The Journey from Discovery to Scientific Change: Scientific Communities, Shared Models, and Specialised Vocabulary

ABSTRACT

Scientific communities as social groupings and the role that such communities play in scientific change and the production of scientific knowledge is currently under debate. I examine theory change as a complex social interaction among individual scientists and the scientific community, and argue that individuals will be motivated to adopt a more radical or innovative attitude when confronted with striking similarities between model systems and a more robust understanding of specialised vocabulary. Two case studies from the biological sciences, Barbara McClintock and Stanley Prusiner, help motivate the idea that sharing of models and specialised vocabulary fill the gap between discovery and scientific change by promoting the dispersal of important information throughout the scientific community.

Acknowledgements

The author would like to thank a great many people who have been instrumental in this project. First, the author would like to thank Roberta Millstein, who encouraged and continually supported the project. The three unnamed reviewers of this journal were both diligent and helpful, a combination not praised enough. Thanks to James Griesemer and the Griesemer-Millstein Philosophy of Biology Lab for continual discussion and support. Finally, the author appreciates the countless conference and workshop attendees who have helped the project progress, including those at the International Society for the History, Philosophy and Social Studies of Biology Conference, the Society for Philosophy of Science in Practice Conference, the Greater Philadelphia Philosophy Consortium Conference on Thomas Kuhn, and the History and Philosophy of Science and Technology Conference at the University of Toronto.

ORCID

Sarah M. Roe http://orcid.org/0000-0002-9414-9660

Notes

1 See Jacobs (2002, 2006) for details regarding Kuhn, Peirce, Royce, Polanyi, and Fleck’s use of the term ‘scientific community’.

2 Examples include, but are not limited to, Peirce ([1887] 1992), Polanyi (1951), Allen (1966), Royce (1968), Havelock (1969), Price (1969), Ravetz (1971), Feyerabend (1975), Gralewska-Vickery (1976), Cole (1979), Fleck (1979), Garvey (1979), Knorr-Cetina (1981), Zuckerman, Cole, and Bruer (1991), Staley (2004), and Rehg (2009).

3 The same could be said of Darden (1991). The book offers an interesting case study, Mendelian genetics, as a way to better understand theory change in science.

4 DeLanda (2015) argues similarly while focusing on the chemical science. According to DeLanda, fields have three important components: a domain of phenomena, a community of practitioners, and instruments and techniques. As such, scientific fields are broken down similarly, in that they are based around a cluster of common phenomena and scientists within a field share the same techniques instruments and methods.

5 See Bechtel (1986) regarding the integration of scientific disciplines, and strategies and examples of such integration.

6 Examples include, but are not limited to, Watkins (1970), Ravetz (1971), Kuhn (1977), Brown (1983), Hull (1988), Hoyningen-Huene (1993), Friedman (2001), D’Agostino (2005, 2010), and Jacobs (2006).

7 I do not mean to offer a complete delineation of all the components necessary for a scientific community. Scientific communities may be different from other scientific groupings, but shared models and specialised vocabulary are minimally required to delineate a communicative cluster of scientists, what we are calling scientific communities.

8 In what is dubbed ‘new mechanistic philosophy’, each ‘new mechanist’ offers a slightly different notion of mechanism. See Machamer, Darden, and Craver (2000, 3); Glennan (2002, S445); Bechtel and Abrahamsen (2005, 423); Craver (2007, 128–129).

9 See Anfinsen (1973) and Rooman et al. (2002) for more specifics on free energy and protein folding.

10 For example, protein-folding software is now available to the public. This software, or computer simulation, contains an explicitly built model system. The users can utilise models that are all governed by specific constraints with the common goal of adding to the scientific understanding of protein folding in general (Pronk et al. 2013).

11 More on prions and protein folding in section 4.

12 Focusing on Kuhnian notions of scientific community, D’Agostino (2005) argues that individual members of scientific communities can be members of multiple communities. Perhaps most interestingly, he goes on to show how an individual member can perform multiple particular roles within the hierarchy of a single community.

13 For a more contemporary example, see Piccinini and Craver (2011) regarding mechanisms sketches and the integration of neuroscience and psychology.

14 See Woody (2004) for more discussion regarding how model systems, or as she calls them scientific representation schemes, can reflect a community’s epistemic aims and pragmatic concerns.

15 Chargaff, Zamenhof, and Green (1950) discovered the ratio of the base pairs, or the pairing of base pairs that allowed for insight regarding the structure of DNA. In other words, Chargaff introduced a constraint on the community’s model system.

16 Craver and Darden (2013, 161–185) argue similarly regarding shared mechanistic models.

17 For case studies that exemplify this, see Shapin (1994), Galison (1997), and Knorr-Cetina (1999).

18 One further benefit to this schema is that it can greatly reduce the time and effort spent interpreting other scientists’ models and theories. In this way, the sharing of similar models and specialised vocabulary enhances a scientist’s ability to contribute to scientific knowledge (Fuller 2002, 206).

19 D’Agostino (2008, 2010) utilises both social psychology and organisation theory to better understand the proper balance of these two attitudes.

20 See Galison (1997, esp. ch. 9) for a detail discussion regarding the coordinating of action and belief, as well as real scientific case studies of such occurrences.

21 It should be noted that I am not interested in scientific disagreement, broadly construed. Instead, I want to focus on how scientists communicate their findings to a community that, initially, does not have the specialised language and other skills necessary to accept the novel idea. I am sure scientific disagreement does ensue, and often, but I am interested in cases where disagreement cannot even happen yet, because, to borrow from Kuhn, the scientists are speaking a different language. Thank you to Philip Kitcher for pointing this out during personal communication.

22 Kusch (2002, 73–74) argues similarly when he discusses background communities, in which a scientist’s attitude toward a model, hypothesis, term, etc. can vary. See Fuller (2002, 208–216) for a variety of types of scientific consensus.

23 I am focusing on only one way in which scientific change and communication may happen, but still hope to enrich our current understanding of scientific discovery, change and knowledge.

24 For more regarding McClintock’s model-building practices and the diversity of models within her model system, see Comfort (2001, 222). There, Comfort discusses McClintock’s particular mechanisms for genomic rearrangement. Also, Comfort (2001, 223, fig. 8.6) shows one of McClintock’s physical model schemas. See McClintock (1978) for more particulars.

25 It should be noted that McClintock was modelling several important mechanisms at the time. I have only offered a few, but I wish to stress the point that models often come in closely related systems. McClintock’s research is a good example of this.

26 Other possible factors include, presentation and communication style, particular and advanced research background, gender discrimination, etc. (Keller 1983; Comfort 2001). For the purposes of this paper, I focus on differences in models (and model building) as well as terminology, but I do not mean to argue that these are the only reasons for McClintock’s difficulties. Instead, I argue that these are important contributing factors.

27 I limit the discussion to human-centred prion diseases for simplicity.

28 Most notably, Prusiner’s two Nobel prizes, countless articles/findings, and numerous new research avenues.

29 There are further concerns. For example, it has been established that one of the major routes of transmission is along the gastrointestinal tract. However, recently it has been shown that the PrP is rapidly destroyed by alimentary track fluids (Jeffrey 2006). Other studies showed that living microglia from an infected brain had no detectable prions, yet contained maximal levels of infectivity (Baker, Martin, and Manuelidis 2002). One study showed that ‘PrP neither encodes nor alters agent-specific characteristics’ (Arjona et al. 2004). Also, blocking the formation of prions by an antimalaria drug does not lengthen victims’ lives (Collinge et al. 2009).

30 Unfortunately, length constraints only allow for illustration of two cases case. However, the same patterns occur with other scientists as well, most notably, Charles Darwin. See Hull (1973) and Roe (Forthcoming).