the helical form (commonly right-handed) present in many proteins, deduced by Pauling and Corey from x-ray diffraction studies of proteins such as a-keratin; the helix is stabilized by hydrogen bonds between, differet eupeptide bonds, R1R2C = O and HN(R3)R4' groups, symbolized by the center dot in R1R2C = O · HN(R3)R4. In a true a helix, there are 3.6 amino acid residues per turn of the helix and an increase of 1.5 ? per residue.

thalassemia due to one of two or more genes that depress (severely or moderately) synthesis of a-globin chains by the chromosome with the abnormal gene. Heterozygous state: severe type, thalassemia minor with 5–15% of Hb Bart at birth, only traces of Hb Bart in adult; mild type, 1–2% of Hb Bart at birth, not detectable in adult. Homozygous state: severe type, erythroblastosis fetalis and fetal death, only Hb Bart and Hb H present; mild type not clinically defined.

the initial negative deflection in the electroretinogram, presumably reflecting retinal photoreceptor activity; an atrial deflection in an electrogram recorded from within the atrium of the heart; the first positive deflection of the atrial and venous pulses due to atrial systole. Further informationAlways consult your healthcare provider to ensure the information displayed on this page applies to your personal circumstances.

adrenergic receptors in effector tissues capable of selective activation and blockade by drugs; conceptually derived from the ability of certain agents, such as phenoxybenzamine, to block only some adrenergic receptors and of other agents, such as methoxamine, to activate only the same adrenergic receptors. Such receptors are designated as a-receptors. Their activation results in physiologic responses such as increased peripheral vascular resistance, mydriasis, and contraction of pilomotor muscles.