ライフサイエンスコーパス: aplasia

1 al aplasia and rudimentary uterus (Mullerian aplasia).

2 BM failure characterized by cytopenia and BM aplasia.

3 eases in platelet counts without intervening aplasia.

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

5 from hemorrhage in patients with bone marrow aplasia.

6 is, hypogammaglobulinemia, and pure red cell aplasia.

7 limb deformities and renal malformations or aplasia.

8 nt graft rejection was accompanied by marrow aplasia.

9 , a thin hypocellular retina and optic nerve aplasia.

10 ng Synthokine after radiation-induced marrow aplasia.

11 d by congenital limb defects and scalp cutis aplasia.

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

13 nd maturation, typically without evidence of aplasia.

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

15 antly with increased risk of renal dysplasia/aplasia.

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

17 erebellar vermis, ranging from hypoplasia to aplasia.

18 f risks associated with interventions during aplasia.

19 hy without concomitant development of B-cell aplasia.

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

21 eature in biopsies from patients with marrow aplasia.

22 curred at dose level 1 with prolonged marrow aplasia.

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

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

25 residual leukemic bone marrow blasts during aplasia.

26 one dog showed rejection and died of marrow aplasia.

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

28 otherapy or those associated with inevitable aplasia.

29 ajor cardiovascular defects and thymus gland aplasia.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

44 5 monoclonal antibody can produce persistent aplasia and whether it could facilitate syngeneic or all

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

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

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

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

49 Chronic red cell aplasia can develop in immunocompromised patients includ

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

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

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

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

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

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

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

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

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

59 Aplasia cutis manifests with localized skin defects at b

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

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

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

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

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

65 80 percent in the incidence of pure red-cell aplasia due to Eprex.

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

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

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

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

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

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

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

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

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

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

76 SMG aplasia in Fgf8 ectoderm conditional mutants indicates t

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

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

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

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

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

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

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

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

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

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

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

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

89 7 adult patients with acquired pure red cell aplasia (median age, 64 years; range, 22 to 84 years).

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

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

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

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

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

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

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

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

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

99 Angiography revealed unilateral aplasia of the internal carotid artery.

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

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

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

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

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

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

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

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

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

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

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

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

112 Additionally, cerebellar aplasia or hypoplasia characteristic of Joubert syndrome

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

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

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

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

117 1 deletion mutants is associated with thymus aplasia or hypoplasia.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

156 75 cases of epoetin-associated pure red-cell aplasia were reported for Eprex, 11 cases for Neorecormo

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

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