate and myometrial artery relaxation was increased compared to c

34 hannels play an adaptive role in maintaining myometrial artery vasodilator sensitivity under chronic

35 altitude during pregnancy showed diminished myometrial artery vasodilatory responses to endothelium-

36 In addition, cultured myometrial as well as leiomyoma smooth muscle cells rapi

37 we investigated human term pregnant nonlabor myometrial biopsies for transcriptome, enhancer histone

38 tein expression using immunohistochemstry in myometrial biopsies from pregnant women.

39 s of these findings for the co-ordination of myometrial [Ca2+]i signalling and contractility are disc

40 4 (TRPV4) channel as a critical regulator of myometrial calcium (Ca(2+)) entry and contractility.

41 Lactate is increased in myometrial capillary blood from women in slow or non-pro

42 We previously identified myometrial caspase-3 (CASP3) as a potential regulator of

43 Polymerase chain reaction of mouse myometrial cDNA identified four alternatively spliced si

44 Critically, simvastatin inhibited myometrial cell contraction, basally and during inflamma

45 The pregnant human myometrial cell line PHM1-41 and primary cultured uterin

46 We identify 23 myometrial cell subpopulations, including contractile an

47 We observe altered myometrial cell-to-cell communication as an aging hallma

48 overexpression of miR-200a in cultured human myometrial cells (hTERT-HM) suppressed STAT5b and increa

49 n nuclear factor-kappaB (NF-kappaB) in human myometrial cells are time-dependent.

50 xytocin response in hTERT-immortalized human myometrial cells by 35% and induced robust oxytocin resp

51 Cytokine stimulation of cultured myometrial cells did not induce iNOS expression or nitri

52 on of the proquiescent Galphas gene in human myometrial cells following stimulation with the proinfla

53 Here we report that myometrial cells from human and mouse express bitter tas

54 nd survive when directly mixed with unsorted myometrial cells in monolayer culture.

55 In human myometrial cells in vitro, the P4/HDAC inhibitor combina

56 Gap junctions between myometrial cells increase dramatically during the final

57 Estrogen/progesterone treatment of mature myometrial cells induced expression of WNT11 and WNT16,

58 induced robust oxytocin responses in primary myometrial cells obtained from patients at the time of C

59 ng revealed that CGRP-Rs are abundant in the myometrial cells of pregnant women who are not in labor,

60 n of the canonical TAS2R signaling system in myometrial cells produces profound relaxation of myometr

61 bour contractions require synchronization of myometrial cells through gap junctions (GJs).

62 In primary myometrial cells treated with phorbol ester, transient i

63 In isolated single mouse myometrial cells, a phenotypical bitter tastant (chloroq

64 ated agonist activity in estrogen-responsive myometrial cells, as determined by induction of prolifer

65 In LMSP cells cocultured with mature myometrial cells, estrogen-progesterone selectively indu

66 In human myometrial cells, knockdown of TAS2R14 but not TAS2R10 i

67 K1 and IK2 were unevenly distributed between myometrial cells, most cells possessing either IK1 (30 c

68 EST in silencing ESR1 expression in cultured myometrial cells, our results support the development of

69 In human myometrial cells, simvastatin reduced proinflammatory me

70 In hTERT-immortalized human myometrial cells, which endogenously express WT OXTR, tr

71 lock oxytocin-induced contractility in human myometrial cells.

72 zyme in in vitro cultures of amnion-WISH and myometrial cells.

73 8%, respectively, in amnion-derived WISH and myometrial cells.

74 ression facilitated PLCL2 gene expression in myometrial cells.

75 ly expressed in the submyometrial stroma and myometrial connective tissues during this period.

76 Myometrial connexin-43 gap junctions are scarce througho

77 onists to determine the relationship between myometrial contractility (spontaneous and oxytocin-induc

78 o OT, prostaglandins (PGs) play key roles in myometrial contractility and cervical ripening.

79 he myometrium suggests that CRH may modulate myometrial contractility and hence parturition.

80 reveal new roles for Kir7.1 in regulation of myometrial contractility and melanocortin signaling.

81 n the physiological range potently decreases myometrial contractility as a result of its inhibition o

82 our initial expectations, TNF did not induce myometrial contractility but did inhibit the relaxation

83 In summary, adiponectin inhibits myometrial contractility consistent with the possibility

84 Spontaneous myometrial contractility declined after 24 h but was les

85 e concentrations, plays a role in regulating myometrial contractility during labour.

86 e inflammation and its subsequent effects on myometrial contractility in experimental preterm labor.

87 en proposed to play a role in the control of myometrial contractility in pregnancy.

88 ose-response curves showed that 5-HT-induced myometrial contractility is drastically increased in lat

89 and the ability of cAMP agonists to repress myometrial contractility is lost with prolonged exposure

90 X43 promoters contribute to the induction of myometrial contractility leading to parturition.

91 hat adiponectin receptors (AdipoRs) decrease myometrial contractility via AMPK to promote uterine qui

92 athogen-derived ligands may directly promote myometrial contractility via Rho/ROCK signaling, thus co

93 patterns, (2) relationships between ECoG and myometrial contractility, and (3) 24 h ECoG patterns at

94 on-induced preterm labor, decreased baseline myometrial contractility, and diminished lipopolysacchar

95 ascular endothelium activation, induction of myometrial contractility, and PGE(2) release in vitro.

96 Acute cAMP elevation inhibits myometrial contractility, but the mechanisms responsible

97 e intra-uterine components of labor, namely, myometrial contractility, cervical ripening, and decidua

98 efined the functional consequence of this on myometrial contractility.

99 nd the impact of prolonged cAMP elevation on myometrial contractility.

100 role in parturition by stimulating not only myometrial contraction and cervical ripening but also th

101 Myometrial contraction is a central feature of labor.

102 the effector mechanisms of labor, including myometrial contraction, cervical dilation, and fetal mem

103 racellular acid pH transients that accompany myometrial contraction.

104 re frequent but shorter duration spontaneous myometrial contractions (P < 0.05) and an attenuated con

105 ulation of extracellular lactate will reduce myometrial contractions and could therefore contribute t

106 of tissues, but the effects of CGRP on human myometrial contractions and the changes in CGRP receptor

107 and maintenance therapy, as it inhibits both myometrial contractions and the proinflammatory effects

108 identify a separate role for AMPK regulating myometrial contractions that may influence labor onset.

109 us research has suggested that cAMP inhibits myometrial contractions via protein kinase A (PKA) activ

110 atin reduces PTB incidence in mice, inhibits myometrial contractions, and exhibits key anti-inflammat

111 cyclic adenosine monophosphate which favours myometrial contractions.

112 nd that prolonged cAMP elevation can prevent myometrial contractions.

113 lationship was found between ECoG cycles and myometrial contracture cycles.

114 rs involved in controlling the expression of myometrial CREM splice variants.

115 ptor type 2 (Amhr2)-Cre causes oviductal and myometrial defects.

116 meostasis and in pathogenesis of orbital and myometrial diseases characterized by persistent myofibro

117 pseudocapsule of leiomyomas despite diffuse myometrial distribution.

118 Age-associated myometrial dysfunction can prompt complications during p

119 Electrocorticogram (ECoG) and myometrial electromyogram (EMG) were recorded continuous

120 eous onset of labour was determined from the myometrial EMG.

121 placental contrast material enhancement with myometrial enhancement as a reference.

122 postcontrast images and precedes substantial myometrial enhancement.

123 base resolution via integrating the pregnant myometrial epigenome and large-scale patient genomes wit

124 ies in mice indicate a dynamic change of the myometrial epigenome and transcriptome during pregnancy

125 hich is a likely mechanism for modulation of myometrial excitability during pregnancy.

126 Myometrial excitability is governed by ion channels, and

127 te the effect of stretch on human myometrium.Myometrial explants, prepared from biopsies obtained at

128 the presence of active ARF6 and ARF1 in all myometrial extracts.

129 d fluorescence-activated cell sorting, human myometrial fibroblasts were successfully separated into

130 At a cellular level, myometrial fibroblasts, and decidual endothelial and str

131 ct transcriptomic landscapes and pathways in myometrial function and labor, which may help further th

132 l causes remain uncertain, although impaired myometrial function has been implicated.

133 a production has the potential for modifying myometrial function in pathological settings, particular

134 delayed progesterone withdrawal and impaired myometrial function.

135 -layer cell pairs, the voltage dependence of myometrial gap junction conductance is more apparent at

136 However, the regulatory systems underlying myometrial gene expression patterns throughout gestation

137 etrium and may thus be useful in achieving a myometrial gene expression profile that favors uterine q

138 e events allowed for a premature increase in myometrial GJA1 levels, elevated contractile responsiven

139 Using immortalized human myometrial (hTERT-HM) cells stably expressing wild-type

140 essing human GPR10 in the myometrium develop myometrial hyperplasia with excessive extracellular matr

141 There were no instances of myometrial infarction.

142 nicians for an accurate estimate of the deep myometrial infiltration already in the diagnosis phase w

143 m of mouse parturition is thought to involve myometrial infiltration by amniotic fluid (AF) macrophag

144 The ability of TRPV4 to modulate both myometrial inflammation and contractility, processes cen

145 ient for both SRC-1 and SRC-2 had suppressed myometrial inflammation, increased serum progesterone, a

146 These data suggest that changes in myometrial iNOS expression may participate in the regula

147 , 0.5 cm) and enhancement of the endometrial-myometrial interface and a signal void in the lumen on g

148 1.8 cm) with enhancement of the endometrial-myometrial interface and latticelike enhancement travers

149 Optimal cutoffs for MTV in predicting deep myometrial invasion (20 mL) and the presence of lymph no

150 e uterus to the cervix with greater than 50% myometrial invasion (MMI; Fig 1 ).

151 15 for all) and independently predicted deep myometrial invasion (P < 0.015) and lymph node metastase

152 lying MTV cutoffs for the prediction of deep myometrial invasion and lymph node metastases may increa

153 nerated, and MTV cutoffs for predicting deep myometrial invasion and lymph node metastases were calcu

154 acteristic curves for identification of deep myometrial invasion and lymph node metastases were gener

155 ly in endometrial polyps than in carcinomas; myometrial invasion and necrosis showed high predictive

156 Myometrial invasion and overall stage were compared by u

157 ior diagnostic accuracy in the assessment of myometrial invasion and significantly higher staging acc

158 association between inaccurate assessment of myometrial invasion and standard pitfalls with DW MR ima

159 more sensitive than US for the detection of myometrial invasion and the type of abnormal placentatio

160 lls associated with inaccurate assessment of myometrial invasion at T1- and T2-weighted imaging, DW M

161 P = .001), and the proportion of tumors with myometrial invasion compared with those with none (92% v

162 Posttest probabilities of deep myometrial invasion for grades 1, 2, or 3 increased to 6

163 e proposed a radiomic-based model to predict myometrial invasion for ultrasound images.

164 tly affects the posttest probability of deep myometrial invasion in patients with all grades of endom

165 mean weighted pretest probabilities of deep myometrial invasion in patients with tumor grades 1, 2,

166 The depth of myometrial invasion is a well-established and crucial pr

167 all female mice as early as age 1 month with myometrial invasion occurring by 3 months.

168 Patients with grade 3 cancer and >/= 50% myometrial invasion or cervical stroma invasion may bene

169 r women with grade 1 or 2 cancer and >/= 50% myometrial invasion or grade 3 cancer and < 50% myometri

170 age I, endometrioid grade 3 cancer with deep myometrial invasion or lymphovascular space invasion, or

171 The threshold of TVR associated with myometrial invasion was assessed by using receiver opera

172 pathology reports, pretest probabilities for myometrial invasion were correlated with tumor grade.

173 The mean pretest probabilities of deep myometrial invasion were derived from seven articles (1,

174 LRs for the prediction of myometrial invasion with contrast-enhanced MR imaging we

175 n or equal to 25% allowed prediction of deep myometrial invasion with sensitivity of 100% and specifi

176 phovascular space), disease stage (including myometrial invasion), patients' characteristics (age and

177 For assessing the depth of myometrial invasion, diagnostic accuracy, sensitivity, a

178 for women with grade 1 or 2 cancer and < 50% myometrial invasion, especially when no other high-risk

179 In the assessment of myometrial invasion, however, contrast-enhanced MR imagi

180 For myometrial invasion, kappa values were 0.75 with DW MR i

181 gnostic factors such as grade 3 tumors, deep myometrial invasion, lymph node metastasis (LNM), and ex

182 gists independently interpreted the depth of myometrial invasion, overall stage, and presence of pitf

183 , and TLG were significantly related to deep myometrial invasion, presence of lymph node metastases,

184 , older women had a higher frequency of deep myometrial invasion, serous tumour histology, and p53-ab

185 metrial invasion or grade 3 cancer and < 50% myometrial invasion, vaginal brachytherapy is as effecti

186 d endometrial adenocarcinoma as evidenced by myometrial invasion.

187 grade, lymphovascular invasion, and depth of myometrial invasion.

188 mas (UL) are benign tumors that arise in the myometrial layer of the uterus.

189 rast, IGFBP-5 hybridization occurs over both myometrial layers before implantation, but decreases in

190 Gland formation and myometrial layers were significantly reduced, and the st

191 Hypertrophy of the myometrial longitudinal muscle was also dramatically dim

192 of NF-kappaB, TNF, and IL-10 in decidual and myometrial macrophages in C57BL/6J mice.

193 trophysiological recordings demonstrate that myometrial maxi-K current is suppressed in term-pregnant

194 Myometrial mitochondrial copy number was reduced in olde

195 RANKL expression in LM compared to adjacent myometrial (MM) tissue.

196 unidentified sPTB genes that are involved in myometrial muscle relaxation and inflammatory responses

197 a a stretch-initiated contraction mechanism (myometrial myogenic response).

198 These mothers exhibited decreased myometrial NF-kappaB activation, PGF2alpha, and expressi

199 WNT/beta-catenin pathway that enables mature myometrial or leiomyoma cells to send mitogenic signals

200 gen/progesterone receptor levels than mature myometrial or leiomyoma cells.

201 rigenesis, involving LMSP and differentiated myometrial or leiomyoma cells.

202 Those seeking a conclusive account of myometrial pacemaking mechanisms, or indeed a definitive

203 image was also evaluated for the presence of myometrial perfusion defects and new fibroids.

204 At 1 and 4 months, myometrial perfusion returned to normal, but leiomyoma p

205 Intriguingly, the predominant myometrial PG produced just prior to labor is prostacycl

206 Intriguingly, the predominant myometrial PG produced just prior to labor is prostacycl

207 ion; such differences may reflect an altered myometrial phenotype in failed IOL and open new areas of

208 Here, we have investigated the myometrial phosphoproteome and found an altered phenotyp

209 but the influence of adiponectin on uterine myometrial physiology is unknown.

210 We address advances in the understanding of myometrial physiology, focusing on excitation and the ef

211 ed during preterm labour, and stimulation of myometrial Piezo1 in an organ bath with the agonist Yoda

212 We measured serum levels of lipoxin A(4) and myometrial protein release using ELISA, quantified lipox

213 Human myometrial proteins and phosphorylation events were diff

214 relevance of uterine UPR-ERSR in maintaining myometrial quiescence and regulating the timing of partu

215 A switch from myometrial quiescence to myometrial activation is requir

216 that were previously thought to affect only myometrial quiescence, can promote myometrial activation

217 t time are thought to include maintenance of myometrial quiescence, regulation of plasma volume, and

218 ar microenvironment to maintain the required myometrial quiescence.

219 cription factor binding motifs include known myometrial regulators AP-1, STAT, NFkB, and PGR among ot

220 PKA is not the sole mediator of cAMP-induced myometrial relaxation and that prolonged prophylactic el

221 These data suggest that cAMP-induced myometrial relaxation is not solely dependent on PKA act

222 t PKA activity is necessary for cAMP-induced myometrial relaxation, and that prolonged cAMP elevation

223 role of PKA in mediating cAMP-induced human myometrial relaxation, and the impact of prolonged cAMP

224 (1 h) application of cAMP agonists promoted myometrial relaxation, but this was weakly related to PK

225 versus vehicle; P = 0.0313) without inducing myometrial relaxation.

226 However, the ion channels controlling the myometrial resting membrane potential and the mechanism

227 This work is the first to describe the myometrial S-nitrosylproteome in both pregnant and nonpr

228 Elucidation of the myometrial S-nitrosylproteome provides a list of mechani

229 nvitro contractility were performed on human myometrial samples from term, preterm, labour and not in

230 We also analysed myometrial samples from women with spontaneous preterm l

231 The myometrial segments of the uteroplacental arteries have

232 the period of invasion, particularly in the myometrial segments where the key failure occurs.

233 GRP-Rs in myometrium, and resulting enhanced myometrial sensitivity to CGRP, may play a role in maint

234 s dependent on extracellular Ca(2+) entry in myometrial SMC.

235 lcium are essential for contraction of human myometrial smooth muscle (HMSM) and hence parturition.

236 ndothelin-1 as both a constrictor of uterine myometrial smooth muscle and a proinflammatory mediator.

237 and in decidualizing uterine endometrium and myometrial smooth muscle at even earlier postimplantatio

238 ctivated K+ (maxi-K) channels modulate human myometrial smooth muscle cell (hMSMC) excitability; howe

239 e at least partly a result of changes in the myometrial smooth muscle cell (MSMC) resting membrane po

240 hanism by which oxytocin may act to modulate myometrial smooth muscle cell excitability.

241 qually effective at inhibiting leiomyoma and myometrial smooth muscle cell proliferation.

242 e serotonin-mediated gene regulations in the myometrial smooth muscle cell.

243 onal tumor arising from a single transformed myometrial smooth muscle cell; however, it is not known

244 Human myometrial smooth muscle cells (HMSMCs) in culture were

245 protein 1 (LRP1), in cultured primary human myometrial smooth muscle cells (hMSMCs).

246 Pharmacological inhibition of TRPV4 in human myometrial smooth muscle cells (SMC) blunted lipopolysac

247 ose assigned female at birth, originate from myometrial smooth muscle cells and cause heavy menstrual

248 Employing transient transfection of human myometrial smooth muscle cells and HeLa cells, as well a

249 NOS isoforms were not detectable in human myometrial smooth muscle cells cultured from term non-la

250 l patch clamp technique, in freshly isolated myometrial smooth muscle cells from pregnant women at te

251 y, xenografts comprised of LMSP and unsorted myometrial smooth muscle cells grew into relatively larg

252 Serotonin treatment of rat uterine myometrial smooth muscle cells induced inositol phosphat

253 of the gene for interstitial collagenase in myometrial smooth muscle cells is absolutely dependent u

254 as xenografts comprised of LMMP and unsorted myometrial smooth muscle cells produced smaller tumors (

255 human pregnant myometrium and cultured human myometrial smooth muscle cells, by immunoblotting, immun

256 ontributor to the electrical excitability of myometrial smooth muscle cells.

257 L-1beta-stimulated COX-2 expression in human myometrial smooth muscle cells.

258 al vasculature, with no staining detected in myometrial smooth muscle cells.

259 ngineer MED12 Gly44 mutations in UF-relevant myometrial smooth muscle cells.

260 e and our understanding of the regulation of myometrial smooth muscle contraction-relaxation is incom

261 nalling system in modulating the response of myometrial smooth muscle in complicated pregnancies.

262 ma is thought to arise from a single mutated myometrial smooth muscle stem cell.

263 potent vasoconstrictor capable of increasing myometrial smooth muscle tone, has been shown to be up-r

264 inflammatory cytokines and that it increases myometrial smooth muscle tone.

265 nce that nitric oxide-mediated relaxation of myometrial smooth muscle, unlike vascular or gastrointes

266 This transition requires that the uterine (myometrial) smooth muscle cells increase their excitabil

267 In human myometrial specimens, inferred PGR activities are positi

268 gonist, AdipoRon, potently inhibited uterine myometrial strip contractions in physiologic organ bath.

269 gated its effects and mechanism of action on myometrial strips from term pregnant rats.

270 tions acutely when added to freshly obtained myometrial strips in 2 out of 9 cases, but Western blot

271 e direct AMPK activator A769662 also relaxed myometrial strips.

272 Putative myometrial super enhancers are mostly colocalized with p

273 d oocytes, and found ratio of endometrial to myometrial thicknesses in abdominal ultrasonic transvers

274 om other combined MRI predictors of PAS (eg, myometrial thinning, intraplacental T2-hypointense bands

275 d not detect message for ERG2 and 3 in whole myometrial tissue extracts.

276 pharmacologic TRVP4 agonists is increased in myometrial tissue from miRNA203 (-/-) mice compared to c

277 nexin 43 through cAMP/PKA signaling in human myometrial tissue in organ and cell culture.

278 nexin 43 through cAMP/PKA signaling in human myometrial tissue in organ and cell culture.

279 Gene expression in myometrial tissue revealed increased levels of inflammat

280 ctile response to oxytocin in pregnant human myometrial tissue strips, which was inhibited by the IP

281 ocin-augmented contractions of ex vivo human myometrial tissue strips.

282 noblotting of extracts from freshly isolated myometrial tissue, affinity-enriched for NOS proteins by

283 ls in UL-affected tissue compared to matched myometrial tissue.

284 tically as compared with the matching normal myometrial tissue.

285 coordinately expressed with labour onset in myometrial tissue.

286 likely to be due to TREK channels, in murine myometrial tissues and myocytes using PCR, Western blots

287 activation of conventional CD4(+) T cells in myometrial tissues and the infiltration of activated mac

288 Myometrial tissues from P(4)-treated 18.5 dpc pregnant m

289 Myometrial tissues obtained from term, pre-labour electi

290 estigated 94 leiomyomas and 60 corresponding myometrial tissues using exon arrays, whole genome seque

291 in leiomyoma tissues compared with adjacent myometrial tissues.

292 ability to mimic estrogen action in uterine myometrial tissues.

293 aberrations but not in any of the 9 matching myometrial tissues.

294 oduced NO is not likely to be a modulator of myometrial tone during human pregnancy.

295 ng a conserved role of PGR in regulating the myometrial transcriptome between species.

296 ng of the molecular events that regulate the myometrial transition from the quiescent pregnant state

297 In six patients thought to have myometrial tumor invasion at MR imaging, five tumors wer

298 maging appears accurate in the prediction of myometrial tumor involvement and in showing the relation

299 sed (P <.001), with no significant change in myometrial vascularity.

300 ein was restricted to the endothelium of the myometrial vasculature, with no staining detected in myo