ライフサイエンスコーパス: MCHC

1 owever, current methods for RBC analysis and MCHC quantification rely on bulk measurements.

2 l associations of HBE1 variants with HCT and MCHC, the alpha-globin gene cluster variants with RBC an

3 ount, mean corpuscular volume (MCV), MCH and MCHC] and the G6PD locus on Xq28 [lead SNP rs1050828; P

4 The top significant SNP for HCT, MCH, and MCHC was found within a genomic region mainly populated

5 ha-globin gene cluster variants with RBC and MCHC, and a variant at the ARHGEF3 locus with PLT, as we

6 can explain the inverse relationship between MCHC and RBC thickness determined from >250 animal speci

7 l mean corpuscular hemoglobin concentration (MCHC) and contributes significantly to pathology.

8 , mean corpuscular hemoglobin concentration (MCHC) and red blood cell count (RBC).

9 Mean corpuscular hemoglobin concentration (MCHC) decreased and the percent high-density red cells w

10 o mean corpuscular hemoglobin concentration (MCHC) in SS and AA RBCs when normalized to the maximal v

11 Mean corpuscular hemoglobin concentration (MCHC) is an important pathological metric in both identi

12 e mean corpuscular hemoglobin concentration (MCHC) should be more therapeutically effective than drug

13 r mean corpuscular hemoglobin concentration (MCHC) to a high of 72.4% for red blood cell (RBC) number

14 , mean corpuscular hemoglobin concentration (MCHC), red cell distribution width (RDW), the percentage

15 d Mean Corpuscular Hemoglobin Concentration (MCHC).

16 r mean corpuscular hemoglobin concentration (MCHC).

17 RDW) and mean cell hemoglobin concentration (MCHC).

18 n mean corpuscular hemoglobin concentration (MCHC).

19 uscular hemoglobin (MCH), MCH concentration (MCHC), mean corpuscular volume (MCV), platelet count (PL

20 ; mean corpuscular hemoglobin concentration [MCHC], >46 g/dL) that contains many irreversibly sickled

21 F, Hct, Hb, and mean corpuscular Hb content (MCHC) from prefortification (1988-1994) and postfortific

22 V), and mean corpuscular hemoglobin content (MCHC) was performed in wan/wan mice from an F2 intercros

23 ne supplementation reduces red cell density (MCHC) in S+S-Antilles mice is by inhibiting the Ca(++)-a

24 ed with their results regarding T2DM, except MCHC.

25 he maximal volume-stimulated (VS(max)) flux (MCHC < 270 g/L [27 g/dL]).

26 ct (population median); #4) estimate Hct (Hb/MCHC); #5) assume SFOL = 0 and estimate Hct; and #6) pre

27 ferences in the mean corpuscular hemoglobin (MCHC) and platelet number at day 10 and white blood cell

28 ced Cl-dependent RVD that resulted in higher MCHC in SS than AA reticulocytes.

29 SS RBCs but KCC-mediated RVD produces higher MCHC in SS than AA reticulocytes.

30 kness must be reduced as appropriate for its MCHC.

31 ing normal density (ND; 1.080 to 1.090 g/mL; MCHC, 32 to 36 g/dL) SS discocytes to repetitive oxygena

32 termediate density (ID; 1.090 to 1.114 g/mL; MCHC, 36 to 46 g/dL).

33 g water as an internal standard, we quantify MCHC of healthy RBCs and RBCs infected with Plasmodium y

34 s were used to track changes in reticulocyte MCHC during KCC-mediated regulatory volume decrease (RVD

35 tes to the disease process by increasing the MCHC and rendering the cells more susceptible to polymer

36 Swelling to MCHC of 260 g/L (26 g/dL) produced Cl-dependent RVD that

37 a = - 0.36, 95% CI - 0.61 to - 0.10) whereas MCHC increased in the OD group as compared to decrease i