1 ve a normal total blood volume but a reduced red cell mass.

2 cated PHD2 as the key PHD isoform regulating red cell mass.

3 ion resulting from hypoxia-induced increased red cell mass.

4 y the knowledge it also enlarges circulating red cell mass and increases platelet aggregability.

5 ency, and point to multifactorial control of red cell mass by PHD2.

6                         In six participants, red cell mass decreased by 7% to 10% within a few days o

7  acute plethora in microgravity, astronauts' red-cell mass falls too rapidly to be explained by dimin

8                                   Changes in red cell mass, hematocrit, hemoglobin concentration, ret

9 iotensin-converting enzyme inhibitors reduce red cell mass in renal transplant recipients with erythr

10 ly hemolyzed, allowing rapid adaptation when red cell mass is excessive for a new environment.

11          The central pathway for controlling red cell mass is the PHD (prolyl hydroxylase domain prot

12 tral pathway for oxygen-dependent control of red cell mass is the prolyl hydroxylase domain protein (

13                It is usually considered that red-cell mass is controlled by erythropoietin-driven bon

14 ly changes in concentration and not absolute red cell mass of haemoglobin can be identified; and disa

15 HIF-1alpha) and HIF-2alpha levels, increased red cell mass, propensity to thrombosis, and early morta

16 e diagnosed as PV owing to an elevated Cr-51 red cell mass (RCM), JAK2 positivity, and at least 1 min

17 nous erythropoietin prevented the changes in red cell mass, serum ferritin level, and(13)C-heme.

18 ation, the erythropoietic response increases red cell mass such that arterial O2 content (C(aO2)) is

19 ic conditions are characterized by increased red cell mass, which is caused by circulating serum fact