Fresnel's laws,ceteris paribus

This article is about structural realism, historical continuity, laws of nature, and ceteris paribus clauses. Fresnel's Laws of optics support Structural Realism because they are a scientific structure that has survived theory change. However, the history of Fresnel's Laws which has been depicted in debates over realism since the 1980s is badly distorted. Specifically, claims that J. C. Maxwell or his followers believed in an ontologically-subsistent electromagnetic field, and gave up the aether, before Einstein's annus mirabilis in 1905 are indefensible. Related claims that Maxwell himself did not believe in a luminiferous aether are also indefensible. This paper corrects the record. In order to trace Fresnel's Laws across significant ontological changes, they must be followed past Einstein into modern physics and nonlinear optics. I develop the philosophical implications of a more accurate history, and analyze Fresnel's Laws' historical trajectory in terms of dynamic ceteris paribus clauses. Structuralists have not embraced ceteris paribus laws, but they continue to point to Fresnel's Laws to resist anti-realist arguments from theory change. Fresnel's Laws fit the standard definition of a ceteris paribus law as a law applicable only in particular circumstances. Realists who appeal to the historical continuity of Fresnel's Laws to combat anti-realists must incorporate ceteris paribus laws into their metaphysics.     

The New Mexico whiptail, Cnemidophorus neomexicanus (Squamata: Teiidae), in the Great Basin of north central Utah

We report the discovery of established populations of Cnemidophorus neomexicanus in the Salt Lake City area. These are the 1st records of this species in Utah and in the Great Basin and are far from all other known populations of the species. We conclude that C. neomexicanus was introduced in the Salt Lake City area, perhaps within the last 30 years.     

Mox2 is a component of the genetic hierarchy controlling limb muscle development.

The skeletal muscles of the limbs develop from myogenic progenitors that originate in the paraxial mesoderm and migrate into the limb-bud mesenchyme. Among the genes known to be important for muscle development in mammalian embryos are those encoding the basic helix-loop-helix (bHLH) myogenic regulatory factors (MRFs; MyoD, Myf5, myogenin and MRF4) and Pax3, a paired-type homeobox gene that is critical for the development of limb musculature. Mox1 and Mox2 are closely related homeobox genes that are expressed in overlapping patterns in the paraxial mesoderm and its derivatives. Here we show that mice homozygous for a null mutation of Mox2 have a developmental defect of the limb musculature, characterized by an overall reduction in muscle mass and elimination of specific muscles. Mox2 is not needed for the migration of myogenic precursors into the limb bud, but it is essential for normal appendicular muscle formation and for the normal regulation of myogenic genes, as demonstrated by the downregulation of Pax3 and Myf5 but not MyoD in Mox2-deficient limb buds. Our findings show that the MOX2 homeoprotein is an important regulator of vertebrate limb myogenesis.     

Expression of two myogenic regulatory factors myogenin and MyoD1 during mouse embryogenesis

MyoD1 and myogenin are muscle-specific proteins which can convert non-myogenic cells in culture to differentiated muscle fibres, implicating them in myogenic determination. The pattern of expression of MyoD1 and myogenin during the early stages of muscle formation in the mouse embryo in vivo and in limb-bud explants cultured in vitro, indicates that they may have different functions in different types of muscle during development.     

Glucose/galactose malabsorption caused by a defect in the Na+/glucose cotransporter

Glucose/galactose malabsorption (GGM) is an autosomal recessive disease manifesting within the first weeks of life and characterized by a selective failure to absorb dietary glucose and galactose from the intestine. The consequent severe diarrhoea and dehydration are usually fatal unless these sugars are eliminated from the diet. Intestinal biopsies of GGM patients have revealed a specific defect in Na(+)-dependent absorption of glucose in the brush border. Normal glucose absorption is mediated by the Na+/glucose cotransporter in the brush border membrane of the intestinal epithelium. Cellular influx is driven by the transmembrane Na+ electrochemical potential gradient; thereafter the sugar moves to the blood across the basolateral membrane via the facilitated glucose carrier. We have previously cloned and sequenced a Na+/glucose cotransporter from normal human ileum and shown that this gene, SGLT1, resides on the distal q arm of chromosome 22. We have now amplified SGLT1 complementary DNA and genomic DNA from members of a family affected with GGM by the polymerase chain reaction. Sequence analysis of the amplified products has revealed a single missense mutation in SGLT1 which cosegregates with the GGM phenotype and results in a complete loss of Na(+)-dependent glucose transport in Xenopus oocytes injected with this complementary RNA.