Threshold Encrypted Mempools: Limitations and Considerations

Encrypted mempools are a class of solutions aimed at preventing or reducing negative externalities of MEV extraction using cryptographic privacy. Mempool encryption aims to hide information related to pending transactions until a block including the transactions is committed, targeting the prevention of frontrunning and similar behaviour. Among the various methods of encryption, threshold schemes are particularly interesting for the design of MEV mitigation mechanisms, as their distributed nature and minimal hardware requirements harmonize with a broader goal of decentralization. This work looks beyond the formal and technical cryptographic aspects of threshold encryption schemes to focus on the market and incentive implications of implementing encrypted mempools as MEV mitigation techniques. In particular, this paper argues that the deployment of such protocols without proper consideration and understanding of market impact invites several undesired outcomes, with the ultimate goal of stimulating further analysis of this class of solutions outside of pure cryptograhic considerations. Included in the paper is an overview of a series of problems, various candidate solutions in the form of mempool encryption techniques with a focus on threshold encryption, potential drawbacks to these solutions, and Osmosis as a case study. The paper targets a broad audience and remains agnostic to blockchain design where possible while drawing from mostly financial examples

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Activation of apoptotic pathways in experimental acute afterload-induced right ventricular failure

Objective: The pathobiology of persistent right ventricular failure observed after an acute increase in right ventricular afterload remains incompletely understood. We hypothesized that persistent right ventricular dysfunction might be related to activation of apoptotic pathways. Design: Prospective, randomized, controlled animal study. Setting: University research laboratory. Subjects: Mongrel dogs. Interventions: Fourteen anesthetized dogs were randomized to a transient 90-min pulmonary artery constriction operation to induce persistent right ventricular failure or to a sham operation followed 30 mins later by hemodynamic measurements and sampling of cardiac tissue. Measurements and main results: We evaluated effective arterial elastance to estimate right ventricular afterload and end-systolic elastance to estimate right ventricular contractility. Transient increase in pulmonary artery pressure persistently increased effective arterial elastance from 0.75 ± 0.08 to 1.37 ± 0.18 mm Hg/mL and decreased end-systolic elastance from 1.06 ± 0.09 to 0.49 ± 0.09 mm Hg/mL, end-systolic elastance/effective arterial elastance from 1.44 ± 0.06 to 0.34 ± 0.03, and cardiac output from 3.78 ± 0.16 to 1.46 ± 0.10 L/min, indicating right ventricular failure. At the pathobiologic level, we assessed apoptosis by real-time quantitative polymerase chain reaction, Western blotting, enzyme-linked immunosorbent assay, and immunohistochemistry. As compared with the sham-operated group, and with the left ventricle in animals with persistent right ventricular failure, there were decreased right ventricular and septal expressions of Bcl-2 with no changes in expressions of Bax, resulting in an increased Bax/Bcl-2 ratio. Right ventricular and septal Bcl-XL, and right ventricular Bcl-w gene expressions were decreased as compared with the sham-operated group, whereas Bak gene expression did not change. There were activations of right ventricular caspases-8 and-9 and of right ventricular and septal caspase-3. Diffuse right ventricular and septal apoptosis was confirmed by terminal deoxynucleotidyl transferase dUTP nick-end labeling staining. There were also increased right ventricular and septal protein expressions of tumor necrosis factor-alpha. Conclusions: Acute afterload-induced persistent right ventricular failure appears to be related to an early activation of apoptotic pathways and to a local overexpression of tumor necrosis factor-alpha, a proinflammatory cytokine. Copyright © 2010 by the Society of Critical Care Medicine and Lippincott Williams & Wilkins.SCOPUS: ar.jinfo:eu-repo/semantics/publishe

Synthesis and Crystallographic Characterization of a Maleimide Derivative of Tryptamine

While mechanosynthesis of the target compound, 1-[2-(1H-indol-3-yl)-ethyl]-pyrrole-2,5-dione, C14 H12 N2 O2, did not yield the desired product, it instead resulted in an open intermediate. On the other hand, synthesis starting from the activated maleic anhydride yielded the final maleimide compound. The outcome of the mechanosynthesis has been evaluated by powder X-ray diffraction, and structures of both the final product and open intermediate have been confirmed using single-crystal crystallography

Endogenous angiotensin II in the regulation of hypoxic pulmonary vasoconstriction in anaesthetized dogs

INTRODUCTION: The role played by several vasoactive mediators that are synthesized and released by the pulmonary vascular endothelium in the regulation of hypoxic pulmonary vasoconstriction (HPV) remains unclear. As a potent vasoconstrictor, angiotensin II could be involved. We tested the hypothesis that angiotensin-converting enzyme inhibition by enalaprilat and type 1 angiotensin II receptor blockade by candesartan would inhibit HPV. METHODS: HPV was evaluated in anaesthetized dogs, with an intact pulmonary circulation, by examining the increase in the Ppa–Ppao gradient (mean pulmonary artery pressure minus occluded pulmonary artery pressure) that occurred in response to hypoxia (inspiratory oxygen fraction of 0.1) at constant pulmonary blood flow. Plasma renin activity and angiotensin II immunoreactivity were measured to determine whether activation or inhibition of the renin–angiotensin system was present. RESULTS: Administration of enalaprilat and candesartan did not affect the Ppa–Ppao gradient at baseline or during hypoxia. Plasma renin activity and angiotensin II immunoreactivity increased during hypoxia, and subsequent measurements were consistent with effective angiotensin-converting enzyme inhibition after administration of enalaprilat, and with angiotensin receptor blockade after administration of candesartan. CONCLUSION: These results suggest that, although the renin–angiotensin system was activated in hypoxia, angiotensin II is not normally involved in mediating acute HPV