ライフサイエンスコーパス: giant cell

1 Ns establish feeding sites in roots known as giant cells.

2 ng an area of carcinoma with osteoclast-like giant cells.

3 ifferentiated carcinoma with osteoclast-like giant cells.

4 amyloid by macrophage-derived multinucleated giant cells.

5 ifferentiated carcinoma with osteoclast-like giant cells.

6 the multinucleate and acytokinetic state of giant cells.

7 lls were also present, with few foreign body giant cells.

8 cogen trophoblast and sinusoidal trophoblast giant cells.

9 ransform into macrophages and multinucleated giant cells.

10 oblasts I and II, and sinusoidal trophoblast giant cells.

11 extent, epithelioid cells and multinucleated giant cells.

12 GLABROUS11 (HDG11), control the identity of giant cells.

13 macrophages in the formation of foreign body giant cells.

14 ons with abnormal dendritic trees resembling giant cells.

15 l cortical tuber and its unique constituent, giant cells.

16 : axo-axonic cells, neurogliaform cells, and giant cells.

17 tem cells, and trophoblast stem cell-derived giant cells.

18 le formation of multinucleate bone-resorbing giant cells.

19 s that included macrophages and foreign body giant cells.

20 eolar septa with poorly formed granulomas or giant cells.

21 DNA content in endoreduplicating trophoblast giant cells.

22 ulomatous lymphohistiocytic choroiditis with giant cells.

23 bility to form TRAP positive, multinucleated giant cells.

24 on the cell surface of TSCs and trophoblast giant cells.

25 monolayer permeability and the formation of giant cells 3x to 5x normal size.

26 ranulomatous inflammation with multinucleate giant cells, accompanied by increased accumulation of ne

27 ranulomatous inflammation with multinucleate giant cells, accompanied by increased accumulation of T

28 ecognized in tubers beyond the classic tuber giant cell and demonstrates cell-specific abnormalities

29 OR signaling responses of LECs, resulting in giant cell and LEC permeability responses.

30 l review of surgically resected atria showed giant cell and lymphocytic infiltrates, lymphocytic myoc

31 ia (OP) pattern developed, with foreign-body giant cells and granulomas.

32 y spectral karyotyping, LMP1 induced "outre" giant cells and hypoploid "ghost" cells.

33 OSL1 expression is restricted to trophoblast giant cells and invasive trophoblast cells.

34 imitless differentiation into multinucleated giant cells and provide useful suggestions for the devel

35 how that distinct enhancers are expressed in giant cells and small cells, indicating that these cell

36 e find that Cited2 in sinusoidal trophoblast giant cells and syncytiotrophoblasts is likely to have a

37 eptible hosts addresses establishment of the giant cells and there is limited information on the earl

38 ncaseating granulomas lacking multinucleated giant cells and, in 1 patient, CD68-positive and CD1a-ne

39 arance of large polyploid cells (trophoblast giant cells), and the expression of trophoblast differen

40 ges, wound-healing macrophages, foreign body giant cells, and bone-resorbing osteoclasts.

41 Giant cells are associated with constitutive mammalian t

42 Multinucleated giant cells are formed by the fusion of macrophages and

43 We found that multinucleated giant cells are formed in the inflamed mouse peritoneum

44 brain pathology of TSC, cortical tubers and giant cells are fully developed at late gestational ages

45 hat comprise SIVE lesions and multinucleated giant cells are present in the CNS early, before SIVE le

46 cans of 20 patients with A-AION secondary to giant cell arteritis (biopsy-proven), 20 patients with N

47 Giant cell arteritis (GCA) and Takayasu's arteritis (TAK

48 Polymyalgia rheumatica (PMR) and giant cell arteritis (GCA) are related inflammatory diso

49 Giant cell arteritis (GCA) causes autoimmune inflammatio

50 This article aims to provide a review of giant cell arteritis (GCA) clinical features, differenti

51 Granuloma formation in giant cell arteritis (GCA) emphasizes the role of adapti

52 Giant cell arteritis (GCA) is an immune-mediated disease

53 Giant cell arteritis (GCA) is the most common form of va

54 Giant cell arteritis (GCA) is the most common systemic v

55 Giant cell arteritis (GCA) is the most common type of pr

56 ies suggest that extracranial involvement of giant cell arteritis (GCA) may be more extensive than pr

57 conducted a large-scale genetic analysis on giant cell arteritis (GCA), a polygenic immune-mediated

58 In giant cell arteritis (GCA), vasculitic damage of the aor

59 (ESR), and bilateral AION were suggestive of giant cell arteritis (GCA).

60 lasms, inflammation, pituitary apoplexy, and giant cell arteritis (GCA).

61 artery biopsies taken from individuals with giant cell arteritis (GCA).

62 Giant cell arteritis (GCA, also called temporal arteriti

63 Associated with increased RAO were giant cell arteritis (odds ratio [OR], 7.73; CI, 2.78-21

64 -positive results than in patients with GCA giant cell arteritis -negative results ( TAB temporal ar

65 re significantly higher in patients with GCA giant cell arteritis -positive results than in patients

66 is accurate in the initial diagnosis of GCA giant cell arteritis .

67 lthough large vessel inflammatory disorders (giant cell arteritis and Takayasu arteritis) are the mos

68 ulated in inflamed arteries of patients with giant cell arteritis and Takayasu arteritis, and serum l

69 of large-vessel vasculitides, including both giant cell arteritis and Takayasu arteritis, and the aor

70 thic arthritis, adult-onset Still's disease, giant cell arteritis and Takayasu arteritis, as well as

71 n clinically available tests: pentraxin-3 in giant cell arteritis and Takayasu's arteritis; von Wille

72 There were 87,794 patients with giant cell arteritis and/or polymyalgia rheumatica (n =

73 Because intracerebral VZV vasculopathy and giant cell arteritis are strongly associated with produc

74 ological aortic involvement in patients with giant cell arteritis correlates with the significant det

75 Giant cell arteritis is a granulomatous vasculitis of th

76 The clinical presentation of giant cell arteritis is occasionally nonspecific; patien

77 ring peripheral blood mononuclear cells from giant cell arteritis patients into immunodeficient NSG m

78 range 1.52 for polymyalgia rheumatica and/or giant cell arteritis to 2.82 for systemic lupus erythema

79 GCA giant cell arteritis was diagnosed or excluded clinicall

80 bilateral amaurosis in whom the diagnosis of giant cell arteritis was suggested by perineural enhance

81 onsent, 185 patients suspected of having GCA giant cell arteritis were included in a prospective thre

82 atory vasculopathy affecting large arteries (giant cell arteritis).

83 Giant cell arteritis, a chronic autoimmune disease of th

84 vasculitides, such as Takayasu arteritis and giant cell arteritis, affect vital arteries and cause cl

85 ymptoms and 2 of 203 (1.0%) for treatment of giant cell arteritis, and 1 of 193 (0.5%) for the pathop

86 al detachment, acute angle-closure glaucoma, giant cell arteritis, and central retinal artery occlusi

87 er virus (VZV) vasculopathy produces stroke, giant cell arteritis, and granulomatous aortitis, and it

88 g from the vasculitides (Takayasu arteritis, giant cell arteritis, and polyarteritis nodosa) to ather

89 tic arthritis, polymyalgia rheumatica (PMR), giant cell arteritis, ankylosing spondylitis, and Sjogre

90 k factors for RAO in cardiac surgery include giant cell arteritis, carotid stenosis, stroke, hypercoa

91 This issue provides a clinical overview of giant cell arteritis, focusing on diagnosis, treatment,

92 ous arteritis characterizes the pathology of giant cell arteritis, granulomatous aortitis, and intrac

93 biopsy (TAB), performed for the diagnosis of giant cell arteritis, has a low reported rate of complic

94 As in giant cell arteritis, recent evidence supports the role

95 n temporal arteries (TAs) from patients with giant cell arteritis, varicella zoster virus (VZV) is se

96 In giant cell arteritis, vessel-wall infiltrating CD4 T cel

97 rely affect the temporal arteries, mimicking giant cell arteritis, while, to our knowledge, the assoc

98 istochemical and gene expression analyses of giant cell arteritis-affected temporal arteries revealed

99 asculitis mimicking polyarteritis nodosa and giant cell arteritis.

100 unced in the age-related vasculitic syndrome giant cell arteritis.

101 ic infiltrates in patients with panarteritic giant cell arteritis.

102 an isolated condition or in association with giant cell arteritis.

103 ith T cells and monocytes from patients with giant cell arteritis.

104 n the older individuals and in patients with giant cell arteritis.

105 f 216 respondents (5.1%; 95% CI, 2.2%-8.0%), giant cell arteritis; and 10 of 218 respondents (4.6%; 9

106 disorder; multiple myeloma; acute leukemia; giant cell arteritis; dialysis; esophageal, stomach, pan

107 Giant-cell arteritis (GCA) is a large-vessel vasculitis

108 ment of large arteries is well-documented in giant-cell arteritis (GCA), but the risk for cardiovascu

109 Giant-cell arteritis commonly relapses when glucocortico

110 Giant-cell arteritis is associated with increased risks

111 , Sweet's syndrome, polyarteritis nodosa, or giant-cell arteritis) or a hematologic condition (myelod

112 n show findings relevant to the diagnosis of giant-cell arteritis.

113 ant to the diagnosis of challenging cases of giant-cell arteritis.

114 ucocorticoid-free remission in patients with giant-cell arteritis.

115 ticoid tapering was studied in patients with giant-cell arteritis.

116 he pathogenesis and organelle dysfunction of giant cells, as well as epilepsy control in patients wit

117 ence of retinal features was associated with giant cell astrocytoma (37.1% vs. 14.6%; P = 0.018), ren

118 more than 35% of patients with subependymal giant cell astrocytoma (SEGA) associated with tuberous s

119 of these proteins in tuber and subependymal giant cell astrocytoma (SEGA) specimens in TSC.

120 , and either serial growth of a subependymal giant cell astrocytoma, a new lesion of 1 cm or greater,

121 uction in volume of the primary subependymal giant-cell astrocytoma, as assessed on independent centr

122 resection or other therapy for subependymal giant-cell astrocytoma.

123 Subependymal nodules (SENs) and subependymal giant cell astrocytomas (SEGAs) are common brain lesions

124 ore severe than TSC1, with more subependymal giant cell astrocytomas and angiomyolipomas, higher inci

125 of everolimus in patients with subependymal giant cell astrocytomas associated with tuberous scleros

126 pport the use of everolimus for subependymal giant cell astrocytomas associated with tuberous scleros

127 pport the use of everolimus for subependymal giant cell astrocytomas associated with tuberous scleros

128 In the brain, growth of subependymal giant cell astrocytomas can cause life-threatening sympt

129 50% reduction in the volume of subependymal giant cell astrocytomas versus none in the placebo group

130 more likely to have concomitant subependymal giant cell astrocytomas, renal angiomyolipomas, cognitiv

131 s including angiomyolipomas and subependymal giant cell astrocytomas.

132 greater relative to baseline in subependymal giant cell astrocytomas.

133 ificantly reduced the volume of subependymal giant cell astrocytomas.

134 rked reduction in the volume of subependymal giant-cell astrocytomas and seizure frequency and may be

135 int was the change in volume of subependymal giant-cell astrocytomas between baseline and 6 months.

136 n is the standard treatment for subependymal giant-cell astrocytomas in patients with the tuberous sc

137 or older with serial growth of subependymal giant-cell astrocytomas were eligible for this open-labe

138 d into a male recipient, among the nuclei of giant cells at sites of osteolysis.

139 targets as well as a better understanding of giant cell biology.

140 spider silk meshes with increased numbers of giant cells compared with controls with initial decompos

141 (LGCs) are a specific type of multinucleated giant cell containing a characteristic horseshoe-shaped

142 ifferentiated carcinoma with osteoclast-like giant cells could be a marker of a poor prognosis.

143 was associated with: 1) lower multinucleated giant cell count (P = 0.04); 2) lower density of mesench

144 we have identified a new mutant with ectopic giant cells covering the sepal epidermis.

145 Resistance destroys the giant cells created in the plant's roots by the nematode

146 y in the promotion of spongiotrophoblast and giant cell differentiation and establish a new mechanism

147 gulation of Hox gene expression, trophoblast giant cell differentiation, paternal X chromosome inacti

148 mitotic cell cycle progression and promoting giant cell differentiation, respectively.

149 Intriguingly, formation of giant cells due to failed mitosis/cytokinesis is common

150 We previously reported giant-cell encephalitis in subtype B and C R5 simian-hum

151 : arrest of cell proliferation, formation of giant cells, excessive DNA replication in the absence of

152 od derived macrophage adhesion, foreign body giant cell (FBGC) formation and inflammatory cytokine an

153 Foreign body giant cells (FBGCs) are inflammatory and destructive mul

154 face, generation of destructive foreign body giant cells (FBGCs), and generation of fibrous tissue th

155 gnaling mechanisms modulating multinucleated giant cell formation and function are necessary for the

156 crophage fusion receptor, that contribute to giant cell formation and function.

157 aling responses and blocked permeability and giant cell formation in ANDV-infected monolayers.

158 demonstrated to be required for foreign body giant cell formation in the foreign body response.

159 , rather than neoplastic, and able to induce giant cell formation similar to that of normal mesenchym

160 nhanced viral replication and multinucleated giant cell formation upon infection of rhesus macrophage

161 elements that are responsible for sustained giant cell formation via receptor activator of NF-kappaB

162 zed by macrophage infiltration, foreign body giant cell formation, and fibrotic encapsulation of the

163 nvolves macrophage activation, proceeding to giant cell formation, fibroblast activation, and collage

164 ANK autocrine loop that determines sustained giant cell formation.

165 IL-15 treatment and LGC-type multinucleated giant cell formation.

166 ons to regulate IL-4-directed multinucleated giant cell formation.

167 participate in both RANKL- and IL-4-induced giant cell formation.

168 lacked the ability to induce multinucleated giant cell formation.

169 afts in the cell membrane, and inhibition of giant-cell formation and release of viral progeny.

170 true multicellularity, and multiple types of giant-celled forms.

171 activity of giant cell pathway genes LOSS OF GIANT CELLS FROM ORGANS, DEFECTIVE KERNEL1, and Arabidop

172 in, several observations indicate that these giant cells function primarily in immunity.

173 y spongiotrophoblast relative to trophoblast giant cells (GCs) within the junctional zone, markedly r

174 vo formed 'pseudo-organs' containing several giant cells (GCs).

175 a (I-PG) (n = 5), 3) peri-implant peripheral giant cell granuloma (I-PGCG) (n = 9), 4) T-RL (n = 44),

176 (n = 21), and 6) tooth-associated peripheral giant cell granuloma (T-PGCG) (n = 23).

177 ANDV-infected LECs became viable mononuclear giant cells, >4 times larger than normal, in response to

178 us SIV-p28(+) macrophages and multinucleated giant cells had fewer MAC387(+) monocytes/macrophages.

179 We found that the vacuolated giant cells had multiple signs of organelle dysfunction,

180 Giant cells had very large irregular somata and long, th

181 though SRC-3 expression in mouse trophoblast giant cells has been documented, its role in the functio

182 However, an animal model that replicates giant cells has not yet been described.

183 ifferentiated carcinoma with osteoclast-like giant cells have been described in the literature.

184 nvolving mainly osteoclasts and foreign body giant cells have revealed a number of common factors, fo

185 Giant cells have undergone endoreduplication, a speciali

186 Granulomas with a core containing giant cells, human CD68(+) macrophages, and high bacilli

187 Giant cell identity is established upstream of cell cycl

188 tic neoplasm and the presence of pleomorphic giant cells in an undifferentiated carcinoma with osteoc

189 e salivary gland imaginal ring cells and the giant cells in Drosophila larvae.

190 We found similar vacuolated giant cells in human tuber specimens.

191 extraembryonic ectoderm, and in trophoblast giant cells in the E6.5 embryo.

192 mbryonic tissue, specifically in trophoblast giant cells in the parietal yolk sac.

193 phages and was unable to form multinucleated giant cells in this cell line.

194 y promotes fusion of human monocytes to form giant cells in vitro, we determined whether A(1)R occupa

195 ntical epidermal cells to differentiate into giant cells interspersed between smaller cells.

196 ar fusion of macrophages into multinucleated giant cells is a distinguishing feature of the granuloma

197 n leading to the formation of multinucleated giant cells is a hallmark of chronic inflammation.

198 Langhans multinucleated giant cells (LGCs) are a specific type of multinucleated

199 a dehydration-rehydration process generated giant cell-like hybrid vesicles, whereas the injection o

200 vour differentiation towards the trophoblast giant cell lineage, whereas lack of Plet1 preferentially

201 Multinucleated giant cells (MGCs) are implicated in many diseases inclu

202 m cells formed up to 45% more multinucleated giant cells (MGCs) in vitro compared to WT, which concur

203 resulting in the formation of multinucleated giant cells (MGCs) is a multistage process that requires

204 unction of osteoclasts (OCs), multinucleated giant cells (MGCs) of the monocytic lineage, is bone res

205 es spontaneously matured into multinucleated giant cells (MGCs), a property not exhibited by monocyte

206 polesis of lymphocytes within multinucleated giant cells (MGCs), MGC death, and fibrinoid necrosis an

207 ocytes, and the occurrence of multinucleated giant cells (MGCs).

208 monocytes fuse to form large, multinucleated giant cells (MGCs).

209 ing macrophage fusion to form multinucleated giant cells (MNG).

210 bit signs of cytopathology or multinucleated giant cell (MNGC) formation, which were observed in wild

211 tion of granulomas containing multinucleated giant cells (MNGCs) and cell death.

212 ity to induce the formation of multinucleate giant cells (MNGCs) in multiple cell types.

213 to stimulate the formation of multinucleated giant cells (MNGCs).

214 ic tumor featuring prominent osteoclast-like giant cells, mononuclear osteoclast precursors, and spin

215 Our work involved 51 patients with giant cell myocarditis (35 women) aged 52+/-12 years.

216 Giant cell myocarditis (GCM) typically causes fulminant

217 However, viruses have not been implicated in giant cell myocarditis (GCM).

218 Giant cell myocarditis presented as nonfatal ventricular

219 ended for patients with cardiac sarcoidosis, giant cell myocarditis, and myocarditis associated with

220 cular tachyarrhythmias are characteristic of giant cell myocarditis, but their true incidence, predic

221 In giant cell myocarditis, the risk of life-threatening ven

222 to analyze (1) our experience in diagnosing giant-cell myocarditis and (2) the outcome of patients o

223 Giant-cell myocarditis often escapes diagnosis until aut

224 cutive patients with histologically verified giant-cell myocarditis treated in our hospital since 199

225 Patients with giant-cell myocarditis, eosinophilic myocarditis, or car

226 l biopsies are frequently needed to diagnose giant-cell myocarditis.

227 ils (n = 4), polymorphonuclears (n = 1), and giant cells (n = 1).

228 resulting in the formation of multinucleated giant cells occurs in a variety of chronic inflammatory

229 ogical examination revealed that trophoblast giant cells of aborting mice phagocytosed infected red b

230 We show that the ectopic giant cells of sec24a-2 are highly endoreduplicated and

231 egions of the genome in parietal trophoblast giant cells (p-TGCs) of the mouse placenta.

232 hat their formation requires the activity of giant cell pathway genes LOSS OF GIANT CELLS FROM ORGANS

233 entiation towards the syncytiotrophoblast or giant cell pathway in Plet1-low and Plet1-high cells, re

234 her cell types can generate a multinucleated giant cell phenotype with bone resorbing activity.

235 4%), tubulitis (82%), tubular rupture (62%), giant cell reaction (60%), and cortical and medullary in

236 nt, complement-dependent, macrophage-derived giant cell reaction that swiftly removes massive viscera

237 Medullary inflammation, giant cell reaction, and the extent of cast formation co

238 n leading to the formation of multinucleated giant cells remains unclear.

239 ic conditions alone enhance permeability and giant cell responses of ANDV-infected MECs and LECs thro

240 lysis of cultured cells and nematode-induced giant cells revealed a failure in mitotic exit, with the

241 inflammation characterized by multinucleated giant cells, some of which displayed elastophagocytosis

242 nvasive spiral artery-associated trophoblast giant cells (SpA-TGCs) surrounding maternal blood vessel

243 r specification of spiral artery trophoblast giant cells (SpA-TGCs) that invade and remodel maternal

244 fusogenicity on HSV and cause multinucleated giant cells, termed syncytia.

245 placentation with enrichment in trophoblast giant cells (TGCs) and other trophoblast-derived cell su

246 The mammalian trophoblast giant cells (TGCs) exploit their size to form a barrier

247 tiation defects and fail to form trophoblast giant cells (TGCs) in vitro.

248 ferentiation of blastomeres into trophoblast giant cells (TGCs), suggesting that geminin regulates tr

249 Mature osteoclasts are multinucleated giant cells that are generated from the fusion of circul

250 distinct but largely overlapping subsets of giant cells that are in direct contact with maternal art

251 treated LNCaP-AI cells formed multinucleated giant cells that contain clusters of nuclear vesicles in

252 Osteoclasts are multinucleated giant cells that resorb bone, ensuring development and c

253 ferous tubules, forming large multinucleated giant cells that underwent apoptosis.

254 es evidenced no reactivity of osteclast-like giant cells to epithelial markers but showed a positive

255 cells with a diversity of sizes ranging from giant cells to small cells.

256 ltinuclear cells, also known as foreign body giant cells, to respond to the biomaterial implants.

257 Giant cell tumor (GCT) of bone is a histologically benig

258 DT) or aggressive fibromatosis, tenosynovial giant cell tumor (TGCT) or diffuse-type pigmented villon

259 n the molecular pathogenesis of tenosynovial giant cell tumor (TGCT) or pigmented villonodular synovi

260 ing in osteosarcoma and, less frequently, in giant cell tumor of bone (GCT).

261 The neoplastic stromal cells of giant cell tumor of bone (GCTB) carry a mutation in H3F3

262 gmented villonodular synovitis (dtPVNS), and giant cell tumor of bone (GCTB).

263 served in DSRCT, solitary fibrous tumor, and giant cell tumor of bone suggests that future evaluation

264 PURPOSE OF REVIEW: Giant cell tumor of tendon sheath and pigmented villonod

265 th the pathological features of tenosynovial giant-cell tumor.

266 Tenosynovial giant cell tumors (TGCT), are rare colony stimulating fa

267 located and highly expressed in tenosynovial giant cell tumors (TGCTs), and this observation allowed

268 Our findings are mirrored in G34W-containing giant cell tumors of bone where patient-derived stromal

269 In contrast, in 92% (49/53) of giant cell tumors of bone, we found histone H3.3 alterat

270 tension cohort of patients with tenosynovial giant-cell tumors (extension study).

271 tension study, 12 patients with tenosynovial giant-cell tumors had a partial response and 7 patients

272 Treatment of tenosynovial giant-cell tumors with PLX3397 resulted in a prolonged r

273 (CSF1) gene is elevated in most tenosynovial giant-cell tumors.

274 of the jaw (17 [3%]), anaemia (6 [1%]), bone giant cell tumour (6 [1%]), and back pain (5 [1%]).

275 Diffuse-type tenosynovial giant cell tumour (dt-GCT) of the soft tissue (alternati

276 Tenosynovial giant cell tumour (TGCT), a rare, locally aggressive neo

277 Giant cell tumour of bone (GCTB) is a very rare, aggress

278 mal tumours ranging from chondroblastoma and giant cell tumour of bone to chondrosarcoma, malignant p

279 Diffuse-type tenosynovial giant-cell tumour is a rare, locally aggressive, and dif

280 Giant-cell tumour of bone (GCTB) is a rare, locally aggr

281 tologically proven diffuse-type tenosynovial giant-cell tumour of large joints.

282 y of patients with diffuse-type tenosynovial giant-cell tumour provides a comprehensive and up-to-dat

283 Patients with localised-type tenosynovial giant-cell tumour were excluded.

284 gical treatment of diffuse-type tenosynovial giant cell tumours is not a definitive treatment for eve

285 s in patients with diffuse-type tenosynovial giant-cell tumours.

286 i adheres, invades, and forms multinucleated giant cells, ultimately leading to cell toxicity.

287 pted seminiferous epithelium, multinucleated giant cells, uncleared apoptotic germ cells and decrease

288 Giant cells undergo endocycles, replicating their DNA wi

289 tive mTOR signaling induces the formation of giant cells via phosphorylation of S6K, and mTOR regulat

290 The percentage of multinucleated giant cells was lower in brain-injured patients without

291 bone were present, but no foreign body-type giant cells were identified.

292 microglia are infected as are multinucleated giant cells when present.

293 essential in patterning the highly elongated giant cells, which are interspersed between small cells,

294 the oocyte of the frog Xenopus tropicalis, a giant cell with an equally giant nucleus.

295 exhibit an expansion of parietal trophoblast giant cells with a concomitant decrease in the area of t

296 ls except horizontal cells, which persist as giant cells with aberrant centrosome content, DNA damage

297 Numerous pleomorphic giant cells with an immunohistochemical sarcomatoid prof

298 rogenitor cells develop into highly enlarged giant cells with enlarged vacuoles.

299 enty-seven percent of these osteoclasts were giant cells with pyknotic nuclei that were adjacent to s

300 On the remaining surface, multinucleated giant cells with varying intensity of tartrate-resistant