Inferring State Machine from the Protocol Implementation via Large Language Model

State machines play a pivotal role in augmenting the efficacy of protocol analyzing to unveil more vulnerabilities. However, the task of inferring state machines from network protocol implementations presents significant challenges. Traditional methods based on dynamic analysis often overlook crucial state transitions due to limited coverage, while static analysis faces difficulties with complex code structures and behaviors. To address these limitations, we propose an innovative state machine inference approach powered by Large Language Models (LLMs). Utilizing text-embedding technology, this method allows LLMs to dissect and analyze the intricacies of protocol implementation code. Through targeted prompt engineering, we systematically identify and infer the underlying state machines. Our evaluation across six protocol implementations demonstrates the method's high efficacy, achieving an accuracy rate exceeding 90% and successfully delineating differences on state machines among various implementations of the same protocol. Importantly, integrating this approach with protocol fuzzing has notably enhanced AFLNet's code coverage by 10% over RFCNLP, showcasing the considerable potential of LLMs in advancing network protocol security analysis. Our proposed method not only marks a significant step forward in accurate state machine inference but also opens new avenues for improving the security and reliability of protocol implementations

Purine metabolites regulate leukemic cell sensitivity toward cytarabine

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Abstract 102: Apolipoprotein E Receptor 2 In Endothelium Affords Protection From Both Atherosclerosis And Insulin Resistance

Introduction: Apolipoprotein E Receptor 2 (ApoER2) is an LDL receptor family member that mediates the actions of apolipoprotein E (apoE) and other ligands. The LRP8 gene that encodes ApoER2 is a major gene locus for premature atherosclerosis and myocardial infarction. Studies were designed to determine how ApoER2 in endothelial cells impacts cardiovascular and metabolic health. Hypothesis: Based on prior cell culture studies, the hypothesis was that endothelial ApoER2 is atheroprotective. How endothelial ApoER2 impacts adiposity or glucose homeostasis is more difficult to predict. Methods: In vivo studies were done in control ApoER2 floxed mice (ApoER2 fl/fl ) and mice deficient in ApoER2 in endothelial cells (ApoER2 ΔEC ). Studies of endothelial cell insulin uptake and transcytosis were performed in human aortic and skeletal muscle endothelial cells (HAEC and HSMEC). Results: Atherosclerotic lesion severity on LDLR -/- background was increased in ApoER2 ΔEC mice compared to ApoER2 fl/fl , and this was not related to differences in circulating lipids. Intravital microscopy revealed that leukocyte-endothelial cell adhesion is increased in ApoER2 ΔEC , and vascular TNFα and IL-1β expression was exaggerated. There was no impact of endothelial ApoER2 silencing on adiposity. However, standard chow-fed ApoER2 ΔEC mice displayed marked glucose intolerance and insulin resistance. Both pancreatic insulin secretion and hepatic insulin sensitivity were normal. Alternatively, in ApoER2 ΔEC mice skeletal muscle glucose disposal was decreased by 41%, and this was due to a 55% fall in insulin delivery to muscle. Using human apoE3 ex vivo, apoE stimulated a 279% increase in insulin uptake in HAEC, and the finding was confirmed in HSMEC. Insulin transcytosis rose 209% with apoE, and apoE enhancement of insulin transport was fully ApoER2-dependent. Conclusions: Endothelial ApoER2 affords atheroprotection by decreasing leukocyte-endothelial cell adhesion and inflammatory gene expression in the vessel wall. Endothelial ApoER2 also has antidiabetic action, and this is due to the promotion of endothelial insulin transport to skeletal muscle. Targeting of the related mechanisms may provide protection from both cardiovascular and metabolic disease. </jats:p

A Study on the Impact of Personality Traits on Behavior of Game Players Toward Spending on In-game Microtransactions

This study examined how personality influences consumer behavior of electronic game players. Participants ( N  = 479) were respectively placed into four groups called microtransaction group (if they had made any in-game microtransactions, n  = 192), free-game group (if they had only played entirely free games, n  = 124), pay-to-play group (if they had only played games that needed just one-time payment upon purchase, n  = 19), and non-microtransaction group (if they had not made any in-game microtransactions although the games provided such services, n  = 144). The results indicated that the microtransaction group had higher levels of extraversion and openness than the non-microtransaction group. Additionally, the microtransaction group showed higher levels of dispositional greed and narcissism than all other groups. However, there were no significant differences in agreeableness, conscientiousness, neuroticism, or self-control among the groups. The study also found that the possibility of making in-game microtransactions decreased with age. These findings have important implications for game developers and marketers, who may use this information to tailor their products and marketing strategies to specific personality types and age groups

Abstract 624: Endothelial Scavenger Receptor Class B, Type I (SR-BI) Mediates LDL Uptake by the Artery Wall and Promotes Atherosclerosis in Hypercholesterolemic Mice

In endothelial cells, high density lipoprotein cholesterol (HDL) binding to scavenger receptor class B, type I (SR-BI) promotes the production of the antiatherogenic signaling molecule nitric oxide (NO) and also endothelial repair. To study how SR-BI in endothelium impacts atherosclerosis, we bred newly-created floxed SR-BI mice, vascular endothelial cadherin promoter-driven Cre recombinase transgenic (VECad-Cre), and apoE -/- mice to generate apoE -/- with normal endothelial SR-BI expression (SR-BI ECIN ;apoE -/- ) or selective deletion of SR-BI from endothelium (SR-BI ECOUT ;apoE -/- ). At weaning all mice were placed on an atherogenic diet (20% fat, 1.25% cholesterol), and plasma lipid profiles and atherosclerosis were evaluated 8 weeks later. Endothelial deletion of SR-BI did not alter the plasma lipid profile. Surprisingly, male SR-BI ECOUT ;apoE -/- mice displayed 63% less atherosclerosis in the en face aorta than male SR-BI ECIN ;apoE -/- mice, aortic root lesions were comparably affected, and similar findings were obtained in females. Recognizing that SR-BI binds both HDL and low density lipoprotein cholesterol (LDL), to then discern how endothelial SR-BI promotes atherosclerosis we determined using Di-I-labeled oxidized LDL (oxLDL) if SR-BI influences oxLDL uptake by endothelial cells. Such uptake is the first step in the endothelial transcytosis that delivers LDL to the artery wall to initiate atherogenesis. OxLDL uptake by primary human aortic endothelial cells was blunted by 87% by SR-BI blocking antibody, and it was also decreased by SR-BI deletion via siRNA, and by the chemical inhibitor of SR-BI BLT-1. Furthermore, SR-BI blocking antibody and BLT-1 caused marked declines in endothelial oxLDL transcytosis. Moreover, 4 hours following IV administration, oxLDL uptake in aorta was decreased by 84% in SR-BI ECOUT ;apoE -/- versus SR-BI ECIN ;apoE -/- mice. These collective findings indicate that endothelial SR-BI plays an important role in atherogenesis, and that it likely does so by mediating LDL uptake into the artery wall. They further suggest that there are mechanisms that govern LDL transport across endothelium that may be targeted to provide novel means to combat atherosclerosis. </jats:p