The rise of the Marburg phoenix: Karl Vorlaender\u27s Kantian/Marxian synthesis as key in the debate over capitalism vs. economic democracy

Mainstream economics has long avoided two issues pressing on the discipline and on society: Ownership of the means of production and ethics. While Adam Smith clearly presented his Wealth of Nations as a normative adjunct to his Theory of Moral Sentiments, he left alone the question of ownership. While Karl Marx presented a detailed critique of the theory and practice of capitalism, he failed to produce an explicit ethical theory to explain why capitalism is unacceptable. In 1971 there appeared a work that would have great impact on the academic world, John Rawls\u27 A Theory of Justice. Here was a large contractarian treatise explaining what justice was. Operating as Kantian agents in an original position, people could supposedly find room for both capitalism and worker ownership in a society defined as just by Rawls. David Ellerman, whose innovative Property & Contract in Economics appeared in 1992, makes the case for economic democracy on Kantian grounds as well but with no prevarication (unlike Rawls): Only worker ownership can be ethically justified. Meanwhile Marxists, harboring no affinity for capitalism, are out in the cold without an explicit ethical system to back their views. After the horrors of Stalinism and State Socialism under the former Soviet Union, the Marxists have an amoral theory that can offer guidance in the economic realm to no one in the old Soviet Union. Rawls\u27 theory of justice is susceptible to Marxist criticism at one point in particular, though. Rawls claims that people in the original position would choose primary goods that every rational man is presumed to want : rights and liberties, powers and opportunities, income and wealth, and self-respect. Marxists claim that Marx\u27s historicist thesis can undermine the validity of choosing these goods; conceptions of rationality are determined by specific historical circumstances. Therefore, Rawls would have to show how his theory of (individualistic) rationality would not become obsolete as the old society with its idea of rationality metamorphoses into a new society with a new conception of rationality. Though Rawls cannot provide a conception of rationality that would transcend historical circumstance, Marxists are mired in the belief that they have no such conception in their heritage. But they have. If they will finally allow Karl Vorlaender the audience he deserves, they will see that Vorlaender has provided an ingenious Kantian/Marxian synthesis that explains why it is rational, on (neo)Kantian grounds, to select the communitarian values espoused by Marx. With this theory in their arsenal, Marxists can undermine Rawls\u27 theory of justice, claim an ethical (Kantian) heritage, and unite with Ellerman in ending the debate over capitalism vs. economic democracy. Only worker-ownership (a.k.a. economic democracy) will be left ethically justifiable

Fluorogermanium(IV) salts of graphite. A system in equilibrium with elemental fluorine

Pyrolytic graphite is not intercalated by GeF{sub 4} alone but is intercalated by GeF{sub 4}/F{sub 2} mixtures to yield, at the intercalation limit, at 20{sup o}, a first-stage material, C{sub 12}GeF{sub 5-6}, which is in equilibrium with gaseous fluorine. GERMANIUM tetrafluoride is a superior fluoride ion acceptor since it can stabilize the O{sub 2}{sup +} ion and the NF{sub 4}{sup +} ion in salts. It is this superior fluoride-ion acceptor capability which must account for our observation that pyrolytic graphite readily intercalates GeF{sub 4} in the presence of fluorine, but does not do so, even with high pressures of GeF{sub 4}, if fluorine is absent, Similar experiments, in which SiF{sub 4} was substituted for GeF{sub 4}, failed to bring about any silicon fluoride intercalation. It has long been known that GeF{sub 4} is a superior fluoride ion acceptor to SiF{sub 4} since, with SF{sub 4}, the former yields the salt (SF{sub 3}{sup +}){sub 2}GeF{sub 6}{sup 2-}, whereas the silicon analogue is not stable at ordinary temperatures and pressures (in spite of the lattice energy of the silicon analogue being slightly more favorable by virtue of the smaller size of SiF{sub 6}{sup 2-})

Elevations of intracellular calcium reflect normal voltage-dependent behavior, and not constitutive activity, of voltage-dependent calcium channels in gastrointestinal and vascular smooth muscle

In smooth muscle, the gating of dihydropyridine-sensitive Ca2+ channels may either be stochastic and voltage dependent or coordinated among channels and constitutively active. Each form of gating has been proposed to be largely responsible for Ca2+ influx and determining the bulk average cytoplasmic Ca2+ concentration. Here, the contribution of voltage-dependent and constitutively active channel behavior to Ca2+ signaling has been studied in voltage-clamped single vascular and gastrointestinal smooth muscle cells using wide-field epifluorescence with near simultaneous total internal reflection fluorescence microscopy. Depolarization (−70 to +10 mV) activated a dihydropyridine-sensitive voltage-dependent Ca2+ current (ICa) and evoked a rise in [Ca2+] in each of the subplasma membrane space and bulk cytoplasm. In various regions of the bulk cytoplasm the [Ca2+] increase ([Ca2+]c) was approximately uniform, whereas that of the subplasma membrane space ([Ca2+]PM) had a wide range of amplitudes and time courses. The variations that occurred in the subplasma membrane space presumably reflected an uneven distribution of active Ca2+ channels (clusters) across the sarcolemma, and their activation appeared consistent with normal voltage-dependent behavior. Indeed, in the present study, dihydropyridine-sensitive Ca2+ channels were not normally constitutively active. The repetitive localized [Ca2+]PM rises (“persistent Ca2+ sparklets”) that characterize constitutively active channels were observed rarely (2 of 306 cells). Neither did dihydropyridine-sensitive constitutively active Ca2+ channels regulate the bulk average [Ca2+]c. A dihydropyridine blocker of Ca2+ channels, nimodipine, which blocked ICa and accompanying [Ca2+]c rise, reduced neither the resting bulk average [Ca2+]c (at −70 mV) nor the rise in [Ca2+]c, which accompanied an increased electrochemical driving force on the ion by hyperpolarization (−130 mV). Activation of protein kinase C with indolactam-V did not induce constitutive channel activity. Thus, although voltage-dependent Ca2+ channels appear clustered in certain regions of the plasma membrane, constitutive activity is unlikely to play a major role in [Ca2+]c regulation. The stochastic, voltage-dependent activity of the channel provides the major mechanism to generate rises in [Ca2+]

Pressure-dependent regulation of Ca2+ signaling in the vascular endothelium

The endothelium is an interconnected network upon which hemodynamic mechanical forces act to control vascular tone and remodeling in disease. Ca2+ signaling is central to the endothelium's mechanotransduction and networked activity. However, challenges in imaging Ca2+ in large numbers of endothelial cells under conditions that preserve the intact physical configuration of pressurized arteries have limited progress in understanding how pressure-dependent mechanical forces alter networked Ca2+ signaling. We developed a miniature wide-field, gradient-index (GRIN) optical probe designed to fit inside an intact pressurized artery which permitted Ca2+ signals to be imaged with subcellular resolution in a large number (∼200) of naturally-connected endothelial cells at various pressures. Chemical (acetylcholine) activation triggered spatiotemporally-complex, propagating IP3-mediated Ca2+ waves that originated in clusters of cells and progressed from there across the endothelium. Mechanical stimulation of the artery, by increased intraluminal pressure, flattened the endothelial cells and suppressed IP3-mediated Ca2+ signals in all activated cells. By computationally modeling Ca2+ release, endothelial shape changes were shown to alter the geometry of the Ca2+ diffusive environment near IP3 receptor microdomains to limit IP3-mediated Ca2+ signals as pressure increased. Changes in cell shape produce a geometric, microdomain-regulation of IP3-mediated Ca2+ signaling to explain macroscopic pressure-dependent, endothelial-mechanosensing without the need for a conventional mechanoreceptor. The suppression of IP3-mediated Ca2+ signaling may explain the decrease in endothelial activity as pressure increases. GRIN imaging provides a convenient method that provides access to hundreds of endothelial cells in intact arteries in physiological configuration