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1 l associations of HBE1 variants with HCT and MCHC, the alpha-globin gene cluster variants with RBC an
2 ount, mean corpuscular volume (MCV), MCH and MCHC] and the G6PD locus on Xq28 [lead SNP rs1050828; P
3 ha-globin gene cluster variants with RBC and MCHC, and a variant at the ARHGEF3 locus with PLT, as we
4 can explain the inverse relationship between MCHC and RBC thickness determined from >250 animal speci
7 Mean corpuscular hemoglobin concentration (MCHC) decreased and the percent high-density red cells w
8 o mean corpuscular hemoglobin concentration (MCHC) in SS and AA RBCs when normalized to the maximal v
9 r mean corpuscular hemoglobin concentration (MCHC) to a high of 72.4% for red blood cell (RBC) number
12 uscular hemoglobin (MCH), MCH concentration (MCHC), mean corpuscular volume (MCV), platelet count (PL
13 ; mean corpuscular hemoglobin concentration [MCHC], >46 g/dL) that contains many irreversibly sickled
14 V), and mean corpuscular hemoglobin content (MCHC) was performed in wan/wan mice from an F2 intercros
15 ne supplementation reduces red cell density (MCHC) in S+S-Antilles mice is by inhibiting the Ca(++)-a
20 ing normal density (ND; 1.080 to 1.090 g/mL; MCHC, 32 to 36 g/dL) SS discocytes to repetitive oxygena
22 s were used to track changes in reticulocyte MCHC during KCC-mediated regulatory volume decrease (RVD
23 tes to the disease process by increasing the MCHC and rendering the cells more susceptible to polymer
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