The variable that affect motor programming time may be studied by changing the nature of the response and measuring the subsequent changes in reaction time (RT). One notion of motor programming suggests that aiming responses with reduced target size and/or increased target amplitude require more "complex" motor programs that require longer RTs. In a series of five experiments which movement time (MT) was experimentally varied target size neither influences RT when the movement amplitude was 2 or 30 cm nor when the target sizes differed by as much as a factor of 16:1. Increasing the movement amplitude from 15 to 30 cm also had no influence on RT. Movement time, however, did affect RT, with 200-msec movements having longer RTs than 120-msec movements. Target size and movement amplitude did not appear to be factors that influence programming time or program complexity.
Transforming growth factor-alpha (TGF-alpha), a member of the epidermal growth factor (EGF) family, is a potent mitogen for several cell types. To investigate the possible role of TGF-alpha in the development of midgestation human fetal lung, we studied its distribution with immunohistochemistry and determined levels of steady-state TGF-alpha mRNA by Northern analysis of cellular RNA isolates from lung. Lung was obtained from fetuses at 10 to 22 wk of gestation (n = 14) and immunostained for TGF-alpha. TGF-alpha was localized in epithelial cells at all gestational ages examined. Immunostaining was particularly prominent in bronchiolar epithelial cells. TGF-alpha immunoreactivity was also associated with arterial smooth muscle cells, as well as with nerves. Occasional chondrocytes were also associated with TGF-alpha immunoreactivity. Total cellular RNA was isolated from lung tissue obtained from additional fetuses at gestational ages 10 to 24 wk (n = 22). TGF-alpha mRNA was present in RNA extracts of all fetal lungs studied. We conclude that TGF-alpha is probably produced in human fetal lung during mid-gestation. The prominent immunostaining of bronchiolar epithelial cells for TGF-alpha is consistent with its playing a role in distal airway formation.
OHOR' IX IT', R = I, R' = H X , R = H, R ' = H XI. R = H. R' = Ac XII; R = I,' R' = AC salt of S-amino-8-isoyuiriolinol (V) was treated with potassium iodide and iodine. Treatminerit of the complex reaction mixt,ure with sodium sulfite and sodium hydroxide followed by neutralization gave a precipitate which, on acetylation with acetic anhydride in pyridine, afforded the pure phenol wetmate VI in an over-all yield of 577,. Alkaline hydrolysis of VI gave a quantitative yield of the monoiodopheriol VI1 as the free base; t'he corresponding hydrochloride was obtained by hydrolysis of VI mit'h hydrochloric acid. Iodination of t'his hydrochloride TVith iodine chloride in ethanol3 finally produced the desired ;j,T-diiodo-8-isoquiiiolinol (111) as its hydrochloride in 667, yield. It should be mentioned also that the catalytic reduction (in alkaline solution4) of VI1 gave 8-hydroxyisoquinolinol (YIII) which was identical with the jsoquiriolinol prepared according to Robinson.' The easily accessible 5-isoquinolinol (IX)5 was selected as the starting material for the synthesis of 6,8diiodo-5-isoquiiiolinol (IT). Iodination of IX with iodine chloride in ethanol resulted in a mixture of iodinated products from which a pure monoiodo derivat'ive was isolated in t'he form of its hydrochloride. Struct'ure X mas teritat'ively assigned to this compound which was also characterized as its free base and acetate XI. When the iodination was carried out in 3 N hydrochloric acid instead of ethanol, a product was obtained which, after acetylation with acetic anhydride in pyridine, afforded the pure diiodo acetate XI1 in 53% over-all yield. A41kali~ie hydrolysis of XI1 yielded, quantitatively, the desired 6,8-diiodo-5-isoquinoliiiol (IV). The structural assignments of the compounds described are supported by spectroscopic data (see Experimental Section)., 411 of the iodoisoquiriolines prepared (except XII) were tested against Endaiiioeba histolytica in vitro. I n addition, compounds 111, IT.', arid XI1 were examined for their effect in vivo against the iritracecal E. hisfolyfica I<-9 infection of mearilirig rats using the (2) L. F. Fieser and E. L. hIartin, [ J . Bm. Chem. Soc., 67, 1840 (1935 I ohtained this compound by electrolytic reduction of 5nitroisoquinoline. These authors did not know ahether their starting material n-as 5or 8-nitroisoquinoline. From the work of F. T . Tyson [ibid., 61, 183 (1939)], it was concluded that the compound in question was 5-nitroisoquinoline; Dewar and P. 31. hlaitlis, J . Chem. Soc., 2,521 (1957). hI. J( 3 ) Cf.
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