Figure 4.
Figure 4. Amelioration of spleen, liver, and kidney pathology in –383 γ-βA– corrected mice. (A) Spleen, liver, and kidney sections were analyzed at low (10×/0.45 NA objective for spleen and kidney, 40×/0.75 NA objective for liver) and high (100×/1.40 NA oil objective) magnification. In –383 γ-βA–corrected mice, normal splenic red and white pulp is observed, and virtually no pools of sickle erythrocytes or infarcts are evident. In livers of –383 γ-βA animals, focal areas of necrosis and aggregation of sickled erythrocytes are not observed; also, extramedullary hematopoiesis and hemosiderin deposition are absent. Kidneys of –383 γ-βA mice appear normal and free of the disruptive vascular RBC pooling. All sections were stained with hematoxylin-eosin. (B) Correction of splenomegaly in –383 γ-βA–corrected mice. Data from –1400 γ-βA–corrected mice are identical to –383 γ-βA–corrected animals.

Amelioration of spleen, liver, and kidney pathology in –383 γ-βA– corrected mice. (A) Spleen, liver, and kidney sections were analyzed at low (10×/0.45 NA objective for spleen and kidney, 40×/0.75 NA objective for liver) and high (100×/1.40 NA oil objective) magnification. In –383 γ-βA–corrected mice, normal splenic red and white pulp is observed, and virtually no pools of sickle erythrocytes or infarcts are evident. In livers of –383 γ-βA animals, focal areas of necrosis and aggregation of sickled erythrocytes are not observed; also, extramedullary hematopoiesis and hemosiderin deposition are absent. Kidneys of –383 γ-βA mice appear normal and free of the disruptive vascular RBC pooling. All sections were stained with hematoxylin-eosin. (B) Correction of splenomegaly in –383 γ-βA–corrected mice. Data from –1400 γ-βA–corrected mice are identical to –383 γ-βA–corrected animals.

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