ライフサイエンスコーパス: aplasia

1 al aplasia and rudimentary uterus (Mullerian aplasia).

2 athy, pulmonary haemorrhage, and bone marrow aplasia).

3 educe long-term side effects, such as B-cell aplasia.

4 disruption leads to deafness due to cochlear aplasia.

5 O products, reduce the risk of pure red cell aplasia.

6 ant and may be associated with pure red cell aplasia.

7 residual leukemic bone marrow blasts during aplasia.

8 one dog showed rejection and died of marrow aplasia.

9 receptors (fgfr1/2(Mes-/-)) results in renal aplasia.

10 ajor cardiovascular defects and thymus gland aplasia.

11 eases in platelet counts without intervening aplasia.

12 D and died of IFN-gamma-mediated bone marrow aplasia.

13 from hemorrhage in patients with bone marrow aplasia.

14 is, hypogammaglobulinemia, and pure red cell aplasia.

15 limb deformities and renal malformations or aplasia.

16 nt graft rejection was accompanied by marrow aplasia.

17 , a thin hypocellular retina and optic nerve aplasia.

18 ng Synthokine after radiation-induced marrow aplasia.

19 T101 expansion correlates with CR and B-cell aplasia.

20 uration of leukemia free survival and B cell aplasia.

21 s had CAR transgenes and 59 (77%) had B-cell aplasia.

22 CAR T-cell therapy, despite long-term B-cell aplasia.

23 ving no cochlear portion identifies cochlear aplasia.

24 ne suppression arising from bystander T cell aplasia.

25 itting FKBP1A(KO) 19CAR-T cell-driven B cell aplasia.

26 BM failure characterized by cytopenia and BM aplasia.

27 ll occurred in the setting of ongoing B-cell aplasia.

28 nd maturation, typically without evidence of aplasia.

29 f risks associated with interventions during aplasia.

30 otherapy or those associated with inevitable aplasia.

31 d by congenital limb defects and scalp cutis aplasia.

32 progenitor cells (HPCs), leading to fatal BM aplasia.

33 , the most common of which was pure red-cell aplasia.

34 antly with increased risk of renal dysplasia/aplasia.

35 s, in BM progenitor cells, leading to severe aplasia.

36 erebellar vermis, ranging from hypoplasia to aplasia.

37 hy without concomitant development of B-cell aplasia.

38 lar T-cell dose developed a predicted B-cell aplasia.

39 eature in biopsies from patients with marrow aplasia.

40 curred at dose level 1 with prolonged marrow aplasia.

41 Four (22%) patients died from prolonged aplasia (1), fungal pneumonia (1), or multiorgan failure

42 most commonly associated with pure red cell aplasia, (2) the presence of clonal cytogenetic abnormal

43 osis 29 d after RLT and another of sepsis in aplasia 34 d after RLT), CXCR4-directed RLT resulted in

44 follow-up shows that long periods of B cell aplasia, a marker of in vivo CAR activity, are associate

45 model where GVHD lethality is due to marrow aplasia, alloreactive CD8+ TCR Tg T cells induced signif

46 FOXN1 deficiency leads to thymic aplasia, alopecia, and nail dystrophy, accounting for th

47 eficiency phenotype due to congenital thymic aplasia and alopecia universalis.

48 disease myelodysplasia can be confused with aplasia and can also evolve from aplastic anemia.

49 aratus, including cleft palate, thymus gland aplasia and cardiac outflow tract malformations.

50 n may develop that presents as pure red cell aplasia and chronic anemia.

51 t variant in SAMD9L in an infant with B cell aplasia and clinical autoinflammatory features who died

52 w failure syndrome characterized by red cell aplasia and congenital anomalies.

53 ct heart defects, thymus gland hypoplasia or aplasia and craniofacial anomalies.

54 ation-induced soluble markers of bone marrow aplasia and endothelial damage.

55 , trabecular bone reduced, and hematopoietic aplasia and erythrocyte-filled vascular sinusoids were a

56 pan-T cell antigens may be limited by T cell aplasia and fratricide, necessitating "rescue" allogenei

57 ts with persistent CAR T cell-induced B cell aplasia and hypogammaglobulinaemia.

58 oma experience prolonged and profound B-cell aplasia and hypogammaglobulinemia, placing them at a hig

59 n B cells, there is the potential for B-cell aplasia and hypogammaglobulinemia.

60 ine hematopoietic cells leads to bone marrow aplasia and lethality.

61 ion of the Msx2 gene resulted in optic nerve aplasia and microphthalmia in all transgenic animals.

62 SAMD9L patients often experienced transient aplasia and monosomy 7, whereas MECOM patients presented

63 of immune aplastic anemia, with bone marrow aplasia and peripheral cytopenia.

64 induced inflammatory markers for bone marrow aplasia and pro-sepsis markers showed early elevation wi

65 y giving rise to NPHP with cerebellar vermis aplasia and retinal degeneration.

66 male carriers with this mutation had vaginal aplasia and rudimentary uterus (Mullerian aplasia).

67 reatment strategy for T-ALL, avoiding T cell aplasia and the need for genome engineering that complic

68 NCRNA) disease, characterized by optic nerve aplasia and total blindness.

69 5 monoclonal antibody can produce persistent aplasia and whether it could facilitate syngeneic or all

70 ly, median clefts of the hands and feet, and aplasia and/or hypoplasia of the phalanges, metacarpals,

71 points: before the conditioning regimen, at aplasia, and at engraftment.

72 duration of hypogammaglobulinemia and B-cell aplasia, and event-free survival and overall survival at

73 ing transient aplastic crisis, pure red cell aplasia, and hydrops fetalis.

74 and persistence of AUTO3, duration of B cell aplasia, and overall and event-free survival.

75 also known as MIDAS (microphthalmia, dermal aplasia, and sclerocornea).

76 vival, stringent event-free survival, B-cell aplasia, and toxicity were assessed in all patients who

77 mal dominant GATA3 mutations can cause renal aplasia as part of the hypoparathyroidism, renal dysplas

78 MRIs, which showed the extent of the vaginal aplasia before surgery, showed the engineered organs and

79 between rituximab therapy and pure red cell aplasia, but the diagnostic and therapeutic utility of t

80 , and the subject achieved peripheral B cell aplasia by day 15 post-infusion.

81 Chronic red cell aplasia can develop in immunocompromised patients includ

82 orrect anemia in patients with pure red-cell aplasia caused by antierythropoietin antibodies.

83 vaginal organs in four patients with vaginal aplasia caused by Mayer-Rokitansky-Kuster-Hauser syndrom

84 complexities of the humanized mouse, marrow aplasia caused by TBI could be alleviated by cell therap

85 n anemia (DBA) is a rare congenital red-cell aplasia characterized by anemia, bone-marrow erythroblas

86 haracterized by progressive bone marrow (BM) aplasia, chromosomal instability, and acquisition of mal

87 f Gdf6 in a mouse model resulted in cochlear aplasia, closely resembling the human phenotype.

88 e (AOS), characterized by the combination of aplasia cutis congenita (ACC) and terminal transverse li

89 Aplasia cutis congenita (ACC) is a congenital epidermal

90 Aplasia cutis congenita (ACC) manifests at birth as a de

91 al disorder characterized by the presence of aplasia cutis congenita (ACC) of the scalp vertex and te

92 n ischemic contracture (CVIC) and unilateral aplasia cutis congenita (ACC) type VII of the forearm pr

93 alformation disorder consisting primarily of aplasia cutis congenita of the vertex scalp and transver

94 e characterized by facial lesions resembling aplasia cutis in a preauricular distribution along the l

95 Aplasia cutis manifests with localized skin defects at b

96 (AOS), a rare disease with major features of aplasia cutis of the scalp and terminal transverse limb

97 approaches have led to the identification of aplasia cutis-causing mutations in genes that have previ

98 c variants give rise to dental anomalies and aplasia cutis.

99 ll-associated neurotoxicity syndrome, B-cell aplasia, cytopenias, and infections.

100 The cytokine-release syndrome and B-cell aplasia developed in both patients.

101 icities were reversible and prolonged B-cell aplasia did not occur.

102 host disease-like colitis, and pure red cell aplasia, different from the pattern observed in CVID pat

103 80 percent in the incidence of pure red-cell aplasia due to Eprex.

104 Celsr1- or Vangl2-deficient mice show valve aplasia due to failure of endothelial cells to undergo r

105 over a 3-year period with congenital vaginal aplasia due to MRKHS.

106 ed with patients maintaining a median B cell aplasia duration of 8.4 years.

107 diagnosis: FSGS, obstructive uropathy (OU), aplasia/dysplasia/hypoplasia (A/D/H), and reflux nephrop

108 f HSCT: pre-transplant homoeostasis, induced aplasia, early settling and engraftment of infused cells

109 es fifth disease, acute and chronic red cell aplasia, fetal hydrops, arthropathy, and other disorders

110 found in a patient who developed bone marrow aplasia following treatment with allogeneic chimeric ant

111 ineous patient with diabetes and bone marrow aplasia from a family with two affected siblings, wherea

112 reports of epoetin-associated pure red-cell aplasia from the Food and Drug Administration and from t

113 runcal cardiac defects, thymic hypoplasia or aplasia, hypocalcemia, and characteristic facial feature

114 arget, off-tumour toxicities, such as B-cell aplasia, hypogammaglobulinaemia, and persistent or bipha

115 ers characterized by various degrees of limb aplasia/hypoplasia and joint dysplasia in humans.

116 aft-versus-host disease in 2 dogs and marrow aplasia in 1.

117 Finally, this is the first example of renal aplasia in a conditional knockout model.

118 ne leukemia virus-C (FeLV-C) causes red cell aplasia in cats, likely through its interaction with its

119 SMG aplasia in Fgf8 ectoderm conditional mutants indicates t

120 ity and the elimination of persistent B-cell aplasia in immune-competent mice.

121 a infectiosum) in children and pure red cell aplasia in immunocompromised patients.

122 domain, and mutations in TFAP2A cause cutis aplasia in individuals with branchiooculofacial syndrome

123 h retinal degeneration and cerebellar vermis aplasia in Joubert syndrome are poorly understood.

124 ene expressed at high levels, caused adrenal aplasia in newborn mice.

125 re attributed to study drug toxicity (marrow aplasia in one patient and colitis in one patient); no f

126 impairment ranged from lobular hypoplasia to aplasia in some cases and was associated with the amount

127 Unlike B cell depletion, T-cell aplasia is highly toxic.

128 Unlike B cell depletion, pan-T cell aplasia is prohibitively toxic.

129 rome), liver fibrosis, and cerebellar vermis aplasia (Joubert syndrome) in approximately 10% of patie

130 One dose-limiting toxic effect (aplasia lasting 8 weeks) occurred at level 4, but the ma

131 o deletion of Med12 causes rapid bone marrow aplasia leading to acute lethality.

132 ine hematopoietic cells leads to bone marrow aplasia, leukopenia, anemia, and early lethality.

133 syndrome, is characterized by red blood cell aplasia, macrocytic anemia, clinical heterogeneity, and

134 7 adult patients with acquired pure red cell aplasia (median age, 64 years; range, 22 to 84 years).

135 isodes of HPV B19-induced transient red cell aplasia occurred with the following clinical events: fev

136 Thymic hypoplasia/aplasia occurs as a part of DiGeorge syndrome, which has

137 e synthesis may be involved in pure red cell aplasia of DBA.

138 the development of stratified epithelia and aplasia of multiple ectodermal appendages, as well as or

139 mbryonic day 15/16 with severe hypoplasia or aplasia of multiple organs and widespread patterning def

140 -/-) develop malformations and hypoplasia or aplasia of multiple organs, including the craniofacial s

141 lity (ID), hypertrichosis, and hypoplasia or aplasia of nails and terminal phalanges.

142 lation of Fgf4 expression, and hypoplasia or aplasia of specific skeletal elements.

143 mation (SHFM) is characterized by hypoplasia/aplasia of the central digits with fusion of the remaini

144 sing a VEGF-C/D trap and displaying complete aplasia of the dural lymphatic vessels, macromolecule cl

145 tions of the upper and lower extremities and aplasia of the hands and feet.

146 n results in hypoplasia of the neocortex and aplasia of the hippocampal anlagen.

147 Angiography revealed unilateral aplasia of the internal carotid artery.

148 Transgenic mice also manifested aplasia of the interparietal bone and decreased ossifica

149 t a case of the right-sided aortic arch with aplasia of the left brachiocephalic trunk in a 64-year-o

150 tual disability, epilepsy, and hypoplasia or aplasia of the nails of the thumb and great toe.

151 of T cells, hypocalcemia with hypoplasia or aplasia of the parathyroids, and a variety of central ne

152 mal-dominant disorder characterized by cutis aplasia of the scalp; minor anomalies of the external ea

153 and cardiovascular anomalies, hypoplasia or aplasia of the thymus with associated deficiency of T ce

154 ized by severe short stature with hypoplasia/aplasia of the ulna and fibula, has been postulated to b

155 t least one morphologic variant (thinning or aplasia) of a muscle of the levator ani complex was note

156 se Diamond Blackfan Anemia (DBA), a red cell aplasia often associated with physical abnormalities.

157 itary PHPV, as well as bilateral optic nerve aplasia (ONA) or hypoplasia (ONH), for mutations in ATOH

158 CAR-T persistence were observed with B-cell aplasia ongoing in 15 of 20 patients at last follow-up.

159 well understood, but congenital venous valve aplasia or agenesis may play a role in some cases.

160 normalities and in two fetuses with scapular aplasia or hypoplasia (one fetus had both facial and sca

161 Additionally, cerebellar aplasia or hypoplasia characteristic of Joubert syndrome

162 chronic kidney disease who had pure red-cell aplasia or hypoplasia due to antierythropoietin antibodi

163 ry to the widely held perception that thymus aplasia or hypoplasia is a characteristic feature of Pax

164 e (GPS) is a rare disorder in which patellar aplasia or hypoplasia is associated with external genita

165 e is a congenital condition characterized by aplasia or hypoplasia of the uterus and vagina in women

166 The syndrome is marked by thymic aplasia or hypoplasia, parathyroid hypoplasia, or congen

167 1 deletion mutants is associated with thymus aplasia or hypoplasia.

168 ogenesis, which subsequently leads to kidney aplasia or hypoplasia.

169 A standard-risk group of 19 patients with aplasia or in remission at transplantation demonstrated

170 o girdle reduction combined with hypoplasia, aplasia or mirror symmetry of all limb segments.

171 anatomical malformations (such as epididymal aplasia) or extrinsic compression of the ejaculatory duc

172 is marked by parathyroid hypoplasia, thymic aplasia, or hypoplasia and congenital cardiac abnormalit

173 donor red cell engraftment and pure red cell aplasia (PRCA) are well-recognized complications of majo

174 Acquired pure red cell aplasia (PRCA) can be associated with lymphoproliferativ

175 espectively, before developing pure red cell aplasia (PRCA) confirmed by bone marrow biopsy.

176 Pure red cell aplasia (PRCA) is a rare complication in patients with c

177 Pure red-cell aplasia (PRCA) is a rare hematologic disease characteriz

178 Pure red cell aplasia (PRCA) is a rare hematological disorder with mul

179 Pure red cell aplasia (PRCA) is a syndrome defined by a normocytic nor

180 IVIG) therapy in patients with pure red cell aplasia (PRCA) related to human parvovirus B19 (HPV-B19)

181 odies to epoetin, resulting in pure red cell aplasia (PRCA).

182 leading to the development of pure red cell aplasia (PRCA).

183 ting that the specific cause of vermal hypo-/aplasia precedes this defect.

184 oss of Top1 in TECs causes congenital thymic aplasia, precipitating T cell immunodeficiency.

185 Rs1 mice display fibrous dysplasia, BM aplasia, progressive loss of HSC numbers, and impaired m

186 ontrolled induction of tumor suppressor gene aplasia Ras homolog member I (ARHI) results in autophagi

187 ontrolled induction of tumor suppressor gene aplasia Ras homolog member I (ARHI) results in autophagi

188 imprinted Ras-related tumor suppressor gene aplasia Ras homolog member I (ARHI; also known as DIRAS3

189 of adenovirus-specific donor T cells during aplasia resulted in rapid and complete clearance of the

190 s effect of rituximab therapy: pure red cell aplasia resulting from chronic parvovirus B19 infection.

191 nt early death from radiation-induced marrow aplasia) results from more committed progenitors.

192 ions decline following CTL019-induced B-cell aplasia, several vaccine/pathogen-specific serum immunog

193 over, Yap and Taz CKO embryos had cerebellar aplasia similar to Dandy-Walker spectrum malformations o

194 ction, 33 (85%) of 39 patients showed marrow aplasia, six (15%) received re-induction.

195 d GVHD-induced lethality characterized by an aplasia syndrome.

196 ine, were more likely to achieve bone marrow aplasia than those with lower S-phase fractions (P = .01

197 CTL019 is frequently associated with B-cell aplasia that can persist for years.

198 splant recipients can cause chronic red cell aplasia that generally responds to IVIG therapy.

199 l maturation characterized by a rapid thymic aplasia that started after birth.

200 ia (DBA) is a rare macrocytic red blood cell aplasia that usually presents within the first year of l

201 Blackfan anemia (DBA), an inherited red cell aplasia, the bone marrow is characterized by a paucity o

202 Prolonged neutrophil aplasia thus occurs in patients with systemic immune dys

203 The mean (+/-SD) duration of B-cell aplasia was 112+/-47 days.

204 The probability of ongoing B-cell aplasia was 70% (95% CI 46-84; seven events) at 12 month

205 hat a patient would have relapse-free B-cell aplasia was 73% (95% CI, 57 to 94).

206 Pure red-cell aplasia was defined as transfusion-dependent anemia with

207 stration, the country in which pure red-cell aplasia was identified, and the date on which pure red-c

208 Protracted B-cell aplasia was not required for durable responses.

209 incidence of Eprex-associated pure red-cell aplasia was reached in 2001, interventions designed in r

210 and 1998, antibody-associated pure red-cell aplasia was reported in three patients who had undergone

211 ntified, and the date on which pure red-cell aplasia was reported.

212 mbryogenesis, whereas no reduction of vessel aplasia was seen, implying recovery is attributable to r

213 Prolonged aplasia was the dose-limiting toxicity, and the maximum-

214 ry and therapeutic response of pure red cell aplasia we have studied 37 patients.

215 s from 2 families with nonsyndromic cochlear aplasia, we identified homozygous 221-kb and 338-kb dele

216 tion of SDF-1 or its receptor lead to marrow aplasia, we investigated the effect of SDF-1 on megakary

217 erebral cortex and brainstem, and cerebellar aplasia were observed.

218 75 cases of epoetin-associated pure red-cell aplasia were reported for Eprex, 11 cases for Neorecormo

219 Biallelic Smc3 loss induced bone marrow aplasia with premature sister chromatid separation and r

220 actyly type B (BDB) is characterized by nail aplasia with rudimentary or absent distal and middle pha