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1 ed by 2 intriguing features: ketogenesis and erythrocytosis.
2 ceptor) was administered to 23 patients with erythrocytosis.
3 nguish polycythemia vera from other-forms of erythrocytosis.
4 ribute to the pathogenesis of posttransplant erythrocytosis.
5 omboembolic events compared to those without erythrocytosis.
6  the ERK2-DBP domain in mice caused baseline erythrocytosis.
7 ks regenerative erythropoiesis to pathogenic erythrocytosis.
8 ted EpoR protects against JAK2(V617F)-driven erythrocytosis.
9 ociated with an increased risk of developing erythrocytosis.
10 nts of the O2-sensing pathway cause familial erythrocytosis.
11 myeloproliferative neoplasm characterized by erythrocytosis.
12 re widely used and have been shown to induce erythrocytosis.
13 rance regarding the safety of SGLT2i-induced erythrocytosis.
14 amongst high altitude natives with excessive erythrocytosis.
15  majority of these patients display isolated erythrocytosis.
16 tion for why Tibetans are not predisposed to erythrocytosis.
17 n, to splenic erythropoiesis and to dramatic erythrocytosis.
18 ain, adrenal glands, and pancreas as well as erythrocytosis.
19 re, severe lower-urinary-tract symptoms, and erythrocytosis.
20 o erythropoietin and the resultant excessive erythrocytosis.
21 che, and tinnitus) in the setting of extreme erythrocytosis.
22 excluded to avoid confounding from secondary erythrocytosis.
23 ve been identified in patients with familial erythrocytosis.
24 7Arg, identified from patients with familial erythrocytosis.
25 henotype displayed by patients with familial erythrocytosis.
26 and CMS(-) individuals had similar levels of erythrocytosis.
27 le knockout of Phd1 and Phd3 led to moderate erythrocytosis.
28 po protein in the serum, which led to severe erythrocytosis.
29 n reported to date, associated with familial erythrocytosis.
30 ght be an important contributor to excessive erythrocytosis.
31 ans use phlebotomy as their first choice for erythrocytosis.
32 with autosomal dominantly inherited familial erythrocytosis.
33 n distinguishing PV from nonclonal causes of erythrocytosis.
34 mia vera (PV) but not in those with reactive erythrocytosis.
35 thality at 12-16 days associated with marked erythrocytosis.
36 or (EpoR), which is associated with familial erythrocytosis.
37 ic role for angiotensin II in posttransplant erythrocytosis.
38 ronic myelogenous leukemia, 6 with secondary erythrocytosis, 2 with iron-deficiency anemia, 4 with he
39 ngiectasias; (2) elevated erythropoietin and erythrocytosis; (3) monoclonal gammopathy; (4) perinephr
40 tation that abolishes the PXLE motif display erythrocytosis, a reflection of HIF pathway dysregulatio
41  hematopoiesis, and substantially suppressed erythrocytosis and angiogenic sprouting.
42 e models of erythropoietic stress, including erythrocytosis and beta-thalassemia.
43 hat certain PHD2 variants linked to familial erythrocytosis and cancer are highly selective for CODD
44 tion of HIF ultimately underlies PHD2-driven erythrocytosis and challenge the currently held uncertai
45            We have screened 78 patients with erythrocytosis and found 8 of Bangladeshi and Pakistani
46 irculating EPO from patients with hereditary erythrocytosis and from healthy newborns were analyzed b
47                      These data suggest that erythrocytosis and granulocytosis in JAK2(V617F) mice ar
48  with other adverse effects, such as causing erythrocytosis and gynaecomastia, worsening obstructive
49 erences, and odds ratios (ORs) for new-onset erythrocytosis and hemoglobin increase greater than 0.5
50 r (HIF) prolyl-4-hydroxylase 2 (PHD2), cause erythrocytosis and in rare cases the development of neur
51 s (SGLT2i) use in diabetic patients leads to erythrocytosis and increases the incidence of arterial a
52 myeloproliferative neoplasm characterized by erythrocytosis and is almost universally associated with
53 a volume is frequently expanded, masking the erythrocytosis and making diagnosis difficult if this es
54 er and R1063H from the father, and exhibited erythrocytosis and megakaryocytic atypia but normal plat
55             PV is typically characterized by erythrocytosis and often leukocytosis and thrombocytosis
56 ygous progenitors activate STAT5, leading to erythrocytosis and polycythemia.
57 of SGLT2 inhibitors to promote ketonemia and erythrocytosis and potentially underlies their actions t
58            We describe a patient with marked erythrocytosis and prominent mitochondrial alterations a
59 isplay, in a mutation dose-dependent manner, erythrocytosis and pulmonary hypertension with a high de
60 rs promote gluconeogenesis, ketogenesis, and erythrocytosis and reduce uricemia, the hallmarks of nut
61            CMS is characterized by excessive erythrocytosis and related clinical symptoms.
62 ance wild-type (WT) NF-E2 function and cause erythrocytosis and thrombocytosis in a murine model.
63 en identified in familial forms of nonclonal erythrocytosis and thrombocytosis, respectively.
64 rocytes, anemia, and iron overload and PV by erythrocytosis and thrombosis.
65  delivery (by stimulating erythropoietin and erythrocytosis) and decrease oxygen consumption.
66  in upregulation of the erythropoietin gene, erythrocytosis, and augmented hypoxic ventilatory respon
67 apnea, ocular neovascularization, hereditary erythrocytosis, and cancer.
68  white fat, low blood pressure, compensatory erythrocytosis, and hepatic steatosis in Shp2(fat-/-) mi
69 ignificant minority of physicians undertreat erythrocytosis, and little consensus exists regarding th
70 nosis of several diseases, including anemia, erythrocytosis, and thalassemias.
71 ltitude populations suffering from excessive erythrocytosis, Andeans with chronic mountain sickness,
72 w kindred with dominantly inherited familial erythrocytosis associated with heterozygosity for a dele
73 ature neonates and in patients with acquired erythrocytosis associated with liver diseases.
74 e previously identified and characterized an erythrocytosis-associated HIF2A mutation, G537W.
75    More recently, we reported two additional erythrocytosis-associated HIF2A mutations, G537R and M53
76 f these two mutants as well as a third novel erythrocytosis-associated mutation, P534L.
77                           In addition, human erythrocytosis-associated mutations in the zinc finger o
78            Studies of humans have identified erythrocytosis-associated, heterozygous point mutations
79 oietin (EPO), a glycoprotein that stimulates erythrocytosis, at the level of transcription and also p
80 ons, and astrocytes that displayed excessive erythrocytosis because of severe overproduction of EPO,
81 that JAK2 E846D predominantly contributes to erythrocytosis, but is not sufficient for the full patho
82 f 21 (52%) study participants with excessive erythrocytosis, but were undetectable in high altitude o
83 po pathway, whereas PHD2 deficiency leads to erythrocytosis by activating the renal Epo pathway.
84 s conditional knock-outs of Phd2 reveal that erythrocytosis can be induced by homozygous and heterozy
85                      We found that secondary erythrocytosis can be related to variants in EPO that le
86 ressure of O(2) in the blood, accompanied by erythrocytosis characterized by elevated erythropoietin
87 T2i use was associated with a higher risk of erythrocytosis compared with DPP-4is and GLP-1RAs; howev
88 ropoiesis and suggest that levels of Epo and erythrocytosis could represent noninvasive surrogate mar
89          The primary outcome was the risk of erythrocytosis, defined by elevated hemoglobin and hemat
90 m a biological continuum, with the degree of erythrocytosis determined by physiological or genetic mo
91 U-E pathway is the major pathway involved in erythrocytosis driven by the oncogenic JAK2 mutant JAK2(
92  and humans who lack functional IRP1 develop erythrocytosis due to erythropoietin (EPO) overproductio
93                                    Excessive erythrocytosis (EE) is a major hallmark of patients suff
94  Andean highlanders suffering from excessive erythrocytosis (EE); however, the mechanistic link betwe
95  in terms of age, smoking history, degree of erythrocytosis, ejection fraction or use of aspirin or w
96       Phd2(P294R/+) mice display a degree of erythrocytosis equivalent to that seen in Phd2(+/-) mice
97                                     Familial erythrocytosis (familial polycythemia) inherited as an a
98                             Primary familial erythrocytosis (familial polycythemia) is a rare myelopr
99 region are associated with dominant familial erythrocytosis (FE), a benign clinical condition charact
100 PD reminiscent of human PV, characterized by erythrocytosis, granulocytosis, extramedullary hematopoi
101      Among SGLT2i users, those who developed erythrocytosis had increased incidence of thromboembolic
102                           Rare patients with erythrocytosis have mutations in the genes encoding for
103                                              Erythrocytosis (hemoglobin >16.5 mg/dL in men or >16.0 m
104 ssense mutations in HIF-2alpha as a cause of erythrocytosis, highlight the importance of this HIF-alp
105  as of JAK1 V658F, and prevents induction of erythrocytosis in a JAK2 V617F myeloproliferative neopla
106 sociated with a significantly higher risk of erythrocytosis in both male (hemoglobin > 16.5 g/dL: HR
107 sociated with a significantly higher risk of erythrocytosis in both male (HR 1.605 [1.573, 1.636] and
108 eveloped a pronounced polycythemia vera-like erythrocytosis in conjunction with microcytosis.
109 dominant JAK2V617F-homzygous subclone drives erythrocytosis in many PV patients, with alternative mec
110 of the mutants, K539I and N622I, resulted in erythrocytosis in mice.
111 t options for both controlling the degree of erythrocytosis in polycythemia vera (PV) patients as wel
112 f A3669G likely contribute to development of erythrocytosis in PV and provide a potential target for
113 5881G>T was found to segregate with isolated erythrocytosis in the affected family and this mutation
114 Conversion was complicated by posttransplant erythrocytosis in two patients.
115          However, unlike secondary causes of erythrocytosis, in PV, the plasma volume is frequently e
116 multisystem involvement, including secondary erythrocytosis, increased thrombotic and bleeding diathe
117                                The resultant erythrocytosis is driven by increased numbers of early e
118 basis for the observed phenotype of isolated erythrocytosis is heterozygosity for a novel nonsense mu
119                                              Erythrocytosis is present in most patients, but excessiv
120                 The Phd2(P294R/+)-associated erythrocytosis is reversed in a Hif2a(+/-), but not a Hi
121   A link between elevated TAL1 and excessive erythrocytosis is suggested by erythroid progenitor cell
122 ell mass in renal transplant recipients with erythrocytosis is unclear.
123 nd congenital polycythemia (PFCP or familial erythrocytosis) is a rare proliferative disorder of eryt
124 l polycythemia (PFCP; also known as familial erythrocytosis) is characterized by elevated red blood c
125                   Our findings indicate that erythrocytosis, leukocytosis, and moderate splenomegaly
126 HSC but it can present initially as isolated erythrocytosis, leukocytosis, thrombocytosis, or any com
127     Increased production of red blood cells (erythrocytosis) occurred in both mouse and primate model
128                                    Secondary erythrocytosis often results from conditions that cause
129 hrombocytosis and primary myelofibrosis, but erythrocytosis only occurs in PV.
130 rent in PTE compared with non posttransplant erythrocytosis or normal controls.
131 ions that MPN disease, manifesting either as erythrocytosis or thrombocytosis, can be initiated clona
132 men with (study group) and without excessive erythrocytosis (packed-cell volume >65%) living in Cerro
133 ggest that PHD1/3 double deficiency leads to erythrocytosis partly by activating the hepatic HIF-2alp
134 eral aspects of the human disease, including erythrocytosis, pathologic angiogenesis in the brain and
135 progenitors of PTE versus non posttransplant erythrocytosis patients and by 32% in PTE patients versu
136                               More recently, erythrocytosis patients with heterozygous point mutation
137 rs in the peripheral blood of posttransplant erythrocytosis patients.
138                     Among SGLT2i initiators, erythrocytosis prevalence in the SGLT2i vs DPP-4i cohort
139           The pathogenesis of posttransplant erythrocytosis (PTE) has been elusive.
140 d in the pathogenesis of posttransplantation erythrocytosis (PTE).
141  treatment of choice for posttransplantation erythrocytosis (PTE).
142 esult of insufficient (anemia) or excessive (erythrocytosis) red blood cell production.
143 on (WBC, platelets), as well as in secondary erythrocytosis (SE), a group of heterogeneous disorders
144  patients with PV, 7 patients with secondary erythrocytosis (SE), and 10 normal controls.
145 e a Swedish family with dominant FE in which erythrocytosis segregates with a new truncation in the n
146 issense mutation in PHD2 is the cause of the erythrocytosis, show that this occurs through haploinsuf
147 elps distinguish PV from secondary causes of erythrocytosis, such as tobacco smoking or sleep apnea.
148 h continuous injections of Epo results in an erythrocytosis that is not seen in HM mice.
149              We identified six families with erythrocytosis that was associated with circulating EPO
150 tly, among SGLT2i patients treated for their erythrocytosis, the men who discontinued SGLT2i had incr
151   A well-characterized example is congenital erythrocytosis-the non-pathogenic hyper-production of re
152 linical development to control PV associated erythrocytosis, thereby reducing the need for therapeuti
153 gression to MF in JAK2V617F mice, decreasing erythrocytosis, thrombocytosis, megakaryocyte hyperplasi
154 tations in JAK2 and clinically presents with erythrocytosis, variable degrees of systemic and vasomot
155                                    New-onset erythrocytosis was not associated with an increased risk
156 compared with DPP-4is and GLP-1RAs; however, erythrocytosis was not associated with thrombotic events
157 f PHD2 in mice leads to HIF-2alpha-dependent erythrocytosis, whereas HIF-1alpha protects these mice,
158 tients with ICD codes of polycythemia and/or erythrocytosis who had testing done for the presence of
159 at contrasts with both the Andean "classic" (erythrocytosis with arterial hypoxemia) and the more rec
160  by E846D above a threshold level leading to erythrocytosis with megakaryocyte abnormalities.
161                       PV is characterized by erythrocytosis with suppressed endogenous erythropoietin
162 and the close association of ketogenesis and erythrocytosis with the cardioprotective and renoprotect
163 ) code-based diagnosis of "polycythemia" or "erythrocytosis" with the true clinical diagnosis of thes
164                            Outcomes included erythrocytosis within 1 year of initiating SGLT2is, as w
165  (AT1) antagonist, ameliorate posttransplant erythrocytosis, without altering serum erythropoietin le

 
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