We report the improved detectivity of AlxGa1−xN-based solar-blind p–i–n photodiodes with high zero-bias external quantum efficiency. The zero-bias external quantum efficiency was ∼42% at 269 nm, and increased to ∼46% at a reverse bias of −5 V. In addition, the photodiodes exhibited a low dark current density of 8.2×10−11 A/cm2 at a reverse bias of −5 V, which resulted in a large differential resistance. The high quantum efficiency and large differential resistance combine to yield a high detectivity of D*∼2.0×1014 cm Hz1/2 W−1. These results are attributed to the use of an Al0.6Ga0.4N window n region, which allows improved transmission to the absorption region, and to improved material quality.

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To evaluate the role of erythrocyte (RBC) membrane proteins in the invasion and maturation of Plasmodiumfalckqarum, we have studied, in culture, abnormal RBCs containing quantitative or qualitative membrane protein defects. These defects included hereditary spherocytosis (HS) due to decreases in the content of spectrin [HS(Sp+)], hereditary elliptocytosis (HE) due to protein 4.1 deficiency [HE(4.10)], HE due to a spectrin aI domain structural variant that results in increased content of spectrin dimers [HE(Spav"')], and band 3 structural variants. Parasite invasion, measured by the initial uptake of [3H1hypoxanthine 18 hr after inoculation with merozoites, was normal in all of the pathologic RBCs. In contrast, RBCs from six HS(Sp+) subjects showed marked growth inhibition that became apparent after the first or second growth cycle. Preincubation of HS(Sp+) RBCs in culture for 3 days did not alter these results. Normal parasite growth was observed in RBCs from one HS subject with normal membrane spectrin content. The extent of decreased parasite growth in HS(Sp+) RBCs closely correlated with the extent of RBC spectrin deficiency (r = 0.90). Homogeneous subpopulations of dense HS RBCs exhibited decreased parasite growth to the same extent as did HS whole blood. RBCs from four HE subjects showed marked parasite growth inhibition, the extent of which correlated with the content of spectrin dimers (r = 0.94). RBCs from two unrelated subjects with structural variants of band 3 sustained normal parasite growth. Decreased growth in the pathologic RBCs was not the result of decreased ATP or glutathione levels or of increased RBC hemolysis. We conclude that abnormal parasite growth in these RBCs is not the consequence of metabolic or secondary defects. Instead, we suggest that a functionally and structurally normal host membrane is indispensable for parasite growth and development.Several erythrocyte (RBC) genetic defects, particularly those with polymorphic gene frequencies, have most likely been expanded in human populations by the selective pressure of Plasmodium falciparum malaria (1). Among these are a and ,B thalassemias, ovalocytosis, glucose-6-phosphate dehydrogenase deficiency, and hemoglobinopathies produced by the presence of hemoglobin (Hb) S, Hb C, and Hb E. Advances have been made in our understanding by which these RBC genetic defects partially protect the bearer from the effects of the malaria infection.Hereditary spherocytosis (HS) and hereditary elliptocytosis (HE) MATERIALS AND METHODSSubject Material. HS and HE subjects were referred because of either acute anemia that occurred during the course of a mild febrile illness or chronic anemia. All HS subjects (AR, MR, MB, FB, LM, MP, and DM) had palpable spleen tips, except for AR, who had been splenectomized. All HS subjects and HE subjects AL, Sr., AL, Jr., and DW had elevated reticulocyte counts. HS was confirmed by RBC osmotic fragility tests, detection of increased abnormally dense RBCs (3), and spherocytes on blood smears. HE was confir...

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