Enlightenment, state, and sovereignty: Kant’s political philosophy

In Kant scholarship, there has long been a debate about the connection between his political and ethical thought. In his works concerned with political theory, such as the Metaphysics of Morals, Perpetual Peace, or An Answer to the Question: What is Enlightenment?, he concerns himself with coercively enforceable principles by which a society can be organised. In his works on ethics, such as The Groundwork to a Metaphysics of Morals, or The Critique of Practical Reason, he is concerned with principles of morality, which require free and unconstrained action. Prima facie, the realms of politics and ethics in Kant’s thought thus appear to be incompatible. This thesis will close the gap between Kant’s ethics and politics through an examination of his anthropological works. The thesis will argue that Kant’s philosophical understanding of human nature, i.e. his “philosophical” anthropology, necessitates a connection between his ethics and politics. The project begins with a reading of Kant’s anthropological texts to show that his concern with human nature was directly related to politics and to ethics. This will allow the thesis to then discuss the way in which human nature necessitates politics as a condition of possibility for ethical deliberation to occur. Finally, having shown the necessity of politics for ethics, and thus their necessary connection, the thesis will present an overview of Kant’s political philosophy in light of this connection to show precisely the way in which politics supports rational ethical deliberation. These considerations will allow for the debate about the connection between Kant’s politics and ethics to be settled, and provide us with an understanding of the depth of Kant’s concern with human nature

Apamin inhibits NO-induced relaxation of the spontaneous contractile activity of the myometrium from non-pregnant women

<p>Abstract</p> <p>There is now considerable evidence for the involvement of K⁺channels in nitric oxide (NO) induced relaxation of smooth muscles including the myometrium. In order to assess whether apamin-sensitive K⁺channels play a role in NO – induced relaxation of the human uterus, we have studied the effect of specific blockers of these channels on the relaxation of myometrium from non-pregnant women. In vitro isometric contractions were recorded in uterine tissues from non-pregnant premenopausal women who had undergone hysterectomy. Apamin (10 nM) and scyllatoxin (10 nM) did not alter spontaneous myometrial contractions. However, 15-min pretreatment of the myometrium strips with apamin completely inhibited relaxation caused by diethylamine-nitric oxide (DEA/NO). The pretreatment with scyllatoxin significantly reduced (about 2.6 times) maximum relaxation of the strips induced by DEA/NO (p < 0.05). These results strongly suggest that, beside Ca²⁺and voltage dependent charybdotoxin-sensitive (CTX-sensitive) K⁺channels, apamin-sensitive K⁺channels are also present in the human non-pregnant myometrium. These channels offer an additional target in the development of new tocolytic agents.</p

Lobe-specific increases in malondialdehyde DNA adduct formation in the livers of mice following infection with Helicobacter hepaticus

Helicobacter hepaticus infection is associated with chronic hepatitis and the development of liver tumours in mice. The underlying mechanism of this liver carcinogenesis is not clear but the oxidative stress associated with H. hepaticus infection may result in induction of lipid peroxidation and the generation of malondialdehyde. Malondialdehyde can react with deoxyguanosine in DNA resulting in the formation of the cyclic pyrimidopurinone N-1,N-2 malondialdehyde-deoxyguanosine (M(1)dG) adduct. This adduct has the potential to cause mutations that may ultimately lead to liver carcinogenesis. The objective of this study was to determine the control and infection-related levels of M(1)dG in the liver DNA of mice over time, using an immunoslot-blot procedure. The level of M(1)dG in control A/J mouse livers at 3, 6, 9 and 12 months averaged 37.5, 36.6, 24.8 and 30.1 adducts per 10(8) nucleotides, respectively. Higher levels of M(1)dG were detected in the liver DNA of H. hepaticus infected A/JCr mice, with levels averaging 40.7, 47.0, 42.5 and 52.5 adducts per 10(8) nucleotides at 3, 6, 9 and 12 months, respectively. There was a significant age dependent increase in the level of M(1)dG in the caudate and median lobes of the A/JCr mice relative to control mice. A lobe specific distribution of the M(1)dG adduct in both infected and control mice was noted, with the left lobe showing the lowest level of the adduct compared with the right and median lobes at all time points. In a separate series of mice experimentally infected with H. hepaticus, levels of 8-hydroxy-deoxyguanosine were significantly greater in the median compared with the left lobe at 12 weeks after treatment. In conclusion, these results suggest that M(1)dG occurs as a result of oxidative stress associated with H. hepaticus infection of mice, and may contribute to liver carcinogenesis in this model