AL 288-1 - Lucy or Lucifer: Gender confusion in the Pliocene
1974-1977; al-288-1; Anthropology; australopithecine; australopithecus-afarensis; body size; collections; dimensions; dimorphism; ethiopia; Evolutionary Biology; hadar formation; Lucy; obstetrics; pelvic size; pelvis; primates; reconstruction; sexual
Hausler & Schmid (1995) challenged the long held opinion that AL 288-1 (Australopithecus afarensis), popularly known as "Lucy," was female. They concluded that AL 288-1 was most probably male ("Lucifer") and, by extension, the hypodigm for A. afarensis consists of two species which differ from one another in body size; in their opinion, AL 288-1 was most probably a male of the smaller of the two species. Hausler & Schmid based their conclusion on an obstetric analysis of AL 288-1 and Sts 14 (A. africanus) and on a comparison of the two australopithecine pelves with those of modern humans. This study evaluates the pelvic anatomy and probable sex of AL 288-1 by both assessing the obstetric adequacy of its pelvis and critically reviewing Hausler & Schmid's (1995, 1997) analyses of australopithecine pelvic dimorphism and relative body size of AL 288-1. Three results are shown. First, using Hausler & Schmid's own data, AL 288-1's and Sts 14's pelves are seen not to be dimorphic with respect to each other, as are human males and females, but they are in fact comparable in both size and shape. Second, AL 288-1's pelvis would have been obstetrically adequate, even with an inferred newborn brain size (as suggested by Hausler & Schmid) for A. afarensis that is likely overestimated. Third, AL 288-1 is shown to be one of the smallest adult individuals in A. afarensis. We conclude that AL 288-1 and Sts 14 were the same sex, and that the name "Lucy" correctly identifies AL 288-1's gender as female. (C) 1998 Academic Press.
Tague R G; Lovejoy C O
Journal of Human Evolution
1998
1998-07
Journal Article
<a href="http://doi.org/10.1006/jhev.1998.0223" target="_blank" rel="noreferrer noopener">10.1006/jhev.1998.0223</a>
Androgen-receptor defect abolishes sex differences in nitric oxide and reactivity to vasopressin in rat aorta
aorta; arginine vasopressin; binding; brain; dependent gender differences; dimorphism; Endothelium; endothelium-derived relaxing factor; estrogen; gonadal steroid hormones; hormones; l-arginine; muscle; Physiology; Sport Sciences; testicular feminized rat; testicular feminized rat; vasoconstriction
Contractions of rat thoracic aorta to vasopressin WP) are threefold higher in females (F) than in males (M), primarily because nitric oxide (NO) attenuation of contraction is greater in M. To determine the role of the androgen receptor (AR) in this mechanism, vascular reactivity to VP was examined in thoracic aorta of the testicular-feminized male (Tfm) rat, which has an X-linked, recessive defect in AR function in affected M. Maximal contraction of normal aortas to VP was fourfold higher in F (4,128 +/- 291 mg/mg ring wt) than in M (971 +/- 133 mg); maximal response of Tfm (3,967 +/- 253 mg) was similar to that of normal F. N-G-nitro-L-arginine methyl ester increased maximal response to VP threefold in M but had no effect in F or Tfm. In contrast, maximal contraction of normal aortas to phenylephrine was 43% higher in M (4,011 +/- 179 mg) than in F (2,809 +/- 78 mg); maximal response of Tfm (2,716 +/- 126 mg) was similar to that of normal F. N-G-nitro-L-arginine methyl ester increased maximal response to phenylephrine by >50% in F and Tfm but had no effect in M. Maximal contractile response to 80 mM KCl did not differ among M, F, or Tfm. Thus androgens and normal vascular AR function are important in the greater NO-mediated attenuation of reactivity to VP in M than in F rat aorta, which may involve specific modulation of endothelial VP signal transduction pathways and NO release by androgens. These data also establish the importance of the Tfm rat as a model to study the effects of androgens on cardiovascular function.
Stallone J N; Salisbury R L; Fulton C T
Journal of Applied Physiology
2001
2001-12
Journal Article
<a href="http://doi.org/10.1152/jappl.2001.91.6.2602" target="_blank" rel="noreferrer noopener">10.1152/jappl.2001.91.6.2602</a>