ライフサイエンスコーパス: erythrocytosis

1 ain, adrenal glands, and pancreas as well as erythrocytosis.

2 re, severe lower-urinary-tract symptoms, and erythrocytosis.

3 majority of these patients display isolated erythrocytosis.

4 o erythropoietin and the resultant excessive erythrocytosis.

5 excluded to avoid confounding from secondary erythrocytosis.

6 ve been identified in patients with familial erythrocytosis.

7 7Arg, identified from patients with familial erythrocytosis.

8 henotype displayed by patients with familial erythrocytosis.

9 le knockout of Phd1 and Phd3 led to moderate erythrocytosis.

10 po protein in the serum, which led to severe erythrocytosis.

11 n reported to date, associated with familial erythrocytosis.

12 ght be an important contributor to excessive erythrocytosis.

13 ans use phlebotomy as their first choice for erythrocytosis.

14 with autosomal dominantly inherited familial erythrocytosis.

15 n distinguishing PV from nonclonal causes of erythrocytosis.

16 mia vera (PV) but not in those with reactive erythrocytosis.

17 thality at 12-16 days associated with marked erythrocytosis.

18 or (EpoR), which is associated with familial erythrocytosis.

19 ic role for angiotensin II in posttransplant erythrocytosis.

20 ceptor) was administered to 23 patients with erythrocytosis.

21 nguish polycythemia vera from other-forms of erythrocytosis.

22 ribute to the pathogenesis of posttransplant erythrocytosis.

23 ronic myelogenous leukemia, 6 with secondary erythrocytosis, 2 with iron-deficiency anemia, 4 with he

24 hematopoiesis, and substantially suppressed erythrocytosis and angiogenic sprouting.

25 e models of erythropoietic stress, including erythrocytosis and beta-thalassemia.

26 hat certain PHD2 variants linked to familial erythrocytosis and cancer are highly selective for CODD

27 We have screened 78 patients with erythrocytosis and found 8 of Bangladeshi and Pakistani

28 These data suggest that erythrocytosis and granulocytosis in JAK2(V617F) mice ar

29 er and R1063H from the father, and exhibited erythrocytosis and megakaryocytic atypia but normal plat

30 isplay, in a mutation dose-dependent manner, erythrocytosis and pulmonary hypertension with a high de

31 ance wild-type (WT) NF-E2 function and cause erythrocytosis and thrombocytosis in a murine model.

32 en identified in familial forms of nonclonal erythrocytosis and thrombocytosis, respectively.

33 rocytes, anemia, and iron overload and PV by erythrocytosis and thrombosis.

34 in upregulation of the erythropoietin gene, erythrocytosis, and augmented hypoxic ventilatory respon

35 apnea, ocular neovascularization, hereditary erythrocytosis, and cancer.

36 white fat, low blood pressure, compensatory erythrocytosis, and hepatic steatosis in Shp2(fat-/-) mi

37 ignificant minority of physicians undertreat erythrocytosis, and little consensus exists regarding th

38 nosis of several diseases, including anemia, erythrocytosis, and thalassemias.

39 w kindred with dominantly inherited familial erythrocytosis associated with heterozygosity for a dele

40 e previously identified and characterized an erythrocytosis-associated HIF2A mutation, G537W.

41 More recently, we reported two additional erythrocytosis-associated HIF2A mutations, G537R and M53

42 f these two mutants as well as a third novel erythrocytosis-associated mutation, P534L.

43 Studies of humans have identified erythrocytosis-associated, heterozygous point mutations

44 oietin (EPO), a glycoprotein that stimulates erythrocytosis, at the level of transcription and also p

45 ons, and astrocytes that displayed excessive erythrocytosis because of severe overproduction of EPO,

46 that JAK2 E846D predominantly contributes to erythrocytosis, but is not sufficient for the full patho

47 f 21 (52%) study participants with excessive erythrocytosis, but were undetectable in high altitude o

48 po pathway, whereas PHD2 deficiency leads to erythrocytosis by activating the renal Epo pathway.

49 s conditional knock-outs of Phd2 reveal that erythrocytosis can be induced by homozygous and heterozy

50 ressure of O(2) in the blood, accompanied by erythrocytosis characterized by elevated erythropoietin

51 ropoiesis and suggest that levels of Epo and erythrocytosis could represent noninvasive surrogate mar

52 m a biological continuum, with the degree of erythrocytosis determined by physiological or genetic mo

53 in terms of age, smoking history, degree of erythrocytosis, ejection fraction or use of aspirin or w

54 Phd2(P294R/+) mice display a degree of erythrocytosis equivalent to that seen in Phd2(+/-) mice

55 Familial erythrocytosis (familial polycythemia) inherited as an a

56 Primary familial erythrocytosis (familial polycythemia) is a rare myelopr

57 region are associated with dominant familial erythrocytosis (FE), a benign clinical condition charact

58 PD reminiscent of human PV, characterized by erythrocytosis, granulocytosis, extramedullary hematopoi

59 Rare patients with erythrocytosis have mutations in the genes encoding for

60 ssense mutations in HIF-2alpha as a cause of erythrocytosis, highlight the importance of this HIF-alp

61 as of JAK1 V658F, and prevents induction of erythrocytosis in a JAK2 V617F myeloproliferative neopla

62 eveloped a pronounced polycythemia vera-like erythrocytosis in conjunction with microcytosis.

63 dominant JAK2V617F-homzygous subclone drives erythrocytosis in many PV patients, with alternative mec

64 of the mutants, K539I and N622I, resulted in erythrocytosis in mice.

65 f A3669G likely contribute to development of erythrocytosis in PV and provide a potential target for

66 5881G>T was found to segregate with isolated erythrocytosis in the affected family and this mutation

67 Conversion was complicated by posttransplant erythrocytosis in two patients.

68 The resultant erythrocytosis is driven by increased numbers of early e

69 basis for the observed phenotype of isolated erythrocytosis is heterozygosity for a novel nonsense mu

70 Erythrocytosis is present in most patients, but excessiv

71 The Phd2(P294R/+)-associated erythrocytosis is reversed in a Hif2a(+/-), but not a Hi

72 A link between elevated TAL1 and excessive erythrocytosis is suggested by erythroid progenitor cell

73 ell mass in renal transplant recipients with erythrocytosis is unclear.

74 nd congenital polycythemia (PFCP or familial erythrocytosis) is a rare proliferative disorder of eryt

75 l polycythemia (PFCP; also known as familial erythrocytosis) is characterized by elevated red blood c

76 Increased production of red blood cells (erythrocytosis) occurred in both mouse and primate model

77 rent in PTE compared with non posttransplant erythrocytosis or normal controls.

78 ions that MPN disease, manifesting either as erythrocytosis or thrombocytosis, can be initiated clona

79 men with (study group) and without excessive erythrocytosis (packed-cell volume >65%) living in Cerro

80 ggest that PHD1/3 double deficiency leads to erythrocytosis partly by activating the hepatic HIF-2alp

81 eral aspects of the human disease, including erythrocytosis, pathologic angiogenesis in the brain and

82 progenitors of PTE versus non posttransplant erythrocytosis patients and by 32% in PTE patients versu

83 More recently, erythrocytosis patients with heterozygous point mutation

84 rs in the peripheral blood of posttransplant erythrocytosis patients.

85 The pathogenesis of posttransplant erythrocytosis (PTE) has been elusive.

86 d in the pathogenesis of posttransplantation erythrocytosis (PTE).

87 treatment of choice for posttransplantation erythrocytosis (PTE).

88 esult of insufficient (anemia) or excessive (erythrocytosis) red blood cell production.

89 patients with PV, 7 patients with secondary erythrocytosis (SE), and 10 normal controls.

90 e a Swedish family with dominant FE in which erythrocytosis segregates with a new truncation in the n

91 issense mutation in PHD2 is the cause of the erythrocytosis, show that this occurs through haploinsuf

92 h continuous injections of Epo results in an erythrocytosis that is not seen in HM mice.

93 f PHD2 in mice leads to HIF-2alpha-dependent erythrocytosis, whereas HIF-1alpha protects these mice,

94 at contrasts with both the Andean "classic" (erythrocytosis with arterial hypoxemia) and the more rec

95 by E846D above a threshold level leading to erythrocytosis with megakaryocyte abnormalities.

96 PV is characterized by erythrocytosis with suppressed endogenous erythropoietin

97 (AT1) antagonist, ameliorate posttransplant erythrocytosis, without altering serum erythropoietin le