Maxwell's role in turning the concept of model into the methodology of modeling

This is a contribution towards a history and philosophy of modeling in its early stages in electromagnetism. In 1873, James Clerk Maxwell (1831–1879) hinted at the methodology of modeling at the end of his Treatise on Electricity and Magnetism. We focus on Maxwell's impact on physicists who immediately followed him, specifically Oliver Lodge (1851–1940) and George Francis FitzGerald (1851–1901). We begin with the role that the scientific concept of model played in the late nineteenth century, as assessed by Ludwig Boltzmann (1844–1906). We then discuss the role of hypothesis as a methodology, the appeal to (dynamical) illustration, and the way Maxwell applied model and working model in his studies of electromagnetism. We show that for Maxwell these key terms were kept distinct, but Lodge did not maintain these distinctions and, in this regard, FitzGerald followed Lodge. Notwithstanding Lodge's influence, Fitzgerald modified Maxwell's theory based on the mechanical model he designed, thereby implicitly taking the first step towards modeling. This methodology consists in drawing consequences from the (mechanical) model to the (electrodynamic) theory and modifying the latter in light of the functioning of the former. At the core of our argument is the thesis that it was a methodological novelty to move from the concept of model to the methodology of modeling. The introduction of modeling as a new methodology into physics in the late nineteenth century was a major event which deserves proper recognition.     

谈“十四五”生态保护与绿色发展的生态关系

 从“十四五”保护与发展的生态关系角度，探讨了生态保护与绿色发展的十大生态关系，阐述了生态保护和绿色发展中的一系列有关生态关系的生态智慧及生态技术，并对长江、黄河等流域的生态保护和修复提出了相关建议。     

The influence of chronic nicotine treatment on stress-induced gastric ulceration and emptying rate in rats.

Ten-day treatment with nicotine (5, 25 or 50 micrograms/ml drinking water) dose-dependently intensified gastric ulceration induced by cold-restraint, and emptying rate. Stomach contractions produced by graded doses of bethanechol i.v. were elevated further by nicotine treatment. It is suggested that chronic nicotine administration produces hypersensitivity of the gastric muscarinic receptors; stomach hypermotility contributes to the ulcer-worsening action of the alkaloid.     

Overcompensation and population cycles in an ungulate.

Although theoretical studies show that overcompensatory density-dependent mechanisms can potentially generate regular or chaotic fluctuations in animal numbers, the majority of realistic single-species models of invertebrate populations are not overcompensatory enough to cause sustained population cycles. The possibility that overcompensation may generate cycles or chaos in vertebrate populations has seldom been considered. Here we show that highly overcompensatng density-dependent mortality can generate recurrent population crashes consistent with those observed in a naturally limited population of Soay sheep. The observed interval of three or more years between crashes points to sharp 'focusing' of mortality over a narrow range of population density.     

Retrograde transport of endocytosed Shiga toxin to the endoplasmic reticulum.

Shiga toxin and some other protein toxins that act on targets in the cytosol have previously been shown to enter the trans-Golgi network. Transport by this route may be necessary for translocation of the toxin to the cytosol and for intoxication, but it is not known whether the enzymatically active part of the toxins actually enters the cytosol from the trans-Golgi network. It has been suggested that such toxins are transported in a retrograde manner to the endoplasmic reticulum and that translocation occurs in this organelle, but retrograde transport of endocytosed material beyond the trans-Golgi network has never been demonstrated. Here we show that in butyric acid-treated A431 cells endocytosed Shiga toxin is not only transported to the trans-Golgi network, but also to all Golgi stacks, to the endoplasmic reticulum and to the nuclear envelope. Furthermore, butyric acid sensitizes the cells to Shiga toxin, which is consistent with the possibility that retrograde transport is required for translocation of the toxin to the cytosol.