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1 ed serum amyloid A production or EPO-induced reticulocytosis.
2 rastingly, produced greater splenomegaly and reticulocytosis.
3 et, coincided with pronounced iron-deficient reticulocytosis.
4  Hemolytic anemia was defined as anemia with reticulocytosis (ACR criterion).
5                     Tg58 x Tg98 mice exhibit reticulocytosis, an elevated white blood cell count and
6               AHSP-gene-ablated mice exhibit reticulocytosis and abnormal erythrocyte morphology with
7 rescent erythrodontia, hemolytic anemia with reticulocytosis and extramedullary erythropoiesis, and,
8 r than 2-g/dL increase in Hb, and diminished reticulocytosis and extramedullary erythropoiesis.
9  and hemoglobin nadirs and provided enhanced reticulocytosis and faster recovery, compared with contr
10 < .05), and greater ERFE was associated with reticulocytosis and Hb repletion (P< .01).
11               Here, we demonstrated that low reticulocytosis and suppressed erythropoietin (Epo)-indu
12                            Infection induced reticulocytosis and the premature egress of immature pro
13 eductions in Hoxa7(-/-) mice correlated with reticulocytosis and thrombocytopenia without anemia.
14  Peripheral blood counts revealed a profound reticulocytosis and thrombocytosis despite normal serum
15 reased hematocrit and red blood cell counts, reticulocytosis, and bilirubinemia, leading secondarily
16  treated with eculizumab, persistent anemia, reticulocytosis, and biochemical evidence of hemolysis a
17 e of hyperparasitemia, more profound anemia, reticulocytosis, and death 14 to 21 days after infection
18 ased BMP, improvement in anemia with reduced reticulocytosis, and decreased ex vivo sickling.
19 bly sickled cells in their peripheral blood, reticulocytosis, and other phenotypic features of SCA.
20 o naive mice, and the development of anemia, reticulocytosis, and RBC turnover was determined.
21 rized by hypochromic red blood cells (RBCs), reticulocytosis, and splenomegaly.
22 topenia, platelet dysfunction, splenomegaly, reticulocytosis, and unbalanced hemoglobin chain synthes
23 and increased RBC turnover with compensatory reticulocytosis, but anemia was not as severe as that in
24        In both strains, parasitemia preceded reticulocytosis, but reticulocytes remained refractory t
25              In immunocompetent C.B-17 mice, reticulocytosis developed early, despite a marginal and
26                           Likewise, an early reticulocytosis developed in resistant BALB/cBy and B10.
27  and C-reactive protein) and did not exhibit reticulocytosis during the weeks following discharge.
28                                    Increased reticulocytosis, enhanced ex vivo erythrocyte sickling,
29 tion; this treatment concomitantly decreased reticulocytosis, erythropoietin abundance and splenomega
30 ly in RBCs and causes microcytic anemia with reticulocytosis, implicating Rac GTPases as dynamic regu
31 ticulocytes are rarely infected, the delayed reticulocytosis in susceptible strains may result from p
32 hroid progenitors and, ultimately, transient reticulocytosis in the circulation.
33                          Both rats developed reticulocytosis, increased hemoglobin, and bone marrow h
34                                          Low reticulocytosis, indicating reduced red blood cell (RBC)
35 nt of sickle-associated hemolytic anemia and reticulocytosis, key pathophysiological biomarkers of SC
36 isease associated with significantly greater reticulocytosis, leukocytosis, neutrophilia and thromboc
37                       Marked anemia, despite reticulocytosis, moderate to mild weight loss and some m
38 use recovery from anaemia requires transient reticulocytosis, our findings imply that in malarious re
39 y perturbed erythroid development and led to reticulocytosis plus heightened splenic erythropoiesis.
40  Increased levels of circulating Epo lead to reticulocytosis, polycythemia, and suppression of hepati
41 globin levels into the normal range, reduced reticulocytosis, reversal of splenomegaly and up to 7% b
42 displayed microcytic hypochromic anemia with reticulocytosis that was partially compensated by avid e
43 ociated with decreased RBCs volume (MCV) and reticulocytosis; the flow-cytometric assay showed good c
44 s a reflection of parasitemia level, but low reticulocytosis was evident despite differences in paras
45 vated serum IgM or the presence of anemia or reticulocytosis which is mainly seen in response to auto
46 tra-medullary erythropoiesis and concomitant reticulocytosis, which protected mice from lethal experi
47  expression were not caused by a decrease in reticulocytosis with HU therapy.
48 s were well tolerated and appeared to effect reticulocytosis, with a peak at day 11 or 15 in most pat