The Bangwa Queen: Interpretations, Constructions, and Appropriations of Meaning of the Esteemed Ancestress Figure from the Cameroon Grassfields

Senior Project submitted to The Division of Social Studies of Bard College. Senior Project submitted to The Division of Languages and Literature of Bard College

Rethinking Cyberspace Operations: Widespread Electromagnetic Jamming by States Indicates Cyber Interference Is Not a Use of Force

Determining if a cyberspace operation by a State actor is an act of war (i.e., use of force under the U.N. Charter) has led to a misguided approach. In 2012, twenty legal experts that published the Tallinn Manual got it wrong. By utilizing the “effects-based approach” they attempted to equate the effects a cyber operation causes to that of a missile to determine if a use of force has occurred. While their underlying premise, that existing international law should be applied to cyber operations, was sound, the analytical approach is flawed. This paper explores how the analytical model used by the Tallinn Manual ignored relevant international law and failed to appreciate the role of State practice. First, the U.N. Charter better addresses this issue. Specifically, Article 41 of the UN Charter states the complete or partial interruption of postal, telegraphic, radio, and other means of communication is not us of armed force. This indicates cyber operations that cause interference, like distributed denial of service, are not a use of force. Second, there is considerable State practice in the area of electromagnetic jamming that States do not consider it a use of force. By ignoring the U.N. Charter and eighty years of State practice for all forms of electromagnetic interference, these experts fail to analyze cyber operations through the normal Law of Armed Conflict framework

Regulation of stimulated cyclic AMP synthesis by urocanic acid

Urocanic acid (UCA) has been shown to mediate the UVB radiation-induced immunosuppression initiated in the skin by UV-induced isomerization from the trans to the cis isomer. However, the mechanism by which cis-UCA acts is still unclear. Therefore, the present study was undertaken to determine the effect of trans- and cis-UCA on cyclic adenosine 3′,5′-monophosphate (cAMP) synthesis in human dermal fibroblasts, Golden Syrian hamster hepatocytes and in the human adenocarcinoma cell line, HT29. Neither trans- nor cis-UCA was able to stimulate cAMP synthesis directly in any of the models tested. In human dermal fibroblasts, cis-UCA, in contrast to trans-UCA, specifically inhibited cAMP synthesis induced by either prostaglandin (PG) E1 or PGE2 with a maximum inhibitory effect of 25-30% at cis-UCA concentrations greater than 1 μM and half-maximum inhibitory effect (EC50) observed at 35 nM. The effect of cis-UCA was not to stimulate phosphodiesterase and cAMP breakdown. The inhibitory effect of cis-UCA (an imidazole derivative) was not mediated through stimulation of the α2-adrenergic receptor. The inhibitory effect of cis-UCA on stimulated cAMP synthesis was a function of the cell density and was only significant when the fibroblasts were confluent or postconfluent. In contrast to the studies with human dermal fibroblasts, an inhibitory effect of cis-UCA was not observed in either isolated hamster hepatocytes or HT29 cells, in which cAMP synthesis was stimulated by glucagon and vasoactive intestinal peptide, respectively. These results point to a possible regulation of cAMP synthesis in fibroblasts as one mechanism by which cis-UCA exerts its biological effect in the skin

Regulation of Stimulated Cyclic AMP Synthesis by Urocanic Acid

Urocanic acid (UCA) has been shown to mediate the UVB radiation-induced immunosuppression initiated in the skin by UV-induced isomerization from the trans to the cis isomer. However, the mechanism by which cis-UCA acts is still unclear. Therefore, the present study was undertaken to determine the effect of trans- and cis-UCA on cyclic adenosine 3′,5′-monophosphate (cAMP) synthesis in human dermal fibroblasts, Golden Syrian hamster hepatocytes and in the human adenocarcinoma cell line, HT29. Neither trans- nor cis-UCA was able to stimulate cAMP synthesis directly in any of the models tested. In human dermal fibroblasts, cis-UCA, in contrast to trans-UCA, specifically inhibited cAMP synthesis induced by either prostaglandin (PG) E1 or PGE2 with a maximum inhibitory effect of 25-30% at cis-UCA concentrations greater than 1 μM and half-maximum inhibitory effect (EC50) observed at 35 nM. The effect of cis-UCA was not to stimulate phosphodiesterase and cAMP breakdown. The inhibitory effect of cis-UCA (an imidazole derivative) was not mediated through stimulation of the α2-adrenergic receptor. The inhibitory effect of cis-UCA on stimulated cAMP synthesis was a function of the cell density and was only significant when the fibroblasts were confluent or postconfluent. In contrast to the studies with human dermal fibroblasts, an inhibitory effect of cis-UCA was not observed in either isolated hamster hepatocytes or HT29 cells, in which cAMP synthesis was stimulated by glucagon and vasoactive intestinal peptide, respectively. These results point to a possible regulation of cAMP synthesis in fibroblasts as one mechanism by which cis-UCA exerts its biological effect in the skin