ライフサイエンスコーパス: proliferative

1 were capable of self-renewal and were poorly proliferative.

2 cells are less exhausted and more active and proliferative.

3 nable to transplant leukemia but were highly proliferative.

4 anscriptional networks to reinforce the anti-proliferative activities of p53.

5 ioma stem cells, promoting both invasive and proliferative activities, as well as therapeutic resista

6 rogen receptors, which were linked to higher proliferative activity according to some reports.

7 e transition, with lower ROS content marking proliferative activity and differentiation.

8 These BMP7-LCs exhibit proliferative activity and increased sensitivity to bact

9 se but high CXCR4 expression, indicating low proliferative activity associated with poor migration to

10 tivated, Ascl1-targeted NSCs undergo limited proliferative activity before they become exhausted.

11 and exhibited potent, but delayed, in vitro proliferative activity in a G-CSF-dependent cell line.

12 activator, phenformin, potentiates its anti-proliferative activity in cancer cells.

13 n the total phenolic compounds with the anti-proliferative activity, for both cell lines, was observe

14 stem cells undergo a programmed cessation of proliferative activity.

15 The same being observed for the higher anti-proliferative activity/cytotoxicity of HE extracts on Ca

16 ents, even mutations that confer substantial proliferative advantage cannot persist, but are expelled

17 consistent with a simple model in which the proliferative advantage conferred by positively selected

18 genicity of 70% and a corresponding 250-fold proliferative advantage over spheroid technologies.

19 lation leads to the emergence of a threshold proliferative advantage, below which mutants cannot pers

20 ly, COX6B2-expressing cancer cells display a proliferative advantage, particularly in low oxygen.

21 Introducing mutants with a proliferative advantage, we demonstrate the existence of

22 3D growth, whereas overexpression provided a proliferative advantage.

23 ical components that are responsible for the proliferative alterations in the different forms of reti

24 tation of miR-181a-5p and miR-324-5p reduces proliferative and angiogenic responses in patient-derive

25 tor that plays a key role in determining the proliferative and differential state of multiple cell ty

26 tem cell aging, which is typified by reduced proliferative and differentiative capacity, is not well

27 ellate cells (qHSCs) transdifferentiate into proliferative and fibrogenic activated myofibroblastic p

28 lls induced substantial apoptosis along with proliferative and growth defects upon the loss of Fbw7.

29 veal the effect of different environments on proliferative and immature cells.

30 s to assess the effect of the environment on proliferative and immature cells: (a) the comparison of

31 e cells: (a) the comparison of raw totals of proliferative and immature cells; (b) these totals stand

32 brain cancer that contains subpopulations of proliferative and invasive cells that coordinately drive

33 nscription factor DeltaNp63 confers distinct proliferative and invasive epithelial-to-mesenchymal tra

34 tantly, amoeboid melanoma cells express both proliferative and invasive gene signatures.

35 s tumor cell plasticity by switching between proliferative and invasive states in cancer.

36 st lethal primary brain cancer, is extremely proliferative and invasive.

37 This beige APC population is proliferative and marked by cell-surface proteins, inclu

38 er partial hepatectomy (PHx), inducing acute proliferative and metabolic stress.

39 SiLAT1 and JPH203 suppressed cell proliferative and migratory and invasive abilities in bl

40 es to the observed down- and upregulation of proliferative and migratory genes, respectively.

41 Vascular smooth muscle cells going from a proliferative and motile circular shape to a contractile

42 D2(-/-) mice had lower proliferative and neural precursor responses.

43 tate epithelial cells, which produced highly proliferative and poorly differentiated malignant tumors

44 ecreased oxidative stress, activation of pro-proliferative and pro-neurogenic genes (KI67, Nestin, So

45 e surface of endothelial cells (EC) triggers proliferative and prosurvival intracellular signaling, w

46 (NFE2L1) transcription factors, which exert proliferative and protective functions, respectively.

47 The gastrointestinal tract is a highly proliferative and regenerative tissue.

48 potential pathogenic roles of these reactive proliferative and senescent cholangiocyte subpopulations

49 We report that HyperD-ALL blasts are low proliferative and show a delay in early mitosis at prome

50 presenting moderate anti-inflammatory, anti-proliferative, and antimicrobial activities.

51 anti-migratory treatment alone, but the anti-proliferative/anti-migratory combination generally showe

52 active meristems, a process known as global proliferative arrest (GPA).

53 suppressor protein is a potent activator of proliferative arrest and cell death.

54 notype, amplify the impact of cell-intrinsic proliferative arrest and contribute to impaired tissue r

55 Quiescence is a state of reversible proliferative arrest in which cells are not actively div

56 sion, and induced cancer-cell senescence and proliferative arrest.

57 umed tumor suppressor pathway that imposes a proliferative barrier (the Hayflick limit) during tumori

58 rats, the administration of BrdU impairs the proliferative behavior of neuroepithelial cells.

59 increases found for TP53 and NOTCH1 mutants (proliferative bias 1-5%).

60 precursors and regulates the post-selection proliferative burst, differentiation and functions of iN

61 t CD8(+) epidermal T(RM) cells have a higher proliferative capability and are bioenergetically more s

62 distribution of a benign tumor with limited proliferative capability indicates that metastatic disse

63 tion was associated with a rapid loss of the proliferative capability of the crypt progenitor cells i

64 wing tumor cells with augmented survival and proliferative capacities.

65 rogenitors is required for maintaining their proliferative capacity and for the production of proper

66 In addition, proliferative capacity as well as markers of injury and

67 idermal DeltaNp63alpha expression along with proliferative capacity in a conditional FIH-1 transgenic

68 clones exhibit lateral migration, and their proliferative capacity is supported by Pdgfra+ fibroblas

69 Neocortex expansion is largely based on the proliferative capacity of basal progenitors (BPs), which

70 uld represent a mechanism that moderates the proliferative capacity of human hippocampal progenitors,

71 transport iron and that their absence limits proliferative capacity of mammalian cells.

72 Here, we report that the proliferative capacity of MYC-driven normal and neoplast

73 region-specific sets of genes to control the proliferative capacity of neural progenitors, ensuring t

74 sion of any one of these lncRNAs reduces the proliferative capacity of the cells.

75 ines of evidence have challenged the lack of proliferative capacity of the differentiated cardiomyocy

76 eir telomere length set point determines the proliferative capacity of their differentiated progeny.

77 process postinjury, despite having a higher proliferative capacity than large airway epithelial cell

78 tact phagocytosis, and lymphocyte counts and proliferative capacity were normal.

79 ls of exhaustion markers, and display robust proliferative capacity.

80 self-renewability, enhanced multipotency and proliferative capacity.

81 rs, limited cytokine production, and reduced proliferative capacity.

82 MCMV challenge, in part due to a diminished proliferative capacity.

83 with increased endogenous GLS2 and restored proliferative capacity.

84 exhausted CD4, CD8 T and NK cells are major proliferative cell components in the TME, the crosstalk

85 These PGCC re-entered the proliferative cell cycle and grew in cell number when tr

86 ynergistic determinants of a switch from the proliferative cell cycle to polyploid growth and multinu

87 high DNA methylation changes related to the proliferative cell history, defines patients with differ

88 postmitotic cells - including neurons - and proliferative cells - such as astrocytes and microglia,

89 apy for acute myeloid leukemia (AML) targets proliferative cells and efficiently induces complete rem

90 lly mutated in tumor samples is increased in proliferative cells compared to quiescent cells.

91 For all methods, the numbers of proliferative cells did not differ statistically among t

92 tinct venom-expressing cell types as well as proliferative cells expressing homologs of known mammali

93 rough the formation of a blastema, a mass of proliferative cells that can grow and develop into the l

94 Intestinal stem cells (ISCs) are highly proliferative cells that fuel the continuous renewal of

95 ill-defined population consisting of highly proliferative cells that, contrary to human SCs, do not

96 ver the shaped scaffold and cultured as stem/proliferative cells to expand them and cover the scaffol

97 roliferative history of the cell was: highly proliferative cells were more likely to arrest than to d

98 nnose metabolism affects the function of non-proliferative cells, such as inflammatory macrophages.

99 quently acquire the characteristics of young proliferative cells.

100 CD5bright phenotype, known to be enriched in proliferative cells.

101 can cause acute and chronic inflammatory and proliferative changes in mouse and nonhuman primate mode

102 fects, her9 mutants also possessed a reduced proliferative ciliary marginal zone, and decreased and d

103 higher levels of mtDNA were observed in stem/proliferative compartments compared with differentiated

104 or not CAR-T integration itself enhances the proliferative competence of individual T cells by rewiri

105 pression of YAP phospho-mutants dampened the proliferative competence of OE CMs.

106 ial injections acquire selectively increased proliferative competency in the brain, with reduced orth

107 nd respective CH development under different proliferative conditions.

108 of thyroid cancer, lymphoma, and a range of proliferative conditions.

109 avour, leading to collateral sensitivity and proliferative costs.

110 eostasis, TM keratinocytes transit through a proliferative CP state and exhibit directional lateral m

111 gut epithelium from microbial dysbiosis and proliferative crypt damage.

112 the muscularis mucosa, in close proximity to proliferative crypts, are a source of WNT and RSPONDIN l

113 e activity, but not deacetylase activity, in proliferative cultured muscle and adipose cells in compa

114 s in Thymus extracts and their in vitro anti-proliferative/cytotoxic activities.

115 IFNAR1 reduction significantly rescued the proliferative defects of ADAR1 loss.

116 c deletion of one FMRE in human cells caused proliferative deficiencies and transcriptional deregulat

117 tumor progression by leading the invasion of proliferative DeltaNp63-high EMT cells in heterogeneous

118 55; 95% CI, 1.32-1.82), as did patients with proliferative diabetic retinopathy (CVA: HR, 2.53; 95% C

119 ovide the real-world outcomes of people with proliferative diabetic retinopathy (PDR) in India and hi

120 The hallmark of proliferative diabetic retinopathy (PDR) is retinal neov

121 roliferative diabetic retinopathy (NPDR) and proliferative diabetic retinopathy (PDR) were excellent

122 retinopathy (PVR) (n = 30), PVR (n = 16) and proliferative diabetic retinopathy (PDR) with tractional

123 agulation (PRP) in treatment-naive eyes with proliferative diabetic retinopathy (PDR).

124 nd has been implicated in the progression of proliferative diabetic retinopathy (PDR).

125 mediator of aberrant retinal angiogenesis in proliferative diabetic retinopathy and its modulation ha

126 scularization, which underlies diseases like proliferative diabetic retinopathy and retinopathy of pr

127 statistically significant increased risk for proliferative diabetic retinopathy in the multivariate m

128 Eyes with proliferative diabetic retinopathy or severe nonprolifer

129 ify neovascularization (NV) in patients with proliferative diabetic retinopathy using swept-source op

130 ho underwent primary vitrectomy for TRD from proliferative diabetic retinopathy were studied.

131 h vison loss due to vitreous hemorrhage from proliferative diabetic retinopathy who were enrolled fro

132 ants whose eyes had vitreous hemorrhage from proliferative diabetic retinopathy, there was no statist

133 ctomy is performed in treating patients with proliferative diabetic retinopathy.

134 nt tumor tissues reveals no evidence of less proliferative diploid/2N lesions in Type 1 tumors.

135 tions, and death, which overall results in a proliferative disadvantage relative to normal cells in t

136 xpression reflects disease biology of highly proliferative disease and distinct IP but does not appea

137 temic survey to exclude systemic plasma cell proliferative diseases.

138 thelial structure as they undergo both early proliferative divisions and later neurogenic divisions.

139 al DR (NDR) (N = 19), or moderate/severe non-proliferative DR (NPDR) (N = 11).

140 f 107 subjects which are comprised of 38 non-proliferative DR (NPDR), 28 without DR (NoDR), and 41 co

141 liferative DR (NPDR) group (n = 48); and the proliferative DR (PDR) group (n = 41).

142 R (NPDR; n = 125), severe NPDR (n = 20), and proliferative DR (PDR; n = 72) were included.

143 % moderate NPDR, 37.5% severe NPDR and 14.7% proliferative DR [PDR]) were reviewed.

144 (NPDR), moderate NPDR, proliferative DR, and proliferative DR with fibrosis.

145 ate NPDR, 4 eyes had severe NPDR, 9 eyes had proliferative DR, and 4 eyes were normal controls.

146 d nonproliferative DR (NPDR), moderate NPDR, proliferative DR, and proliferative DR with fibrosis.

147 and 12 diabetic patients with severe NPDR to proliferative DR.

148 Braf-driven nevus formation, analyzing both proliferative dynamics and single-cell gene expression,

149 eals the emergence of a population of highly proliferative ECs that likely arise from multiple miEC p

150 Interestingly, the anti-proliferative effect of PRMT5 inhibition was also partia

151 In vitro, DMOG had no proliferative effect on HC, but conditioned supernatant

152 come activated and differentiate into highly proliferative effector T cells.

153 We also evaluated the anti-proliferative effects (IC(50)) of these samples on tripl

154 Mechanistically, the pro-proliferative effects of LYCAT were mediated by an incre

155 Exogenous T3 stimulates proliferative ERK1/2 signaling in apical cardiomyocytes,

156 these hormonal effects, ultimately blocking proliferative estrogen signaling (i.e., oral contracepti

157 s results in a cell-autonomous defect in the proliferative expansion of myoblasts.

158 ation rapidly and potently inhibited the pro-proliferative extracellular signal-regulated kinase (ERK

159 FoxM1 inhibitor, reduced FoxM1 regulated pro-proliferative factors and cell proliferation in vitro, a

160 cularly ROR scores are determined largely by proliferative features.

161 enes (AREG and CCND1), suggesting these were proliferative FLC cell clusters.

162 operated Ca(2+) entry (SOCE) and drive fibro-proliferative gene programs during cardiovascular remode

163 Consistently, NRG1 treatment induces a proliferative gene signature and promotes organoid forma

164 Paradoxically, FLs originate from highly proliferative germinal center (GC) B cells with prolifer

165 We report that proliferative glomerulonephritis arose only in the prese

166 e cohort included the following 26 patients: proliferative glomerulonephritis with MIg deposits (PGNM

167 The mechanisms whereby leaf anlagen undergo proliferative growth and expansion to form wide, flat le

168 e benefits of cardiomyocyte enlargement over proliferative growth of the heart and the physiological

169 in granulocytes suggested ~20 years of added proliferative history of HSCs in recipients compared wit

170 addition was not predictive of outcome, the proliferative history of the cell was: highly proliferat

171 s sufficient to extend lifespan and preserve proliferative homeostasis in the gut with age.

172 noma broadly distributed into angiogenic and proliferative/ immunogenic clades.

173 n the apoptotic index and an increase in the proliferative index (2.3 and 56.9%, respectively) compar

174 several parameters (ie, tumor size, grading, proliferative index, localization, mesoappendiceal invas

175 e staining for GFAP, Olig2, and a high Ki-67 proliferative index.

176 ing CCT2 were more invasive and had a higher proliferative index.

177 they must overcome a final telomere-mediated proliferative lifespan barrier called replicative crisis

178 reased tumor thickness and expression of the proliferative marker Ki-67 and the reactive oxygen speci

179 t cancer cells grown in 3D downregulated the proliferative marker Ki67 (P < 0.05) and exhibited decre

180 Expression levels of two proliferative markers, phospho-histone H3 and Ki-67, wer

181 of the interplay between circadian rhythms, proliferative metabolism and cancer, highlighting potent

182 Silencing HNF1alpha reduced the proliferative, migratory, invasive and colony forming ca

183 000 protein profiles, finding that immature, proliferative monocyte-lineage cells with reduced antige

184 Initially, these cells are seeded as a proliferative monolayer over the shaped scaffold and cul

185 These proliferative neonatal cardiomyocytes display a unique t

186 ation trajectory and identified three highly proliferative oligopotent progenitor populations downstr

187 expressing any of six of the most prominent proliferative oncogenes, including the receptor tyrosine

188 -MSI defined regions of a hypoxic core and a proliferative outer layer from metabolite distribution.

189 mal cells are released from organs under non-proliferative pathological conditions, correlating with

190 lies at the nexus of most, if not all, known proliferative pathways.

191 Highly proliferative Periostin (Postn)+ lineage CFs were found

192 d-glass opacities and consolidation, and the proliferative phase would manifest as a tendency toward

193 n chronic ulcers than in acute wounds at the proliferative phase.

194 ion of intestinal stem cells in two distinct proliferative phases via the steroid receptors EcR and U

195 bpopulation acquires a ductular reactive and proliferative phenotype, while another subpopulation und

196 e activated and acquire highly migratory and proliferative phenotypes.

197 ant antral cells, SCJ cells contain a highly proliferative pool of immature Lgr5(-)CD44(+) cells, whi

198 Fs are heterogeneous and include a transient proliferative Postn+ population required for cardiac ner

199 The surviving cells retained proliferative potential and the ability to be reinfected

200 rontal lobe, exhibit striking differences in proliferative potential in the brain.

201 Our findings thus suggest that proliferative potential of adipocyte precursors is limit

202 However, the proliferative potential of adipocyte progenitors in vivo

203 e leads to telomere shortening and a reduced proliferative potential of alveolar type II cells and cl

204 uptake rate has been further related to the proliferative potential of cancer, specifically the prol

205 ar teeth were digested enzymatically and the proliferative potential of human PDLMSCs and GMSCs was c

206 /SA) mice, which was associated with reduced proliferative potential of infected Stat3(SA/SA) gastric

207 of ARID1A alone did not significantly affect proliferative potential or rate of apoptosis, ARID1A-def

208 increased progenitor diversity and enhanced proliferative potential play important roles in human ne

209 ap1(-/-) osteoblasts have significantly less proliferative potential than Keap1(+/-) osteoblasts.

210 nondividing state without compromising their proliferative potential, which requires changes to core

211 e time cells spend in the earlier pro-memory/proliferative (PP) state is a fixed and inherent propert

212 l role of metalloproteinase dysregulation in proliferative, premalignant Hi-Myc prostatic glands.

213 Proliferative pressure drives migrating cells to attach

214 xl2 as both a critical regulator of myogenic proliferative processes and a susceptible gene target du

215 mechanism regulating proinflammatory and pro-proliferative processes in the initiation of experimenta

216 and miR-221, 2 activators of profibrotic and proliferative processes, increased the most, at 4- and 2

217 display characteristics of normally discrete proliferative progenitor and anterior, differentiated ca

218 Further, iAs-exposed proliferative progenitor cells exhibited NRF2 pathway ac

219 ays collaborate to trigger the commitment of proliferative progeny by fueling LEF1- and MITF-dependen

220 m cells (McSCs) become activated to generate proliferative progeny that differentiate into pigment-pr

221 a+ fibroblasts, generating migratory but non-proliferative progeny.

222 controversial: some groups described its pro-proliferative properties, but others illustrated its inh

223 roRNAs (miRNAs) are well-known activators of proliferative quiescence and terminal differentiation.

224 eration, suggesting that HNF4alpha maintains proliferative quiescence in the liver, at least, in part

225 utricles and contributes to maintaining the proliferative quiescence that appears to underlie the pe

226 ling eventually may be harnessed to overcome proliferative quiescence that limits regeneration in mam

227 tems seem to exhibit a similar decoupling of proliferative replenishment divisions and consuming neur

228 Whether telomere attrition reducing proliferative reserve in blood-cell progenitors is causa

229 ted a homeostatic-like morphology, decreased proliferative response and reduced expression of neurode

230 fails to induce a robust transcriptional and proliferative response in the heart.

231 ardiomyocyte endowment of P8 hearts, but the proliferative response is confined to cardiomyocytes of

232 ets, inhibition of EGFR or HB-EGF blocks the proliferative response not only to HB-EGF but also to gl

233 e, PPI treatment decreased the IL-13-induced proliferative response of esophageal epithelial cells.

234 tion of liver injury biomarkers and enhanced proliferative response of peripheral blood mononuclear c

235 ls of long-term graft recipients generated a proliferative response to donor Ags at a similar magnitu

236 like growth factor (HB-EGF) in the beta-cell proliferative response to glucose, a beta-cell mitogen a

237 n and were required not only for the ensuing proliferative response, but also for tumor cell growth a

238 Despite such disparities in proliferative response, Myc is bound to DNA at open elem

239 longation factor (P-TEFb), instating a large proliferative response.

240 in skeletal myoblasts resulted in increased proliferative responses characterized by activation of m

241 rogeny that expressed hair cell markers, but proliferative responses declined postnatally.

242 activity primes individual cells for optimal proliferative responses following Ag exposure.

243 anzyme B(+)/IFN-gamma(+), CD4(+), and CD8(+) proliferative responses to peptide pools in most individ

244 latory acclimatization and carotid body cell proliferative responses to sustained hypoxia.

245 rimental hypoxic PH, proinflammatory and pro-proliferative responses were dependent on complement (al

246 tor (VEGF) has transformed therapy for these proliferative retinopathies.

247 s and regeneration and glia proliferation in proliferative retinopathies.

248 a lower HR of cataract surgery in eyes with proliferative retinopathy (0.903; 95% CI, 0.725-1.124),

249 Proliferative retinopathy can present variably in VKH pa

250 inical features and outcome of management of proliferative retinopathy in 2 patients with VKH.

251 Proliferative retinopathy is an uncommon feature of Vogt

252 ell-controlled type-2 diabetics, free of pre-proliferative retinopathy, were included.

253 d females with VKH presented with unilateral proliferative retinopathy.

254 regeneration, this finding elucidates a pro-proliferative role of KLF4 during the postirradiation re

255 nismal changes, intercellular signaling, and proliferative safeguards.

256 ng, sestrins induce the reprogramming of non-proliferative senescent-like CD27(-)CD28(-)CD8(+) T cell

257 dentified higher B-cell content and a strong proliferative signal in subgroup A and enriched T-cell,

258 From sustained proliferative signaling and the activation of invasion a

259 minimizes the activation of inflammatory and proliferative signaling pathways, including the NF-kappa

260 er that promotes both pro-apoptotic and anti-proliferative signaling, and they highlight the utility

261 cells and their microenvironment to sustain proliferative signaling, evade growth suppressors, resis

262 t effects on cell cycle progression and cell proliferative signaling.

263 primary cilia presents a conundrum: how are proliferative signals conveyed through an organelle that

264 Although proliferative, SOD1 myoblasts demonstrated delayed and r

265 During the proliferative stage, macrophages produce canonical Wnt l

266 e of switching from a quiescent to an active proliferative state during angiogenesis.

267 pment, cardiomyocytes undergo a shift from a proliferative state in the fetus to a more mature but qu

268 ry state being more motile than cells in the proliferative state.

269 ion of CD8 T cells with highly cytotoxic and proliferative states and no evidence of regulatory T cel

270 le phenotype switching between migratory and proliferative states, with cells in the migratory state

271 is a potential in vivo target for measuring proliferative status in cancer.

272 ET could provide an in vivo measure of tumor proliferative status, and we hypothesized that uptake wo

273 hus, SMC5/6 functions are critical in highly proliferative stem cells during organism development.

274 allowed response to hypertrophic as well as proliferative stimuli.

275 Tissue alterations are accompanied by a pro-proliferative stimulus mediated by AKT signaling.

276 dividual are exposed to different degrees of proliferative stress and environments, ie, in long-term

277 mental brain enlargement are inherently more proliferative than control NPCs.

278 Recurrent tumors were generally less proliferative than pre-treatment tumors as measured via

279 The presence of proliferative tissue in contact with the lens was found

280 In young telomerase mutants, proliferative tissues exhibit DNA damage and p53-depende

281 tatic outgrowth and switches clusters from a proliferative to a collective migratory state.

282 ptional output in cells transitioning from a proliferative to cell-lineage specifying phenotype.

283 neural stem and progenitor cells (NSCs) from proliferative to differentiative divisions to generate n

284 scription factor (MITF) is a hallmark of the proliferative-to-invasive phenotype switch, although how

285 on generally showed improvement over an anti-proliferative treatment alone.

286 ty of responses to an application of an anti-proliferative treatment.

287 deficiencies to induce the dissemination of proliferative tumor cells.

288 native T(1) corresponded to regions dense in proliferative undifferentiated neuroblasts, whereas regi

289 dently protective against the development of proliferative VAO.

290 presented with tractional RD associated with proliferative vitreo-retinopathy.

291 pes, such as rhegmatogenous RD (RRD) without proliferative vitreoretinopathy (PVR) (n = 30), PVR (n =

292 ence of male sex, foveal detachment, grade C proliferative vitreoretinopathy (PVR), inferior retinal

293 ay of symptom onset, and presence of primary proliferative vitreoretinopathy (PVR).

294 of operated eyes) due to variable degrees of proliferative vitreoretinopathy (PVR).

295 Proliferative vitreoretinopathy in turn increases the ri

296 rd PPV (vitreous hemorrhage, dense cataract, proliferative vitreoretinopathy, giant retinal tear, amo

297 ounger than 18 years and those with advanced proliferative vitreoretinopathy, giant retinal tear, tra

298 Eyes with proliferative vitreoretinopathy, giant retinal tears, pr

299 Eyes with proliferative vitreoretinopathy, previous glaucoma surge

300 from other epidermal sites and has discrete proliferative zones with a three-dimensional hierarchy o