Pluralism without Genic Causes?

Since the fundamental challenge that I laid at the doorstep of the pluralists was to defend, with nonderivative models, a strong notion of genic cause, it is fatal that Waters has failed to meet that challenge. Waters agrees with me that there is only a single cause operating in these models, but he argues for a notion of causal ‘parsing’ to sustain the viability of some form of pluralism. Waters and his colleagues have some very interesting and important ideas about the sciences, involving pluralism and parsing or partitioning causes, but they are ideas in search of an example. He thinks he has found an example in the case of hierarchical and genic selection. I think he has not

Session 2: Female Orgasms and Evolutionary Theory

Proceedings of the Pittsburgh Workshop in History and Philosophy of Biology, Center for Philosophy of Science, University of Pittsburgh, March 23-24 2001 Session 2: Female Orgasms and Evolutionary Theor

Pluralism without Genic Causes?

Since the fundamental challenge that I laid at the doorstep of the pluralists was to defend, with nonderivative models, a strong notion of genic cause, it is fatal that Waters has failed to meet that challenge. Waters agrees with me that there is only a single cause operating in these models, but he argues for a notion of causal ‘parsing’ to sustain the viability of some form of pluralism. Waters and his colleagues have some very interesting and important ideas about the sciences, involving pluralism and parsing or partitioning causes, but they are ideas in search of an example. He thinks he has found an example in the case of hierarchical and genic selection. I think he has not

The ‘Alice in Wonderland’ mechanics of the rejection of (climate) science:simulating coherence by conspiracism

Science strives for coherence. For example, the findings from climate science form a highly coherent body of knowledge that is supported by many independent lines of evidence: greenhouse gas (GHG) emissions from human economic activities are causing the global climate to warm and unless GHG emissions are drastically reduced in the near future, the risks from climate change will continue to grow and major adverse consequences will become unavoidable. People who oppose this scientific body of knowledge because the implications of cutting GHG emissions—such as regulation or increased taxation—threaten their worldview or livelihood cannot provide an alternative view that is coherent by the standards of conventional scientific thinking. Instead, we suggest that people who reject the fact that the Earth’s climate is changing due to greenhouse gas emissions (or any other body of well-established scientific knowledge) oppose whatever inconvenient finding they are confronting in piece-meal fashion, rather than systematically, and without considering the implications of this rejection to the rest of the relevant scientific theory and findings. Hence, claims that the globe “is cooling” can coexist with claims that the “observed warming is natural” and that “the human influence does not matter because warming is good for us.” Coherence between these mutually contradictory opinions can only be achieved at a highly abstract level, namely that “something must be wrong” with the scientific evidence in order to justify a political position against climate change mitigation. This high-level coherence accompanied by contradictory subordinate propositions is a known attribute of conspiracist ideation, and conspiracism may be implicated when people reject well-established scientific propositions

Severe Weather Event Attribution: Why values won’t go away

We start by reviewing the complicated situation in methods of scientific attribution of climate change to extreme weather events. We emphasize the social values involved in using both so-called ``storyline'' and ordinary probabilistic or ``risk-based'' methods, noting that one important virtue claimed by the storyline approach is that it features a reduction in false negative results, which has much social and ethical merit, according to its advocates. This merit is critiqued by the probabilistic, risk-based, opponents, who claim the high ground; the usual probabilistic approach is claimed to be more objective and more ``scientific'', under the grounds that it reduces false positive error. We examine this mostly-implicit debate about error, which apparently mirrors the old Jeffrey-Rudner debate. We also argue that there is an overlooked component to the role of values in science: that of second-order inductive risk, and that it makes the relative role of values in the two methods different from what it first appears to be. In fact, neither method helps us to escape social values, and be more scientifically ``objective'' in the sense of being removed or detached from human values and interests. The probabilistic approach does not succeed in doing so, contrary to the claims of its proponents. This is important to understand, because neither method is, fundamentally, a successful strategy for climate scientists to avoid making value judgments

ISOANTIGENS OF THE H-2 AND Tla LOCI OF THE MOUSE : INTERACTIONS AFFECTING THEIR REPRESENTATION ON THYMOCYTES

H-2 and TL isoantigens of the mouse are specified by the closely linked genetic loci H-2 and Tla. A. study of their representation on thymocytes was performed in order to reveal any interactions between the determinant genes or their products affecting the synthesis or disposition of these components of the thymocyte surface. The method employed was quantitative absorption of cytotoxic antibody by viable thymocytes. The phenotypic expression of TL antigens was found to reduce the demonstrable amount of certain H-2 antigens to as little as 34% of the quantity demonstrable on TL- thymocytes. A reduction was observed in all three H-2 types tested, (H-2b, H-2a, and H-2k). As antigenic modulation (change of TL phenotype from TL+ to TL-, produced by TL antibody) is known to entail a compensatory increase in H-2(D) antigen, it is concluded that the TL phenotype, rather than the Tla genotype, influences the surface representation of H-2 antigens. The two known TL+ phenotypes of thymocytes (TL.2 and TL.1,2,3) depress H-2 equally. The H-2 specificities affected are those determined by the D end of the E-2 locus, which is adjacent to Tla; antigens of the K end, which is distal to Tla, are not depressed. The reduction of demonstrable H-2 antigen on the thymocytes of TL+ x TL- progeny is half that of thymocytes of TL+ x TL+ progeny and the reduction affects equally the products of both H-2 alleles (cis and trans in relation to Tla), indicating that the mechanism of H-2 reduction by TL is extrachromosomal. Whether it involves diminished synthesis of H-2 or steric masking by TL at the cell membrane is unknown, but in either case the reciprocal relation of TL and H-2(D) antigens implies that they probably occupy adjacent positions on thymocytes and that the gene order, H-2(K): H-2(D):Tla is reflected in cell surface structure. Extrachromosomal interaction, apparently involving control of synthesis, occurs also within the TL system of antigens. Thymocytes of TL.2 x TL.1,2,3 progeny express the full homozygous quantity of antigens TL.1 and TL.3 (but not of TL.2), in contrast to the half-quantity present in thymocytes of TL- x TL.1,2,3 progeny. Another example of interaction is implicit in the finding that thymocytes of TL-1,2,3 x TL.1,2,3 progeny have more TL.2 antigen than thymocytes of TL.2 x TL.2 progeny, but in this instance there is nothing to indicate whether the mechanism is chromosomal or extrachromosomal. Thus the quantitative surface representation of at least some H-2 and TL antigens is influenced by the cellular complement of H-2:Tla genes as a whole. Comparison of H-2 heterozygous thymocytes with H-2 homozygous thymocytes in quantitative absorption tests shows (a) more than the expected 50% of each parental-type H-2 antigen on heterozygous cells, and (b) a greater suppression of H-2 by TL in H-2 heterozygotes in comparison with H-2 homozygotes. Both results may be explained on the basis of differences in the density of H-2 antigenic sites and consequent differences in the efficiency of absorption of H-2 antibody. These considerations may be useful in other contexts, e.g. in estimating the representation of Rh antigens on the red cells of human subjects homozygous and heterozygous for Rh components

THE GIX SYSTEM : A CELL SURFACE ALLO-ANTIGEN ASSOCIATED WITH MURINE LEUKEMIA VIRUS; IMPLICATIONS REGARDING CHROMOSOMAL INTEGRATION OF THE VIRAL GENOME

This report concerns a cell surface antigen (GIX; G = Gross) which exhibits mendelian inheritance but which also appears de novo in cells that become productively infected with MuLV (Gross), the wild-type leukemia virus of the mouse. In normal mice, GIX is a cell surface allo-antigen confined to lymphoid cells and found in highest amount on thymocytes. Four categories of inbred mouse strains can be distinguished according to how much GIX antigen is expressed on their thymocytes. GIX- strains have none; in the three GIX+ categories, GIX3, GIX2, and GIX1, the amounts of GIX antigen present (per thymocyte) are approximately in the ratios 3:2:1. A study of segregating populations derived mainly from strain 129 (the prototype GIX3 strain) and C57BL/6 (the prototype GIX- strain) revealed that two unlinked chromosomal genes are required for expression of GIX on normal lymphoid cells. The phenotype GIX+ is expressed only when both genes are present, as in 129 mice. C57BL/6 carries neither of them. At one locus, expression of GIX is fully dominant over nonexpression (GIX fully expressed in heterozygotes). At the second locus, which is linked with H-2 (at a distance of 36.4 ± 2.7 units) in group IX (locus symbol GIX), expression is semidominant (50% expression of GIX in heterozygotes); gene order T:H-2:Tla:GIX. As a rule, when cells of GIX- mice or rats become overtly infected with MuLV (Gross), an event which occurs spontaneously in older mice of certain strains and which also commonly accompanies malignant transformation, their phenotype is converted to GIX+. This invites comparison with the emergence of TL+ leukemia cells in TL- mouse strains which has been observed in previous studies and which implies that TL- → TL+ conversion has accompanied leukemic transformation of such cells. So far the only example of GIX- → GIX+ conversion taking place without overt MuLV infection is represented by the occurrence of GCSA-:GIX+ myelomas in BALB/c (GCSA:GIX-) mice. Unlike the other Gross cell surface antigen described earlier, GCSA, which is invariably associated with MuLV (Gross) infection and never occurs in its absence, GIX antigen sometimes occurs independently of productive MuLV infection; for example, thymocytes and some leukemias of 129 mice are GCSA-:GIX+, and MuLV-producing sarcomas may be GCSA+:GIX-. The frequent emergence of cells of GIX+ phenotype in all mouse strains implies that the structural gene coding for GIX antigen is common to all mice. There is precedent for this in the TL system, in which two of the Tla genes in linkage group IX appear to be ubiquitous among mice, but are normally expressed only in strains of mice carrying a second (expression) gene. It is not yet certain whether either of the two segregating genes belongs to the MuLV genome rather than to the cellular genome. This leaves the question whether MuLV may have a chromosomal integration site still debatable. But there is a good prospect that further genetic analysis will provide the answer and so elucidate the special relationship of leukemia viruses to the cells of their natural hosts