The role of movement in the development of joints and related structures: the head and neck in the chick embryo

Development ◽  
1969 ◽  
Vol 22 (3) ◽  
pp. 349-371
Author(s):  
P. D. F. Murray ◽  
Daniel B. Drachman

Skeletal muscle contractions are necessary during embryonic life for the normal development of joints. The general features of joint development in immobile limbs were first studied with the techniques of grafting and organ culture. (Murray, 1926; Murray & Selby, 1930; Fell, 1925; Fell & Canti, 1934; Hamburger & Waugh, 1940; Lelkes, 1958). However, these methods of necessity entail a drastic alteration in the environment of the developing articulations, which may result in gross distortions of the skeletal structures themselves. More recently, neuromuscular blocking agents have been used to produce paralysis of chick embryos in ovo. When administered intravenously, these pharmacological substances produce profound paralysis, which may be continued for prolonged periods during embryonic development (Drachman & Coulombre, 1962a, b). Drachman & Sokoloff (1966) have analyzed the primary development of the knee, ankle and toe joints of the chick embryo by the use of these methods.

1984 ◽  
Vol 224 (3) ◽  
pp. 769-777 ◽  
Author(s):  
A Ferioli ◽  
C Harvey ◽  
F De Matteis

The ability of drugs to cause uroporphyria in hepatocytes from 17-day-old chick embryos has been investigated and the response of the cells in culture compared with that of the intact liver of the embryos in ovo. In this chick-embryo system, drugs that cause accumulation of uroporphyrin within 19-24 h can only do so in culture; in contrast, 2-allyl-2-isopropylacetamide and 3,5-diethoxycarbonyl-1,4-dihydrocollidine, which stimulate production of protoporphyrin, are effective both in culture and in ovo. A role of exogenous iron in worsening drug-induced uroporphyria was demonstrated in cultures of hepatocytes; iron also caused preferential accumulation of uroporphyrin from added 5-aminolaevulinate in the absence of a porphyrogenic chemical. Uroporphyria was induced in cultures of hepatocytes by drugs of widely different structures, suggesting that the primary molecular target with which they interact may be relatively aspecific in its binding characteristics. These results are briefly discussed, and two alternative hypotheses for the drug-induced effect in uroporphyrinogen metabolism are considered.


1981 ◽  
Vol 198 (2) ◽  
pp. 321-329 ◽  
Author(s):  
U Giger ◽  
U A Meyer

The role of haem synthesis during induction of hepatic cytochrome P-450 haemoproteins was studied in chick embryo in ovo and in chick embryos hepatocytes cultured under chemically defined conditions. 1. Phenobarbitone caused a prompt increase in the activity of 5-aminolaevulinate synthase, the rate-limiting enzyme of haem biosynthesis, and in the concentration of cytochrome P-450. This induction response occurred without measurable initial destruction of the haem moiety of cytochrome P-450. 2. When intracellular haem availability was enhanced by exogenous haem or 5-aminolaevulinate, phenobarbitone-medicated induction of cytochrome P-450 was not affected in spite of the well known repression of 5-aminolaevulinate synthase by haem. These data are consistent with the concept that haem does not regulate the synthesis of cytochrome P-450 haemoproteins. 3. Acetate inhibited haem biosynthesis at the level of 5-aminolaevulinate formation. When intracellular haem availability was diminished by treatment with acetate, phenobarbitone-medicated induction was decreased. 4. This inhibitory effect of acetate on cytochrome P-450 induction was reversed by exogenous haem or its precursor 5-aminolaevulinate. These data suggest that inhibition of haem biosynthesis does not decrease synthesis of apo-cytochrome P-450. Moreover, they indicate that exogenous haem can be incorporated into newly formed aop-cytochrome P-450.


2016 ◽  
Vol 30 (5) ◽  
pp. e45-e46
Author(s):  
Marina Pieri ◽  
Alessandro Belletti ◽  
Giovanni Affronti ◽  
Veronica Dalessandro ◽  
Ada Carla Alba ◽  
...  

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