Human developmental anatomy has been organized as structured lists of the major constituent tissues present during each of Carnegie stages 1-20 (E1-E50, ∼ 8500 anatomically defined tissue items). For each of these stages, the tissues have been organized as a hierarchy in which an individual tissue is catalogued as part of a larger tissue.Such a formal representation of knowledge is known as an ontology and this anatomical ontology can be used in databases to store, organize and search for data associated with the tissues present at each developmental stage.The anatomical data for compiling these hierarchies comes from the literature, from observations on embryos in the Patten Collection (Ann Arbor, MI, USA) and from comparisons with mouse tissues at similar stages of development.The ontology is available in three versions. The first gives hierarchies of the named tissues present at each Carnegie stage (http://www.ana.ed.ac.uk/anatomy/database/humat/) and is intended to help analyse both normal and abnormal human embryos; it carries hyperlinked notes on some ambiguities in the literature that have been clarified through analysing sectioned material. The second contains many additional subsidiary tissue domains and is intended for handling tissue-associated data (e.g. gene-expression) in a database. This version is available at the humat site and at http://genex.hgu.mrc.ac.uk/Resources/intro.html/), and has been designed to be interoperable with the ontology for mouse developmental anatomy, also available at the genex site. The third gives the second version in GO ontology syntax (with standard IDs for each tissue) and can be downloaded from both the genex and the Open Biological Ontology sites (http://obo.sourceforge.net/)

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1 This study has compared the effects of exogenous and endogenous prostaglandins on the two phases of contraction of the guinea-pig vas deferens produced by electrical field stimulation. Prostaglandin E2 (PGE2), sulprostone and arachidonic acid dose-dependently and completely inhibited the first (fast) phase of contraction, with ICs5s of 2.6 nM, 0.65 nm and 2.2 14M, respectively.2 Following desensitization of the receptor for adenosine triphosphate (ATP) with a, f-methylene ATP, PGE2, sulprostone and arachidonic acid dose-dependently inhibited the second (slow) phase of contraction of the guinea-pig vas deferens produced by electrical field stimulation, but the inhibition was incomplete (up to only 30%). Indomethacin (2.8 uM) reduced the effect of arachidonic acid. On its own, indomethacin (0.3 to 6.0 pM) had no consistent effect although, on some tissues, a slight potentiation of the contractions was seen. 3 Cicaprost (a PGI2 analogue) at low concentrations (0.5 to 30 nM) potentiated the first phase of contraction but even at high concentrations, had no consistent effect on the second phase of contraction of the guinea-pig vas deferens produced by electrical field stimulation. 4 PGE2, sulprostone and cicaprost potentiated contractions of the guinea-pig vas deferens produced by exogenous ATP. PGE2-and sulprostone also potentiated contractions produced by exogenous noradrenaline, whereas cicaprost had no consistent effect on the response to noradrenaline. 5 These findings indicate that prostaglandins of the E-series inhibit the second phase of contraction as well as the first phase of contraction of the guinea-pig vas deferens produced by electrical field stimulation. However, the extent of the inhibition is much less for the second phase than for the first phase. The reasons for this differential action of PGE are not clear. 6 Cicaprost potentiates the first phase but not the second phase of contraction. Since cicaprost potentiates the contractions produced by exogenous ATP, but not by exogenous noradrenaline, by an action presumably on post-junctional IP receptors, the potentiating action of cicaprost on the first phase of contraction produced by electrical field stimulation would appear to be satisfactorily explained through the action of cicaprost on these post-junctional IP receptors. 7 Exogenous arachidonic acid is apparently converted predominantly to PGE2 by the vas deferens, since the action of arachidonic acid mimicked that of PGE2 and was reduced by indomethacin. However, there was little evidence thatufficient PGE2 is generated during a short period (15 s) of sympathetic nerve stimulation for it to have any-significant inhibitory effect on the size of the contractions produced.