ライフサイエンスコーパス: hydrops

1 iated with a high risk of developing corneal hydrops.

2 This may present prenatally as non-immune hydrops.

3 identified risk factors for developing acute hydrops.

4 al grafts after transplantation for resolved hydrops.

5 presented with moderate to severe anemia or hydrops.

6 largement, leading to low cardiac output and hydrops.

7 r insidiously, consistent with endolymphatic hydrops.

8 abyrinth with the formation of endolymphatic hydrops.

9 irth at 7 months, again with nonimmune fetal hydrops.

10 l was similar in eyes with and without prior hydrops.

11 Eleven cases of corneal hydrops (5.8%) occurred in our series during a mean foll

12 Stage 5 demonstrates hydrops; 5a, acute onset: Descemet's membrane rupture an

13 vival rates compared with eyes without prior hydrops: 86.5% +/- 4.0% vs 86.5% +/- 2.6% at 1 year, 61.

14 either in the presence or in the absence of hydrops (95 percent confidence interval, 86 to 100 perce

15 e-free survival rates with and without prior hydrops: 98.6% +/- 1.3% vs 97.1% +/- 1.3% at 1 year, 97.

16 Eleven fetuses had severe hydrops; all had polyhydramnios and a structurally abnor

17 t the time of PK in 44.6% of eyes with prior hydrops and 7.6% without prior hydrops (P < .001).

18 es were corneal neovascularization following hydrops and complications following PK.

19 ignificant predictors of in utero death were hydrops and earlier diagnosis, and of postnatal death we

20 multivariable analysis of all cases included hydrops and endocardial fibroelastosis.

21 red with whites, who were at a lower risk of hydrops and endocardial fibroelastosis.

22 ent compression of the right ventricle (RV); hydrops and low cardiac output are often associated.

23 neal features in eyes that developed corneal hydrops and those that did not develop this complication

24 n the duration of corneal edema during acute hydrops, and have improved the survival of corneal graft

25 Fetal lung masses associated with hydrops are nearly 100% fatal.

26 e, acute and chronic red cell aplasia, fetal hydrops, arthropathy, and other disorders.

27 Four with hydrops at presentation died perinatally, despite initia

28 nd posterior corneal pathology such as acute hydrops, Descematocele and pre-Descemet's dystrophies.

29 Attempts are being made to prevent fetal hydrops due to congenital heart defects, to recruit hypo

30 nctata, CHILD syndrome, lathosterolosis, and hydrops-ectopic calcification-moth-eaten skeletal dyspla

31 throderma and limb defects (CHILD syndrome), hydrops-ectopic calcification-moth-eaten skeletal dyspla

32 rlier diagnosis, and of postnatal death were hydrops, endocardial fibroelastosis, and lower ventricul

33 al effusions (2 of 2), ascites (6 of 8), and hydrops fetalis (5 of 8).

34 erited form of lymphatic-related (nonimmune) hydrops fetalis (LRHF).

35 etuses with incessant tachycardia and either hydrops fetalis (n=24) or ventricular dysfunction (n=2)

36 efects in the formation of the heart lead to hydrops fetalis and are likely the cause of embryonic le

37 /-) embryos die at midgestation with extreme hydrops fetalis and cardiovascular abnormalities, includ

38 The Calcrl-/- embryos exhibit extreme hydrops fetalis and cardiovascular defects, including th

39 m of GLD with a high incidence of non-immune hydrops fetalis and childhood onset of facial and four l

40 t with severe nonimmune hemolytic anemia and hydrops fetalis at birth.

41 a complicated by ventricular dysfunction and hydrops fetalis carries a significant risk of morbidity

42 The majority of hydrops fetalis cases are nonimmune conditions that pres

43 Hydrops fetalis describes fluid accumulation in at least

44 vious sibling born with hemolytic anemia and hydrops fetalis died on the second day of life.

45 s in 8 group A versus 0 group B (P < 0.007), hydrops fetalis in 8 group A versus 0 group B (P < 0.007

46 absence of Adm may be one cause of nonimmune hydrops fetalis in humans.

47 re the correction of alpha-thalassemia major hydrops fetalis in transgene-free iPS cells using zinc f

48 In utero infection may result in hydrops fetalis or congenital anemia.

49 icular tachycardia, even when accompanied by hydrops fetalis or ventricular dysfunction.

50 Hemoglobin (Hb) Bart's hydrops fetalis syndrome (BHFS) resulting from alpha(0)-

51 nd neonatal deaths associated with nonimmune hydrops fetalis uncovered 2 heterozygous missense varian

52 oglobin [Hb] H disease) or lethal (Hb Bart's hydrops fetalis).

53 that is characterized by multiple anomalies, hydrops fetalis, and death within the first 8 wk of life

54 of diverse pathological outcomes, including hydrops fetalis, fetal myocarditis, meningoencephalitis,

55 lly relevant thalassemias (hemoglobin Bart's hydrops fetalis, hemoglobin H disease, beta-thalassemia

56 h homozygous mutants develop polyhydramnios, hydrops fetalis, spina bifida occulta and osteochondrody

57 oss of beta-glucuronidase activity can cause hydrops fetalis, with in utero or postnatal death of the

58 unexplained cases of severe neonatal NSHA or hydrops fetalis.

59 linical and electrophysiologic predictors of hydrops fetalis; and 3) to describe the medium-term foll

60 d moderate anemia; and 31, including 12 with hydrops, had severe anemia.

61 d in vivo imaging of the cornea during acute hydrops has led to an enhanced understanding of the path

62 Effective management of acute corneal hydrops in keratoconus is based on recognizing and addre

63 In fact, prenatal hydrops is a common manifestation of MPS VII because of

64 Acute corneal hydrops is an incompletely understood complication of ke

65 V-IgG in fetuses with B19V-derived anemia or hydrops is most likely due to a limited materno-fetal tr

66 Eyes with prior hydrops (n = 74) had lower endothelial rejection-free su

67 ted hereditary stomatocytosis and non-immune hydrops of unknown aetiology.

68 evere childhood manifestations include fetal hydrops or sudden infant death syndrome.

69 es with prior hydrops and 7.6% without prior hydrops (P < .001).

70 er gestation at presentation correlated with hydrops (p < 0.02, p < 0.05), but mechanism of tachycard

71 In fetuses without hydrops that are at risk because of maternal red-cell al

72 uctural changes that take place during acute hydrops, the factors that influence its duration, and se

73 examining 3D T2 sequences, and endolymphatic hydrops was identified on delayed post-contrast FLAIR se

74 Hydrops was present in 12 of 30 fetuses.

75 rization, a frequent complication of corneal hydrops, was associated with increased risk of endotheli

76 l were significantly associated with corneal hydrops, whereas the presence of corneal scarring was a

77 86 to 100 percent for the 23 fetuses without hydrops), with a false positive rate of 12 percent.