Cells existing already during gastrulation are associated with valve formation days later. The Wnt/beta-catenin signaling in PP cells is normally repressed by Wnt antagonists and Hex is up-regulated. The antagonism occurring at the receptor level is bypassed by Li exposure by its intracellular inactivation of GSK-3 directly to augment Wnt signaling.

We have identified the presence of the hypoxia marker EF5 in the stage 4/5 chick heart fields. This suggests that cardiac cell differentiation occurs in a relatively anaerobic environment. Monocarboxylate transporter (MCT) studies in adult cardiac myocytes have demonstrated that MCTs catalyze proton-linked pyruvate and lactate transport activity. 5A11/Basigin is an ancillary protein that targets MCTs to the plasma membrane for their function. MCT-4 expression is most evident in cells with a high glycolytic rate associated with hypoxic energy production. Subsequent to the immunohistochemical localization of EF5 in the early heart field, we continued in our analysis during stages 5 to 12 for the expression of indicators of cellular glycolytic metabolism in the developing heart, such as MCT-4, MCT-1, and 5A11 (Basigin/CD147). Our observations indicate that MCT-4 and 5A11/Basigin are expressed early, in a differential left-right pattern, in the bi-lateral plate mesoderm, as the cardiac compartment is forming. At stage 11, MCT-4/5A11 continues to be highly expressed in the myocardial wall of the looping heart, but not in the dorsal mesocardium. RT-PCR analyses for MCT-1, -4, and 5A11 indicate that MCT-4 and 5A11 are expressed throughout precardiac, embryonic, and fetal stages in the heart. MCT-1 is first detected in the heart on embryonic day 3 and then remains expressed throughout development to hatching. These results indicate that cardiac precursor cells are equipped for differentiating in a hypoxic environment using anaerobic metabolism for energy production. Developmental Dynamics 235:124 -131, 2006.

Administration of testosterone propionate (TP) to neonatal female rats induces a syndrome of sterility, characterized by acyclicity and anovulation (Barraclough & Gorski, 1961;Gorski, 1966;Lobi & Gorski, 1969). This study shows the ability of the uterus of androgenized female rats to respond to oestradiol by change in weight and by formation of specific oestrogen-induced proteins (IP) (Barnea & Gorski, 1970).To study the response of the uterus to oestradiol, groups of 15 normal dioestrous and 15 androgenized (1\m=.\25mg TP s.c. on postnatal day 3) adult female rats were hemihysterectomized (ipsilateral ovary removed simultaneously) and the excised uterine tissue was cleaned and weighed. These animals were then injected twice daily with 4 \g=m\g oestradiol benzoate for 5 days. On the 6th day, all animals were killed and the remaining uterine horn was excised, cleaned and weighed. Another group of nine androgenized and ten oestrous females were bilaterally ovariectomized. Six days later, one uterine horn was excised and weighed and oestrogen administered as above.This experiment confirms the findings of Wrenn, Wood & Bitman (1969) that the initial weight of the uterus is similar in normal dioestrous female (NF) and in androgenized female (AF) rats (NF = 113-9± 11-4 (s.e.m.) mg; AF = 114-4 + 4-9). The uterus of the normal female responded to oestradiol treatment by a 62% increase in wet weight (184-7 + 13-6 mg; < 0-001), but that of the AF rats did not (weight = 122-0 ±4-7 mg). In response to ovariectomy, uteri from both NF and AF rats responded by decreases in wet weight to similar levels (NF = 59-3+1-74; AF = 63-9 + 2-1). Administration of oestradiol increased uterine weight in ovari¬ ectomized rats to levels approaching oestrogen-injected, hemihysterectomized rats (NF = 152-83 ± 7-1 ; AF = 119-3 ± 3-7). These results suggest that the uterus from AF rats is tonically maximally stimulated and is less responsive to oestradiol than the normal uterus, although the response to oestrogen after ovariectomy and uterine atrophy is apparently similar.To test the ability of androgenized rats to respond to oestradiol by the formation of IP, we used the double-labelling method exactly as described by Katzenellenbogen & Gorski (1972). One uterus from a 3-day ovariectomized normal or ovariectomized and androgenized female was incubated in 1 ml Eagle's HeLa tissue culture medium. Control uteri were incubated in the absence of steroid and in the presence of 5/¿Ci L-[4,5-14CJleucine (312 mCi/mmol)/ml while experimental tissues were incubated in medium containing 3-7 IO-8 M-oestradiol-17/? and 20/¿Ci L-[3HJleucine (2-0 Ci/mmol)/ml. Three control and three experimental uteri were

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