Biology Reference
In-Depth Information
The models of such a structure usually constitute a series of idealized proto-
typical mechanisms and variations (some of which may be mutants) that bear
family or similarity resemblances to each other, and characteristically each has
a (relatively) narrow scope of straightforward application to (few) pure types.
The models are typically interlevel in the sense of levels of aggregation, con-
taining component parts which are often specified in intermingled body part
(e.g., head or tail), cellular (e.g., neuron or axon), and biochemical (e.g., receptor
or ions) terms. Stages of temporal development in the models may represent
either deterministic, causally probabilistic, random (Markovian), or even mixed
connections. This probabilistic character of some causal connections (a failure
of strict determinism) should be distinguished from the conceptually distinct
failure of the exact match of a model to a nonpure type to which, nonetheless,
it is closest given available knowledge. Such a match can be close, however,
exhibiting a strong analogy between a model and an organism (or population of
organisms). I argued at length (in my 1980) that this new type of theory, which
I termed a 'theory of the middle range' (with apologies to R.K. Merton (1968)
who first used that term in a somewhat different context), both is found and
should be expected to be found in the biomedical sciences. The term 'middle
range' seemed appropriate for two reasons: first, the theories were not broad
sweeping general theories but they were not summaries of data either; they were
midway between these extremes. Second, in terms of levels of aggregation of
the entities in such theories, the theories were not about high-level populations
evolving in evolutionary time and not about specific DNA sequences or spe-
cific enzymes functioning in well-defined biochemical pathways, but were at
the level of the organelle, the gene as characterized by functional products, the
cell, and the organ. Thus though interlevel, their levels of aggregation tended to
concentrate in the 'middle range.'
Though the Waddington and von Bertalanffy programs have not been con-
firmed in the typical accomplishments and representations in molecular biology
in general, and molecular genetics in particular, there are interesting advances
that fall between those searches for broad theories couched in mathematically
precise differential equation form, and the narrow classes of mechanisms, usu-
ally described in qualitative multilevel causal language, that constitute the vast
majority of current biomedical explainers. In traditional population genetics, one
important exception is the ability to develop a powerful axiomatization of the
subject that does bear strong analogies to equation based theories of physics.
(For a detailed example see the Jacquard axiomatization of population genetics
summarized in Schaffner (1993), Chapter 8.)
There are several other theories that are equation-based which can be identified
in contemporary biomedicine; and in the remainder of this paper I discuss
two of these in detail. My view is that these can disclose some important
ways that very general and quantitative principles can be applied fruitfully
